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Study Guide
Study Guide for
for

Pathophysiology Concepts
of Altered Health States
Eighth Edition
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Managing Editor: Annette Ferran

Senior Production Editor: Debra Schiff
Director of Nursing Production: Helen Ewan
Senior Managing Editor/Production: Erika Kors
Manufacturing Coordinator: Karin Duffield
Compositor: Aptara

8th Edition

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Copyright © 2005, 2002 by Lippincott Williams & Wilkins. Copyright © 1998 by Lippincott-
Raven Publishers. Copyright © 1994 by J. B. Lippincott Company. All rights reserved. This book
is protected by copyright. No part of this book may be reproduced or transmitted in any form or
by any means, including as photocopies or scanned-in or other electronic copies, or utilized by
any information storage and retrieval system without written permission from the copyright
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in this book prepared by individuals as part of their official duties as U.S. government employees
are not covered by the above-mentioned copyright. To request permission, please contact
Lippincott Williams & Wilkins at 530 Walnut Street, Philadelphia PA 19106, via email at
permissions@lww.com or via website at lww.com (products and services).

9 8 7 6 5 4 3 2 1

Printed in the United States of America

ISBN: 978-0-7817-6913-6

Care has been taken to confirm the accuracy of the information presented and to describe
generally accepted practices. However, the authors, editors, and publisher are not responsible for
errors or omissions or for any consequences from application of the information in this book
and make no warranty, expressed or implied, with respect to the currency, completeness, or ac-
curacy of the contents of the publication. Application of this information in a particular situa-
tion remains the professional responsibility of the practitioner; the clinical treatments described
and recommended may not be considered absolute and universal recommendations.
The authors, editors, and publisher have exerted every effort to ensure that drug selection
and dosage set forth in this text are in accordance with the current recommendations and prac-
tice at the time of publication. However, in view of ongoing research, changes in government
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the reader is urged to check the package insert for each drug for any change in indications and
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mended agent is a new or infrequently employed drug.
Some drugs and medical devices presented in this publication have Food and Drug Adminis-
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Preface

This Study Guide was written by Brian Kipp, demonstrate your comprehension of the infor-
PhD, and Jo Anne Kirk, MSN, RN, to accompany mation.
the eighth edition of Pathophysiology: Concepts of
Altered Health States by Carol Mattson Porth and
Glenn Matfin. The Study Guide is designed to APPLYING YOUR KNOWLEDGE
help you practice and retain the knowledge
The second section of each Study Guide chapter
you’ve gained from the textbook, and it is struc-
consists of case study–based exercises that ask you
tured to integrate that knowledge and give you a
to begin to apply the knowledge you’ve gained
basis for applying it in your practice. The follow-
from the textbook chapter and reinforced in the
ing types of exercises are provided in each chap-
first section of the Study Guide chapter. A case
ter of the Study Guide.
study scenario based on the chapter’s content is
presented, and then you are asked to answer some
ASSESSING YOUR questions, in writing, related to the case study.
UNDERSTANDING The questions could cover lab values, next steps
in treatment, anticipated diagnoses, and the like.
The first section of each Study Guide chapter
concentrates on the basic information of the
textbook chapter and helps you to remember key PRACTICING FOR NCLEX
concepts, vocabulary, and principles.
The third and final section of the Study Chapters
• Fill in the Blanks helps you practice NCLEX-style questions while
Fill-in-the-blank exercises test important chapter further reinforcing the knowledge you have been
information, encouraging you to recall key gaining and testing for yourself through the text-
points. book chapter and the first two sections of the
study guide chapter. In keeping with the NCLEX,
• Labeling the questions presented are multiple-choice and
Labeling exercises are used where you need to re- scenario-based, asking you to reflect, consider,
member certain visual representations of the con- and apply what you know and to choose the best
cepts presented in the textbook. answer out of those offered.
• Matching
Matching questions test your knowledge of the ANSWER KEYS
definition of key terms.
The answers for all of the exercises and questions
• Sequencing in the Study Guide are provided at the back of
Sequencing exercises ask you to remember partic- the book, so you can assess your own learning as
ular sequences or orders, for instance of normal you complete each chapter.
or abnormal physiologic processes. We hope you will find this Study Guide to be
helpful and enjoyable, and we wish you every
• Short Answers
success in your studies and future profession.
Short-answer questions cover facts, concepts,
procedures, and principles of the chapter. These The Publishers
questions ask you to recall information as well as

iii
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Contents

CHAPTER 1 CHAPTER 9
Concepts of Health and Disease 1 Stress and Adaptation 44

CHAPTER 2 CHAPTER 10
Concepts of Altered Health in Alterations in Temperature
Children 5 Regulation 49

CHAPTER 3 CHAPTER 11
Concepts of Altered Health in Older Activity Tolerance and Fatigue 55
Adults 10
CHAPTER 12
CHAPTER 4 Blood Cells and the Hematopoietic
Cell and Tissue Characteristics 15 System 60

CHAPTER 5 CHAPTER 13
Cellular Adaptation, Injury, and Death 20 Disorders of Hemostasis 64

CHAPTER 6 CHAPTER 14
Genetic Control of Cell Function Disorders of Red Blood Cells 69
and Inheritance 26
CHAPTER 15
CHAPTER 7 Disorders of White Blood Cells and
Genetic and Congenital Disorders 31 Lymphoid Tissues 75

CHAPTER 8 CHAPTER 16
Neoplasia 37 Mechanisms of Infectious Disease 80

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vi CONTENTS

CHAPTER 17 CHAPTER 27
Innate and Adaptive Immunity 85 Structure and Function of the
Respiratory System 145
CHAPTER 18
CHAPTER 28
Inflammation, Tissue Repair, and
Wound Healing 91 Respiratory Tract Infections, Neoplasms,
and Childhood Disorders 151
CHAPTER 19
CHAPTER 29
Disorders of the Immune
Response 97 Disorders of Ventilation and Gas
Exchange 157
CHAPTER 20
CHAPTER 30
Acquired Immunodeficiency
Syndrome 103 Structure and Function of the
Kidney 164
CHAPTER 21
CHAPTER 31
Structure and Function of the
Cardiovascular System 108 Disorders of the Fluid and Electrolyte
Balance 169
CHAPTER 22
CHAPTER 32
Disorders of Blood Flow in the
Systemic Circulation 114 Disorders of Acid-Base Balance 175

CHAPTER 23 CHAPTER 33
Disorders of Blood Pressure Disorders of Renal Function 180
Regulation 120
CHAPTER 34
CHAPTER 24 Acute Renal Failure and Chronic
Disorders of Cardiac Function 126 Kidney Disease 186

CHAPTER 25 CHAPTER 35
Disorders of Cardiac Conduction Disorders of the Bladder and Lower
and Rhythm 134 Urinary Tract 190

CHAPTER 26 CHAPTER 36
Heart Failure and Circulatory Structure and Function of the
Shock 139 Gastrointestinal System 195
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CONTENTS vii

CHAPTER 37 CHAPTER 46
Disorders of Gastrointestinal Disorders of the Female Reproductive
Function 200 System 249

CHAPTER 38 CHAPTER 47
Disorders of Hepatobiliary and Exocrine Sexually Transmitted Infections 255
Pancreas Function 207
CHAPTER 48
CHAPTER 39
Organization and Control of Neural
Alterations in Nutritional Function 259
Status 214
CHAPTER 49
CHAPTER 40
Somatosensory Function, Pain,
Mechanisms of Endocrine and Headache 266
Control 219
CHAPTER 50
CHAPTER 41
Disorders of Motor Function 274
Disorders of Endocrine Control of
Growth and Metabolism 223 CHAPTER 51
Disorders of Brain Function 281
CHAPTER 42
Diabetes Mellitus and the Metabolic CHAPTER 52
Syndrome 229
Sleep and Sleep Disorders 288
CHAPTER 43
CHAPTER 53
Structure and Function of the Male
Genitourinary System 235 Disorders of Thought, Mood, and
Memory 293
CHAPTER 44
CHAPTER 54
Disorders of the Male Genitourinary
System 239 Disorders of Visual Function 300

CHAPTER 45 CHAPTER 55
Structure and Function of the Female Disorders of Hearing and Vestibular
Reproductive System 243 Function 308
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viii CONTENTS

CHAPTER 56 CHAPTER 59
Structure and Function of the Disorders of the Musculoskeletal
Musculoskeletal System 313 Function: Rheumatic Disorders 328

CHAPTER 57 CHAPTER 60
Disorders of the Musculoskeletal Function: Structure and Function of the Skin 333
Trauma, Infection, and Neoplasms 318
CHAPTER 61
CHAPTER 58
Disorders of Skin Integrity and
Disorders of Musculoskeletal Function: Function 338
Developmental and Metabolic
Disorders 324
Answer Key 345
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CHAPTER
Concepts of Health
and Disease

SECTION I: LEARNING SECTION II: ASSESSING YOUR

OBJECTIVES UNDERSTANDING
1. State the World Health Organization defini- Activity A Fill in the blanks.
tion of health
1. Pathophysiology is the study of
2. State a definition of pathophysiology and its manifestations via changes in cells,
tissues, and organs.
3. Characterize the disease process in terms of
etiology, pathogenesis, morphology, clinical 2. The World Health Organization defines the
manifestations, and prognosis state of as a state of complete
physical, mental, and social well-being and not
4. Explain the meaning of reliability, validity,
merely the absence of disease and infirmity.
sensitivity, specificity, and predictive value as
it relates to observations and tests used in the 3. The term can be defined as an
diagnosis of disease interruption, cessation, or disorder of a body
system or organ structure.
5. Define the term epidemiology
4. The multiple factors that predispose a patient
6. Compare the meaning of the terms incidence
to a particular disease are known as
and prevalence as they relate to measures of
.
disease frequency
5. are present at birth but may not
7. Compare the sources of information and
be relevant until later stages of development.
limitations of mortality and morbidity
statistics 6. Defects or damage that occurs after birth are
termed defects.
8. Characterize the natural history of a disease
7. The description as to the nature or cause of a
9. Differentiate primary, secondary, and tertiary
health problem that is arrived at following
levels of prevention
examination is the .
10. Propose ways in which practice guidelines
8. is not clinically apparent and is
can be used to improve health care
not destined to become clinically apparent.
is manifested by signs and
symptoms.

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2 UNIT 1 CONCEPTS OF HEALTH AND DISEASE

9. is the study of disease occur- Activity D Briefly answer the following.

rence in a population.
1. Define the term pathophysiology. Compare and
10. is a measure of the existing dis- contrast that definition with definitions for
ease in a population, whereas is physiology and pathology.
reflective of the development of new cases.

Activity B Match the key terms in Column A

with their definitions in Column B.
Column A Column B
2. Explain what is meant by the term clinical
1. Etiology a. Predicted outcome course. In your answer, address the differences
of a disease process between an acute disorder and chronic disease.
2. Mortality
b. Causes of disease
3. Pathogenesis
c. Fundamental struc-
4. Morphology ture or form of cells
or tissues
5. Cohort
d. Signs and symp- 3. Differentiate between a congenital condition
6. Morbidity toms of a disease and an acquired defect.
7. Clinical e. Group of persons
manifestations that shares certain
characteristics
8. Prognosis
f. Sequence of cellular
9. Evidence-based and tissue events
practice 4. What is the difference between syndromes and
g. Characteristics of
sequelae?
10. Prevention death-producing ef-
fects of a disease
h. Effects of disease on
patient’s life
i. Using current and
best information in 5. What is the importance of risk factors and how
treatment they are determined for a given population?
j. Halting disease
progress or develop-
ment

Activity C
1. Diagnosing and treating a disease involves a
complex set of steps that a clinician must per- SECTION III: APPLYING YOUR
form in order to provide a patient with the
best care possible. Make a flowchart of the
KNOWLEDGE
evaluation process of the health status of an
Activity E Consider the following scenario and
afflicted patient as a clinician would.
answer the questions.
A nurse from a local hospital has been asked to
present an educational event for a community
group. They have asked her to speak on commu-
nicable diseases.
1. When presenting to this group, the nurse
should include information on what aspects of
the topic?

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CHAPTER 1 CONCEPTS OF HEALTH AND DISEASE 3

2. One member of the group asks, “The nurse a problem; written directives for care; or a
who takes care of my mother said that she uses combination thereof.
‘evidence-based guidelines’ when she cares for d. They take the place of both written orders
her patients. What does that mean?” How by the doctor and the nursing care plan.
would the nurse answer this question?
5. There are three fundamental types of preven-
tion used in health care: primary, secondary,
and tertiary. Which of the following state-
SECTION IV: PRACTICING ments accurately describes secondary preven-
FOR NCLEX tion?
a. Secondary prevention detects disease early,
Activity F Answer the following questions. and most is done in clinical settings.
1. A disease agent can affect more than one b. Secondary prevention goes beyond treating
organ of the body, and more than one disease the problem with which the person pre-
agent can affect the same organ of the body. sents.
Therefore, the majority of diseases c. Secondary prevention is often accom-
a. are multifactorial in origin. plished outside the health care system at
b. are complicated and hard to diagnose. the community level.
c. are simple and easy to diagnose. d. Secondary prevention takes place within
health care systems and involves the ser-
d. have a single cause.
vices of a number of different types of
2. Which science is called on to study the risk health care professionals.
factors in multifactorial diseases?
6. Why are some diseases termed syndromes?
a. Scientology
a. They have complications.
b. Morphology
b. They leave sequelae such as lesions as
c. Histology residual effects.
d. Epidemiology c. They are a compilation of signs and symp-
3. What do morbidity and mortality statistics toms characteristic of a specific disease
refer to? state.
a. Long-term consequences and recovery d. They are a group of disease states that has
rates of a disease the same etiology.
b. Cause of death and impact on the family 7. Which of the following is the term given to
because of a disease the progression and projected outcome of a
c. Functional effects and death-producing disease without medical intervention?
characteristics of a disease a. Prognosis
d. Effects a disease has on a person’s life and b. Morbidity
treatment c. Natural history
4. Which of the following statements accurately d. Risk factors
describes clinical practice guidelines, or evi-
8. Pathogenesis is the term used to describe the se-
dence-based practice guidelines? Mark all that
quence of cellular and tissue events that occurs
apply.
from the time of first contact with an etiologic
a. They are intended to inform practitioners agent until the disease becomes evident. What
and clients in making decisions about is another way of defining pathogenesis?
health care for specific clinical circum-
a. What sets the disease process in motion
stances.
b. Multiple factors that predispose to a partic-
b. They should review various outcomes;
ular disease
weigh various outcomes, both positive and
negative; and make recommendations. c. The causes of disease
c. They can take the form of algorithms, d. How the disease process evolves
which are step-by-step methods for solving

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4 UNIT 1 CONCEPTS OF HEALTH AND DISEASE

9. Signs and symptoms describe the structural and 10. Diagnostic tests are used to gain information
functional changes that accompany a disease. about the patient that is pertinent to the pre-
Symptoms are what the patient describes to senting signs and symptoms. Diagnostic tests
the caregiver. Signs are what the caregiver ob- are judged for their validity, reliability, sensi-
serves. Which of the following would not be tivity, specificity, and predictive value. In the
considered signs and symptoms? field of clinical laboratory measurements,
a. Headache and dizziness standardization is aimed at increasing the
trueness and reliability of measured values.
b. Elevated white cell count and fever of
Standardization relies on which of the follow-
101.5F
ing? Mark all that apply.
c. Pain and difficulty swallowing
a. In vitro laboratory equipment
d. Black eye and green thumb
b. Reference measurement procedures
c. Written standards
d. U.S. Food and Drug Administration
approval

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CHAPTER
Concepts of Altered
Health in Children

SECTION I: LEARNING 13. Describe the growth and development of

early childhood
OBJECTIVES
14. Discuss the common health problems of early
1. Characterize the use of percentiles to describe childhood
growth and development during infancy and
15. Define middle to late childhood
childhood
16. Characterize the growth and development
2. Describe the major events that occur during
that occurs during middle to late childhood
prenatal development from fertilization to birth
17. Discuss the common health problems of mid-
3. Define the terms low birth weight, small for ges-
dle to late childhood
tational age, and large for gestational age
18. Define what is meant by the period known as
4. Identify reasons for abnormal intrauterine
adolescence
growth
19. Characterize the physical and psychosocial
5. Describe assessment methods for determina-
changes that occur during adolescence
tion of gestational age
20. Cite the developmental tasks that adolescents
6. Describe the use of the Apgar score in evaluat-
need to fulfill
ing infant well-being at birth
21. Describe common concerns of parents regard-
7. Describe the causes and manifestations of
ing their adolescent child
neonatal hypoglycemia
22. Discuss how the changes that occur during
8. List three injuries that can occur during the
adolescence can influence the health care
birth process
needs of the adolescent
9. Describe physical growth and organ develop-
ment during the first year of life
SECTION II: ASSESSING YOUR
10. Explain how the common health care needs
of the premature infant differ from the health
UNDERSTANDING
care needs of the term newborn or infant
Activity A Fill in the blanks.
11. Differentiate between organic and nonor-
1. The phrase
ganic failure to thrive syndrome
describes a process whereby a fertilized ovum
12. Define early childhood becomes an adult person.

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6 UNIT 1 CONCEPTS OF HEALTH AND DISEASE

2. The development of an embryo to a fetus pro- Activity B Consider the following figure and
gresses through three distinct phases. In the answer the questions.
first phase, occurs as a process of
increasing cell numbers and elaboration of Grams
cell material. In the second stage, 5000
4750
cells interact, move, and form
4500
organs and tissues. During the third stage, the tational age
4250 r ge s
tissues into functional organs e fo 90th%
4000 rg
La
capable of adult function. 3750
3500
3. The is a system of evaluating an 3250 nal age
estatio
infant’s well-being at birth. 3000 or g
ef 10th%
2750 at

ri
4. Cranial injuries, skull fractures, and broken

op
2500

pr
clavicles are all . 2250 Ap stational
age
ge
2000 for
5. The leading complication in newborn infants all
1750 m

S
is . It is caused by a lack of sur- 1500
factant production. 1250
1000
6. is defined as paroxysmal ab-
750
dominal pain manifested by loud crying, re- 500
traction of legs, and extreme irritability.
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
7. During middle to late childhood, children Weeks of gestation
typically gain approximately
Preterm Term Postterm
and grow an average of per year.
8. In adolescence, the risk of infection
due to the competency level of 1. Using this chart, determine whether a child
the immune system. born at 37 weeks and weighing 1,750 g is large,
appropriate, or small for gestational age.
9. Skin infections are much more common in
adolescence due to increased frequency of 2. Using this chart, determine whether a child
. born at 40 weeks and weighing 2,700 g is large,
appropriate, or small for gestational age.
10. The causes of childhood are un-
doubtedly multifactorial, but ultimately re- Activity C Match the key terms in Column A
flect an imbalance between the amount of with their definitions in Column B.
calories the child consumes in food and bev-
erages and the calories that the child uses. Column A Column B
1. Low birth a. Use of six external
weight physical signs and
six neuromuscular
2. Development
signs to evaluate
3. Physical the development
growth of an infant at
term
4. Morpho-
genesis

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CHAPTER 2 CONCEPTS OF ALTERED HEALTH IN CHILDREN 7

5. Neurulation b. Unossified mem- 3. Respiratory distress syndrome is the result of

branous tissue in low or absent surfactant production. What is
6. Ballard
the fetal skull the function of surfactant in the respiratory
method
c. Changes in the system?
7. Fontanels body as a whole
8. Infantile d. Fetal undergrowth
hypoglycemia or below the 10th
percentile
9. Jaundice
e. Blood sugar level 4. Sudden infant death syndrome (SIDS) affects
10. Small for below 40 to 45 children younger than 1 year. The actual
gestational mg/dL cause is still unknown, but risk factors have
age
f. Formation of the been postulated. List the risk factors for
neural plate, SIDS.
neural folds, and
their closure
g. Sign of excessive
circulating levels
of unconjugated,
lipid-soluble 5. Failure to thrive (FTT) refers to inadequate
bilirubin growth due to inability to obtain or use essen-
tial nutrients. Nonorganic causes include ne-
h. Weight of 2500 g
glect and abuse. Explain what is meant by an
or less at birth
organic cause of FTT.
i. Changes in body
function and psy-
chosocial behavior
j. Development of
form
6. Physiological jaundice is normal for the neonate.
When does it become a concern, and why?
Activity D Briefly answer the following.

1. Prior to birth, fetuses, and following birth, in-

fants, are checked for growth and development.
Describe the progression of testing methods
and the differing interpretations of data.

SECTION III: APPLYING YOUR

KNOWLEDGE
2. The clavicle is the most frequently fractured bone
in the birth process. Explain why this is true Activity E Consider the following scenario and
and what would make it more likely to occur. answer the questions.
A 6-year-old girl is brought to the clinic for a
well-child examination. While doing your physi-
cal assessment, you notice dental caries on and
between the teeth.

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8 UNIT 1 CONCEPTS OF HEALTH AND DISEASE

1. What education would be given to this child c. second week after conception to the 12th
and her family pertinent to her developmental week of pregnancy.
stage? d. second week after fertilization to the 8th
week after fertilization.
3. A pregnancy lasts 10 lunar months, or 38
weeks from the date of fertilization. When is
an infant considered to be “term”?
2. What common health concerns should you be a. When it is born between the beginning of
aware of when examining a child of this age? the 38th week and the end of the 41st week
b. When it is born between the beginning of
the 36th week and the end of the 40th week
c. When it weighs between 2500 and 4500 g
d. When it weighs between 3000 and 4000 g
3. What is the major task, as defined by Erickson, 4. Common concerns of adolescence include
at this developmental stage? conflicts with parents, conflicts with siblings,
concerns about school, and concerns about
peers and peer relationships. Of major con-
cern to them is the establishment of a per-
sonal identity. This is a time when many of
their concerns manifest themselves in psy-
chosomatic illnesses. What are the illnesses
reported most by adolescents?
SECTION IV: PRACTICING
a. Headache, stomachache, and insomnia
FOR NCLEX
b. Headache, insomnia, and dental caries
Activity F Answer the following questions. c. Stomachache, dental caries, and leg pain
d. Insomnia, skeletal pain, and headache
1. A mother brings her 2-year-old son in for a
well-child check. After weighing and measur- 5. Small for gestational age infants are more
ing the toddler, the nurse mentions that the prone to episodes of hypoglycemia than in-
child falls within 1 standard deviation of the fants who are considered appropriate for ges-
mean in both height and weight. What does tational age. What factor is considered to be
this mean? the most likely cause of these hypoglycemic
a. The toddler is the same height and weight episodes?
as 75% of other toddlers that age and a. They are too small for their pancreas to
weight. produce the insulin their body requires.
b. The toddler is the same height and weight b. They do not have enough brown fat to
as 68% of other toddlers that age and maintain their body temperature.
weight. c. They have depleted glycogen stores in their
c. The toddler is small and underweight for liver.
his age. d. Their bodies are so small that their pan-
d. The toddler is tall and overweight for his creas produces too much insulin for their
age. body requirements.
2. A nurse is teaching a class on fetal development 6. Middle to late childhood, ages 6 to 12 years
to a group of pregnant women. The nurse of age, brings with it a more developed im-
knows to include in her teaching that the em- mune system. Yet, this is when acute or
bryonic period in fetal development is from the chronic conditions can appear for the first
a. moment of conception to the 8th week of time. Which of the following diseases often
pregnancy. appears in middle to late childhood?
b. moment of implantation to the 6th week a. Pneumonia
of pregnancy b. Nephrotic syndrome

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CHAPTER 2 CONCEPTS OF ALTERED HEALTH IN CHILDREN 9

c. Cerebral palsy the history, and autopsy of the body. SIDS

d. Asthma accounts for more infant deaths, after the
neonatal period, than any other cause. What
7. The anterior fontanel of an infant is an area are the risk factors for SIDS?
of unossified membranous material that is
a. Being Native American and placing the in-
considered “open” when the infant is born. It
fant on its back to sleep
is the largest of several areas, or fontanels, in
an infant’s skull. When does the anterior b. Being Asian and exposing the infant to en-
fontanel close, or ossify? vironmental cigarette smoke
a. 18 months to 2 years of age c. Mother’s use of drugs during pregnancy
and placing the infant in the prone posi-
b. 1 to 2 years of age
tion to sleep
c. 6 to 9 months of age
d. Breast-feeding and placing the infant on its
d. 2 to 3 years of age back to sleep
8. Early childhood is the period when the child 11. Macrosomic infants, or those who are large
is from 18 months to 5 years of age. Infec- for gestational age, born to diabetic mothers
tious diseases and injuries are major health face which of the following risk factors for
problems during this period in a child’s life. complications during the neonatal period?
Which of the following is considered a com- Mark all that apply.
municable disease?
a. Hypoglycemia
a. Diaper rash
b. Polycythemia
b. Chickenpox
c. Birth trauma
c. Urinary tract infection
d. Birth asphyxia
d. Croup
12. When planning an educational event for a
9. Bacterial infections in newborns have nonspe- group of women having their first babies, a
cific signs and symptoms in the early stages. nurse knows to include which information
Often, it is the nurse who notes that some- about intrauterine growth retardation? Mark
thing “just isn’t right” with the newborn. For all that apply.
optimal outcomes of these infections, it is
a. The terms small for gestational age and
imperative to have early diagnosis and treat-
intrauterine growth retardation are used
ment. Maternal group B streptococcus (GBS)
interchangeably, but do not mean the
infections are transmitted to the infant during
same thing.
birth. When are GBS infections treated?
b. Eighty percent of newborns fall between
a. During pregnancy to the mother to pre-
the 10th and the 90th percentile of the
vent transmission of the bacteria to the
Colorado Growth Curve.
newborn and after birth to the infant pro-
phylactically c. Intrauterine growth retardation can occur
at any time during the pregnancy.
b. During the intrapartal period to the
mother to help prevent transmission of the d. An infant who is “small for gestational
bacteria to the newborn and after birth to age” weighs less then 80% of all other
the infant prophylactically newborns.
c. During postpartum care to the mother and 13. During adolescence, the anterior pituitary
at discharge to the infant gland produces gonadotropic hormones that
d. During the intrapartal period to the affect target organs, causing the secretion of
mother to help prevent transmission of the sex hormones. It is the sex hormones that
bacteria to the newborn and at discharge cause the appearance of both primary and
to the infant as a prophylactic agent secondary sex characteristics. Sex hormones,
including androgens, stimulate the body to
10. Sudden infant death syndrome (SIDS) is de- do other things, such as conclude
fined as the death of an infant younger than growth. They cause epiphyseal
1 year that remains unexplained even after closure of bones and discontinuation of
investigation of the death scene, review of skeletal growth.

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3
CHAPTER

Concepts of Altered
Health in Older Adults

SECTION I: LEARNING 13. Compare information obtained from func-

tional assessment with that obtained from a
OBJECTIVES physical examination used to arrive at a med-
ical diagnosis
1. State a definition for young-old, middle-old,
and old-old, and characterize the changing 14. Cite the differences between chronic and
trend in the elderly population transient urinary incontinence
2. State a philosophy of aging that incorporates 15. State four risk factors for falls in older individ-
the positive aspects of the aging process uals
3. Discuss theories of biologic aging 16. List five symptoms of depression in older adults
4. Describe common skin changes that occur 17. Name a tool that can be used for assessing
with aging cognitive function
5. Explain how muscle changes that occur with 18. State the difference between delirium and
aging affect high-speed performance and en- dementia
durance
19. Characterize drug therapy in the older adult
6. Describe the process of bone loss that occurs population
with aging
20. List five factors that contribute to adverse
7. State the common changes in blood pressure drug reactions in the elderly
regulation that occur with aging
21. Cite cautions to be used in prescribing med-
8. List the changes in respiratory function that ications for the elderly
occur with aging
9. Relate aging changes in neural function to
the overall function of the body SECTION II: ASSESSING YOUR
10. Briefly discuss the effects of aging on vision,
UNDERSTANDING
hearing, taste, and smell
Activity A Fill in the blanks.
11. Describe changes that occur in the gastroin-
1. Because there is great diversity in the health
testinal tract with aging
of older adults, they are categorized into sub-
12. State the significance of decreased lean body groups of young-old, from years
mass on interpretation of the glomerular fil- of age; middle-old, from years of
tration rate using serum creatinine levels age; and old-old, from years of

10
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CHAPTER 3 CONCEPTS OF ALTERED HEALTH IN OLDER ADULTS 11

age to reflect more accurately the changes in 16. The signature symptom of depression is a
function that occur over time. mood.
2. Developmental or genetic theories of aging 17. Major depression is a common consequence
are termed . of and occurs in about one-third
of afflicted patients.
3. theories maintain that the
changes result from an accumulation of ran- 18. is a syndrome of acquired, per-
dom events or damage from environmental sistent impairment in several domains of in-
agents or influences. tellectual function.
4. Cellular aging resides with an enzyme called 19. is defined as an organic mental
that is believed to govern chro- syndrome featuring a cognitive impairment,
mosomal aging. disturbances of attention, reduced level of
consciousness, increased or decreased psy-
5. The theory of aging holds that
chomotor activity, and a disorganized sleep-
aging results partially from oxidative metabo-
wake cycle.
lism and the effects of free radical damage.
20. Drug toxicity is common in elderly patients
6. Areas of the skin that are repeatedly exposed
due to decreases in and
to the sun experience changes in the dermis.
decreases in lean muscle mass.
fibers rearrange and degenerate,
resulting in decreased skin strength and elas-
Activity B Match the key terms in Column A
ticity.
with their definitions in Column B.
7. Decreases in height as a person ages can be at-
tributed to compression of the . Column A Column B
8. In elderly individuals, stiffening of the arter- 1. Telomerase a. Yellow insoluble de-
ies results in a chronic elevation of posits of intracellular
2. Stochastic
pressure. material
theory of
9. A progressive loss of in the lung aging b. Govern chromoso-
is caused by changes in the amount of elastin mal aging through
3. Superoxide its action on
and composition of collagen fibers and results
in decreased VO2 max. 4. Osteoporosis telomeres
c. Decreased bone mass
10. , or hearing loss, occurs as a re- 5. Sedatives
sult of aging plus auditory stressors, trauma, d. Key component of
6. Dementia oxidative stress-
environmental influences, otologic diseases,
and genetic influences. 7. Orthostatic related aging
hypotension e. Mitochondrial dam-
11. , or dry mouth, is a common af-
age is one example
fliction of the elderly and is caused by de- 8. Lipofuscin
of this type of aging
creased salivary secretions.
9. Wear and f. Accumulated dam-
12. The age-associated loss of parietal cells in the tear theory age to vital parts of
stomach results in , a decrease in of aging the cell leads to
hydrochloric acid secretion. aging and death
10. Alzheimer
13. Age-related decreases in renal blood flow re- disease g. Associated with an
sult in a decreased rate, which increased prevalence
can confuse a diagnosis. of falling
14. The index is commonly used to h. A syndrome of ac-
assess the mental and biological status of an quired, persistent im-
elderly patient. pairment in several
domains of intellec-
15. A decrease in bladder capacity, in bladder and tual function
sphincter tone, and in the ability to
detrusor muscle contractions are
common causes of incontinence.

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12 UNIT 1 CONCEPTS OF HEALTH AND DISEASE

i. Significant drop in 6. Explain the differences between dementia and

systolic pressure on Alzheimer disease.
assumption of the
upright position
j. Chronic, progres-
sive neurologic dis-
order of unknown
cause with symp-
toms of dementia
SECTION III: APPLYING YOUR
Activity C Briefly answer the following. KNOWLEDGE
1. The process of aging is one of slow steady de-
Activity D Consider the following scenario and
cline. Using the oxidative free radical theory of
answer the questions.
aging as a guide, describe the changes as they
develop in the circulatory system to result in An elderly gentleman is brought to the emer-
higher blood pressure. gency room by his daughter after she found him
lying on the floor of his house. The daughter tells
you that she has been afraid that her father
would fall and now he has.
1. The daughter asks the nurse what she can do
to help prevent her father from falling again.
2. The process of aging is often likened to a dis-
How should the nurse respond?
ease state. Explain how disease and aging are
different.

2. While conducting the physical assessment, the

nurse notices that the gentleman’s affect is flat,
3. There are numerous theories of how humans
he responds to questions only briefly, and says
age. One such class of theories is the stochastic
that he has lost weight over the past few months.
theory of aging. Explain the concept of DNA
For what would the nurse further assess?
repair and how it fits into this theory.

4. As humans age, muscular strength declines.

Provide a rational for why we lose our strength SECTION IV: PRACTICING
as we age.
FOR NCLEX
Activity E Answer the following questions.
1. With aging, the skin acquires an overall thin
and transparent quality while becoming dry
5. The elderly are more prone to falling. Explain and wrinkled. Which of the following skin
the degeneration of sensory processes behind disorders are common among the older adult
the increased risk of falling. population?
a. Keratoses and skin cancers
b. Skin cancers and xenobiotic
c. Dermatitis and xenomas
d. Xenomas and keratoses

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CHAPTER 3 CONCEPTS OF ALTERED HEALTH IN OLDER ADULTS 13

2. There are many factors that determine the 6. One of the major indexes of kidney function
effect of aging on cardiac function in normal is the serum creatinine level. It is used as an
healthy persons. Which of these statements is indication of the glomerular filtration rate
not true about aging and cardiac function? (GFR), and is often used when prescribing
a. There is a decrease in responsiveness to - and calculating drug doses for medications
adrenergic stimulation and circulating that are eliminated through the kidneys. In
catecholamines. older adults, why does this have important
implications?
b. There is an increase in systemic vascular
resistance and left ventricular afterload. a. Serum creatinine levels progressively in-
crease as a person ages.
c. There is a decrease in the maximal heart
rate and maximal cardiac output. b. GFR increases as a person ages without a
corresponding increase in serum creatinine
d. There is a decrease in systemic vascular re-
levels.
sistance and left ventricular afterload.
c. Both GFR and serum creatinine levels de-
3. Hearing loss in the elderly is characterized by crease as a person ages.
a gradual, progressive onset of bilateral and
d. GFR decreases without an increase in
symmetric sensorineural hearing loss of high-
serum creatinine levels as a person ages.
frequency tones. This occurs at various rates
in different people. Which sign, in the el- 7. As men age, benign prostatic hypertrophy
derly, is indicative of hearing impairment? (BPH) becomes common. As the size of the
a. Speech discrimination is difficult. prostate increases, BPH can cause both ob-
structive and irritative symptoms. All of the
b. Repetition is more evident.
following are obstructive symptoms of BPH
c. Speech is slower and softer. except for which one?
d. Shouting occurs when it is not necessary. a. Urge incontinence
4. Both the sense of smell and the sense of taste b. Postvoid dribbling
seem to decline in the elderly. However, in c. Hesitancy
many cases, what is perceived as a decline in
d. Retention
ability to taste is actually a decline in the abil-
ity to smell. With a decline in the sense of 8. In the elderly population, depression is a sig-
taste and smell, the elderly are at risk for nificant but underestimated health problem.
which of the following? Statistics show that at least 25% of commu-
a. Taking the wrong medication nity-dwelling elderly people are believed to
have depressive symptoms. Which of the fol-
b. Being unable to smell smoke if there is a
lowing symptoms are indicative of depression
fire
in older people?
c. Living in unhealthy and unclean condi-
a. Fatigue and loss of energy
tions
b. Appetite and weight changes
d. Eating food that is spoiled and not cooked
properly c. Sleep disturbance and irritable mood
d. All of the above
5. A complex and devastating problem in ap-
proximately 5% to 10% of the elderly popula- 9. Although there are many causes contributing
tion is dementia. Dementia is a syndrome of to the diagnosis of dementia in the elderly
acquired, persistent impairment in several do- population, it is believed that up to 70% of
mains of intellectual function. Which of the these cases involve Alzheimer disease.
following is not affected in a person with de- Alzheimer disease is a chronic, progressive,
mentia? neurologic disorder of unknown etiology.
a. Ability to interact with others Two changes occur in the brain of Alzheimer
patients: plaques that develop between neu-
b. Visuospatial ability
rons, called senile plaques, and neurofibrillary
c. Physical changes of aging tangles that develop within the neurons
d. Problem-solving ability themselves. Which diagnostic test is used to
determine specifically if the elderly patient

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14 UNIT 1 CONCEPTS OF HEALTH AND DISEASE

has Alzheimer disease or another form of de- a. A careful evaluation A. a, d, e, c, b

mentia? of the need to medicate B. e, a, d, c, b
a. The Mini-Mental State Examination b. The cost of the drug C. a, d, c, b, e
b. There is no specific test to confirm the as compared to a generic D. d, b, c, a, e
diagnosis drug if it is available
c. A complete metabolic panel performed on c. Timing of the dose
the patient’s blood
d. Analysis of the current
d. The auscultation of bruits in the carotid
medication regimen
arteries
and disease state
10. A nurse is preparing an educational event for
e. Providing written and
the elderly population at a local senior center.
verbal education on
The nurse knows that it is important to in-
the medication
clude information on polypharmacy because
of which of these factors? 13. Atrophic gastritis and decreased secretion of
a. Psychotropic drugs administered to older intrinsic factor are more common with aging
adults with dementia may cause a decrease and can result in a malabsorption of vitamin
in any confusion they are experiencing. B12. A deficiency of vitamin B12 can cause
which of these to occur? Mark all that apply.
b. Polypharmacy increases the risk of drug in-
teractions and adverse drug reactions and a. Peripheral neuropathy
has been found to decrease compliance b. Lack of intrinsic factor
with drug regimens. c. Pernicious anemia
c. Nonsteroidal anti-inflammatory medica- d. Improved coordination
tions given to an older adult with hyper-
tension can cause orthostatic hypotension. 14. Depression can occur as a result of many dif-
ferent physical illnesses. Which of these ill-
d. Beta-blocking agents administered to an
nesses can cause depression in the elderly?
individual with chronic obstructive pul-
Mark all that apply.
monary disease may reduce the severity of
bronchoconstriction. a. Pancreatic cancer
b. Congestive heart failure
11. Falls in the elderly are all too common. One
of the major causes of falls in the elderly pop- c. Hypocholesteremia
ulation, although often overlooked, is med- d. Hyperthyroidism
ication. Match the type of medication with its
15. Changes in the micturition cycle that accom-
physiologic result.
pany the aging process make the older adult
Type of Medication Physiologic Result prone to urinary incontinence. Urinary in-
continence can have many contributing
1. Antihypertensive a. Fatigue
causes, including which of the following?
2. Diuretic b. Electrolyte Mark all that apply.
disturbances
3. Sedative a. Increased ability to inhibit detrusor con-
c. Confusion tractions
4. Hypnotic d. Impaired b. Impaired mobility and a slower reaction
alertness time
c. A decrease in bladder capacity
12. Several factors come into effect when making
decisions about medication use in the elderly, d. Medications, such as long-acting sedatives
not the least of which is preventing harm. and hypnotics
Choose the answer that places the following
decision-making factors in the correct order.

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CHAPTER
Cell and Tissue
Characteristics

SECTION I: LEARNING 13. Explain the process of cell differentiation in

terms of development of organ systems in the
OBJECTIVES embryo and the continued regeneration of
tissues in postnatal life
1. State why the nucleus is called the “control
center” of the cell 14. Explain the function of stem cells
2. List the cellular organelles and state their 15. Describe the characteristics of the four differ-
functions ent tissue types
3. State four functions of the cell membrane 16. Explain the function of intercellular adhe-
sions and junctions
4. Trace the pathway for cell communication,
beginning at the receptor and ending with the 17. Characterize the composition and functions
effector response, and explain why the process of the extracellular components of tissue
is often referred to as signal transduction
5. Compare the functions of G-protein–linked,
ion-channel–linked, and enzyme-linked cell SECTION II: ASSESSING YOUR
surface receptors UNDERSTANDING
6. Describe the phases of mitotic cell division
Activity A Fill in the blanks.
7. Relate the function of ATP to cell metabolism
1. is composed of water, proteins,
8. Compare the processes involved in anaerobic lipids, carbohydrates, and electrolytes.
and aerobic metabolism 2. All cells have a nucleus, whereas
9. Discuss the mechanisms of membrane trans- cells do not.
port associated with diffusion, osmosis, endo- 3. The nucleus contains , which
cytosis, and exocytosis and compare them serves as the template for making the
with active transport mechanisms , which is later used to direct the
10. Describe the function of ion channels synthesis of in the cytoplasm.
11. Describe the basis for membrane potentials 4. Ribosomes serve as the site for
synthesis in the cytoplasm.
12. Explain the relationship between membrane
permeability and generation of membrane 5. endoplasmic reticulum is stud-
potentials ded with ribosomes attached to specific bind-
ing sites on the membrane.

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16 UNIT 2 CELL FUNCTION AND GROWTH

6. The complex modifies proteins 10. First h. Division of cells follow-

and packages them into secretory granules messenger ing mitosis
bound for the membrane. i. Organelles that metabo-
7. contain powerful hydrolytic en- lize misfolded proteins
zymes that are used to break down excess and j. Carbohydrate and pro-
worn-out cell parts as well as foreign substances. tein layer that
participates in cell
8. Peroxisomes contain a special enzyme that
recognition
degrades __________.
2.
9. Mitochondria are the site of cellular
, the product of which is the for- Column A Column B
mation of .
1. Diffusion a. Secondary active trans-
10. Transport along the axon of neuronal cells port where substances
2. Osmosis
takes place along the primary cytoskeletal are moved in the same
component . 3. Active direction
transport b. Any type of transport
11. Actin and myosin are examples of functional
within muscle cells. 4. Passive across the cell mem-
transport brane that requires en-
12. Integral proteins span the entire lipid bilayer, ergy as it moves
whereas proteins are bound to 5. Cotransport material against the
one side of the membrane or the other. concentration gradient
6. Facilitated
13. The four tissues of the body are , diffusion c. Secondary active trans-
, , and . port where substances
7. Primary
are moved in the oppo-
14. The differences in permeability of active
site direction
is responsible for the generation transport
of membrane potential. Permeability is regu- d. The coupling of the
8. Secondary transport of one solute
lated by ion channels.
active to a second solute
15. Of the four tissue types, only transport
e. Transport across the
and tissue is excitable.
9. Counter- cell membrane through
transport a protein channel that
Activity B Match the key terms in Column A
does not require ATP
with their definitions in Column B. 10. Symport
f. The diffusion of water
1.
g. Any type of transport
Column A Column B across the cell mem-
brane that does not re-
1. tRNA a. Site of synthesis of
quire energy
lipid molecules
2. Cytokinesis h. Direct use of ATP in the
b. Transfer RNA
3. Tubulin transport of a solute
c. Hormone or neuro-
i. Utilization of the en-
4. Glycocalyx transmitter
ergy derived from the
5. G protein d. Second messenger that primary active trans-
mediates cellular re- port of one solute for
6. Smooth sponses the cotransport of a
endoplasmic
e. Separation of the second solute
reticulum
chromosome pairs j. Passive movement of
7. Anaphase f. Protein subunit of mi- solute down the con-
8. Centrioles crotubules centration gradient
g. Used to direct
9. Proteasomes
chromosomes in
dividing cells

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CHAPTER 4 CELL AND TISSUE CHARACTERISTICS 17

Activity C Put the phases of the cell cycle in aerobic metabolism, explain how alterations in
the correct order, starting with the beginning of oxygen delivery to the tissues are detrimental.
interphase.
1. G2 phase
2. Anaphase
3. Telophase 3. Tissues must maintain their shape and integrity
4. S phase in order to function. Explain from the cellular
level to the tissue level what is responsible for
5. Prophase maintaining tissue shape and structure.
6. Metaphase
7. G1 phase

4. Signal transduction is a complex and varied

Activity D Consider the following figure. process. Describe the process starting at the
first messenger and ending in a physiological
response. Be sure to include the various possi-
1. bilities at both the receptor level and the sec-
ond messenger level.

Extracellular
fluid

5. Large molecules or particles are ingested or re-

leased from cells. Describe the basics of inges-
tion and release.

Cytosol

SECTION III: APPLYING YOUR

In this figure, label phospholipid by layer, an
individual phospholipid, an integral protein, a
KNOWLEDGE
peripheral protein, a channel protein, a
Activity F Consider the following scenario and
glycoprotein, and a glycolipid.
answer the questions.
Activity E Briefly answer the following. Fourteen-year-old Thomas Kirk is brought to the
clinic for a routine physical before starting to
1. The cell cycle is regulated by three protein
play sports in school. He is 77 in. tall and weighs
complexes and their interactions. List each
200 lb. Tom states, “I have tried to lose weight so
protein type and describe how it influences the
I can wrestle at a lower weight, and I just don’t
progression through the cell cycle.
understand why I still weigh 200 pounds. My sci-
ence teacher said it’s because I have white fat and
not brown fat.” How would you explain to Tom
about the two kinds of adipose tissue in his body?

2. In many diseases, the root cause is ischemia

(low blood flow) or hypoxia (decreased deliv-
ery of oxygen). Using what you know about

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18 UNIT 2 CELL FUNCTION AND GROWTH

SECTION IV: PRACTICING c. Receptor membrane

FOR NCLEX d. Bilayer membrane
6. Some messengers, such as thyroid hormone
Activity G Answer the following questions. and steroid hormones, do not bind to mem-
1. There are two forms of endoplasmic reticu- brane receptors but move directly across the
lum (ER) found in a cell. They are the rough lipid layer of the cell membrane and are car-
and the smooth ER. What does the rough ER ried to the cell nucleus. What do they do at
do in a cell? the cell nucleus?
a. Produces proteins a. Transiently open or close ion channels
b. Combines protein with other components b. Influence DNA activity
of the cytoplasm c. Stabilize cell function
c. Exports protein from the cell d. Decrease transcription of mRNA
d. Destroys ribosomes 7. The Krebs cycle provides a common pathway
2. The Golgi complex, or Golgi bodies, consists for the metabolism of nutrients by the body.
of stacks of thin, flattened vesicles or sacs The Krebs cycle forms two pyruvate mole-
within the cell. These Golgi bodies are found cules. Each pyruvate molecule formed in the
near the nucleus and function in association cytoplasm from one molecule of glucose
with the ER. What is one purpose of the Golgi yields another molecule of what?
complex? a. FAD
a. To produce bile b. NADH  H
b. To receive proteins and other substances c. ATP
from the cell surface by a retrograde trans- d. H2O
port mechanism
8. When cells use energy to move ions against
c. To produce excretory granules
an electrical or chemical gradient, the process
d. To produce small carbohydrate molecules is called what?
3. In Tay-Sachs disease, an autosomal recessive a. Passive transport
disorder, hexosaminidase A, which is the b. Neutral transport
lysosomal enzyme needed for degrading the
c. Cotransport
GM2 ganglioside found in nerve cell mem-
branes, is deficient. Although GM2 ganglio- d. Active transport
side accumulates in many tissues, where does 9. Groups of cells that are closely associated in
it do the most harm? structure and have common or similar func-
a. Brain and retinas tions are called tissues. What are the types of
b. Retinas and heart tissue in the human body?
c. Nervous system and retinas a. Connective and muscle tissue
d. Nervous system and brain b. Binding and connecting tissue
c. Nerve and exothelial tissue
4. The mitochondria are literally the “power
plants” of the cell because they transform or- d. Exothelial and muscle tissue
ganic compounds into energy that is easily 10. Endocrine glands are epithelial structures that
accessible to the cell. What do the mitochon- have had their connection with the surface
dria do? obliterated during development. How are
a. Make energy these glands described?
b. Form proteasomes a. Ductile and produce secretions
c. Need DNA from other sources to replicate b. Ductless and produce secretions
d. Extract energy from organic compounds c. Ductile and release their glandular prod-
ucts by exocytosis
5. The cell membrane is also called what?
d. Ductless and release their glandular prod-
a. Plasma membrane
ucts by exocytosis
b. Nuclear membrane

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CHAPTER 4 CELL AND TISSUE CHARACTERISTICS 19

11. Each skeletal muscle is a discrete organ made 14. Cells in multicellular organisms need to com-
up of hundreds or thousands of muscle fibers. municate with one another to coordinate
Although muscle fibers predominate, substan- their function and control their growth. The
tial amounts of connective tissue, blood ves- human body has several means of transmit-
sels, and nerve fibers are also present. What ting information between cells, what are
happens during muscle contraction? they? Mark all that apply.
a. When activated by GTP, the cross-bridges a. Direct communication between adjacent
swivel in a fixed arc, much like the oars of cells
a boat, as they become attached to the b. Express communication between cells
actin filament.
c. Autocrine and paracrine signaling
b. During contraction, each cross-bridge un-
d. Endocrine or synaptic signaling
dergoes its own cycle of movement, form-
ing a bridge attachment and releasing it; 15. The human body has nondividing cells that
the same sequence of movement repeats it- have left the cell cycle and are not capable of
self when the cross-bridge reattaches to the mitotic division once an infant is born. What
same cell. are the nondividing cells? Mark all that apply.
c. The thick myosin and thin actin filaments a. Mucous cells
slide over each other, causing shortening b. Neurons
of the muscle fiber.
c. Skeletal muscle cells
d. Calcium-calmodulin complexes produce
d. Cardiac muscle cells
the sliding of the filaments that form
cross-bridges with the thin actin filaments. 16. Smooth muscle is often called
muscle because it contracts spontaneously or
12. The three main parts of a cell are the nucleus,
through activity of the autonomic nervous
the , and the cell membrane.
system.
13. Bilirubin is a normal major pigment of bile;
its excess accumulation within cells is evi-
denced clinically by a yellowish discoloration
of the skin and sclera, a condition called
.

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5
CHAPTER

Cellular Adaptation,
Injury, and Death

SECTION I: LEARNING 11. Describe three types of reversible cell changes

that can occur with cell injury
OBJECTIVES
12. Define free radical and reactive oxygen species
1. Cite the general purpose of changes in cell
13. Relate free radical formation and oxidative
structure and function that occur as the result
stress to cell injury and death
of normal adaptive processes
14. Describe cell changes that occur with is-
2. Describe cell changes that occur with atro-
chemic and hypoxic cell injury
phy, hypertrophy, hyperplasia, metaplasia,
and dysplasia and state general conditions 15. Relate the effects of impaired calcium home-
under which the changes occur ostasis to cell injury and death
3. Cite three sources of intracellular accumula- 16. Differentiate cell death associated with necro-
tions sis and apoptosis
4. Compare the pathogenesis and effects of dys- 17. Cite the reasons for the changes that occur
trophic and metastatic calcifications with the wet and dry forms of gangrene
5. Describe the mechanisms whereby physical
agents such as blunt trauma, electrical forces,
and extremes of temperature produce cell in- SECTION II: ASSESSING YOUR
jury UNDERSTANDING
6. Differentiate between the effects of ionizing
and nonionizing radiation in terms of their Activity A Fill in the blanks.
ability to cause cell injury 1. Cells may adapt to the environment by un-
7. Explain how the injurious effects of biologic dergoing changes in ,
agents differ from those produced by physical , and .
and chemical agents 2. There are two types of genes involved in
8. State the mechanisms and manifestations of adapting to the environment: the
cell injury associated with lead poisoning genes that are necessary for nor-
mal function of a cell, and the genes that
9. Identify the causes and outcomes of mercury control cellular .
toxicity
3. Atrophy is seen as a decrease in cell
10. State how nutritional imbalances contribute .
to cell injury

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CHAPTER 5 CELLULAR ADAPTATION, INJURY, AND DEATH 21

4. Denervation will result in cellular 20. Acidosis develops and denatures the enzy-
. matic and structural proteins of the cell
during necrosis.
5. Hypertrophy is an _________ in cell size.
6. An increase in muscle mass associated with Activity B Consider the following figure.
exercise is an example of .
7. An increase in the number of cells in an
organ or tissue is known as cellular Nucleus
.
Basement
8. Liver regrowth is an example of membrane
hyperplasia.
9. or hyperplasia is
due to excessive hormonal stimulation or ex-
cessive growth factors.
10. represents a reversible change in
which one adult cell type is replaced by an-
other adult cell type.
11. Metaplasia usually occurs in response to
chronic and and
allows for substitution of cells that are better
able to survive stressful or harmful condi-
tions.
12. Deranged cell growth of a specific tissue that
results in cells that vary in size, shape, and or-
ganization is known as .
13. Dysplasia is strongly implicated as a precursor
of .
14. Intracellular represent the
buildup of substances that cells cannot imme-
diately use or eliminate.
15. radicals are highly reactive
chemical species having an unpaired electron
in the outer valence shell of the molecule.
16. deprives the cell of oxygen and
interrupts oxidative metabolism and the gen-
eration of ATP.
17. Reversible cellular injury is seen as either cel-
lular or accumula-
tion.
18. differs from apoptosis in that it
involves unregulated enzymatic digestion of
cell components, loss of cell membrane in-
tegrity with uncontrolled release of the prod- The figure represents cellular adaptation. Label
ucts of cell death into the intracellular space, each adaptation, and state whether it is a physio-
and initiation of the inflammatory response. logic, pathologic, or both.

19. The increased levels may inap-

propriately activate a number of enzymes
with potentially damaging effects.

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22 UNIT 2 CELL FUNCTION AND GROWTH

Activity C Match the key terms in Column A 3. Lead was recently found in paint used to give
with their descriptions in Column B. children’s toys their brilliant colors. Why is
this a concern?
Column A Column B
1. Metastatic a. Macroscopic deposi-
calcification tion of calcium salts
in injured tissue
2. Reactive oxygen
species (ROS) b. Oxygen-containing
4. List and describe the three major mechanisms
molecules that are
3. Antioxidants of cellular injury.
highly reactive
4. Apoptosis c. Ice crystal forma-
tion in cytosol
5. Dystrophic
calcification d. Natural and syn-
thetic molecules
6. Temperature- that inhibit the re- 5. Oxidative stress has been implicated as the
induced injury actions of ROS with causative agent in numerous disease states and
7. Ischemia biological structures the cause of physiological aging. Explain how
e. Occurs in normal oxidative stress can cause damage and why it
8. Molecular aging is a concern.
tissues as the result
9. Ionizing of increased serum
radiation calcium levels
10. Cellular aging f. Impaired oxygen
delivery
g. Programmed cell 6. Explain why one of the complications of hy-
death poxia is the development of acidosis and how
h. Causes injury due to acidosis will damage the tissue.
changes in electron
stability
i. Aging focused on
mutations and/or
changes in gene ex-
pression 7. Apoptosis occurs under normal stimulation or
as the result of cellular injury. There are two
j. Aging due to short- pathways for apoptosis to occur. What are
ened telomeres they, and what major protein is involved?
Activity D Briefly answer the following.
1. Why does chronically damaged tissue result in
calcification?

SECTION III: APPLYING YOUR

KNOWLEDGE
2. List the five categories of cellular injury.
Activity E Consider the following scenario and
answer the question.
A 50-year-old male is about to receive chemother-
apy drugs for a tumor in his liver. He states that
he has heard that chemotherapy drugs can hurt
normal cells in his body and cells in his tumor.
The client asks how this happens.

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CHAPTER 5 CELLULAR ADAPTATION, INJURY, AND DEATH 23

1. How can chemotherapy drugs injure normal d. When the body stimulates gene expression
cells? to begin a progressive decrease in left ven-
tricular muscle mass
3. Metastatic calcification occurs in normal tis-
sues as the result of increased serum calcium
levels (hypercalcemia). Anything that in-
creases the serum calcium level can lead to
calcification in inappropriate places such as
the lung, renal tubules, and blood vessels.
SECTION IV: PRACTICING What are the major causes of hypercalcemia?
FOR NCLEX a. Diabetes mellitus and Paget disease
Activity F Answer the following questions. b. Hypoparathyroidism and vitamin D intoxi-
cation
1. Many molecular mechanisms mediate cellular
c. Hyperparathyroidism and immobilization
adaptation. Some are factors produced by
other cells, and some are produced by the d. Immobilization and hypoparathyroidism
cells themselves. These mechanisms depend 4. Mercury is a toxic substance, and the hazards
largely on signals transmitted by chemical of mercury-associated occupational and acci-
messengers that exert their effects by altering dental exposures are well known. What is the
the function of a gene. Many adaptive cellular primary concern for the general public in re-
responses alter the expression of “differentia- gard to mercury poisoning today?
tion” genes. What can cells do because of this?
a. Amalgam fillings in the teeth
a. A cell is able to change size or form with-
b. Mercury from thermometers and blood
out compromising its normal function.
pressure machines
b. A cell incorporates its change in function
c. Mercury found in paint that was made be-
and passes this change on to other cells
fore 1990
like it.
d. Fish such as tuna and swordfish
c. A cell is able to pass its change on to a
“housekeeping” cell. 5. Small amounts of lead accumulate to reach
d. A cell dies once the stimulus to change has toxic levels in the human body. Lead is found
been removed. in many places in the environment and is
still a major concern in the pediatric popula-
2. Hypertrophy may occur as the result of nor- tion. What would you teach the parents of a
mal physiologic or abnormal pathologic con- child who is being tested for lead poisoning?
ditions. The increase in muscle mass
a. Keep your child away from peeling paint.
associated with exercise is an example of
physiologic hypertrophy. Pathologic hyper- b. Keep your child away from anything ceramic.
trophy occurs as the result of disease condi- c. Do not let your child read newspapers.
tions and may be adaptive or compensatory. d. Do not let your child tour a mine on a
Examples of adaptive hypertrophy are the school field trip.
thickening of the urinary bladder from long-
continued obstruction of urinary outflow and 6. In a genetic disorder called xeroderma pigmen-
the myocardial hypertrophy that results from tosum, an enzyme needed to repair sunlight-
valvular heart disease or hypertension. What induced DNA damage is lacking. This autosomal
is compensatory hypertrophy? recessive disorder is characterized by what?
a. When the body increases its major organs a. Patches of pink, leathery pigmentation
during times of malnutrition that replace normal skin after a sunburn
b. When one kidney is removed, the remaining b. Extreme photosensitivity and a greatly in-
kidney enlarges to compensate for the loss creased risk of skin cancer in sun-exposed
skin
c. When the body controls myocardial
growth by stimulating actin expression to c. White, scaly patches of skin that appear on
enlarge the heart African American people after they have a
sunburn

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24 UNIT 2 CELL FUNCTION AND GROWTH

d. Photosensitivity and a decreased risk of 10. Biologic agents differ from other injurious
skin cancer in sun-exposed skin agents in that they are able to replicate and
can continue to produce their injurious ef-
7. While presenting a talk to the parents of
fects. How do gram-negative bacteria cause
preschoolers at a local day care center, the
harm to the cell?
nurse is asked about electrical injury to the
body. What should she include in her a. Gram-negative bacilli excrete elaborate ex-
response? Mark all that apply. otoxins that interfere with cellular produc-
tion of ATP.
a. In electrical injuries, the body acts as a de-
flector of the electrical current. b. Gram-negative bacilli release endotoxins
that cause cell injury and increased capil-
b. In electrical injuries, the body acts as a
lary permeability.
conductor of the electrical current.
c. Gram-negative bacilli enter the cell and
c. The most severe damage is caused by light-
disrupt its ability to replicate.
ning and high-voltage wires.
d. Gram-negative bacilli cannot cause harm
d. When a person touches an electrical
to the cell; only gram-positive bacilli can
source, the current passes through the
harm the cell.
body and exits to another receptor.
11. When confronted with a decrease in work de-
8. A man presents to the emergency room after
mands or adverse environmental conditions,
being out in below zero weather all night. He
most cells are able to revert to a smaller size
asks the nurse why the health care team is
and a lower and more efficient level of func-
concerned about his toes and feet. How
tioning that is compatible with survival. This
would the nurse respond?
decrease in cell size is called .
a. Cold causes injury to the cells in the body
by injuring the blood vessels, making 12. Match the pigments (Column A) with their
them leak into the surrounding tissue. description (Column B).
b. After being out in the cold all night, his Column A Column B
toes and feet are frozen, and it will be very
1. Icterus a. A yellow discoloration
painful to warm them again; in addition,
of tissue
the health care team is concerned that he 2. Lipofuscin
might be a drug addict. b. A blue lead line along
3. Carbon the margins of the gum
c. “It is obvious that you are a homeless per-
son, and we were wondering how often 4. Melanin c. A brown or dark-
this has happened to you before and when brown pigment found
it will happen again.” in the skin and hair
d. “Your toes and feet are frozen, and there is d. A yellow-brown pig-
a concern about the formation of blood ment that accumulates
clots as we warm them again.” in neurons

9. Clinical manifestations of radiation injury re- 13. Match the type of agent causing cell injury
sult from acute cell injury, dose-dependent (Column A) to the example (Column B).
changes in the blood vessels that supply the Column A Column B
irradiated tissues, and fibrotic tissue replace-
ment. What are these clinical manifestations? 1. Physical agent a. Submicroscopic
viruses
a. Radiation cystitis, dermatitis, and diarrhea 2. Chemical agent
from enteritis b. Mechanical forces
3. Biologic agent that produce tis-
b. Dermatitis, diarrhea from enteritis, and
4. Nutritional sue trauma
hunger
factor c. Free radicals
c. Diarrhea from enteritis, hunger, and muscle
spasms d. Vitamin B
deficiency
d. Radiation cystitis, diarrhea from enteritis,
and muscle spasms

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CHAPTER 5 CELLULAR ADAPTATION, INJURY, AND DEATH 25

14. You are a nurse preparing an educational a. Acetaminophen and aspirin

event for a group of single parents. You are b. Immunosuppressant drugs
going to talk about drugs and the damage
c. Alcohol and cigarettes
they can cause to the body. You would know
to include which of these? Mark all that d. Vitamin supplements and antineoplastic
apply. drugs

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16
CHAPTER

Genetic Control of Cell

Function and Inheritance

SECTION I: LEARNING 13. Briefly describe the methods used in linkage

studies, dosage studies, and hybridization
OBJECTIVES studies
1. Describe the structure and function of DNA 14. Describe the goals of the International
HapMap Project
2. Relate the mechanisms of DNA repair to the
development of a gene mutation 15. Describe the process of recombinant DNA
technology
3. Describe the function of messenger RNA, ri-
bosomal RNA, and transfer RNA as they relate 16. Characterize the process of RNA interference
to protein synthesis
4. Cite the effects of post-translational process-
ing on protein structure and function SECTION II: ASSESSING YOUR
5. Explain the role of transcription factors in UNDERSTANDING
regulating gene activity
Activity A Fill in the blank.
6. Define the terms autosomes, chromatin,
meiosis, and mitosis 1. Our genetic information is stored in the struc-
ture of acid.
7. List the steps in constructing a karyotype
using cytogenetic studies 2. acid serves as the template for
protein synthesis.
8. Explain the significance of the Barr body
3. The complete set of proteins encoded by the
9. Construct a hypothetical pedigree for a reces- genome is known as the .
sive and dominant trait according to
Mendel’s laws 4. A precise complementary pairing of
and bases occurs
10. Contrast genotype and phenotype in the double-stranded DNA molecule.
11. Define the terms allele, locus, expressivity, and 5. DNA replication is semiconservative, mean-
penetrance ing that the parental DNA strands dissociate
12. Differentiate between genetic and physical and pair with strands to com-
genomic maps plete mitosis.
6. Human somatic cells contain
pairs of different chromosomes.

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CHAPTER 6 GENETIC CONTROL OF CELL FUNCTION AND INHERITANCE 27

7. In the nucleus, DNA is in the form of Activity B Match the key terms in Column A
, and during mitosis, it con- with their definitions in Column B.
denses into .
1.
8. The genetic code is repeat of
bases. Column A Column B

9. Errors in DNA duplication are known as 1. tRNA a. Used to align amino

. acids with ribosomes
2. Transcription
for the formation of
10. A represents the variations in factors
protein
the genetic code that are responsible for the 3. Penetrance b. Ability of a gene to ex-
differences between individuals.
4. mRNA press its function
11. Messenger RNA is formed in the process of c. Initiate and regulate
. 5. Mitosis
transcription
12. The coding sequence of an mRNA molecule is 6. Meiosis d. Manner in which the
known as . 7. Expressivity gene is expressed
13. MRNA undergoes the process of e. Template that is
8. Chromo-
to form a protein in the cytosol. copied from DNA
somes
f. Replicating germ cells
14. Molecular assist in the folding 9. Multifactorial
of proteins into their three-dimensional con- g. Multiple alleles at dif-
inheritance
formation. ferent loci affect the
10. Single gene outcome
15. The degree to which a gene or particular inheritance h. Organized and con-
group of genes is activated is termed gene
densed DNA
.
i. One pair of genes is
16. Sonic is a gene that participates involved in the trans-
in the left-to-right axis responsible for the mission of informa-
rostral-caudal orientation of the nervous sys- tion
tem.
j. Duplication of
17. Achondroplasia is a condition characterized somatic cells
by short stature with limbs that are dispro-
2.
portionately shorter than the trunk and
caused by mutations or altered levels of Column A Column B
growth factors.
1. Collabo- a. More than one allele
18. The pattern of gene expression and the out- rative affects the same trait
ward presentation is the . genes b. One gene masks the
19. The position of a gene on a chromosome is 2. Multiple phenotypic effects of
called its , and alternate forms alleles another nonallelic gene
of a gene at the same locus are called c. Each gene is mutually
3. Comple-
. dependent on the other
mentary
20. A is a graphic method for por- genes d. Two different genes in-
traying family history of an inherited trait. fluencing the same trait
4. Epistasis interact to produce a
5. Alleles phenotype neither gene
alone could produce
e. Alternate forms of a gene
at the same locus

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28 UNIT 2 CELL FUNCTION AND GROWTH

Activity C Sequencing 4. Humans have both somatic and sex chromo-

somes. How many of each do we have, and
1. The processing of genetic material involves where do they originate?
many well-organized steps. Put the following
in order starting at transcription and ending
with the three-dimensional protein.
a. Transcription
b. Translation begins
5. Only about 2% of the genome encodes instruc-
c. mRNA moves to cytosol
tions for synthesis of proteins. The remainder
d. mRNA is read by ribosome complex consists of noncoding regions that serve to de-
e. Posttranslational processing termine where, when, and in what quantity
f. tRNA moves to ribosome proteins are made. Explain how this occurs,
and describe its significance.
g. Ribosomal subunits come together
h. Formation of peptide bonds
i. Final 3D protein structure

SECTION III: APPLYING YOUR

KNOWLEDGE
Activity D Briefly answer the following. Activity E Consider the following scenario and
answer the question.
1. Gregor Mendel was the first to study and char-
acterize inheritance. Explain what he did and Jessica Jones, an adopted child, has been search-
what he discovered. ing for her parents for many years. She believes
that she has finally found her father but wants to
be 100% sure before she approaches him.
1. Is there any way for her to absolutely identify
her father before she meets him? Discuss the
use of DNA fingerprinting to identify familial
2. Genetic mapping is done to allow us to know
relationships.
the position of certain genes and sequences on
the chromosomes. Explain the difference be-
tween genetic maps and physical maps. In
your explanation, describe the basic methodol-
ogy used to construct these maps.

3. During meiosis, a process takes place that in-

creases genetic variability. Explain how this
occurs. Is it a good or bad thing?

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CHAPTER 6 GENETIC CONTROL OF CELL FUNCTION AND INHERITANCE 29

SECTION IV: PRACTICING different loci, with each gene exerting a small
additive effect in determining a trait?
FOR NCLEX
a. Polygenic inheritance
Activity F Answer the following questions. b. Multifactorial inheritance
1. It is the proteins that the genes encode that c. Monofactorial inheritance
make up the majority of cellular structures d. Collaborative inheritance
and perform most life functions. What is the
6. Two syndromes exhibit mental retardation as
term used to define the complete set of pro-
a common feature. Both disorders have the
teins encoded by a genome?
same deletion in chromosome 15. When the
a. Proteome deletion is inherited from the mother, the in-
b. Protogene fant presents with one syndrome; when the
c. Nucleotomics same deletion is inherited from the father,
Prader-Willi syndrome results. What is the
d. Chromosome
syndrome when the deletion is inherited
2. Below are the steps in cell replication. Put from the mother?
them in the correct order. a. Turner syndrome
a. Complementary molecule A. a, c, b, d b. Angelman syndrome
is duplicated next to each B. b, a, d, c c. Down syndrome
original strand.
C. b, d, a, c d. Fragile X syndrome
b. Two strands of DNA D. d, b, c, a
separate. 7. Homozygotes are what people are called in
whom the two alleles of a given pair are the
c. Mitosis occurs. same (AA or aa). Heterozygotes are what peo-
d. Two strands become four ple who have different alleles (Aa) at a gene
strands. locus are called. What kind of trait is ex-
pressed only in homozygous pairing?
3. Chromosomes contain all the genetic content
a. Dominant trait
of the genome. There are 23 pairs of different
chromosomes in each somatic cell, half from b. Single-gene trait
the mother and half from the father. One of c. Recessive trait
those chromosomes is the sex chromosome. d. Penetrant trait
What are the other 22 pairs of chromosomes
called? 8. The International HapMap Project was cre-
ated with two goals. One is the development
a. Ribosomes
of methods for applying the technology of
b. Helixes these projects to the diagnosis and treatment
c. Autosomes of disease. The other is to map which of the
d. Haploids many closely related single nucleotide poly-
morphisms in the human genome?
4. On rare occasions, accidental errors in dupli-
a. Codons
cation of DNA occur. What are these called?
b. Triplet code
a. Codons
c. Alleles
b. Ribosomes
d. Haplotypes
c. Endonucleases
d. Mutations 9. DNA fingerprinting is based in part on recom-
binant DNA technology and, in part, on
5. Most human traits are determined by multi- those techniques originally used in medical
ple pairs of genes, many with alternate codes genetics to detect slight variations in the
accounting for some dissimilar forms that genomes of different individuals. These tech-
occur with certain genetic disorders. What niques are used in forensic pathology to com-
type of inheritance involves multiple genes at pare specimens from the suspect and the

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30 UNIT 2 CELL FUNCTION AND GROWTH

forensic specimen. What is being compared 13. One of the first products to be produced
when DNA fingerprinting is used in forensic using recombinant DNA technology was
pathology? human ____________.
a. Banding pattern 14. Cytogenetics is the study of the structure and
b. Triplet code numeric characteristics of the cell’s chromo-
c. Haplotypes somes. Chromosome studies can be done on
any tissue or cell that grows and divides in
d. Chromosomes
culture. What are the characteristics of a
10. There are two main approaches used in gene chromosomal study? Mark all that apply.
therapy: Transferred genes can replace defec- a. The completed picture of a chromosomal
tive genes, or they can selectively inhibit study is called karyotyping.
deleterious genes. What are the compounds
b. Human chromosomes are divided into
usually used in gene therapy?
three types according to the position of the
a. mRNA sequences centromere.
b. Cloned DNA sequences c. Special laboratory techniques are used to
c. Sterically stable liposomes culture body cell. They are then fixed and
d. Single nucleotide polymorphisms stained to display identifiable banding pat-
terns.
11. The human genome sequence is almost ex-
d. Complementary genes and collaborative
actly (99.9%) the same in all people. What is
genes are easily recognized.
believed to account for the differences in
each human’s behaviors, physical traits, and 15. Genetics has its own set of definitions. Match
their susceptibility to disease is the small vari- the word with its definition.
ation (0.01%) in gene sequence. This is 1. Genotype a. Traits, physical or
termed a ____________. biochemical, asso-
2. Phenotype
12. Like DNA, RNA is a long string of nucleotides ciated with a spe-
encased in a large molecule. However, there 3. Pharmaco- cific genotype
are three aspects of its structure that makes it genetics that are recogniz-
different from DNA. What are these aspects? able
4. Somatic cell
Mark all that apply. hybridization b. How drugs re-
a. RNA’s double strand is missing one pair of spond to an indi-
5. Penetrance vidual’s inherited
chromosomes.
characteristics
b. The sugar in each nucleotide of RNA is
ribose. c. Genetic informa-
tion contained in
c. RNA is a single-stranded molecule.
the base sequence
d. RNA’s thymine base is replaced by uracil. triplet code
d. Ability of a gene
to express its
function
e. Fusion of human
somatic cells with
those of a differ-
ent species to
yield a cell con-
taining the chro-
mosomes of both
species

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CHAPTER
Genetic and Congenital
Disorders

SECTION I: LEARNING 10. State the cautions that should be observed

when considering use of drugs during preg-
OBJECTIVES nancy, including the possible effects of alco-
hol abuse, vitamin A derivatives, and folic
1. Define the terms congenital, allele, gene locus,
acid deficiency on fetal development
gene mutation, genotype, phenotype, homozy-
gous, heterozygous, polymorphism, gene pene- 11. List four infectious agents that cause congeni-
trance, and gene expression tal defects
2. Describe three types of single-gene disorders 12. Describe the process of genetic assessment
and their patterns of inheritance
13. Cite the rationale for prenatal diagnosis
3. Explain the genetic abnormality responsible
14. Describe methods used in arriving at a pre-
for the fragile X syndrome
natal diagnosis, including ultrasonography,
4. Contrast disorders due to multifactorial in- amniocentesis, chorionic villus sampling,
heritance with those caused by single-gene percutaneous umbilical fetal blood sam-
inheritance pling, and laboratory methods to determine
the biochemical and genetic makeup of the
5. Describe three patterns of chromosomal
fetus
breakage and rearrangement
6. Trace the events that occur during meiosis
and explain the events that lead to trisomy or
monosomy
SECTION II: ASSESSING YOUR
UNDERSTANDING
7. Describe the chromosomal and major clinical
characteristics of Down, Turner, and Klinefel- Activity A Fill in the blanks.
ter syndromes
1. defects, also known as birth de-
8. State the primary mechanism of altered body fects, are abnormalities of structure, function,
function in mitochondrial gene disorders and or metabolism that are present at birth.
relate it to the frequent involvement of
neural and muscular tissues 2. Genetic disorders are caused either by an
alteration in that disrupts the
9. Cite the most susceptible period of intrauter- single-gene sequence or
ine life for development of defects due to en- rearrangements.
vironmental agents

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32 UNIT 2 CELL FUNCTION AND GROWTH

3. Genes are expressed in an individual as domi- Activity B Consider the following figures.
nant, recessive, or pairs of
alleles. 1.

4. A gene is a biochemical event,

such as nucleotide change, deletion, or inser-
tion, that produces a new allele.
A
5. Genetic disorders arise in two ways:
from parents or Lost
due to an acquired mutation.
6. Someone who carries a gene responsible for a
disease but who does not manifest the disease
is said to be a . B

7. syndrome is an autosomal dom-

inant disorder of connective tissue.
8. X-linked inheritance patterns are predomi-
nantly .
C
9. Specific chromosomal abnormalities can be
linked to more than identifiable
syndromes. Pericentric Paracentric

10. Chromosomal disorders may take the form of

alterations in the of one or more
chromosomes or in an number D Lost
of chromosomes.
11. occurs when there are simulta-
neous breaks in two chromosomes from dif-
ferent pairs, with exchange of chromosome
parts. In the reciprocal type, there is no loss
of information. E

Fragments

In the figure, label the abnormality (deletion,

ring formation, isochromosomal translocation,
Robertsonian translocation, inversion, balanced
translocation).

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CHAPTER 7 GENETIC AND CONGENITAL DISORDERS 33

2. Activity D Briefly answer the following

questions.
1. Inheritance of a genetic disease depends on
the location of the mutation within the
karyotype. What are the potential methods
of inheritance? What will determine the like-
lihood of the offspring developing the dis-
ease? Does the sex of the offspring make any
difference?

Is this pedigree for an autosomal dominant, auto-

somal recessive, or sex-linked disease?

Activity C Match the key concepts in Column

A with their descriptions in Column B. 2. Multifactorial inheritance patterns involve
many different genes and their interactions
Column A Column B with the environment. Predicting such disor-
1. Single-gene a. Single set of chro- ders is difficult, but they do display several
disorders mosomes characteristics. Explain these characteristics.

2. Multifactorial b. Disorders are mani-

inheritance fested only when
both members of
3. Autosomal the gene pair are af-
dominant fected 3. Chromosomal abnormalities are among the most
disorder
c. Traits carried by common reasons for first trimester spontaneous
4. Haploid multiple genes and abortions as well as more than 60 different dis-
influenced by the eases. Structural changes are a common form of
5. Chromosomal
environment chromosomal abnormalities. Explain what a
abnormality
d. Outward expression structural change is and list the potential causes.
6. Autosomal of a gene
recessive
e. Affected parent has
7. Polymorphism a 50% chance of
transmitting the
8. Phenotype
disorder to each off-
4. Why are alterations in sex chromosomes better
9. Mutation spring
tolerated than alterations of autosomal chro-
10. Mitochondrial f. Follow a non- mosomes?
disorders Mendelian pattern
of inheritance
g. Trisomy
h. Disorders caused by
a defective or mu-
tant allele at a sin- 5. Mitochondrial genetic abnormalities are not
gle-gene locus transmitted via Mendelian genetics. In addi-
tion, they tend to affect the brain and muscle
i. Biochemical event
tissue. Explain why these two characteristics of
such as nucleotide
mtDNA inheritance are true.
change, deletion, or
insertion
j. Genes have more
than one normal al-
lele at the same
locus

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34 UNIT 2 CELL FUNCTION AND GROWTH

SECTION III: APPLYING YOUR 3. The parents of an infant boy ask the nurse
why their son was born with a cleft lip and
KNOWLEDGE palate. The nurse responds that cleft lip and
palate are defects that are caused by many
Activity E Consider the following scenario and
factors. The defect may also be caused by ter-
answer the questions.
atogens. Which teratogens can cause cleft lip
A 37-year-old woman is 2 months pregnant and and palate?
has a history of alcohol intake of one to two a. Mumps
drinks per day. She states, “My coworker told me
b. Pertussis
that drinking alcohol can harm my baby.”
c. Rubella
1. She asks you how having a drink or two every
d. Measles
day can harm her baby. What would you re-
spond? 4. Sometimes an individual that developed
from a single zygote is found to have two or
more kinds of genetically different cell pop-
ulations. These individuals are called what?
a. Mutants
b. Monosomies
2. Discuss the effects of fetal alcohol syndrome.
c. Aneuploidy
d. Mosaic
5. With increasing age, there is a greater chance
of a woman being exposed to damaging envi-
ronmental agents such as drugs, chemicals,
and radiation. These factors may act on the
SECTION IV: PRACTICING aging oocyte to cause what in a fetus?
FOR NCLEX a. Down syndrome
b. Marfan syndrome
Activity F Answer the following questions.
c. Patau syndrome
1. Chromosomes carry 46 genes, 23 from the d. Turner syndrome
mother and 23 from the father. These genes
are paired, and if both members of the gene 6. From 15 to 60 days after conception, the em-
pair are identical, the person is considered bryo is most susceptible to adverse influences.
homozygous. What is the person considered This period is referred to as what?
if both members of the gene pair are not a. Period of susceptibility
identical? b. Period of organogenesis
a. Heterozygous c. Period of fetal anomalies
b. Phenotypic d. Period of hormonal imbalance
c. Codominant 7. Teratogenic substances cause abnormalities
d. Mutant during embryonic and fetal development.
These substances are divided into three
2. An adolescent presents at the clinic with
classes. These classes are called what?
complaints of pedunculated lesions project-
ing from the skin on his trunk area. The nurse a. Period of organogenesis, third trimester,
knows that this is a sign of what? second month
a. Marfan syndrome b. Outside environmental substances, inside
environmental substances, internal envi-
b. Neurofibromatosis type 1
ronmental substances
c. Down syndrome
c. Radiation, drugs and chemical substances,
d. Klinefelter syndrome infectious agents
d. Drugs and chemical substances, smoking,
bacteria and viruses

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CHAPTER 7 GENETIC AND CONGENITAL DISORDERS 35

8. Infections with the TORCH agents are re- d. To allow parents at risk for having a child
ported to occur in 1% to 5% of newborn in- with a specific defect to begin a pregnancy
fants in the United States and are among the with the assurance that knowledge about the
major causes of neonatal morbidity and mor- presence or absence of the disorder in the
tality. Which of these are clinical and patho- fetus can be confirmed by testing and to pro-
logic manifestations of TORCH? vide information on where they can have
a. Microcephaly, hydrocephalus, spina bifida the pregnancy terminated if they so choose
b. Pneumonitis, myocarditis, macrocephaly 11. Match the genetic disorder (Column A) with
c. Hydrocephalus, macrocephaly, thrombocy- its kind of disorder (Column B).
topenia Column A Column B
d. Microcephaly, hydrocephalus, thrombocy-
1. Marfan a. Single-gene
topenia
syndrome disorder
9. The birth of a child with a defect brings with it
2. Huntington’s b. Autosomal domi-
two issues that must be resolved quickly. The
chorea nant
traumatized parents need emotional support
from the nurse and guidance in how to resolve 3. Tay-Sachs c. Autosomal reces-
these two issues. What are these issues? disease sive disorders
a. The immediate and future care of the af- 4. Fragile d. Sex-linked
fected child and the possibility of future chil- X syndrome disorders
dren in the family having a similar defect
b. The immediate and future care of the af- 12. Although multifactorial traits cannot be pre-
fected child and the possibility of the dicted with the same degree of accuracy as
child’s death the Mendelian single-gene mutations, charac-
teristic patterns exist. What are these charac-
c. The possibility of future children having a
teristic patterns? Mark all that apply.
similar defect and the possibility of this
child’s death a. Multifactorial congenital malformations
tend to involve a single organ or tissue de-
d. The need for financial resources and the
rived from the same embryonic develop-
possibility of this child’s death
mental field.
10. Genetic counseling and prenatal screening b. The risk of recurrence in future pregnan-
are tools both for the parents of a child with a cies is for the same or a similar defect.
defect and for those couples who want a child
c. The risk increases with increasing inci-
but are at high risk for having a child with a
dence of the defect among relatives.
genetic problem. What are the objectives of
prenatal screening? d. Multifactorial congenital malformations
are always present at birth.
a. To detect fetal abnormalities and to provide
information on where they can have the 13. is a rare metabolic disorder that
pregnancy terminated if they so choose affects approximately 1 in every 15,000 in-
b. To detect fetal abnormalities and to pro- fants in the United States. The disorder is
vide parents with information needed to caused by a deficiency of the liver enzyme
make an informed choice about having a phenylalanine hydroxylase. Without a special
child with an abnormality diet, these children will die.
c. To provide parents with information
needed to make an informed choice about
having a child with an abnormality and
to assure the prospective parents that any
defect in their hoped for child can be
identified

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36 UNIT 2 CELL FUNCTION AND GROWTH

14. After conception, development is influenced 15. The U.S. Food and Drug Administration
by the environmental factors that the embryo passed a law in 1983 classifying drugs accord-
shares with the mother. Some of these factors ing to their proven teratogenicity. Listed as
can act on the developing fetus and cause de- follows are the classes of drugs in random
fects. These factors include which of the fol- order. Put them in order according to their
lowing? Mark all that apply. teratogenicity.
a. Drugs a. Class X A. b, d, c, e, a
b. Weather B. a, b, c, d, e
b. Class A
c. Air pollution C. b, c, d, a, e
c. Class C
d. Radiation D. a, e, b, c, d
d. Class B
e. Class D

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CHAPTER
Neoplasia

SECTION I: LEARNING 13. State the importance of cancer stem cells, an-
giogenesis, and the cell microenvironment in
OBJECTIVES cancer growth and metastasis
1. Define neoplasm and explain how neoplastic 14. Explain how host factors such as heredity,
growth differs from the normal adaptive levels of endogenous hormones, and immune
changes seen in atrophy, hypertrophy, and system function increase the risk for develop-
hyperplasia ment of selected cancers
2. Distinguish between cell proliferation and 15. Relate the effects of environmental factors
differentiation such as chemical carcinogens, radiation,
and oncogenic viruses to the risk of cancer
3. Describe the phases of the cell cycle
development
4. Explain the function of cyclins, cyclin-
16. Identify concepts and hypotheses that may
dependent kinases, and cyclin-dependent
explain the processes by which normal cells
kinase inhibitors in terms of regulating the
are transformed into cancer cells by
cell cycle
carcinogens
5. Describe the properties of stem cells
17. Describe the many possible ways by which
6. Cite the method used for naming benign and cancer acts to disrupt organ function
malignant neoplasms
18. Characterize the mechanisms involved in the
7. State at least five ways in which benign and anorexia and cachexia, fatigue and sleep dis-
malignant neoplasms differ orders, anemia, and venous thrombosis expe-
rienced by patients with cancer
8. Relate the properties of cell differentiation to
the development of a cancer cell clone and 19. Define the term paraneoplastic syndrome and
the behavior of the tumor explain its pathogenesis and manifestations
9. Trace the pathway for hematologic spread of 20. Cite three characteristics of an ideal screening
a metastatic cancer cell test for cancer.
10. Use the concepts of growth fraction and dou- 21. Describe the four methods that are used in
bling time to explain the growth of cancerous the diagnosis of cancer
tissue
22. Differentiate between the methods used for
11. Describe various types of cancer-associated grading and staging of cancers.
genes and cancer-associated cellular and mol-
23. Explain the mechanism by which radiation
ecular pathways
exerts its beneficial effects in the treatment of
12. Describe genetic events and epigenetic factors cancer
that are important in tumorigenesis

37
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38 UNIT 2 CELL FUNCTION AND GROWTH

24. Describe the adverse effects of radiation and is uncoordinated with that of the normal
therapy tissues.
25. Differentiate between the action of direct 10. tumors do not usually cause
DNA-interacting and indirect DNA-interacting death unless the location interferes with the
chemotherapeutic agents and cell cycle– function of a vital organ.
specific and cell cycle–independent drugs
11. Malignant neoplasms are less well
26. Describe the three mechanisms whereby bio- and have the ability to break loose, enter the
therapy exerts its effects circulatory or lymphatic systems, and form sec-
ondary malignant tumors at other sites.
27. Describe three examples of targeted therapy
used in the treatment of cancer 12. Tumors are usually named by adding the suf-
fix to the parenchymal tissue
28. Cite the most common types of cancer affect-
type from which the growth originated.
ing infants, children, and adolescents
13. A is growth that projects from a
29. Describe how cancers that affect children dif-
mucosal surface.
fer from those that affect adults.
14. The term is used to designate a
30. Discuss possible long-term effects of radiation
malignant tumor of epithelial tissue origin.
therapy and chemotherapy on adult survivors
of childhood cancer 15. There are two categories of malignant neo-
plasms, and
cancers.
SECTION II: ASSESSING YOUR 16. The term is used to describe the
UNDERSTANDING loss of cell differentiation in cancerous tissue.
17. A characteristic of cancer cells is the ability to
Activity A Fill in the blanks. proliferate even in the absence of
1. Cancer is a disorder of altered cell .
and . 18. The complex acting with other
2. The process of cell division results in cellular proteins has been proposed to be involved
. with cell migration, apoptosis, and cell cycle
regulation.
3. is the process of specialization
whereby new cells acquire the structure and 19. The types of genes involved in cancer are nu-
function of the cells they replace. merous, with two main categories being the
, which control cell growth and
4. Proteins called control entry replication, and tumor genes,
and progression of cells through the cell which are growth-inhibiting regulatory genes.
cycle.
20. is the only known retrovirus to
5. Kinases are enzymes that cause cancer in humans.
proteins.
21. Tumor cells must double times
6. Continually renewing cell populations rely before a palpable mass is formed.
on cells of the same lineage that
have not yet differentiated to the extent that 22. A common manifestation of solid tumors is
they have lost their ability to divide. the cancer syndrome.

7. cells remain incompletely undif- 23. As cancers grow, they compress and erode
ferentiated throughout life. blood vessels, causing and
, along with frank bleeding and
8. stem cells are pluripotent cells sometimes hemorrhage.
derived from the inner cell mass of the blasto-
cyst stage of the embryo. 24. is a common side effect of many
cancers. It is related to blood loss, hemolysis,
9. The term refers to an abnormal impaired red cell production, or treatment
mass of tissue in which the growth exceeds effects.

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CHAPTER 8 NEOPLASIA 39

25. A tissue involves the removal of Activity C Match the key terms in Column A
a tissue specimen for microscopic study. with their definitions in Column B.
26. therapy uses high-energy parti- 1.
cles or waves to destroy or damage cancer
cells. Column A Column B
27. is a systemic treatment that en- 1. Malignant a. Defines the differentia-
ables drugs to reach the site of the tumor and mass tion potential of stem
other distant sites. cells
2. Cellular
potency b. Undefined or less differ-
entiated cellular mass
Activity B Consider the following figure. 3. Renewal
c. Mass of cells due to
4. Proliferation overgrowth
Carcinogenic Normal 5. Tumor- d. Process that removes
agent cell senescent and/or dam-
initiating
cells aged cells
e. Stem cells undergoing
6. Tumor numerous mitotic divi-
7. Apoptosis sions while maintain-
ing an undifferentiated
8. Benign state
mass
f. Cancer stem cells
9. Differen- g. Process of cell special-
tiation ization
10. Oncology h. Well-differentiated
mass of cells
i. Study of tumors and
their treatment
j. Process of cell division
2.
Column A Column B
Malignant 1. Protoonco- a. Loss of cell differentia-
neoplasm
gene tion
2. Growth b. Changes in gene ex-
fraction pression without DNA
1. In the flowchart, fill in the missing steps using mutation
3. Tumor
the following terms: DNA damage, alterations c. Variations in size and
suppressor
in genes that control apoptosis, unregulated cell shape of both the cell
gene
differentiation and growth, inactivation of tumor and the nucleus
suppressor genes, activation of growth-promoting 4. Genetic d. Normal gene that can
oncogenes, DNA repair, failure of DNA repair. instability cause cancer if mu-
5. Epigenetic tated
effects e. Promote cancer when
less active
6. Anaplasia
f. Ratio of dividing cells
7. Anchorage to resting cells
dependence g. Tumor suppressor gene
8. Doubling h. Marked by chromoso-
time mal aberrations

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40 UNIT 2 CELL FUNCTION AND GROWTH

9. Pleomor- i. Epithelial cells must 5. Explain how a diminished immune system

phism be anchored to ei- may play a role in carcinogenesis.
ther neighboring
10. p53
cells or the underly-
ing extracellular ma-
trix to live and grow
j. Time it takes for the
total mass of cells in 6. Chemical carcinogens act in two distinct
a tumor to double ways, what are they?

Activity D
1. Put the following terms for cellular potency in
order from the least differentiated to the most 7. Cachexia is marked by a hypermetabolic
differentiated. state. Give two reasons for this, and explain
the consequences.
a. Pluripotent
b. Totipotent
c. Unipotent
d. Multipotent

8. What is paraneoplastic syndrome?

Activity E Briefly answer the following

1. Not all cells in the body can reenter the cell
cycle, but some will do so continuously. In
terms of regeneration and differentiation, 9. List some of the common methods used for
which types of cells will or will not reenter diagnosing cancer.
the cell cycle?

10. Cancers are graded and staged on their char-

2. Compare and contrast benign tumors and acteristics in order to determine a treatment
malignant tumors. regimen. Explain the grading and staging sys-
tem and how it is met.

3. List the five factors used to describe benign

and malignant neoplasm.

SECTION III: APPLYING YOUR

KNOWLEDGE
Activity F Consider the following scenario and
4. Describe the process and routes of metastasis. answer the questions.
Eight-year-old Joe Cheapson has been diagnosed
with acute lymphocytic leukemia. His treatment
plan includes placement of an implanted central
venous catheter and multiple administrations of

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CHAPTER 8 NEOPLASIA 41

chemotherapy. Joe says, “NO! I don’t want to be 3. It is well known that cancer is not a single
stuck with needles all the time.” disease. Thus, it follows that cancer does not
have a single cause. It seems more likely that
1. What would you tell Joe to decrease his
the occurrence of cancer is triggered by the
anxiety?
interactions of multiple risk factors. What are
identified risk factors for cancer?
a. Body type, age, hereditary
b. Radiation, cancer-causing viruses, color of
skin
2. How would you explain the way chemother- c. Hormonal factors, chemicals, immunologic
apy works to Joe’s parents? mechanisms
d. Immunologic mechanisms, cancer-causing
viruses, color of skin
4. Several cancers have been identified as inheri-
table through an autosomal dominant gene.
Generally, people who inherit these genes are
only at increased risk for developing the can-
SECTION IV: PRACTICING FOR cer. There is one type of cancer, however, that
NCLEX is almost certain to develop in someone who
inherits the dominant gene. Which cancer
Activity G Answer the following questions. carries the highest risk of developing in some-
one who carries the gene?
1. The nurse has provided an educational ses-
a. Retinoblastoma
sion with a 56-year-old man, newly diag-
nosed with a benign tumor of the colon. The b. Osteosarcoma
nurse knows that the patient needs further c. Acute lymphocytic leukemia
teaching when he makes which remark? d. Colon cancer
a. “This tumor I have, will I die from it?”
5. One group of chemical carcinogens is called
b. “Even though benign tumors cannot stop indirect-reacting agents. Another term for
growing, they are not considered to be these agents is procarcinogens, which become
cancer.” active only after metabolic conversion. One
c. “Benign tumors still produce normal cells of the most potent procarcinogens is a group
different from other cells around them.” of dietary carcinogens called
d. “This kind of tumor cannot invade other a. Polycyclic aromatic hydrocarbons.
organs or travel to other places in the body b. Aflatoxins.
to start new tumors.”
c. Initiators.
2. The nurse on an oncology floor has just ad- d. Diethylstilbestrol.
mitted a patient with metastatic cancer. The
patient asks how cancer moves from one 6. In some cancers, the presenting factor is an
place in the body to another. What would the effusion, or fluid, in the pleural, pericardial,
nurse answer? or peritoneal space. Research has found that
almost 50% of undiagnosed effusions in peo-
a. “Cancer cells are not able to float around
ple not known to have cancer turn out to be
the original tumor in body fluids.”
malignant. Which cancers are often found be-
b. “Cancer cells enter the body’s lymph sys- cause of effusions?
tem and thereby spread to other parts of
a. Colon and rectal cancers
the body.”
b. Lung and ovarian cancers
c. “Cancer cells are moved from one place in
the body to another by transporter cells.” c. Breast and colon cancers
d. “Cancer cells replicate and form a chain d. Ovarian and rectal cancers
that spreads from the original tumor site to
the site of the metastatic lesion.”

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42 UNIT 2 CELL FUNCTION AND GROWTH

7. Tumor markers are used for screening, estab- 11. Cancer is a disorder of altered cell differentia-
lishing prognosis, monitoring treatment, and tion and growth. The term
detecting recurrent disease. Which serum refers to an abnormal mass of tissue in which
tumor markers have been proven to be the growth exceeds and is uncoordinated
among the most useful in clinical practice? with that of the normal tissues.
a. Prostate-specific antigen and deoxyribonu- 12. A woman diagnosed with breast cancer asks
cleic acid the nurse how a malignant tumor in her
b. Deoxyribonucleic acid and carcinoembry- breast could spread to other parts of her body.
onic antigen The nurse answers that a malignant neoplasm
c. Alpha-fetoprotein and human chorionic is comprised of less well-differentiated cells
gonadotropin that have which of the following abilities?
Mark all that apply.
d. Chorionic gonadotropin and cyclin-
dependent kinases a. They break loose.
b. They reinvade their original site.
8. Cranial radiation therapy (CRT) has been
used to treat brain tumors, acute lymphocytic c. They enter the circulatory or lymphatic
leukemia, head and neck soft tissue tumors, system.
and retinoblastoma in children. Childhood d. They are excreted through the alimentary
cancer survivors who had CRT as therapy for canal.
their cancers are prone to growth hormone e. They form secondary malignant tumors at
deficiency. In adults, with what is growth other sites.
hormone deficiency associated?
13. Cancer cells differ from normal cells in many
a. Hypocalcemia
ways. They have lost the ability to accurately
b. Cardiovascular longevity communicate with other cells, and they do
c. Hyperinsulinemia not have to be anchored to other cells to sur-
d. Dyslipidemia vive. How else are they different from other
cells? Mark all that apply.
9. A big difference in the treatment of child-
a. Cancer cells have an increased tendency to
hood cancer as opposed to adult cancer is
stick together.
that chemotherapy is the most widely used
treatment therapy for childhood cancer. b. Cancer cells have an unlimited life span.
What is the reason for this? c. Cancer cells have lost contact inhibition.
a. Pediatric tumors are more responsive to d. Cancer cells need increased amounts of
chemotherapy than adult cancers. growth factor to proliferate.
b. Children do not tolerate other forms of e. Cancer cells are genetically unstable.
therapy as well as adults do.
14. Match the following types of cancer with
c. Children do not complain about the nau- their screening tests.
sea and vomiting caused by chemotherapy
like adults do. Type of Cancer Screening Test
d. Children think losing their hair is “cool.” 1. Malignant a. Mammography
melanoma b. Self-examination
10. The inherent properties of a tumor that deter-
mine how the tumor responds to radiation is 2. Prostatic c. Pap smear
called radiosensitivity. When radiation is d. Prostate-specific
3. Cervical
combined with cytotoxic drugs, it has been antigen
noted that there is a radiosensitizing effect on 4. Breast
tumor cells. Which drug is considered a
radiosensitizer?
a. Doxorubicin
b. Cisplatin
c. Vincristine
d. Docetaxel

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CHAPTER 8 NEOPLASIA 43

15. Childhood cancers are often diagnosed late in a. Cardiomyopathy and pulmonary fibrosis
the disease process because the signs and b. Cognitive dysfunction and hormonal
symptoms mimic other childhood diseases. dysfunction
However, with the huge strides in treatment
c. Second malignancies and liver failure
methods, increasingly more children survive
childhood cancer. These survivors face the d. Impaired growth and second malignancies
uncertainty that the lifesaving treatment they
received during their childhood may produce
what late effects? Mark all that apply.

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9
CHAPTER

Stress and Adaptation

SECTION I: LEARNING SECTION II: ASSESSING YOUR

OBJECTIVES UNDERSTANDING
1. Cite Cannon’s four features of homeostasis Activity A Fill in the blanks.
2. Describe the components of a control system, 1. The ability of the body to function and main-
including the function of a negative feedback tain under conditions of change
system in the internal and external environments
depends on the thousands of
3. State Selye’s definition of stress
control systems that regulate body function.
4. Define stressor
2. is only achieved through a sys-
5. Cite two factors that influence the nature of tem of carefully coordinated physiologic
the stress response processes that oppose change.
6. Explain the interactions among components 3. Most control systems in the body operate by
of the nervous system in mediating the stress feedback mechanisms.
response
4. Selye described as a state mani-
7. Describe the stress responses of the autonomic fested by a specific syndrome of the body de-
nervous system, the endocrine system, the im- veloped in response to any stimuli that made
mune system, and the musculoskeletal system an intense systemic demand on it.
8. Explain the purpose of adaptation 5. Stress may contribute directly to the produc-
tion or exacerbation of a .
9. List at least six factors that influence a
person’s adaptive capacity 6. There is evidence that the axis,
the hormonal system, and the
10. Relate experience and previous learning to
nervous system are differentially
the process of adaptation
activated, depending on the type and inten-
11. Contrast anatomic and physiologic reserve sity of the stressor.
12. Propose a way by which social support may 7. Humans, because of their highly developed
serve to buffer challenges to adaptation nervous system and intellect, usually have
alternative mechanisms for and
13. Describe the physiologic and psychological
have the ability to control many aspects of
effects of a chronic stress response
their environment.
14. Describe the three states characteristic of
8. The means used to attain this balance are
post-traumatic stress disorder
called .
15. List five nonpharmacologic methods of
treating stress

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CHAPTER 9 STRESS AND ADAPTATION 45

9. is considered a restorative func- d. Stressor that pro-

tion in which energy is restored and tissues duces a response
are regenerated. e. Enhances stress-
10. is commonly used in excess and induced release of
can suppress the immune system. vasopressin from
the posterior pitu-
Activity B Consider the following figure. itary
f. Ability of body
systems to in-
crease their func-
tion given the
need to adapt
g. Regulation of
heart rate and va-
somotor tone
h. Suppresses os-
teoblast activity,
hematopoiesis,
and protein syn-
thesis
i. Stimulates the
adrenal gland to
synthesize and se-
1. In this figure, trace the activation of the hypo- crete the glucocor-
thalamus to the release of corticotrophin to the ticoid hormones
effect on the adrenal gland and to the final re- j. Increases water re-
lease of cortisol. Also, label the locus ceruleus. tention by the
kidneys and pro-
duces vasocon-
Activity C Match the key terms in Column A striction of blood
with their definitions in Column B. vessels
Column A Column B
Activity D Briefly answer the following.
1. Conditioning a. Personality char-
factors acteristic that in- 1. How does the body regulate and maintain
cludes a sense of homeostasis? Give one example.
2. Antidiuretic
having control
hormone
over the environ-
3. Baroreflex ment
4. Allostasis b. Factors used to cre-
ate a new balance
5. Physiologic 2. Describe the stages of general adaptation syn-
between a stressor
reserve drome.
and the ability to
6. Angiotensin II deal with it
c. Physiologic
7. Hardiness
changes in the
8. Cortisol neuroendocrine,
autonomic, and
9. ACTH
immune systems
10. Coping in response to real
mechanisms or perceived chal-
lenges to home-
ostasis

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46 UNIT 3 DISORDERS OF INTEGRATIVE FUNCTION

3. Stress will activate numerous body systems. SECTION IV: PRACTICING FOR
Many are based in neuroendocrine activity.
List the effects of neuroendocrine activation in
NCLEX
response to stress.
Activity F Answer the following questions.
1. The control systems of the body act in many
ways to maintain homeostasis. These control
systems regulate the functions of the cell and
integrate the functions of different organ sys-
4. Trained athletes use physiologic and anatomic tems. What else do they do?
reserves to achieve top-level performance. Ex- a. Control life processes
plain and give examples of how this is accom-
b. Feed cells under stress
plished.
c. Act on invading organisms
d. Shut down the body at death
2. It has long been known that our bodies need
a stable internal environment to function op-
5. What are the physiologic and anatomic causes
timally. What serves to fulfill this need?
of post-traumatic stress disorder? a. Organ systems
b. Control systems
c. Biochemical messenger systems
d. Neurovascular systems
3. The general adaptation syndrome is what
occurs in the body in response to stressors.
SECTION III: APPLYING YOUR When the body’s defenses are depleted, signs
KNOWLEDGE of “wear and tear” or systemic damage ap-
pear. Which diseases have been linked to
Activity E Consider the following scenario and stress and are believed to be encouraged by
answer the questions. the body itself when it can no longer adapt to
stress in a healthy manner?
Mr. Jones is a 33-year-old patient brought to the
emergency room by his brother. He presents with a. Psychotic disorders
a history of increased irritability, difficulty con- b. Osteogenesis sarcomas
centrating, an exaggerated startle reflex, and in- c. Rheumatic disorders
creased vigilance and concern over his safety. His d. Infections of the head and neck
brother tells the triage nurse, “Ever since he
moved here, he keeps asking why he lived and 4. A number of responses to the release of neu-
his family didn’t.” rohormones occur when the body encounters
stress, including which of the following?
1. What information should the nurse gather
when obtaining the health history of Mr. Jones? a. Increase in appetite
b. Decreased cerebral blood flow
c. Decrease in awareness
d. Inhibition of reproductive function

2. What nursing interventions are needed when

caring for Mr. Jones?

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CHAPTER 9 STRESS AND ADAPTATION 47

5. Chronic and excessive activation of the stress 9. The acute stress response can be detrimental
response has been shown to play a part in the in people with preexisting physical or mental
development of long-term health problems. health problems. In which of these clients
The stress response can also result from could the acute stress response cause further
chronic illness. Which health problems have problems?
been linked to a stress response that is a. Client who is post resection of a brain
chronic and excessive? tumor
a. Suicide and immune disorders b. Client who is schizophrenic and off
b. Depression and renal disease medication
c. Immune disorders and brain tumors c. Client with a broken femur
d. Suicide and thrombosis in the extremities d. Client with heart disease
6. Our body’s response to psychologic perceived 10. Some clients experience chronic activation of
threats is not regulated to the same degree as the stress response as a result of severe
our body’s response to physiologic perceived trauma. Which of the following is the disor-
threats. The psychologic responses may be der that can occur when the stress response is
a. appropriate and limited. chronically activated?
b. inappropriate and sustained. a. Post-traumatic stress disorder
c. regulated by a positive feedback system. b. Chronic renal insufficiency
d. the result of a baroreflex-mediated response. c. Schizophrenia
d. Post delivery depression
7. Adaptation implies that an individual has
successfully created a new balance between 11. In a organism, it is necessary for
the stressor and the ability to deal with it. the composition of the internal environment
The safety margin for adaptation of most to be compatible with the survival needs of
body systems is considerably greater than the individual cells.
that needed for normal activities. What is the
12. Selye suggested that stress could have positive
method of adaptation that allows the body to
influences on the body, and these periods of
live with only one of a pair of organs (i.e.,
positive stress are called .
one lung or one kidney)?
a. Genetic endowment 13. The first goal of treatment of stress disorders
is to aid clients in avoiding those coping
b. Physiologic reserve
mechanisms that cause their health to be at
c. Anatomic reserve risk. Second, the treatment of stress disorders
d. Health status should engage them in alternative strategies
that reduce stress. Which are nonpharmaco-
8. Psychosocial factors can impact the body’s
logic treatments of stress disorders? Mark all
response to stress either positively or nega-
that apply.
tively. It has been shown that social networks
play a part in the psychosocial and physical a. Lithium therapy
integrity of a person. How do social networks b. Music therapy
affect how the body deals with stress? c. Education therapy
a. By stepping in and making decisions for d. Massage therapy
the person
b. By reapportioning the finances of the
person
c. By mobilizing the resources of the person
d. By protecting the person from other inter-
nal stressors

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48 UNIT 3 DISORDERS OF INTEGRATIVE FUNCTION

14. Match the following terms with their 15. It is believed that there is an interaction
definitions. between the neuroendocrine system and the
immune system. It has been postulated that
Term Definition
these interactions play a significant role in
1. Corticotropin- a. Increased corti- autoimmune diseases. These systems have
releasing costeroid pro- what in common? Mark all that apply.
factor duction and a. They share common signal pathways.
atrophy of the
2. Fight-or-flight b. Hormones and neuropeptides can change
thymus
response what immune cells do.
b. Endocrine regu-
3. Allostatic c. Mediators of the immune system can
lator of pituitary
load modify neuroendocrine function.
and adrenal ac-
tivity and neu- d. They are symbiotic systems and cannot
4. Endocrine-
rotransmitter work without each other.
immune
interactions involved in au-
tonomic ner-
vous system
activity, metab-
olism, and
behavior
c. Physiologic
changes in the
neuroendocrine,
autonomic, and
immune sys-
tems occurring
in response to
real or perceived
challenges to
homeostasis
d. Most rapid of
the stress re-
sponses, repre-
senting the basic
survival re-
sponse

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10

CHAPTER
Alterations in
Temperature Regulation

SECTION I: LEARNING 12. Compare the mechanisms of malignant

hyperthermia and neuroleptic malignant
OBJECTIVES syndrome
1. Differentiate between body core temperature 13. Define hypothermia
and skin temperature and relate the differ-
14. Compare the manifestations of mild, moder-
ences to methods used for measuring body
ate, and severe hypothermia and relate them
temperature
to changes in physiologic functioning that
2. Describe the physiologic mechanisms that occur with decreased body temperature
control the gain and loss of heat from the
15. Describe the causes of heat loss and hy-
body
pothermia in the newborn infant and patient
3. Define the terms conduction, radiation, convec- undergoing surgery
tion, and evaporation, and relate them to the
mechanisms for gain and loss of heat from
the body
SECTION II: ASSESSING YOUR
4. Characterize the physiology of fever UNDERSTANDING
5. Describe the four stages of fever
Activity A Fill in the blanks.
6. Explain what is meant by intermittent, remit-
tent, sustained, and relapsing fevers 1. Core body temperature is normally main-
tained within a range of C.
7. State the relation between body temperature
and heart rate 2. Core body and skin temperatures are sensed
and integrated by thermoregulatory regions
8. Differentiate between the physiologic mecha- within the .
nisms involved in fever and hyperthermia
3. is the body’s main source of
9. State the definition of fever of unknown heat production.
source in children 0 to 36 months of age
4. Contraction of the muscles of
10. State the definition for fever in the elderly the skin, which raises skin hairs and produces
and cite possible mechanisms for altered goose bumps, also aids in heat conservation
febrile response in the elderly by reducing the surface area available for heat
11. Compare the characteristics of fevers caused loss.
by infectious agents and drug-related fevers

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50 UNIT 3 DISORDERS OF INTEGRATIVE FUNCTION

5. It has been shown that small elevations in 17. Systemic may result from expo-
temperature, such as those that occur with sure to prolonged cold.
, enhance immune function.
18. General agents lower the meta-
6. PGE2 binds to receptors in the hypothalamus bolic rate and decrease vasoconstriction and
to induce changes in its set-point via the sec- shivering thresholds, putting the patient at
ond messenger . greater risk for .
7. PGE2 that is produced by the 19. A gradual decline in and
cells is believed to cause an immediate rise in occurs as hypothermia
temperature. progresses.
8. A fever that has its origin in the central ner-
Activity B Consider the following figure and
vous system is sometimes referred to as a
answer the questions.
.
9. An is one in which temperature
returns to normal at least once every 24
˚F ˚C
114
hours.
44
110
10. A 1C rise in temperature produces a
beats/minute increase in heart 42
rate. 106
40
11. The syndrome, which is charac- 102
terized by periodic fever, aphthous, pharyngi- 38
tis, and cervical adenopathy occurring every 98
21 to 28 days, is the most common cause of 36
recurrent fevers in children younger than 94
34
5 years.
90 32
12. work at the hypothalamus, pre-
sumably by blocking the activity of cyclooxy-
genase, an enzyme that is required for the 86 30
conversion of arachidonic acid to
82 28
.
13. Slight elevations in temperature in 26
78
patients should be considered
24
significant. 74
14. describes an increase in body
temperature that occurs without a change in 1. On the temperature strip in the figure, mark
the set-point of the hypothalamic thermoreg- the following temperature points or ranges:
ulatory center. a. Where thermoregulation is lost
15. The is the temperature that the b. Where thermoregulation is impaired
body senses when both temperature and hu- c. Where normal temperature is located
midity are combined.
d. Where regulation is impaired by fever
16. Heat exhaustion is related to a gradual loss e. Threshold for the upper limits of survival
of and , usually
after prolonged and heavy exertion in a hot
environment.

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CHAPTER 10 ALTERATIONS IN TEMPERATURE REGULATION 51

Activity C Match the key terms in Column A Activity D Put the stages of a fever in the
with their definitions in Column B. proper order:

Column A Column B a. Defervescence

b. Prodrome
1. Convection a. Shift metabolism
to heat production c. Flush
2. Radiation
b. Water that diffuses d. Chill
3. Subcutaneous through the skin
tissues independent of
4. Shivering sweating
c. Point held by hy- Activity E Briefly answer the following.
5. Thyroid
pothalamus relat-
hormone 1. Blood flow changes in order to maintain core
ing to normal
6. Insensible body temperature body temperature. Explain how these changes
perspiration occur in hot and cold environments.
d. Initiated by im-
7. Arteriovenous pulses from the
shunts hypothalamus,
can produce a
8. Set-point three- to fivefold
9. Conduction increase in body 2. Describe the symptoms associated with each
temperature. stage of a fever.
10. Evaporation
e. Transfer of heat
through air
f. Insulate the core
from swings in en-
vironmental tem-
perature 3. Why do children experience fevers more
g. Heat transfer commonly?
through the circu-
lation of air cur-
rents
h. Use of body heat
to convert water 4. List and explain the possible causes of hyper-
on the skin to thermia.
water vapor
i. Allow blood to
move directly
from the arterial
to the venous sys-
tem to rapidly de- 5. What are the possible mechanisms of fever
crease heat produced by drugs?
j. Direct transfer of
heat from one
molecule to an-
other

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52 UNIT 3 DISORDERS OF INTEGRATIVE FUNCTION

6. List and describe the conditions that con- c. Hot and cold
tribute to hypothermia. d. Unpleasant and pleasant
2. Fever and hyperthermia describe conditions
in which body temperature is higher than the
normal range. When does hyperthermia
occur?
7. Explain the mechanisms and steps of rewarm- a. When the body temperature is 39.5°C
ing a hypothermic patient. b. When the body’s set-point is unchanged,
but the temperature goes up
c. When the body’s set-point changes to a
higher set-point
d. When body temperature is greater than
37.6C

SECTION III: APPLYING YOUR 3. Pyrogens are substances that produce fever in
the body. Substances such as bacterial prod-
KNOWLEDGE ucts, bacterial toxins, or whole microorgan-
isms enter the body and stimulate the host
Activity F Consider the following scenario and
cells to produce certain mediators. What are
answer the questions.
these called?
George Collins, 79 years old, is brought to the a. Exogenous pyrogens
clinic by his son. He presents with a history of
b. Outer pyrogens
fever and cough. His son states, “I am really wor-
ried about my father; he’s not eating well, and c. Endogenous pyrogens
sometimes he coughs so hard he can’t get his d. Set-point pyrogens
breath.”
4. Neurogenic fevers begin in the central ner-
1. What information should the nurse gather vous system. By what characteristics are neu-
when obtaining the health history of Mr. rogenic fevers known?
Collins? a. High temperatures that respond quickly to
antipyretic therapy
b. Temperatures that go up and down for no
apparent reason
c. Variable temperatures that are associated
2. What physical examination should the nurse with sweating
perform? d. High temperatures that are not associated
with sweating
5. The term submersion hypothermia is used when
cooling follows acute asphyxia, as occurs in
cases of near-drowning. Children have been
reported to survive after being submerged
from 10 to 40 minutes. This situation is be-
SECTION IV: PRACTICING lieved to be possible because of the rapid
FOR NCLEX cooling process following a particular reflex.
What is the name of that reflex?
Activity G Answer the following questions. a. Diving reflex
1. There are two types of stimuli that affect the b. Moro reflex
raising or lowering of body temperature. c. Bainbridge reflex
What are these stimuli? d. Oculocephalic reflex
a. Innocuous and noxious
b. Strong and weak

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CHAPTER 10 ALTERATIONS IN TEMPERATURE REGULATION 53

6. Most febrile illnesses are due to common in- 10. The pathophysiology of heat stroke is be-
fections and are relatively easy to diagnose. lieved to result from the direct effect of heat
In certain instances, however, it is difficult to on body cells and the release of cytokines
establish the cause of a fever. In these in- (e.g., interleukins, tumor necrosis factor, in-
stances, the elevation in temperature is re- terferon) from heat-stressed endothelial cells,
ferred to as a fever of unknown origin (FUO). leukocytes, and epithelial cells that protect
What is a common cause of FUO? against tissue injury. Which of the following
a. Disseminated intravascular coagulation conditions cannot be caused by heat stroke?
b. Malignancies a. Disseminated intravascular clotting and
acute renal failure
c. Pulmonary emboli
b. Acute respiratory distress and
d. Femoral artery emboli
rhabdomyoma
7. Sometimes recurrent fevers occur but do not c. Rhabdomyolysis and multiorgan failure
follow a strictly periodic pattern. Causes of
d. Disseminated intravascular clotting and
these recurrent fevers include genetic disor-
multiorgan failure
ders such as familial Mediterranean fever.
What are the characteristics of familial 11. Drug fever is a fever that can occur with the
Mediterranean fever? administration of a specific drug, and then
a. Early age of onset (20 years) and seizures disappear when the drug is discontinued.
Which of the following is a way that drugs
b. Episodic bouts of peritonitis and duration
can induce fever? Mark all that apply.
of 1 week
a. Drugs can cause heat dissipation.
c. Early age of onset (20 years) and high
fever b. Drugs can act as direct pyrogens.
d. Episodic bouts of peritonitis and low fever c. Drugs can induce an autoimmune
response.
8. Antipyretic drugs, such as aspirin, ibuprofen,
d. Drugs can injure tissues directly.
and acetaminophen, are often used to allevi-
ate the discomforts of fever and protect vul- 12. A sign that the body is losing heat occurs
nerable organs, such as the brain, from with the contraction of the ______ muscles of
extreme elevations in body temperature. The the skin. This raises skin hairs and produces
use of aspirin is limited in children, however, goose bumps; it also aids in heat conservation
because it can sometimes cause which of the by reducing the surface area available for heat
following diseases? loss.
a. Münchhausen syndrome 13. The four successive stages of fever are listed in
b. Guillain-Barré syndrome random order as follows. Choose the answer
c. Angelman syndrome that places them in correct order.
d. Reye syndrome a. Prodromal A. c,d,a,b
9. Fever in infants and young children is not an b. Defervescence B. a,b,c,d
uncommon event. Many trips to the pediatri- C. dcab
c. Chill
cian’s office occur because of fever in children D. a,c,d,b
ages 1 day to 3 years. Which sign or symptom d. Flush
does not indicate fever in an infant?
a. Avid feeding
b. Hypoventilation
c. Cyanosis
d. Poor tissue oxygenation

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54 UNIT 3 DISORDERS OF INTEGRATIVE FUNCTION

14. Diagnosing the primary cause is one of sev- 15. Malignant hyperthermia is a disorder in
eral methods used to treat fever. What are which the body’s core temperature can rise by
some other methods? Mark all that apply. 1C every 5 minutes. Although it is often
a. Modification of external environment to caused by a halogenated anesthetic agent in
decrease heat transfer to external environ- combination with succinylcholine, there are
ment also nonoperative precipitating factors. What
nonoperative factors can precipitate malig-
b. Support of hypermetabolic state that ac-
nant hyperthermia? Mark all that apply.
companies fever
a. Trauma
c. Protection of vulnerable body organs and
systems b. Exercise
d. Modification of internal environment to c. Infection
decrease heat transfer to external environ- d. Environmental heat stress
ment

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11

CHAPTER
Activity Tolerance
and Fatigue

SECTION I: LEARNING 12. Describe the time course events of the physio-
logic changes associated with immobility and
OBJECTIVES prolonged bed rest.
1. Differentiate among aerobic, isometric, and 13. Identify physical assessment findings that are
flexibility exercises related to the effects of immobility and pro-
longed bed rest
2. Describe the physiologic and psychological
responses to exercise 14. Describe treatment interventions that coun-
teract the negative effects of immobility and
3. Define the term maximal oxygen consumption
prolonged bed rest
and state how it is measured
4. Describe methods that can be used to assess a
person’s activity tolerance and ability to en-
gage in an exercise program
SECTION II: ASSESSING YOUR
UNDERSTANDING
5. Describe the physiologic effects of exercise in
the elderly population Activity A Fill in the blanks.
6. Define fatigue and describe its manifestations 1. is defined as the process of en-
7. Differentiate acute from chronic fatigue ergy expenditure for the purpose of accom-
plishing an effect.
8. List at least four health problems that are as-
sociated with chronic fatigue 2. exercise involves the body’s
ability to transport use of oxygen for energy
9. Define chronic fatigue syndrome and describe during prolonged strenuous exercise.
assessment findings, presenting symptoms,
and laboratory values associated with the 3. Although training has long
disorder been accepted as a means of developing
strength and muscle mass, its beneficial rela-
10. Discuss treatment modalities for chronic fa- tionship to health factors and chronic dis-
tigue syndrome eases has only recently been recognized.
11. Describe the effects of immobility and pro- 4. is determined by the rate at
longed bed rest on cardiovascular, pul- which oxygen is delivered to the working
monary, renal, metabolic, musculoskeletal, muscles.
gastrointestinal, and sensory function.

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56 UNIT 3 DISORDERS OF INTEGRATIVE FUNCTION

5. Exercise produces an increase in heart rate 19. The development of is the third
and stroke volume, which in turn increases major complication of bed rest.
.
20. Adverse effects of prolonged immobility and
6. An increase in venous return stimulates right bed rest include a decreased , or-
atrial stretch receptors, which stimulate the thostatic intolerance, dehydration, and sensory
response and increase cardiac deprivation, as well as the potential for devel-
output. opment of thrombophlebitis, ,
, and pressure ulcers.
7. is defined as the ability of mus-
cle groups to produce force against resistance.
Activity B Match the key concepts in Column
8. fibers are larger and better A with their definitions in Column B.
suited for high-intensity work, but they fa-
Column A Column B
tigue more easily.
1. Phospho- a. Common side effect
9. Persons with congestive heart failure typically
creatine of disease state
experience symptoms of breathlessness, exer-
tional fatigue, and exercise intolerance result- 2. Iometric b. Effect of epinephrine
ing in of skeletal muscles. exercise during exercise to in-
crease blood vessel
10. The enzyme catalyzes the trans- 3. Venous health
fer of the high-energy phosphate groups from distention
c. Loss of body heat by
ATP to creatine-forming creatine phosphate
4. Increased evaporation
and ADP.
fibrinolysis d. Multiples of the basal
11. During intense physical activity, blood flow is metabolic rate
5. Sweating
shunted away from the toward
e. Complication of bed
the active skeletal muscles. 6. Chronic
rest
fatigue
12. Strenuous exercise also lowers the production f. Originally designed
of the nonessential amino acid , 7. Human for patients with
which serves as an energy source for lympho- Activity chronic obstructive
cytes and macrophages. Profile pulmonary disease
13. Elevation in body temperature, cytokine re- 8. Metabolic g. Sustained muscle con-
lease, and increased levels of various equivalents traction is generated
hormones may result in a tem- against an immovable
9. Acute fatigue
porary depression of the body’s innate im- load with no change
mune defenses during intense exercise. 10. Ergometry in length
14. Current evidence supports a 5% to 15% h. Procedure for deter-
· mining physical per-
per decade in VO2max in men
and women beginning at age 25 years. formance capacity
i. May serve as a protec-
15. Activity can be viewed as not
tive function
having sufficient physical or psychological
energy reserve to endure or complete required j. High-energy phos-
or desired daily activities. phate bonds and is
unique to muscle
16. The physiologic basis of fibers
includes factors such as diaphragmatic,
motor, or neurologic mechanisms.
17. fatigue has a rapid onset and is
quickly relieved on cessation of activity.
18. Once believed to increase the restorative
process, prolonged has now
shown to hinder healing.

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CHAPTER 11 ACTIVITY TOLERANCE AND FATIGUE 57

Activity C Briefly answer the following. SECTION III: APPLYING YOUR

1. What are the physiologic and psychological KNOWLEDGE
benefits of exercise?
Activity D Consider the following scenario
and answer the questions.
James Whitlow, a 75-year-old marathon runner,
has suffered a fractured hip in a fall. Postopera-
tively, Mr. Whitlow sustains complications, in-
2. How does exercise increase the functional cluding a myocardial infarction and a pulmonary
state of blood vessels? embolus. He is on bed rest at this time.
1. What is the recommended approach to this
patient’s care? What does it include?

3. As we age, our ability to perform declines. Ex-

plain the role of skeletal muscle degeneration
in this age-related decline.
2. Because bed rest affects all systems in the
body, what are the concerns of Mr. Whitlow’s
caregiver?

4. Compare and contrast acute and chronic fa-

tigue.

SECTION IV: PRACTICING

FOR NCLEX
5. The diagnosis of chronic fatigue syndrome
Activity E Answer the following questions.
(CFS), a debilitating condition faced by many
adults, is on the rise. Explain the pathophysi- 1. There are two types of muscle fibers in skele-
ology of CFS and why there are no definitive tal muscle. Which type of muscle fiber is af-
treatments. fected most by prolonged immobility or bed
rest?
a. Long muscle fibers
b. Fast-twitch muscle fibers
c. Short muscle fibers
6. What are the mechanisms of orthostatic hy- d. Slow-twitch muscle fibers
potension following bed rest?
2. People with congestive heart failure need to
be on a closely monitored exercise regimen.
What is the reason for this?
a. Fast-twitch muscle fibers are used more
than slow-twitch muscle fibers.
b. Decreased fatigability is caused by early de-
pendence on anaerobic metabolism and
excessive intramuscular acidification.

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58 UNIT 3 DISORDERS OF INTEGRATIVE FUNCTION

c. Anaerobic metabolism, coupled with vaso- 6. Many types of fatigue are reported by clients
constrictor response, can cause an in- with a wide variety of disease disorders. What
creased afterload on the heart. is an identified cause of fatigue in clients with
d. Anaerobic metabolism inhibits the vaso- forced immobility, neuromuscular disorders,
constrictor response and decreases after- and wasting syndromes?
load on the heart. a. Insomnia caused by nocturia and pain
3. A treatment plan for people with peripheral b. Interference with the oxygen-carrying ca-
vascular disease has been proposed. Which of pacity of the blood
the following should it include? c. Loss of muscle mass, muscle strength, and
a. Weight training to strengthen the vastus endurance
lateralis d. Pain related to extended immobility
b. Isometric exercise to increase cardiac en- 7. Bed rest causes deconditioning responses to
durance occur that affect all body systems. What is
c. Aerobic exercise to decrease respiratory one important factor to remember when deal-
stress ing with the inactivity of immobility?
d. Exercise training to increase angiogenesis a. These responses occur slowly and can be
quickly overcome.
4. The sweat produced by both a trained person
and a nontrained person normally contains b. These responses can be stopped by fre-
sodium chloride in large amounts. What hap- quent turning and repositioning.
pens when sweat is produced in a trained per- c. These responses occur rapidly and can be
son? quickly overcome.
a. Sweat production begins before the core d. These responses occur rapidly and take a
temperature rises, and the sweat produced long time to overcome.
is dilute and conserves sodium chloride.
8. Disuse of a muscle and muscle atrophy con-
b. Sweat is produced within 5 to 6 minutes of tribute to the weakening and wasting of mus-
the start of exercise, and the sweat, being cle tissue. What else do they contribute to?
high in sodium chloride, depletes the body
a. Joint contractures
of sodium chloride.
b. Gastrointestinal hyperactivity
c. Sweat is produced within 1 to 2 minutes of
the start of exercise, and the sweat, being c. Venous hyperresponsiveness
high in sodium chloride, depletes the body d. Neural decompensation
of sodium chloride.
9. Chronic fatigue syndrome (CFS) is a disease
d. Sweat production begins after the core with an unknown etiology and no definitive
temperature rises, and the sweat, being treatments. Even the diagnosis of CFS is diffi-
high in sodium chloride, depletes the body cult because the diagnostic criteria are many
of sodium chloride. and require concurrent occurrence of specific
5. Elderly people sometimes have decreased car- symptoms. What is a concurrent symptom
diac output. What is believed to be the cause needed for the clinical diagnosis of CFS?
of this condition? a. Multijoint pain with swelling or redness
a. Natural decrease in the load the respiratory b. Muscle pain
system can handle as a person ages c. Long periods of refreshing sleep
b. Natural decrease in the maximal heart rate d. Malaise lasting more than 24 hours unre-
as a person ages lated to exertion
c. Natural occurrence of increased resistance
in the major blood vessels as a person ages
d. Natural destruction in peripheral blood
vessels as a person ages

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CHAPTER 11 ACTIVITY TOLERANCE AND FATIGUE 59

10. All systems in the body are affected by bed 13. There are several ways of assessing activity
rest or immobility. For the immune system, tolerance and fatigue. One of these is a proce-
research has demonstrated that interleukin dure for determining physical performance
(IL)-1, IL-6, and tumor necrosis factor-alpha capacity called .
are increased during immobility or bed rest.
14. What are the major complications of bed
What are these mediators associated with?
rest? Mark all that apply.
a. Hyperresponsiveness in the central ner-
a. Venous stasis with the potential for devel-
vous system
opment of deep venous thrombosis
b. Reduction in inflammatory reactions and
b. Redistribution and change in blood vol-
bone wasting
ume
c. Hyperinflammatory reactions and tissue
c. Increased cardiac workload
injury
d. Increased intestinal function and diarrhea
d. Tissue wasting and decreasing bone density
e. Orthostatic hypotension
11. There are two main types of exercise. Aerobic
exercise involves rhythmic changes in large 15. There is a direct proportional response be-
muscle groups. Isometric, or , ex- tween bone density and the stress placed on
ercise involves a sustained muscle contraction them according to law.
against an immovable load.
12. During exercise, the respiratory system in-
creases the rate of exchange of oxygen and
carbon dioxide. This is caused by a series of
physiologic responses. Listed as follows in ran-
dom order are the physiologic responses caus-
ing the increased rate of exchange of oxygen
and carbon dioxide. Choose the answer that
puts these responses in order of occurrence.
a. Larger volume of blood under increased
pressure is delivered to the lungs.
b. Respiratory rate increases four- to fivefold.
c. Cardiac output increases.
d. More pulmonary capillary beds open.
e. Tidal volume increases five- to sevenfold.
f. Minute ventilation increases 20 to 30 times
its resting value.
g. Better perfusion of the alveoli occur.
h. Oxygen and carbon dioxide exchange
more efficiently.
A. a, e, f, g, d, c, b, h
B. g, h, a, b, d, f, e, c
C. b, e, f, c, a, d, g, h
D. d, a, g, b, e, f, c, h

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12
CHAPTER

Blood Cells and the

Hematopoietic System

SECTION I: LEARNING 4. is the most abundant of the

plasma proteins.
OBJECTIVES
5. The blood cells are not all true ,
1. Describe the composition and functions of hence the term “formed elements.”
plasma
6. Red blood cells contain the protein
2. Name the formed elements of blood and cite , which is used to transport
their function and life span oxygen.
3. Trace the process of hematopoiesis from stem 7. facilitates the formation of car-
cell to mature blood cell bonic acid from carbon dioxide and water,
which, in turn, dissociates into bicarbonate
4. Cite information gained from a complete
and hydrogen ions.
blood count
8. Leukocytes have granules that contain
5. State the purpose of the erythrocyte sedimen-
degradative enzymes known as .
tation rate
9. contain complement activators,
6. Describe the procedure used in bone marrow
bactericidal agents, peroxidases, and other
aspiration
hydrolytic enzymes.
10. In parasitic infections, the use
surface markers to attach themselves to the
SECTION II: ASSESSING YOUR parasite and then release hydrolytic enzymes
UNDERSTANDING that kill it.

Activity A Fill in the blanks. 11. The function of lymphocytes in the lymph
nodes or spleen is to defend against microor-
1. The percentage of packed red blood cells in a ganisms through the response.
given volume of blood is known as the 12. The T lymphocytes differentiate in the
. .
2. Plasma, being a liquid, is water 13. The , precursors of the mononu-
by weight, proteins by weight, clear phagocyte system, are often referred to
and other small molecular sub- as when they enter the tissues.
stances.
14. Thrombocytes are circulating cell fragments
3. The produces plasma proteins. of the large that are derived
from the myeloid stem cell.
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CHAPTER 12 BLOOD CELLS AND THE HEMATOPOIETIC SYSTEM 61

15. Under normal conditions, the numbers and h. Contain heparin

total mass for each type of circulating blood i. Last 8–9 days in
cell remain relatively . circulation
j. Stem cell line for
Activity B Consider the following figure.
granulocytes, ery-
throcytes, and
megakaryocytes

Activity D Put the following stem cells in

order from least differentiated (left) to fully
committed cells (right).
a. Macrophage
b. Monoblast
c. Pluripotent stem cell
d. Myeloid stem cell
e. Monocyte colony-forming units

Activity E Briefly answer the following:

1. Explain the importance of stem cells and how
they contribute to hematopoietic homeostasis.

In the test tube, label the layers as they separate

out of whole blood.
• Plasma 2. Erythropoiesis is regulated by special receptors
• Formed elements in the kidney. Explain how this relates to en-
• Erythrocytes durance athletes training at high elevation.
• Buffy coat

Activity C Match the key terms in Column A

with their definitions in Column B.
Column A Column B
1. Erythrocytes a. Increase during aller-
2. Leukocytes
gic reactions SECTION III: APPLYING YOUR
b. Include granulocytes, KNOWLEDGE
3. Lymphoid lymphocytes, and
4. Neutrophils monocytes Activity F Consider the following scenario
c. Stem cell line of im- and answer the question.
5. Eosinophils
mune cells Sally Moore, 12 years old, is scheduled to have a
6. Basophils d. Immune cells bone marrow transplant to treat her acute lym-
7. Lymphocytes e. Largest white blood phoid leukemia. The nurse explains to Sally that,
cell after she has the transplant, she will get a transfu-
8. Monocytes
f. Most numerous of sion of blood that has been specially treated with
9. Thrombocytes formed elements something called growth factors.
10. Myeloid g. Nuclei in three to
five lobes

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62 UNIT 4 DISORDERS OF THE HEMATOPOIETIC SYSTEM

1. Sally asks the nurse why she has to have 5. Some cytokines stimulate the growth and pro-
growth factors in the blood. How does the duction of new blood cells. Other cytokines
nurse answer Sally? support the proliferation of stem cells in the
human body. Which cytokines support the
proliferation of stem cells in the human body?
a. Interleukins, interferons, and tumor necro-
sis factor
b. Granulocytes, B-cell growth factor, and
interferons
SECTION IV: PRACTICING c. Interleukins, T-cell growth factor, and
colony-stimulating factors
FOR NCLEX
d. Transforming growth factor, interferons,
Activity G Answer the following questions. and tumor necrosis factor

1. The globulins that make up part of the 6. The erythrocyte sedimentation rate is a com-
plasma of the blood have three distinct pur- monly performed blood test used for monitor-
poses. What are the gamma globulins? ing the clinical course of a disease. It is a
measurement of how rapidly red blood cells
a. Antibodies of the immune system
will aggregate and drop to the bottom of a tube
b. Transporters of iron and copper as a sediment in anticoagulated blood. What
c. Transporters of bilirubin and steroids influences the rate of fall that would give infor-
d. Autoantibodies of the immune system mation about the clinical course of a disease?
a. The rate of fall is faster in the presence of
2. What are the biconcave disks in the blood
cytokines that are increased in an inflam-
that carry oxygen?
matory disease.
a. Neutrophils
b. The rate of fall is faster in the presence of
b. Erythrocytes fibrinogen that is increased in an inflam-
c. Eosinophils matory disease.
d. Leukocytes c. The rate of fall is faster in the presence of
macrophages that are increased in an in-
3. Pluripotent stem cells for an invaluable
flammatory disease.
source of reserve cells for the entire
hematopoietic system. Between these cells d. The rate of fall is faster in the presence of
and the unipotential cells are several levels of growth factors that are increased in an in-
differentiation. What are these unipotential flammatory disease.
cells called? 7. Although the usual site for a bone marrow
a. Embryonic stem cells test is the posterior iliac crest, other sites in-
b. Immature neural cells clude the anterior iliac crest and the sternum.
What are the dangers of using the sternum
c. Colony-forming units
for a bone marrow test in children?
d. Blood cell precursors
a. Potential for hemorrhage
4. Stem cell transplantation has been shown to b. Danger of perforating the lungs
provide potential cures for diseases such as
c. Danger of perforating the mediastinum
aplastic anemia and the leukemias. What are
the sources of stem cells used for transplant? d. Potential for infection in the chest cavity
a. Peripheral blood cells and immature em- 8. Normally, there is a relatively constant number
bryonic cells of each type of circulating blood cell. What reg-
b. Bone marrow and immature neural cells ulates the number of each type of blood cell?
c. Umbilical cord blood and yellow bone a. Immune system
marrow b. Hematopoietic system
d. Peripheral blood and yellow bone marrow c. Pluripotent stem cells
d. Cytokines

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CHAPTER 12 BLOOD CELLS AND THE HEMATOPOIETIC SYSTEM 63

9. To have stem cells for transplantation, clients 13. There are many components reported on in a
are given specific agents to increase the quan- complete blood count (CBC). Fill in the fol-
tity and migration of the cells from the bone lowing abbreviations’ definitions.
marrow. What is the agent used to accom-
plish this? Abbreviation Definition

a. Cytokine growth factor Hgb

b. Human leukocyte antigen growth factor Hct
c. Platelet growth factor
MCV
d. Human growth factor
MCHC
10. The cloning of the genes for most of the
hematopoietic growth factors has been ac- MCH
complished. The recombinant proteins that
are produced are used in a wide range of clini- 14. What are the components of blood? Mark all
cal problems. What diseases have these pro- that apply.
teins been used to fight? a. Electrolytes
a. AIDS and autoimmune disorders b. Enzymes
b. Aplastic anemia and the anemia of kidney c. Ascites
failure d. Bile
c. Anemia of cancer and Parkinson disease
15. Organ, blood, and bone marrow transplants,
d. Aplastic anemia and the anemia of Hunt- once an experimental phenomenon in medi-
ington disease cine, are now being done every day. Our abil-
11. Plasma, because of its water volume, is the ve- ity to match the tissues of one client with
hicle used by the body to distribute those of another person is being more finely
. This is one of the means by developed by researchers around the world.
which the body warms and cools itself. Organ, blood, and bone marrow transplants
are lifesaving procedures that come from
12. For each plasma protein, fill in its purpose what sources? Mark all that apply.
and the percent it makes up of plasma.
a. A histocompatible donor
Protein Percent Purpose b. A heterologous donor
Albumin c. The patients themselves

Globulins d. An autologous donor

Fibrinogen

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13
CHAPTER

Disorders of
Hemostasis

SECTION I: LEARNING 15. Explain the physiologic basis of acute dissem-

inated intravascular coagulation
OBJECTIVES
1. Describe the five stages of hemostasis
2. Explain the formation of the platelet plug
SECTION II: ASSESSING YOUR
UNDERSTANDING
3. State the purpose of blood coagulation
4. State the function of clot retraction Activity A Fill in the blanks.

5. Trace the process of fibrinolysis 1. The term refers to the stoppage

of blood flow.
6. Compare normal and abnormal clotting
2. Platelets have a cell membrane, but have no
7. Describe the causes and effects of increased and cannot reproduce.
platelet function
3. The platelet shape is maintained by micro-
8. State two conditions that contribute to in- tubules and and
creased clotting activity filaments that support the cell membrane.
9. State the mechanisms of drug-induced 4. The release of from platelets re-
thrombocytopenia and idiopathic thrombo- sults in the proliferation and growth of vascu-
cytopenia and the differing features of the lar endothelial cells, smooth muscle cells, and
disorders in terms of onset and resolution fibroblasts, and is important in vessel repair.
10. Describe the manifestations of thrombocy- 5. The combined actions of and
topenia lead to the expansion of the en-
11. Characterize the role of vitamin K in coagula- larging platelet aggregate, which becomes the
tion primary hemostatic plug.

12. State three common defects of coagulation 6. The is a stepwise process result-
factors and the causes of each ing in the conversion of the soluble plasma
protein, fibrinogen, into fibrin.
13. Differentiate between the mechanisms of
bleeding in hemophilia A and von Wille- 7. Most of the coagulation factors are proteins
brand disease synthesized in the .

14. Describe the effect of vascular disorders on 8. It has been suggested that some of these nat-
hemostasis ural anticoagulants may play a role in the
bleeding that occurs with .

64
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CHAPTER 13 DISORDERS OF HEMOSTASIS 65

9. represents an exaggerated form Activity B Consider the following figures:

of hemostasis that predisposes to thrombosis
and blood vessel occlusion. Intrinsic system
(blood or vessel injury)
10. , elevated levels of blood lipids
and cholesterol, hemodynamic stress, dia-
betes mellitus, and immune mechanisms may
cause vessel damage, platelet adherence, and, Extrinsic system
eventually, thrombosis. (tissue factor)
Ca++
11. The common clinical manifestations of essen- Ca++
tial are thrombosis and hemor-
rhage.
12. In persons with inherited defects in factor V,
Ca++
the mutant factor Va cannot be inactivated
by .
Ca++
13. Secondary factors that lead to increased
and thrombosis are venous sta-
sis due to prolonged bed rest and immobility,
myocardial infarction, cancer, hyperestro-
genic states, and oral contraceptives.
14. from mucous membranes of the
nose, mouth, gastrointestinal tract, and uter- 1. In the above figure, place the activated factors
ine cavity is characteristic of platelet bleeding and proteins in their respective places: Xlla,
disorders. Xla, IXa, Xa, Vlla, thrombin, prothrombin,
15. A reduction in platelet number is referred to fibrinogen, and fibrin.
as .
16. destruction may be caused by
antiplatelet antibodies, resulting in thrombo-
Intrinsic pathway Extrinsic pathway
cytopenia. (Endothelial injury) (Tissue injury)
17. thrombocytopenic purpura re- Trauma
Burns Trauma
sults in platelet antibody formation and ex- Gram-negative sepsis Obstetric complications
cess destruction of platelets. Hypoxia Complications of cancer
Acidosis
18. may result from inherited disor- Shock
Vasculitis
ders of adhesion or acquired defects caused
by drugs, disease, or extracorporeal circula-
tion.
19. Hemophilia A is an recessive
disorder that primarily affects males.
20. In liver disease, synthesis of these
is reduced, and bleeding may result. Plasmin
Thrombocytopenia
generation
21. Vitamin C deficiency, results in ,
where poor collagen synthesis and failure of Fibrinolysis
Clotting factor
degradation
the endothelial cells to be cemented together
properly causes a fragile wall and bleeding. Hemolytic Tissue Fibrin degradation
anemia ischemia products
22. Common clinical conditions that may cause (inhibit thrombin
include obstetric disorders, and platelet aggregation)
massive trauma, shock, sepsis, and malignant
disease.

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66 UNIT 4 DISORDERS OF THE HEMATOPOIETIC SYSTEM

2. In the preceding figure explaining the patho- Activity E Briefly answer the following.
physiology of disseminated intravascular coag-
ulation, insert the following terms where 1. Explain the five stages of hemostasis.
appropriate: thrombosis, bleeding, thrombin
generation, platelet consumption, intravascu-
lar fibrin deposition, and plasminogen activa-
tion.

Activity C Match the key terms in Column A 2. Describe the process of platelet activation and
with their definitions in Column B. plug formation.

Column A Column B
1. Thrombin a. Breaks down
fibrin
2. Fibrinolysis
b. May be caused by 3. The coagulation cascade is activated in multi-
3. Thrombocytosis aplastic anemia ple ways and is integral in maintaining hemo-
4. Thromboxane
stasis. Explain the general stimulation and end
c. Enzyme that con-
A2 results.
verts fibrinogen
to fibrin
5. Plasmin
d. Factor VIII defi-
6. Antiphospho- ciency
lipid syndrome
e. Stimulates vaso-
7. Megakaryocytes constriction 4. There are many causes of bleeding disorders.
f. Autoantibodies One of the more clinically relevant is drug-
8. Factor X
that result in in- induced thrombocytopenia. Explain how drugs
9. Hemophilia A creased coagula- such as quinine, quinidine, and certain sulfa-
tion activity containing antibiotics may induce thrombocy-
10. Thrombocy-
topenia.
topenia g. Process of blood
clot dissolution
h. Converts pro-
thrombin to
thrombin
i. Describe eleva- 5. Disseminated intravascular coagulation is a se-
tions in the vere condition that is characterized by wide-
platelet count spread coagulation and bleeding. Explain how
above the disease is initiated, and describe its pro-
1,000,000/L gression.
j. Thrombocyte
precursor

Activity D
1. Write the correct sequence of the terms listed
in the boxes provided.
a. Clot retraction SECTION III: APPLYING YOUR
b. Clot dissolution KNOWLEDGE
c. Activation of coagulation cascade
Activity F Consider the following scenario
d. Formation of platelet plug
and answer the questions.
e. Vessel spasm
Parents of a 17-year-old boy with hemophilia
have brought him to the emergency department
because he is having an exacerbation.

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CHAPTER 13 DISORDERS OF HEMOSTASIS 67

1. What are the two most important nursing ob- a. Binds to factor X
jectives when caring for them? b. Promotes the inactivation of clotting factors
c. Binds to factor Xa
d. Promotes the inactivation of factor VIII
5. The process of clot retraction squeezes serum
from the clot, thereby joining the edges of
2. In planning teaching for the client and his the broken vessel. Through the action of
family, the nurse knows to include what? actin and myosin, filaments in platelets con-
tribute to clot retraction. Failure of clot retrac-
tion is indicative of what?
a. Absence of factor Xa
b. Low platelet count
c. Overabundance of factor Xa
d. High platelet count
SECTION IV: PRACTICING
6. Thrombocytosis is used to describe elevations
FOR NCLEX in the platelet count above 1,000,000/L. It is
Activity G Answer the following questions.
either a primary or a secondary thrombocyto-
sis. Secondary thrombocytosis can occur as a
1. Many different proteins, enzymes, and hor- reactive process due to what?
mones are involved in maintaining hemosta- a. Crohn disease
sis. Which protein is required for platelet
b. Lyme disease
adhesion?
c. Hirschsprung disease
a. von Willebrand factor
d. Megacolon
b. Growth factors
c. Ionized calcium 7. A 57-year-old man is diagnosed with throm-
bocytopenia. The nurse knows that thrombo-
d. Platelet factor 4
cytopenia refers to a decrease in the number
2. There are two pathways that can be activated of circulating platelets. The nurse also knows
by the coagulation process. One pathway be- that thrombocytopenia can result from what?
gins when factor XII is activated. The other a. Decreased platelet production
pathway begins when there is trauma to a
b. Increased platelet survival
blood vessel. What are these pathways?
c. Decreased sequestration of platelets
a. Clotting and bleeding pathways
d. Increased platelet production
b. Extrinsic and intrinsic pathways
c. Inner and outer pathways 8. A young man has been diagnosed with hemo-
philia A, and the nurse is planning his dis-
d. Factor and trauma pathways
charge teaching. She knows to include what
3. Anticoagulant drugs prevent thromboembolic information in her discharge teaching?
disorders. How does warfarin, one of the anti- a. Only use NSAIDs for mild pain
coagulant drugs, act on the body?
b. Prevent trauma to the body
a. Alters vitamin K, reducing its ability to par-
c. The client will not be on IV factor VIII
ticipate in the coagulation of the blood
therapy at home
b. Increases prothrombin
d. It is an X-linked dominant disorder
c. Increases vitamin K–dependent factors in
the liver 9. A teenage girl, seen in the clinic, is diagnosed
with nonthrombocytopenic purpura. The girl
d. Increases procoagulation factors
states, “You have taken a lot of blood from
4. Heparin is an anticoagulant given by injec- me. Which of my tests came back abnormal?”
tion to prevent the formation of blood clots. How should the nurse respond?
How does heparin work?

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68 UNIT 4 DISORDERS OF THE HEMATOPOIETIC SYSTEM

a. Your complete blood count (CBC) with dif- 13. is a natural mucopolysaccharide
ferential showed a shift to the left. anticoagulant that occurs in the lungs and in-
b. Your CBC with differential showed that testinal mucosa.
you do not have enough iron. 14. When platelets adhere to the vessel wall, they
c. Your CBC with differential showed a nor- release growth factors that cause smooth
mal platelet count. muscle to grow. This is a major factor in caus-
d. Your CBC with differential showed a nor- ing atherosclerosis. What are the factors that
mal hematocrit. influence platelets to adhere to the vessel
wall? Mark all that apply.
10. Disseminated intravascular coagulation is a
a. Hemodynamic stress
grave coagulopathy resulting from the over-
stimulation of clotting and anticlotting b. High cholesterol
processes in response to what? c. Diabetes
a. Disease or injury d. Low blood lipids
b. Septicemia and acute hypertension e. Smoking
c. Neoplasms and nonpoisonous snakebites 15. In a client with disseminated intravascular
d. Severe trauma and acute hypertension coagulation, microemboli form, causing ob-
struction of blood vessels and tissue hypoxia.
11. The following five stages of hemostasis are
Common clinical signs may be due to what?
given in random order. Put them into their
Mark all that apply.
correct order.
a. Circulatory failure
a. Clot dissolution a. c, a, b, e, d
b. Immunologic failure
b. Blood coagulation b. a, c, b, d, e
c. Renal failure
c. Vessel spasm c. c, e, b, d, a
d. Right ventricular failure
d. Clot retraction d. e, c, d, b, a
e. Respiratory failure
e. Formation of platelet plug
12. The coagulation cascade is the third compo-
nent of the hemostatic process. It is a step-
wise process resulting in the conversion of
the soluble plasma protein, fibrinogen, into
fibrin. This multistep process ensures that a
massive episode of clotting does
not occur by chance.

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14

CHAPTER
Disorders of Red
Blood Cells

SECTION I: LEARNING 13. Compare characteristics of the red blood cells

in acute blood loss, hereditary spherocytosis,
OBJECTIVES sickle cell disease, iron-deficiency anemia,
and aplastic anemia
1. Trace the development of a red blood cell
from erythroblast to erythrocyte 14. Differentiate red cell antigens from antibodies
in persons with type A, B, AB, or O blood
2. Discuss the function of iron in the formation
of hemoglobin 15. Explain the determination of the Rh factor
3. Describe the formation, transport, and elimi- 16. List the signs and symptoms of a blood trans-
nation of bilirubin fusion reaction
4. Explain the function of the enzyme glucose- 17. Define the term polycythemia
6-phosphate dehydrogenase in the red blood
18. Compare causes of polycythemia vera and
cell
secondary polycythemia
5. State the meaning of the red blood cell count,
19. Describe the manifestations of polycythemia
percentage of reticulocytes, hemoglobin,
hematocrit, mean corpuscular volume, and 20. Cite the function of hemoglobin F in the
mean corpuscular hemoglobin concentration neonate and describe the red blood cell
as it relates to the diagnosis of anemia changes that occur during the early neonatal
period
6. Describe the manifestations of anemia and
their mechanisms 21. Cite the factors that predispose to hyper-
bilirubinemia in the infant
7. Explain the difference between intravascular
and extravascular hemolysis 22. Describe the pathogenesis of hemolytic dis-
ease of the newborn
8. Compare the hemoglobinopathies associated
with sickle cell disease and thalassemia 23. Compare conjugated and unconjugated
bilirubin in terms of production of en-
9. Explain the cause of sickling in sickle cell disease
cephalopathy in the neonate
10. Cite common causes of iron-deficiency ane-
24. Explain the action of phototherapy in the
mia in infancy, adolescence, and adulthood
treatment of hyperbilirubinemia in the
11. Describe the relation between vitamin B12 de- neonate
ficiency and megaloblastic anemia
25. State the changes in the red blood cells that
12. List three causes of aplastic anemia occur with aging

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70 UNIT 4 DISORDERS OF THE HEMATOPOIETIC SYSTEM

SECTION II: ASSESSING YOUR and the defective synthesis of one of the
polypeptide chains that form the globin por-
UNDERSTANDING tion of hemoglobin, as in the .
Activity A Fill in the blanks. 14. Hereditary is caused by abnor-
malities of the spectrin and ankyrin mem-
1. The shape of an erythrocyte
brane proteins that lead to a gradual loss of
provides a larger surface area for oxygen diffu-
the membrane surface.
sion than would a spherical cell of the same
volume, and the thinness of the 15. are caused by deficient synthesis
enables oxygen to diffuse rapidly between the of the  chain and by deficient
exterior and the innermost regions of the cell. synthesis of the  chain.
2. The rate at which hemoglobin is synthesized 16. The most common inherited enzyme defect
depends on the availability of that results in hemolytic anemia is a defi-
for heme synthesis. ciency of .
3. During its transformation from normoblast to 17. anemia results from dietary defi-
reticulocyte, the red blood cell accumulates ciency, loss of iron through bleeding, or in-
hemoglobin as the condenses creased demands.
and is finally lost.
18. Iron deficiency in adults in the Western
4. Mature red blood cells have a life span of ap- world is usually the result of .
proximately months.
19. anemias are caused by impaired
5. The red blood cell relies on the DNA synthesis that results in enlarged red
pathway for its metabolic needs. blood cells due to impaired maturation and
division.
6. Large doses of nitrites can result in high levels
of , causing pseudocyanosis and 20. anemia is a specific form of
tissue hypoxia. megaloblastic anemia caused by atrophic gas-
tritis.
7. The measures the total number
of red blood cells in a microliter of blood. 21. describes a disorder of pluripo-
tential bone marrow stem cells that results in
8. The measures the volume of red
a reduction of all three hematopoietic cell
blood cell mass in 100 mL of plasma volume.
lines.
9. The is the concentration of he-
22. is an abnormally high total red
moglobin in each cell.
blood cell mass with a hematocrit greater
10. is defined as an abnormally low than 50%.
number of circulating red blood cells or level
23. At birth, changes in the red blood cell indices
of hemoglobin.
reflect the transition to extrauterine life and
11. Tissue can give rise to fatigue, the need to transport from the
weakness, dyspnea, and, sometimes, angina. lungs.
12. anemia is characterized by the 24. Jaundice in infants is the result of increased
premature destruction of red blood cells, the red blood cell breakdown and the inability of
retention in the body of iron and the other the immature liver to bilirubin.
products of hemoglobin destruction, and an
25. The diagnosis of in the elderly
increase in erythropoiesis.
requires a complete physical examination, a
13. Two main types of hemoglobinopathies can complete blood count, and studies to rule out
cause red blood cell hemolysis: the abnormal comorbid conditions such as malignancy,
substitution of an amino acid in the hemo- gastrointestinal conditions that cause bleed-
globin molecule, as in anemia, ing, and pernicious anemia.

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CHAPTER 14 DISORDERS OF RED BLOOD CELLS 71

Activity B Consider the following figure. 7. B12 deficiency e. Caused by defi-

cient globin pro-
8. Erythropoiesis
duction
Spleen 9. Jaundice f. Regulator of red
10. Normochromic blood cell pro-
cell duction
g. Normal hemoglo-
Hemoglobin bin concentra-
tion in red blood
cell
h. Yellow discol-
oration of skin
due to high levels
of bilirubin
i. Transports iron
Liver to plasma
j. Receiving blood
from yourself

Activity D Briefly answer the following.

Bone
1. Hemoglobin is the oxygen-carrying protein
marrow found in red blood cells. Describe the molecu-
lar structure of hemoglobin. Also, explain how
oxygen interacts with hemoglobin.

In this figure, fill in the steps associated with red

blood cell breakdown and secretion from the
body. Begin by labeling where heme and the glo- 2. Red blood cells (RBCs) have a finite life span.
bin proteins separate. Trace the iron as it is recy- How long is the life span, and what is the fate
cled or as it is conjugated by the liver. of RBCs?

Activity C Match the key terms in Column A

with their definitions in Column B.

Column A Column B
1. Thalassemia a. Decreases he- 3. What are the three categories of anemic
moglobin affin- effects?
2. 2, 3-Diphospho-
ity for oxygen
glycerate
b. Common cause
3. Erythropoietin of megaloblastic
4. Mean corpus- anemias
cular volume c. Measure of size 4. Describe and explain the two consequences of
of red blood cell sickle cell disease.
5. Transferrin
d. Red blood cell
6. Autologous production
donation

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72 UNIT 4 DISORDERS OF THE HEMATOPOIETIC SYSTEM

5. Anemia is a common side effect of cancer 2. The nurse would also explain to Mrs. McFee
treatments. Which type of anemia usually de- that two people always check the donor blood
velops, and why? against the recipient information before it is
transfused at least two times. Once, when it
leaves the laboratory, and, again, before it is
infused into the patient. Why is this attention
given to checking the blood?

6. Polycythemia vera is a neoplastic disorder of

red blood cells. Describe the complications
that arise from the rapid increase in hemat-
ocrit.

SECTION IV: PRACTICING

FOR NCLEX
7. Infantile jaundice is caused by the underdevel- Activity F Answer the following questions.
oped liver being unable conjugate bilirubin.
What are the treatment methods for infantile 1. All cells of the body age and are replaced in a
jaundice, and how do they work? natural order. When red blood cells (RBCs)
age, they are destroyed in the spleen. During
this process, the iron from their hemoglobin
is released into the circulation and returned
where?
a. To the bone marrow for incorporation into
new RBCs
b. To the liver to bind with oxygen
SECTION III: APPLYING YOUR c. To the lungs to bind with oxygen
KNOWLEDGE d. To the muscles to be stored for strength
Activity E Consider the following scenario 2. Bilirubin is the pigment of bile and is made
and answer the questions. when red blood cells die. There are two
types of bilirubin that can be measured in
Mrs. McFee, a 62-year-old woman, is in the out-
the blood and reported on by the laboratory.
patient procedure area of the hospital. She has a
What does the laboratory reports them as?
long history of rheumatoid arthritis and is to re-
ceive a blood transfusion to treat a chronic dis- a. Conjugated and unconjugated
ease anemia. She appears very nervous as the b. Soluble and insoluble
nurse begins the transfusion. She states, “My c. Positive and negative
friends have told me that there are serious
d. Direct and indirect
things that can happen to you because of a
transfusion.” 3. Neonatal hyperbilirubinemia is an increased
level of bilirubin in the infant’s blood. It is
1. The nurse would respond that there are several
usually a benign condition characterized by
side effects that need to be watched for during
what?
a blood transfusion. Together, the nurse and
Mrs. McFee will watch for what types of symp- a. A yellow, jaundiced color
toms of a transfusion reaction? b. Failure to thrive
c. Brain damage
d. A reddish, ruddy complexion
4. Anemia resulting from blood loss can be re-
versed if the blood loss is not so severe that it
results in death. How long does it take for the

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CHAPTER 14 DISORDERS OF RED BLOOD CELLS 73

red blood cell concentration to return to a. Uremic toxins and retained nitrogen
normal? b. Bleeding tendencies and lack of fibrinogen
a. 8 to 10 days in blood
b. 3 to 4 weeks c. Hemodialysis and decreased nitrogen
c. 10 to 14 days d. Hemolysis of red blood cells and lack of
d. 5 to 6 weeks fibrinogen in blood

5. During chronic blood loss, iron-deficiency 10. When an Rh-negative mother gives birth to
anemia occurs. Most patients are asympto- an Rh-positive infant, the mother usually
matic until their hemoglobin falls below 8 produces antibodies that will attack any sub-
g/dL. The red blood cells that the body does sequent pregnancies in which the fetus is Rh
produce have too little hemoglobin. What is positive. When subsequent babies are Rh pos-
the term for the resulting anemia? itive, erythroblastosis fetalis occurs. What is
another name for erythroblastosis fetalis?
a. Macrocytic hyperchromic
a. Microcytic disease of the newborn
b. Macrocytic hypochromic
b. Hemolytic iron-deficiency anemia
c. Microcytic hypochromic
c. Hemolytic disease of the newborn
d. Microcytic hyperchromic
d. Macrocytic disease of the newborn
6. In hemolytic anemia, the red blood cells are
destroyed prematurely. What distinguishes al- 11. Pernicious anemia is believed to be an autoim-
most all types of hemolytic anemia? mune disease that destroys the gastric mucosa.
This results in chronic atrophic gastritis and
a. Normocytic hypochromic cells
the production of antibodies that interfere
b. Microcytic normochromic cells with binding to intrinsic factor.
c. Macrocytic hyperchromic cells
12. Sickle cell disease is an inherited disorder seen
d. Normocytic normochromic cells in African American people. It is marked by
7. When hemolytic anemia has intravascular the characteristic sickling of red blood cells.
hemolysis, it can be characterized in different This causes both chronic hemolytic anemia
ways. Which of the following is not a charac- and occlusion of blood vessels. Which are
terization of hemolytic anemia with intravas- considered to be triggers of an episode of sick-
cular hemolysis? ling? Mark all that apply.
a. Hemoglobinemia a. Infection
b. Jaundice b. Stress
c. Hemosiderinuria c. Heat
d. Spherocytosis d. Dehydration
e. Alkalosis
8. Aplastic anemia is a serious anemia that is a
disorder of the pluripotential bone marrow 13. The indices of the red blood cell (RBC) are
stem cells and causes all three hematopoietic used to differentiate the anemias by size and
cell lines to be reduced. What is the treatment color of cell. Match the term for a RBC with
for aplastic anemia in the young and severely its definition:
affected client?
Term Definition
a. No treatment
1. Mean corpuscular a. The concen-
b. Bone marrow transplant
hemoglobin tration of he-
c. Spleen transplant concentration moglobin in
d. Liver transplant 2. Mean cell each cell
hemoglobin b. The mass of
9. When a client is in chronic renal failure, he
3. Mean corpuscular the RBC
or she almost always has anemia because of a
volume
deficiency of erythropoietin. What else con- c. The volume
tributes to the anemia experienced by clients or size of the
in chronic renal failure? RBCs

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74 UNIT 4 DISORDERS OF THE HEMATOPOIETIC SYSTEM

14. A pregnant woman at her first prenatal visit a. Headache

complains to the nurse that she is always b. Dusky red appearance
tired. The nurse knows that fatigue is one
c. Ability to concentrate better
symptom of anemia. What are other symp-
toms of anemia? Mark all that apply. d. Cyanosis of trunk
a. Faintness e. Hearing difficulty
b. Dim vision 16. Thalassemia can be classed as major or minor.
c. Ruddy skin In thalassemia major, it is necessary to start
therapy as early as 6 months of
d. Bradycardia
age. If therapy is not started in infants who
15. Polycythemia vera most often occurs in men present with this disease, severe growth retar-
with a median age of 62 years. It is a neoplas- dation will occur.
tic disease of the bone marrow that is charac-
terized by which of the following signs and
symptoms? Mark all that apply.

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15

CHAPTER
Disorders of White
Blood Cells and
Lymphoid Tissues

SECTION I: LEARNING 10. Use the predominant white blood cell type
and classification of acute or chronic to de-
OBJECTIVES scribe the four general types of leukemia
1. Describe the different types of white blood 11. Explain the manifestations of leukemia in
cells and structures of the lymphoid system terms of altered cell differentiation
where they circulate
12. Describe the following complications of acute
2. Trace the development of the different white leukemia and its treatment: leukostasis,
blood cells from their origin in the pluripo- tumor lysis syndrome, hyperuricemia, and
tent bone marrow stem cell to their circula- blast crisis
tion in the bloodstream
13. Relate the clonal expansion of immunoglobu-
3. Define the terms leukopenia, neutropenia, gran- lin-producing plasma cells and accompany-
ulocytopenia, and aplastic anemia ing destructive skeletal changes that occur
with multiple myeloma in terms of manifes-
4. Cite two general causes of neutropenia
tations and clinical course of the disorder
5. Describe the mechanism of symptom produc-
tion in neutropenia
6. Use the concepts regarding the central and SECTION II: ASSESSING YOUR
peripheral lymphoid tissues to describe the UNDERSTANDING
site of origin of the malignant lymphomas,
leukemias, and plasma cell dyscrasias Activity A Fill in the blanks.
7. Explain how changes in chromosomal struc- 1. The white blood cells include the
ture and gene function can contribute to the , monocyte/macrophages, and
development of malignant lymphomas, lymphocytes.
leukemias, and plasma cell dyscrasias
2. T lymphocytes mature in the .
8. Contrast and compare the signs and symptoms
3. The B lymphocytes differentiate to form im-
of non-Hodgkin and Hodgkin lymphomas
munoglobulin-producing cells.
9. Describe the measures used in treatment of
4. Another population of lymphocytes includes
non-Hodgkin and Hodgkin lymphomas
the cells, which do not share

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76 UNIT 4 DISORDERS OF THE HEMATOPOIETIC SYSTEM

the specificity or characteristics of the T or B 18. The leukemias involve imma-

lymphocytes, but have the ability to lyse tar- ture lymphocytes and their progenitors,
get cells. which originate in the bone marrow but infil-
trate the spleen, lymph nodes, central ner-
5. The granulocyte and monocyte cell lines
vous system, and other tissues.
derive from the stem cells and
the lymphocytes from the stem 19. Cytogenetic studies have shown that recur-
cells. rent chromosomal changes occur in more
than one-half of all cases of .
6. The body’s lymphatic system consists of the
lymphatic vessels, lymphoid tissue and lymph 20. usually have a sudden and
nodes, , and . stormy onset with signs and symptoms re-
lated to depressed bone marrow function.
7. T lymphocytes travel to the thymus, where
they differentiate into helper T 21. There are two types of acute leukemia: acute
cells and cytotoxic T cells. and acute .
8. In anemia, the myeloid stem 22. are malignancies involving pro-
cells are affected, resulting in anemia, throm- liferation of more fully differentiated myeloid
bocytopenia, and agranulocytosis. and lymphoid cells.
9. Alloimmune neonatal neutropenia is neu- 23. Chronic lymphocytic leukemia, a clonal ma-
tropenia that occurs after transplacental lignancy of , is the most com-
transfer of maternal directed at mon form of leukemia in adults in the
an infant’s neutrophils. Western world.
10. Early signs of infection of in- 24. The diagnostic hallmark of chronic lympho-
clude mild skin lesions, stomatitis, pharyngi- cytic leukemia is isolated .
tis, and diarrhea.
25. It is generally believed that chronic myeloge-
11. is a self-limiting lymphoprolifer- nous leukemia develops when a single,
ative disorder caused by the Epstein-Barr pluripotential, hematopoietic stem cell ac-
virus. quires a chromosome.
12. can involve lymphocytes, gran- 26. are characterized by expansion
ulocytes, and other blood cells. of a single clone of immunoglobulin-produc-
ing plasma cells and a resultant increase in
13. originate in peripheral lym-
serum levels of a single monoclonal im-
phoid structures such as the lymph nodes,
munoglobulin or its fragments.
where B and T lymphocytes undergo differen-
tiation and proliferation. 27. The development of lesions in
multiple myeloma is believed to be related to
14. cell lymphomas are the most
an increase in expression by osteoblasts of the
common type of lymphoma in the Western
receptor activator of the nuclear factor-B.
world.
28. One of the characteristics resulting from
15. Four variants of classical Hodgkin lymphoma
the proliferating osteoclasts in multiple
have been described: sclerosis,
myeloma is the unregulated production of
mixed cellularity, rich, and lym-
a monoclonal antibody referred to as the
phocyte depleted.
.
16. Persons with are staged accord-
ing to the number of lymph nodes that are Activity B Match the key terms in Column A
involved; whether the lymph nodes are on with their definitions in Column B.
one or both sides of the diaphragm; and
whether there is disseminated disease involv- Column A Column B
ing the bone marrow, liver, lung, or skin.
1. Heterophil a. Neoplasm involving B
17. The are malignant neoplasms of or T cells
2. Leukopoiesis
cells originally derived from hematopoietic b. Translocation on
precursor cells. chromosome 8

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CHAPTER 15 DISORDERS OF WHITE BLOOD CELLS AND LYMPHOID TISSUES 77

3. Burkitt c. Found in more 4. There are two major differences between

lymphoma than 90% of per- Hodgkin lymphoma and non-Hodgkin lym-
sons with chronic phoma. What are they?
4. Non-Hodgkin
myelogenous
lymphomas
leukemia
5. Neutropenia d. Production of
6. Reed-Sternberg white blood cells
cells e. Used for the diag-
5. What are the potential causes of leukemia?
nosis of infectious
7. Kostmann
mononucleosis
syndrome
f. An abnormally
8. Philadelphia low number of
chromosome neutrophils
9. Blast cells g. Immature precur- 6. Compare and contrast acute lymphocytic
sor cells leukemia and acute myelocytic leukemia.
10. ZAP-70
h. Definitive marker
for Hodgkin lym-
phoma
i. An arrest in
myeloid matura- 7. Describe the progression of chronic myeloge-
tion nous leukemia through its three stages.
j. Normal T cell pro-
tein, abnormal in
chronic lympho-
cytic leukemia

Activity C Briefly answer the following. 8. What are the potential causes of multiple
myeloma?
1. Neutrophils are very important as a first line of
defense against viral/bacterial infection. Ex-
plain what a neutrophil does and the condi-
tion that results from a deficiency of
neutrophils.

SECTION III: APPLYING YOUR

KNOWLEDGE
2. Describe the pathogenesis of infectious
Activity D Consider the following scenario
mononucleosis.
and answer the questions.
Two-year-old Lucy has been diagnosed with acute
lymphocytic leukemia and admitted to your unit
for treatment. How would you answer when the
parents ask these questions?
3. Describe the clinical manifestations of non-
Hodgkin lymphoma, and relate the symptoms 1. “What caused Lucy’s leukemia?”
to the pathologic cause.

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78 UNIT 4 DISORDERS OF THE HEMATOPOIETIC SYSTEM

2. “What kind of treatment will Lucy have?” a. Peripheral nerve palsies

b. Rupture of the spleen
c. Rupture of the lymph nodes
d. Severe bacterial infections
6. You are presenting an educational event to a
group of cancer patients. What would you
cite as the most commonly occurring hema-
SECTION IV: PRACTICING tologic cancer?
FOR NCLEX a. Acute lymphocytic leukemia
b. Hodgkin lymphomas
Activity E Answer the following questions.
c. Non-Hodgkin lymphomas
1. Progenitor cells, or parent cells, for
d. Mantle cell lymphoma
myelopoiesis and lymphopoiesis are derived
from which of the following? 7. Endemic Burkitt lymphoma occurs in regions
a. Pluripotent stem cells of Africa where what other infections are
common?
b. Unipotent cells
a. Herpes zoster and Epstein-Barr virus
c. Multipotential progenitor cells
b. Herpes zoster and streptococcal
d. Myeloproliferative cells
c. Malaria and streptococcal
2. What is the name of the region of the lymph
d. Epstein-Barr virus and malaria
nodes that contains most of the T cells?
a. Primary follicles 8. Acute lymphoblastic leukemia (ALL) and
acute myelogenous leukemia (AML) are two
b. Paracortex
distinct disorders with similar presenting clin-
c. Secondary follicles ical features. What clinical feature do ALL
d. Primary cortex and AML share?
3. Kostmann syndrome is a severe congenital a. Night sweats
neutropenia. Which of the following is char- b. Weight gain
acteristic of this condition? c. High fever
a. Bone marrow disorders d. Polycythemia
b. Severe viral infections
9. Definitive diagnosis of multiple myeloma in-
c. Autoimmune disorders cludes the triad of bone marrow plasmacyto-
d. Severe bacterial infections sis, lytic bone lesions, and what?
4. Drug-induced neutropenia is a disease that a. Oligoclonal bands in the cerebrospinal
has significantly increased in incidence over fluid
the past several decades. What is the attribut- b. Bence-Jones proteins in the urine
ing factor in the increased incidence of drug- c. Serum M-protein depression
induced neutropenia?
d. BCR-ABL fusion protein in serum
a. Treatment of cancer by chemotherapeutic
drugs 10. Chronic lymphocytic leukemia (CLL) com-
monly causes hypogammaglobulinemia. This
b. Decrease in the use of street drugs
makes clients with CLL more susceptible to
c. Destruction of tissue cells by cocaine infection. What are the most common infec-
d. New drugs developed to treat autoimmune tious organisms that attack clients with CLL?
diseases a. Acne rosacea
5. Infectious mononucleosis is a lymphoprolif- b. Pseudomonas aeruginosa
erative disorder caused by the Epstein-Barr c. Staphylococcus aureus
virus that is usually self-limiting and non-
d. Escherichia coli
lethal. Which of the following complications
can arise during this mostly benign disease?

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CHAPTER 15 DISORDERS OF WHITE BLOOD CELLS AND LYMPHOID TISSUES 79

11. Large granular lymphocytes, or natural killer a. Cushing syndrome

cells, have the ability to target b. Neurofibromatosis
cells.
c. Fanconi anemia
12. Which lymphatic tissue is associated with d. Down syndrome
mucous membranes and called mucus-associ-
e. Prader-Willi syndrome
ated lymphatic tissue (or MALT)? Mark all
that apply. 14. Tumor lysis syndrome, the massive necrosis
a. Genitourinary systems and central nervous of malignant cells that can occur during the
system initial phase of treatment of acute lym-
phoblastic leukemia, can lead to metabolic
b. Respiratory passages and cardiovascular
disorders that are life threatening. Which
system
metabolic disorders can occur because of
c. Alimentary canal and genitourinary sys- tumor lysis syndrome? Mark all that apply.
tems
a. Hyperuricemia
d. Cardiovascular system and central nervous
b. Hypokalemia
system
c. Acidosis
13. You are speaking to a group of genetic stu-
d. Alkalosis
dents touring your hospital’s laboratory. You
talk about the possibility of a genetic predis- e. Hypocalcemia
position for the leukemias being suggested 15. Secondary malignancies in survivors of
because of the increased incidence of the dis- Hodgkin lymphoma have been attributed
ease among a number of congenital disorders. mainly to therapy.
Which congenital disorders are these? Mark
all that apply.

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16
CHAPTER

Mechanisms of
Infectious Disease

SECTION I: LEARNING 10. State the two criteria used in the diagnosis of
an infectious disease
OBJECTIVES
11. Explain the differences among culture, serol-
1. Define the terms host, infectious disease, colo- ogy, and antigen, metabolite, or molecular
nization, microflora, virulence, pathogen, and detection methods for diagnosis of infectious
saprophyte disease
2. Describe the concept of host–microorganism 12. Cite three general intervention methods that
interaction using the concepts of commensal- can be used in treatment of infectious ill-
ism, mutualism, and parasitic relationships nesses
3. Describe the structural characteristics and 13. State four basic mechanisms by which antibi-
mechanisms of reproduction for prions, otics exert their action
viruses, bacteria, fungi, and parasites
14. Differentiate bactericidal from bacteriostatic
4. Use the concepts of incidence, portal of entry,
15. List the infectious agents considered to pose
source of infection, symptomatology, disease
the highest level of bioterrorism threat
course, site of infection, agent, and host char-
acteristics to explain the mechanisms of in- 16. Describe the effect of international travel on
fectious diseases the spread of infection
5. Differentiate between incidence and preva- 17. State an important concept in containment
lence and among endemic, epidemic, and of infections due to bioterrorism and global
pandemic travel
6. Describe the stages of an infectious disease
after the potential pathogen has entered the
body SECTION II: ASSESSING YOUR
7. List the systemic manifestations of infectious UNDERSTANDING
disease
Activity A Fill in the blanks.
8. Describe mechanisms and significance of an-
timicrobial and antiviral drug resistance 1. The colonizing bacteria acquire nutritional
needs and shelter, and the host is not ad-
9. Explain the actions of intravenous im- versely affected by the relationship; an inter-
munoglobulin and cytokines in the treatment action such as this is called .
of infectious illnesses

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CHAPTER 16 MECHANISMS OF INFECTIOUS DISEASE 81

2. The term describes the presence, of the pathogen, repair of damaged tissue,
multiplication, and subsequent injury within and resolution of associated symptoms.
a host by another living organism.
17. Inflammation of an anatomic location is
3. A relationship is one in which usually designated by adding the suffix
only the infecting organism benefits from the to the name of the involved
relationship and the host either gains noth- tissue in an infection.
ing from the relationship or sustains injury
18. The suffix is used to designate
from the interaction.
the presence of a substance in the blood.
4. All microorganisms can be
19. factors are substances or prod-
pathogens capable of producing an infectious
ucts generated by infectious agents that
disease when the health and immunity of the
enhance their ability to cause disease.
host have been severely weakened.
20. In contrast to , endotoxins do
5. The various prion-associated diseases produce
not contain protein, are not actively released
very similar symptomatology and pathology
from the bacterium during growth, and have
in the host and are collectively called
no enzymatic activity.
diseases.
6. are the smallest obligate intra- Activity B Consider the following figure.
cellular pathogens.
7. Bacteria are autonomously replicating unicel- Death
lular organisms known as Critical threshold
because they lack an organized nucleus.
8. characteristics and microscopic replication of pathogens
Severity of illness

morphology are used in combination to Chronic disease

describe bacteria.
9. The are an eccentric category of
bacteria that are mentioned separately be- Clinical
cause of their unusual cellular morphology threshold
and distinctive mechanism of motility. Subclinical disease

10. The are unicellular prokaryotes

capable of independent replication.
11. Serious infections are rare and
usually initiated through puncture wounds or
inhalation.
12. The fungi can be separated into two groups, In this figure, label the areas that represent the
and , based on course through which a disease progresses: reso-
rudimentary differences in their morphology. lution, acute phase, convalescent phase, incuba-
tion phase, infection, and prodromal phase.
13. Parasitic infection results from the ingestion
of highly resistant cysts or spores that are
Activity C Match the key terms in Column A
shed in the of an infected host.
with their definitions in Column B.
14. The is the initial appearance of
symptoms in the host. 1.
15. The period during which the host experiences Column A Column B
the maximum impact of the infectious 1. Microflora
a. Describes the act of es-
process corresponding to rapid proliferation
2. Host tablishing an infection
and dissemination of the pathogen is known
as the . 3. Infection b. Microorganisms that live
with a host
16. The is characterized by the con- 4. Disease
tainment of infection, progressive elimination

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82 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

5. Colonization c. Microorganisms so 9. Facultatively h. Virus capable of

virulent that they are anaerobic transforming a cell
6. Virulence
rarely found bacteria i. Sexually transmitted
7. Pathogens in the absence of dis- genital infections
10. Chlamydia
ease
8. Saprophytes trachomatis j. Cannot live long out-
d. Presence, multiplica- side strict growth re-
9. Prions tion, and subsequent quirements
10. Rickettsiaceae injury within a host by
another living organ-
Activity D Write the correct sequence of the
ism
following in the boxes provided.
e. Disease-producing po-
tential of a microor- a. Viral DNA copy is integrated into the host
ganism chromosome
f. Any organism capable b. Host cell lysis
of supporting the nu- c. Reactivation of virus
tritional and physical
d. Entry into the host cell
growth requirements
of another e. Viral RNA genome is first translated into DNA
g. Condition of an or- f. Replication of virus
ganism that impairs
normal physiologic
function
h. Harmless, free-living
organisms Activity E Briefly answer the following.
i. Disease-causing pro-
1. Explain the general mechanism of cellular
tein particles that lack
viral infection and replication. Differentiate
a demonstrable
between those that cause lysis and those that
genome
do not. Also, explain the concept of a latent
j. Organisms combining virus.
characteristics of viral
and bacterial agents to
produce disease in hu-
mans
2.
Column A Column B 2. Describe the various methods of infiltration
1. Plasmids a. Organisms are less taken by organisms that will cause infection,
than one-third the from the organism entering the host to the
2. Mycoplasmas manifestation of the disease state.
size of bacteria
3. Fastidious b. Cause Rocky Moun-
bacteria tain spotted fever
4. Ectoparasites c. Flu viruses
5. Orthomy- d. Herpesvirus and
xoviridae paramyxoviruses 3. Explain the concept of “disease course,” and
e. Infest external body list all the stages that the disease course takes.
6. Enveloped
surfaces
viruses
f. Bacterial DNA that
7. Rickettsiaceae may increase viru-
8. Oncogenic lence
viruses g. Bacteria that can
adapt metabolism

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CHAPTER 16 MECHANISMS OF INFECTIOUS DISEASE 83

4. What is the goal of treatment in regard to in- a. Infectious disease

fective organisms? Provide the common meth- b. Mutual disease
ods of treatment.
c. Communicable disease
d. Commensal disease
2. The infectious agents that cause Rocky Moun-
tain spotted fever and epidemic typhus are
transmitted to the human body via vectors
5. Explain the categorization of organisms that such as ticks. What are these infectious agents?
carry the potential for bioterrorism.
a. Viruses
b. Rickettsiaceae
c. Chlamydiaceae
d. Anaplasmataceae
3. Severe acute respiratory syndrome (SARS), a
highly transmissible respiratory infection,
SECTION III: APPLYING YOUR crossed international borders in the winter of
2002. What terms are used to describe the
KNOWLEDGE outbreak of SARS?
Activity F Consider the following scenario a. Pandemic and nosocomial
and answer the questions. b. Regional and endemic
You are a nurse working for a public health c. Epidemic and pandemic
agency. You have been asked to give a talk to the d. Nosocomial and endemic
local rotary club about infectious diseases. In
4. The clinical picture, or presentation of a
your presentation, you are going to include infor-
disease in the body, is called what?
mation about treatment of these diseases.
a. Virulence of the disease
1. In discussing the role of antibiotics in the
b. Source of the disease
treatment of infectious diseases, you would in-
clude definitions of bactericidal and bacterio- c. Diagnosis of the disease
static. What are these definitions? d. Symptomatology of the disease
5. There are two criteria that have to be met in
order for a diagnosis of an infectious disease
to occur. What are these two criteria?
a. Recovery of probable pathogen and docu-
2. What drugs are used for HIV infections? How mentation of signs and symptoms compat-
are these drugs classified? ible with an infectious process
b. Propagation of a microorganism outside
the body and testing to see what destroys it
c. Identification by microscopic appearance
and Gram stain reaction
d. Serology and an antibody titer specific to
the serology
SECTION IV: PRACTICING 6. Levels A, B, and C are levels assigned to po-
FOR NCLEX tential agents of bioterrorism. What are these
categorical assignments based on?
Activity G Answer the following questions. a. Safety to terrorist
1. What is the term for parasitic relationships b. Transmissibility
between microorganisms and the human c. Environmental impact
body in which the human body is harmed? d. Ease of use to terrorist

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84 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

7. Global infectious diseases are now being rec- 11. Transmissible neurodegenerative diseases
ognized. These diseases, known as endemic to such as Creutzfeldt-Jakob disease are associ-
one part of the world, are now being found in ated with .
other parts of the world due to international
12. infections refer to vertically
travel and a global marketplace. Which of the
transmitted infections, that is, infections that
following is considered a global infectious
are transmitted from mother to infant.
disease?
a. Coxsackie disease 13. Match the category of infectious diseases with
its source.
b. Respiratory syncytial disease
c. West Nile virus Category Source
d. Hand, foot, and mouth disease 1. Zoonoses a. Passed from
mother to child
8. Which of the following sequences accurately 2. Perinatal
at birth
describes the stages of a disease? infections
b. Health care
a. Incubation, prodromal, current, recovery, 3. Opportunistic facility
and resolution
4. Nosocomial c. Passed from ani-
b. Subacute, prodromal, acute, postacute, and
mals to humans
convalescent
d. Acquired from
c. Prodromal, subacute, acute, postdromal,
client’s own body
and resolution
d. Incubation, prodromal, acute, convales- 14. Infectious agents produce products or sub-
cent, and resolution stances called virulence factors that make it
easier for them to cause disease. Which of
9. Sometimes the host’s white blood cells are these are virulence factors? Mark all that
unable to eliminate the microorganism, but apply.
the body is able to contain the dissemination
a. Invasive factors
of the pathogen. What is this called?
b. Prodromal factors
a. Abscess
c. Adhesion factors
b. Pimple
d. Toxins
c. Lesion
e. Evasive factors
d. Acne
15. Evasive factors, one type of virulence factor,
10. Escherichia coli produces an exotoxin called
are factors produced by infectious microor-
Shiga toxin that enters the body when you
ganisms to keep the host’s immune system
eat undercooked hamburger meat and fruit
from destroying the microorganism. Which
juices that are not pasteurized. What can
of these are evasive factors? Mark all that
E. coli infection cause?
apply.
a. Nephritic syndrome
a. Capsules
b. Hemorrhagic colitis
b. Phospholipases
c. Hemolytic thrombocytopenia
c. Collagenases
d. Neuroleptic malignant syndrome
d. Slime
e. Mucous layers

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17

CHAPTER
Innate and Adaptive
Immunity

SECTION I: LEARNING 14. Describe the antigen-presenting functions of

macrophages and dendritic cells
OBJECTIVES
15. Contrast and compare the development and
1. Discuss the function of the immune system function of the T and B lymphocytes
2. Contrast and compare the general properties 16. State the function of the five classes of im-
of innate and adaptive immunity munoglobulins
3. Describe the cells of the immune system 17. Differentiate between the central and periph-
eral lymphoid structures
4. Characterize the chemical mediators that or-
chestrate the immune response 18. Describe the function of cytokines involved
in the adaptive immune response
5. Characterize the function of the innate im-
mune system 19. Compare passive and active immunity
6. Describe components of the innate immune 20. Explain the transfer of passive immunity
system including epithelial barriers, soluble from mother to fetus and from mother to in-
chemical agents, and cellular components fant during breast-feeding
7. Describe the recognition systems for 21. Characterize the development of active im-
pathogens in innate immunity munity in the infant and small child
8. State the types and functions of leukocytes 22. Describe changes in the immune response
that participate in innate immunity that occur with aging
9. Describe the functions of the various cy-
tokines involved in innate immunity
10. Define the role of the complement system in
SECTION II: ASSESSING YOUR
immunity and inflammation. UNDERSTANDING
11. State the properties associated with adaptive Activity A Fill in the blanks.
immunity
1. The has evolved in multicellular
12. Define and describe the characteristics of an organisms to defend against bacteria, viruses,
antigen and other foreign substances.
13. Characterize the significance and function of
major histocompatibility complex molecules

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86 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

2. Although the immune response is normally 15. are cytokines that stimulate the
protective, it can also produce undesirable migration and activation of immune and in-
effects such as when the response is excessive, flammatory cells.
as in , or when it recognizes self-
16. Cytokines that stimulate bone marrow
tissue as foreign, as in disease.
pluripotent stem and progenitor or precursor
3. As the first line of defense, im- cells to produce large numbers of platelets,
munity consists of the physical, chemical, erythrocytes, lymphocytes, neutrophils,
molecular, and cellular defenses. monocytes, eosinophils, basophils, and den-
dritic cells are known as .
4. immunity is the second major
immune defense. 17. The mucous membrane linings of the gas-
trointestinal, respiratory, and urogenital
5. Substances that elicit adaptive immune re-
tracts are protected by sheets of tightly
sponses are called .
packed cells that block the entry
6. immunity, generated by B lym- of microbes.
phocytes, is mediated by molecules called an-
18. The binding of to the pattern
tibodies and is the principal defense against
recognition receptors on leukocytes initiates
extracellular microbes and toxins.
the signaling events that lead to innate im-
7. immunity is mediated by spe- munity and tissue changes associated with
cific T lymphocytes and defends against acute inflammation.
intracellular microbes such as viruses.
19. is the coating of a microorgan-
8. Dendritic cells and function as ism with soluble molecules that tag the
antigen-presenting cells for adaptive immu- microorganism for more efficient recognition
nity. by phagocytes.
9. The key cells of innate immunity are 20. are substances foreign to the
, , and natural killer host that can stimulate an immune response.
cells.
21. Antibodies comprise a class of proteins called
10. are the early responding cells of .
innate immunity.
22. immunity depends on matura-
11. During an inflammation response, the mono- tion of B lymphocytes into plasma cells,
cyte leaves the blood vessel; transforms into a which produce and secrete antibodies.
tissue ; and phagocytoses bacte-
23. The serves as a master regulator
ria, damaged cells, and tissue debris.
for the immune system.
12. cells and cells are
24. T cells suppress immune re-
the only cells in the body capable of specifi-
sponses by inhibiting the proliferation of
cally recognizing different antigenic determi-
other potentially harmful self-reactive
nants of microbial agents and other
lymphocytes.
pathogens.
25. The central lymphoid organs, the
13. are part of the innate immune
and the , provide
system and may be the first line of defense
the environment for immune cell production
against viral infections.
and maturation.
14. cells are specialized, bone mar-
26. The white pulp layer of the con-
row–derived leukocytes found in lymphoid
tains concentrated areas of B and T lympho-
tissue that are important intermediaries be-
cytes permeated by macrophages and
tween the innate and adaptive immune sys-
dendritic cells.
tems.

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CHAPTER 17 INNATE AND ADAPTIVE IMMUNITY 87

Activity B Consider the following figure. f. Physical barrier of

skin to infection
Antigen g. Disrupts virus infec-
tions
h. Small cationic pep-
Variable region tides found in the
(heavy chain)
stomach
Fab
Constant region
i. Regulates the pro-
(heavy chain) duction of cy-
tokines and
adhesion molecules
j. Hydrolytic enzyme
Variable
region capable of cleaving
(light chain) the walls of bacter-
Constant
ial cell
region
(light chain)
2.
Column A Column B
Fc
1. Epitopes a. Processing a com-
Heavy plex antigen into
2. CD4
chain epitopes and then
3. Perforans displaying the for-
eign and self-pep-
4. Cell-mediated
1. What does this figure depict? Discuss the sig-
tides on their
immunity
nificance of the different parts depicted in the membranes
5. Antigen b. Dependent on B
model.
presentation cells
6. Antibody- c. Self-recognition
Activity C Match the key terms in Column A
with their definitions in Column B. mediated proteins
immunity d. Type of T helper cell
1.
7. Major e. Dependent on T
Column A Column B histocom- cells
1. Mucins a. Pathogen-associated patibility f. Pore-forming mole-
molecular pattern complex cules
2. Lysozyme
receptors 8. Haptens g. Immunologically
3. Epithelial b. Renders bacteria  active sites on anti-
9. CD8
barrier and other cells sus- gens
ceptible to phagocy- 10. Tolerance h. Combine with
4. Defensins
tosis larger protein mole-
5. Collectins cules and serve as
c. Traps and washes
6. Cilia away potential in- antigens
vaders i. Ability of the im-
7. Toll-like
receptors d. Epithelial protru- mune system to be
sion that moves nonreactive to self-
8. Opsonins mucus to throat antigens
9. NF- e. Surfactant proteins j. Cytotoxic T cells
in respiratory track
10. Interferons

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88 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

Activity D Briefly answer the following. 8. Compare and contrast active versus passive
immunity.
1. How do the cells of the immune system com-
municate with each other?

2. What is the innate immune system, and what SECTION III: APPLYING YOUR
is its function?
KNOWLEDGE
Activity E Consider the following scenario and
answer the question.
A young mother has her 2-week-old infant at the
3. What is the general function of neutrophils clinic for a well-baby check-up. She is concerned
and macrophages in the inflammatory re- because her baby has been exposed to chicken-
sponse? pox. She states, “What am I going to do? I didn’t
know my friend’s son had just gotten over the
chickenpox. Will my baby get chickenpox?”
1. In talking with this mother, the nurse explains
passive immunity. What key points will the
4. What are the methods of initiating the com- nurse be sure to mention?
plement system, and what are the results of ac-
tivation?

5. What is the function of MHC proteins, and SECTION IV: PRACTICING

how are they classified? FOR NCLEX
Activity F Answer the following questions.
1. Natural killer cells are specialized lympho-
cytes that are one of the major parts of which
immunity?
6. Explain how a macrophage participates in
antigen presentation. a. Innate
b. Adaptive
c. Humoral
d. Cell mediated
2. Both innate and adaptive immunity have
7. How many classes of antibody are there? Give cells that produce cytokines. Cytokines medi-
a brief definition of function for each one. ate the actions of many cells in both innate
and adaptive immunity. How are the actions
of cytokines described?
a. Rapid and self-limiting
b. Pleiotropic and redundant
c. Cell specific and targeted
d. Dendritic and morphologic

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CHAPTER 17 INNATE AND ADAPTIVE IMMUNITY 89

3. Stem cells in the bone marrow produce T 8. The laboratory finds IgA in a sample of cord
lymphocytes or T cells, and release them into blood from a newborn infant. This finding is
the vascular system. The T cells then migrate important because it signifies what?
where to mature? a. Fetal reaction to an infection acquired at
a. Spleen birth
b. Liver b. Maternal reaction to an infection in the
c. Thymus fetus
d. Pancreas c. Maternal exposure to an infection in a sex-
ual partner
4. Cell-mediated immunity is involved in resis-
d. Fetal reaction to exposure to an intrauter-
tance to infectious diseases caused by bacteria
ine infection
and some viruses. It is also involved in cell-
mediated hypersensitivity reactions. Which 9. The daughter of a 79-year-old woman asks
of these does not cause a cell-mediated hyper- the nurse why her mother gets so many infec-
sensitivity reaction? tions. The daughter states, “My mother has
a. Latex always been healthy, but now she has pneu-
monia. Last month she got cellulitis from a
b. Poison ivy
bug bite she scratched. The month before
c. X-ray dye that was some other infection. How come she
d. Blood transfusion seems to get sick so often now?” What is the
nurses’ best response?
5. Passive immunity is immunity that is trans-
ferred from another source and lasts only a. “As people get older, their immune system
weeks to months. What is an example of pas- doesn’t respond as well as it did when they
sive immunity? were younger.”
a. An injection of gamma-globulin b. “About the time we are 75 or 76 years old,
our immune system quits working.”
b. An immunization
c. “Your mother just seems to be prone to in-
c. Exposure to poison ivy
fections.”
d. Allergy shots
d. “Your mother gets infections frequently
6. An essential property of the immune system because she wants attention from you.”
is self-regulation. An immune response that is
10. The results of recent research suggest that a
not adequate can lead to immunodeficiency,
key role in the origin of some diseases is
whereas an immune response that is exces-
played by inflammation. Inflammation has a
sive can lead to conditions from allergic re-
role in the beginnings of which of these
sponses to autoimmune diseases. Which of
diseases?
these is not an example of a breakdown of the
self-regulation of the immune system? a. Osteoporosis
a. Multiple sclerosis b. Rheumatoid arthritis
b. Huntington disease c. Osteogenesis imperfecta
c. Systemic lupus d. Hydronephrosis
d. Fibromyalgia 11. , or immunogens, are substances
foreign to the host that can stimulate an
7. One of the self-regulatory actions of the im-
immune response.
mune system is to identify self-antigens and
be nonreactive to them. What is this ability
of the immune system defined as?
a. Antigen specificity
b. Nonreactivity
c. Tolerance
d. Antigen diversity

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90 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

12. Each immunoglobulin has a different role 13. The mucous membrane linings of the gas-
in the immune response. Match each trointestinal, respiratory, and urogenital
immunoglobulin with its role. tracts are protected by sheets of tightly
packed cells that block the entry
Immunoglobulin Role
of microbes and destroy them by secreting
1. IgG a. First circulating antimicrobial enzymes, proteins, and pep-
immunoglobulin to tides.
2. IgA
appear in response to
14. In both innate and adaptive immune sys-
3. IgM an antigen and first
tems, cells communicate information about
antibody type made by
4. IgD invading organisms by the secretion of chem-
a newborn
ical mediators. Which are these mediators?
5. IgE b. Involved in inflamma- Mark all that apply.
tion, allergic responses,
a. Virulence factors
and combating para-
sitic infections b. Chemokines
c. Serves as an antigen c. Colony-stimulating factors
receptor for initiating d. Coxiella
the differentiation of
15. There are many cells that comprise the pas-
B cells
sive and adaptive immune systems. Which
d. Protects against bacte- cells are responsible for the specificity and
ria, toxins, and viruses memory of adaptive immunity? Mark all that
in body fluids and apply.
activates the comple-
a. Phagocytes
ment system
b. T lymphocytes
e. Primary defense
against local infections c. Dendritic cells
in mucosal tissues d. Natural killer cells
e. B lymphocytes

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18

CHAPTER
Inflammation, Tissue
Repair, and Wound
Healing

SECTION I: LEARNING 10. Explain the effects of soluble mediators and

the extracellular matrix on tissue repair and
OBJECTIVES wound healing
1. State the five cardinal signs of acute inflam- 11. Trace the wound-healing process through the
mation and describe the physiologic mecha- inflammatory, proliferative, and remodeling
nisms involved in production of these signs phases
2. Describe the vascular changes in an acute in- 12. Explain the effects of malnutrition; ischemia
flammatory response and oxygen deprivation; impaired immune
and inflammatory responses; and infection,
3. Characterize the interaction of adhesion mol-
wound separation, and foreign bodies on
ecules, chemokines, and cytokines in leuko-
wound healing
cyte adhesion, migration, and phagocytosis,
which are part of the cellular phase of inflam- 13. Discuss the effect of age on wound healing
mation
4. List four types of inflammatory mediators and
state their function SECTION II: ASSESSING YOUR
5. Contrast acute and chronic inflammation UNDERSTANDING
6. Define the systemic manifestations of inflam- Activity A Fill in the blanks.
mation, including the characteristics of an
acute-phase response 1. is a protective response in-
tended to eliminate the initial cause of cell
7. Define the terms parenchymal and stromal as injury, remove the damaged tissue, and gen-
they relate to the tissues of an organ erate new tissue.
8. Compare labile, stable, and permanent cell 2. The cardinal signs of inflammation are
types in terms of their capacity for regenera- , , ,
tion and .
9. Describe healing by primary and secondary
intention

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92 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

3. In addition to the cardinal signs that appear 18. Aspirin and the nonsteroidal anti-inflamma-
at the site of injury, manifesta- tory drugs reduce inflammation by inactivat-
tions may occur as chemical mediators pro- ing the first enzyme in the
duced at the site of inflammation gain pathway for prostaglandin synthesis.
entrance to the circulatory system.
19. Eating oily fish and other foods that are high
4. inflammation is of relatively in results in partial replacement
short duration, lasting for a few minutes, of arachidonic acid in inflammatory cell
whereas inflammation is of a membranes, which leads to decreased produc-
longer duration, lasting for days to years. tion of arachidonic acid–derived inflamma-
tory mediators.
5. Acute inflammation involves two major com-
ponents: the and 20. fragments contribute to the in-
stages. flammatory response by causing vasodilation,
increasing vascular permeability; and enhanc-
6. Increased circulating white blood cells are a
ing the activity of phagocytes.
condition known as .
21. Activation of the system results
7. produce prostaglandins and
in release of bradykinin, which increases vas-
leukotrienes, platelet activating factor, in-
cular permeability and causes contraction of
flammatory cytokines, and growth factors
, dilation of blood vessels, and
that promote regeneration of tissues.
.
8. changes that occur with inflam-
22. , a cytokine that will induce en-
mation involve the arterioles, capillaries, and
dothelial cells to express adhesion molecules
venules of the microcirculation.
and release cytokines, chemokines, and reac-
9. The selectins function in adhesion of tive oxygen species, is released from mast
to endothelial cells. cells.
10. The integrins promote and 23. The radical, radi-
cell-to-extracellular matrix interactions. cal, and radical are the major
free oxygen radicals produced within the cell.
11. Chemotaxis is dynamic and energy-directed
process of directed . 24. At higher levels, free radical mediators can
produce .
12. Groups of proteins that direct the trafficking
of leukocytes during the early stages of 25. The acute inflammatory response involves
inflammation or injury are known as the production of ; they can be
. serous, hemorrhagic, fibrinous, membranous,
or purulent.
13. The pathways generate toxic
oxygen and nitrogen products. 26. Agents that evoke chronic inflammation typi-
cally are low-grade, persistent infections or
14. The plasma-derived mediators of inflamma-
irritants that are unable to or
tion include the factors and the
.
proteins.
27. The function of the acute phase protein
15. Histamine causes of arterioles
is believed to be protective, in
and increases the of venules.
that it binds to the surface of invading mi-
16. The family of inflammatory me- croorganisms and targets them for destruc-
diators consists of prostaglandins, tion by complement and phagocytosis.
leukotrienes, and related metabolites.
28. Body organs and tissues are composed of two
17. The induce inflammation and types of structures: and
potentiate the effects of histamine and other .
inflammatory mediators.

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CHAPTER 18 INFLAMMATION, TISSUE REPAIR, AND WOUND HEALING 93

29. are those that continue to divide 1. What does this figure represent? Explain the
and replicate throughout life, replacing cells process that is depicted.
that are continually being destroyed.
30. Cells that are capable of undergoing regenera-
tion when confronted with an appropriate
stimulus and are thus capable of reconstitut-
ing the tissue of origin are termed
.
31. tissue is a glistening red, moist
Activity C Match the key terms in Column A
connective tissue that contains newly formed
with their definitions in Column B.
capillaries, proliferating fibroblasts, and resid-
ual inflammatory cells. Column A Column B
32. The elderly have reduced and 1. Endothelial a. Increase in the
synthesis, impaired wound con- cells blood during aller-
traction, and slower reepithelialization of gic reactions
2. Eosinophils
open wounds. b. Leukocyte accumu-
3. Edema lation
33. The is often born with imma-
ture organ systems and minimal energy stores 4. Neutrophils c. Regulate leukocyte
but high metabolic requirements—a condi- extravasation
5. Exudate
tion that predisposes to impaired wound d. Stimulate inflam-
healing. 6. Nitric oxide matory reaction in
7. Margination response to injury
Activity B Consider the following figure. or infection
8. Thrombocytes
e. Circulating cells
Injured tissue,
inflammatory mediators
9. Mast cells similar to mast cells
10. Basophils f. Primary phagocyte
Cell membrane phospholipids that arrives early at
the site of inflam-
Corticosteroid
medications mation
Arachidonic acid g. Stimulator of
vasodilation
Lipoxygenase
h. Activation affects
Cyclooxygenase
pathway pathway vascular permeabil-
Aspirin, NSAIDs ity, chemotactic,
adhesive, and prote-
Leukotrienes
(LTC4, LTD4, LTE4) Prostaglandins Thromboxane
olytic properties
(PGI2, PGF2a) (TxA2)
i. Swelling due to
Induces smooth muscle movement of fluid
contraction
Constricts pulmonary
Induces vasodilation and
bronchoconstriction
Vasoconstriction
Bronchoconstriction
from vasculature
airways Inhibits inflammatory Promotes platelet into tissues
Increases microvascular cell function function
permeability j. Outpouring of a
protein-rich fluid
into the tissue and
extravascular space

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94 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

Activity D Put the following events in the 6. Explain and describe the two types of chronic
proper order: inflammation.

a. Chemotaxis
b. Margination and adhesion to endothelium
c. Activation and phagocytosis
d. Transmigration across endothelium
7. What is the purpose of the acute phase re-
sponse of inflammation?

Activity E Briefly answer the following.

1. The cardinal signs of inflammation result from
the physiologic processes of the inflammatory
cells and protein systems. List the signs, and 8. Explain the concept of wound healing by first
give a brief explanation as to its cause. and second intent.

2. Describe and differentiate between acute and

chronic inflammation.
SECTION III: APPLYING YOUR
KNOWLEDGE
Activity F Consider the following scenario
and answer the questions.
3. The vascular response of inflammation follows
one of three patterns. Describe these patterns, You are the nurse caring for a burn victim who
and explain why it is necessary to have multi- has sustained second- and third-degree burns
ple responses. over 50% of his body. The family is asking you
questions about the care that is being given to
their relative.
1. A family member asks about the drainage she
sees on the bandages. What would you tell
her?
4. Many leukocytes have the ability to phagocy-
tose foreign material and dispose of it. The
process involves three steps. List and explain
these steps.

2. Several days post injury, a family member asks

why the client is not eating. What kind of in-
formation would you give her?
5. There are many mediators of the inflamma-
tory system. They may be grouped by func-
tion. Describe each group, and give a brief
example of each.

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CHAPTER 18 INFLAMMATION, TISSUE REPAIR, AND WOUND HEALING 95

SECTION IV: PRACTICING are the phases of wound healing? Mark all
that apply.
FOR NCLEX
a. Activation phase
Activity G Answer the following questions. b. Proliferative phase
1. The cardinal signs of inflammation include c. Nutritional phase
swelling, pain, redness, and heat. What is the d. Inflammatory phase
fifth cardinal sign of inflammation? e. Maturational phase
a. Loss of function
5. Hyperbaric treatment for wound healing is
b. Altered level of consciousness used for wounds that have problems in heal-
c. Sepsis ing due to hypoxia or infection. It works by
d. Fever raising the partial pressure of oxygen in
plasma. How does hyperbaric oxygen treat-
2. The cells that are associated with allergic dis- ment enhance wound healing?
orders and the inflammation associated with
a. Destruction of anaerobic bacteria
immediate hypersensitive reactions are
known as what? Mark all that apply. b. Increased action of eosinophils
a. Macrophages c. Promotion of angiogenesis
b. Eosinophils d. Decrease in fibroblast activity
c. Mast cells 6. As a nurse in the emergency department, you
d. Neutrophils would know that research has shown that the
possibility of infection in a bite wound is tied
e. Basophils
to what caused the bite, the location of the
3. Inflammation can be either acute or chronic. bite, and the type of injury inflicted by the
The immune system is believed to play a role bite. Which bite would have the highest pos-
in chronic inflammation and may be one of sibility of infection?
the reasons chronic inflammation may persist a. Bite inflicted by a child
for days to months to years. Why is the risk
b. Wound caused by a cat bite
of scarring and deformity greater in chronic
inflammation than it is in acute inflamma- c. Bite inflicted by an adult
tion? d. Wound caused by a dog bite
a. Chronic inflammation is the persistent de- 7. Wound healing is more difficult for persons
struction of healthy tissue. at both ends of the age spectrum, although
b. Fibroblasts instead of exudates proliferate the reasons differ. In the elderly, wound heal-
in chronic inflammation. ing is impaired or delayed because of struc-
c. Typically, agents that evoke chronic in- tural and functional changes in the skin that
flammation are infections or irritants that occur with aging and the chronicity of
penetrate deeply and spread rapidly. wounds in the elderly. Why do neonates and
small children have problems with wound
d. Chronic inflammation is often the result of
healing?
allergic reactions.
a. Their bodies are not yet capable of an in-
4. A class of student nurses is hearing a lecture flammatory response.
on wound healing. The professor explains
b. Their skin is fragile.
about primary and secondary healing. The
professor continues to talk about the phases c. They do not have the reserves needed.
of wound healing and states that in both pri- d. Their immune systems are hypersensitive
mary and secondary healing the phases of to infectious agents.
wound healing occur at different rates. What

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96 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

8. All wounds are considered contaminated at 10. Inflammation can be either local or systemic.
the time they occur. Usually, the natural de- What are the most prominent systemic mani-
fenses in our bodies can deal with the invad- festations of inflammation?
ing microorganisms; however, there are times a. Fever, leukocytosis or leukopenia, and the
when a wound is badly contaminated and acute phase response
host defenses are overwhelmed. What hap-
b. Fever, leukocytosis or leukopenia, and the
pens to the healing process when host de-
transition phase response
fenses are overwhelmed by infectious agents?
c. Widening pulse pressure, thrombocytope-
a. The inflammatory response is shortened
nia, and the recovery phase response
and does not complete destruction of the
invading organisms. d. Widening pulse pressure, thrombocytope-
nia, and the latent phase response
b. Fibroblast production becomes malignant
due to hypersensitization by invading or-
ganisms.
c. The formation of granulation tissue is im-
paired.
d. Collagen fibers cannot draw tissues to-
gether.
9. During the acute inflammatory response,
there is a period called the transient phase
where there is increased vascular permeabil-
ity. What is considered the principal media-
tor of the immediate transient phase?
a. Histamine
b. Arachidonic acid
c. Fibroblasts
d. Cytokines

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19

CHAPTER
Disorders of the
Immune Response

SECTION I: LEARNING 9. Discuss the rationale for matching of human

leukocyte antigen or major histocompatibil-
OBJECTIVES ity complex types in organ transplantation
1. State the difference in causes of primary and 10. Compare the immune mechanisms involved
secondary immunodeficiency disorders in allogeneic transplant rejection
2. Compare and contrast pathology and mani- 11. Describe the mechanisms and manifestations
festations of humoral (B-cell), cellular (T-cell), of graft-versus-host disease
and combined T- and B-cell immunodefi-
12. Relate the mechanisms of self-tolerance to the
ciency disorders
possible explanations for development of
3. State the function of the complement system autoimmune disease
and relate it to the manifestations of comple-
13. Name four or more diseases attributed to
ment deficiencies and hereditary angioneu-
autoimmunity
rotic edema
14. Describe three or more postulated mecha-
4. State the proposed mechanisms of dysfunc-
nisms underlying autoimmune disease
tion and manifestations of phagocytosis dis-
orders 15. State the criteria for establishing an autoim-
mune basis for a disease
5. Differentiate between adaptive immune re-
sponses that protect against microbial agents
and hypersensitivity responses
6. Describe the immune mechanisms involved
SECTION II: ASSESSING YOUR
in a type I, type II, type III, and type IV hy- UNDERSTANDING
persensitivity reaction
Activity A Fill in the blanks.
7. Describe the pathogenesis of allergic rhinitis,
food allergy, serum sickness, Arthus reaction, 1. Under normal conditions, the
contact dermatitis, and hypersensitivity response deters or prevents disease.
pneumonitis 2. can be defined as an abnormal-
8. Characterize the differences in latex allergy ity in the immune system that renders a
caused by a type I, IgE-mediated hypersensi- person susceptible to diseases normally
tivity response and that caused by a type IV, prevented by an intact immune system.
cell-mediated response

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98 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

3. The immune system is com- 16. Severe combined immunodeficiency disease

prised of the phagocytic leukocytes, natural is more commonly found in
killer cells, and complement proteins. because it is X linked.
4. The immune response is com- 17. Hereditary angioneurotic edema is a form of
posed mainly of T and B cells and responds to deficiency.
infections more slowly, but more specifically
18. Chronic cirrhosis of the liver would reduce
than the innate immune system.
the production of complement proteins; this
5. The adaptive immune system is further type of deficiency would be classified as
divided into the and .
immune systems.
19. Chédiak-Higashi syndrome is an abnormality
6. A large number of primary immunodeficiency of of phagocytes.
diseases have been mapped to the
20. Chronic granulomatous disease is a group of
chromosome.
inherited disorders that greatly reduce or in-
7. Defects in humoral immunity increase the activate the ability of phagocytic cells to pro-
risk of recurrent infections. duce the .
8. During the first few months of life, infants are 21. disorders refer to excessive or in-
protected from infection by IgG antibodies appropriate activation of the immune system.
that originate in circulation
22. Type I hypersensitivity reactions to antigens
during fetal life.
are referred to as .
9. Of all the primary immunodeficiency dis-
23. is a systemic life-threatening hy-
eases, those affecting produc-
persensitivity reaction characterized by wide-
tion are the most frequent.
spread edema, vascular shock secondary to
10. Abnormal immunoglobulin loss can occur vasodilation, and difficulty breathing.
with chronic disease; due to
24. Persons with allergic conditions
abnormal glomerular filtration, patients lose
tend to have high serum levels of IgE and in-
serum IgA and IgG in their urine.
creased numbers of basophils and mast cells.
11. Secondary humoral immunodeficiency’s can
25. Allergic is characterized by
also result from a number of , in-
symptoms of sneezing, itching, and watery
cluding chronic lymphocytic leukemia, lym-
discharge from the nose and eyes.
phoma, and multiple myeloma that interfere
with normal immunoglobulin production. 26. There are three different types of antibody-
mediated mechanisms involved in
12. T cells can be functionally divided into two
reactions: opsonization and
subtypes: and T
complement- and antibody receptor–
cells.
mediated phagocytosis, complement- and
13. Collectively, protect against antibody receptor–mediated inflammation,
fungal, protozoan, viral, and intracellular bac- and antibody-mediated cellular dysfunction.
terial infections; control malignant cell prolif-
27. With destruction, cells that are
eration; and are responsible for coordinating
coated with low levels of IgG antibody are
the overall immune response.
killed by a variety of effector cells, which bind
14. Disorders that affect both B and T lympho- to their target by their receptors for IgG, and
cytes, with resultant defects in both humoral cell lysis occur without phagocytosis.
and cell-mediated immunity, fall under the
28. hypersensitivity reactions are
broad classification of syn-
responsible for the vasculitis seen in certain
drome.
autoimmune diseases such as systemic lupus
15. In , genetic mutations lead to erythematous or the kidney damage seen
absence of all T- and B-cell function and, in with acute glomerulonephritis.
some cases, a lack of natural killer cells.

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CHAPTER 19 DISORDERS OF THE IMMUNE RESPONSE 99

29. sickness is a systemic immune Activity B Consider the following figure.

complex disorder that is triggered by the de-
position of insoluble antigen-antibody com-
plexes in blood vessels, joints, heart, and Bone marrow
kidney tissue.
30. A term used by pathologists and immunolo-
gists to describe localized tissue necrosis
caused by immune complexes is the Pre-T cells

.
31. Hypersensitivity reactions that are mediated
Thymus
by specifically sensitized T lymphocytes are
divided into two basic types—direct cell-
mediated cytotoxicity and delayed-type hy-
persensitivity—and generally classified as
.
32. Allergic denotes an inflamma-
tory response confined to the skin that is ini-
tiated by reexposure to an allergen to which a
person had previously become sensitized.
33. A major barrier to is the process
of rejection in which the recipient’s immune A
system recognizes the graft as foreign and at-
tacks it. B

34. Transplanted tissue can be categorized as an C

graft if donor and recipient are
the same person, graft if the In this figure, label and diagram the process of T
donor and recipient are identical twins, and cell selection. Be sure to include the end result of
if the donor and recipient are each pathway.
related or unrelated but share similar human
leukocyte antigen types. Activity C Match the key terms in Column A
with their definitions in Column B.
35. occurs when immunologically
competent cells or precursors are transplanted Column A Column B
into recipients who are immunologically
1. DiGeorge a. Essentially unde-
compromised.
syndrome tectable levels of all
36. diseases represent a group of dis- serum im-
2. Secondary
orders that are caused by a breakdown in the munoglobulins
immunod-
ability of the immune system to differentiate b. Complement-
eficiency
between self- and nonself-antigens. mediated immune
3. Hyper-IgM disorders
37. The ability of the immune system to differen-
syndrome
tiate self from nonself is called . c. Decreases in one or
4. X-linked more IgG subgroups
38. Loss of self-tolerance with development of
agammaglo- d. Repeated bouts of
is characteristic of a number of
bulinemia upper respiratory
autoimmune disorders.
5. Selective IgA and middle ear
deficiency infections

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100 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

6. Adenosine e. Partial or complete Activity E Briefly answer the following.

deaminase failure of develop-
deficiencies ment of the thymus 1. What is the difference between a primary and
and T-cell and parathyroid a secondary immunodeficiency?
cytokine glands
receptor f. In levels of serum
mutations and secretory IgA
7. Transient g. Antibody-mediated
hypogamma- disorders 2. Why does it take up to 6 months for the symp-
globulinemia h. Acquired later in life toms of a primary immunodeficiency to ap-
of infancy pear?
i. Terminal differenti-
8. Ataxia- ation of mature B
telangiectasia cells to plasma cells
is blocked
9. Common
variable j. Ig-E–mediated dis-
immuno- orders
3. Explain how a patient can become sensitized
deficiency k. Lymphopenia and a to an allergen (antigen) in a type I hypersensi-
decrease in the ratio tivity reaction.
10. Immuno-
of CD4 helper T
globulin G
cells to CD8 sup-
subclass
pressor T cells
deficiency
l. Low IgG and IgA
11. Wiskott-Aldrich levels, high IgM
syndrome concentrations 4. Compare the direct cell-mediated cytotoxicity
12. Type I m. Cause of severe of type IV hypersensitivity reactions with the
hypersensitivity combined immun- delayed-type hypersensitivity reactions.
reaction odeficiency disease
13. Type II n. Susceptible to infec-
hypersensitivity tions caused by
reaction encapsulated
microorganisms
14. Type III 5. What is severe combined immunodeficiency
o. T-cell–mediated disease?
hypersensitivity
disorders
reaction
15. Type IV
hypersensitivity
reaction

Activity D Put the normal sequence of actions

of a polymorphonuclear phagocyte in order in
the following boxes. SECTION III: APPLYING YOUR
1. Phagocytosis
KNOWLEDGE
2. Kill the ingested pathogens Activity F Consider the following scenario and
3. Chemotaxis answer the questions.
4. Generate microbicidal substances A 30-year-old woman has just been diagnosed
5. Adherence with systemic lupus erythematosus. She presents
with arthritis, a “butterfly rash,” weight loss,
weakness, and fatigue. She is distraught and
states, “How can the doctor be sure that I have
this disease?”

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CHAPTER 19 DISORDERS OF THE IMMUNE RESPONSE 101

1. The correct response to this patient about the a. DiGeorge syndrome

diagnosis would include information about b. Y-linked hyper-IgM syndrome
which test?
c. X-linked agammaglobulinemia
d. Y-linked agammaglobulinemia
4. Combined immunodeficiency syndrome is a
disorder in which both B and T lymphocytes
are affected. This results in defects in both
2. When planning patient education for this humoral and cell-mediated immunity. What
woman, what medications would the nurse could be the cause of this disorder?
tell the patient about?
a. Multiple misplaced genes that influence
lymphocyte development and response
b. A single mutation in any gene that influ-
ences major histocompatibility antigens
c. A single misplaced gene that influences
major histocompatibility
d. Multiple mutations in genes that influence
SECTION IV: PRACTICING lymphocyte development and response
FOR NCLEX 5. Combined immunodeficiency syndrome
(CIDS) is distinguished by low, not absent, T-
Activity G Answer the following questions. cell function. These diseases are usually asso-
ciated with other disorders and arise from
1. Infants are born with a passive immunity that
diverse genetic causes. Which of the follow-
occurs when immunoglobulin antibodies
ing diseases is considered a CIDS?
cross the placenta from the maternal circula-
tion prior to birth. Which immunoglobulin is a. Pierre-Robin syndrome
capable of crossing the placenta? b. Angelman syndrome
a. IgM c. Ataxia-telangiectasia
b. IgD d. Adair-Dighton syndrome
c. IgG 6. The immune system typically responds to in-
d. IgE vaders of all types in our bodies. However, it
can also cause tissue injury and disease. What
2. Drug-induced secondary hypogammaglobu-
is this effect called?
linemia are reversible. Which drugs produce
hypogammaglobulinemia? Mark all that a. Hypersensitivity action
apply. b. Antigen reaction
a. Phenytoin c. Mediator response action
b. Corticosteroids d. Allergen stimulating reaction
c. Carbamazepine 7. Some people are so sensitive to certain anti-
d. Disease-modifying antirheumatic drugs gens that they react within minutes by devel-
e. Interferon-beta 1a drugs oping itching, hives, and skin erythema,
followed shortly thereafter by bronchospasm
3. Primary cell-mediated disorders of the im- and respiratory distress. What is this com-
mune system cause severe problems with in- monly known as?
fections. Children with these disorders rarely
a. Antigen reaction
survive beyond childhood without a bone
marrow transplant. Which of the following is b. Anaphylactic reaction
a disease that involves primary cell-mediated c. Hyposensitive reaction
disorders of the immune system? d. Arthus reaction

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102 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

8. A systemic immune complex disorder that is 10. A transplant reaction that occurs immediately
caused by insoluble antigen-antibody com- after transplantation is caused by
plexes being deposited in blood vessels, the antibodies.
joints, the heart, or kidney tissue is called
11. It has been postulated that an autoimmune
what?
disease needs a “trigger event” for it to clini-
a. Anti-immune disease cally manifest itself in the body. What are
b. Systemic lupus erythematosus these “trigger events” believed to be? Mark all
c. Serum sickness that apply.
d. Antigen-antibody sickness a. A. microorganism or virus
b. A self-antigen from a previously se-
9. The incidence of latex allergy is skyrocketing
questered body tissue
because of diseases such as HIV. It is known
that the use of latex examining gloves has c. A breakdown in the antigen-antibody re-
played a major role in the increasing inci- sponse
dence of latex allergy. What plays a signifi- d. A chemical substance
cant role in the allergic response to latex e. A systemic ability for self-tolerance
gloves?
a. Baking powder used inside the gloves
b. Airborne pieces of latex
c. Latex proteins that attach to clothing
d. Cornstarch powder used inside the gloves

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20

CHAPTER
Acquired
Immunodeficiency
Syndrome

SECTION I: LEARNING 10. Explain the possible significance of a positive

antibody test for HIV infection
OBJECTIVES
11. Differentiate between the enzyme immunoas-
1. Briefly trace the history of the AIDS epidemic say (enzyme-linked immunosorbent assay)
and Western blot antibody detection tests for
2. State the virus responsible for AIDS and ex-
HIV infection
plain how it differs from most other viruses
12. Describe the methods used in the early man-
3. Describe the mechanisms of HIV transmis-
agement of HIV infection
sion and relate them to the need for public
awareness and concern regarding the spread 13. Compare the actions of the reverse transcrip-
of AIDS tase inhibitors (e.g., nucleoside reverse tran-
scriptase inhibitors, nucleotide analog reverse
4. Describe the structure of HIV and trace its
transcriptase inhibitors), non-nucleoside re-
entry and steps in replication within the
verse transcriptase inhibitors, protease in-
CD4 T lymphocyte
hibitors, and fusion inhibitors in terms of
5. Describe the alterations in immune function controlling HIV replication
that occur in persons with AIDS
14. Enumerate some of the psychosocial issues as-
6. Describe the CDC HIV/AIDS classification sys- sociated with HIV/AIDS
tem
15. Discuss the vertical transmission of HIV from
7. Relate the altered immune function in per- mother to child and recommended preven-
sons with HIV infection and AIDS to the de- tion measures
velopment of opportunistic infections,
16. Cite problems with the diagnosis of HIV in-
malignant tumors, nervous system manifesta-
fection in the infant
tions, the wasting syndrome, and metabolic
disorders 17. Compare the progress of HIV infection in in-
fants and children with HIV infection in
8. Discuss the transmission of HIV
adults
9. Describe preventive strategies to decrease the
transmission of HIV

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104 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

SECTION II: ASSESSING YOUR 11. infections begin to occur as the

immune system becomes severely compro-
UNDERSTANDING mised.
Activity A Fill in the blanks. 12. The most common causes of respiratory dis-
ease in persons with HIV infection are
1. AIDS is a disease caused by infection with
, Pneumocystis carinii pneumo-
and is characterized by pro-
nia, and pulmonary .
found with associated
infections, malignancies, wast- 13. syndrome is common in per-
ing, and central nervous system degenera- sons with HIV infection or AIDS.
tion.
14. The term is frequently used to
2. HIV is a that selectively attacks describe the body composition changes with
the T lymphocytes, the immune or without the other metabolic derange-
cells responsible for orchestrating and coordi- ments.
nating the immune response to infection.
15. The development of or
3. HIV is transmitted from one person to an- behaviors will prevent HIV transmission.
other through contact,
16. The most accurate and inexpensive method
contact, or .
for identifying HIV is the test.
4. contact is the most frequent
17. The test is more specific than
way that HIV is transmitted.
the HIV antibody test.
5. Because HIV is found in , the use
18. Polymerase chain reaction is a technique for
of needles, syringes, and other drug injection
detecting HIV .
paraphernalia is a direct route for transmis-
sion. 19. The medications that are currently available
to treat HIV the amount of virus
6. Occupational risk of infection for health care
in the body, but they do not
workers is most often associated with
HIV.
or of blood from a
patient with HIV. 20. Many people with HIV have preexisting men-
tal health conditions like or
7. HIV infects a limited number of cell types in
disorders as well as alcohol and
the body, including a subset of lymphocytes
other drug problems.
called , , and
cells. 21. for HIV DNA is used most often
to diagnose HIV in infants younger than 18
8. CD4 T cell recognizes foreign antigens and
months.
helps activate and
immunity.
9. Treatment of HIV/AIDS relies on the use of
agents that steps of the HIV
replication process.
10. HIV replication involves the killing of the
cell and the release of copies of
HIV into the bloodstream.

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CHAPTER 20 ACQUIRED IMMUNODEFICIENCY SYNDROME 105

Activity B Match the key terms in Column A CD4 T cell; DNA synthesis via reverse
with their definitions in Column B. transcriptase; attachment and uncoating of the
virus, allowing the genetic material to enter the
Column A Column B host cell; translation of mRNA into a protein;
1. HIV-associated a. Demyelinating dis- assemblage of new HIV; integration into the host
neurocognitive ease of the central DNA.
disorders nervous system
2. Mycobacterium b. Malignancy of the
tuberculosis endothelial cells
that line small Activity D Briefly answer the following.
3. Human blood vessels
papillomavirus 1. How does HIV make a patient immunodefi-
c. Organism com- cient?
4. Pneumocystis mon in the envi-
carinii ronment that
causes pneumonia
5. Progressive
in AIDS patients
multifocal
leukoen- d. Usually a late com-
cephalopathy plication of HIV 2. What is the typical course of HIV?
manifested via de-
6. Toxoplasma crease in neural
gondii speed
7. Kaposi sarcoma e. Most common
cause of death for
8. HIV-associated 3. What is the goal of highly active antiretroviral
people with HIV
dementia therapy (HAART)?
f. Brain parasite
9. Streptococcus
g. Causes bacterial
pneumoniae
pneumonia in
AIDS patients
h. Syndrome of cog-
nitive impairment 4. What are the primary classes of medication
with motor dys- used in HAART, and what is the goal of each?
function
i. Causes cervical
and anal carci-
noma

5. What is the most common route of HIV infec-

Activity C Put the following steps of viral tion for children?
replication in the correct order.
Cleavage of protein product into separate
proteins for new viruses; transcription of viral
DNA into mRNA; binding of the virus to the

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106 UNIT 5 INFECTION, INFLAMMATION, AND IMMUNITY

SECTION III: APPLYING YOUR 2. The HIV virus, once inside the body, repli-
cates through an eight-step process. Take the
KNOWLEDGE eight steps that are listed and put them in the
correct order.
Activity E Consider the following scenario and
answer the questions. a. DNA synthesis
b. Binding of virus to CD4 T cell
A 15-year-old boy is coming to the clinic with his
parents after being diagnosed with HIV/AIDS. c. Cleavage
The client and his family want to learn about the d. Assembly and release from CD4 T cell
treatment plan that is being recommended. e. Integration
1. As the nurse, you are preparing the educa- f. Transcription
tional plan for the family. What essential ele- g. Translation
ments will you include in the education of the
h. Internalization
client and family?
3. A new patient presents at the clinic with the
following history: a CD4 cell count of 400
cells/L, generalized lymphadenopathy, and
a positive HIV test 8 years ago. Based on this
information, you would know that the pa-
2. At this clinic visit, you know that a baseline tient is in what phase of the HIV infection?
evaluation will be performed. What will this a. Latent phase
evaluation include?
b. Overt AIDS phase
c. Primary infection phase
d. Conversion phase
4. A 21-year-old woman diagnosed with
HIV/AIDS 4 years ago now presents with
cytomegalovirus. The nurse explains to the
woman that this infection is caused by a com-
SECTION IV: PRACTICING mon organism that normally does not cause
FOR NCLEX infection in someone with a healthy immune
system. This type of infection is called what?
Activity F Answer the following questions. a. HIV infection
1. You are a school nurse teaching a health class b. Opportunistic infection
to a group of high school students. You are c. Autoimmune infection
preparing a lecture on HIV/AIDS. You would d. Suppression infection
know to include what information about the
transmission of AIDS in your lecture? Mark all 5. In the United States, the most common
that apply. opportunistic infection in people with
HIV/AIDS infections is respiratory infection.
a. AIDS is transmitted through the bite of an
When the CD4 level drops below 200
insect.
cells/L, it is time to start prophylaxis. What
b. AIDS is transmitted through sexual con- is the drug of choice for prophylaxis?
tact.
a. Trimethobenzamide
c. AIDS is transmitted through blood-to-
b. Triamterene
blood contact.
c. Trimethoprim-sulfate
d. AIDS is transmitted from the mother to her
unborn baby. d. Trimipramine
e. AIDS is transmitted through nonsexual
household contact.

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CHAPTER 20 ACQUIRED IMMUNODEFICIENCY SYNDROME 107

6. Kaposi sarcoma is an opportunistic malig- treatment includes combinations of two, three,

nancy that is found on the skin, in the oral or more drugs. What is this treatment called?
cavity, in the gastrointestinal tract, and in the a. DHHS treatment
lungs of immunocompromised people. Many
b. Anti-AIDS treatment
people with skin lesions caused by Kaposi sar-
coma also have gastrointestinal involvement. c. HAART treatment
What are the presenting symptoms of Kaposi d. HEELP treatment
sarcoma in the gastrointestinal tract? Mark all
10. A client presents at the clinic complaining of
that apply.
unplanned weight loss of up to 10% of her
a. Bleeding body weight. She states that she has had diar-
b. Rectal burning rhea, more than twice a day. She goes on to
c. Pain say the she has fever and weakness that “just
won’t go away.” After a complete history and
d. Diarrhea
physical, an enzyme-linked immunoab-
e. Obstruction sorbent assay test is ordered. This order is
7. While doing patient education at a public based on what suspected diagnosis?
health clinic, a nurse teaches about sexually a. Wasting syndrome
transmitted disease prevention. In the educa- b. AIDS syndrome
tion is a segment on HIV/AIDS. Which of the
c. Beal syndrome
following statements from a client would in-
dicate that more teaching is needed? d. WAGAR syndrome
a. “Latex condoms provide protection from 11. Psychosocial issues are faced by every patient
HIV/AIDS.” diagnosed with HIV/AIDS and their families.
b. “There is no cure for HIV/AIDS.” These issues include which of the following?
Mark all that apply.
c. “Natural or lambskin condoms are as pro-
tective as latex condoms.” a. Condemnation of risk behaviors
d. “Adopting risk-free or low-risk behavior is b. Helplessness
the best protection against HIV/AIDS.” c. Lack of control
8. A 20-year-old male presents at the clinic com- d. Decreased strain on relationships with sup-
plaining of severe fatigue, night sweats, and port persons
fever. While taking the client’s history, he re- e. Acceptance of lifestyle
ports having multiple sexual partners and un-
12. Perinatal transmission of HIV/AIDS from the
protected sex. HIV/AIDS is suspected. What
mother to the baby have dropped drastically
diagnostic test would be ordered to confirm
with the advent of new treatment methods
the diagnosis?
and drug therapies. What increases the risk of
a. Complete metabolic panel perinatal transmission of the virus?
b. Western blot assay a. Low viral load
c. ALEA b. High CD4 counts
d. Eastern blot assay c. Breast-feeding
9. The treatment of HIV/AIDS is complicated be- d. Mother in primary phase of disease
cause different drugs act on different stages of
the replication cycle of the virus. Therefore,

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21
CHAPTER

Structure and Function

of the Cardiovascular
System

SECTION I: LEARNING 8. Define the terms preload and afterload

OBJECTIVES 9. State the formula for calculating the cardiac
output and explain the effects that venous re-
1. Compare the function and distribution of turn, cardiac contractility, and heart rate have
blood flow and blood pressure in the systemic on cardiac output
and pulmonary circulations
10. Describe the cardiac reserve and relate it to
2. State the relation between blood volume and the Frank-Starling mechanism
blood pressure in arteries, veins, and capillar-
11. Compare the structure and function of arter-
ies of the circulatory system
ies and veins
3. Define the term hemodynamics and describe
12. Describe the structure and function of vascu-
the effects of blood pressure, vessel radius,
lar smooth muscle
vessel length, vessel cross-sectional area, and
blood viscosity on blood flow 13. Use the equation blood pressure  cardiac
output  peripheral vascular resistance to ex-
4. Use the law of Laplace to explain the effect of
plain the regulation of arterial blood pressure
radius size on the pressure and wall tension
in a vessel. 14. Define autoregulation and characterize mech-
anisms responsible for short-term and long-
5. Use the term compliance to describe the char-
term regulation of blood flow
acteristics of arterial and venous blood vessels
15. Describe mechanisms involved in the
6. Describe the structural components and func-
humoral control of blood flow
tion of the pericardium, myocardium, endo-
cardium, and the heart valves and fibrous 16. Define the term microcirculation
skeleton
17. Describe the structure and function of the
7. Draw a figure of the cardiac cycle, incorporat- capillaries
ing the volume, pressure, phonocardio-
18. Explain the forces that control the fluid ex-
graphic, and electrocardiographic changes
change between the capillaries and the inter-
that occur during atrial and ventricular sys-
stitial spaces
tole and diastole

108
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CHAPTER 21 STRUCTURE AND FUNCTION OF THE CARDIOVASCULAR SYSTEM 109

19. Describe the structures of the lymphatic sys- 7. Because it is a closed system, the effective
tem and relate them to the role of the lym- function of the circulatory system requires
phatics in controlling interstitial fluid volume that the outputs of both sides of the heart
pump the amount of blood over
20. Describe the roles of the medullary vasomo-
time.
tor and cardioinhibitory centers in control-
ling the function of the heart and blood 8. Blood flow in the circulatory system depends
vessels on a blood that is sufficient to
fill the blood vessels and a dif-
21. Relate the performance of baroreceptors and
ference across the system that provides the
chemoreceptors in the control of cardiovascu-
force to move blood forward.
lar function
9. The term refers to the principles
22. Describe the distribution of sympathetic and
that govern blood flow in the circulatory
parasympathetic nervous system in the inner-
system.
vation of the circulatory system and their
effects on heart rate and cardiac contractility 10. Because flow is directly related to the radius,
small changes in vessel radius can produce
23. Relate the role of the central nervous system
changes in flow to an organ or
in terms of regulating circulatory function
tissue.
11. is the resistance to flow caused
by the friction of molecules in a fluid.
SECTION II: ASSESSING YOUR
UNDERSTANDING 12. blood flow may predispose to
clot formation as platelets and other coagula-
Activity A Fill in the blanks. tion factors are exposed to the endothelial
lining of the vessel.
1. The circulatory system delivers
and nutrients needed for metabolic processes 13. Wall tension is inversely related to wall thick-
to the tissues, carries products ness, such that the the vessel
from the tissues to the kidneys and other wall, the lower the tension.
excretory organs for elimination, and circu- 14. The total quantity of blood that can be stored
lates electrolytes and needed to in a given portion of the circulation for each
regulate body function. millimeter rise in pressure is termed compli-
2. The circulatory system can be divided into ance and reflects the of the
two parts: the circulation and blood vessel.
the circulation. 15. The and valves
3. The circulation consists of the control the movement of blood out of the
right heart, the pulmonary artery, the pul- ventricles.
monary capillaries, and the pulmonary veins. 16. The electrical activity, recorded on the ECG,
4. The circulation consists of the the mechanical events of the
left heart, the aorta and its branches, the cardiac cycle.
capillaries that supply the brain and periph- 17. The aorta is highly and, as such,
eral tissues, and the systemic venous system stretches during systole to accommodate the
and the vena cava. blood that is being ejected from the left heart
5. The pressure of the pulmonary during systole.
circulation allows blood to move through the 18. is marked by ventricular relax-
lungs more slowly, which is important for gas ation and filling.
exchange.
19. The difference between the end diastolic and
6. The function as collection end systolic volumes (approximately 70 mL)
chambers for blood, and the are is called the .
the main pumping chambers of the heart.
20. The stroke volume divided by the end dias-
tolic volume is the fraction.

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110 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

21. The efficiency of the heart as a pump is often cells and provide a pathway for passage of
measured in terms of the or the substances through the capillary wall.
amount of blood the heart pumps each
35. The key factor that restrains fluid loss from
minute.
the capillaries is the pressure
22. The refers to the maximum per- generated by the plasma proteins.
centage of increase in cardiac output that can
36. The neural control centers for the integration
be achieved above the normal resting level.
and modulation of cardiac function and
23. The mechanism allows the blood pressure are located bilaterally in the
heart to adjust its pumping ability to accom- .
modate various levels of venous return.
37. The neural control of the circulatory system
24. The determines the frequency occurs primarily through the
with which blood is ejected from the heart. and divisions of the autonomic
nervous system.
25. The outermost layer of a vessel, the
, is composed primarily of 38. When the intracranial pressure rises to levels
loosely woven collagen fibers. The middle that equal intraarterial pressure, blood vessels
layer, the , is largely a smooth to the vasomotor center become compressed,
muscle layer. The innermost layer, the initiating the central nervous system is-
, consists of a single layer of flat- chemic response. This is known as the
tened endothelial cells. .
26. The represents the energy that is
Activity B Consider the following figures.
transmitted from molecule to molecule along
the length of the vessel.
27. With peripheral arterial disease, there is a
delay in the transmission of the reflected
wave so that the pulse in ampli-
tude.
28. Pressure in the right atrium is called the
.
29. in the veins of extremities pre-
vent retrograde flow with the help of skeletal
muscles that surround and intermittently
compress the leg veins to move blood forward
to the heart.
30. of blood flow is mediated by
changes in blood vessel tone due to changes Posterior
in flow through the vessel or by local tissue
factors.
31. An increase in local blood flow is called
.
32. In the heart and other vital structures,
Anterior
channels exist between some of
the smaller arteries. 1. Label the following structures.
33. The term refers to the functions • Pericardium
of the smallest blood vessels, the capillaries, • Pleura
and the neighboring lymphatic vessels. • Right ventricle
34. Water-filled junctions, called the
, join the capillary endothelial

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CHAPTER 21 STRUCTURE AND FUNCTION OF THE CARDIOVASCULAR SYSTEM 111

• Right coronary artery Activity C Match the key terms in Column A

• Right atrium with their definitions in Column B.
• Subclavian vein
• External jugular vein Column A Column B
• Internal jugular vein 1. Diastole a. Contractile phase of
• Intraventricular septum cardiac cycle
• Aortic arch 2. Pericardium
b. Sac that covers the
• Left atrium 3. End diastolic heart
• Left coronary artery volume
• Left ventricle c. Ventricular filling
• Superior vena cava 4. Preload d. Resting phase of car-
5. Myocardium diac cycle
e. Semilunar and atri-
6. Cardiac output
oventricular
7. Heart valves f. Residual blood vol-
8. End systolic ume following con-
volume traction
g. Resistance to ejec-
9. Systole
tion of blood from
10. Afterload heart
h. Heart rate  stroke
volume
i. Muscular wall of
heart
j. Volume in heart
following passive
filling phase

2. Label the following structures. Activity D Briefly answer the following.

• Chordae tendineae 1. What are the factors involved in regulating the
• Tricuspid valve flow of blood, and how are they related?
• Superior vena cava
• Inferior vena cava
• Pulmonic valve
• Papillary muscle
• Left pulmonary artery
• Right pulmonary artery 2. The velocity of blood in the circulatory system
• Pulmonary veins varies considerably between large vessels and
• Aortic valve capillaries. Normally, when fluid flows from a
• Mitral valve large vessel to a smaller vessel, the velocity in-
• Left atrium creases, but this does not occur in the circula-
• Right atrium tory system. Why, and for what purpose?
• Left ventricle
• Right ventricle
• Descending aorta
• Papillary muscles

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112 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

3. What is the importance of the Frank-Starling SECTION IV: PRACTICING

mechanism?
FOR NCLEX
Activity F Answer the following questions.
1. Blood volume is dictated by age and body
weight. Neonates have a higher blood volume
4. How is blood vessel diameter controlled? per kilogram than does an adult. What is the
blood volume range per kilogram in an adult?
a. 70 to 75 mL/kg
b. 85 to 90 mL/kg
c. 60 to 65 mL/kg
5. What are the factors that travel in the blood- d. 90 to 100 mL/kg
stream that will regulate blood flow? Indicate
2. Resistance to flow is determined by the blood
whether it is a dilator or a vasoconstrictor.
vessels and the blood vessel itself. An equation
has been developed for understanding the rela-
tionship between the diameter of the blood
vessel, the viscosity of the blood, and resis-
tance. What is the equation called?
a. Laplace law
b. Poiseuille law
SECTION III: APPLYING YOUR c. Laminar law
KNOWLEDGE d. Pierre law
Activity E Consider the following scenario 3. The distensibility of the blood vessel is the
and answer the question. major factor in which of the vessels character-
istics?
As a nurse on the telemetry floor, you are caring
for a 77-year-old man who was admitted with a a. Wall tension
cardiac dysrhythmia. He has spent the day hav- b. Compliance
ing diagnostic tests performed and complains of c. Laminar blood flow
being very tired and feeling weak. He states, “I
d. Resistance
feel like I am suffocating; I think I am going to
die.” You note that his telemetry is showing ST 4. When intracranial pressure (ICP) equals in-
segment elevations. You have read his chart and traarterial pressure, the central nervous system
know that he has a history of variant angina. ischemic response is initiated. This response is
directed at raising arterial pressure above ICP,
1. You know that variant angina is caused by se-
thereby reestablishing blood flow to the
vere spasms of the coronary artery. What med-
vasomotor center of the brain. What is this
ications would you expect to give this client to
response called?
reverse the spasm of the artery?
a. Cushing law
b. Cushing response
c. Cushing reflex
d. Cushing syndrome

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CHAPTER 21 STRUCTURE AND FUNCTION OF THE CARDIOVASCULAR SYSTEM 113

5. The troponin complex is one of a number of 10. Nitroglycerin is the drug of choice in treating
important proteins that regulate actin-myosin angina. What does nitroglycerin release into
binding. Troponin works in striated muscle to the vascular smooth muscle of the target
help regulate calcium-mediated contraction of tissues?
the muscle. Which of the troponin complexes a. Antithrombin factor
are diagnostic of a myocardial infarction?
b. Platelet aggregating factor
a. Troponin C and Troponin T
c. Calcium channel blocker
b. Troponin A and Troponin I
d. Nitric oxide
c. Troponin T and Troponin I
11. Colloidal osmotic pressure acts differently
d. Troponin A and Troponin C
than the osmotic effects of the plasma
6. The stroke volume is the amount of blood proteins. What is its action?
ejected with every contraction of the ventricle. a. Pulls fluid back into the capillary
It is broken down into quarters. What is the
b. Pushes fluid into the extracellular spaces
approximate amount of the stroke volume per
quarter? c. Controls the direction of the fluid flow in
the large arteries
a. 25%, 25%, 25%, and 25%
d. Pulls fluid into the interstitial spaces
b. 50%, 30%, 20%, and little blood
c. 40%, 40%, 10%, and 10% 12. The lymph system correlates with the vascu-
lar system without actually being part of the
d. 60%, 20%, 20%, and little blood
vascular system. Among other things, the
7. Downstream peripheral pulses have a higher lymph system is the main route for the
pulse pressure because the pressure wave trav- absorption of fats from the gastrointestinal
els faster than the blood itself. What occurs in system. The lymph system empties into the
peripheral arterial disease? right and left thoracic ducts, which are the
a. The pulse decreases rather than increases in points of juncture with the vascular system.
amplitude. What are these points of juncture?
b. The reflected wave is transmitted more a. Bifurcation of the common carotid arteries
rapidly through the aorta. b. Internal and external jugular veins
c. Downstream peripheral pulses are increased c. Junctions of the subclavian and internal
even more than normal. jugular veins
d. Downstream peripheral pulses are greater d. Junctions of the subclavian and pulmonary
than upstream pulses. veins
8. Cardiac output (CO) is used to measure the ef- 13. The heart and blood vessels receive both sym-
ficiency of the heart as a pump. What is the pathetic and parasympathetic innervation
equation used to express CO? from neural control. What controls the
a. CO  HR  AV parasympathetic-mediated slowing of the
heart rate?
b. CO  SV  HR
a. Vasomotor center
c. CO  AV  SV
b. Cardioinhibitory center
d. CO  HR  EF
c. Medullary center
9. As the needs of the body change, the heart’s
d. Innervation center
ability to increase output necessarily needs to
change. This ability in the heart depends on
what factors? Mark all that apply.
a. Cardiac reserve
b. Cardiac contractility
c. Heart rate
d. Preload
e. Afterload

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22
CHAPTER

Disorders of Blood Flow

in the Systemic
Circulation

SECTION I: LEARNING 11. Compare the mechanisms and manifestations

of ischemia associated with atherosclerotic
OBJECTIVES peripheral vascular disease, Raynaud phe-
nomenon, and thromboangiitis obliterans
1. Describe the functions of the endothelial cells
(i.e., Buerger disease)
and define the term endothelial dysfunction
12. Distinguish between the pathology and mani-
2. Describe the function of vascular smooth
festations of aortic aneurysms and dissection
muscle and its role in vascular repair
of the aorta
3. List the five types of lipoproteins and state
13. Describe venous return of blood from the
their function in terms of lipid transport and
lower extremities, including the function of
development of atherosclerosis
the muscle pumps and the effects of gravity,
4. Describe the role of lipoprotein receptors in and relate to the development of varicose
removal of cholesterol from the blood veins
5. Cite the criteria for diagnosis of hypercholes- 14. Differentiate primary from secondary varicose
terolemia veins
6. Describe possible mechanisms involved in 15. Characterize the pathology of venous insuffi-
the development of atherosclerosis ciency and relate to the development of stasis
dermatitis and venous ulcers
7. List risk factors in atherosclerosis
16. List the four most common causes of lower
8. List the vessels most commonly affected by
leg ulcer
atherosclerosis and describe the vessel
changes that occur 17. Cite risk factors associated with venous
thrombosis and describe the manifestation of
9. State the signs and symptoms of acute arterial
the disorder and its treatment
occlusion
10. Describe the pathology associated with the
vasculitides and relate it to four disease condi-
tions associated with vasculitis

114
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CHAPTER 22 DISORDERS OF BLOOD FLOW IN THE SYSTEMIC CIRCULATION 115

SECTION II: ASSESSING YOUR 14. The uptake of low-density lipoprotein by

macrophages in the arterial wall can result in
UNDERSTANDING the accumulation of insoluble cholesterol es-
ters, the formation of foam cells, and the de-
Activity A Fill in the blanks.
velopment of .
1. Although the heart is the center of the cardio-
15. High-density lipoprotein is synthesized in the
vascular system, transport blood
liver and is often referred to as the
throughout the body.
.
2. Endothelial cells form a continuous lining for
16. Lipoprotein measurements are particularly
the entire vascular system called the
important in persons at high risk for develop-
.
ment of .
3. Vascular smooth muscle cells, which form the
17. Many types of primary hypercholesterolemia
predominant cellular layer in the tunica
have a basis.
media, produce or
of blood vessels. 18. Causes of hyperlipoproteinemia
include obesity with high-calorie intake and
4. The term denotes a reduction in
diabetes mellitus.
arterial flow to a level that is insufficient to
meet the oxygen demands of the tissues. 19. Excess calories consistently
high-density lipoprotein and less consistently
5. refers to an area of ischemic
low-density lipoprotein.
necrosis in an organ produced by occlusion of
its arterial blood supply or its venous 20. is a type of arteriosclerosis or
drainage. hardening of the arteries.
6. Elevated levels of blood are im- 21. The major risk factor for atherosclerosis is
plicated in the development of atherosclero- .
sis with its attendant risk of heart attack and
22. is closely linked with coronary
stroke.
heart disease and sudden death.
7. Because and are
23. Considerable interest in the role of
insoluble in plasma, they are encapsulated by
in the etiology of atherosclerosis
a stabilizing coat of water-soluble lipopro-
has emerged over the last few years.
teins.
24. is a serum marker for systemic
8. The transport cholesterol and
inflammation.
triglyceride to various tissues for energy uti-
lization, lipid deposition, steroid hormone 25. inhibits elements of the antico-
production, and bile acid formation. agulant cascade and is associated with en-
dothelial damage, which is believed to be an
9. Some of the apoproteins activate the
important first step in the development of
enzymes that facilitate the re-
atherosclerosis.
moval of lipids from the lipoproteins.
26. Activated macrophages release
10. There are two sites of lipoprotein synthesis:
that oxidize low-density lipoprotein.
the and the .
27. Small vessel are sometimes asso-
11. transfer their triglycerides to the
ciated with antineutrophil cytoplasmic anti-
cells of adipose and skeletal muscle tissue.
bodies.
12. Low-density lipoprotein, sometimes called
28. An is a freely moving particle
the , is the main carrier of cho-
such as a blood clot that breaks loose and
lesterol.
travels in the larger vessels of the circulation
13. Low-density lipoprotein is removed from the until lodging in a smaller vessel and occlud-
circulation either by or by ing blood flow.
cells.

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116 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

29. is an inflammatory arterial dis- Activity C Match the key terms in Column A
order that causes thrombus formation. with their definitions in Column B.
30. is a functional disorder caused Column A Column B
by intense vasospasm of the arteries and arte-
rioles in the fingers and, less often, the toes. 1. Chylomicrons a. Necrosis of the
blood vessel wall
31. An is an abnormal localized di- 2. C-reactive
protein b. Main carrier of cho-
latation of a blood vessel. lesterol
32. An aneurysm may also be , with 3. Familial
c. Derived from the
the first evidence of its presence being associ- hypercholes-
metabolism of di-
ated with vessel . terolemia
etary methionine
33. Aortic dissection involves into 4. Xanthomas d. Elevated levels of
the vessel wall with longitudinal tearing of 5. Hypercholes- blood cholesterol
the vessel wall to form a blood-filled channel. terolemia e. LDL-related arte-
34. Venous prevent the retrograde riosclerosis
6. Vasculitis
flow of blood. f. Carries large
7. Very amounts of triglyc-
35. The most common cause of secondary vari- low-density erides
cose veins is . lipoprotein
g. Caused by LDL
36. leads to tissue congestion, 8. Homocysteine receptor deficiency,
edema, and eventual impairment of tissue which prevents up-
nutrition. 9. Atherosclerosis
take of LDL
37. Virchow described the triad that has come to 10. Low-density h. Transfer triglyc-
be associated with venous thrombosis: lipoprotein erides to skeletal
, , and . (LDL) muscle, smaller
than very low-den-
Activity B Consider the following figure. sity lipoproteins
i. Elevated levels asso-
LUMEN ciated with arterial
disease
j. Cholesterol deposits

SHOULDER
Activity D Put the following sequence of
events of atherosclerotic pathogenesis in
chronologic order:
formation of fibrofatty plaque, foam cell forma-
tion, endothelial injury, complicated lesion,
development of fatty streak.

Activity E Briefly answer the following.

In this figure, label the following: media, lym- 1. Describe the role of the endothelium.
phocytes, endothelial cells, smooth muscle cells,
macrophages, CAP region, and necrotic core.

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CHAPTER 22 DISORDERS OF BLOOD FLOW IN THE SYSTEMIC CIRCULATION 117

2. Describe the causation of secondary hyper- the ED, the patient’s blood pressure and pulse
lipoproteinemia. were unobtainable in his left arm, and his pain
and syncope were worse. The nurse suspects a di-
agnosis of a dissecting aneurysm of the descend-
ing aorta.
1. What orders would the nurse expect to receive
from the physician to confirm a diagnosis of a
3. Describe the general mechanisms of drug ther-
dissecting aneurysm?
apy to lower serum low-density lipoprotein
levels.

2. Once the diagnosis of dissecting aneurysm is

confirmed, what would be the priority nursing
4. What are the seven signs and symptoms of
action for this patient?
acute arterial occlusion?

5. What are the physical effects of Raynaud phe-

nomenon?
SECTION IV: PRACTICING
FOR NCLEX
Activity G Answer the following questions.

6. How do skeletal muscles of the leg contribute 1. A variety of etiologies are responsible for alter-
to returning blood to the heart? ing the blood flow in the systemic circulation.
Match the disturbance of blood flow with the
cause.
Disturbance in Blood Flow Cause
1. Abnormal vessel a. Atherosclerosis
dilation (arterial)
2. Pathologic b. Raynaud phe-
nomenon
SECTION III: APPLYING YOUR changes in
(vasospasm)
vessel wall
KNOWLEDGE c. Venous throm-
3. Acute vessel
bosis (venous)
Activity F Consider the following scenario and obstruction
answer the questions. d. Varicose veins
4. Pathologic (venous)
A 72-year-old man is brought to the emergency changesin vessel
e. Vasculitis
department (ED) by his wife. She says that her wall
(arterial)
husband “just started moaning and complaining
5. Abnormal vessel f. Arterial
of pain in his back.” She goes on to say that “she
dilation aneurysms
has never seen him in this much pain.” In the
triage area of the ED, the client’s blood pressure 6. Acute vessel (arterial)
was mildly elevated. He complained of syncope obstruction
that became worse over time. On admission to

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118 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

2. Where in the body is lipoprotein is synthe- disorders are common pathways for tissue
sized? Mark all that apply. and organ involvement in many different
a. Small intestine disease conditions. What is the most
common of the vasculitides?
b. Large intestine
a. Polyarteritis nodosa
c. Pancreas
b. Raynaud disease
d. Liver
c. Temporal arteritis
3. A 35-year-old man presents to the emergency
d. Varicose veins
department complaining of chest pain for the
past 2 hours. He describes the pain as crush- 6. A 69-year-old man is admitted to the floor
ing, like a huge weight is on his chest. He also following a popliteal embolectomy. He asks
states that the pain goes up into his neck and the nurse why he had to have surgery on his
down his left arm. An acute myocardial in- leg. What is the best response by the nurse?
farction (MI) is diagnosed. When taking his a. “The doctor wanted to look into your
history, the following things are noted: artery to make sure everything was okay.”
• Hyperlipoproteinemia for past 7 years b. “Didn’t the doctor explain everything to
• Family history of early MI you before your surgery?”
• Cholesterol deposits along the tendons c. “The artery that runs behind your knee
(diagnosed 1 year ago) was blocked by a blood clot, and the doc-
• Atherosclerosis (diagnosed 6 months ago) tor removed it.”
• Diabetes mellitus (type 1) (diagnosed at age
d. “Your upper leg wasn’t getting enough
16 years)
blood, so the doctor had to fix it.”
The nurse suspects which of the following
7. A 45-year-old woman with a diagnosis of
diagnosis will be made?
multiple sclerosis comes to the clinic com-
a. Familial hypercholesterolemia (type 2A) plaining of coldness and pain in her fingers.
b. Homozygotic cutaneous xanthoma She says that her fingers turn blue and then
c. Adult onset hypercholesterolemia (type red, and they throb and tingle. The nurse
1A) would expect what diagnosis and treatment
for this patient? Mark all that apply.
d. Secondary hyperlipoproteinemia
a. Raynaud disease; protecting the digits from
4. Atherosclerosis begins in an insidious manner cold
with symptoms becoming apparent as long as
b. Arterial thrombosis; streptokinase
20 to 40 years after the onset of the disease.
Although an exact etiology of the disease has c. Peripheral artery disease; aspirin
not been identified, epidemiologic studies d. Raynaud phenomenon; stop smoking
have shown that there are predisposing risk
8. Aortic aneurysms take varied forms and can
factors to this disease. What is the major risk
occur anywhere along the aorta. What are the
factor for developing atherosclerosis?
types of aneurysm termed abdominal aortic
a. Male sex aneurysms? Mark all that apply.
b. Hypercholesterolemia a. Berry aneurysms
c. Familial history of premature coronary b. Dissecting aneurysms
heart disease
c. Saccular aneurysms
d. Increasing age
d. Fusiform aneurysms
5. A group of vascular disorders called vasculi- e. Bifurcating aneurysms
tides cause inflammatory injury and necrosis
of the blood vessel wall (i.e., vasculitis). These

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CHAPTER 22 DISORDERS OF BLOOD FLOW IN THE SYSTEMIC CIRCULATION 119

9. A 56-year-old woman presents at the clinic 10. Venous thrombosis most commonly occurs
complaining of the unsightliness of her vari- in the lower extremities. Risk factors for ve-
cose veins and wants to know what can be nous thrombosis include which of the follow-
done about them. The nurse explains that the ing?
treatment for varicose veins includes which a. Stasis of blood, hypercoagulability, inflam-
of the following interventions? mation
a. Surgical or fibrotherapy b. Hypocoagulability, vessel wall injury, in-
b. Sclerotherapy or surgery creased pressure on deep veins
c. Trendelenburg therapy or sclerotherapy c. Vessel wall injury, hypocoagulability, de-
d. Surgery or Trendelenburg therapy creased venous blood flow
d. Stasis of blood, hypercoagulability, vessel
wall injury

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23
CHAPTER

Disorders of Blood
Pressure Regulation

SECTION I: LEARNING 9. Describe behavior modification strategies

used in the prevention and treatment of hy-
OBJECTIVES pertension
1. Define the terms systolic blood pressure, dias- 10. List the different categories of drugs used to
tolic blood pressure, pulse pressure, and mean ar- treat hypertension and state their mecha-
terial blood pressure nisms of action in the treatment of high
blood pressure
2. Explain how cardiac output and peripheral
vascular resistance interact in determining 11. Explain the changes in blood pressure that ac-
systolic and diastolic blood pressure company normal pregnancy and describe the
four types of hypertension that can occur
3. Describe the mechanisms for short-term and
during pregnancy
long-term regulation of blood pressure
12. Cite the criteria for the diagnosis of high
4. Describe the requirements for accurate and
blood pressure in children
reliable blood pressure measurement in terms
of cuff size, determining the maximum infla- 13. Define systolic hypertension and relate the
tion pressure, and deflation rate circulatory changes that occur with aging
that predispose to the development of sys-
5. Cite the definition of hypertension put forth
tolic hypertension
by the seventh report of the Joint National
Committee on Detection, Evaluation, and 14. Define the term orthostatic hypotension
Treatment of Hypertension
15. Describe the cardiovascular, neurohumoral,
6. Differentiate essential, systolic, secondary, and muscular responses that serve to
and malignant forms of hypertension maintain blood pressure when moving from
the supine to standing position
7. Describe the possible influence of genetics,
age, race, obesity, diet and sodium intake, 16. Explain how fluid deficit, medications, aging,
and alcohol consumption on the develop- disorders of the ANS, and bed rest contribute
ment of essential hypertension to the development of orthostatic hypoten-
sion
8. Cite the risks of hypertension in terms of tar-
get-organ damage

120
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CHAPTER 23 DISORDERS OF BLOOD PRESSURE REGULATION 121

SECTION II: ASSESSING YOUR the pressure against which the heart must
pump as it ejects blood into the systemic cir-
UNDERSTANDING culation.
Activity A Fill in the blanks. 13. Chronic hypertension leads to ,
a common cause of chronic kidney disease.
1. blood pressure reflects the
rhythmic ejection of blood from the left ven- 14. Hypertension is a major risk factor for
tricle into the aorta. stroke and intracerebral
.
2. The pressure at the height of the pressure
pulse is pressure, and the lowest 15. The main objective for treatment of essential
pressure is the pressure. hypertension is to achieve and maintain arte-
rial blood pressure below .
3. The difference between the systolic and dias-
tolic pressure (approximately 40 mm Hg) is 16. lower blood pressure initially by
called the . decreasing vascular volume and cardiac out-
put.
4. The represents the average pres-
sure in the arterial system during ventricular 17. The blockers are effective in
contraction and relaxation. treating hypertension because they are car-
dioselective and thus decrease heart rate and
5. The mean arterial blood pressure is deter-
cardiac output.
mined mainly by the and the
. 18. The drugs inhibit the move-
ment of calcium into cardiac and vascular
6. The renin-angiotensin-aldosterone system
smooth muscle.
plays a central role in blood pressure by in-
creasing and . 19. Elevated pressures during favor
the development of left ventricular hypertro-
7. The extracellular fluid volume and arterial
phy, increased myocardial oxygen demands,
blood pressure are regulated around an
and eventual left heart failure.
point, which represents the nor-
mal pressure for a given individual. 20. Many of the conditions causing
hypertension can be corrected or cured by
8. The role that the play in blood
surgery or specific medical treatment.
pressure regulation is emphasized by the fact
that many hypertension medications produce 21. The use of pills is probably the
their blood pressure lowering effects by in- most common cause of secondary hyperten-
creasing and sion in young women.
elimination.
22. hypertension is characterized by
9. hypertension is the term ap- sudden marked elevations in blood pressure,
plied to 95% of cases in which no cause for with diastolic values above 120 mm Hg com-
hypertension can be identified. In plicated by evidence of acute or rapidly pro-
hypertension, the elevation of gressive life-threatening organ dysfunction.
blood pressure results from some other disorder.
23. is defined as an elevation in
10. A diagnosis of hypertension is made if the blood pressure and proteinuria developing
systolic blood pressure is or after 20 weeks of gestation.
higher and the diastolic blood pressure is
24. Any disease condition that reduces blood vol-
or higher.
ume, impairs mobility, results in prolonged
11. The risk factors include a family inactivity, or impairs autonomic nerve system
history of hypertension, race, and age-related function may also predispose to .
increases in blood pressure.
25. drugs and drugs
12. An elevation in blood pressure increases the are the most common cause of chronic
workload of the by increasing orthostatic hypotension.

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122 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

Activity B Consider the following figures. 2. In this figure, fill in the following terms that
apply to maintaining blood pressure on
standing:
Arterial blood pressure

• Action of skeletal muscle pumps

Cardiac output Peripheral vascular resistance • Compression of veins
Sympathetic
• Increased venous return
Stroke volume Heart rate
activity
• Pooling of blood in lower body
• Decreased venous return to the heart
Heart
Vagal and • Decreased cardiac output
sympathetic activity
• Drop in blood pressure
• Increased heart rate
Baroreceptors
• Increased cardiac output
Venous return Angiotensin II
• Vasoconstriction
Blood volume Adrenal gland • Blood pressure returns to normal
Aldosterone

Salt and water

retention Activity C Match the key terms in Column A
with their definitions in Column B.
Renin-angiotensin
mechanism Column A Column B
Kidney

1. Dippers a. Abnormal drop in

1. What does this figure depict? What do the blood pressure on
solid lines and the dashed lines represent? 2. Systolic
assumption of the
hypertension
standing position
3. Vasopressin b. Noninvasive blood
4. Angiotensin- pressure measure-
converting ment
enzyme c. Persons with flat
inhibitors blood pressure pro-
file
5. Postural
hypotension d. Increases renal
water retention
6. Indirect
e. Diastolic pressure
auscultatory
over 90 mm Hg
method
f. Strong vasoconstric-
7. Diastolic tor, reduces sodium
hypertension excretion
8. Coarctation g. Narrowing of the
of the aorta aorta
9. Angiotensin II h. Systolic pressure
over 140 mm Hg
10. Nondippers
i. Persons whose blood
pressure follows cir-
cadian rhythms
j. Block formation of
angiotensin II

Assumption of the upright position

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CHAPTER 23 DISORDERS OF BLOOD PRESSURE REGULATION 123

Activity D SECTION III: APPLYING YOUR

1. Put the sequence and actions of the RAAS sys- KNOWLEDGE
tem in chronological order.
Activity F Consider the following scenario and
a. Water retention answer the questions.
b. Stimulation of juxtaglomerular apparatus
An 87-year-old African American male is brought
c. Conversion of angiotensinogen to angio- to the clinic by his son for a routine physical exam.
tensin I His son states, “Dad has been complaining of feel-
d. Conversion of angiotensin I to angiotensin ing dizzy, and he is afraid he is going to fall.”
II by angiotensin-converting enzyme When taking the patient’s vital signs, the nurse
e. Increased vascular resistance, release of notes that the his blood pressure has reached or-
aldosterone thostatic levels and needs further evaluation.
f. Release of renin 1. What assessments need to be made in further
g. Decrease in blood pressure evaluating this patient?
h. Na retention, stimulation of ADH release

Activity E Briefly answer the following.

1. Explain the short-term regulation of blood
pressure. 2. The son asks what his father’s treatment will
be to correct this condition. What is the
nurse’s best response?

2. Why does the kidney play a major role in the

development of secondary hypertension?
3. The son asks what else can be done to help his
father if it is not possible to correct the cause
of the orthostatic hypertension. What is the
nurse’s best response?

3. How does the RAAS system influence blood

pressure?

SECTION IV: PRACTICING

4. Why are the elderly predisposed to hyperten- FOR NCLEX
sion?
Activity G Answer the following questions.
1. For people who suffer from hypertension and
other diseases that affect blood pressure, im-
portant information about the status of their
disease is gathered from measurements in-
cluding systolic and diastolic pressures, pulse
pressure, and mean arterial pressure.

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124 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

What is the mean arterial pressure estimated 5. A client with malignant hypertension is at
to be when the blood pressure is 130/85 risk for a hypertensive crisis, including the
mm Hg? cerebral vascular system often causing cere-
a. 90 bral edema. As the nurse caring for this pa-
tient, what are the signs and symptoms you
b. 95
would assess for?
c. 100
a. Papilledema and lethargy
d. 105
b. Headache and confusion
2. Although the etiology of essential hyperten- c. Restlessness and nervousness
sion is mainly unknown, several risk factors
d. Stupor and hyperreflexia
have been identified. These risk factors fall
under the categories of constitutional risk 6. Pregnancy-induced hypertension is a serious
factors and lifestyle factors. What are the condition affecting between 5% and 10% of
primary risk factors for essential hyperten- pregnant women. The most serious classifica-
sion? Mark all that apply. tion of hypertension in pregnancy is
a. Race and excessive sodium chloride intake preeclampsia-eclampsia. It is a pregnancy-
specific syndrome that can have both
b. Type 2 diabetes and obesity
maternal and fetal manifestations. What
c. Age and high intake of potassium is a life-threatening manifestation of the
d. Race and smoking preeclampsia-eclampsia classification of
e. Family history and excessive alcohol con- pregnancy-induced hypertension?
sumption a. Hepatocellular necrosis
3. A 37-year-old woman is admitted to your b. Thrombocytopenia
unit with a differential diagnosis of rule out c. HELLP syndrome
pheochromocytoma. What are the most com- d. Decreased renal filtration rate
mon symptoms you would expect this pa-
tient to exhibit? 7. In infants and children, secondary hyperten-
sion is the most common form of hyperten-
a. Nervousness and periodic severe headache
sion. What is the most common cause of
b. Variability in blood pressure and weight loss hypertension in an infant?
c. Excessive sweating and pallor a. Cerebral vascular bleed
d. Periodic severe headache and marked vari- b. Coarctation of the aorta
ability in blood pressure
c. Pheochromocytoma
4. The extended, severe exposure of the walls of d. Renal artery thrombosis
the blood vessels to the exaggerated pressures
that occur in malignant hypertension cause 8. Hypertension in the elderly is a common find-
injuries to the walls of the arterioles. Blood ing. This is due to the age-related rise in systolic
vessels in the renal system are particularly vul- blood pressure. Among the aging processes,
nerable to this type of damage. Because hyper- what is a contributor to hypertension?
tension is a chronic disease, and it is associated a. Baroreceptor sensitivity
with autoregulatory changes in the blood flow b. Aortic softening
to major organs, what would be the initial
c. Decreased peripheral vascular resistance
treatment goal for malignant hypertension?
d. Increased renal blood flow
a. Partial reduction in blood pressure to less
critical values
b. Reduction to normotensive levels of blood
pressure
c. Rapid decrease in blood pressure to less
critical levels
d. Slow, gradual decrease in blood pressure to
normotensive blood pressures

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CHAPTER 23 DISORDERS OF BLOOD PRESSURE REGULATION 125

9. A 75-year-old male presents at the clinic for a 10. The rennin-angiotensin-aldosterone system is
routine physical check-up. He is found to be a negative feedback system that plays a cen-
hypertensive. While taking his blood pressure tral role in blood pressure regulation. How
in the sitting, standing, and lying positions, the does the end result of this feedback loop regu-
nurse notes that the brachial artery is pulseless late blood pressure in the body?
at a high cuff pressure, but she can still feel it. a. Vasodilates blood vessels to decrease blood
What condition would the nurse suspect? pressure
a. Essential hypertension b. Vasoconstricts blood vessels to increase
b. Pseudohypertension blood pressure
c. Orthostatic hypertension c. Increases salt and water retention by the
d. Secondary hypertension kidney
d. Decreases salt and water retention by the
kidney

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24
CHAPTER

Disorders of
Cardiac Function

SECTION I: LEARNING 10. Differentiate among the pathophysiologic

changes that occur with hypertrophic car-
OBJECTIVES diomyopathy, arrhythmogenic right ventric-
ular cardiomyopathy, dilated
1. Characterize the function of the pericardium
cardiomyopathies, and myocarditis
2. Compare the clinical manifestations of acute
11. List four causes of secondary cardiomyopathy
pericarditis and chronic pericarditis
12. Describe the treatment strategies of both pri-
3. Describe the physiologic impact of pleural ef-
mary and secondary cardiomyopathy
fusion on cardiac function and relate it to the
life-threatening nature of cardiac tamponade 13. Distinguish between the roles of infectious
organisms and the immune system in infec-
4. Relate the pathophysiology of constrictive
tive endocarditis and rheumatic fever
pericarditis to its clinical manifestations
14. Describe the relation between the infective
5. Describe blood flow in the coronary circula-
vegetations associated with infective endo-
tion and relate it to the determinants of my-
carditis and the extracardiac manifestations
ocardial oxygen supply and demand
of the disease
6. Define the term acute coronary syndrome and
15. Describe the long-term effects of rheumatic
distinguish among chronic stable angina, un-
fever and primary and secondary prevention
stable angina, non–ST-segment elevation
strategies for rheumatic fever and rheumatic
myocardial infarction, and ST-segment eleva-
heart disease
tion infarction in terms of pathology, sympto-
matology, ECG changes, and serum cardiac 16. State the function of the heart valves and re-
markers late alterations in hemodynamic function of
the heart that occur with valvular disease
7. Compare the treatment goals for stable
angina and the acute coronary syndromes 17. Compare the effects of stenotic and regurgi-
tant mitral and aortic valvular heart disease
8. Define the term cardiomyopathy as it relates to
on cardiovascular function
both the mechanical and electrical function
of the myocardium 18. Compare the methods of and diagnostic in-
formation obtained from cardiac auscultation
9. Describe the role of genetics in the etiology of
and echocardiography as they relate to valvu-
the primary cardiomyopathies
lar heart disease

126
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CHAPTER 24 DISORDERS OF CARDIAC FUNCTION 127

19. Trace the flow of blood in the fetal circulation, 7. In most cases, coronary artery disease is
state the function of the foramen ovale and caused by .
ductus arteriosus, and describe the changes in
8. Myocardial blood flow, in turn, is largely
circulatory function that occur at birth
regulated by the of the my-
20. Compare the effects of left-to-right and right- ocardium and mechanisms that
to-left shunts on the pulmonary circulation control vessel dilation.
and production of cyanosis
9. There is little oxygen reserve in the blood;
21. Describe the anatomic defects and altered therefore, coronary arteries must increase
patterns of blood flow in children with atrial their flow to meet the metabolic needs of the
septal defects, ventricular septal defects, en- myocardium during periods of .
docardial cushion defects, pulmonary stenosis,
10. The is the most frequently used
tetralogy of Fallot, patent ductus arteriosus,
cardiovascular diagnostic procedure.
transposition of the great vessels, coarctation
of the aorta, and single-ventricle anatomy 11. uses ultrasound signals that are
inaudible to the human ear.
22. Describe the prevalence of the condition and
issues of concern for adults with congenital 12. is by far the most common
heart disease. cause of coronary artery disease.
23. Describe the manifestations related to the 13. There are two types of atherosclerotic lesions:
acute, subacute, and convalescent phases of the plaque, which obstructs
Kawasaki disease blood flow, and the plaque,
which can rupture and cause platelet adhe-
sion and thrombus formation.
SECTION II: ASSESSING YOUR 14. Coronary artery disease is commonly divided
UNDERSTANDING into two types of disorders: and
.
Activity A Fill in the blanks. 15. The classic ECG changes that occur with acute
1. The is a double-layered serous coronary syndrome involve ,
membrane that isolates the heart from other , and .
thoracic structures, maintains its position in 16. Acute severe ischemia reduces the
the thorax, prevents it from overfilling, and and shortens the duration of the
serves as a barrier to infection. action potential in the ischemic area.
2. Pericardial fluid acts as a lubricant that pre- 17. The have high specificity for
vents forces from developing as myocardial tissue and have become the pri-
the heart contracts and relaxes. mary biomarker for the diagnosis of myocar-
3. The manifestations of acute in- dial infarction.
clude a triad of chest pain, pericardial friction 18. myocardial infarction is charac-
rub, and ECG changes. terized by the ischemic death of myocardial
4. Pericardial refers to the accumu- tissue associated with atherosclerotic disease
lation of fluid in the pericardial cavity, usually of the coronary arteries.
because of an inflammatory and/or infectious 19. Irreversible myocardial cell death occurs after
process. minutes of severe ischemia.
5. Pericardial effusion can lead to cardiac 20. Infarcted and noninfarcted areas of the heart
, in which there is compression muscle in patients with ST-segment elevation
of the heart due to the accumulation of fluid, myocardial infarction can change size, shape,
pus, or blood in the pericardial sac. and thickness, a term referred to as
6. In pericarditis, fibrous, calcified .
scar tissue develops between the visceral and
parietal layers of the serous pericardium.

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128 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

21. The gastrointestinal symptoms of ST-segment 33. The function of the heart is to
elevation myocardial infarction are believed promote directional flow of blood through
to be related to the severity of the pain and the chambers of the heart.
stimulation.
34. Mitral valve represents the in-
22. The medication used to alleviate angina, complete opening of the mitral valve during
, is given because of its vasodilat- diastole with left atrial distention and im-
ing effect. paired filling of the left ventricle.
23. is a mechanical technique to re- 35. Mitral valve is characterized by
move atherosclerotic tissue during angio- incomplete closure of the mitral valve, with
plasty. the left ventricular stroke volume being
divided between the forward stroke volume
24. Partial or complete rupture of a
that moves into the aorta and the regurgitant
is a rare but often fatal complication of trans-
stroke volume that moves back into the left
mural myocardial infarction.
atrium during systole.
25. is the initial manifestation of is-
36. Most persons with mitral valve
chemic heart disease in approximately half of
are asymptomatic, and the disorder is discov-
persons with coronary artery disease.
ered during a routine physical examination.
26. Typically, chronic stable angina is provoked
37. Increased resistance to ejection of blood from
by or stress and re-
the left ventricle into the aorta characterizes
lieved within minutes by rest or the use of ni-
aortic valve .
troglycerin.
38. Aortic is the result of an incom-
27. The cardiomyopathies include
petent aortic valve that allows blood to flow
hypertrophic cardiomyopathy, arrhythmo-
back to the left ventricle during diastole.
genic right ventricular cardiomyopathy, left
ventricular noncompaction cardiomyopathy, 39. The major development of the
inherited conduction system disorders, and occurs between the fourth and seventh weeks
ion channelopathies. of gestation, and most congenital heart de-
fects arise during this time.
28. The cardiomyopathies, which
include dilated cardiomyopathy, are of both 40. Congenital heart defects produce their effects
genetic and nongenetic origin. mainly through abnormal shunting of
, production of ,
29. The physiologic abnormality in
and disruption of blood flow.
is reduced left ventricular chamber size, poor
compliance with reduced stroke volume that 41. Congenital heart defects that result in a left-
results from impaired diastolic filling, and dy- to-right shunt are usually categorized as
namic obstruction of left ventricular outflow. disorders because they do not
compromise oxygenation of blood in the pul-
30. cardiomyopathies are character-
monary circulation.
ized by atrophic and hypertrophic myocardial
fibers and interstitial fibrosis. 42. A defect is an opening in the
ventricular septum that results from an in-
31. is the most common and, fre-
complete separation of the ventricles during
quently, the first manifestation of rheumatic
early fetal development.
fever.
43. disease, also known as mucocu-
32. The manifestation of rheumatic
taneous lymph node syndrome, is an acute
fever is Sydenham chorea, where the child
febrile disease of young children.
often is fidgety, cries easily, begins to walk
clumsily, and drops things.

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CHAPTER 24 DISORDERS OF CARDIAC FUNCTION 129

Activity B Consider the following figure.

Superior Right Superior

vena Left pulmonary vena
cava pulmonary veins cava
Aortic veins
arch Aortic valve Coronary
Left sinus
Inferior
atrium vena
cava

Right
atrium Right
atrium

Right
Left ventricle
Right ventricle
ventricle

In this figure, label the coronary arteries. 10. Pulsus j. Exaggeration of the
paradoxus normal variation in
the pulse during the
Activity C Match the key terms in Column A inspiratory phase of
with their definitions in Column B. respiration
1. 2.
Column A Column B Column A Column B
1. Unstable a. Chest pain due to a 1. Restrictive a. Ventricular en-
angina coronary artery spasm cardiomyopathy largement, a re-
b. ST-segment elevation duction in
2. Effusive- 2. Ion channelo-
myocardial infarction ventricular wall
constrictive pathies
thickness, and im-
pericarditis c. Decreased blood flow
3. Myocarditis paired systolic
to tissue
3. Ischemia function
d. Accumulation of fluid 4. Arrhythmo-
4. Pericardial genic right b. An inflammation
in the pericardial cavity
effusion ventricular of the heart
e. Invasion of the heart
cardiomyopathy c. Disproportionate
5. Prinzmetal valves and the mural
thickening of the
angina endocardium by a mi- 5. Dilated cardio-
ventricular sep-
crobial agent myopathy
6. Cardiac tum and left ven-
tamponade f. Mechanical compres- 6. Stress cardio- tricle
sion of the heart myopathy
7. Silent d. Occurs during the
g. Occurs in the absence last trimester of
myocardial 7. Hypertrophic
of anginal pain pregnancy or the
ischemia cardiomyopathy
h. Combination of first 6 months
8. Heart attack effusion-tamponade 8. Left ventricular after delivery
and constriction noncompaction
9. Infective
endocarditis i. Chest pain occurring
while at rest

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130 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

9. Secondary e. Conduction disor- 2. What factors determine myocardial oxygen

cardiomyopathy ders in the heart supply and demand?
resulting from ab-
10. Peripartum
normal membrane
cardiomyopathy
potentials (long
QT/short QT syn-
dromes)
f. Left ventricular 3. How does an atherosclerotic plaque stimulate
dysfunction in re- thrombosis?
sponse to profound
psychological or
emotional stress
g. Ventricular filling
restricted because 4. What changes are seen in the blood (serum)
of excessive rigid- during acute coronary syndromes?
ity of the ventricu-
lar walls
h. Heart muscle dis-
ease that affects
primarily the right
ventricle 5. Describe the pathologic process that is seen in
i. Heart muscle dis- unstable angina/non–ST-segment elevation
ease in the presence myocardial infarction.
of a multisystem
disorder
j. Failure of trabecu-
lar compaction in
the developing
6. What is the damage that results from an
myocardium
acute myocardial infarction, and what are the
Activity D factors that determine severity?

1. Construct a flowchart using the following con-

ditions and manifestations of coronary heart
disease:
• Chronic ischemic heart disease
• Acute coronary syndrome 7. What is meant by “reperfusion therapy,” and
• Stable angina what is its goal?
• Unstable angina
• Variant angina
• Non-ST-segment elevation
• Silent myocardial ischemia
• ST-segment elevation
• Q-wave AMI 8. What is the definition of a cardiomyopathy
• No ST-elevation (according to the American Heart Association)?

Activity E Briefly answer the following.

1. Why does pericardial effusion demonstrate
signs of right-sided heart failure?

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CHAPTER 24 DISORDERS OF CARDIAC FUNCTION 131

9. What is the relationship between strep throat SECTION IV: PRACTICING

and heart valve disorders?
FOR NCLEX
Activity G Answer the following questions.
1. Nearly everyone with pericarditis has chest
pain. With acute pericarditis, the pain is
10. Describe the clinical manifestation of patent abrupt in onset and sharp, and radiates to the
ductus arteriosus. neck, back, abdomen, or sides. What can be
done to ease the pain of acute pericarditis?
a. Have patient sit up and lean forward
b. Have patient change positions to unaf-
fected side
11. Describe the tetralogy of Fallot. c. Have patient breath deeply
d. Have patient swallow slowly and frequently
2. Cardiac tamponade is a serious life-
threatening condition that can arise from a
number of other conditions. What is a key
diagnostic finding in cardiac tamponade?
a. Increase in stroke volume
SECTION III: APPLYING YOUR b. Pulsus paradoxus
KNOWLEDGE c. Narrowed pulse pressure
d. Rise in systolic blood pressure
Activity F Consider the following scenario and
answer the questions. 3. The scar tissue that occurs between the layers
of the pericardium becomes rigid and con-
A 55-year-old woman is brought to the emer- strictive from scar tissue in constrictive peri-
gency department by ambulance complaining of carditis. What is a physiologic sign of
severe, acute chest pain. The patient states, “It constrictive pericarditis?
just came on all of a sudden. Like someone sit-
ting on my chest crushing me.” An ECG shows a. Kussmaul breathing
ST segment elevation, and the presumptive diag- b. Pulsus paradoxus
nosis is acute ST-segment elevation myocardial c. Kussmaul sign
infarction (STEMI). d. Widening pulse pressure
1. While taking a history on this patient, what 4. Unstable plaque, a condition of atheroscle-
symptoms should the nurse pay particular at- rotic heart disease, occurs in unstable angina
tention to because they are further indications and myocardial infarction. Unstable plaque
of a STEMI? can rupture, causing platelet aggregation and
thrombus formation. What are the major de-
terminants of the vulnerability of plaque to
rupture? Mark all that apply.
a. Size of lipid-rich core
b. Preponderance of smooth muscle cells
2. What are the emergency department goals of c. Presence of inflammation
management for a patient with a STEMI?
d. Decrease in blood pressure and coronary
blood flow
e. Thickness of fibrous cap

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132 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

5. A patient with a suspected myocardial infarc- 9. During an acute myocardial infarction (MI),
tion (MI) is brought to the emergency depart- there is ischemic damage to the heart muscle.
ment by ambulance. As the nurse caring for The location and extent of the ischemic dam-
this patient, what lab work would you expect age is the major predictor of complications,
to receive an order for to confirm a diagnosis ranging from cardiac insufficiency to death,
of MI? following an MI. What is the “window of op-
a. Creatine kinase marker portunity” in restoring blood flow to the af-
fected area so as to diminish the ischemic
b. Complete blood components
damage to the heart and maintain the viabil-
c. Calcium level ity of the cells?
d. Troponin level a. 10 to 20 minutes
6. Unstable angina/non–ST-segment elevation b. 30 to 40 minutes
myocardial infarction is a clinical syndrome c. 20 to 40 minutes
that ranges in severity between stable angina to
d. 10 to 30 minutes
myocardial infarction (MI). It is classified ac-
cording to its risk of causing an acute MI and is 10. Angina pectoris is a chronic ischemic coro-
diagnosed based on what? Mark all that apply. nary artery disease that is characterized by a
a. Severity of pain and abruptness of onset symptomatic paroxysmal chest pain or pres-
sure sensation associated with transient my-
b. Serum biomarkers
ocardial ischemia. What precipitates an attack
c. Coexisting chronic conditions of angina pectoris?
d. ECG pattern a. Exposure to heat
e. Blood flow angiography b. Sedentary lifestyle
7. When an acute myocardial infarction (MI) oc- c. Abrupt change in position
curs, many physiologic changes occur very d. Emotional stress
rapidly. What causes the loss of contractile
function of the heart within seconds of the 11. The diagnosis of chronic stable angina is
onset of an MI? based on a detailed pain history, the presence
of risk factors, invasive and noninvasive stud-
a. Conversion from aerobic to anaerobic me-
ies, and laboratory studies. What test is not
tabolism
used in the diagnosis of angina?
b. Overproduction of energy capable of sus-
a. Serum biochemical markers
taining normal myocardial function
b. Cardiac catheterization
c. Conversion from anaerobic to aerobic me-
tabolism c. Echocardiogram
d. Inadequate production of glycogen with d. Nuclear imaging studies
mitochondrial shrinkage 12. Cardiomyopathies are classified as either pri-
8. ST-elevated myocardial infarction (STEMI) is mary or secondary. The primary cardiomy-
accompanied by severe, crushing pain. Mor- opathies are further classified as genetic,
phine is the drug of choice used to treat the mixed, or acquired. Identify the following
pain of STEMI when the pain cannot be re- conditions as genetic, acquired, or mixed.
lieved with oxygen and nitrates. Why is mor- Hypertrophic cardiomyopathy
phine considered the drug of choice in STEMI? Left ventricular noncompaction
a. Action increases autonomic nervous sys- Myocarditis
tem activity
Dilated cardiomyopathy
b. Action decreases metabolic demands of the
Peripartum cardiomyopathy
heart
c. Action increases anxiety, thus increasing
metabolic demands of heart
d. Action relieves pain and gives sense of de-
pression

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CHAPTER 24 DISORDERS OF CARDIAC FUNCTION 133

13. It is known that more than 100 distinct my- 16. Mitral valve prolapse occurs frequently in the
ocardial diseases can demonstrate clinical fea- population at large. Its treatment is aimed at
tures associated with dilated cardiomyopathy relieving symptoms and preventing complica-
(DCM). What is the most common identifi- tions of the disorder. Which drug is used in
able cause of DCM in the United States? the treatment of mitral valve prolapse to re-
a. Hepatic cardiomyopathy lieve symptoms and aid in preventing com-
plications?
b. Alcoholic cardiomyopathy
a. -adrenergic blocking drugs
c. Cardiotoxic cardiomyopathy
b. Calcium channel blocking drugs
d. Exercise-induced cardiomyopathy
c. Antianxiety drugs
14. In infective endocarditis, vegetative lesions
d. Broad-spectrum antibiotic drugs
grow on the valves of the heart. These vegeta-
tive lesions consist of a collection of infec- 17. Heart failure in an infant usually manifests it-
tious organisms and cellular debris enmeshed self as tachypnea or dyspnea, both at rest and
in the fibrin strands of clotted blood. What on exertion. When does this most commonly
are the possible systemic effects of these vege- occur with an infant?
tative lesions? a. During bathing
a. They can block the heart valves from clos- b. During feeding
ing completely.
c. During burping
b. They can keep the heart valves from open-
d. During sleep
ing.
c. They can fragment and cause cerebral em- 18. Tetralogy of Fallot is a congenital condition
boli. of the heart that manifests in four distinct
anomalies of the infant heart. It is considered
d. They can fragment and make the lesions
a cyanotic heart defect due to the right-to-left
larger.
shunting of the blood through the ventricular
15. Antibodies directed against the M protein of septal defect. A hallmark of this condition is
certain strains of streptococcal bacteria seem the “tet spells” that occur in these children.
to cross-react with glycoprotein antigens in What is a tet spell?
the heart, joint, and other tissues to produce a. A stressful period right after birth that oc-
an autoimmune response resulting in curs without evidence of cyanosis
rheumatic fever and rheumatic heart disease.
b. A hyperoxygenated period when the infant
This occurs through what phenomenon?
is at rest
a. Aschoff reaction
c. A hypercyanotic attack brought on by peri-
b. Sydenham reaction ods of stress
c. C-reactive mimicry d. A hyperpneic attack in which the infant
d. Molecular mimicry loses consciousness

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25
CHAPTER

Disorders of Cardiac
Conduction and Rhythm

SECTION I: LEARNING 12. Describe the methods used in diagnosis of

cardiac arrhythmias
OBJECTIVES
13. Explain the mechanisms, criteria for use, and
1. Describe the cardiac conduction system and benefits of antiarrhythmic drugs, internal
relate it to the mechanical functioning of the cardioverter-defibrillator therapy, ablation
heart therapy, and surgical procedures in the treat-
ment of persons with recurrent, symptomatic
2. Characterize the four phases of a cardiac ac-
arrhythmias
tion potential and differentiate between the
fast and slow responses
3. Draw an ECG tracing and state the origin of SECTION II: ASSESSING YOUR
the component parts of the tracing UNDERSTANDING
4. Provide a rationale for the importance of
careful lead placement and monitoring of is- Activity A Fill in the blanks.
chemic events 1. Specialized cells generate im-
5. Describe the possible mechanisms for ar- pulses at a faster rate than other types of
rhythmia generation heart tissue, and the conduction tissue trans-
mits these impulses at a more rapid rate than
6. Compare sinus arrhythmias with atrial ar- other cardiac cell types.
rhythmias
2. Coronary heart disease that
7. Characterize the effects of atrial flutter and blood flow through the vessels supplying tis-
atrial fibrillation on heart rhythm sues of the conduction system can induce se-
8. Describe the significance of long QT syn- rious and sometimes fatal disturbances in
drome cardiac rhythm.

9. Describe the characteristics of first-, second-, 3. Blood supply to the sinoatrial node is pro-
and third-degree heart block vided by means of the artery.

10. Compare the effects of premature ventricular 4. The , which supplies the ventri-
contractions, ventricular tachycardia, and cles, has large fibers that allow for rapid con-
ventricular fibrillation on cardiac function duction and almost simultaneous excitation.

11. Cite the types of cardiac conditions that can 5. represents the period during
be diagnosed using the ECG which the negative potential inside the cell
reverses and becomes positive.

134
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CHAPTER 25 DISORDERS OF CARDIAC CONDUCTION AND RHYTHM 135

6. involves reestablishment of the 20. The long QT syndrome may result in

resting membrane potential. and sudden cardiac death.
7. The longer length of the of car- 21. A is caused by a ventricular ec-
diac muscle is important in maintaining the topic pacemaker and leaves the ventricle un-
alternating contraction and relaxation that is able to repolarize sufficiently to respond to
essential to the pumping action of the heart the next impulse that arises in the sinoatrial
and for the prevention of fatal arrhythmias. node.
8. The records the potential differ- 22. is dangerous because it elimi-
ence in charge between two electrodes as de- nates atrial kick and can cause a reduction in
polarization and repolarization waves move diastolic filling time to the point where cardiac
through the heart and are conducted to the output is severely diminished or nonexistent.
skin surface.
23. In ventricular fibrillation, the ventricle
9. The six limb leads view the electrical forces as but does not contract.
they pass through the heart on the
24. refers to abnormalities of im-
plane, and the six chest leads
pulse conduction.
provide a view of the electrical forces as they
pass through the heart on the 25. -degree block may be the result
plane. of disease in the atrioventricular node, such
as ischemia or infarction, or of infections,
10. Many forms of cardiac diagnostic criteria are
such as rheumatic fever or myocarditis.
ECG .
26. heart disease is the primary
11. There are two types of disorders of the cardiac
cause for the development of ventricular
conduction system: disorders of
fibrillation.
and disorders of .
27. tachycardia is characterized by
12. If the sinoatrial (SA) node fires more slowly or
ventricular tachycardia, syncope, and sudden
SA node conduction is blocked, then another
death occurring in familial or sporadic cases
site that is capable of takes over
in the absence of cardiac disease or ECG ab-
as pacemaker.
normalities.
13. Almost all tachyarrhythmias are the result of
28. The correction of conduction defects, brady-
a phenomenon known as .
cardias, and tachycardias can involve the use
14. Arrhythmias that arise because of anatomic of an electronic , ,
reentry are . or .
15. In normal , a P wave precedes
Activity B Consider the following figure.
each QRS complex, and the RR intervals re-
main relatively constant over time.
16. are contractions that originate
in the atrial conduction pathways or atrial
muscle cells and occur before the next ex-
pected sinoatrial node impulse.
U
17. Paroxysmal supraventricular tachycardias Baseline
originate above the bifurcation of the
and have a sudden onset and
termination.
18. In typical atrial flutter, the ECG reveals a de-
fined pattern in leads aVF, V1, In this figure, label the following:
and V5.
• P wave
19. is characterized by chaotic im- • QRS complex
pulses propagating in different directions and
causing disorganized atrial depolarization
without effective atrial contraction.

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136 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

• T wave Activity D Put the events of cardiac

• Delay in atrioventricular node conduction in the order in which the structures
• Atrial depolarization are depolarized.
• Ventricular depolarization
• Ventricular repolarization Atrioventricular node depolarization
Bundle branches
Activity C Match the key terms in Column A Sinoatrial node depolarization
with their definitions in Column B.
Bundle of His
Column A Column B Purkinje fibers

1. Automaticity Activity E Briefly answer the following.

a. Failure of the sinoa-
2. Sinus 1. Describe the phases of the cardiac action po-
trial node to dis-
bradycardia tential and relate each phase to the ECG.
charge
3. ECG b. Conduction link be-
4. Sinus arrest tween the atria and
ventricles is lost
5. Bradyarrhy-
c. Disorders of cardiac
thmias
rhythm 2. What is believed to be the cause(s) of many ar-
6. Sick sinus d. Prolonged PR interval rhythmias?
syndrome
e. Ability of certain
7. Ectopic cells to sponta-
pacemaker neously initiate an
action potential
8. Arrhythmia
f. Intermittent failure 3. Describe the treatment options for atrial fibril-
9. Sinus tachy- of conduction of one
cardia lation.
or more P waves
10. Tachyarrhy- g. Decreased systemic
thmias perfusion
11. First-degree h. Heart rate 100
atrioventri- beats/minute
4. Explain the effects on the cardiac cell mem-
cular block i. Graphic recording of
brane that result in long QT syndrome.
the electrical activity
12. Second-degree
of the heart
atrioventri-
cular block j. Excitable focus out-
side the normally
13. Third-degree functioning sinoa-
atrioventri- trial node 5. What is an exercise stress test, and what is its
cular block
k. Bradycardia- purpose?
tachycardia syndrome
l. Heart rate 60
beats/minute
m. Reduce the diastolic
filling time
6. What is the physiologic aim of pharmacologic
treatment of arrhythmia?

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CHAPTER 25 DISORDERS OF CARDIAC CONDUCTION AND RHYTHM 137

SECTION III: APPLYING YOUR 2. Respiratory sinus arrhythmia is considered a

more optimal rhythm than a rhythm where
KNOWLEDGE all RR intervals are equal. In respiratory sinus
arrhythmia, what is the variation in cardiac
Activity F Consider the following scenario and
cycles related to?
answer the questions.
a. Intraabdominal pressure changes that
A 75-year-old woman is brought to the emer- occur with respiration
gency department by ambulance. She has a 6-
b. Intrathoracic pressure changes that occur
month history of atrial fibrillation. She is
with respiration
complaining of palpitations and extreme fatigue.
The paramedic reports that she has a wet sound- c. Intraabdominal pressure changes due to
ing, nonproductive cough. Her respiratory rate is vagal nerve stimulus
35 breaths/minute; her heart rate is variable with d. Intrathoracic pressure changes due to inad-
a ventricular rate ranging from 80 to 160 equate oxygenation
beats/minute. Her ECG confirms atrial fibrillation.
3. In children, what is sick sinus syndrome most
1. What medications would the nurse expect this commonly associated with?
patient to be taking? a. Congenital heart defects prior to corrective
cardiac surgery
b. Destruction of the sinoatrial node
c. Congenital heart defects following correc-
tive cardiac surgery
2. What treatment is used to convert atrial fibril- d. Destruction of the atrioventricular node
lation to sinus rhythm, and what are the com-
4. Atrial fibrillation is the most common chronic
plications of this treatment?
arrhythmia whose incidence increases with
age. Atrial fibrillation may present as asymp-
tomatic to severe symptomatology. What is
the treatment of atrial fibrillation dependent
on? Mark all that apply.
a. Recency of onset
b. Etiology
SECTION IV: PRACTICING
c. Persistence of arrhythmia
FOR NCLEX
d. Size of pulse deficit
Activity G Answer the following questions. e. Atrial rate
1. ECG monitoring has been found to be more 5. Torsade de pointes is a specific type of poly-
sensitive than a patient’s report of symptoms morphic ventricular tachycardia in which
when identifying transient ongoing myocar- the polarity of the QRS complex swings be-
dial ischemia. Why is this? tween positive and negative, often on a beat-
a. Most ECG-detected ischemic events are to-beat basis. It is the result of the long QT
clinically silent. syndrome and can cause sudden cardiac
death. Which medication is not linked to tor-
b. The ECG can look at ischemic events from
sade de pointes as a causative agent?
different directions.
a. Verapamil
c. ECG monitoring is reliable only when the
patient remains still. b. Procainamide
d. Most ECG-detected ischemic events cause a c. Digitalis
great deal of pain. d. Tetracycline

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138 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

6. In second-degree atrioventricular block, there a. ECG ischemic-type ST segment changes

is a relationship between the P waves and the b. ECG ischemic-type QRS changes
QRS complex resulting in recurring PR inter-
c. ECG documented conduction abnormali-
vals. What does this mean?
ties
a. The association of P waves and QRS com-
d. ECG documented hemodynamic hyperre-
plexes is not random.
actions
b. The relationship between the P waves and
the QRS complexes is a widening PR inter- 10. Antiarrhythmic drugs are classified into four
val. major groups. The drugs in one may act simi-
larly on cardiac conduction their hemody-
c. The association of P waves and QRS com-
namic action may vary significantly. Match
plexes is random.
the name of the drug to its classification and
d. The relationship between the P waves and use in the following chart:
the QRS complexes is a narrowing PR inter-
Uses: supraventricular arrhythmias and tach-
val.
yarrhythmias; slowing the sinoatrial node
7. Brugada syndrome, an autosomal dominant pacemaker and inhibiting conduction in the
disorder, manifests in adulthood as ST seg- atrioventricular node; supraventricular and
ment elevation, right bundle branch block, ventricular arrhythmias; treating ventricular
and susceptibility to ventricular tachycardia. arrhythmias only; treatment of serious ven-
In Brugada syndrome, the timing of cardiac tricular arrhythmias
events is significant. When do these cardiac Classifications: Class IA, Class IB, Class II,
events typically occur? Class III, Class IV
a. During exercise
Drug Use Class
b. When first arising in the morning
c. Just before bedtime at night Procainamide

d. During sleep or rest Atenolol

8. A Holter monitor is a small ECG recording de- Amiodarone

vice used for long-term monitoring of cardiac Diltiazem
activity, usually for up to 48 hours. These de-
vices are used in correlation with event mark- Lidocaine
ers (on the device itself) and activity logs, or
diaries of the person’s activities. What cardiac 11. When a patient has a recurrent, life-threaten-
problems is a Holter monitor useful in docu- ing arrhythmia originating either supraven-
menting? Mark all that apply. tricularly or ventricularly, ablation therapy is
a. Conduction abnormalities an option for treatment. What does ablation
therapy do?
b. Acquired cardiac deficiencies
a. Removes hyperexcitable cardiac tissue
c. Congenital cardiac problems
through open heart surgery
d. ST segment changes
b. Isolates and destroys arrhythmogenic
e. PR interval changes cardiac tissue
9. An exercise stress test challenges the heart to c. Identifies and excises ischemic cardiac
respond to the increased demands of exercise tissue
in a controlled and monitored environment. d. Uses a catheter technique to reestablish
Not only do exercise stress tests show changes conductivity to mild infarcts
in heart rate, blood pressure, and perceived
level of exercise, but they have also been
found useful in determining what?

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26

CHAPTER
Heart Failure and
Circulatory Shock

SECTION I: LEARNING ventricular assist devices, heart transplanta-

tion, and other surgical alternatives to the
OBJECTIVES treatment of selected types of heart failure
1. Define heart failure 10. State a clinical definition of shock
2. Describe the contractile properties of the 11. Compare the causes, pathophysiology, and
myocardium chief characteristics of cardiogenic, hypov-
olemic, obstructive, and distributive shock
3. Explain how the Frank-Starling mechanism,
sympathetic nervous system, renin- 12. Describe the complications of shock as they
angiotensin-aldosterone mechanism, natri- relate to the lungs, kidneys, gastrointestinal
uretic peptides, endothelins, and myocardial tract, and blood clotting
hypertrophy and remodeling function as
13. State the rationale for treatment measures to
adaptive and maladaptive mechanisms in
correct and reverse shock
heart failure
14. Define multiple organ dysfunction syndrome
4. Differentiate high-output versus low-output
and cite its significance in shock
heart failure, systolic versus diastolic heart
failure, and right-sided versus left-sided heart 15. Describe the causes of heart failure in infants
failure in terms of causes, impact on cardiac and children
function, and major manifestations
16. Cite how the aging process affects cardiac
5. Differentiate chronic heart failure from acute function and predisposes to ventricular dys-
heart failure syndromes function
6. Describe the manifestations of heart failure 17. State how the signs and symptoms of heart
and relate to the function of the heart failure may differ between younger and older
7. Describe the methods used in diagnosis and adults
assessment of cardiac function in persons
with heart failure
8. Relate the pharmacologic actions of an-
SECTION II: ASSESSING YOUR
giotensin-converting enzyme inhibitors and UNDERSTANDING
receptor blockers, -adrenergic–blockers, di-
uretics, digoxin, and vasodilatory agents to Activity A Fill in the blanks.
the treatment of heart failure 1. has been defined as a complex
9. Relate the use of cardiac resynchronization, syndrome that results from any functional or
implantable cardioverter-debrillators, left
139
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140 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

structural disorder of the heart that causes de- 14. Among the conditions that cause diastolic
creased pumping. dysfunction are those that the
ventricle (e.g., pericardial effusion, constric-
2. Among the most common causes of heart
tive pericarditis), those that wall
failure are , , dilated
thickness and reduce chamber size (e.g.,
cardiomyopathy, and heart dis-
myocardial hypertrophy, hypertrophic car-
ease.
diomyopathy), and those that
3. Endurance athletes have cardiac diastolic relaxation (e.g., aging, ischemic
reserves. heart disease).
4. can be expressed as the product 15. Diastolic dysfunction can be aggravated by
of the heart rate and stroke volume. and can be improved by a re-
duction in heart rate.
5. The heart rate is regulated by a balance be-
tween the activity of the ner- 16. Heart failure can be classified according to the
vous system, which produces an increase in of the heart that is primarily
heart rate, and the nervous affected.
system, which slows it down.
17. A major effect of right-sided heart failure is
6. The is a function of preload, the development of .
afterload, and myocardial contractility.
18. As venous distention progresses in right-sided
7. is the percentage of blood heart failure, blood backs up in the
pumped out of the ventricles with each veins that drain into the inferior
contraction. vena cava, and the liver becomes engorged.
8. In systolic ventricular dysfunction, myocar- 19. is the most common cause of
dial contractility is impaired, leading to a right ventricular failure.
in the ejection fraction and
20. The most common causes of
cardiac output.
ventricular dysfunction are acute myocardial
9. Diastolic ventricular dysfunction is character- infarction and cardiomyopathy.
ized by a ejection fraction but
21. is an uncommon type of heart
impaired diastolic ventricular relaxation,
failure that is caused by an excessive need for
leading to a decrease in ventricular filling that
cardiac output.
ultimately causes a decrease in preload, stroke
volume, and cardiac output. 22. is caused by disorders that im-
pair the pumping ability of the heart, such as
10. With both systolic and diastolic ventricular
ischemic heart disease and cardiomyopathy.
dysfunction, are usually able to
maintain adequate resting cardiac function 23. Elevated levels have been
until the later stages of heart failure. shown to be predictive of the development of
heart failure.
11. The rise in preload seen in systolic dysfunc-
tion is believed to be a compensatory mecha- 24. The development of constitutes
nism to help maintain stroke volume via the one of the principal mechanisms by which
mechanism despite a drop in the heart compensates for an increase in
ejection fraction. workload.
12. Systolic dysfunction commonly results from 25. A gradual or rapid change in heart failure
conditions that impair the per- signs and symptoms resulting in a need for
formance of the heart (e.g., ischemic heart urgent therapy is defined as
disease, cardiomyopathy), produce a syndrome.
(e.g., valvular insufficiency, ane-
26. dyspnea is a sudden attack of
mia), or generate a (e.g., hyper-
dyspnea that occurs during sleep.
tension, valvular stenosis) on the heart.
27. is the most dramatic symptom
13. In dysfunction, cardiac output
of acute heart failure syndromes.
is compromised by the abnormal filling of the
ventricle.

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CHAPTER 26 HEART FAILURE AND CIRCULATORY SHOCK 141

28. In acute or severe left-sided failure, cardiac 41. is associated with impaired left
output may fall to levels that are insufficient ventricular filling that is due to changes in
for providing the with adequate myocardial relaxation and compliance.
oxygen.
Activity B Match the key terms in Column A
29. Ascites is a common manifestation associated
with their definitions in Column B.
with ventricular failure and
long-standing elevation of systemic venous 1.
pressures.
Column A Column B
30. Central cyanosis is caused by conditions that
1. Inotropy a. Volume or loading
impair of the arterial blood.
conditions of the
2. Cardiac
31. In persons with ventricular dysfunction, sud- ventricle at the end
output
den death is caused most commonly by of diastole
tachycardia or fibrillation. 3. Afterload b. Right heart failure
32. Measurements of are recom- 4. Pulmonary occurs in response to
mended to confirm the diagnosis of heart fail- congestion chronic pulmonary
ure, to evaluate the severity of left ventricular disease
5. Cardiac
compromise and estimate the prognosis and c. Ability to increase
reserve
predict future cardiac events such as sudden cardiac output dur-
death, and to evaluate the effectiveness of 6. Cor pulmo- ing increased activity
treatment. nale d. Force that the con-
33. -Adrenergic receptor blocking drugs are used 7. High-output tracting heart muscle
to decrease dysfunction associ- failure must generate to
ated with activation of the sympathetic ner- eject blood from the
8. Preload filled heart
vous system.
9. Systolic e. Failure that is caused
34. can be described as an acute fail-
dysfunction by an excessive need
ure of the circulatory system to supply the pe-
for cardiac output
ripheral tissues and organs of the body with 10. Endothelin
an adequate blood supply, resulting in cellu- f. Amount of blood the
lar hypoxia. ventricles eject each
minute
35. The most common cause of cardiogenic
g. Ejection fraction less
shock is .
than 40%
36. shock is characterized by dimin- h. Potent vasoconstric-
ished blood volume such that there is inade- tors
quate filling of the vascular compartment.
i. Common sign of left
37. shock is characterized by loss of ventricular failure
blood vessel tone, enlargement of the vascu- j. Contractile perfor-
lar compartment, and displacement of the mance of the heart
vascular volume away from the heart and
central circulation. 2.

38. A defect in the vasomotor center in the brain Column A Column B

stem or the sympathetic outflow to the blood 1. Hydrothorax a. Periodic breathing
vessels is known as . characterized by grad-
2. Cyanosis
39. Anaphylactic shock results from an ual increase in depth,
-mediated reaction in which 3. Cheyne- followed by a de-
vasodilator substances such as histamine are Stokes crease resulting in
released into the blood. respiration apnea
4. Dyspnea b. Bronchospasm due
40. heart defects are the most com-
to congestion of the
mon cause of heart failure in children.
bronchial mucosa

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142 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

5. Cardiac c. Bluish discoloration Activity D Briefly answer the following.

asthma of the skin
1. How is cardiac contractility regulated?
6. Circulatory d. Labored breathing
failure e. Transudation of fluid
into the peritoneal
7. Orthopnea
cavity
8. Ascites f. Hypoperfusion of or-
gans and tissues 2. Why is it advisable to test cardiac function
g. Transudation of fluid during exercise (stress) rather than at rest?
into the pleural cavity
h. Shortness of breath
when supine
3.
Column A Column B 3. How does diastolic dysfunction produce the
1. Cardiogenic a. Acute failure of the
typical signs and symptoms that characterize
shock circulatory system to the condition?
supply the peripheral
2. Obstructive
tissues and organs of
shock
the body with an ade-
3. Distributive quate blood supply
shock b. Caused by excessive 4. Often, the early signs of heart failure are silent.
4. Hypovolemic vasodilation with This is due to the many compensatory mecha-
shock maldistribution of nisms of the cardiovascular system. Explain,
blood flow briefly, how these mechanisms work and why,
5. Circulatory
c. Caused by alteration in the end, they only serve to make the heart
shock
in cardiac function failure worse.
d. Caused by a decrease
in blood volume
e. Caused by obstruction
of blood flow through
the circulatory system
5. What are the common manifestations of heart
Activity C failure? Why?
1. The pathophysiology of right- and left-sided
heart failure has distinct features. Construct a
flowchart of the following symptoms and their
causes:
• Right heart failure
6. What effect does diuretic therapy have on
• Left heart failure
heart failure?
• Orthopnea
• Cyanosis
• Activity intolerance
• Anorexia
• Weight loss
• Impaired liver function
7. What are the cellular consequences of shock?
• Gastrointestinal tract congestion
• Impaired gas exchange
• Pulmonary edema
• Dependent edema and ascites
• Congestion of peripheral tissues
• Decreased cardiac output
• Pulmonary congestion

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CHAPTER 26 HEART FAILURE AND CIRCULATORY SHOCK 143

8. What are the five major complications of se- 4. Acute myocardial c. Right ventricular
vere shock? infarction dysfunction
5. Paget disease d. Low-output fail-
6. Cardiomyopathy ure
e. High-output
failure
f. Systolic dysfunc-
tion
SECTION III: APPLYING YOUR 2. What are the signs and symptoms of heart
KNOWLEDGE failure? Mark all that apply.
a. Fluid retention
Activity E Consider the following scenario and
b. Ruddy complexion
answer the questions.
c. Fatigue
The parents of a 1-month-old boy born with
d. Bradycardia
tetralogy of Fallot are in the emergency depart-
ment with their child, who is exhibiting a respira- e. Chronic productive cough
tory rate of 65 breaths/minute, heart rate of 160 3. When an acute event occurs and the circula-
beats/minute, and urine output of 1 cc/kg/hour. tory system can no longer provide the body
The child is diaphoretic, his extremities are cool, with adequate perfusion of its tissues and or-
and he is lethargic and will not eat. The sus- gans, cellular hypoxia occurs, and the body
pected diagnosis is heart failure. goes into shock. What are the causes of shock
1. What diagnostic tests would the nurse expect in the human body? Mark all that apply.
to be ordered for this child? a. Maldistribution of blood flow
b. Hypovolemia
c. Excessive vasoconstriction
d. Obstruction of blood flow
e. Hypervolemia
2. What drugs are used in the treatment of heart
4. What are the physiologic signs and symptoms
failure in infants and children, and what are
of cardiogenic shock? Mark all that apply.
the dosages based on?
a. Decreased mean arterial blood pressures
b. Increased urine output related to increased
renal perfusion
c. Increased central venous pressure
d. Hypercapnic lips and nail beds
e. Increased extraction of O2 from hemoglobin
SECTION IV: PRACTICING
5. In hypovolemic shock, the main purpose of
FOR NCLEX treatment is correcting or controlling the un-
derlying cause of the hypovolemia and im-
Activity F Answer the following questions.
proving the perfusion of the tissues and
1. Match the following conditions with the type organs of the body. Which of the following
of heart failure they cause. treatments is not a primary form of therapy
for hypovolemic shock?
Condition Type of Heart Failure
a. Surgery
1. Valvular a. Diastolic
b. Administration of IV fluids and blood
insufficiency dysfunction
c. Vasoconstrictive drugs
2. Ischemic heart b. Left ventricular
disease dysfunction d. Infusion of blood and blood products
3. Aortic or mitral
stenosis

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144 UNIT 6 DISORDERS OF CARDIOVASCULAR FUNCTION

6. Neurogenic shock, or spinal shock, is a phe- 9. What is the primary physiologic result of
nomenon caused by the inability of the vaso- obstructive shock?
motor center in the brain stem to control a. Left ventricular hypertrophy
blood vessel tone through the sympathetic out-
b. Elevated right heart pressure
flow to the blood vessels. In neurogenic shock,
what happens to the heart rate and the skin? c. Right atrial hypertrophy
a. Heart rate slower than normal; skin warm d. Decreased right heart pressure
and dry 10. An important factor in the mortality of severe
b. Heart rate faster than normal; skin cool shock is acute renal failure. What is the
and moist degree of renal damage related to in shock?
c. Heart rate slower than normal; skin cool a. Loss of perfusion and duration of shock
and moist b. Loss of perfusion and degree of immune-
d. Heart rate slower than normal; skin warm mediated response
and dry c. Severity and duration of shock
7. Anaphylactic shock is the most severe form of d. Severity of shock and degree of immune-
systemic allergic reaction. Immunologically mediated response
medicated substances are released into the
11. The pathogenesis of multiorgan dysfunction
blood, causing vasodilation and an increase
syndrome (MODS) is not clearly understood
in capillary permeability. What physiologic
at this time. Supportive management is cur-
response often accompanies the vascular re-
rently the focus of treatment in this disorder.
sponse in anaphylaxis?
What is not a major risk factor in MODS?
a. Uterine smooth muscle relaxation
a. Advanced age
b. Laryngeal edema
b. Alcohol abuse
c. Bronchodilation
c. Respiratory dysfunction
d. Gastrointestinal relaxation
d. Infarcted bowel
8. Sepsis is a growing incidence in the United
12. What is the primary cause of heart failure in
States. Its pathogenesis includes neutrophil
infants and children?
activation that kills microorganisms. Neu-
trophils also injure the endothelium, releasing a. Idiopathic heart disease
mediators that increase vascular permeability. b. Structural heart defects
What else do neutrophils do in sepsis? c. Hyperkalemia
a. Release nitric oxide d. Reaction to medications
b. Vasoconstrict the capillary bed
c. Cause bradycardia
d. Activate erythropoiesis

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27

CHAPTER
Structure and Function of
the Respiratory System

SECTION I: LEARNING 10. Differentiate between the determinants of

airway resistance and lung compliance and
OBJECTIVES their effect on the work of breathing
1. State the difference between the conducting 11. Define inspiratory reserve, expiratory reserve,
and the respiratory airways vital capacity, residual lung volume, and
FEV1.0
2. Trace the movement of air through the air-
ways, beginning in the nose and oropharynx 12. Trace the exchange of gases between the air
and moving into the respiratory tissues of the in the alveoli and the blood in the pulmonary
lung capillaries
3. Describe the function of the mucociliary 13. Differentiate between pulmonary and alveolar
blanket ventilation
4. Compare the supporting structures of the 14. Explain why ventilation and perfusion must
large and small airways in terms of cartilagi- be matched
nous and smooth muscle support
15. Cite the difference between dead air space
5. State the function of the two types of alveolar and shunt
cells
16. List four factors that affect the diffusion of
6. Differentiate the function of the bronchial gases in the alveoli
and pulmonary circulations that supply the
17. Explain the difference between PO2 and
lungs
hemoglobin-bound oxygen and O2 saturation,
7. Describe the basic properties of gases in rela- and oxygen content
tion to their partial pressures and their pres-
18. Explain the significance of a shift to the
sures in relation to volume and temperature
right and a shift to the left in the oxygen–
8. State the definition of intrathoracic, in- hemoglobin dissociation curve
trapleural, and intra-alveolar pressures, and
19. Compare the neural control of the respiratory
state how each of these pressures changes in
muscles, which control breathing, with that
relation to atmospheric pressure during inspi-
of cardiac muscle, which controls the pump-
ration and expiration
ing action of the heart
9. Use the law of Laplace to explain the need for
20. Describe the function of the chemoreceptors
surfactant in maintaining the inflation of
and lung receptors in the regulation of venti-
small alveoli
lation

145
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146 UNIT 7 DISORDERS OF RESPIRATORY FUNCTION

21. Trace the integration of the cough reflex from of gas exchange between the air and the
stimulus to explosive expulsion of air that blood.
constitutes the cough
11. The pulmonary circulation arises from the
22. Describe the type of periodic breathing artery and provides for the gas
known as Cheyne-Stokes breathing exchange function of the lungs.
23. Define dyspnea and list three types of condi- 12. Particulate matter entering the lung is partly
tions in which dyspnea occurs removed by vessels, as are the
plasma proteins that have escaped from the
pulmonary capillaries.
SECTION II: ASSESSING YOUR 13. It is stimulation, through the
UNDERSTANDING vagus nerve, that is responsible for the
slightly constricted smooth muscle tone in
Activity A Fill in the blanks. the normal resting lung.

1. The primary function of the respiratory system 14. Stimulation of the nervous sys-
is . tem causes airway relaxation, blood vessel
constriction, and inhibition of glandular
2. Functionally, the respiratory system can be secretion.
divided into two parts: the air-
ways, through which air moves as it passes 15. The pressure exerted by a single gas in a mix-
between the atmosphere and the lungs, and ture is called the .
the tissues of the lungs, where 16. Air moves between the atmosphere and the
gas exchange takes place. lungs because of a .
3. The airways consist of the nasal 17. The pressure in the pleural cavity is called the
passages, mouth and pharynx, larynx, tra- pressure.
chea, bronchi, and bronchioles.
18. The maneuver is used to study
4. The air we breathe is , the cardiovascular effects of increased in-
, and as it moves trathoracic pressure on peripheral venous
through the conducting airways. pressures, cardiac filling, and cardiac output,
5. The produced by the epithelial as well as poststrain heart rate and blood
cells in the conducting airways forms a layer pressure responses.
that protects the respiratory system by 19. Lung refers to the ease with
entrapping dust, bacteria, and other foreign which the lungs can be inflated.
particles that enter the airways.
20. The is the volume of air inspired
6. The vocal folds and the elongated opening (or exhaled) with each breath.
between them are called the .
21. The maximum amount of air that can be in-
7. The walls of the trachea are supported by spired in excess of the normal tidal volume
horseshoe- or C-shaped rings of (TV) is called the , and the maxi-
cartilage, which prevent it from collapsing mum amount that can be exhaled in excess
when the pressure in the thorax becomes of the normal TV is the .
negative.
22. The is the amount of air a per-
8. Each primary bronchus, accompanied by the son can breathe in beginning at the normal
pulmonary arteries, veins, and lymph vessels, expiratory level and distending the lungs to
enters the lung through a slit called the the maximal amount.
.
23. The equals the inspiratory re-
9. Each is supplied by a branch of serve volume plus the tidal volume plus the
a terminal bronchiole, an arteriole, the pul- expiratory reserve volume and is the amount
monary capillaries, and a venule. of air that can be exhaled from the point of
10. The are the terminal air spaces maximal inspiration.
of the respiratory tract and the actual sites

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CHAPTER 27 STRUCTURE AND FUNCTION OF THE RESPIRATORY SYSTEM 147

24. The is the amount of air that is Activity B Consider the following figure.
exchanged in 1 minute.
25. ventilation refers to the total ex-
change of gases between the atmosphere and
the lungs; ventilation is the
exchange of gases within the gas exchange
portion of the lungs.
26. Even at low lung volumes, some air remains
in the alveoli of the lower portion of the
lungs, preventing their .
27. refers to the air that is moved
with each breath but does not participate in
gas exchange.
28. Both dead air space and shunt produce a
of ventilation and perfusion.
29. Although the lungs are responsible for the In this figure of the respiratory system, label the
exchange of gases with the external environ- following structures:
ment, the transports gases be-
tween the lungs and body tissues. • Secondary bronchi
• Tracheal cartilage
30. carries about 98% to 99% of • Left primary bronchus
oxygen in the blood and is the main trans- • Terminal bronchioles
porter of oxygen. • Segmental bronchi
31. Oxygen binds with the heme
groups on the hemoglobin molecule. Activity C Match the key terms in Column A
with their definitions in Column B.
32. Hemoglobin’s affinity for oxygen is influ-
enced by , concen- Column A Column B
tration, and body .
1. Mediastinum a. Mucus lining of the
33. Carbon dioxide is transported in the blood in conducting airways
2. Elastic recoil
three forms as (10%), attached b. Form part of respi-
to (30%), and as 3. Epiglottis ratory membrane
(60%).
4. Type I pneu- c. Pressure inside the
34. The pacemaker properties of the respiratory mocytes airways and alveoli
center result from the cycling of the two d. Trachea, bronchi,
5. Angiogenesis
groups of respiratory neurons: the and bronchioles
center in the upper pons and 6. Mucociliary
e. Synthesize pul-
the center in the lower pons. blanket
monary surfactant
35. The automatic regulation of ventilation is 7. Alveolar f. Space between lungs
controlled by input from two types of sensors pressure that contains heart,
or receptors: and blood vessels, lymph
8. Brush cells
receptors. nodes, nerves, and
9. Tracheo- esophagus
36. The content in the blood regu-
bronchial
lates ventilation through its effect on the pH
of the extracellular fluid of the brain. 10. Type II
pneumocytes
37. is a subjective sensation or a
person’s perception of difficulty in breathing (continues)
that includes the perception of labored
breathing and the reaction to that sensation.

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148 UNIT 7 DISORDERS OF RESPIRATORY FUNCTION

g. Ability of the elastic 5. In the clinic, what type of blood is used for
components of the blood gas measurements, and why?
lung to recoil to their
original position
h. Routes liquids and
foods into the
esophagus
6. What causes us to cough?
i. Formation of new
blood vessels
j. Act as receptors
that monitor the air
quality of the lungs
Activity D Put these respiratory structures in
anatomic order:
SECTION III: APPLYING YOUR
a. Nasopharynx KNOWLEDGE
b. Trachea
c. Epiglottis Activity F Consider the following scenario and
answer the questions.
d. Alveoli
e. Respiratory bronchiole Seventy-nine-year-old Mr. Borden is brought to
the clinic by his daughter, who says, “I am wor-
f. Intrapulmonary bronchus
ried about him. He is so stubborn, he just won’t
g. Extrapulmonary bronchus complain. When he walks, he gets so short of
breath. I don’t think he is getting enough oxy-
Activity E Briefly answer the following. gen!” Mr. Borden’s O2 level is 87%, and his nail
1. Describe the pleura and explain its function. beds are dusky with a delayed capillary refill
time. There is no clubbing to Mr. Borden’s fin-
gertips.
1. How would the nurse explain generalized hy-
poxia to Mr. Borden’s daughter?
2. Describe the events of the respiratory cycle.

2. What diagnostic tests would the doctor order

to confirm a diagnosis of generalized hypoxia?
3. What is the function of pulmonary surfactant?

4. What is the mathematical formula used to

describe the diffusion of gas across the respira- SECTION IV: PRACTICING
tory membrane? FOR NCLEX
Activity G Answer the following questions.
1. The lungs are the working structures of the
respiratory system, and they have several

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CHAPTER 27 STRUCTURE AND FUNCTION OF THE RESPIRATORY SYSTEM 149

functions. What are the functions of the 6. Our ability to oxygenate the tissues and or-
lungs? Mark all that apply. gans of our bodies depends on our ability to
a. To produce heparin ventilate, or exchange gases in our respiratory
system. The resultant distribution of ventila-
b. To activate vasoactive substances
tion of the areas of the body open to the ex-
c. To convert angiotensin I to angiotensin II change of gases in our respiratory system
d. To activate bradykinin depends on what?
e. To convert glucose to glycogen a. Effects of gravity intrathoracic pressure
2. Bronchial blood vessels have several func- b. Body position and alveolar pressure
tions. They warm and humidify incoming air c. Effects of gravity and body position
as well as distribute blood to the conducting d. Intrathoracic pressure and alveolar
airways and the supporting structures of the pressure
lung. What is it that makes bronchial blood
vessels unique in the body? 7. Alveolar oxygen levels directly impact the
blood vessels in the pulmonary circulation. In
a. They can undergo angiogenesis.
a person with lung disease, there is vasocon-
b. They drain blood into the bronchiole arteries. striction throughout the lung, causing a gen-
c. They participate in gas exchange. eralized hypoxia. What can prolonged
d. They carry oxygenated blood to the lung hypoxia lead to?
tissues. a. Hypertension and increased workload on
the left heart
3. Match the respiratory pressures with their
definitions. b. Pulmonary hypertension and left ventricu-
lar hypertrophy
Pressure Definition
c. Hypertension and increased workload on
1. Alveolar a. Pressure in the the right heart
pressure thoracic cavity d. Pulmonary hypertension and increased
2. Intrapleural b. Pressure inside the workload on the right heart
pressure airways and alveoli
8. When there is a mismatch of ventilation and
3. Transpulmonary of the lungs
perfusion within the lung itself, insufficient
pressure c. Difference be- ventilation occurs. There is a lack of enough
4. Intrathoracic tween the intra- oxygen to adequately oxygenate the blood
pressure alveoli and flowing through the alveolar capillaries, thus
intrapleural creating a physiologic shunt. What causes a
pressures physiologic right-to-left shunting of blood in
d. Pressure in the the respiratory system?
pleural cavity a. Destructive lung disease or heart failure
4. What does the equation C  V/P stand for? b. Obstructive lung disease or heart failure
a. Surface tension inside the lungs c. Heart failure or pulmonary hypertension
b. Lung compliance d. Heart failure or regional hypoxia
c. Airway resistance 9. Blood transports both oxygen and carbon
d. Change in peak expiratory flow dioxide in a physically dissolved form to the
tissues and organs of the body. It is the mea-
5. An 82-year-old man with chronic obstructive
surements of the components of the gases in
pulmonary disease is at the clinic for a regular
the blood that are used as indicators of the
check-up. Because of his diagnosis, the nurse
body’s status by health care workers. Why is
would expect his respiratory rate under nor-
it commonly the blood in the arteries that is
mal circumstances to be what?
measured for its components rather than the
a. Tachypneic blood in the veins?
b. 18–20 beats/minute
c. 18–20 beats/minute
d. Hyperpneic

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150 UNIT 7 DISORDERS OF RESPIRATORY FUNCTION

a. Arterial blood most adequately measures d. Endorphins

the metabolic demands of the tissues along e. Emotion
with the gas exchange function of the
lungs. 11. There are several actions the body makes to
initiate a cough. Put these actions into the
b. Venous blood measures the metabolic
correct order.
demands of the tissues rather than the gas
exchange function of the lungs. a. Elevation of intrathoracic pressures
c. Arterial blood only measures the gas ex- b. Rapid opening of glottis
change function of the lung after it has c. Closure of glottis
met the metabolic demands of the tissues. d. Rapid inspiration of large volume of air
d. Venous blood only measures the hypoxic e. Forceful contraction of abdominal and
reflex of the body, not the gas exchange expiratory muscles
function of the lungs.
12. Dyspnea is defined as an uncomfortable sen-
10. Respiration has both automatic and volun- sation or difficulty in breathing that is subjec-
tary components that are sent to the respira- tively defined by the client. Which of the
tory center of the brain from a number of following disease states is not characterized by
sources. What physiologic forces can exert dyspnea?
their influence on respiration through the
a. Pneumonia
lower brain centers? Mark all that apply.
b. Emphysema
a. Fever
c. Myasthenia gravis
b. Cold
d. Multiple sclerosis
c. Pain

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28

CHAPTER
Respiratory Tract
Infections, Neoplasms,
and Childhood Disorders

SECTION I: LEARNING 9. Describe the manifestations of lung cancer

and list two symptoms of lung cancer that
OBJECTIVES are related to the invasion of the medi-
astinum
1. Describe the transmission of the common
cold from one person to another 10. Define the term paraneoplastic and cite three
paraneoplastic manifestations of lung cancer
2. Describe the causes, manifestations, and
treatment of acute and chronic sinusitis 11. Characterize the effect of age on treatment of
lung cancer
3. Relate the characteristics of the influenza
virus to its contagious properties and the 12. Trace the development of the respiratory tract
need for a yearly “flu shot” through the five stages of embryonic and fetal
development
4. Characterize community-acquired pneumo-
nia, hospital-acquired pneumonia, and pneu- 13. Cite the function of surfactant in lung func-
monia in immunocompromised persons in tion in the neonate
terms of pathogens, manifestations, and
14. Cite the possible cause and manifestations
prognosis
of respiratory distress syndrome and bron-
5. Describe the properties of the immunologic chopulmonary dysplasia
properties of the tubercle bacillus, and differ-
15. Describe the physiologic basis for sternal and
entiate between primary tuberculosis and
chest wall retractions and grunting, stridor,
reactivated tuberculosis on the basis of their
and wheezing as signs of respiratory distress
pathophysiology
in infants and small children
6. State the mechanism for the transmission of
16. Compare croup, epiglottitis, and bronchiolitis
fungal infections of the lung
in terms of incidence by age, site of infection,
7. Cite risk factors associated with lung cancer and signs and symptoms
8. Compare small cell lung cancer and 17. List the signs of impending respiratory failure
non–small cell lung cancer in terms of in small children
histopathology, prognosis, and treatment
methods

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152 UNIT 7 DISORDERS OF RESPIRATORY FUNCTION

SECTION II: ASSESSING YOUR infection that was not present or incubating
on admission to the hospital.
UNDERSTANDING
15. The term host is usually applied
Activity A Fill in the blanks. to persons with a variety of underlying de-
fects in host defenses.
1. are the most frequent cause of
respiratory tract infections. 16. disease is a form of bronchopneu-
monia, an infection that normally occurs by
2. Viral infections can damage ep-
acquiring the organism from the environment.
ithelium, airways, and lead to
secondary infections. 17. The primary atypical pneumonias are caused
by a variety of agents, the most common
3. The common cold is a viral infection of the
being pneumonia.
respiratory tract.
18. is the world’s foremost cause of
4. Outbreaks of colds due to are
death from a single infectious agent.
most common in early fall and late spring.
19. Mycobacteria are similar to other bacterial or-
5. are popular over-the-counter
ganisms except for an outer
treatments for colds because of their action in
coating that makes them more resistant to
drying nasal secretions.
destruction.
6. refers to inflammation of the
20. tuberculosis is a form of the dis-
nasal passages and sinusitis as inflammation
ease that develops in previously unexposed,
of the sinuses.
and therefore, unsensitized persons.
7. The lower content in the sinuses
21. The most frequently used screening methods
facilitates the growth of organisms, impairs
for pulmonary tuberculosis are the
local defenses, and alters the function of
tests and chest .
immune cells.
22. is caused by the dimorphic fun-
8. Host antibodies to and
gus Histoplasma capsulatum and is one of the
prevent or ameliorate infection
most common fungal infections in the
by the influenza virus.
United States.
9. The influenza viruses can cause three types of
23. respiratory infections produce
infections: an uncomplicated
pulmonary manifestations that resemble
respiratory infection, pneumo-
tuberculosis.
nia, and a respiratory viral infection followed
by a infection. 24. The number of Americans who develop lung
cancer is decreasing, primarily due to a
10. Because influenza is so highly contagious,
decrease in .
prevention relies primarily on .
25. Cigarette smoking causes more than
11. Avian strains of the influenza virus do not
of the cases of lung cancer.
usually cause outbreaks of disease in humans
unless a of the virus genome has 26. are aggressive, locally invasive,
occurred within an intermediate mammalian and widely metastatic tumors that arise from
host such as a pig. the epithelial lining of major bronchi.
12. The term describes inflamma- 27. The are small round to oval cells
tion of parenchymal structures of the lung, that are approximately the size of a lympho-
such as the alveoli and the bronchioles. cyte and grow in clusters that exhibit neither
glandular nor squamous organization.
13. refers to consolidation of a part
or all of a lung lobe, and signi- 28. The include squamous cell car-
fies a patchy consolidation involving more cinomas, adenocarcinomas, and large cell
than one lobe. carcinomas.
14. Hospital-acquired, or , pneumo- 29. is characterized by inspiratory
nia is defined as a lower respiratory tract stridor, hoarseness, and a barking cough.

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CHAPTER 28 RESPIRATORY TRACT INFECTIONS, NEOPLASMS, AND CHILDHOOD DISORDERS 153

30. By the weeks of gestation, suffi- 5. Hemagglutinin d. Attachment protein

cient terminal air sacs are present to permit that allows the in-
6. Squamous cell
survival of the premature infant. fluenza virus to enter
7. Paraneoplastic epithelial cells in the
Activity B Consider the following figures. syndrome respiratory tract
8. Atypical e. Symptoms that de-
pneumonias velop when sub-
stances released by
9. Neuraminidase some cancer cells
10. Reye syndrome disrupt the normal
function
f. Viral and my-
coplasma infection
g. Facilitates influenza
viral replication and
release from the cell
h. Fatty liver with
encephalitis
i. Highly aggressive
lung cancer
j. Carcinoma associ-
ated with the
Sphenoidal paraneoplastic
sinus
syndromes that pro-
Activity D duce hypercalcemia

Inhalation of
tubercle bacillus

In these figures, label the following structures:

• Frontal sinus
• Ethmoid sinuses Primary Secondary
• Maxillary sinus tuberculosis tuberculosis
• Superior turbinate
• Middle turbinate
Development of
• Inferior turbinate cell-mediated
immunity
Activity C Match the key terms in Column A
with their definitions in Column B.
Positive skin
Column A Column B test

1. Small cell lung a. Audible crowing

cancers sound during inspi-
ration
2. Typical
pneumonias b. False-negative tu-
berculin skin tests
3. Stridor
c. Result from infec-
4. Anergy tion by bacteria

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154 UNIT 7 DISORDERS OF RESPIRATORY FUNCTION

Use the following terms to complete the flow- 7. Describe the pathogenic mechanisms of
chart: Mycobacterium tuberculosis hominis.
• Reinfection
• Ghon complex
• Granulomatous inflammatory response
• Healed dormant lesion
• Cell-mediated hypersensitivity response
8. How is lung cancer categorized?
• Reactivated tuberculosis
• Progressive or disseminated tuberculosis

Activity E Briefly answer the following.

1. How is the cold virus spread?
9. What causes the varied manifestations of
lung cancer?

2. How does the influenza virus reinfect some-

one? How is it so contagious?
10. What is the result of the absence of surfactant
in premature infants?

3. What is a common complication of influenza

(usually of the elderly or those with car-
diopulmonary disease)?
SECTION III: APPLYING YOUR
KNOWLEDGE
Activity F Consider the following scenario and
4. What type of pneumonia results from inhala- answer the questions.
tion or aspiration of nasopharyngeal secre- Mr. Jones, a 68-year-old man, presents to the
tions during sleep? clinic with lack of appetite and weight loss of
30 pounds over the past 6 months. He has a
history of a chronic, nonproductive cough; short-
ness of breath, which is worse on exertion; and
wheezing. He tells the nurse that he is now
coughing up “bloody stuff,” and he wants to
5. What are the pathophysiologic stages of know what is wrong with him. When asked
pneumococcal pneumonia infection? about pain he says, “I get heartburn once in
awhile, but the pain is dull instead of burning.”
Routine laboratory work is ordered, and the only
abnormal finding is hypercalcemia. The sus-
pected diagnosis is squamous cell cancer of the
lung.
6. How is Mycobacterium tuberculosis hominis
spread? 1. What diagnostic tests would the nurse expect
to be ordered?

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CHAPTER 28 RESPIRATORY TRACT INFECTIONS, NEOPLASMS, AND CHILDHOOD DISORDERS 155

2. Mr. Jones wants to know how his cancer will a. Epidemic in Southeast Asia
be treated. The nurse knows that treatments b. Inability to develop a vaccine for the newly
are available. Which treatments are used for infected poultry
squamous cell cancer (non–small cell lung
c. Initiation of a pandemic
cancer) of the lung?
d. Several small pockets of infection so wide-
spread that they will be hard to control
4. Community-acquired pneumonia can be cat-
egorized according to several indexes. What
are these indexes? Mark all that apply.
a. Radiologic findings
SECTION IV: PRACTICING b. Serologic findings
FOR NCLEX c. Age
d. Presence of coexisting disease
Activity G Answer the following questions. e. Need for hospitalization in long-term care
1. A 23-year-old woman goes to the drugstore to facility
buy a medication to ease the symptoms of 5. An immunocompromised host is open to
her cold. Her friends have told her to buy a pneumonia from all types of organisms.
medication with an antihistamine in it to There is, however, a correlation between spe-
help dry up her runny nose and make it easier cific types of immunologic deficits and spe-
to breath. The woman talks with the pharma- cific invading organisms. What organism is
cist, who has known her for many years. The most likely to cause pneumonia in an im-
pharmacist recommends that she does not munocompromised host with neutropenia
buy a cold medication with a decongestant in and impaired granulocyte function?
it. Why would he do that?
a. -Hemolytic Streptococcus gram-positive
a. Client has history of hypothyroidism bacilli
b. Client has history of hypotension b. Eosinophilic Bacillus subtilis
c. Client has history of type 1 diabetes c. Haemophilus influenza
mellitus
d. Staphylococcus aureus
d. Client has history of juvenile rheumatoid
arthritis 6. Elderly people are susceptible to pneumonia
in all its varieties. The symptoms the elderly
2. The early stages of influenza pass by as if the exhibit can be different than those of other
infection were any other viral infection. age groups who have pneumonia. What signs
What is the distinguishing feature of an in- and symptoms are elderly people with pneu-
fluenza viral infection that makes it different monia less likely to experience than people
from other viral infections? with pneumonia in other age groups?
a. Slow onset of upper respiratory symptoms a. Marked elevation in temperature
b. Rapid onset of profound malaise b. Loss of appetite
c. Slow onset of fever and chills c. Deterioration in mental status
d. Rapid onset of productive cough d. Pleuritic pain
3. Influenza A subtype H5N1 has been docu- 7. Tuberculosis is a highly destructive disease
mented in poultry in both East and Southeast because the tubercle bacillus activates a tissue
Asian countries. This form of avian flu (bird hypersensitivity to the tubercular antigens.
flu) is highly contagious from bird to bird, but What does the destructive nature of tubercu-
is rarely passed from human to human. There losis cause in a previously unexposed im-
is a large amount of concern that the H5N1 munocompetent person?
strain might mutate, making it easier to be
a. Cavitation and rapidly progressing pul-
passed from human to human, carrying with
monary lesions
it a high mortality rate. What is the main con-
cern if the H5N1 strain does mutate? b. Caseating necrosis and cavitation

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156 UNIT 7 DISORDERS OF RESPIRATORY FUNCTION

c. Rapidly progressing lesions and purulent 10. Premature infants who are treated with me-
necrosis chanical ventilation, mostly for respiratory
d. Caseating necrosis and purulent pul- distress syndrome, are at risk for developing
monary lesions bronchopulmonary dysplasia (BPD), a
chronic lung disease. What are the signs and
8. Coccidioidomycosis is a pulmonary fungal in- symptoms of BPD?
fection resembling tuberculosis. Less severe
a. Rapid, shallow breathing and chest retrac-
forms of the infection are treated with oral
tions
antifungal medications. For persons with pro-
gressive disease, what is the drug of choice? b. Weight loss and barrel chest
a. IV fluconazole c. Tachycardia and slow, shallow breathing
b. IV bacillus Calmette-Guérin d. Barrel chest and rapid weight gain
c. IV amphotericin B 11. For each of the following conditions, identify
d. IV rifampin where it occurs in the respiratory tract of
children (upper airway or lower airway.)
9. Non-small cell lung cancers mimic small cell
Epiglottitis
lung cancers through their abilities to do
what? Acute bronchiolitis
a. Synthesize bioactive products and produce Asthma
panneoplastic syndromes Spasmodic croup
b. Neutralize bioactive products that produce Laryngotracheobronchitis
paraneoplastic syndromes
12. What is the underlying cause of respiratory
c. Produce paraneoplastic syndromes and failure in a child with bronchiolitis?
synthesize adrenocorticotropic hormone
a. Obstructive process
d. Synthesize bioactive products and produce
b. Impaired gas exchange
paraneoplastic syndromes
c. Hypoxemia and hypercapnia
d. Metabolic acidosis

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29

CHAPTER
Disorders of Ventilation
and Gas Exchange

SECTION I: LEARNING bronchial asthma and relate them to current

methods for treatment of the disorder
OBJECTIVES
11. Explain the changes in pulmonary function
1. Define the terms hypoxemia and hypercapnia studies that occur with chronic airway disease
2. Characterize the mechanisms whereby disor- 12. Explain the distinction between chronic
ders of ventilation and diffusion cause hypox- bronchitis and emphysema in terms of
emia and hypercapnia pathology and clinical manifestations
3. Compare the manifestations of hypoxemia 13. State the chief manifestations of bronchiectasis
and hypercapnia
14. Describe the genetic abnormality responsible
4. Characterize the pathogenesis and manifesta- for cystic fibrosis and relate it to the manifes-
tions of transudative and exudative pleural tations of the disorder
effusion, chylothorax, and hemothorax
15. State the difference between chronic obstruc-
5. Differentiate among the causes and manifes- tive pulmonary diseases and chronic restric-
tations of spontaneous pneumothorax, sec- tive lung diseases in terms of their pathology
ondary pneumothorax, and tension and manifestations
pneumothorax
16. Cite the characteristics of occupational dusts
6. Describe the causes of pleurisy and differenti- that determine their pathogenicity in terms
ate the characteristics of pleural pain from of the production of pneumoconiosis
other types of chest pain
17. Describe the causes of hypersensitivity pneu-
7. Describe the causes and manifestations of monitis
atelectasis
18. Characterize the organ involvement in
8. Describe the physiology of bronchial smooth sarcoidosis
muscle as it relates to airway disease
19. State the most common cause of pulmonary
9. Describe the interaction between heredity, embolism and the clinical manifestations of
alterations in the immune response, and en- the disorder
vironmental agents in the pathogenesis of
20. Describe the pathophysiology of pulmonary
bronchial asthma
arterial hypertension and state three causes of
10. Characterize the acute- or early-phase and secondary pulmonary hypertension
late-phase responses in the pathogenesis of
21. Describe the alterations in cardiovascular func-
tion that are characteristic of cor pulmonale

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22. Describe the pathologic lung changes that 10. is a specific type of pleural effu-
occur in acute respiratory distress syndrome sion in which there is blood in the pleural
and relate them to the clinical manifestations cavity.
of a general definition of respiratory failure
11. Primary atelectasis of the newborn implies
23. Differentiate between the causes and manifes- that the lung has never been .
tations of hypoxemic and hypercapnic/
12. Obstructive airway disorders are caused by
hypoxemic respiratory failure
disorders that limit airflow.
24. Describe the treatment of respiratory failure
13. Bronchial is a chronic disorder of
the airways that causes episodes of airway ob-
struction, bronchial hyperresponsiveness, and
SECTION II: ASSESSING YOUR airway inflammation that are usually reversible.
UNDERSTANDING 14. Recent research has focused on the role of
in the pathogenesis of bronchial
Activity A Fill in the blanks. asthma.
1. The primary function of the respiratory sys- 15. pulmonary disease is character-
tem is to remove appropriate amounts of ized by chronic and recurrent obstruction of
from the blood entering the airflow in the pulmonary airways.
pulmonary circulation and to add adequate
amounts of to the blood leaving 16. In chronic obstructive pulmonary disease,
the pulmonary circulation. and of the
bronchial wall, along with excess mucus se-
2. involves the movement of fresh cretion, obstruct airflow and cause mismatch-
atmospheric air to the alveoli for delivery pro- ing of ventilation and perfusion.
vision of O2 and removal of CO2.
17. is believed to result from the
3. As a general rule, of the blood breakdown of elastin and other alveolar wall
primarily depends on factors that promote components by enzymes called
diffusion of O2 from the alveoli into the pul- that digest proteins.
monary capillaries, whereas pri-
marily depends on the minute ventilation 18. A hereditary deficiency in ac-
and elimination of CO2 from the alveoli. counts for approximately 1% of all cases of
chronic obstructive pulmonary disease and is
4. refers to a reduction in blood O2 more common in young persons with em-
levels. physema.
5. Hypoxemia produces its effects through tissue 19. The earliest feature of chronic bronchitis is
and the compensatory mecha- in the large airways, associated
nisms that the body uses to adapt to the low- with hypertrophy of the submucosal glands
ered oxygen level. in the trachea and bronchi.
6. The body compensates for chronic hypox- 20. Persons with predominant emphysema are
emia by increased , pulmonary classically referred to as “ ,” a ref-
, and increased production of erence to the lack of cyanosis, the use of
cells. accessory muscles, and pursed-lip breathing.
7. can occur in a number of disor- 21. Persons with a clinical syndrome of chronic
ders that cause hypoventilation or mismatch- bronchitis are classically labeled
ing of ventilation and perfusion resulting in “ ,” a reference to cyanosis and
increased arterial CO2. fluid retention associated with right-sided
8. Elevated levels of PCO2 produce a decrease in heart failure.
and respiratory . 22. is a permanent dilation of the
9. refers to an abnormal collection bronchi and bronchioles caused by destruc-
of fluid in the pleural cavity. tion of the muscle and elastic supporting tis-
sue, resulting from a vicious cycle of infection
and inflammation.

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CHAPTER 29 DISORDERS OF VENTILATION AND GAS EXCHANGE 159

23. is an autosomal recessive disor- Complete the flowchart using the following
der involving fluid secretion in the exocrine items:
glands in the epithelial lining of the respira- • Destruction of elastic fibers in lung
tory, gastrointestinal, and reproductive tracts. • Decreased 1-antitrypsin activity
• Action inhibited by 1-antitrypsin
24. The diffuse diseases are a diverse
• Inherited 1-antitrypsin deficiency
group of lung disorders that produce similar
• Release of elastase
inflammatory and fibrotic changes in the in-
• Attraction of inflammatory cells
teralveolar septa of the lung.
25. The interstitial lung disorders exert their Activity C Match the key terms in Column A
effects on the and with their definitions in Column B.
connective tissue found between the delicate
1.
interstitium of the alveolar walls.
Column A Column B
26. Pulmonary develops when a
blood-borne substance lodges in a branch of 1. Ventilation a. Ratio of carbon diox-
the pulmonary artery and obstructs the flow, ide production to
2. PF ratio
almost all of which are thrombi that arise oxygen consumption
from deep vein thrombosis. 3. Cyanosis b. Difference between
27. Chest pain, dyspnea, and increased respira- 4. Respiratory arterial PO2 and the
tory rate are the most frequent signs and quotient fraction of inspired
symptoms of . oxygen
5. Empyema
c. Infection of the
28. is a disorder characterized by an
6. Hypercapnia pleura
elevation of pressure within the pulmonary
circulation, namely, the pulmonary arterial 7. Venous d. Movement of gas
system. oxygen into or out of lungs
saturation e. Increase in the car-
29. Continued exposure of the pulmonary vessels
bon dioxide content
to is a common cause of pul- 8. Pneumo-
of the arterial blood
monary hypertension. thorax
f. Reflects the body’s
30. can be viewed as a failure in the 9. Hypoxemia extraction and uti-
gas exchange due to pump failure, lung fail- lization of O2 at the
10. Pleuritis
ure, or both. tissue levels
g. Air in pleural space
Activity B Consider the following figure.
h. Decreased oxygena-
tion
Smoking i. Results from an exces-
sive concentration of
reduced hemoglobin
j. Infection in the
pleural cavity
2.
Column A Column B
1. Cor pulmonale a. Lung tissue de-
struction resulting
2. Pneumo-
from a vicious
conioses
Macrophages cycle of infection
and neutrophils 3. CFTR and inflammation
4. ARDS b. Caused by the in-
halation of inor-
5. Atelectasis ganic dusts and
Emphysema
particulate matter

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160 UNIT 7 DISORDERS OF RESPIRATORY FUNCTION

6. Mismatching c. Symptoms are in- 2. What are the clinical features of atelectasis?
of ventilation creased mucus
and perfusion production, ob-
struction of small
7. Bronchiectasis
airways, and a
8. Emphysema chronic productive
cough 3. Explain what is meant by the acute response
9. Sarcoidosis
d. Incomplete expan- and the late phase reactions of asthma.
10. Chronic sion of a lung or
bronchitis portion of a lung
e. Right heart failure
resulting from pri-
mary lung disease 4. What factors are causative to the development
f. Granulomas found of bronchiectasis?
in the lung and
lymphatic system
g. Cystic fibrosis
transmembrane
regulator
h. Enlargement of air 5. Describe the pathogenic mechanism of cystic
spaces and destruc- fibrosis.
tion of lung tissue
i. Acute respiratory
distress syndrome
j. When areas of the
lung are ventilated 6. What are the effects of a pulmonary embolism
but not perfused, on lung tissue?
or when areas are
perfused but not
ventilated

Activity D Put the events of IgE-mediated

asthma reaction in order in the following boxes: 7. Describe the disease-producing changes of
acute respiratory distress syndrome.
a. Infiltration of inflammatory cells
b. Mast cell activation
c. Bronchospasm
d. Increased airway responsiveness
e. Exposure to allergen
f. Airway inflammation
SECTION III: APPLYING YOUR
KNOWLEDGE
Activity E Briefly answer the following. Activity F Consider the following scenario and
answer the questions.
1. What are the mechanisms of hypoxemia?
The parents of a 14-year-old girl come to the
emergency department after being notified by
the school nurse that their daughter had a

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CHAPTER 29 DISORDERS OF VENTILATION AND GAS EXCHANGE 161

“spell” at school and was taken to the hospital 2. When CO2 levels in the blood rise, a state of
by ambulance. When they arrive, their daugh- hypercapnia occurs in the body. What factors
ter is sitting up on the stretcher, has oxygen on contribute to hypercapnia? Mark all that
at 1 L/min, and is answering questions asked by apply.
the nurse. a. Alteration in CO2 production
1. The doctor talks to the family and tells them b. Abnormalities in respiratory function
that he suspects their daughter has asthma. c. Disturbance in gas exchange function
What diagnostic tests would the nurse expect
d. Decrease in CO2 production
to be ordered to confirm the diagnosis of
asthma? e. Changes in neural control of respiration
3. The complications of a hemothorax can af-
fect the total body. Left untreated, what can a
moderate or large hemothorax cause?
a. Calcification of the lung tissue
2. The parents mention to the nurse that their b. Fibrothorax
daughter values her independence. They want c. Pleuritis
to know how her treatment plan will impact d. Atelectasis
it. How would the nurse correctly respond?
4. Talc lung can occur from injected or inhaled
talc powder that has been mixed with heroin,
methamphetamine, or codeine as filler. What
are people with talc lung very susceptible to?
a. Hemothorax
b. Chylothorax
c. Fibrothorax
SECTION IV: PRACTICING
d. Pneumothorax
FOR NCLEX
5. Pleuritis, an inflammatory process of the
Activity G Answer the following questions. pleura, is common in infectious processes
that spread to the pleura. Which are the
1. There can be many reasons for a patient to
drugs that may be used for treating pleural
present with hypoxemia. For a patient’s PO2
pain? Mark all that apply.
to fall, a respiratory disease is usually in-
volved. Often, patients have involvement a. Indomethacin
from more than one mechanism. Match the b. Aspirin
mechanism involved with the end result (hy- c. Acetaminophen
poxemia or decreased levels of PO2).
d. Inderal

Mechanism Outcome 6. Atelectasis is the term used to designate an

incomplete expansion of a portion of the
Decreased oxygen in air lung. Depending on the size of the collapsed
Inadequate circulation area and the type of atelectasis occurring,
through pulmonary capillaries you may see a shift of the mediastinum and
trachea. Which way does the mediastinum
Hypoventilation and trachea shift in compression atelectasis?
Disease in respiratory system a. Toward the affected lung
Mismatched ventilation b. Toward the mediastinum
and perfusion c. Away from the affected lung
Dysfunction of neurologic d. Away from the trachea
system

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162 UNIT 7 DISORDERS OF RESPIRATORY FUNCTION

7. Like adults, infants and small children have d. Biologic nature of the dust particle
asthma and need to be medicated. There are e. Ability of particle to incite lung destruction
special systems manufactured for the delivery
of inhaled medications to children. At what 12. There are cytotoxic drugs used in the treat-
age is it recommended that children begin ment of cancer that cause pulmonary damage
using a metered-dose inhaler with a spacer? because of their direct toxicity and because
they stimulate an influx of inflammatory cells
a. 3–5 years
into the alveoli. Which cardiac drug is known
b. 4–6 years for its toxic effect in the lungs?
c. 2–4 years a. Amiodarone
d. 5–7 years b. Inderal
8. Chronic obstructive pulmonary disease c. Methotrexate
(COPD) is a combination of disease processes. d. Busulfan
What disease processes have been identified
as being part of COPD? 13. A pulmonary embolism occurs when there
is an obstruction in the pulmonary artery
a. Emphysema and asthma
blood flow. Classic signs and symptoms of
b. Chronic obstructive bronchitis and a pulmonary embolism include dyspnea,
emphysema chest pain, and increased respiratory
c. Chronic obstructive bronchitis and asthma rate. What is a classic sign of pulmonary
d. Chronic bronchitis and emphysema infarction?
a. Mediastinal shift to the left
9. Bronchiectasis is considered a secondary
chronic obstructive pulmonary disease and, b. Pleuritic pain
with the advent of antibiotics, it is not a com- c. Tracheal shift to the right
mon disease entity. In the past, bronchiecta- d. Pericardial pain
sis often followed specific diseases. Which
disease did it not follow? 14. Pulmonary hypertension is usually caused by
long-term exposure to hypoxemia. When pul-
a. Necrotizing bacterial pneumonia
monary vessels are exposed to hypoxemia,
b. Complicated measles what is their response?
c. Chickenpox a. Pulmonary vessels dilate
d. Influenza b. Pulmonary vessels constrict
10. Cystic fibrosis (CF) is an autosomal recessive c. Pulmonary vessels spasm
disorder involving the secretion of fluids in d. Pulmonary vessels infarct
specific exocrine glands. The genetic defect in
CF inclines a person to chronic respiratory 15. The management of cor pulmonale is di-
infections from a small group of organisms. rected at the underlying lung disease and
Which organisms create chronic infection in heart failure. Why is low-flow oxygen ther-
a child with cystic fibrosis? apy part of the management of cor pul-
monale?
a. Pseudomonas aeruginosa and Escherichia coli
a. It stimulates the body to breathe on its
b. Staphylococcus aureus and hepatitis C
own.
c. Haemophilus influenzae and influenza A
b. It inhibits the respiratory center of the
d. Pseudomonas aeruginosa and Staphylococcus brain from initiating tachypnea.
aureus
c. It reduces pulmonary hypertension and
11. What etiologic determinants are important in polycythemia associated with chronic lung
the development of the pneumoconioses? disease.
Mark all that apply. d. It reduces pulmonary hypertension and
a. Chemical nature of the dust particle formation of pulmonary embolism.
b. Size of dust particle
c. Density of dust particle

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CHAPTER 29 DISORDERS OF VENTILATION AND GAS EXCHANGE 163

16. Acute lung injury and acute respiratory dis- 17. Acute respiratory failure is commonly sig-
tress syndrome (ARDS) are distinguishable naled by varying degrees of hypoxemia and
from each other by the extent of hypoxemia hypercapnia. Respiratory acidosis develops
involved. What is the clinical presentation of manifested by what?
ARDS? Mark all that apply. a. Decrease in cerebral blood flow
a. Diffuse bilateral infiltrates of lung tissue b. Arterial vasoconstriction
without cardiac dysfunction
c. Increase in cardiac contractility
b. Rapid onset
d. Increase in cerebral spinal fluid pressure
c. Signs of respiratory distress
d. Increase in respiratory rate
e. Hypoxemia refractory to treatment

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30
CHAPTER

Structure and Function

of the Kidney

SECTION I: LEARNING 13. Explain the concept of the glomerular filtra-

tion rate
OBJECTIVES
14. Explain the value of serum creatinine levels
1. Describe the location and gross structure of in evaluating renal function
the kidney
15. Describe the methods used in cystoscopic ex-
2. Explain why the kidney receives such a large amination of the urinary tract, ultrasono-
percentage of the cardiac output and de- graphic studies of the urinary tract, computed
scribe the mechanisms for regulating renal tomographic scans, magnetic resonance
blood flow imaging studies, excretory urography, and
renal angiography
3. Describe the structure and function of the
glomerulus and tubular components of the
nephron in terms of regulating the composi-
tion of the extracellular fluid compartment
SECTION II: ASSESSING YOUR
UNDERSTANDING
4. Explain the function of sodium in terms of
tubular transport mechanisms Activity A Fill in the blanks.
5. Describe how the kidney produces concen- 1. The are paired, bean-shaped or-
trated or diluted urine gans that lie outside the peritoneal cavity in
6. Characterize the function of the juxta- the back of the upper abdomen.
glomerular complex 2. The is the place where blood
7. Relate the function of the kidney to drug vessels and nerves enter and leave the kidney.
elimination 3. are the functional units of the
8. Explain the endocrine functions of the kidney kidney.

9. Relate the sodium reabsorption function of 4. The contains the glomeruli and
the kidney to action of diuretics convoluted tubules of the nephron and blood
vessels.
10. Describe the characteristics of normal urine
5. The medulla consists of the ,
11. Explain the significance of casts in the urine that are divided by the columns of the cortex.
12. Explain the value of urine specific gravity in 6. Each kidney is supplied by a single renal
evaluating renal function artery that arises on either side of the
.

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CHAPTER 30 STRUCTURE AND FUNCTION OF THE KIDNEY 165

7. The afferent arterioles that supply the 21. Renal is the volume of plasma
arise from the intralobular that is completely cleared each minute of any
arteries. substance that finds its way into the urine.
8. The is a unique, high-pressure 22. functions in the regulation of
capillary filtration system. sodium and potassium elimination.
9. are low-pressure vessels that are 23. Atrial natriuretic peptide contributes to the
adapted for reabsorption rather than filtration. regulation of elimination.
10. The passes through each of 24. The kidneys regulate body pH by conserving
these segments before reaching the pelvis of base and eliminating
the kidney. ions.
11. The is regulated by the constric- 25. is an end product of protein me-
tion and relaxation of the afferent and effer- tabolism.
ent arterioles.
26. The synthesis of is stimulated by
12. Substances move from the tubular filtrate tissue hypoxia, which may be brought about
into the tubular cell along a by anemia, residence at high altitudes, or im-
gradient, but they require facilitated trans- paired oxygenation of tissues due to cardiac
port or carrier systems to move across the or pulmonary disease.
membrane into the interstitial
27. represents excessive protein ex-
fluid, where they are absorbed into the per-
cretion in the urine.
itubular capillaries.
28. Urine- provides a valuable index
13. uses a carrier system in which
of the hydration status and functional ability
the downhill movement of one substance
of the kidneys.
such as sodium is coupled to the uphill move-
ment of another substance such as glucose or 29. levels in the blood and urine
an amino acid. can be used to measure glomerular filtration
rate.
14. In the tubule, there is almost
complete reabsorption of nutritionally impor- 30. , therefore, is not only related to
tant substances from the filtrate. the glomerular filtration rate, but, unlike cre-
atinine, is also influenced by protein intake,
15. The plasma level at which the substance
gastrointestinal bleeding, and hydration status.
appears in the urine is called the .
16. The establishes a high concen- Activity B Match the key terms in Column A
tration of osmotically active particles in the with their definitions in Column B.
interstitium surrounding the medullary col-
Column A Column B
lecting tubules where the antidiuretic hor-
mone exerts its effects. 1. Countertrans- a. Originate in the
port superficial part of
17. The thick portion of the loop of Henle con-
the cortex
tains a cotransport system. 2. Glomerular
filtration rate b. Originate deeper
18. The tubule is relatively imper- in the cortex
meable to water, and reabsorption of sodium 3. Vasopressin
c. Contribute to reg-
chloride from this segment further dilutes the
4. Cortical ulation of
tubular fluid.
nephrons glomerular blood
19. The assists in maintenance of flow
5. Vitamin D
the extracellular fluid volume by controlling d. Milliliters of fil-
the permeability of the medullary collecting 6. Principal cells trate formed per
tubules. minute
20. Increased activity causes con-
striction of the afferent and efferent arteri-
oles, and thus a decrease in renal blood flow.

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166 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

7. Juxtamedullary e. Movement of one 3. How does the juxtaglomerular apparatus regu-

nephrons substance enables the late glomerular filtration rate?
movement of a sec-
8. Counter-
ond substance in the
current
opposite direction
9. Transport f. Maximum amount of
maximum substance that can be
reabsorbed per unit of 4. What are the actions of atrial natriuretic
10. Mesangial
time peptide?
cells
g. Site of aldosterone
action
h. Flow of fluids in op-
posite directions
i. Stimulate expression 5. What are the endocrine functions of the kidney?
of aquaporin-2
channels
j. Converted to active
form in kidney

Activity C 6. How do Na+ blockers function as a diuretic?

1. Put the components of the renin-angiotensin-

aldosterone system in order from stimulation
to end hormone action:
• Conversion of angiotensin I to angiotensin
II by angiotensin-converting enzyme
• Decreased glomerular filtration rate
• Sodium and water retention SECTION III: APPLYING YOUR
• Angiotensin II stimulates release of antidi- KNOWLEDGE
uretic hormone and aldosterone
• Juxtaglomerular release of renin Activity E Consider the following scenario and
• Conversion of angiotensinogen to an- answer the questions.
giotensin I by renin An 18-year-old woman is brought to the emer-
gency department by her friends. Her blood
Activity D Briefly answer the following. pressure is 115/85 mm Hg, pulse is 99, and respi-
1. Describe the three layers of the glomerular ratory rate in 35 breaths/minute. The girl is
membrane. doubled over, and she is holding her abdomen
saying, “I hurt so bad; I hurt so bad.” Her
friends deny the girl has been using recreational
drugs. They tell the triage nurse that the girl
started complaining that her side hurt about
3 hours prior to the trip to the emergency de-
2. Describe the various methods of transport partment. Asked if the girl’s parents had been
across the epithelial layer of the renal tubule. notified, the friends tell the triage nurse that
they have been unable to reach the girl’s par-
ents. On examination, a suspected diagnosis of
kidney impairment is arrived at.

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CHAPTER 30 STRUCTURE AND FUNCTION OF THE KIDNEY 167

1. What tests would the nurse expect to be c. Normal electrolyte and pH composition of
ordered to either confirm or deny the the blood
diagnosis? d. Rate of renal blood flow
e. Rate at which sodium is excreted from the
body
4. It is known that high levels of uric acid in the
blood can cause gout, whereas high levels in
the urine can cause kidney stones. What
2. The girl says, “My father just had a kidney medication competes with uric acid for secre-
stone removed. Is that what I have?” What tion into the tubular fluid, thereby reducing
noninvasive test should the nurse order to rule uric acid secretion?
out a kidney stone? a. Ibuprofen
b. Acetaminophen
c. Aspirin
d. Advil
5. Many drugs are eliminated in the urine.
These drugs cannot be bound to plasma pro-
SECTION IV: PRACTICING teins if the glomerulus is going to filter them
out of the blood. In what situation would it
FOR NCLEX be necessary to create either an alkaline or an
acid diuresis in a patient?
Activity F Answer the following questions.
a. When there are nontherapeutic drug levels
1. Many substances are filtered out of the blood in the patient’s blood
and then reabsorbed into the blood in the b. If the patient is noncompliant with the
kidneys. What is the plasma level at which a medication regimen
specific substance can be found in the urine?
c. In the event that a loading dose of a spe-
a. Renal threshold cific drug must be used and kept in the
b. Renal clearance patient’s system for a long time
c. Renal filtration rate d. In the case of a drug overdose
d. Renal transport level 6. The anemia that occurs with end-stage kid-
2. You are admitting a 45-year-old female with a ney disease is often caused by the kidneys
presumptive diagnosis of diabetes mellitus to themselves. What inability of the kidneys
the floor. While taking her history, she men- causes anemia in end-stage kidney disease?
tions that she has been eating a lot of sweets a. Inability to produce erythropoietin
lately. How would you expect this diet to b. Inability to produce rennin
affect her renal system?
c. Inability to produce angiotensin
a. Decrease tubular reabsorption
d. Inability to inactivate vitamin D
b. Increase renal blood flow
7. Diuretics can either block the reabsorption of
c. Decrease renal blood flow
components of the urine, or they can block
d. Increase sodium excretion the reabsorption of water back into the body.
3. The renal clearance of a substance is mea- What does the increase in urine flow from the
sured independently. What are the factors body depend on with a patient on diuretics?
that determine renal clearance of a sub- a. Amount of water reabsorption back into
stance? Mark all that apply. the body
a. Ability of the substance to be filtered in the b. Amount of sodium and chloride reabsorp-
glomeruli tion that it blocks
b. Capacity of the renal tubules to reabsorb or c. Amount of sodium and chloride that it
secrete the substance excretes through the kidney
d. Amount of water excreted by the body

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168 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

8. Urine-specific gravity is normally 1.010 to a. Blood urea nitrogen level

1.025 with adequate hydration. When there is b. 24-Hour urine test
loss of renal concentrating ability due to im-
c. Urine test—first void in AM
paired renal function, low concentration levels
are exhibited. When would the nurse consider d. Serum creatinine
low levels of concentration to be significant? 10. When the urologist wants to directly visualize
a. At noon the bladder, urethra, and ureteral orifices,
b. First void in morning what diagnostic test would he use?
c. Last void at night a. Cystoscopy
d. After a nap b. Ultrasonography
c. Echocardiogram
9. An elderly man is brought into the clinic by
his daughter who states, “My father hasn’t d. Laparoscopy
been himself lately. Now I think he looks a
little yellow.” What test would the nurse ex-
pect to have ordered to check this man’s crea-
tinine level?

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31

CHAPTER
Disorders of Fluid and
Electrolyte Balance

SECTION I: LEARNING 9. Describe measures that can be used in assessing

body fluid levels and sodium concentration
OBJECTIVES
10. Describe the causes, manifestations, and
1. Define the terms electrolyte, ion, and nonelec- treatment of psychogenic polydipsia
trolytes
11. Describe the relationship between antidi-
2. Differentiate the intracellular from the extra- uretic hormone and aquaporin-2 channels in
cellular fluid compartments in terms of distri- reabsorption of water by the kidney
bution and composition of water,
12. Compare the pathology, manifestations, and
electrolytes, and other osmotically active
treatment of diabetes insipidus and the syn-
solutes
drome of inappropriate antidiuretic hormone
3. Cite the rationale for the use of concentration
13. Compare and contrast the causes, manifesta-
rather than absolute values in describing elec-
tions, and treatment of isotonic fluid volume
trolyte content of body fluids
deficit, isotonic fluid volume excess, hypona-
4. Relate the concept of a concentration gradi- tremia with water excess, and hypernatremia
ent to the processes of diffusion and osmosis with water deficit
5. Describe the control of cell volume and the 14. Characterize the distribution of potassium in
effect of isotonic, hypotonic, and hypertonic the body and explain how extracellular potas-
solutions on cell size sium levels are regulated in relation to body
gains and losses
6. Describe factors that control fluid exchange
between the vascular and interstitial fluid 15. State the causes of hypokalemia and hyper-
compartments and relate them to the devel- kalemia in terms of altered intake, output,
opment of edema and third spacing of extra- and transcellular shifts
cellular fluids
16. Relate the functions of potassium to the man-
7. Describe the manifestations and treatment of ifestations of hypokalemia and hyperkalemia
edema
17. Describe methods used in diagnosis and treat-
8. State the functions and physiologic mecha- ment of hypokalemia and hyperkalemia
nisms controlling body water levels and
18. Describe the associations among intestinal
sodium concentration, including the effective
absorption, renal elimination, bone stores,
circulating volume, sympathetic nervous sys-
and the functions of vitamin D and parathy-
tem, renin-angiotensin-aldosterone system,
roid hormone in regulating calcium, phos-
and antidiuretic hormone
phorus, and magnesium levels

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170 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

19. State the difference between ionized and 9. The difference between the calculated and
bound or chelated forms of calcium in terms measured osmolality is called the
of physiologic function .
20. Describe the mechanisms of calcium gain and 10. proteins and other organic com-
loss and relate them to the causes of hypocal- pounds cannot pass through the membrane.
cemia and hypercalcemia
11. The membrane pump continu-
21. Relate the functions of calcium to the mani- ously removes three Na+ ions from the cell for
festations of hypocalcemia and hypercal- every two K+ ions that are moved back into
cemia the cell.
22. Describe the mechanisms of phosphorus gain 12. refers to the movement of water
and loss and relate them to causes of hy- through capillary pores because of a mechani-
pophosphatemia and hyperphosphatemia cal, rather than an osmotic, force.
23. Relate the functions of phosphorus to the 13. The represents an accessory
manifestations of hypophosphatemia and route whereby fluid from the interstitial
hyperphosphatemia spaces can return to the circulation.
24. Describe the mechanisms of magnesium gain 14. is a palpable swelling produced
and loss and relate them to the causes of by expansion of the interstitial fluid volume.
hypomagnesemia and hypermagnesemia
15. Edema due to decreased capillary colloidal os-
25. Relate the functions of magnesium to the motic pressure is usually the result of inade-
manifestations of hypomagnesemia and hy- quate production or abnormal loss of
permagnesemia .
16. edema occurs at times when the
accumulation of interstitial fluid exceeds the
SECTION II: ASSESSING YOUR absorptive capacity of the tissue gel.
UNDERSTANDING 17. represent an accumulation or
trapping of body fluids that contribute to
Activity A Fill in the blanks. body weight but not to fluid reserve or
1. The consists of fluid contained function.
within the billions of cells in the body. 18. Water losses that occur through the skin and
2. The contains all fluids outside lungs are referred to as because
the cells, including those in the interstitial or they occur without a person’s awareness.
tissue spaces and blood vessels. 19. Most sodium losses occur through the
3. are substances that dissociate in .
solution to form ions. 20. The major regulator of sodium and water bal-
4. Particles that do not dissociate into ions such ance is the maintenance of the .
as glucose and urea are called . 21. The renin-angiotensin-aldosterone system
5. is the movement of charged or exerts its action through and
uncharged particles along a concentration .
gradient. 22. is primarily a regulator of water
6. is the movement of water across intake and a regulator of water
a semipermeable membrane. output.

7. refers to the osmolar concentra- 23. involves compulsive water

tion in 1 L of solution and to drinking and is usually seen in persons with
the osmolar concentration in 1 kg of water. psychiatric disorders, most commonly, schiz-
ophrenia.
8. The predominant osmotically active particles
in the extracellular fluid are and 24. is caused by a deficiency of or a
its associated anions (Cl and HCO3). decreased response to antidiuretic hormone.

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CHAPTER 31 DISORDERS OF FLUID AND ELECTROLYTE BALANCE 171

25. Disorders of sodium concentration produce a 39. The signs and symptoms of potassium
change in the osmolality of the extracellular are closely related to a decrease
fluid (ECF) with movement of water from the in neuromuscular excitability.
ECF compartment into the intracellular fluid
40. acts to sustain normal plasma
(ICF) compartment, known as ,
levels of calcium and phosphorus by increas-
or from the ICF compartment into the ECF
ing their absorption from the intestine. It is
fluid compartment, known as .
also necessary for normal bone formation.
26. When the effective circulating blood volume
41. serves as a cofactor in the gener-
is compromised, the condition is often
ation of cellular energy and is important in
referred to as .
the function of second messenger systems.
27. cause sequestering of extracellu-
42. The manifestations of acute
lar fluid in the serous cavities, extracellular
reflect the increased neuromuscular
spaces in injured tissues, or lumen of the gut.
excitability.
28. Fluid volume excess represents an
43. The manifestations of result
expansion of the extracellular
from a decrease in cellular energy stores due
fluid compartment with increases in both
to deficiency in ATP and impaired oxygen
interstitial and vascular volumes.
transport due to a decrease in red blood cell
29. represents a plasma sodium 2,3-diphosphoglycerate.
concentration of less than 135 mEq/L.
44. Many of the signs and symptoms of a phos-
30. hyponatremia represents reten- phorus excess are related to a
tion of water with dilution of sodium while deficit.
maintaining the extracellular fluid volume
45. acts as a cofactor in many intra-
within a normal range.
cellular enzyme reactions, including the
31. MDMA (ecstasy) and its metabolites have transfer of high-energy phosphate groups in
been shown to produce enhanced release of the generation of ATP from adenosine
from the hypothalamus. diphosphate.
32. implies a plasma sodium level of
Activity B Consider the following figure.
more than 145 mEq/L.
33. Hypernatremia represents a deficit of
in relation to the body’s sodium
stores.
Blood volume
Serum osmolality
34. The effects of aldosterone on potassium elim-
ination are mediated through a
located in the late distal and cortical collect-
ing tubules of the kidney.
35. The is determined by the ratio
of intracellular fluid to extracellular fluid
potassium concentration.
36. With severe , the resting mem-
brane approaches the threshold potential,
causing sustained subthreshold depolarization
Feedback
with a resultant inactivation of the sodium
channels and a net decrease in excitability. Complete this flowchart using the following terms:
37. The renal processes that conserve potassium • Extracellular water volume
during interfere with the kid- • Thirst
ney’s ability to concentrate urine. • Secretion of antidiuretic hormone
38. Chronic hyperkalemia is usually associated • Reabsorption of water by the kidney
with . • Water ingestion

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172 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

Activity C Match the key terms in Column A 4. Circulatory c. Hypotonic dilution

with their definitions in Column B. overload d. Failure of the neg-
5. Hyponatremia ative feedback sys-
1.
tem that regulates
Column A Column B 6. Baroreceptors the release and in-
7. Nephrogenic hibition of antidi-
1. Cations a. Effective osmolal-
diabetes uretic hormone
ity same as the in-
2. Osmotic insipidus e. Renal insensitivity
tracellular fluid
pressure to antidiuretic
b. Effect that the os- 8. Osmoreceptors
3. Capillary hormone
motic pressure of a
colloidal 9. Atrial f. Decrease in the
solution has on
osmotic natriuretic ability to sense
cell size because of
pressure peptide thirst
water movement
4. Tonicity across the cell 10. Hypodipsia g. Respond to changes
membrane in extracellular fluid
5. Generalized osmolality by swel-
c. Positively charged
edema ling or shrinking
ions
6. Glomerulo- d. Negatively charged h. Acts at the cortical
nephritis ions collecting tubules
to increase sodium
7. Isotonic e. Osmotic pressure
reabsorption
solution generated by the
plasma proteins i. Increases sodium
8. Obligatory excretion by the
that do not pass
urine output kidney
through the pores
9. Anions of the capillary wall j. Respond to
f. Increased perme- pressure-induced
10. Lymphedema
ability of glomeru- stretch of the ves-
lus to proteins sel walls
g. Pressure by which Activity D
water is drawn
1. Draw a flowchart that puts the following
into a solution
steps of calcium concentration by parathy-
through a semiper-
roid hormone in order. Include the involved
meable membrane
organs: parathyroid glands, bone, kidney, and
h. Urine output that intestine.
is required to elim-
inate wastes • Increased serum calcium
• Increased intestinal calcium absorption
i. Edema due to im-
• Activated vitamin D
paired lymph
• Decreased calcium elimination
drainage
• Release of calcium from bone
j. Result of increased • Decreased serum calcium
vascular volume • Release of parathyroid hormone
2.
Activity E Briefly answer the following.
Column A Column B
1. Compare and contrast the intracellular fluid
1. Syndrome of a. State of fluid vol-
and the extracellular fluid.
inappropriate ume excess affect-
antidiuretic ing cardiac
hormone function
2. Aldosterone b. Hypertonic con-
centration
3. Hypernatremia

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CHAPTER 31 DISORDERS OF FLUID AND ELECTROLYTE BALANCE 173

2. What are the forces that control the move- SECTION III: APPLYING YOUR
ment of water between the capillary and inter-
stitial spaces?
KNOWLEDGE
Activity F Consider the following scenario and
answer the questions.
The parents of a 10-year-old girl arrive at the
burn unit to see their child for the first time since
3. What are the physiologic mechanisms that her admission. The client was admitted 8 hours
produce edema? ago with second- and third-degree burns over
60% of her body. She is edematous and in pain.
1. The parents state, “When we left here, just a
few hours ago, she wasn’t all swollen like that.
What causes all that swelling?” What answer
4. How are sodium and water levels maintained
would you give?
in the body?

2. The doctor explains to the parents that be-

5. What are the three types of polydipsia?
cause their daughter has a large burned area,
she has lost a large amount of fluid. The con-
cern for the client is not only the burn, but
also a disorder called fluid volume deficit.
After the doctor leaves, the parents ask the
nurse whether the doctor is sure their daugh-
6. What are the physical manifestations of an ter has fluid volume deficit. What should the
isotonic volume expansion? nurse know about fluid volume deficit?

7. What are the changes seen in an ECG during

hypokalemia, and why are they present? SECTION IV: PRACTICING
FOR NCLEX
Activity G Answer the following questions.
1. Edema is an excess in the interstitial fluid vol-
8. What are the systemic effects of hypercal- ume. What mechanisms play a part in the
cemia? formation of edema? Mark all that apply.
a. Mechanisms that increase capillary
permeability
b. Mechanisms that increase capillary
filtration pressure
c. Mechanisms that increase capillary
colloidal osmotic pressure
d. Mechanisms that produce obstruction to
the flow of lymph
e. Mechanisms that decrease capillary
colloidal osmotic pressure

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174 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

2. Match the following elements with their ac- can occur if fluid volume deficit is corrected
tions in the body. too rapidly?
Element Action in the body a. Nerve cells absorb too much sodium and
cease to function
1. Sodium a. Increases the absorp-
b. Brain cells shut down to prevent cerebral
tion of calcium from
2. Potassium edema
the intestine
3. Calcitriol c. Fluid volume increases at a rate the body
b. Required for cellular
cannot tolerate
4. Phosphorus energy metabolism
d. Cerebral edema occurs with potentially se-
c. Metabolizes glucose,
5. Magnesium vere neurologic impairment
fat, and protein
d. Regulates the extracel- 7. Potassium is the major cation in the body. It
lular fluid volume plays many important roles, including the ex-
citability of nerves and muscles. Where is this
e. Maintains the osmotic
action particularly important?
integrity of cells
a. Heart
3. The effective circulating volume is the major
b. Brain
regulator of water balance in the body. What
else does it regulate? c. Lungs
a. Sodium d. Liver
b. Magnesium 8. Vitamin D, although officially classified as a
c. Calcium vitamin, functions as a hormone in the body.
What other hormone is necessary in the body
d. Potassium
for vitamin D to work?
4. Psychogenic polydipsia is most commonly a. Thyroid hormone
seen in people with schizophrenia. It is a dis-
b. Parathyroid hormone
ease that involves compulsive water drinking
without thirst and excessive urine output. c. Antidiuretic hormone
It may be worsened by things that cause by d. Angiotensin II
excessive antidiuretic hormone (ADH) secre-
9. The sodium-phosphate cotransporter (NPT2)
tion. What may be reasons that there is exces-
creates the action by which phosphate is reab-
sive ADH secretion in the body?
sorbed from the filtrate in the proximal tubule.
a. Excessive sleeping combined with irregular NPT2 is inhibited by phosphatonin. What
eating condition can cause an overproduction of
b. Antipsychotic medications and smoking phosphatonin resulting in hypophos-
c. Increased need in the aquaporin channel phatemia?
and coffee drinking a. Tumor-induced osteomyelitis
d. Antipsychotic medications and coffee b. Tumor-induced hypopituitarism
drinking c. Tumor-induced syndrome of antidiuretic
5. There are two types of diabetes insipidus (DI), hormone
neurogenic and nephrogenic. In nephrogenic d. Tumor-induced osteomalacia
DI, there is an inability of the kidney to con-
10. Magnesium levels are important indicators to
centrate urine and to conserve free water.
a variety of bodily functions. What is severe
Nephrogenic DI can be either genetic or ac-
hypermagnesemia associated with?
quired. What are the causes of nephrogenic DI?
a. Muscle and respiratory paralysis
a. Head injury and cranial surgery
b. Cardiac arrest and pulmonary paralysis
b. Oral antidiabetic drugs and smoking
c. Complete heart block and cardiac
c. Lithium and hypokalemia
arrhythmias
d. Hypocalcemia and hypernatremia
d. Cardiac arrhythmias and respiratory
6. In a person with fluid volume deficit, there is paralysis
a dehydration of brain and nerve cells. What

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32

CHAPTER
Disorders of
Acid-Base Balance

SECTION I: LEARNING 11. Explain the use of the plasma anion gap in
differentiating types of metabolic acidosis
OBJECTIVES
12. List common causes of metabolic and respira-
1. State the definition of an acid and a base tory acidosis and metabolic and respiratory
alkalosis
2. Cite the source of metabolic acids
13. Contrast and compare the clinical manifesta-
3. Describe the three forms of carbon dioxide
tions and treatment of metabolic and respira-
transport and their contribution to acid-base
tory acidosis and of metabolic and respiratory
balance
alkalosis
4. Define pH and use the Henderson-Hassel-
balch equation to calculate the pH and to
compare compensatory mechanisms for
regulating pH
SECTION II: ASSESSING YOUR
UNDERSTANDING
5. Describe the intracellular and extracellular
mechanisms for buffering changes in body Activity A Fill in the blanks.
pH
1. Normally, the concentration of body acids
6. Compare the role of the kidneys and respira- and bases is regulated so that the pH of extra-
tory system in regulation of acid-base balance cellular body fluids is maintained within a
7. Explain how interactions between potassium very narrow range of to
and hydrogen cations and between bicarbon- .
ate and chloride anions contribute to the 2. The H concentration is commonly expressed
regulation of pH in terms of the .
8. Differentiate the terms acidemia, alkalemia, 3. Acids are continuously generated as byprod-
acidosis, and alkalosis ucts of processes.
9. Describe a clinical situation involving an 4. Physiologically, these acids fall into two
acid-base disorder in which both primary and groups: the acid H2CO3 and all
compensatory mechanisms are present other acids.
10. Define metabolic acidosis, metabolic alkalo- 5. The content of the blood can be
sis, respiratory acidosis, and respiratory calculated by multiplying the partial pressure
alkalosis of CO2 (PCO2) by its solubility coefficient.

175
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176 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

6. The metabolism of and other 21. Most cases of acidosis are caused
substances results in the generation of fixed by inadequate oxygen delivery, as in shock or
or nonvolatile acids and bases. cardiac arrest.
7. The plasma pH can be calculated using an 22. An overproduction of occurs
equation called the . when carbohydrate stores are inadequate or
when the body cannot use available carbohy-
8. A consists of a weak base and its
drates as a fuel.
conjugate acid pair.
23. The cross the blood-brain bar-
9. It has been estimated that as much as 40% of
rier and directly stimulate the respiratory cen-
buffering of an acute acid load takes place in
ter, causing hyperventilation and respiratory
.
alkalosis.
10. The buffer system is the princi-
24. The enzyme metabolizes
ple extracellular fluid buffer.
methanol and ethylene glycol into their toxic
11. and are the major metabolites.
protein buffers in the vascular compartment.
25. disease is the most common
12. The kidney regulates pH by excreting excess cause of chronic metabolic acidosis.
and reabsorbing .
26. Excessive loss of occurs with
13. There are two important intratubular buffer severe diarrhea; small bowel, pancreatic, or
systems: the phosphate and biliary fistula drainage; ileostomy drainage;
buffer systems. and intestinal suction.
14. is a potent stimulus for H 27. is a systemic disorder caused by
secretion and HCO3 reabsorption. an increase in plasma pH due to a primary ex-
cess in HCO3.
15. acts in the collecting duct to
stimulate H secretion, while increasing Na 28. Metabolic alkalosis also leads to a compen-
reabsorption and K secretion. satory with development of var-
ious degrees of and respiratory
16. Arterial blood gases are used for blood gas
acidosis.
measurements due to venous blood gas
, depending on metabolic 29. Respiratory occurs in acute or
demands. chronic conditions that impair effective alve-
olar ventilation and cause an accumulation of
17. The describes the difference be-
PCO2.
tween the plasma concentration of the major
measured cation (Na) and the sum of the 30. Elevated levels of CO2 produce
measured anions (Cl and HCO3). of cerebral blood vessels, causing headache,
blurred vision, irritability, muscle twitching,
18. The terms and de-
and psychological disturbances.
scribe the clinical conditions that arise be-
cause of changes in dissolved CO2 and HCO3 31. Respiratory is caused by hyper-
concentrations. ventilation or a respiratory rate in excess of
that needed to maintain normal plasma
19. provide a means to control pH
PCO2.
when correction is impossible or cannot be
immediately achieved.
20. involves a decreased plasma
HCO3 concentration, along with a decrease
in pH.

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CHAPTER 32 DISORDERS OF ACID-BASE BALANCE 177

Activity B Consider the following figure.

7.4

6.9 7.9

24 1.2
pH = 6.1 + log10 (ratio HCO3-: H2CO3)
HCO3- H2CO3
(mEq/L) (mEq/L)

A Ratio: HCO3-: H2CO3 = 20:1

7.4 7.4
7.7
6.9 7.9 6.9 7.9

12 0.6

HCO3- 1.2 24 H2CO3

(mEq/L) (mEq/L)
H2CO3 HCO3-
(mEq/L) (mEq/L)

B Ratio: HCO3-: H2CO3 = 10:1 D Ratio: HCO3-: H2CO3 = 40:1

7.4 7.4

6.9 7.9 6.9 7.9

12 0.6 12 0.6

HCO3- H2CO3 HCO3- H2CO3

(mEq/L) (mEq/L) (mEq/L) (mEq/L)

C Ratio: HCO3-: H2CO3 = 20:1 E Ratio: HCO3-: H2CO3 = 20:1

In this diagram, label each scale to reflect the Activity C Match the key terms in Column A
acid-base state and whether there is any compen- with their definitions in Column B.
sation present.
Column A Column B
• Normal, pH 7.4
• Metabolic acidosis 1. Amphoteric a. Molecule that can re-
• Metabolic acidosis with respiratory compensa- lease H
2. Acid
tion b. Acute increases in
• Respiratory alkalosis 3. Whole blood HCO3
• Respiratory alkalosis with renal compensation buffer base
c. Genetic mitochondr-
4. Delta gap ial disorder
5. MELAS d. Ion or molecule that
(myopathy, can accept H

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178 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

encephalopathy, e. Can function as 6. What are symptoms of metabolic acidosis?

lactic acidosis, acid or base
and strokelike f. Increase in plasma
episodes) PCO2
6. Excess base g. Degree to which an
loading acid or base in a
7. Describe the manifestations of respiratory
buffer system disso-
7. Base alkalosis.
ciates
8. Carbonic h. Anion gap of urine
anhydrase
i. Measures the level
9. Hypercapnia of all buffer systems
of the blood
10. Dissociation
constant j. Catalyzes bicarbon-
ate reaction SECTION III: APPLYING YOUR
KNOWLEDGE
Activity D Briefly answer the following.
Activity E Consider the following scenario and
1. List the three ways carbon dioxide is trans-
answer the questions.
ported in the body.
A female college student is brought to the emer-
gency department by her friend. It is reported by
the young woman’s friend that they found her
wandering around outside the dorm, and she did
not know where she was or why she was there.
2. Why does someone with kidney disease need The friend stated that the young woman had
to worry about the integrity of his or her skele- complained of being “very tired” lately and that
tal system? she had lost weight because she was not eating or
drinking. Vital signs are blood pressure 118/78 mm
Hg, respiratory rate 30 beats/minute, and pulse 66.
An arterial blood gas is ordered and results are PO2
of 95, PCO2 35, HCO3 of 20, and a pH of 7.1.
1. What do this patient’s laboratory values indicate?
3. How are pH and K related? How do they serve
as a buffer?

2. The physician orders a blood glucose level to

4. How do the kidneys regulate acid-base bal- be drawn. Why would a blood glucose level be
ance? important for this patient?

5. What are the two types of acid-base disorders?

SECTION IV: PRACTICING
FOR NCLEX
Activity F Answer the following questions.
1. To calculate the H2CO3 content of the blood,
you need to measure the PCO2 (partial

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CHAPTER 32 DISORDERS OF ACID-BASE BALANCE 179

pressure of CO2) by its solubility coefficient. a. Long-term measures that backup first-line
What is the solubility coefficient of CO2? correction mechanisms
a. 0.03 b. Interim measures that permit survival
b. 0.3 c. Short-term measures that depend on first-
c. 0.04 line correction mechanisms
d. 0.4 d. Ways to correct the primary disorder

2. The body regulates the pH of its fluids by 7. Metabolic acidosis has four main causes.
what mechanism? Mark all that apply. Which laboratory test is used to determine
the cause of metabolic acidosis?
a. Chemical buffer systems of the body fluids
a. Acid-base deficit
b. Liver
b. Arterial blood gas
c. Lungs
c. Anion gap
d. Cardiovascular system
d. Serum bicarbonate
e. Kidneys
8. A change in the pH of the body affects all
3. By reabsorbing HCO3 from the glomerular fil-
organ systems. When the pH falls to less than
trate and excreting H from the fixed acids
7.0, what can occur in the cardiovascular
that result from lipid and protein metabolism,
system? Mark all that apply.
the kidneys work to return or maintain the pH
of the blood to normal or near-normal values. a. Vascular bed can vasodilate, causing the
How long can this mechanism function when client to go into shock
there is a change in the pH of body fluids? b. Vascular bed can vasoconstrict to preserve
a. Minutes the primary organs
b. Hours c. Cardiac contractility can increase, causing
cardiac dysrhythmias
c. Days
d. Cardiac contractility can decrease, causing
d. Weeks
cardiac dysrhythmias
4. Laboratory tests give us valuable information
9. Respiratory acidosis occurs when the plasma
about what is happening in the body. What
pH falls below 7.35 and arterial PCO2 rises
laboratory test is a good indicator of the how
above 50 mm Hg. Because CO2 easily crosses
the buffer systems in the body are working?
the blood-brain barrier, what signs and symp-
a. Acid-base test toms of respiratory acidosis might you see?
b. Urine acidity test Mark all that apply.
c. H level test a. Irritability
d. Base excess or deficit test b. Muscle twitching
5. There are both metabolic and respiratory effects c. Psychological disturbances
on the acid-base balance in the body. How do d. Seizures
metabolic disorders change the pH of the body? e. Psychotic breaks
a. Alter the plasma HCO3
10. Respiratory alkalosis is caused by hyperventi-
b. Alter urine H content lation, which is recognized as a respiratory
c. Alter CO2 levels in the lungs rate in excess of that which maintains normal
d. Alter O2 levels in the major organ systems plasma PCO2 levels. What is a common cause
of respiratory alkalosis?
6. The body has built-in compensatory mecha-
a. Hyperventilation syndrome
nisms that take over when correction of pH is
not possible or cannot be immediately b. Hypoventilation syndrome
achieved. What are these compensatory c. Cluster breathing
mechanisms considered? d. Kussmaul breathing

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33
CHAPTER

Disorders of
Renal Function

SECTION I: LEARNING 12. Describe factors that predispose to UTIs in

children, sexually active women, pregnant
OBJECTIVES women, and older adults
1. Define the terms agenesis, hypoplasia, and dys- 13. Compare the manifestations of UTIs in differ-
genesis, and discuss them as they refer to the ent age groups, including infants, toddlers,
development of the kidney adolescents, adults, and older adults
2. Cite the effect of urinary obstruction in the 14. Cite measures used in the diagnosis and treat-
fetus ment of UTIs
3. Describe the inheritance, pathology, and 15. Describe the two types of immune mecha-
manifestations of the different types of poly- nisms involved in glomerular disorders
cystic kidney disease
16. Use the terms proliferation, sclerosis, membra-
4. List four common causes of urinary tract nous, diffuse, focal, segmental, and mesangial to
obstruction explain changes in glomerular structure that
occur with glomerulonephritis
5. Define the term hydronephrosis and relate it to
the destructive effects of urinary tract ob- 17. Relate the proteinuria, hematuria, pyuria,
structions oliguria, edema, hypertension, and azotemia
that occur with glomerulonephritis to
6. Describe the role of urine supersaturation,
changes in glomerular structure
nucleation, and inhibitors of stone formation
in the development of kidney stones 18. Briefly describe the difference among the
nephritic syndromes, rapidly progressive
7. Explain the mechanisms of pain and infec-
glomerulonephritis, nephrotic syndrome,
tion that occur with kidney stones
asymptomatic glomerular disorders, and
8. Describe methods used in the diagnosis and chronic glomerulonephritis
treatment of kidney stones
19. Cite a definition of tubulointerstitial kidney
9. Cite the organisms most responsible for UTIs disease
and state why urinary catheters, obstruction,
20. Differentiate between the defects in tubular
and reflux predispose to infections
function that occur in proximal and distal
10. List three physiologic mechanisms that pro- tubular acidosis
tect against UTIs
21. Explain the pathogenesis of kidney damage
11. Describe the signs and symptoms of UTIs in acute and chronic pyelonephritis

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CHAPTER 33 DISORDERS OF RENAL FUNCTION 181

22. Explain the vulnerability of the kidneys to in- progressive atrophy of the kidney due to ob-
jury caused by drugs and toxins struction of urine outflow.
23. Characterize Wilms tumor in terms of age of 12. Obstruction of the urinary tract may provoke
onset, possible oncogenic origin, manifesta- pain due to of the collecting sys-
tions, and treatment tem and renal capsule.
24. Cite the risk factors for renal cell carcinoma, 13. The most common cause of upper urinary
describe its manifestations, and explain why tract obstruction is urinary .
the 5-year survival rate has been so low
14. In addition to a supersaturated urine, kidney
stone formation requires a that
facilitates crystal aggregation.
SECTION II: ASSESSING YOUR 15. Most kidney stones are stones.
UNDERSTANDING
16. The major manifestation of kidney stones is
Activity A Fill in the blanks. .
17. Urinary tract infections are the
1. Anomalies in and most common type of bacterial infection seen
of the kidneys are the most common form of by health care providers.
congenital renal disorder.
18. Most uncomplicated lower urinary tract in-
2. Dysgenesis refers to a failure of an organ to fections are caused by .
develop normally and to com-
plete failure of an organ to develop. 19. Most urinary tract infections are caused by
bacteria that enter through the .
3. Newborns with renal agenesis often have
characteristic facial features, termed 20. Urinary tract infections are
, resulting from the effects of common in women than men.
oligohydramnios. 21. In urinary tract infections associated with
4. In renal , the kidneys do not de- stasis of urine flow, the obstruction may be
velop to normal size. or .

5. Renal is due to an abnormality 22. -associated bacteriuria remains

in the differentiation of kidney structures the most frequent cause of gram-negative
during embryonic development. septicemia in hospitalized patients.

6. Unilateral renal dysplasia is the 23. An acute episode of is character-

most common cause of an abdominal mass in ized by frequency of urination, lower abdomi-
newborns. nal or back discomfort, and burning and pain
on urination.
7. kidney diseases are a group of
kidney disorders characterized by fluid-filled 24. is the second leading cause of
sacs or segments that have their origin in the kidney failure worldwide, and it ranks third,
tubular structures of kidney. after diabetes and hypertension, as a cause of
chronic kidney disease in the United States.
8. In the form of polycystic kidney
disease, thousands of large cysts are derived 25. The syndromes produce a prolif-
from every segment of the nephron. erative inflammatory response, whereas the
syndrome produces increased
9. The effects of urinary obstruc- permeability of the glomerulus.
tion on kidney structures are determined by
the degree and duration of the obstruction. 26. syndrome is characterized by
sudden onset of hematuria, variable degrees
10. of urine predisposes to infec- of proteinuria, diminished glomerular filtra-
tion, which may spread throughout the uri- tion rate, oliguria, and signs impaired renal
nary tract. function.
11. refers to urine-filled dilatation 27. Acute postinfectious glomerulonephritis usu-
of the renal pelvis and calyces associated with ally occurs after infection with certain strains

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182 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

of group A -hemolytic streptococci and is Activity B Consider the following figure.

caused by of immune complexes.
28. The of postinfectious glomeru-
lonephritis is caused by infiltration of leuko-
cytes, both neutrophils and monocytes;
proliferation of endothelial and mesangial
cells; and, in severe cases, formation of
crescents.
29. syndrome is an uncommon and
aggressive form of glomerulonephritis that is
caused by antibodies to the glomerular base-
ment membrane.
30. syndrome is characterized by
massive proteinuria and lipiduria, along with
an associated hypoalbuminemia, generalized
edema, and hyperlipidemia.
31. glomerulonephritis is caused by
diffuse thickening of the glomerular base-
ment membrane due to deposition of im-
mune complexes.
32. disease is a primary glomeru-
lonephritis characterized by the presence of In this figure, identify the common locations and
glomerular IgA immune complex deposits. causes of urinary tract obstructions:
33. Alport syndrome represents a hereditary • Pregnancy or tumor
defect of the glomerular that • Ureterovesical junction stricture
results in hematuria and may progress to • Kidney stone
chronic renal failure. • Scar tissue
• Neurogenic bladder
34. refers to a group of tubular • Bladder outflow obstruction
defects in reabsorption of bicarbonate ions or
excretion of hydrogen ions (H) that result Activity C Match the key terms in Column A
in metabolic acidosis and its subsequent with their definitions in Column B.
complications, including metabolic bone
disease, kidney stones, and growth failure in Column A Column B
children. 1. Urease a. Low renal mass in
35. Proximal renal tubular acidosis involves a infant
2. Hypogenesis
defect in proximal tubular reabsorption of b. Blood cells in urine
. 3. Oliguria
c. Urea-splitting bac-
36. represents an infection of the 4. Polycystic terial enzyme
upper urinary tract, specifically the renal kidney disease d. Change in renal
parenchyma and renal pelvis. 1 and 2 structure
37. is one of the most common pri- 5. Hydronephrosis e. Dilatation of the
mary neoplasms of young children. renal pelvis and
6. Proteinuria
calyces associated
38. Kidney cancer is suspected when there are 7. Renal dysplasia with progressive
findings of and a renal atrophy
. 8. Nephrolithiasis
f. Very low urine
9. Hematuria production
10. Oligohydram- g. Genes responsible
nios for autosomal

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CHAPTER 33 DISORDERS OF RENAL FUNCTION 183

dominant polycys- 3. Who are the risk factors for urinary tract infec-
tic kidney disease tion higher for?
h. Kidney stone for-
mation
i. Protein loss in urine
j. Low amniotic fluid
levels 4. What are the host defense mechanisms against
the development of a urinary tract infection?
Activity D

5. What are the cellular changes associated with

glomerular disease?
Glomerular damage

6. Describe the disease progress and the produc-

tion of symptoms in poststreptococcal
glomerulonephritis.

7. Describe the mechanisms of a diabetic

nephropathy.

Complete this flowchart using the following items:

• Edema
• Hyperlipidemia
• Increased permeability to proteins
8. How do medications and toxins from the envi-
• Decreased plasma oncotic pressure
ronment damage renal structures?
• Hypoproteinemia
• Compensatory synthesis of proteins by liver

Activity E Briefly answer the following.

1. What is the mechanism of tissue damage in
urinary tract obstructions?

SECTION III: APPLYING YOUR

KNOWLEDGE
Activity F Consider the following scenario and
2. What are the factors involved in kidney stone
answer the questions.
formation?
An elderly woman, hospitalized with a broken
hip, has an indwelling catheter in place. On the
third day of hospitalization, the woman’s urine
becomes cloudy and foul smelling. The nurse

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184 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

knows that catheters have a high incidence of c. Cysts that are re-
causing urinary tract infections in hospitalized stricted to the corti-
patients. comedullary border
1. What orders would the nurse expect to receive d. Cysts that develop in
for this patient? the kidney as a con-
sequence of aging,
dialysis, or other
conditions that affect
tubular function
3. A young woman presents with signs and
2. What actions would the nurse take to prevent symptoms of a urinary tract infection (UTI).
further contamination by the indwelling The nurse notes that this is the fifth UTI in as
catheter? many months. What would this information
lead the nurse to believe?
a. There is possible obstruction in the urinary
tract.
b. The woman has multiple sexual partners.
c. The woman takes too many bubble baths.
SECTION IV: PRACTICING d. The woman does not clean herself properly.
FOR NCLEX 4. Staghorn kidney stones, or struvite stones, are
usually located in the renal pelvis. These
Activity G Answer the following questions. stones are made from what?
1. Congenital disorders of the kidneys are fairly a. Calcium oxalate
common, occurring in approximately 1:1000 b. Magnesium ammonium phosphate
live births. What is the result to the newborn c. Cystine
when bilateral renal dysplasia occurs? Mark
d. Uric acid
all that apply.
a. Potter facies 5. What is the most common cause of a lower
urinary tract infection?
b. Oligohydramnios
a. Staphylococcus saprophyticus
c. Pulmonary hypoplasia
b. Pseudomonas aeruginosa
d. Multicystic kidneys
c. Escherichia coli
e. Renal failure
d. Staphylococcus aureus
2. Match the type of polycystic kidney disorder
with the characteristic cysts. 6. Urinary tract infections (UTIs) in children do
not generally present as they do in adults.
Type of polycystic What are the signs and symptoms of a UTI in
kidney disorder Characteristic cysts a toddler? Mark all that apply.
1. Autosomal a. Small elongated a. Frequency
dominant cysts that form in b. Diarrhea
polycystic the collecting ducts c. Abdominal pain
kidney disease and maintain con-
d. Poor growth
2. Autosomal tact with the
nephron of origin e. Burning
recessive
polycystic b. Tubule wall, which 7. Acute postinfectious glomerulonephritis, as
kidney disease is lined by a single its name implies, follows an acute infection
3. Acquired cysts layer of tubular somewhere else in the body. What is the
cells, expands and most common cause of acute postinfectious
4. Nephronoph-
then rapidly closes glomerulonephritis?
thisis-medullary
the cyst off from a. Escherichia coli
cystic kidney
the tubule of origin
disease b. Staphylococcus aureus

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CHAPTER 33 DISORDERS OF RENAL FUNCTION 185

c. Pseudomonas aeruginosa 10. Drug-related nephropathies occur all too

d. Group A -hemolytic streptococci often. They involve functional and/or struc-
tural changes to the kidney after exposure to
8. Both type 1 and type 2 diabetes mellitus can a drug. What does the tolerance to drugs de-
cause damage to the glomeruli of the kidneys. pend on?
What renal disease is diabetic nephropathy
a. Vesicoureteral reflux
associated with?
b. Glomerular filtration rate
a. Nephrotic syndrome
c. State of hydration
b. Acute glomerulonephritis
d. Proteinuria
c. Nephritic syndrome
d. Acute glomerulonephritis 11. Wilms tumor is a tumor of childhood. It is
usually an encapsulated mass occurring in
9. Acute pyelonephritis is an infection of the renal any part of the kidney. What are the com-
parenchyma and renal pelvis. What is the mon presenting signs of a Wilms tumor?
most common cause of acute pyelonephritis?
a. Hypotension and a large abdominal mass
a. Group A -hemolytic streptococci
b. Vomiting and oliguria
b. Pseudomonas aeruginosa
c. Abdominal pain and diarrhea
c. Haemophilus influenza
d. Large asymptomatic abdominal mass
d. Candida albicans and hypertension

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34
CHAPTER

Acute Renal Failure and

Chronic Kidney Disease

SECTION I: LEARNING 9. Describe the scientific principles underlying

dialysis treatment, and compare hemodialysis
OBJECTIVES with peritoneal dialysis
1. Describe acute renal failure in terms of its 10. Cite the possible complications of kidney
causes, treatment, and outcome transplantation
2. Differentiate the prerenal, intrinsic, and 11. State the goals for dietary management of
postrenal forms of acute renal failure in terms persons with chronic kidney disease
of the mechanisms of development and man-
12. List the causes of CKD in children and de-
ifestations
scribe the special problems of children with
3. Cite the two most common causes of acute kidney failure
tubular necrosis and describe the course of
13. State why CKD is more common in the elderly
the disease in terms of the initiation, mainte-
and describe measures to prevent or delay the
nance, and recovery phases
onset of kidney failure in this population
4. State the most common causes of chronic
14. Describe the treatment of CKD in children
kidney disease
and the elderly
5. Describe the five stages of chronic kidney
disease
SECTION II: ASSESSING YOUR
6. Describe the methods used to arrive at an ac-
curate estimation of the GFR and explain the UNDERSTANDING
rationale for its use in defining the stages of
chronic kidney disease Activity A Fill in the blanks.

7. Explain the physiologic mechanisms underly- 1. represents a rapid decline in

ing the common problems associated with kidney function sufficient to increase blood
chronic kidney disease, including alterations levels of nitrogenous wastes and impair fluid
in fluid and electrolyte balance and disorders and electrolyte balance.
of skeletal, hematologic, cardiovascular, im- 2. The causes of acute renal failure are com-
mune system, neurologic, skin, and sexual monly categorized as ,
function , or .
8. State the basis for adverse drug reactions in 3. failure, the most common form
patients with chronic kidney disease of acute renal failure, is characterized by a
marked decrease in renal blood flow.

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CHAPTER 34 ACUTE RENAL FAILURE AND CHRONIC KIDNEY DISEASE 187

4. Because of their high metabolic rate, the 18. Anorexia, nausea, and vomiting are common
cells are most vulnerable to is- in patients with , along with a
chemic injury. metallic taste in the mouth.
5. Prerenal failure is manifested by a sharp de- 19. Neuropathy is caused by and
crease in urine output and a disproportionate of nerve fibers, possibly caused
elevation of in relation to serum by uremic toxins.
creatinine levels.
20. Normal aging is associated with a decline in
6. failure results from obstruction the and, subsequently, with re-
of urine outflow from the kidneys. duced homeostatic regulation under stressful
conditions.
7. A major concern in the treatment of acute
renal failure is identifying and correcting the
Activity B Consider the following figure.
.
8. Regardless of cause, represents a
loss of functioning kidney nephrons with
progressive deterioration of glomerular filtra-
tion, tubular reabsorptive capacity, and en-
docrine functions of the kidneys.
9. The normal glomerular filtration rate, which
varies with age, gender, and body size, is ap-
proximately mL/min (1.73
mL/min/m2) for normal young healthy
adults.
10. In clinical practice, glomerular filtration rate
is usually estimated using the serum
concentration.
11. Increased excretion of low-molecular-weight
globulins is a marker of disease,
and excretion of , a marker of In this figure, label the sites of prerenal, in-
chronic kidney disease. trarenal, and postrenal causes of renal failure.
12. The state includes signs and
symptoms of altered fluid, electrolyte, and Activity C Match the key terms in Column A
acid-base balance and alterations in regula- with their definitions in Column B.
tory functions. Column A
13. Chronic renal failure can produce Column B
1. Isosthenuria
or fluid , depend- a. Decreased urine pro-
ing on the pathology of the kidney disease. 2. Azotemia
duction
14. In chronic renal failure, the kidneys lose the 3. Creatinine b. Polyuria with urine
ability to regulate excretion. 4. Salt wasting that is almost isotonic
with plasma
15. The acidosis that occurs in persons with kid- 5. Oliguria
ney failure seems to stabilize as the disease c. Increased bone re-
progresses, probably because of the tremen- 6. Uremic sorption and forma-
dous buffering capacity of . encephalo- tion
pathy d. Byproduct of muscle
16. The term renal is used to de-
7. Prostatic metabolism
scribe the skeletal complications of chronic
kidney disease. hyperplasia e. Decreased central ner-
vous system activity
17. is commonly an early manifes- 8. Hemodialysis
f. Presence of excessive
tation of chronic renal failure. 9. Uremia amounts of urea in
10. Osteitis fibrosa the blood

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188 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

g. Impaired tubular reab- 7. How does renal disease cause cardiovascular

sorption of sodium disease?
h. Most common cause
of postrenal failure
i. Use of artificial kidney
to filter blood
j. Accumulation of ni-
trogenous wastes in
the blood SECTION III: APPLYING YOUR
KNOWLEDGE
Activity D Briefly answer the following.
1. Name the most common intrarenal cause of Activity E Consider the following scenario and
renal failure and describe its different forms. answer the questions.
The parents of a hospitalized 4-year-old boy have
just been told that their son has a chronic renal
disease. The nurse is planning discharge teaching
for this family.

2. Describe the progression of acute tubular 1. What would the nurse know to include in the
necrosis. discharge teaching for this child and his family?

3. How is chronic kidney disease classified? 2. The parents inquire about treatment for their
son and the option of kidney transplantation.
What would be the nurse’s best response?

4. Why is chronic kidney disease considered to

have an insidious progression?

SECTION IV: PRACTICING

FOR NCLEX
5. What are the clinical manifestations of Activity F Answer the following questions.
chronic kidney disease?
1. Acute renal failure occurs at a high rate in se-
riously ill people who are in intensive care
units. What is the most common indicator of
acute renal failure?
a. Azotemia and a decrease in the glomerular
6. How is anemia related to chronic kidney filtration rate
disease? b. Proteinuria and a decrease in the glomeru-
lar filtration rate
c. Azotemia and an increase in the glomeru-
lar filtration rate
d. Proteinuria and an increase in the
glomerular filtration rate

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CHAPTER 34 ACUTE RENAL FAILURE AND CHRONIC KIDNEY DISEASE 189

2. Acute tubular necrosis (ATN) is the most com- 7. People with chronic kidney disease have im-
mon cause of intrinsic renal failure. One of paired immune responses to infection due to
the causes of ATN is ischemia. What are the high levels of urea and metabolic wastes in
most common causes of ischemic ATN? the blood. What is one thing that is missing
Mark all that apply. in an immune response in people with
a. Severe hypovolemia chronic kidney disease?
b. Severe hypertension a. Failure to mount a fever with infection
c. Burns b. Failure of a phagocytic response with infec-
tion
d. Overwhelming sepsis
c. Decrease in granulocyte count
e. Severe hypervolemia
d. Impaired humoral immunity response
3. The glomerular filtration rate (GFR) is consid- with infection
ered the best measure of renal function. What
is used to estimate the GFR? 8. Sexual dysfunction in people with chronic
kidney disease (CKD) is believed to be multi-
a. Blood urea nitrogen
factorial. What are believed to be causes of
b. Serum creatinine sexual dysfunction in people with CKD?
c. Albumin level Mark all that apply.
d. Serum protein a. Antihypertensive drugs
4. Chronic kidney disease (CKD) affects many b. Psychological factors
systems in the body. What is the number one c. Uremic toxins
hematologic disorder caused by CKD? d. Inability to vasodilate veins
a. Polycythemia e. High incidence of sexually transmitted
b. Erythrocythemia diseases
c. Anemia 9. In hemodialysis, access to the vascular system
d. Leukocytosis is most commonly through what?
5. Uremic pericarditis is a disorder that accom- a. External arteriovenous shunt
panies chronic kidney disease. What are its b. Internal arteriovenous fistula
presenting signs and symptoms? Mark all that c. Internal arteriovenous shunt
apply.
d. External arteriovenous fistula
a. Pericardial friction rub
10. Dietary restrictions placed on people with
b. Chest pain with respiratory accentuation
chronic kidney disease (CKD) include limit-
c. Fever without infection ing protein in their diet. The recommended
d. Shortness of breath sources of protein for people with CKD in-
e. Thromboangiitis clude what source of protein?
a. Red meat
6. Neuromuscular disorders can be triggered by
chronic kidney disease. For those clients on b. Fowl
dialysis, approximately two-thirds suffer from c. Milk
what peripheral neuropathy? d. Fish
a. Raynaud syndrome
b. Burning hands and feet
c. Tingling and loss of sensation in lower limbs
d. Restless leg syndrome

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35
CHAPTER

Disorders of the Bladder

and Lower Urinary Tract

SECTION I: LEARNING 9. Describe behavioral, pharmacologic, and sur-

gical methods used in treatment of the differ-
OBJECTIVES ent types of incontinence
1. Trace the ascending sensory and descending 10. List the treatable causes of incontinence in
motor impulses between the detrusor muscle the elderly
and external urinary sphincter and the spinal
11. Discuss the difference between superficial and
cord, pontine micturition center, and cerebral
invasive bladder cancer in terms of bladder
cortex
involvement, extension of the disease, and
2. Explain the mechanism of low-pressure urine prognosis
storage in the bladder
12. State the most common sign of bladder cancer
3. List at least three classes of autonomic drugs
and explain their potential effect on bladder
function
SECTION II: ASSESSING YOUR
4. Describe at least three urodynamic studies UNDERSTANDING
that can be used to assess bladder function
5. Describe the causes of and compensatory Activity A Fill in the blanks.
changes that occur with urinary tract ob- 1. The stores urine and controls its
struction elimination from the body.
6. Differentiate lesions that produce storage dys- 2. The bladder is a freely movable organ located
function associated with spastic bladder from on the pelvic floor, just poste-
those that produce emptying dysfunction as- rior to the pubic .
sociated with flaccid bladder in terms of the
level of the lesions and their effects on blad- 3. In the male, the gland sur-
der function rounds the neck of the bladder where it emp-
ties into the urethra.
7. Describe methods used in treatment of neuro-
genic bladder 4. Urine passes from the kidneys to the bladder
through the .
8. Define incontinence and differentiate be-
tween stress incontinence, overactive blad- 5. The tonicity and composition of the urine is
der/urge incontinence, and overflow often quite different from that of the blood,
incontinence. and the of the bladder acts as an
effective barrier to prevent the passage of

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CHAPTER 35 DISORDERS OF THE BLADDER AND LOWER URINARY TRACT 191

water and other urine elements between the 17. A mild form of reflex neurogenic bladder can
bladder and the blood. develop after a .
6. The operates as a reserve mecha- 18. of the detrusor muscle and loss
nism to stop micturition when it is occurring of the perception of bladder fullness permit
and to maintain continence in the face of un- the overstretching of the detrusor muscle that
usually high bladder pressure. contributes to weak and ineffective bladder
contractions seen in detrusor muscle areflexia.
7. The motor component of the neural reflex
that causes bladder emptying is controlled by 19. is the involuntary loss of urine
the nervous system, whereas the during coughing, laughing, sneezing, or lift-
relaxation and storage function of the bladder ing that increases intra-abdominal pressure.
is controlled by the nervous
20. Two mechanisms are believed to contribute
system.
to its symptomatology of overactive bladder:
8. The parasympathetic lower motor neurons central nervous system and neural control
for the detrusor muscle of the bladder are lo- of bladder sensation and emptying,
cated in the segments of the , and those involving the
spinal cord; their axons travel to the bladder smooth muscle of the bladder itself,
by way of the . .
9. The immediate coordination of the normal 21. Approximately 90% of bladder cancers are de-
micturition reflex occurs in the micturition rived from the epithelial cells
center in the , facilitated by de- that line the bladder.
scending input from the forebrain and as-
22. The most common sign of bladder cancer is
cending input from the reflex centers in the
painless .
spinal cord.
10. brain centers enable inhibition Activity B Consider the following figure.
of the micturition center in the pons and Epithelium when Epithelium when
conscious control of urination. bladder is empty bladder is full

11. The receptors are found in the

detrusor muscle; they produce relaxation of the
detrusor muscle, increasing the bladder volume
at which the micturition reflex is triggered.
12. The activation of produces con-
traction of the intramural ureteral muscula-
ture, bladder neck, and internal sphincter.
13. Alterations in bladder function include uri-
nary with retention or stasis of
urine and urinary with involun-
tary loss of urine.
14. The most important cause of urinary obstruc-
tion in males is external compression of the
urethra caused by enlargement of the
.
15. Neurogenic disorders of bladder function are 1. In this diagram of the bladder, please locate
commonly manifested in one of two ways: and label the following:
failure to urine or failure to
• Detrusor muscle
.
• Ureters
16. Spastic bladder is caused by conditions that • Trigone
produce partial or extensive neural damage • Internal sphincter
above the center in the sacral • External sphincter
cord.

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192 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

Activity C Match the key terms in Column A 3. Describe the activities of the pontine micturi-
with their definitions in Column B. tion center and cortical brain centers.

Column A Column B
1. Incontinence a. Muscle-tensing exer-
cises of the pelvic
2. Micturition
muscles
3. Kegel exercises 4. Describe the actions that take place in the
b. Uninhibited spinal
bladder during micturition.
4. Muscarinic reflex–controlled
contraction of the
5. Nocturia bladder without re-
6. Antimus- laxation of the exter-
carinic drugs nal sphincter
c. Decrease bladder 5. What are the necessary factors that every child
7. Detrusor-
contractility and in- must possess in order to attain conscious con-
sphincter
crease outlet resis- trol of bladder function?
dyssynergia
tance
8. May cause d. Cholinergic receptor
urinary found on external
retention sphincter muscle
9. Nicotinic e. Antihistamine
6. Describe the effects of prolonged urinary tract
10. Tricyclic anti- f. Passage of urine
obstruction disorders on the bladder.
depressants g. Decrease detrusor
muscle tone and in-
crease bladder capa-
city
h. Cholinergic receptor
found on striated 7. Why do many women develop incontinence
muscle fibers of following childbirth?
bladder
i. Involuntary loss or
leakage of urine
j. Excessive urination
at night 8. Describe how chronic neurologic disorders can
Activity D Briefly answer the following. contribute to overactive bladder.

1. Describe the structural layers of the bladder.

9. What are the factors associated with age that

contribute to incontinence in the elderly?
2. List the name and function of the major nerves
that regulate bladder function.

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CHAPTER 35 DISORDERS OF THE BLADDER AND LOWER URINARY TRACT 193

SECTION III: APPLYING YOUR a. Up to the age of 12 to 14 years, the capac-

ity of the bladder is the child’s age in years
KNOWLEDGE plus 2.
Activity E Consider the following scenario and b. Up to the age of 5 years, the capacity of the
answer the questions. bladder is the child’s age in years plus 3.
c. The capacity of the bladder is equal to the
A 53-year-old woman with multiple sclerosis pre-
child’s age in years.
sents at the clinic with urinary frequency and
bladder spasms. A urinalysis is negative for infec- d. Age has nothing to do with bladder capac-
tion. A complete history is taken, and a physical ity; it has adult capacity from toddlerhood.
is performed by the primary care physician. The 3. One of the many tests done during urody-
woman asks the nurse why she is having bladder namic studies is the sphincter electromyelo-
spasms and urinary frequency if she does not gram. What does this test study?
have a bladder infection.
a. Ability of the bladder to store urine
1. What would the nurse respond? b. Activity of the voluntary muscles of the
perineal area
c. Pressure of the bladder during filling and
emptying
d. Flow rate during urination
2. What would the nurse expect the doctor to do 4. Urinary obstruction in the lower urinary tract
for this woman? triggers changes to the urinary system to
compensate for the obstruction. What is an
early change the system makes in its effort to
cope with an obstruction?
a. Ability to suppress urination is increased
b. Stretch receptors in the bladder wall be-
come hypersensitive
SECTION IV: PRACTICING c. Bladder begins to shrink
FOR NCLEX d. Bladder contraction weakens
5. What is a common cause of spastic bladder
Activity F Answer the following questions.
dysfunction?
1. You are caring for a 16-year-old boy, newly a. Central nervous system lesions
diagnosed with a spinal cord injury. He asks
b. Constriction of the internal sphincter
you why he can no longer control his blad-
muscles
der. What would you explain to him? Mark
all that apply. c. External sphincter spasticity
a. “Your spinal cord injury has disrupted the d. Vesicoureteral reflux
control your brain has over your bladder.” 6. Acute overdistention of the bladder can occur
b. “You will always have to wear an internal in anyone with a neurogenic bladder that
catheter.” does not empty. How much urine would the
c. “You will have to learn how to in-and-out nurse empty out of the bladder at one time?
catheterize yourself.” a. Everything in the bladder, no matter how
d. “You have a condition known as a relaxed full it is
bladder.” b. No more than 600 cc of urine at one time
e. “You have a condition known as detrusor- c. No more than 500 cc of urine at one time
sphincter dyssynergia.” d. No more than 1000 cc of urine at one time.
2. Children usually achieve bladder control by 7. In women, stress incontinence is a common
age 5 years. Girls generally achieve bladder problem. The loss of the angle between the
control before boys do. What is the general urethrovesical junction and the bladder
rule for bladder capacity in a child?

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194 UNIT 8 DISORDERS OF RENAL FUNCTION AND FLUIDS AND ELECTROLYTES

contributes to stress incontinence. What is 9. Urinary incontinence can be a problem with

the normal angle between the bladder and the elderly. One method of treatment is habit
the urethrovesical junction? training, or bladder training. When using this
a. 90 to 100 degrees treatment with an elderly person, how fre-
quently should they be voiding?
b. 100 to 110 degrees
a. Every 1 to 3 hours
c. 80 to 90 degrees
b. Every 2 to 4 hours
d. 95 to 105 degrees
c. Every 3 to 5 hours
8. Incontinence can be transient. What are the
d. Every 4 to 6 hours
causes of transient urinary incontinence?
Mark all that apply. 10. One of the treatments for bladder cancer in
a. Spinal cord injury situ is the intervesicular administration of
what drug?
b. Confusional states
a. Adriamycin
c. Stool impaction
b. Mitomycin C
d. Diarrhea
c. Bacillus Calmette-Guérin vaccine
e. Recurrent urinary tract infections
d. Thiotepa

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36

CHAPTER
Structure and Function
of the Gastrointestinal
System

SECTION I: LEARNING 11. Describe the function of the gastric secretions

in the process of digestion
OBJECTIVES
12. List three major GI hormones and cite their
1. Describe the anatomic structures of the function
upper, middle, and lower gastrointestinal
13. Describe the site of gastric acid and pepsin
tract
production and secretion in the stomach
2. List the five layers of the gastrointestinal tract
14. Describe the function of the gastric mucosal
wall and describe their function
barrier
3. Characterize the structure and function of the
15. Describe the functions of the secretions of the
peritoneum and describe its attachment to
small and the large intestine
the abdominal wall
16. Discuss the function of gut flora in terms of
4. Characterize the properties of the interstitial
metabolic activities, trophic effects, and pro-
smooth muscle cells that act as pacemakers
tection against invasion by pathogenic
for the GI tract
microorganisms
5. Compare the actions of the enteric and auto-
17. Differentiate digestion from absorption
nomic nervous systems as they relate to
motility of the GI tract 18. Relate the characteristics of the small intes-
tine to its absorptive function
6. Trace a bolus of food through the stages of
swallowing 19. Explain the function of intestinal brush bor-
der enzymes
7. Differentiate tonic and peristaltic movements
in the GI tract 20. Compare the digestion and absorption of
carbohydrates, fats, and proteins
8. Describe the action of the internal and exter-
nal sphincters in the control of defecation 21. Characterize the relationship among
anorexia, nausea, retching, and vomiting
9. State the source and function of water and
electrolytes that are secreted in digestive 22. Describe the neural structures involved in
secretions vomiting and their mediators
10. Explain the protective function of saliva

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196 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

SECTION II: ASSESSING YOUR monitor the chemical composi-

tion of its contents.
UNDERSTANDING
13. Numerous reflexes influence
Activity A Fill in the blanks. motility and secretions of the digestive tract.
1. The major physiologic function of the 14. Swallowing consists of three phases: an
is to digest food and absorb nu- phase, a phase, and
trients into the bloodstream. an phase.
2. The upper esophageal sphincter, the 15. The is the major site for the
sphincter, consists of a circular digestion and absorption of food.
layer of striated muscle.
16. is normally initiated by the
3. The lower esophageal sphincter, the mass movements of the large intestine.
sphincter, lies just above the
17. The tract produces that act
area where the esophagus joins the stomach.
locally, pass into the general circulation for
4. The lies in the left side of the distribution to more distant sites, and inter-
abdomen and serves as a food storage reser- act with the central nervous system by way
voir during the early stages of digestion. of the enteric and autonomic nervous
systems.
5. The small intestine, which forms the middle
portion of the digestive tract, consists of three 18. The primary function of is the
subdivisions: the , , stimulation of gastric acid secretion.
and .
19. has potent growth hormone–
6. Bile and pancreatic juices enter the intestine releasing activity and has a stimulatory effect
through openings for the common bile duct on food intake and digestive function, while
and the main pancreatic duct in the reducing energy expenditure.
.
20. potentiates the action of se-
7. The cells carry out the secretory cretin, increasing the pancreatic bicarbonate
and absorptive functions of the gastrointesti- response to low circulating levels of secretin;
nal tract, and they produce the stimulates biliary secretion of fluid and bicar-
that lubricates and protects the inner surface bonate; and regulates gallbladder contraction
of the alimentary canal. and gastric emptying.
8. fluid forms a moist and slippery 21. The cells secrete hydrochloric
surface that prevents friction between the acid and intrinsic factor, which is necessary
continuously moving abdominal structures. for the absorption of .
9. The contains the blood vessels, 22. The chief cells secrete , an en-
nerves, and lymphatic vessels that supply the zyme that initiates proteolysis or breakdown
intestinal wall. of proteins.
10. Like the self-excitable cardiac muscle cells in 23. G cells secrete .
the heart, some smooth muscle cells of the
24. secrete large amounts of alka-
gastrointestinal tract function as
line mucus that protect the duodenum
cells.
from the acid content in the gastric chyme
11. The nervous system consists of and from the action of the digestive
the myenteric and submucosal plexuses in enzymes.
the wall of the gastrointestinal tract.
25. The stomach and small intestine contain only
12. monitor the stretch and disten- a few species of , probably due to
tion of the gastrointestinal tract wall, and the composition of luminal contents.

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CHAPTER 36 STRUCTURE AND FUNCTION OF THE GASTROINTESTINAL SYSTEM 197

26. The major metabolic function of colonic 1. In the transfers section of the digestive tract,
microflora is the fermentation of locate and label the following layers/
and endogenous mucus structures:
produced by the epithelial cells.
• Mesentery
27. is the process of dismantling • Muscularis mucosae
foods into their constituent parts. • Serosa (mesothelium)
• Longitudinal muscle
28. is the process of moving nutri-
• Circular muscle
ents and other materials from the external
• Submucosa
environment of the gastrointestinal tract to
• Mucosa
the internal environment.
• Serosa (connective tissue)
29. Each villus is covered with cells called • Muscularis externis
that contribute to the absorp-
tive and digestive functions of the small 2.
bowel and goblet cells that provide
mucus.
30. The enterocytes secrete that ad-
here to the border of the villus structures.
31. Triglycerides are broken down by pancreatic
.
32. represents a loss of appetite.
33. is the conscious sensation re-
sulting from stimulation of the medullary
vomiting center that often precedes or
accompanies vomiting.
34. is the sudden and forceful oral
expulsion of the contents of the stomach.

Activity B Consider the following figures.

1.

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198 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

2. In the transfers section of the digestive tract, 3. Describe the two types of contractions seen in
locate and label the following layers/structures: the small intestine.
• Extruded enterocyte
• Enterocyte
• Vein
• Lacteal
• Artery
4. Describe the incretin effect.
• Crypt of Lieberkühn

Activity C Match the key terms in Column A

with their definitions in Column B.
Column A Column B
5. What are the three functions of saliva?
1. Amylase a. Responsible for motil-
ity along the length of
2. Mastication
the gut
3. Mesentery b. Blood vessels, nerves,
4. Interstitial and lymphatic vessels
cells of Cajal that supply the intesti- 6. What is the mechanism of acid secretion by
nal wall the parietal cells of the stomach?
5. Peritoneum
c. Breaks down starch
6. Submucosal d. Result of chemical
plexus breakdown of proteins
7. Haustrations in stomach
e. Chewing of food
8. Chyme 7. How are carbohydrates broken down to
f. Generate slow waves of absorbable units?
9. Myenteric electrical activity
plexus
g. Largest serous mem-
10. Secretin brane in the body
h. Segmental mixing
movements of the
large intestine 8. Describe protein digestion and absorption.
i. Controls function of
each segment of in-
testinal tract
j. Inhibits gastric acid
secretion
Activity D Briefly answer the following.
SECTION III: APPLYING YOUR
KNOWLEDGE
1. Describe the functional divisions of the
gastrointestinal tract. Activity E Consider the following scenario and
answer the question.
The nurse is preparing an educational event for a
group of children in elementary school who are
studying the gastrointestinal tract.
2. What factors are involved in stimulating the 1. What facts would the nurse know to include
emptying of the stomach? for these children?

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CHAPTER 36 STRUCTURE AND FUNCTION OF THE GASTROINTESTINAL SYSTEM 199

SECTION IV: PRACTICING 6. Saliva has more than one function. What are
the functions of saliva? Mark all that apply.
FOR NCLEX
a. Protection
Activity F Answer the following questions. b. Lubrication
1. The circular layer of smooth muscle that lies c. Antibacterial
between the stomach and the small intestine d. Initiate digestion of starches
is called what? e. Initiate digestion of protein
a. Pyloric sphincter
7. The colon is home to between 300 and 500
b. Cardiac sphincter different species of bacteria. What is their
c. Antrum main metabolic function?
d. Cardiac orifice a. Digestion of insoluble fiber
2. Where in the gastrointestinal tract is food b. Fermentation of undigestible dietary
digested and absorbed? residue
a. Colon and ileum c. Compaction of metabolic waste prior to
leaving the body
b. Jejunum and ileum
d. Absorption of calcium
c. Stomach and jejunum
d. Jejunum and colon 8. Absorption is a major function of the gas-
trointestinal (GI) tract. How is absorption
3. Some smooth muscle cells in the gastroin- accomplished in the GI tract?
testinal tract serve as pacemakers. They dis-
a. Osmosis and diffusion
play rhythmic spontaneous oscillations in
membrane potentials. What are these called? b. Active transport and osmosis
a. Peristalsis c. Active transport and diffusion
b. Intestinal spasms d. Diffusion and inactive transport
c. Slow waves 9. Nausea and vomiting can be side effects of
d. Rapid contractility many drugs as well as physiologic distur-
bances within the body. What is a common
4. Defecation is controlled by both an internal cause of nausea?
and an external sphincter. What nerve con-
a. Distention of the stomach
trols the external sphincter?
b. Distention of the cecum
a. Vagus nerve
c. Distention of the jejunum
b. Femoral nerve
d. Distention of the duodenum
c. Phrenic nerve
d. Pudendal nerve 10. Several neurotransmitters have been identi-
fied with nausea and vomiting. In this capac-
5. The stomach secretes two important hor- ity, they act as neuromediators. What
mones in the gastrointestinal tract. One is neuromediator is believed to be involved in
gastrin. What is the second hormone secreted the nausea and vomiting that accompanies
by the stomach? chemotherapy?
a. Ghrelin a. Serotonin
b. Secretin b. Dopamine
c. Incretin c. Acetylcholine receptors
d. Cholecystokinin d. Opioid receptors

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37
CHAPTER

Disorders of
Gastrointestinal Function

SECTION I: LEARNING 10. List risk factors associated with gastric cancer
OBJECTIVES 11. State the diagnostic criteria for irritable bowel
syndrome
1. Define and cite the causes of dysphagia,
12. Compare the characteristics of Crohn disease
odynophagia, and achalasia
and ulcerative colitis
2. Relate the pathophysiology of gastroe-
13. Relate the use of a high-fiber diet in the treat-
sophageal reflux to measures used in the diag-
ment of diverticular disease to the etiologic
nosis and treatment of the disorder in adults
factors for the condition
and children
14. Describe the pathogenesis of the symptoms
3. State the reason for the poor prognosis associ-
associated with appendicitis.
ated with esophageal cancer
15. Compare the causes and manifestations of
4. Describe the anatomic and physiologic
small-volume diarrhea and large-volume
factors that contribute to the gastric mucosal
diarrhea
barrier
16. Explain why a failure to respond to the defe-
5. Differentiate between the causes and manifes-
cation urge may result in constipation
tations of acute and chronic gastritis
17. List five causes of fecal impaction
6. Characterize the proposed role of Helicobacter
pylori in the development of chronic gastritis 18. Differentiate between mechanical and para-
and peptic ulcer and cite methods for diagno- lytic intestinal obstruction in terms of cause
sis and treatment of the infection and manifestations
7. Describe the predisposing factors in develop- 19. Describe the characteristics of the peritoneum
ment of peptic ulcer and cite the three com- that increase its vulnerability to and protect it
plications of peptic ulcer against the effects of peritonitis
8. Describe the goals for pharmacologic treat- 20. List three causes of intestinal malabsorption
ment of peptic ulcer disease and describe their manifestations
9. Cite the etiologic factors in ulcer formation 21. List the risk factors associated with colorectal
related to Zollinger-Ellison syndrome and cancer and cite the screening methods for de-
stress ulcer tection

200
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CHAPTER 37 DISORDERS OF GASTROINTESTINAL FUNCTION 201

SECTION II: ASSESSING YOUR nonsteroidal antiinflammatory agents, alco-

hol, or bacterial toxins.
UNDERSTANDING
14. is denoted by the absence of
Activity A Fill in the blanks. grossly visible erosions and the presence of
chronic inflammatory changes leading even-
1. The functions primarily as a
tually to atrophy of the glandular epithelium
conduit for passage of food and liquid from
of the stomach.
the pharynx to the stomach.
15. Autoimmune gastritis results from the pres-
2. anomalies of the esophagus re-
ence of to components of gas-
quire early detection and correction because
tric gland parietal cells and intrinsic factor.
they are incompatible with life.
16. is a term used to describe a
3. can result from disorders that
group of ulcerative disorders that occur in
produce narrowing of the esophagus, lack of
areas of the upper gastrointestinal tract that
salivary secretion, weakness of the muscular
are exposed to acid-pepsin secretions.
structures that propel the food bolus, or
neural networks coordinating the swallowing 17. The most common complications of peptic
mechanism. ulcer are , perforation and pene-
tration, and gastric outlet .
4. is characterized by a protrusion
of the stomach through the esophageal hiatus 18. Laboratory findings of hypochromic anemia
of the diaphragm. and occult blood in the stools indicate
.
5. The most frequent symptom of
is heartburn. 19. is the major physiologic media-
tor for hydrochloric acid secretion.
6. There is considerable evidence linking gas-
troesophageal reflux with . 20. Persons at high risk for development of
include those with large surface
7. involves mucosal injury to the
area burns, trauma, sepsis, acute respiratory
esophagus, hyperemia, and inflammation.
distress syndrome, severe liver failure, and
8. Symptoms of reflux esophagitis in an major surgical procedures.
include evidence of pain when
21. Gastric is the second most com-
swallowing, hematemesis and anemia due to
mon tumor in the world.
esophageal bleeding, heartburn, irritability,
and sudden or inconsolable crying. 22. is a functional gastrointestinal
disorder characterized by a variable combina-
9. Most squamous cell esophageal carcinomas
tion of chronic and recurrent intestinal
are attributable to and
symptoms not explained by structural or bio-
use.
chemical abnormalities.
10. The stomach lining is usually to
23. The term inflammatory bowel disease is used to
the acid it secretes, a property that allows the
designate two related inflammatory intestinal
stomach to contain acid and pepsin without
disorders: disease and
having its wall digested.
.
11. The are believed to exert their
24. disease is a recurrent, granulo-
effect through improved mucosal blood flow,
matous type of inflammatory response that
decreased acid secretion, increased bicarbon-
can affect any area of the gastrointestinal
ate ion secretion, and enhanced mucus pro-
tract.
duction.
25. Ulcerative colitis is confined to the
12. refers to inflammation of the
and the .
gastric mucosa.
26. deficiencies are common in
13. is most commonly associated
Crohn disease because of diarrhea, steator-
with local irritants such as aspirin or other
rhea, and other malabsorption problems.

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202 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

27. Characteristics of ulcerative colitis are the le- 42. Celiac disease is an immune-mediated disor-
sions that form in the crypts of der triggered by ingestion of
in the base of the mucosal layer. containing grains.
28. of the colon is one of the feared 43. provides a means for direct visu-
complications of ulcerative colitis. alization of the rectum and colon.
29. The complications of result
Activity B Match the key terms in Column A
from massive fluid loss or destruction of in-
with their definitions in Column B.
testinal mucosa.
1.
30. is a condition in which the mu-
cosal layer of the colon herniated through the Column A Column B
muscularis layer.
1. Achalasia a. Swallowing is painful
31. is a complication of diverticulo- b. Most common cause
2. Esophageal
sis in which there is inflammation and gross of chronic gastritis
atresia
or microscopic perforation of the diverticu- in the United States
lum. 3. Odynopha-
c. Ulcer erodes
gia
32. The pain associated with is through all layers of
caused by stretching of the appendix during 4. Gastroeso- the stomach
the early inflammatory process. phageal d. Esophagus is con-
reflux nected to the trachea
33. The usual definition of is exces-
sively frequent passage of stools. 5. Dysphagia e. Backward move-
ment of gastric
34. Toxin-producing bacteria or other agents that 6. Barrett
contents into the
disrupt the normal absorption or secretory esophagus
esophagus
process in the small bowel commonly cause
7. Tracheoeso- f. Upper esophagus
.
phageal ends in a blind
35. diarrhea is often associated with fistulae pouch
conditions such as inflammatory bowel dis-
8. Mallory- g. Difficulty passing
ease, irritable bowel syndrome, malabsorp-
Weiss food into the
tion syndrome, endocrine disorders, or
syndrome stomach
radiation colitis.
9. Perforation h. Squamous mucosa
36. is commonly associated with that lines the esoph-
acute or chronic inflammation or intrinsic 10. Helicobacter agus gradually is re-
disease of the colon, such as ulcerative colitis pylori placed by columnar
or Crohn disease. epithelium
37. can be defined as the infrequent i. Tears in the esopha-
and/or difficult passage of stools. gus at the esopha-
gogastric junction
38. is the retention of hardened or
puttylike stool in the rectum and colon, j. Difficulty in
which interferes with normal passage of feces. swallowing
2.
39. Intestinal obstruction designates an impair-
ment of movement of intestinal contents in a Column A Column B
direction. 1. Fistulas a. Infection by Enta-
40. obstruction results from neuro- moeba histolytica
2. Zollinger-
genic or muscular impairment of peristalsis. Ellison b. Water is pulled into
syndrome the bowel by the hy-
41. Peritonitis is an inflammatory response of the
perosmotic nature
that lines the abdominal cavity 3. Amebiasis of its contents
and covers the visceral organs.
4. Osmotic c. Tubelike passages
diarrhea that form connec-

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CHAPTER 37 DISORDERS OF GASTROINTESTINAL FUNCTION 203

5. Hypergastri- tions between dif- 5. What are the typical characteristics of irritable
nemia ferent sites in the bowel syndrome?
gastrointestinal tract
6. Steatorrheic
d. Hallmark symptom
7. Cobblestone of Crohn disease
appearance
e. Presence of an ex-
8. Penetration cess of gastrin in
6. What is hypothesized to be a cause of inflam-
the blood
9. Adenomatous matory bowel disease (ulcerative colitis and
polyps f. Ulcer crater erodes Crohn disease)?
into adjacent organs
10. Rotavirus
g. Gastrin-secreting
tumor
h. Causes diarrhea in
children
7. What is the mechanism of diverticulosis for-
i. Benign neoplasms mation?
that arise from the
mucosal epithelium
of the intestine
j. Stools contain ex-
cess fat
8. What is the pathophysiology of constipation?
Activity C Briefly answer the following.
1. What is gastroesophageal reflux disease? What
is the mechanism of damage?

9. How does diet expose a patient to colon cancer?

2. Describe how the gastric mucosal barrier func-

tions to protect the stomach from its own se-
cretions.

SECTION III: APPLYING YOUR

KNOWLEDGE
3. Describe the progression and remission of peptic Activity D Consider the following scenario
ulcers. and answer the questions.
A 67-year-old black man presents at the clinic with
complaints of difficulty swallowing foods of any
kind. He states, “It always feels like I have some-
thing caught in my throat.” His medical history is
4. What is the relationship between Helicobacter significant for Barrett esophagus, unintentional
pylori infection and the development of stom- weight loss of 15 pounds over the past 4 months,
ach cancer? and some pain when swallowing. The patient is
scheduled for an esophagoscopy, and a diagnosis
of esophageal cancer is subsequently confirmed.
The physician explains that, depending on the
stage of the tumor, there are options for treatment.
The physician recommends chemotherapy
followed by surgical resection of the tumor.

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204 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

1. The patient arrives for his first treatment of 3. Infants and children commonly have gastroe-
chemotherapy and asks the nurse why he has sophageal reflux. Often, it is asymptomatic
to have chemotherapy before having the and resolves on its own. What are the signs
surgery to remove the tumor. The nurse cor- and symptoms of gastroesophageal reflux in
rectly responds by stating what? infants with severe disease?
a. Consolable crying and early satiety
b. Delayed satiety and sleeping after feeding
c. Tilting of the head to one side and arching
of the back
2. Subsequent studies show that this patient’s d. Inconsolable crying and delayed satiety
tumor has already metastasized. The physi-
4. The stomach secretes acid to begin the diges-
cian recommends that surgery be done right
tive process on the food that we eat. The gas-
away, but emphasizes to the patient that there
tric mucosal barrier works to prevent acids
is no cure for his cancer. The patient arrives
secreted by the stomach from actually damag-
for surgery and asks the preop nurse why he
ing the wall of the stomach. What are the fac-
needs the surgery if it will not cure his cancer.
tors that make up the gastric mucosal barrier?
What would be the correct response by the
Mark all that apply.
nurse?
a. Impermeable epithelial cell surface covering
b. Mechanisms for selective transport of bi-
carbonate and potassium ions
c. Characteristics of gastric mucus
d. Cell coverings that act as antacids
e. Mechanisms for selective transport of hy-
SECTION IV: PRACTICING drogen and bicarbonate ions
FOR NCLEX 5. Helicobacter pylori gastritis has a prevalence in
more than 50% of American adults older than
Activity E Answer the following questions. 50 years and is believed to be caused by a pre-
vious infection when the patient was
1. Esophageal atresia (EA) is the most common
younger. What can chronic gastritis caused
congenital anomaly of the esophagus and is
by H. pylori cause?
incompatible with life. The majority of chil-
dren born with EA also have tracheoe- a. Decreased risk of gastric adenocarcinoma
sophageal fistulae. What are the signs and b. Decreased risk of low-grade B-cell gastric
symptoms of EA in a newborn? lymphoma
a. Cyanosis and respiratory distress c. Duodenal ulcer
b. Poor feeding and tire easily d. Gastric atrophy
c. Episodes of choking and coughing 6. A 39-year-old Caucasian woman presents at
d. Poor feeding and low blood sugar the clinic with complaints of epigastric pain
that is cramplike, rhythmic, and just below the
2. Hiatal hernias can cause severe pain if the
xiphoid. She states that it wakes her up around
hernia is large. Gastroesophageal reflux is a
1 AM and that she is not sleeping well because
common comorbidity of hiatal hernia, and
of it. She further states that this is her third
when this occurs, what might the hernia do?
painful episode in the past year. The nurse sus-
a. Increase esophageal acid clearance pects the patient has a peptic ulcer and expects
b. Retard esophageal acid clearance to receive what orders from the physician?
c. Decrease esophageal acid clearance a. Schedule patient for a complete metabolic
d. Accelerate esophageal acid clearance panel and a complete blood count
b. Schedule patient for laparoscopic examina-
tion

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CHAPTER 37 DISORDERS OF GASTROINTESTINAL FUNCTION 205

c. Schedule patient for a swallow study c. Information on sulfasalazine, including

d. Schedule patient for a lower gastrointesti- dosage, route, frequency, and side effects
nal study of the drug
d. Information on the chemotherapy that
7. A patient in a nursing home complains to her
will be ordered to cure the disease
nurse that she is not feeling well. When asked
to describe how she feels, the patient states 10. Rotavirus is a common infection in children
that she really is not hungry anymore and younger than 5 years. Like other diseases, ro-
seems to have indigestion a lot. The nurse tavirus is most severe in children younger
checks the patient’s chart and finds that her than 24 months. What is a symptom of ro-
vital signs are normal, but that she has lost tavirus infection?
weight over the past 2 months. She also notes a. Mild to moderate fever that gets higher
that there is a history of gastric cancer in the after the second day
patient’s family. The nurse notifies the physi-
b. Vomiting that lasts for the course of the
cian and expects to receive what orders? Mark
disease
all that apply.
c. Fever that disappears after 7 days
a. Schedule a barium x-ray and an endoscopy
d. Vomiting that disappears around the sec-
b. Perform a Papanicolaou smear on the
ond day
patient’s gastric secretions
c. Order cytologic studies to be done during 11. Diverticulitis is the herniation of tissue of the
the endoscopy large intestine through the muscularis layer
of the colon. It is often asymptomatic and is
d. Schedule a lower gastrointestinal study
found in approximately 80% of people older
e. Have the tech do an endoscopic ultrasound than 85 years. Diverticulitis is often asympto-
8. Irritable bowel syndrome is believed to be matic, but when symptoms do occur, what is
present in 10% to 15% of the population in the patient’s most common complaint?
the United States. What is its hallmark a. Lower left quadrant pain with nausea and
symptom? vomiting
a. Nausea and abdominal pain unrelieved by b. Right lower quadrant pain with nausea and
defecation vomiting
b. Abdominal pain relieved by defecation c. Midepigastric pain with nausea and vomit-
with a change in consistency or frequency ing
of stools d. Right lower quadrant pain with rebound
c. Diarrhea and abdominal pain unrelieved tenderness on the left
by defection
12. Diarrhea is described as a change in fre-
d. Abdominal pain relieved by defecation and quency of stool passage to where it is exces-
bowel impaction sively frequent. Diarrhea can be acute or
9. Crohn disease is a recurrent inflammatory chronic, inflammatory or noninflammatory.
disease that can affect any area of the bowel. What are the symptoms of noninflammatory
The characteristic of this disease is granulo- diarrhea? Mark all that apply.
matous lesions that are sharply demarcated a. Small-volume watery stools
from the surrounding tissue. As the nurse car- b. Nonbloody stools
ing for a patient with newly diagnosed Crohn
c. Periumbilical cramps
disease, you would know to include what in
your teaching? d. Nausea and/or vomiting
a. Definition of Crohn disease that indicates e. Large-volume bloody stools
that it is a recurrent disease that affects
only the large intestine
b. Information on which nonsteroidal anti-
inflammatory drugs to take and how often
to take them

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206 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

13. Peritonitis is an inflammatory condition of the 15. One of the accepted methods of screening for
lining of the abdominal cavity. What is one of colorectal cancer is testing for occult blood in
the most important signs of peritonitis? the stool. Because it is possible to get a false-
a. Vomiting of coffee ground–appearing positive result on these tests, you would in-
emesis struct the patient to do what?
b. Translocation of extracellular fluid into the a. Eat a lot of red meat for 3 or 4 days before
peritoneal cavity the test is done.
c. Translocation of intracellular fluid into the b. Take 1,000 mg of vitamin C in supplement
peritoneal cavity form for 1 week prior to testing.
d. Vomiting of bloody emesis c. Eat citrus fruits at least five times a day for
2 days prior to testing.
14. Celiac disease commonly presents in infancy
d. Avoid nonsteroidal anti-inflammatory
as failure to thrive. It is an inappropriate T-
drugs for 1 week prior to testing.
cell–mediated immune response, and there is
no cure for it. What is the treatment of choice
for celiac disease?
a. Removal of protein from the diet
b. Removal of fat from the diet
c. Removal of gluten from the diet
d. Removal of sugar from the diet

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38

CHAPTER
Disorders of
Hepatobiliary and
Exocrine Pancreas
Function

SECTION I: LEARNING acute disease manifestations, development of

chronic disease, and the carrier state
OBJECTIVES
9. Define chronic hepatitis and compare the
1. Describe the lobular structures of the liver pathogenesis of chronic autoimmune and
chronic viral hepatitis
2. State the source and trace the movement of
blood flow into, through, and out of the liver 10. Characterize the metabolism of alcohol by
the liver and state metabolic mechanisms
3. Describe the function of the liver in terms of
that can be used to explain liver injury
carbohydrate, protein, and fat metabolism
11. Summarize the three patterns of injury that
4. Characterize the function of the liver in terms
occur with alcohol-induced liver disease.
of bilirubin elimination and describe the
pathogenesis of unconjugated and conju- 12. Describe the pathogenesis of intrahepatic
gated hyperbilirubinemia biliary tract disease
5. Relate the mechanism of bile formation and 13. Characterize the liver changes that occur with
elimination to the development of cholestasis cirrhosis
6. List four laboratory tests used to assess liver 14. Describe the physiologic basis for portal hy-
function and relate them to impaired liver pertension and relate it to the development
function of ascites, esophageal varices, and splenomegaly
7. State the three ways by which drugs and 15. Relate the functions of the liver to the mani-
other substances are metabolized or inacti- festations of liver failure.
vated in the liver and provide examples of
16. Characterize etiologies of hepatocellular can-
liver disease related to the toxic effects of
cer and state the reason for the poor progno-
drugs and chemical agents
sis in persons with this type of cancer
8. Compare hepatitis A, B, C, D, and E in terms
17. Explain the function of the gallbladder in
of source of infection, incubation period,
regulating the flow of bile into the duodenum

207
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208 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

and relate to the formation of cholelithiasis the that transport fatty acids
(gallstones). and fat-soluble vitamins to the surface of the
intestinal mucosa for absorption.
18. Describe the clinical manifestations of acute
and chronic cholecystitis 10. represents a decrease in bile flow
through the intrahepatic canaliculi and a re-
19. Characterize the effects of choledocholithiasis
duction in secretion of water, bilirubin, and
and cholangitis on bile flow and the potential
bile acids by the hepatocytes.
for hepatic and pancreatic complications
11. Common to all types of obstructive and hepa-
20. Cite the possible causes and describe the man-
tocellular cholestasis is the accumulation of
ifestations and treatment of acute pancreatitis
pigment in the liver.
21. Describe the manifestations of chronic pan-
12. jaundice occurs when red blood
creatitis
cells are destroyed at a rate in excess of the
22. State the reason for the poor prognosis in liver’s ability to remove the bilirubin from
pancreatic cancer the blood.
13. of bilirubin is impaired when-
ever liver cells are damaged, when transport
SECTION II: ASSESSING YOUR of bilirubin into liver cells becomes deficient,
UNDERSTANDING or when the enzymes needed to conjugate
the bile are lacking.
Activity A Fill in the blanks.
14. result in chemical modification
1. The liver, the gallbladder, and the exocrine of reactive drug groups by oxidation, reduc-
pancreas are classified as organs tion, hydroxylation, or other chemical reac-
of the gastrointestinal tract. tions carried out in hepatocytes.
2. Approximately 300 mL of blood per minute 15. Drugs such as alcohol and barbiturates can
enters the liver through the hepatic induce certain members of the
; another 1,050 mL/minute family to increase enzyme production, accel-
enters by way of the . erating drug metabolism, and decreasing the
3. The venous blood delivered by the pharmacologic action of the drug.
comes from the digestive tract 16. , which involve the conversion
and major abdominal organs, including the of lipid-soluble derivatives to water-soluble
pancreas and spleen. substances, may follow phase 1 reactions or
4. A major exocrine function of the liver is proceed independently.
secretion. 17. Direct hepatotoxic reactions result from
5. The most important of liver’s secretory pro- drug metabolism and the generation of
teins is . .

6. Acetyl-coenzyme A units from fat metabolism 18. drug reactions result in decreased
are also used to synthesize and secretion of bile or obstruction of the biliary
acids in the liver. tree.

7. Almost all synthesis in the body 19. refers to inflammation of the

from carbohydrates and proteins occurs in liver.
the liver. 20. Currently, recreational use is the
8. Whenever a greater quantity of carbohydrates most common mode of hepatitis C virus (HCV)
enters the body than can be immediately transmission in the United States and Canada.
used, the excess is converted to The main route of transmission of HCV in the
in the liver. past was through contaminated
or blood products and .
9. Bile salts serve an important function in di-
gestion; they aid in dietary fats, 21. hepatitis is a severe type of
and they are necessary for the formation of chronic hepatitis of unknown origin that is

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CHAPTER 38 DISORDERS OF HEPATOBILIARY AND EXOCRINE PANCREAS FUNCTION 209

associated with high levels of serum im- 36. Acute is a diffuse inflammation
munoglobulins, including autoantibodies. of the gallbladder, usually secondary to ob-
struction of the gallbladder outlet.
22. biliary diseases disrupt the flow
of bile through the liver, causing cholestasis 37. The pancreas is made up of lob-
and biliary cirrhosis. ules that consist of acinar cells, which secrete
digestive enzymes into a system of micro-
23. biliary cirrhosis results from
scopic ducts.
prolonged obstruction of the extrabiliary tree.
38. Acute represents a reversible in-
24. Obesity, type 2 diabetes, the metabolic syn-
flammatory process of the pancreatic acini
drome, and hyperlipidemia are coexisting
brought about by premature activation of
conditions frequently associated with
pancreatic enzymes.
liver disease.
39. is characterized by progressive
25. represents the end stage of
destruction of the exocrine pancreas, fibrosis,
chronic liver disease in which much of the
and, in the later stages, destruction of the en-
functional liver tissue has been replaced by fi-
docrine pancreas.
brous tissue.
40. The most significant and reproducible envi-
26. is characterized by increased re-
ronmental risk factor of pancreatic cancer is
sistance to flow in the portal venous system
.
and sustained portal vein pressure above 12
mm Hg.
Activity B Consider the following figure.
27. Complications of portal hypertension arise
from the pressure and
of the venous channels behind
the obstruction.
28. occurs when the amount of
fluid in the peritoneal cavity is increased.
29. is a complication in persons
with both cirrhosis and ascites.
30. The syndrome refers to a func-
tional renal failure sometimes seen during the
terminal stages of liver failure with ascites.
31. Hepatic refers to the totality of
CNS manifestations of liver failure.
32. Among the factors identified as etiologic
agents in are chronic viral he- In this figure, label the following structures:
patitis, cirrhosis, long-term exposure to envi-
• Liver
ronmental agents such as aflatoxin, and
• Gallbladder
drinking water contaminated with arsenic.
• Cystic duct
33. The is a distensible, pear-shaped, • Common bile duct
muscular sac located on the ventral surface of • Duodenum
the liver. • Tail of pancreas
• Head of pancreas
34. provides a strong stimulus for
• Pancreatic duct
gallbladder contraction and is released when
• Hepatic duct
food enters the intestines.
• Spleen
35. Gallstones are caused by precipitation of sub- • Diaphragm
stances contained in bile, mainly • Ampulla of Vater
and . • Sphincter of Oddi

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210 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

Activity C Match the key terms in Column A c. Inoculation with in-

with their definitions in Column B. fected blood and/or
spread by oral or
1. sexual contact
Column A Column B d. Occurs primarily by
the fecal-oral route
1. Kupffer cells a. Formed from
senescent red e. Most common
2. Albumin cause of chronic
blood cells
3. Gluconeo- hepatitis, cirrhosis,
b. Conversion of
genesis and hepatocellular
amino acids to
cancer in the world
4. Oxidative ketoacids and
deamination ammonia
c. Capable of remov- Activity D
5. Beta oxi-
ing and phagocy-
dation
tosing old and
6. Extrahepatic defective blood cells
cholestasis d. Abnormally high Gluconeogenesis
7. Bilirubin accumulation of
bilirubin in the
8. Jaundice blood
9. Steatosis e. Splitting of fatty
acids into two-
10. Cholestatic
carbon acetyl-
jaundice
coenzyme A Bloodstream

f. Transport protein/ 1. Complete the flowchart above for the hepatic

plasma colloidal pathways for the storage and synthesis of
osmotic pressure glucose:
g. Obstruction of the
• Triglycerides
large bile ducts
• Glucose
that reduces bile
• Amino acids
secretion
• Glycogen
h. Amino acids are • Glycerol
used for producing • Lactic acid
glucose
2. Complete the flowchart on the following page
i. Fatty infiltration of
using the following terms:
the liver
j. Occurs when bile • Increased pressure in peritoneal capillaries
flow is obstructed • Portosystemic shunting of blood
between the liver • Splenomegaly
and the intestine • Ascites
• Development of collateral channels
2. • Shunting of ammonia and toxins into
general circulation
Column A Column B • Anemia
1. Hepatitis A a. Infection is linked to • Leukopenia
hepatitis B • Thrombocytopenia
2. Hepatitis B • Hepatic encephalopathy
b. Does not cause
3. Hepatitis C • Hemorrhoids
chronic hepatitis or
• Esophageal varices
4. Hepatitis D the carrier state
• Caput medusae
5. Hepatitis E • Bleeding

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CHAPTER 38 DISORDERS OF HEPATOBILIARY AND EXOCRINE PANCREAS FUNCTION 211

Portal hypertension

Activity E Briefly answer the following: 6. How does ethanol cause tissue damage?

1. What are the basic functions of the liver?

7. What changes take place in the liver due to

the toxic affects of alcohol?
2. Describe the pathogenesis of cholestasis.

8. What is cirrhosis of the liver?

3. List the major causes and categories of jaun-
dice.

9. What are the factors that lead to the develop-

ment of ascites?
4. What is measured in the serum to assess liver
dysfunction?

10. How does biliary venous obstruction lead to

hemorrhoid formation?
5. Describe the clinical course of viral hepatitis.

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212 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

SECTION III: APPLYING YOUR water, bilirubin, and bile acids by the hepato-
cytes. Cholestasis can have more than one
KNOWLEDGE cause, but, in all types of cholestasis, there
is what?
Activity F Consider the following scenario and
answer the questions. a. Accumulation of bile pigment in the gall-
bladder
A 16-year-old girl is brought to the clinic by her
b. Accumulation of bile pigment in the liver
mother. She complains of recurrent fatigue and
loss of appetite. Her mother states, “I am con- c. Accumulation of bile pigment in the blood
cerned because she has a yellow look in her eyes. d. Accumulation of bile pigment in the portal
It sort of comes and goes.” While taking the pa- vein
tient’s history, the nurse finds that the patient
3. What is considered the normal amount of
became sexually active 1 year ago and has had
serum bilirubin found in the blood?
multiple partners during the past 12 months. On
physical exam, the physician notes an enlarged a. 1–2 mg/dL
liver. The presumptive diagnosis is hepatitis C. b. 0.01–0.02 mg/dL
1. What confirmatory tests would the nurse ex- c. 0.1–0.2 mg/dL
pect to be ordered? d. 0.001–0.002 mg/dL
4. Many drugs are metabolized and detoxified in
the liver. Most drug metabolizing occurs in
the central zones of the liver. What condition
is caused by these drug-metabolizing actions?
2. The patient’s tests come back positive for he- a. Central cirrhosis
patitis C. What medications might be ordered b. Lobular cirrhosis
for this patient? c. Lobular necrosis
d. Centrilobular necrosis
5. Primary biliary cirrhosis is an autoimmune
disease that destroys the small intrahepatic
bile ducts causing cholestasis. It is insidious
in onset and is a progressive disease. What are
the earliest symptoms of the disease?
SECTION IV: PRACTICING a. Unexplained pruritus
FOR NCLEX b. Weight gain
c. Pale urine
Activity G Answer the following questions.
d. Dark stools
1. The liver has many jobs. One of the most im-
portant functions of the liver is to cleanse the 6. One of the jobs the liver performs is to export
portal blood of old and defective blood cells, triglyceride. When the liver’s capacity to ex-
bacteria in the bloodstream, and any foreign port triglyceride is maximized, excess fatty
material. Which cells in the liver are capable acids accumulate in the liver. What is the dis-
of removing bacteria and foreign material ease these excess fatty acids contribute to?
from the portal blood? a. Biliary cirrhosis
a. Kupffer cells b. Nonalcoholic fatty liver disease
b. Langerhans cells c. Cholelithiasis
c. Epstein cells d. Alcoholic fatty liver disease
d. Davidoff cells 7. Ascites is an accumulation of fluid in the peri-
2. Cholestasis is a condition where there is a de- toneal cavity that usually occurs in advanced
crease in bile flow through the intrahepatic cirrhosis. What is the treatment of choice for
canaliculi and a reduction in secretion of ascites?

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CHAPTER 38 DISORDERS OF HEPATOBILIARY AND EXOCRINE PANCREAS FUNCTION 213

a. Paracentesis c. Pieces of hard food trapped in the gall-

b. Thoracentesis bladder
c. Diuretics d. Thickened bile
d. Desmopressin acetate (DDAVP) 10. What laboratory markers are most commonly
used to diagnose acute pancreatitis?
8. A client is suspected of having liver cancer.
What diagnostic tests would be ordered to a. Amylase and cholesterol
confirm the diagnosis? b. Lipase and amylase
a. Serum -fetoprotein c. Lipase and triglycerides
b. Endoscopy d. Cholesterol and triglycerides
c. Ultrasound of liver 11. All diseases have risk factors. What is the
d. MRI of liver most significant environmental risk factor for
pancreatic cancer?
9. Gallstones are made up mostly of cholesterol.
What is believed to be a precursor of gall- a. Air pollution
stones? b. Water pollution
a. Gallbladder sludge c. Cigarette smoking
b. Thinned mucoprotein d. Heavy metal toxicity

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39
CHAPTER

Alterations in
Nutritional Status

SECTION I: LEARNING 12. Discuss the treatment of obesity in terms of

diet, behavior modification, exercise, social
OBJECTIVES support, pharmacotherapy, and surgical
methods
1. Define nutritional status
13. Explain the use of body mass index in evalu-
2. Define calorie and state the number of calories
ating body weight in terms of overnutrition
derived from the oxidation of 1 g of protein,
fat, or carbohydrate 14. List the major causes of malnutrition and
starvation
3. Explain the difference between anabolism
and catabolism 15. State the difference between protein-calorie
starvation (i.e., marasmus) and protein mal-
4. Relate the processes of glycogenolysis and
nutrition (i.e., kwashiorkor)
gluconeogenesis to the regulation of blood
glucose by the liver 16. Explain the effect of malnutrition on muscle
mass, respiratory function, acid-base balance,
5. Define basal metabolic rate and cite factors
wound healing, immune function, bone min-
that affect it
eralization, the menstrual cycle, and testicu-
6. Describe the function of adipose tissue in terms lar function
of energy storage and as an endocrine organ
17. State the causes of malnutrition in the se-
7. State the purpose of the Recommended Di- verely ill or traumatized patients
etary Allowance of calories, proteins, fats, car-
18. Compare the eating disorders of anorexia ner-
bohydrates, vitamins, and minerals
vosa and bulimia nervosa and the complica-
8. Describe methods used for a nutritional as- tions associated with each.
sessment
9. State the factors used in determining body
mass index and explain its use in evaluating SECTION II: ASSESSING YOUR
body weight in terms of undernutrition and UNDERSTANDING
overnutrition
10. Define and discuss the causes of obesity and Activity A Fill in the blanks.
health risks associated with obesity 1. describes the condition of the
11. Differentiate upper and lower body obesity body related to the availability and use of
and their implications in terms of health risk nutrients.

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CHAPTER 39 ALTERATIONS IN NUTRITIONAL STATUS 215

2. is the organized process through 17. increases stool bulk and facili-
which nutrients such as carbohydrates, fats, tates bowel movements.
and proteins are broken down, transformed,
18. The contains the feeding center
or otherwise converted into cellular energy.
for hunger and satiety.
3. The body transforms carbohydrates, fats, and
19. A decrease in blood causes
proteins into the intermediary compound,
hunger.
.
20. measurements provide a means
4. The refers to the metabolic reac-
for assessing body composition, particularly
tions occurring when the body is at rest.
fat stores and skeletal muscle mass.
5. Energy expenditure can be increased by in-
21. The uses height and weight to
creasing and/or nonexercise
determine healthy weight.
activity thermogenesis.
22. Studies have indicated that waist
6. More than 90% of body energy is stored in
at the abdomen is highly corre-
the tissues of the body.
lated with insulin resistance.
7. acts at the level of the hypothal-
23. is defined as having excess body
amus to decrease food intake and increase en-
fat, enlarged fat cells, and even an increased
ergy expenditure through an increase in
number of fat cells.
thermogenesis and sympathetic nervous sys-
tem activity. 24. Research suggests that may be a
more important factor for morbidity and
8. The defines the intakes that
mortality than overweight or obesity.
meet the nutrient needs of almost all healthy
persons in a specific age and gender group. 25. has been found to have little or
no effect on metabolic variables, central obe-
9. (% daily vitamins [DV]) tells the
sity, cardiovascular risk factors, or future
consumer what percent of the DV one serving
amount of weight loss.
of a food or supplement supplies.
26. There is convincing evidence that
10. are required for growth and
physical activity decreases the risk of over-
maintenance of body tissues, enzymes and
weight and obesity.
antibody formation, fluid and electrolyte bal-
ance, and nutrient transport. 27. does afford significant weight
loss, long-term weight loss maintenance, im-
11. The rate of protein breakdown can be esti-
proved quality of life, decreased incidence of
mated by measuring the amount of
associated diseases, and decreased all-cause
in the urine.
mortality.
12. The saturated fatty acids blood
28. Obesity is the most prevalent nutritional dis-
cholesterol, whereas the monounsaturated
order affecting the population
and polyunsaturated fats blood
in the United States.
cholesterol.
29. and are conditions
13. Trans-fatty acids low-density
in which a person does not receive or is un-
lipoprotein cholesterol and
able to use an adequate amount of nutrients
high-density lipoprotein cholesterol.
for body function.
14. There is no specific dietary requirement for
30. Protein and energy malnutrition represents a
.
depletion of the body’s lean tissues caused by
15. are a group of organic com- and/or catabolic stress.
pounds that act as catalysts in various chemi-
31. The child with has a wasted ap-
cal reactions.
pearance, with loss of muscle mass, stunted
16. are involved in acid-base bal- growth, and loss of subcutaneous fat.
ance and in the maintenance of osmotic pres-
32. Bulimia nervosa is defined by
sure in body compartments.
binge eating and activities such as vomiting;

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216 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

fasting; excessive exercise; and use of diuret- 3. Dermatitis c. Hormone that may
ics, laxatives, or enemas to compensate for stimulate hunger
4. Triglycerides
that behavior.
d. Unsaturated oils
5. Marasmus
are partially hydro-
Activity B Match the key terms in Column A
6. Trans-fatty genated
with their definitions in Column B.
acids e. Minerals present in
1. large amounts in
7. Macro-
Column A Column B minerals the body
f. Characterized by
1. Adipocytes a. Amount of nitro-
determined
gen taken in by
2. Anabolism dieting, often ac-
way of protein is
companied by com-
3. Kwashiorkor equivalent to the
pulsive exercise
nitrogen excreted
4. Calorie g. Protein and calorie
b. Malnutrition
5. Diet-induced deficiency
caused by inade-
thermo- quate protein in-
genesis take in the
6. Metabolites presence of fair to Activity C Briefly answer the following.
good energy
7. Nitrogen 1. What are the two types of adipose tissue? How
c. Chemical interme- do they differ?
balance
diates of metabo-
8. Catabolism lism
9. Resting d. Storage and syn-
energy thesis of cell con-
equivalent stituents
e. Amount of energy 2. How is bioimpedance performed, and what
10. Kilocalorie does it do?
needed to raise the
temperature of 1 kg
of water by 1C
f. Fat cells
g. Breakdown of
complex molecules 3. What are the nongenetic causes of obesity?
h. Amount of heat or
energy required to
raise the tempera-
ture of 1 g of water
by 1C
i. Energy used by 4. What are the causes of anorexia?
the body for diges-
tion, absorption,
and assimilation
j. Used for predict-
ing energy expen- 5. What are the criteria for the diagnosis of bu-
diture limia nervosa?
2.
Column A Column B
1. Anorexia a. Mixture of fatty
nervosa acids and glycerol
2. Ghrelin b. Result of a deficiency
of linoleic acid

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CHAPTER 39 ALTERATIONS IN NUTRITIONAL STATUS 217

6. Describe the criteria for a diagnosis of binge- used in the production

eating disorder. of energy
d. Chemical intermediates
for anabolism and cata-
bolism
e. Phase of metabolic stor-
age and synthesis of cell
constituents
SECTION III: APPLYING 2. Adipose tissue is known to be both an en-
YOUR KNOWLEDGE docrine and a paracrine organ because of the
factors it secretes. What are these factors?
Activity D Consider the following scenario Mark all that apply.
and answer the questions. a. Leptin
A 14-year-old girl is brought to the clinic by her b. Growth hormone
mother for a sports physical. The young lady is c. Adipokine
5’4” tall, weighs 95 pounds, and has a small
d. Insulin resistance factor
frame. The nurse notes the client’s weight and
suspects an eating disorder. e. Adiponectin

1. What questions would be appropriate in 3. When nutritional requirements are needed

the nursing history to assess for an eating for a specific group, what dietary require-
disorder? ments are used?
a. Estimated average requirement
b. Adequate intake
c. Recommended dietary allowance
d. Dietary reference intake
2. The nurse knows that the DSM-IV-TR diag- 4. Fat is a necessary part of the diet. The Food
nostic criteria for anorexia nervosa include and Nutrition Board has set what percent of
what? fat as necessary in our diet?
a. 10%
b. 20%
c. 30%
d. 40%
5. It is the hypothalamus that tells us when we
SECTION IV: PRACTICING are hungry or full. Its message is mediated by
FOR NCLEX input from the gastrointestinal tract. There
are also centers in the hypothalamus that reg-
Activity E Answer the following questions. ulate energy balance and metabolism based
on the secretion of what hormones?
1. Match the term with its action. a. Cholecystokinin and glucagonlike peptide-1
Term Action b. Ghrelin and thyroid
1. Anabolism a. Transform fuel sub- c. Thyroid and adrenocortical hormones
strates into cellular d. Adrenocortical hormones and cholecys-
2. Catabolism
energy tokinin
3. Substrate b. Substance on which
4. Metabolite an enzyme acts
c. Breakdown of com-
5. Enzyme
plex molecules into
systems
substances that can be

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218 UNIT 9 DISORDERS OF GASTROINTESTINAL FUNCTION

6. Body mass index (BMI) is the measurement a. Self-induced vomiting

used to determine a person’s healthy weight. b. Compulsive exercise
A BMI between 18.5 and 24.9 is considered
c. Laxative use
the lowest health risk in relation to the
weight of a person. How is the BMI calcu- d. Compulsive working
lated? 9. Childhood obesity is recognized as a major
a. BMI  weight[lb]/height[ft2] problem in the pediatric population. What
b. BMI  weight[kg]/height[ft2] diseases are pediatricians now seeing in their
clients as a direct result of childhood obesity?
c. BMI  weight[lb]/height[m2]
a. Type 1 diabetes
d. BMI  weight[kg]/height[m2]
b. Dyslipidemia
7. Two types of obesity are recognized: upper
c. Hypotension
body obesity and lower body obesity. How is
the type of obesity determined? d. Psychosocial acceptance
a. Waist/hip circumference 10. Malnutrition is not common in the general
b. Chest circumference/weight population in the United States. However, cer-
tain populations are more prone to malnutri-
c. Chest/hip circumference
tion than others are. One of these populations
d. Waist circumference/weight is hospitalized patients. Why is this true?
8. Anorexia nervosa, bulimia nervosa, and binge- a. Appetites are increased by fever and pain.
eating disorder are becoming increasingly b. Special diets can increase appetite.
common, with assessments for these disorders
c. Pain and medications can decrease ap-
being made in children as young as 9 years. In
petite.
the adult population, what means of control-
ling binge eating is most prevalent in men? d. Only healthy diets are served in hospitals.

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40

CHAPTER
Mechanisms of
Endocrine Controls

SECTION I: LEARNING 2. The functions of the endocrine system are

closely linked with those of the
OBJECTIVES system and the system.
1. Characterize a hormone 3. When hormones act locally on cells other
than those that produced the hormone, the
2. Differentiate vesicle-mediated and non–
action is called .
vesicle-mediated mechanisms of hormone syn-
thesis in terms of their stimuli for hormone 4. Hormones can also exert an
synthesis and release action on the cells from which they were
produced.
3. Describe mechanisms of hormone transport
and inactivation 5. Hormones that are released into the blood-
stream circulate either as mole-
4. State the function of a hormone receptor and
cules or as hormones to
the difference between cell surface hormone
transport carriers.
receptors and intracellular hormone receptors
6. Hormones produce their effects through in-
5. Describe the role of the hypothalamus in regu-
teraction with , which in turn
lating pituitary control of endocrine function
are linked to one or more effector systems
6. State the major difference between positive within the cell.
and negative feedback control mechanisms
7. The structure of hormone varies
7. Describe methods used in diagnosis of en- in a manner that allows target cells to re-
docrine disorders spond to one hormone and not to others.
8. hormones attach to intracellular
receptors and form a hormone-receptor com-
SECTION II: ASSESSING YOUR plex that travels to the cell nucleus.
UNDERSTANDING 9. The synthesis and release of anterior pituitary
hormones is regulated by the action of releas-
Activity A Fill in the blanks. ing or inhibiting hormones from the
1. The endocrine system uses chemical sub- , which is the coordinating cen-
stances called as a means of reg- ter of the brain for endocrine, behavioral, and
ulating and integrating body functions. autonomic nervous system function.

219
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220 UNIT 10 DISORDERS OF ENDOCRINE FUNCTION

10. The pituitary gland has been called the Activity D Briefly answer the following.
because its hormones control
the functions of many target glands and cells. 1. What is a hormone?

11. The easiest way to measure hormone levels

during a specific period are by either blood
samples or urine tests to measure
or .
2. What is the structure of a hormone?
Activity B Match the key terms in Column A
with their definitions in Column B.
Column A Column B
1. Autocrine a. Time it takes for the
body to reduce the 3. How do tissues regulate a hormone’s effect?
2. Half-life of a
concentration of the
hormone
hormone by one-half
3. Hormones b. Hormone acts on cell
4. Hypophysis that produced it
c. Hormone affecting
5. Paracrine 4. What are the main types of cell membrane
neighboring cells
receptors, and how do they exert their
6. Second d. The hypothalamus effects?
messenger and the pituitary
7. Hormone e. Highly specialized or-
response ganic molecules pro-
element duced by endocrine
organs that exert their
action on specific tar- 5. Describe the global role of the anterior pitu-
get cells itary hormones.
f. Intracellular signal
g. Activate or suppress
intracellular mecha-
nisms such as gene
activity
6. How does negative feedback regulate hormone
levels?

Activity C Put the steps of hypothalamic-

pituitary-target cell feedback mechanism in
order. Draw a flowchart using these terms:
• Effect
• Target
• Peripheral gland
• Tropic hormone
• Central nervous system input SECTION III: APPLYING YOUR
• Hypothalamus KNOWLEDGE
• Pituitary
• Releasing hormone Activity E Consider the following scenario and
• Hormone answer the questions.
• Other input
An 87-year-old woman has come to the clinic
for a routine physical exam. She says she has
no complaints and is concerned only about a

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CHAPTER 40 MECHANISMS OF ENDOCRINE CONTROLS 221

20-pound weight gain in the past 2 years. She synthesized by nonvesicle-mediated path-
says that she is not as active as she used to be. ways?
She also mentions that she has fallen several a. Neurotransmitters that are also hormones
times and now has a large bruise on her right
b. Renin and angiotensin
hip.
c. Androgens and estrogens
1. The nurse knows that this client is at risk for
d. Pepsin and ghrelin
osteoporosis due to her decrease in activity.
What test would the nurse expect to be or- 4. To prevent the accumulation of hormones in
dered to either confirm or rule out osteoporo- our bodies, the hormones are constantly
sis in this patient? being metabolized and excreted. Where are
adrenal and gonadal steroid hormones
excreted?
a. Feces and urine
b. Bile and lungs
2. With the client’s weight gain over the past c. Cell metabolites and lungs
2 years and her decrease in activity level, the d. Bile and urine
nurse would expect what test to be ordered to
5. The hypophysis is a unit formed by the pitu-
either rule out or confirm type 2 diabetes in
itary and the hypothalamus. These two
this client?
glands are connected by the blood flow in
what system?
a. Hypophyseal portal system
b. Supraoptic portal system
c. Paraventricular portal system
d. Hypothalamic portal system
SECTION IV: PRACTICING 6. The hormone levels in the body need to be
FOR NCLEX kept within an appropriate range. How is this
accomplished for many of the hormones in
Activity F Answer the following questions. the body?
a. Positive feedback loop
1. The endocrine system is closely linked with
both the immune system and the nervous b. Negative feedback loop
system. What neurotransmitter can also act as c. Regulated feedback loop
a hormone? d. Sensory feedback loop
a. Epinephrine
7. Many hormones are measured for diagnostic
b. Norepinephrine reasons by using the plasma levels of the hor-
c. Dopamine mones. What is used today to measure
d. Succinylcholine plasma hormone levels?
a. Nucleotide assay methods
2. When hormones act locally rather than being
secreted into the bloodstream, their actions b. Selective binding methods
are termed what? c. Radioimmunoassay methods
a. Autocratic and paracratic d. Radiolabeled hormone-antibody methods
b. Autocrine and paracrine 8. Sometimes the measurement of hormones is
c. Localized and influential done through a urine sample. What is an
d. Preventers and inhibitors advantage of measuring hormone levels
through a urine sample rather than a blood
3. Hormones can be synthesized by both sample?
vesicle-mediated pathways and nonvesicle-
a. Urine has more accurate measurements of
mediated pathways. What hormones are
hormones

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222 UNIT 10 DISORDERS OF ENDOCRINE FUNCTION

b. There are more hormone metabolites in 10. Imaging has proven useful in both the diag-
urine than in blood nosis and follow-up of endocrine disorders.
c. Blood sampling has more pure hormone Two types of imaging studies are useful when
than urine does dealing with endocrine disorders, isotopic
imaging and nonisotopic imaging. What is an
d. Urine samples are easily obtained
example of isotopic imaging?
9. In an adult with acromegaly, a growth a. MRI
hormone-secreting tumor is suspected. What
b. Thyroid scan
diagnostic test would be used for this client?
c. Renal angiography
a. A growth hormone suppression test
d. Positron emission topography scan
b. A growth hormone stimulation test
c. A growth hormone serum assay test
d. A growth hormone urine assay test

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41

CHAPTER
Disorders of Endocrine
Control of Growth and
Metabolism

SECTION I: LEARNING 10. Explain why children with isosexual preco-

cious puberty are tall-statured children but
OBJECTIVES short-statured adults
1. Describe the mechanisms of endocrine hypo- 11. Characterize the synthesis, transport, and reg-
function and hyperfunction ulation of thyroid hormone
2. Differentiate primary, secondary, and tertiary 12. Diagram the hypothalamic-pituitary-thyroid
endocrine disorders feedback system
3. Discuss the classification of pituitary tumors 13. Describe tests in the diagnosis and manage-
ment of thyroid disorders
4. Describe the clinical features and causes of
hypopituitarism 14. Relate the functions of thyroid hormone to
hypothyroidism and hyperthyroidism
5. State the effects of a deficiency in growth hor-
mone 15. Describe the effects of congenital hypothy-
roidism
6. Differentiate genetic short stature from con-
stitutional short stature 16. Characterize the manifestations and treatment
of myxedematous coma and thyroid storm
7. State the mechanisms of short stature in hy-
pothyroidism, poorly controlled diabetes 17. Describe the function of the adrenal cortical
mellitus, chronic treatment with excessive hormones and their feedback regulation
glucocorticoid hormones, malnutrition, and
18. State the underlying cause of congenital
psychosocial dwarfism
adrenal hyperplasia
8. List three causes of tall stature
19. Relate the functions of the adrenal cortical
9. Relate the functions of growth hormone to hormones to Addison disease (i.e., adrenal
the manifestations of acromegaly and adult- insufficiency) and Cushing syndrome (i.e.,
onset growth hormone deficiency glucocorticoid excess)

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224 UNIT 10 DISORDERS OF ENDOCRINE FUNCTION

SECTION II: ASSESSING YOUR 13. Thyroid hormone has two major functions: it
increases and syn-
UNDERSTANDING thesis, and it is necessary for growth and de-
velopment in children.
Activity A Fill in the blanks.
14. Thyroid hormone increases the
1. Disturbances of endocrine function can
of all body tissues except the retina, spleen,
usually be divided into two categories:
testes, and lungs.
and .
15. Measures of T3, T4, and thyroid-stimulating
2. defects result in endocrine hy-
hormone have been made available through
pofunction due to the absence or impaired
methods.
development of the gland or the absence of
an enzyme needed for hormone synthesis. 16. Congenital hypothyroidism is a common
cause of .
3. Several hormones are essential for normal
body and maturation, including 17. implies the presence of a non-
growth hormone, insulin, thyroid hormone, pitting mucus-type edema caused by the
and androgens. accumulation of hydrophobic extracellular
matrix substances in the connective tissues of
4. Growth hormone cannot directly produce
a number of body tissues.
bone growth; instead, it acts indirectly by
causing the liver to produce . 18. is the clinical syndrome that re-
sults when tissues are exposed to high levels
5. secretion is stimulated by hypo-
of circulating thyroid hormone.
glycemia, fasting, starvation, increased blood
levels of amino acids, and stress conditions 19. The most common cause of hyperthyroidism
such as trauma, excitement, emotional stress, is disease, which is accompa-
and heavy exercise. nied by ophthalmopathy (or dermopathy)
and diffuse goiter.
6. describes children (particularly
boys) who have moderately short stature, 20. Many of the manifestations of hyperthy-
thin build, delayed skeletal and sexual matu- roidism are related to the increase in
ration, and absence of other causes of de- consumption and use of
creased growth. fuels associated with the hyper-
metabolic state, as well as to the increase
7. describes a child who is taller
in sympathetic nervous system activity that
than his or her peers and is growing at a
occurs.
velocity that is within the normal range for
bone age. 21. is manifested by a very high
fever, extreme cardiovascular effects, and se-
8. Growth hormone excess occurring before pu-
vere central nervous system effects.
berty and the fusion of the epiphyses of the
long bones results in . 22. The forms the bulk of the gland
and is responsible for secreting three types of
9. When growth hormone excess occurs in
hormones: the glucocorticoids, the mineralo-
adulthood or after the epiphyses of the long
corticoids, and the adrenal androgens.
bones have fused, the condition is referred to
as . 23. secretion is regulated by the
renin-angiotensin mechanism and by blood
10. Long-term elevation of growth hormone re-
levels of potassium.
sults in of the beta cells, causing
them to literally “burn out.” 24. When produced as part of the stress response,
hormones aid in regulating the
11. sexual development may be
metabolic functions of the body and in con-
idiopathic or may be caused by gonadal,
trolling the inflammatory response.
adrenal, or hypothalamic disease.
25. stimulates glucose production
12. hormones are bound to thyrox-
by the liver, promotes protein breakdown,
ine-binding globulin and other plasma
and causes mobilization of fatty acids.
proteins for transport in the blood.

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CHAPTER 41 DISORDERS OF ENDOCRINE CONTROL OF GROWTH AND METABOLISM 225

26. Primary adrenal insufficiency, or

disease, is caused by destruction of the adrenal
gland.
27. refers to the manifestations of
hypercortisolism from any cause.

Activity B Consider the following figure.

Hypothalamus

Anterior
pituitary

Growth hormone

Liver

IGF-1

Adipose Carbohydrate
tissue metabolism

Bone and Body

Muscle
cartilage organs

Complete the flowchart with the following Activity C Match the key terms in Column A
terms: with their definitions in Column B.
• Antiinsulin effects Column A Column B
• Decreased glucose use
• Decreased adiposity 1. Laron-type a. Growth hormone-
• Growth-promoting actions dwarfism secreting cells
• Increased blood glucose 2. Hypopi- b. Deficiency of all
• Increased lean muscle mass tuitarism pituitary-derived
• Increased linear growth hormones
• Increased lipolysis 3. Cretinism
c. Dry skin and swelling
• Increased protein synthesis 4. Hashimoto around lips and nose as
• Increased size and function thyroiditis well as mental deterio-
ration

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226 UNIT 10 DISORDERS OF ENDOCRINE FUNCTION

5. Panhypopi- d. Manifestations of 4. How is growth hormone release stimulated?

tuitarism untreated congenital How is it inhibited?
hypothyroidism
6. Ophthalmo-
pathy e. Autoimmune disor-
der in which the thy-
7. Goiter roid gland may be
8. Myxedema totally destroyed
5. Describe the stimulation of the thyroid gland,
f. Increase in the size of
9. Somatotropes and explain the mechanism of negative feed-
the thyroid gland
back to inhibit thyroid activity.
10. Pendred g. Eyelid retraction,
syndrome bulging eyes, light
sensitivity, discom-
fort, double vision,
and vision loss
h. Patients with goiter 6. Describe the manifestations of hypothy-
and congenital deaf- roidism.
ness
i. Growth hormone lev-
els are normal or ele-
vated, but there is a
hereditary defect in
insulinlike growth 7. What is the result of adrenal insufficiency?
factor production
j. Decreased secretion
of pituitary
hormones
8. What are the manifestations of Cushing
Activity D Briefly answer the following. syndrome?
1. Explain the grouping of the root causes of
endocrine disorders.

2. What hormones are directly affected by hy-

SECTION III: APPLYING YOUR
popituitarism? What affect does it have on the KNOWLEDGE
rest of the endocrine system?
Activity E Consider the following scenario and
answer the questions.
The parents of a newborn have been notified by
the hospital that they need to bring their new-
born back to the hospital for further testing. The
3. What are the normal actions of growth parents are informed that one of the tests done
hormone? on the baby when it was first born needs to be re-
peated. When the parents arrive at the hospital,
they meet with a pediatrician who explains that
their infant’s thyroid tests have come back ab-
normal and need to be repeated. He goes on to
say that it might be a false-negative result on the
original test and not to worry.

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CHAPTER 41 DISORDERS OF ENDOCRINE CONTROL OF GROWTH AND METABOLISM 227

1. As the nurse prepares to take the infant’s 3. Growth hormone (GH) exerts its effects on
blood, the parents ask what it means if the the body in many ways. Which of these are
first test result is not a mistake. The nurse effects of GH? Mark all that apply.
knows the best information to give the parents a. Enhances fatty acid mobilization
is what?
b. Increases insulin levels
c. Facilitates the rate of protein synthesis
d. Decreases ACTH production
e. Decreases use of fatty acids for fuel

2. The parents want to know what will happen 4. Acromegaly is a disorder that is caused by the
to their baby if the thyroid gland is not work- production of excessive growth hormone in
ing correctly. The nurse correctly answers the adult. Because the person cannot grow
what? taller, the soft tissues continue to grow, present-
ing a very distinctive appearance. What is it
that is distinctive in a person with acromegaly?
a. Small hands and feet compared to length
of arms and legs
b. Broad, bulbous nose and a protruding
lower jaw
c. Slanting forehead and a receding lower jaw
SECTION IV: PRACTICING
d. Protruding lower jaw and forehead
FOR NCLEX
5. Precocious puberty is a disorder that occurs in
Activity F Answer the following questions. both boys and girls. What does precocious
puberty cause in adults?
1. Advances in technology have made it possi-
ble to assess hypothalamic-pituitary function a. Early menopause in females
by newly developed imaging and radioim- b. Early erectile dysfunction problems in males
munoassay methods. When baseline tests are c. Short stature in adults
not sufficient, what suppression test gives
d. Gigantism in adults
information about combined hypothalamic-
pituitary function? 6. When the assessment of thyroid autoantibodies
a. Growth hormone suppression test is performed, what is the suspected diagnosis?
b. ACTH suppression test a. Goiter
c. Cortisol suppression test b. Thyroid tumor
d. Prolactin suppression test c. Congenital hypothyroidism
d. Hashimoto thyroiditis
2. Growth hormone (GH) is secreted by both
adults and children. GH deficiency in chil- 7. An elderly woman is brought to the emer-
dren is treated by injections of GH on a daily gency room by her family. They relate to the
basis. When teaching a family or child to give nurse that the client has had mental status
injections of GH, what is it important to changes and cannot remember her grandchil-
teach them? dren’s names. They go on to say that she is in-
a. Give the injections in the morning so the tolerant of cold and is lethargic. On physical
peak effect is before noon. examination, the nurse notes that the client
has a husky voice, her face is puffy around the
b. Give the injections at bedtime to produce
eyes, and her tongue appears enlarged. What
the greatest effect at night.
diagnosis would the nurse suspect?
c. Give the injections about 3 PM to produce
a. Myxedema
the greatest effect in the evening.
b. Hashimoto thyroiditis
d. Give the injections in the early afternoon
to produce the greatest effect at dinner c. Hyperthyroidism
time. d. Congenital hypothyroidism

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228 UNIT 10 DISORDERS OF ENDOCRINE FUNCTION

8. Hyperthyroidism that is inadequately treated 11. In Addison disease, the majority of the
can cause a life-threatening condition known adrenal cortex has been destroyed. This
as a thyroid storm. What are the manifesta- causes a lack of mineralocorticoids and
tions of a thyroid storm? Mark all that apply. glucocorticoids. Therapy consists of oral
a. Tachycardia replacement with what drug?
b. Very low fever a. Cortisol
c. Delirium b. Aldosterone
d. Bradycardia c. Glucocorticoid
e. Very high fever d. Hydrocortisone

9. At times, it is necessary to give medications 12. In an acute adrenal crisis, the onset of symp-
that suppress the adrenal glands on a long- toms is sudden, and in the case of Addison
term basis. When the suppression of the disease, can be precipitated by exposure to a
adrenals becomes chronic, the adrenal glands minor illness or stress. What are the manifes-
atrophy. What does the abrupt withdrawal of tations of acute adrenal crisis? Mark all that
these suppressive drugs cause? apply.
a. Acute adrenal hyperplasia a. Hypertension
b. Acute adrenal insufficiency b. Muscle weakness
c. Acute adrenal hypoplasia c. Dehydration
d. Acute adrenal cortical hyperplasia d. Altered mental status
e. Vascular collapse
10. Congenital adrenal hyperplasia is a congenital
disorder in which a deficiency exists in any of 13. The hallmark manifestations of Cushing syn-
the enzymes necessary for the synthesis of drome are a moon face, a “buffalo hump” be-
cortisol. Infants of both genders are affected, tween the shoulder blades, and a protruding
although boys are not diagnosed at birth un- abdomen. What other manifestations of
less of enlarged genitalia. Female infants often Cushing syndrome occur?
have ambiguous genitalia because of the over- a. Thin extremities and muscle weakness
secretion of adrenal androgens. What are the
b. Muscle wasting and thickened extremities
manifestations of the ambiguous genitalia
caused by congenital adrenal hyperplasia? c. Muscle weakness and thickened extremi-
ties
a. Small clitoris, fused labia, and urogenital
sinus d. Thin extremities and increased strength
b. Small clitoris, open labia, and urogenital
sinus
c. Enlarged clitoris, fused labia, and urogeni-
tal sinus
d. Enlarged clitoris, open labia, and urogeni-
tal sinus

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42

CHAPTER
Diabetes Mellitus and
the Metabolic Syndrome

SECTION I: LEARNING 11. Differentiate between the causes and clinical

manifestations of diabetic ketoacidosis and
OBJECTIVES the hyperosmolar hyperglycemic state
1. State the functions of glucose, fats, and pro- 12. Describe alterations in physiologic function
teins in meeting the energy needs of the body that accompany diabetic peripheral neuropa-
thy, retinopathy, and nephropathy
2. Characterize the actions of insulin with refer-
ence to glucose, fat, and protein metabolism 13. Describe the causes of foot ulcers in people
with diabetes mellitus
3. Explain what is meant by counter-regulatory
hormones, and describe the actions of 14. Explain the relation between diabetes melli-
glucagon, epinephrine, growth hormone, and tus and infection
the glucocorticoid hormones in regulation of
blood glucose levels
4. Compare the distinguishing features of type 1 SECTION II: ASSESSING YOUR
and type 2 diabetes mellitus, list causes of UNDERSTANDING
other specific types of diabetes, and cite the
criteria for gestational diabetes Activity A Fill in the blanks.
5. Describe what is meant by the term predia- 1. The primary source of energy for the body is
betes .
6. Relate the physiologic functions of insulin to 2. Because the can neither synthe-
the manifestations of diabetes mellitus size nor store more than a few minutes’ sup-
7. Define the metabolic syndrome and describe ply of glucose, normal cerebral function
its associations with the development of type requires a continuous supply from the
2 diabetes circulation.

8. Discuss the role of diet and exercise in the 3. Severe and prolonged can cause
management of diabetes mellitus. brain death.

9. Characterize the blood glucose–lowering 4. Glucose that is not needed for energy is
actions of the hypoglycemic agents used in removed from the blood and stored as
treatment of type 2 diabetes or converted to fat.

10. Name and describe the types (according to 5. When blood glucose levels fall below normal,
duration of action) of insulin as they do between meals, a process called

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230 UNIT 10 DISORDERS OF ENDOCRINE FUNCTION

breaks down glycogen, and 19. diabetes mellitus is a heteroge-

glucose is released. neous condition that describes the presence
of hyperglycemia in association with relative
6. In addition to mobilizing its glycogen stores,
insulin deficiency.
the liver synthesizes glucose from amino
acids, glycerol, and lactic acid in a process 20. Insulin initially stimulates an
called . increase in insulin secretion, often to a level
of modest hyperinsulinemia, as the beta cells
7. Fat is the most efficient form of fuel storage,
attempt to maintain a normal blood glucose
providing kcal/g of stored en-
level.
ergy, compared with the kcal/g
provided by carbohydrates and proteins. 21. Although the insulin resistance seen in per-
sons with type 2 diabetes can be caused by a
8. are essential for the formation
number of factors, it is strongly associated
of all body structures, including genes, en-
with and .
zymes, contractile structures in muscle, bone
matrix, and hemoglobin of red blood cells. 22. A major factor in persons with the metabolic
syndrome that leads to type 2 diabetes is
9. Because cannot be converted to
.
glucose, the body must break down
and use the amino acids as a 23. diabetes mellitus refers to any
major substrate for gluconeogenesis during degree of glucose intolerance that is first
periods when metabolic needs exceed food detected during pregnancy.
intake.
24. The plasma glucose has been
10. Because cell membranes are impermeable to suggested as the preferred diagnostic test be-
glucose, they require a special carrier, called a cause of ease of administration, convenience,
, to move glucose from the blood patient acceptability, and cost.
into the cell.
25. A plasma glucose concentration
11. is the insulin-dependent glucose that is unequivocally elevated (
transporter for skeletal muscle and adipose mg/dL) in the presence of classic symptoms
tissue. of diabetes, such as polydipsia, polyphagia,
polyuria, and blurred vision, is diagnostic of
12. maintains blood glucose be-
diabetes mellitus at any age.
tween meals and during periods of fasting.
26. In uncontrolled diabetes or diabetes with hy-
13. The most dramatic effect of glucagon is its
perglycemia, there is an increase in the level
ability to initiate and
of in circulation.
.
27. Type 1 diabetes mellitus always requires treat-
14. The secretion of growth hormone normally is
ment with , and many people
inhibited by and increased lev-
with type 2 diabetes eventually require similar
els of blood glucose.
therapy.
15. is a disorder of carbohydrate,
28. Diabetic most commonly occurs
protein, and fat metabolism resulting from an
in a person with type 1 diabetes, in whom the
imbalance between insulin availability and
lack of insulin leads to mobilization of fatty
insulin need.
acids from adipose tissue because of the unsup-
16. A fasting plasma glucose of or a pressed adipose cell lipase activity that breaks
2-hour oral glucose tolerance test result of down triglycerides into fatty acids and glycerol.
is considered normal.
29. The is characterized by hyper-
17. diabetes mellitus is characterized glycemia (blood glucose 600 mg/dL), hyper-
by destruction of the pancreatic beta cells. osmolarity (plasma osmolarity 310 mOsm/L)
and dehydration, the absence of ketoacidosis,
18. The term type 1B diabetes is
and depression of the sensorium.
used to describe those cases of beta cell de-
struction in which no evidence of autoimmu- 30. are thought to produce struc-
nity is present. tural defects in the basement membrane of

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CHAPTER 42 DIABETES MELLITUS AND THE METABOLIC SYNDROME 231

the microcirculation and to contribute to eye, Activity C

kidney, and vascular complications.
1. Construct a flowchart, using the terms below,
31. The term is used to describe the that reflects hormonal and hepatic regulation
combination of lesions that often occur con- of blood glucose.
currently in the diabetic kidney.
• decreased blood glucose
32. is characterized by abnormal • removal of glucose from blood
retinal vascular permeability, microaneurysm • decreased glucagon
formation, neovascularization and associated • increased insulin release from beta cells
hemorrhage, scarring, and retinal detachment. • deceased hepatic glucose production
33. Multiple risk factors for , includ- • increased blood glucose
ing obesity, hypertension, hyperglycemia, hy- • decreased insulin and increased glucagon
perinsulinemia, hyperlipidemia, altered platelet and gluconeogenesis
function, endothelial dysfunction, systemic
inflammation, and elevated fibrinogen levels, Activity D Briefly answer the following
frequently are found in people with diabetes. questions.
1. What are the results/actions of insulin
Activity B Match the key terms in Column A release?
with their definitions in Column B.
Column A Column B
1. Incretin a. Three fatty acids linked
effect by a glycerol molecule
2. Somato- b. Produce inhibition of 2. How is insulin secretion from beta cells
statin gastric emptying and stimulated?
glucagon secretion
3. Epinephrine
c. Inhibit the release of
4. Secretago- insulin and glucagon
gues d. Increase insulin release
5. Adiponectin after an oral nutrient 3. Why are patients with type 1 diabetes mellitus
load especially likely to develop ketoacidosis?
6. Triglyceride
e. Agents that cause or
7. Somogyi stimulate secretion
effect f. Inhibits insulin release
8. PPAR- and promotes
glycogenolysis
9. Amylin 4. What is thought to cause type 1 diabetes
g. Stimulate gluconeo-
mellitus?
10. Glucocorti- genesis by the liver
coid h. Increases tissue sensi-
11. Dawn phe- tivity to insulin
nomenon i. Nuclear receptor that
leads to the regulation
of genes controlling free 5. What are the metabolic changes that precede
fatty acids (FFA) levels the development of type 2 diabetes?
and glucose metabolism
j. Cycle of insulin-
induced posthypo-
glycemic episodes
k. Increased levels of fast-
ing blood glucose with-
out precursor
hypoglycemia

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232 UNIT 10 DISORDERS OF ENDOCRINE FUNCTION

6. How does beta cell dysfunction develop in 13. What are the common complications of
type 2 diabetes? chronic diabetes mellitus? How do they
develop?

7. What are the systemic manifestations of

metabolic syndrome? 14. What are the pathologic changes observed in
peripheral neuropathies that are associated
with chronic diabetes mellitus?

8. What are the effects of insulin resistance and

increased glucose production in obese pa-
tients with type 2 diabetes? 15. What are the effects of diabetes mellitus on
renal tissue?

9. What are the three “polys” and why are they

significant?
SECTION III: APPLYING YOUR
KNOWLEDGE
Activity E Consider the following scenario and
10. Why do patients with type 1 diabetes lose answer the questions.
weight? A 16-year-old boy is admitted to your unit with a
new diagnosis of type 1A diabetes mellitus. His
blood sugar on admission is 735; he is lethargic;
his parents state that he has started eating con-
tinuously; and he is urinating much more than
he usually does. They say he has lost 10 pounds
11. How does continuous subcutaneous insulin over the past few months without trying. The
infusion work? patient and his family state that they know
nothing about diabetes and ask you for an
explanation of the disorder.
1. You would know to include what information
in educating the patient and his family about
12. What are the three major challenges to nor- type 1A diabetes mellitus?
mal physiology from diabetic ketoacidosis
(DKA)?

2. The patient asks if there is any cure for type 1A

diabetes. You would know to respond:

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CHAPTER 42 DIABETES MELLITUS AND THE METABOLIC SYNDROME 233

SECTION IV: PRACTICING d. Diabetogenic gene from both parents, en-

vironmental triggering event, and a B lym-
FOR NCLEX phocyte reaction to alpha cell antigens
Activity F Answer the following questions. 5. Type 2 diabetes is caused by metabolic abnor-
malities in the presence of insulin. What are
1. The pancreas is an endocrine organ that is
these metabolic abnormalities? Mark all that
composed of the acini and the islets of
apply.
Langerhans. The islets of Langerhans have
alpha, beta, and delta cells as well as the PP a. Deranged secretion of insulin
cell. Which cells secrete insulin? b. Decreased glucose production by the liver
a. Alpha cells c. Insulin resistance
b. Beta cells d. Increased glucose production by the liver
c. Delta cells e. Hypersensitivity to insulin
d. PP cells 6. Secondary diabetes occurs because of disor-
2. Hormones that counteract insulin’s storage ders that produce hyperglycemia by stimulat-
function when regulating blood glucose dur- ing the hepatic production of glucose or
ing times when glucose intake is limited or decrease the cellular use of glucose. Which
glucose stores are depleted are called counter- disorders can cause secondary diabetes?
regulatory hormones. What are the counter a. Pheochromocytoma and Cushing syndrome
regulatory hormones? Mark all that apply. b. Pancreatic disease and dwarfism
a. Glucocorticoids c. Acromegaly and pancreatic hyperplasia
b. Growth hormone d. Hepatomegaly and pheochromocytoma
c. Catecholamines
7. Gestational diabetes mellitus (GDM) is a dis-
d. Mineralocorticoids order of glucose intolerance that occurs dur-
e. Glucagon ing pregnancy. It is associated with increased
risk for developing type 2 diabetes and with
3. During periods of fasting and starvation, the
fetal abnormalities. What fetal abnormalities
glucocorticoid and other corticosteroid hor-
are associated with GDM?
mones are critical for survival because of their
stimulation of gluconeogenesis by the liver. a. Microsomia and polycythemia
When the glucocorticoid hormones remain b. Macrosomia and hypocalcemia
elevated for extended periods of time what c. Hypercalcemia and hyperbilirubinemia
can occur?
d. Hypoglycemia and hypercalcemia
a. Hepatomegaly
8. What are the hallmark signs of diabetes
b. Portal hypertension
mellitus?
c. Hyperglycemia
a. Polyuria, polydipsia, and pheochromocy-
d. Adrenal hyperplasia toma
4. Type 1A diabetes is now considered an au- b. Polyuria, polyphagia, and polycythemia
toimmune disorder. What factors are consid- c. Polyuria, polydipsia, and polyphagia
ered necessary for type 1A diabetes to occur?
d. Polycythemia, polydipsia, and pheochro-
a. Genetic predisposition, environmental mocytoma
triggering event, and a T lymphocyte-
mediated hypersensitivity reaction against 9. Match the type of oral antidiabetic agent with
some beta cell antigen the name of a drug in its class.
b. Genetic predisposition, physiologic trigger- Type of
ing event, allergic reaction to pancreatic Antidiabetic Agent Drug
alpha cells
1. Insulin a. Exenatide
c. Diabetogenic gene from both parents, secretagogues b. Rosiglitazone
physiologic triggering event, and an aller-
gic reaction to pancreatic delta cells 2. Biguanides c. Metformin

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234 UNIT 10 DISORDERS OF ENDOCRINE FUNCTION

3. -Glucosidase d. Repaglinide 14. Peripheral neuropathies occur in people with

inhibitors e. Acarbose diabetes mellitus. With the loss of sensation
in the lower extremities, diabetics become
4. Thiazolidinediones f. Alogliptin
predisposed to what?
5. Dipeptidyl peptidase a. Denervation of the large muscles of the
4 (DPP-4) enzyme foot and bunions
inhibitors b. Displacement of the submetatarsal fat pad
6. Glucagonlike poly- posteriorly and hammer toes
peptide 1 agonists c. Impairment of temperature and touch
10. Diabetic ketoacidosis (DKA) is a condition sensations
that mostly occurs in type 1 diabetes. What d. Clawing of toes and denervation of the
are the definitive diagnostic criteria for DKA? small muscles of the foot
a. Blood glucose level 350 mg/dL; bicarbon- 15. Diabetics are at higher risk than most of the
ate 05 mEq/L and pH 7.4 population for injury to organ systems in the
b. Blood glucose level 250 mg/dL; bicarbon- body. Which organs are most at risk?
ate 25 mEq/L and pH 7.3 a. Kidneys and eyes
c. Blood glucose level 350 mg/dL; bicarbon- b. Kidneys and liver
ate 05 mEq/L and pH 7.4 c. Liver and eyes
d. Blood glucose level 250 mg/dL; bicarbon- d. Pancreas and eyes
ate 15 mEq/L and pH 7.3
16. Macrovascular disease includes coronary
11. A man is brought into the emergency depart- artery disease, cerebrovascular disease, and
ment by paramedics who state that he passed peripheral vascular disease. People with both
out on the street. The man smells of alcohol type 1 and type 2 diabetes are at high risk for
and when roused says he has not eaten since developing macrovascular disease. What are
yesterday. He is wearing a medic alert bracelet the risk factors for macrovascular disease in
that says he is a diabetic. What diagnosis diabetics? Mark all that apply.
would you suspect?
a. Elevated fibrinogen levels and hyperinsu-
a. Hypoglycemia linemia
b. Hyperglycemia b. Hyperlipidemia and hypotension
c. Hyponatremia c. Hyperglycemia and hypoinsulinemia
d. Hypernatremia d. Decreased fibrinogen levels and systemic
12. Hypoglycemia has a sudden onset with a pro- inflammation
gression of symptoms. What are the signs and 17. Diabetics are hospitalized for a number of rea-
symptoms of hypoglycemia? sons. What is the most common complica-
a. Difficulty problem solving and muscle tion of diabetes requiring hospitalization?
spasms a. Diabetic ketoacidosis
b. Altered cerebral function and headache b. Foot problems
c. Muscle spasms and headache c. Hypertensive crisis
d. Altered cerebral function and muscle d. Macrovascular disease
spasms
18. Infections are common in people with
13. Research has identified a cycle of insulin- diabetes. Which infection is thought to be
induced posthypoglycemic episodes. What related to a neurogenic bladder?
is this phenomenon called?
a. Nephrotic syndrome
a. Dawn phenomenon
b. Urinary retention
b. Joslin phenomenon
c. Pyelonephritis
c. Somogyi effect
d. Urinary incontinence
d. Sunset effect

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43

CHAPTER
Structure and
Function of the Male
Genitourinary System

SECTION I: LEARNING SECTION II: ASSESSING YOUR

OBJECTIVES UNDERSTANDING
1. Characterize the embryonic development of Activity A Fill in the blanks.
the male reproductive organs and genitalia
1. The male system is composed
2. Describe the structure and function of the of the paired gonads, or testes, genital ducts,
testes and scrotum, the genital ducts, accessory accessory organs, and penis.
organs, and penis
2. The testicular cells of a male embryo produce
3. Describe the process of spermatogenesis an , which prevents develop-
ment of the uterus and fallopian tubes in the
4. State the functions of testosterone
male, and testosterone.
5. Draw a diagram illustrating the secretion,
3. stimulates the wolffian ducts to
site of action, and feedback control of go-
develop into the epididymis, vas deferens,
nadotropin-releasing hormone, luteinizing
and seminal vesicles.
hormone, follicle-stimulating hormone and
inhibin 4. After descent of the testes, the
closes almost completely.
6. Describe the function of follicle-stimulating
hormone in terms of spermatogenesis 5. The male consist of the seminal
vesicles, the prostate gland, and the bul-
7. Describe the classification and clinical features
bourethral glands.
of male hypogonadism
6. The is a fibromuscular and glan-
8. Describe the autonomic and nonautonomic
dular organ lying just inferior to the bladder.
nervous system’s control of erection, emission,
and ejaculation 7. refers to the generation of sper-
matozoa or sperm.
9. Describe changes in the male reproductive
system that occur with aging

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236 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

8. is produced and secreted by the

interstitial Leydig’s cells in the testes.
9. All or almost all of the actions of testosterone
and other androgens result from increased
in target tissues.
10. The term has been used to de-
scribe an ill-defined collection of symptoms
in aging men, typically those older than
50 years, who have a relative or absolute
hypogonadism associated with aging.

Activity B Consider the following figures: 2. In the figure above, locate and label the fol-
lowing structures:
• deep penile fascia
• corpus cavernosum
• central artery
• corpus spongiosum
• urethra

Activity C
Match the key terms in Column A with their
definitions in Column B.
Column A Column B
1. SRY gene a. Expulsion of the
sperm from the
2. Cryptorchidism
urethra
3. Follicle- b. Sperm move from
stimulating the epididymis to
hormone the urethra
1. In the figure above, locate and label the follow- 4. Hypogonadism c. Persistent inability to
ing structures: achieve and main-
5. Erectile
• ampulla tain an erection
dysfunction
• urethra d. Androgen deficiency
• spongy urethra 6. Ejaculation
e. Initiation of sper-
• membranous urethra 7. Emission matogenesis
• prostatic urethra
8. Luteinizing f. Controls production
• seminiferous tubules
hormone of testosterone
• epididymis
• ductus deferens g. Becomes engorged
9. Corpora
• ejaculatory duct with blood during
cavernosa
• prostate gland erection
• urinary bladder opening 10. Seminiferous h. Site of sperm pro-
• urinary bladder surface tubules duction
• seminal vesicle i. Failure of the testes
• testis to descend into the
scrotum
j. The sex-determining
region of the Y chro-
mosome

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CHAPTER 43 STRUCTURE AND FUNCTION OF THE MALE GENITOURINARY SYSTEM 237

Activity D Briefly answer the following: 2. The diagnosis of secondary hypogonadism is

confirmed. The patient asks what the treatment
1. What are the endocrine changes that occur to will be. What would be your correct response?
stimulate male puberty?

2. Describe the process of spermatogenesis.

SECTION IV: PRACTICING
FOR NCLEX
Activity F Answer the following questions.
3. What are the side effects of excess synthetic 1. Sperm production by the testes is optimal at
androgens? 2°C to 3°C below body temperature. Two sys-
tems of the body maintain the temperature of
the testes at a level that allows sperm produc-
tion. What is the system that assists in main-
taining the testes at a temperature that allows
sperm production?
4. How does the penis become erect?
a. Pampiniform plexus
b. Testicular artery
c. Cremaster veins
d. Tunica vaginalis
2. Spermatozoa are produced in the seminiferous
tubules of the testes and are moved through
SECTION III: APPLYING YOUR the genital ducts to be stored in the ampulla of
the vas deferens before ejaculation through
KNOWLEDGE the penis. Unlike the female egg, which re-
mains briefly fertile, spermatozoa can remain
Activity E Consider the following scenario and
fertile for up to 42 days. Where are the sperma-
answer the questions.
tozoa stored so they maintain their fertility?
A 35-year-old man comes into the clinic com- a. Vas deferns
plaining of decreased sexual desire and activity,
b. Genital ducts
depression, and fatigue. He states that he and his
wife want to conceive, but he has developed erec- c. Ampulla
tile dysfunction and, over the last 6 months, he d. Epididymis
has lost a lot of his body hair. You consider a pos-
3. The fluid from both the vas deferens and the
sible diagnosis of impaired testosterone secretion
vagina are acidic. From where do the alkaline
or hypogonadism.
secretions that allow mobilization of sperm
1. For what tests would you expect to receive an come?
order? a. Vaginal vault
b. Genital ducts
c. Prostate
d. Urethra

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238 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

4. The penis is a soft, cylindrical shaft that is 7. The practice among some athletes of taking
outside the body. When sexual stimulation synthetic androgens to improve their perfor-
occurs the penis becomes firm and elongated mance in their sport can be physiologically
due to blood being trapped in what? Mark all harmful. What are the undesired effects of
that apply. the androgens taken by athletes in supraphys-
a. Corpus spongiosum iologic doses? Mark all that apply.
b. Corpora spongiosum a. Gynecomastia
c. Corpora cavernosa b. Azoospermia
d. Corpus cavernosa c. Increased testicular size
e. Corpus cavernosum d. Acne
e. Hypogonadism
5. Spermatogenesis, or generation of spermato-
zoa or sperm, begins at approximately 13 8. Sperm begin their life in the Sertoli cells.
years of age and continues as long as a man What factor functions in releasing mature
remains fertile. It is in the seminiferous spermatozoa from the Sertoli cells?
tubules that spermatogenesis takes place. Of a. Prostate secretions
what is the inner lining of the seminiferous
b. Plasminogen activator
tubules composed?
c. Testosterone
a. Epididymal cells
d. Androgen-binding protein
b. Leydig cells
c. Cowper cells 9. What can cause erectile dysfunction?
d. Sertoli cells a. Dysfunction of the pampiniform plexus
b. Damage to Leydig cells
6. The male reproductive system is controlled by
the hypothalamus and the anterior pituitary c. Dysfunction of pudendal nerves
gonadotropic hormones regulated by a nega- d. Damage to the Cowper gland
tive feedback loop. What gonadotropic hor-
10. The male reproductive system undergoes
mones regulate control of the male
changes as aging occurs. What is the term
reproductive system?
used to describe a relative or absolute hypog-
a. Follicle-stimulating hormone and luteiniz- onadism associated with aging?
ing hormone
a. Male menopause
b. Testosterone and antimüllerian hormone
b. Testosterone deficiency
c. Gonadotropic hormone and follicle-
c. Atherogenisis
stimulating hormone
d. Andropause
d. Testosterone and luteinizing hormone

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44

CHAPTER
Disorders of the Male
Genitourinary System

SECTION I: LEARNING 14. Compare the pathology and symptoms of

acute bacterial prostatitis, chronic bacterial
OBJECTIVES prostatitis, and chronic prostatitis/pelvic pain
syndrome
1. State the difference between hypospadias and
epispadias 15. Describe the urologic manifestations and
treatment of benign prostatic hyperplasia
2. Cite the significance of phimosis
16. List the methods used in the diagnosis and
3. Describe the anatomic changes that occur
treatment of prostate cancer
with Peyronie disease
4. Explain the physiology of penile erection and
relate it to erectile dysfunction and priapism
SECTION II: ASSESSING YOUR
5. Describe the appearance of balanitis xerotica UNDERSTANDING
obliterans
6. List the signs of penile cancer Activity A Fill in the blanks.

7. State the physical manifestations and poten- 1. and are congenital

tial risks associated with uncorrected cryp- disorders of the penis resulting from embry-
torchidism ologic defects in the development of the
urethral groove and penile urethra.
8. Compare the cause, appearance, and signifi-
cance of hydrocele, hematocele, spermato- 2. involves a localized and progres-
cele, and varicocele sive fibrosis of unknown origin that affects
the tunica albuginea.
9. State the difference between extravaginal and
intravaginal testicular torsion 3. The manifestations of disease
include painful erection, bent erection, and
10. Describe the symptoms of epididymitis the presence of a hard mass at the site of
11. State the manifestations and possible compli- fibrosis.
cations of mumps orchitis 4. Erection is under the control of the
12. Relate environmental factors to development nervous system, and ejaculation
of scrotal cancer and detumescence (penile relaxation) are under
the nervous system control.
13. State the cell types involved in seminoma,
embryonal carcinoma, teratoma, and chorio-
carcinoma tumors of the testes

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240 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

5. Parasympathetic stimulation results in release symptoms has been directed toward

of , which causes relaxation of sources.
trabecular smooth muscle of the corpora
18. The level of correlates with the
cavernosa, permitting inflow of blood into the
volume and stage of prostate cancer.
sinuses of the cavernosa at pressures approach-
ing those of the system.
Activity B Consider the following figure:
6. is commonly classified as psy-
chogenic, organic, or mixed psychogenic and
A
organic.
7. Erectile dysfunction, now recognized as a
marker for disease, is now con-
sidered a component of the
syndrome.
8. is caused by impaired blood
flow in the corpora cavernosa of the penis.
9. Several risk factors for have
been suggested, including increasing age,
poor hygiene, smoking, human papillo-
mavirus infections, ultraviolet radiation expo- B
sure, and immunodeficiency states.
10. The consequences of include
infertility, malignancy, testicular torsion, and
the possible psychological effects of an empty
scrotum.
11. Sperm concentration and are
decreased in men with varicocele.
12. is an inflammation of the epi- In the figure above, locate and label the struc-
didymis, the elongated cordlike structure that tures responsible for penile erection:
lies along the posterior border of the testis,
whose function is the storage, transport, and • deep dorsal vein
maturation of spermatozoa. • tunica albuginea
• corpora cavernosa
13. refers to a variety of inflamma- • cavernous artery
tory disorders of the prostate gland, some • sinusoidal spaces
bacterial and some not. • circumflex vein
14. The manifestations of include • circumflex artery
fever and chills, malaise, myalgia, arthralgia, • cavernous nerve
frequent and urgent urination, dysuria, and • dorsal nerve
urethral discharge. • dorsal artery
• subtunical venular plexus
15. As with other cancers, it appears that the de-
velopment of cancer is a multi- Activity C Match the key terms in Column A
step process involving genes that control cell with their definitions in Column B.
differentiation and growth.
Column A Column B
16. Men with typically have recur-
rent urinary tract infections with persistence 1. Balanitis a. Inflammation of the
of the same strain of pathogenic bacteria in glans penis
2. Smegma
prostatic fluid and urine. b. Undescended testes
3. Epispadias
17. The cause of noninflammatory prostatitis is c. Accumulation under
unknown, but because of the absence of 4. Hydrocele the phimotic foreskin
inflammation, the search for the cause of

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CHAPTER 44 DISORDERS OF THE MALE GENITOURINARY SYSTEM 241

5. Cryptorchi- d. Excess fluid collects be- 6. How is prostate cancer diagnosed?

dism tween the layers of the
tunica vaginalis
6. Orchitis
e. Infection of the testes
7. Prostatitis
f. Inflammation of the
8. Benign prostate
prostatic g. Tightening of the pe-
hyperplasia nile foreskin
SECTION III: APPLYING YOUR
9. Phimosis h. Opening of the urethra
KNOWLEDGE
is on the dorsal surface
10. Priapism Activity E Consider the following scenario and
of the penis
answer the questions.
i. Involuntary, prolonged,
abnormal, and painful A 50-year-old man presents at the clinic complain-
erection ing of a lump on his penis that has progressed
over the past 4 months until he can no longer re-
j. An age-related, non-
tract the foreskin over his glans. He states the
malignant enlargement
condition is now painful. He is having difficulty
of the prostate gland
urinating, and a discharge is coming from under
his foreskin. He is scheduled for surgery the fol-
Activity D Briefly answer the following
lowing day to relieve the phimosis and biopsy the
questions.
lump. The physician explains the surgery to him
1. What are some of the known causes of erectile and states that, if the lump is malignant, a partial
dysfunction? or total penectomy may be necessary.
1. Before the patient leaves, he asks you what
causes penile cancer. You correctly respond:

2. How do drugs like Viagra treat erectile

dysfunction?
2. The patient is admitted to your unit after hav-
ing a total penectomy for penile cancer with
inguinal lymph node involvement. While car-
ing for him, the client asks you what his prog-
3. What is testicular torsion? What are the nosis is. What would be your correct response
different types? to him?

4. How are testicular cancers staged?

SECTION IV: PRACTICING
FOR NCLEX
Activity F Answer the following questions.

5. How does benign prostatic hyperplasia cause 1. In hypospadias, the treatment of choice is
obstruction of the urethra? surgery to repair the defect. What influences
the timing of the surgical repair? Mark all
that apply.

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242 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

a. Penile size a. Testicular torsion

b. Testicular involvement b. Hypospadias
c. Psychological effects on a child c. Balanitis
d. Presence of an abdominal hernia d. Paraphimosis
e. Anesthetic risk 7. Epididymitis can be sexually transmitted, or
2. A 75-year-old man presents at the clinic com- it can be caused by a variety of other reasons,
plaining of pain during intercourse and an including abnormalities in the genitourinary
upward bowing of his penis during erection. tract. What are the most common causes of
His history includes an inflammation of the epididymitis in young men without underly-
penis that was treated 3 months ago. The ing genitourinary disease?
physician’s physical examination of him a. Chlamydia trachomatis and Candida albicans
notes beads of scar tissue along the dorsal b. Chlamydia trachomatis and Neisseria gonor-
midline of the penile shaft. What would be rhoeae
the suggested diagnosis for this patient?
c. Escherichia coli and Neisseria gonorrhoeae
a. Peyronie disease
d. Candida albicans and Escherichia coli
b. Cavernosa disease
8. Testicular cancer is highly curable if found
c. Balanitic disease
and treated early. What are signs of metasta-
d. Paraphimosic disease tic spread of testicular cancer? Mark all that
3. Priaprism (a prolonged painful erection not apply.
associated with sexual excitement) can occur a. Hemoptysis
at any age. In boys, ages 5 to 10 years, what b. Back pain
are the most common causes of priapism?
c. Neck mass
a. Neoplasms or hemophilia
d. Chest mass
b. Sickle cell disease or neoplasms
e. Hoarse voice
c. Hemophilia or sickle cell disease
9. A 40-year-old man presents at the clinic com-
d. Hypospadias or neoplasms
plaining of painful urination and rectal pain.
4. Cryptorchidism, left untreated, is a high risk His vital signs are as follows: temperature
for testicular cancer and infertility. What are 101.7F; blood pressure 105/74 mm Hg; pulse
the treatment goals for boys with cryp- 98; respiratory rate 22. While taking a history,
torchidism? you note that the patient has had chills,
a. Prevention of testicular cancer malaise, and myalgia. What would you
suspect as a diagnosis?
b. Prevention of an associated inguinal hernia
a. Benign prostatic hyperplasia
c. Easier cancer detection
b. Epididymitis
d. Decreased fertility
c. Acute bacterial prostatitis
5. The mother of a 5-year-old boy brings him
d. Orchitis
into the clinic because of a firm swelling
around one of his testes. What diagnosis is 10. Although the cause of benign prostatic hyper-
suggested? plasia (BPH) is unknown, its incidence in-
a. Peyronie disease creases with age. In which ethnic group is
BPH highest?
b. Cryptorchidism
a. Japanese
c. Priapism
b. Caucasian
d. Hydrocele
c. Native American
6. In the neonatal and pediatric population,
d. African American
there can be many physiologic problems with
the male genitourinary system. What is the
most common acute scrotal disorder in the
pediatric population?

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45

CHAPTER
Structure and
Function of the Female
Reproductive System

SECTION I: LEARNING 12. Describe the physiology of normal

menopause
OBJECTIVES
13. Describe the anatomy of the female breast
1. Describe the anatomic relationship of the
14. Describe the influence of hormones on breast
structures of the external genitalia
development
2. Name the three layers of the uterus and
15. Characterize the changes in breast structure
describe their function
that occur with pregnancy and lactation
3. Cite the location of the ovaries in relation to
the uterus, fallopian tubes, broad ligaments,
and ovarian ligaments SECTION II: ASSESSING YOUR
4. Explain the function of the fallopian tubes UNDERSTANDING
5. State the function of endocervical secretions
Activity A Fill in the blanks.
6. Describe the feedback control of estrogen and
1. The is a rounded, skin-covered
progesterone levels by means of gonadotropin-
fat pad located anterior to the symphysis pubis.
releasing hormone, LH, FSH, and ovarian
follicle function 2. The are analogous to the male
scrotum.
7. List the actions of estrogen and progesterone
3. The begin anteriorly at the
8. Describe the four functional compartments of
hood of the clitoris and end posteriorly at the
the ovary
base of the vagina.
9. Relate FSH and LH levels to the stages of folli-
4. The female is an erectile organ,
cle development and to estrogen and proges-
rich in vascular and nervous supply.
terone production
5. The functions as a route for
10. Describe the endometrial changes that occur
discharge of menses and other secretions.
during the menstrual cycle
6. The is a thick-walled muscular
11. Describe the composition of normal cervical
organ, located between the bladder and the
mucus and the changes that occur during the
rectum.
menstrual cycle

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244 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

7. The uterus is supported on both sides by four 18. As estrogen suppresses FSH, the actions of LH
sets of ligaments: the ligaments, predominate, and the mature follicle bursts;
which run laterally from the body of the the , with the corona radiata, is
uterus to the pelvic sidewalls; the ejected from the follicle.
ligaments, which run from the
19. If fertilization does not take place, the corpus
fundus laterally into each labium majus;
luteum atrophies and is replaced by white
the ligaments, which run from
scar tissue called the ; the hor-
the uterocervical junction to the sacrum;
monal support of the endometrium is with-
and the cervical ligaments.
drawn and occurs.
8. The forms the major portion of
20. In the event of fertilization, is
the uterine wall.
produced by the trophoblastic cells in the
9. The superficial layer of the is blastocyst and prevents luteal regression.
shed during menstruation and regenerated by
21. The functional layer of the
cells of the basal layer.
arises from the basal layer and undergoes pro-
10. The end of the nearest the ovary liferative changes and menstrual sloughing.
forms a funnel-like opening with fringed,
22. The absence of of cervical
finger-like projections, called fimbriae, which
mucus can indicate inadequate estrogen stim-
pick up the ovum after its release into the
ulation of the endocervical glands or inhibi-
peritoneal cavity after ovulation.
tion of the endocervical glands by increased
11. The ovaries have a dual function: they store secretion of progesterone.
the female germ cells, or ova, and produce
23. results from the gradual cessa-
the female sex hormones, and
tion of ovarian function and the resultant
.
diminished levels of estrogen.
12. Growth, prepubertal maturation, the repro-
24. Problems that can arise from menopause are a
ductive cycle, and sex hormone secretion are
result of and include vaginal
regulated by and
dryness, urinary stress incontinence, urgency,
from the anterior pituitary gland.
nocturia, vaginitis, and urinary tract infec-
13. The steroid hormones enter tion.
cells by passive diffusion, bind to specific re-
25. Consequences of long-term estrogen depriva-
ceptor proteins in the cytoplasm, and then
tion include due to an imbal-
move to the nucleus, where they bind to spe-
ance in bone remodeling, and an increased
cific sites on the chromosomes.
risk for disease, which is the
14. Androgens can be converted to estrogens leading cause of death for women after
peripherally, especially in . menopause.
15. Observational studies indicate a possible pre- 26. The are specialized glandular
ventative role of estrogen in the development structures that have an abundant shared ner-
of Alzheimer disease through vous, vascular, and lymphatic supply.
mechanisms to prevent vascular injury, in-
27. stimulates increased vascularity
creased cerebral blood flow, and altered brain
of the breasts and the growth and extension
activation.
of the ductile structures, causing “heaviness”
16. The corpus luteum of the ovary secretes large of the breasts.
amounts of after ovulation.
28. causes marked budding and
17. The local effects of progesterone on reproduc- growth of the alveolar structures.
tive organs include the glandular develop-
ment of the lobular and alveolar tissue of the
breasts and the cyclic glandular development
of the .

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CHAPTER 45 STRUCTURE AND FUNCTION OF THE FEMALE REPRODUCTIVE SYSTEM 245

Activity B Consider the following figures:

1. In the figure above, locate and label the fol- • fallopian tube
lowing structures of the female reproductive • ovary
system: • urinary bladder
• pubic symphysis
• uterus
• clitoris
• cervix
• urethra
• vagina
• vaginal orifice
• anus

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246 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

Frequent site of implantation Site of fertilization

Path of oocyte
Ruptured
ovarian
follicle

Path of sperm

2. In the figure above, locate and label the follow- g. Hormone that stimu-
ing structures of female reproductive organs: lates lactation in the
postpartum period
• ovary
• uterine tube h. Tissue located poste-
• fimbriae rior to the vaginal
• ovarian ligament opening and ante-
• fundus rior to the anus
• suspensory ligament of ovary i. Glands at urethral
• broad ligament opening with lubri-
• uterosacral ligament cating function
• cardinal ligament j. First menstrual
• round ligament of uterus bleeding

Activity C Match the key terms in Column A Activity D Briefly answer the following.
with their definitions in Column B.
1. How and why is the vagina kept at an acidic
Column A Column B pH?
1. Oogenesis a. Technique to exam-
ine properties of cer-
2. Menarche
vical mucus
3. Dyspareunia b. Cessation of men-
4. Perineal body strual cycles 2. What relationship is there between body com-
c. Painful intercourse position and a normal menstrual cycle?
5. Spinnbarkeit
d. Pain accompanying
6. Prolactin the contractions as-
7. Skene glands sociated with menses
e. Sebaceous glands
8. Menopause
that keep the nipple
9. Dysmenorrhea area soft and elastic
10. Montgomery f. Generation of ova by
tubercles mitotic division

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CHAPTER 45 STRUCTURE AND FUNCTION OF THE FEMALE REPRODUCTIVE SYSTEM 247

3. What is the cardioprotective effect of estro- 2. The patient asks if HT can reverse the symp-
gen? toms of aging (e.g., decrease in body hair and
subcutaneous fat) in her body? You would
know that the best response is what?

4. What is the normal role of estrogen in female

development?

SECTION IV: PRACTICING

FOR NCLEX
5. What were the posited benefits of hormone Activity F Answer the following questions.
replacement therapy? How has it been shown
to be incorrect? 1. The female external genitalia are made up of
several components. What is in the vestibule
of the female external genitalia?
a. Bartholin glands
b. Skene glands

6. How does lactation occur? c. Cowper glands

d. Bulbourethral glands
2. Estrogen stimulates the vaginal wall to
thicken and increase the secretion of glyco-
gen. What causes the glycogen in the vagina
to ferment to lactic acid?
a. Escherichia coli
SECTION III: APPLYING YOUR b. Döderlein’s bacilli
KNOWLEDGE c. Candida albicans
d. Staphylococcus aureus
Activity E Consider the following scenario and
answer the questions. 3. The perimetrium reflects over the bladder
wall and forms what?
A 55-year-old woman has just been told by her a. Opening to fallopian tubes
physician that she is going through menopause.
The physician discusses with her the adverse ef- b. The external cervical os
fects menopause can have on a woman’s body c. The pouch of Douglas
and explains that most of these effects are caused d. Bartholin’s pouch
by a significant decrease in the estrogen level of
estrogen in her body. After leaving the clinic, the 4. The fallopian tubes are narrow tubes that at-
patient calls back and, speaking with you, asks tach bilaterally to the uterus. Within the fal-
about hormone replacement therapy. lopian tube, fertilization of the ovum takes
place. The end of the fallopian tube nearest
1. What information about hormone therapy the ovary is funnel-like. What are the fringed,
(HT) would you tell her? fingerlike projections around the funnel-
shaped opening of the fallopian tube called?
a. Fallopian fingers
b. Oviducts
c. Cilia
d. Fimbriae

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248 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

5. The ovarian follicle becomes luteinized once 8. Menopause signals the end of the menstrual
ovulation has taken place. As the corpus lu- cycle. It is caused by the end of ovarian func-
teum, the now empty follicle produces what? tion and the decreased levels of estrogen this
a. Estrogen and progesterone brings to the body. What are problems that
can arise from the onset of menopause? Mark
b. Follicle-stimulating hormone and luteiniz-
all that apply.
ing hormone
a. Nocturia
c. Testosterone and estrogen
b. Urinary stress incontinence
d. Glycogen and testosterone
c. Upper respiratory infection
6. The ovaries secrete both estrogen and proges-
d. Vaginitis
terone. What is one function of progesterone
in the body? e. Urinary retention
a. Causes moderate retention of sodium and 9. What are the small bumps or projections on
water the areolar surface called?
b. Increases body temperature at ovulation a. Cowper cells
c. Reduces levels or rennin b. Bartholin gland
d. Enhances the coagulability of blood c. Climacteric glands
7. Follicle-stimulating hormone (FSH) and d. Montgomery tubercles
luteinizing hormone (LH) produce profound 10. Lactation occurs under the control of the an-
effects on the ovaries. What do high levels of terior pituitary hormone prolactin. What
estrogen do to FSH and LH? causes the ejection of milk from the ductile
a. cFSH and TLH system in the breast?
b. cLH and Testradiol a. Oxytocin
c. c LH and T FSH b. Prolactin
d. c FSH and T renin c. Estrogen
d. Progesterone

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46

CHAPTER
Disorders of the Female
Reproductive System

SECTION I: LEARNING unopposed estrogen stimulation of the en-

dometrium and development of endometrial
OBJECTIVES cancer
1. Compare the abnormalities associated with 11. Compare the location and manifestations of
Bartholin cyst, non-neoplastic epithelial dis- intramural and subserosal leiomyomas
orders, vulvodynia, and cancer of the vulva
12. List the common causes and symptoms of
2. State the role of Döderlein bacilli in main- pelvic inflammatory disease
taining the normal ecology of the vagina
13. Describe the risk factors and symptoms of
3. Describe the conditions that predispose to ectopic pregnancy
vaginal infections and the methods used to
14. State the underlying cause of ovarian cysts
prevent and treat these infections
15. Differentiate benign ovarian cyst from poly-
4. Describe the importance of the cervical trans-
cystic ovary syndrome
formation zone in the pathogenesis of cervi-
cal cancer 16. List the hormones produced by the three
types of functioning ovarian tumors
5. Compare the lesions associated with naboth-
ian cysts and cervical polyps 17. State the reason that ovarian cancer may be
difficult to detect in an early stage
6. List the complications of untreated cervicitis
18. Characterize the function of the supporting
7. Describe the development of cervical cancer
ligaments and pelvic floor muscles in main-
from the appearance of atypical cells to the
taining the position of the pelvic organs, in-
development of invasive cervical cancer and
cluding the uterus, bladder, and rectum
relate to the importance of the Pap smear in
early detection of cervical cancer 19. Describe the manifestations of cystocele, rec-
tocele, and enterocele
8. Cite the rationale for describing cervical can-
cer as a sexually transmitted infection and 20. Explain how uterine anteflexion, retroflexion,
the rationale for use of the HPV vaccine in and retroversion differ from normal uterine
prevention of cervical cancer position
9. Compare the pathology and manifestations 21. Describe the cause and manifestations of
of endometriosis and adenomyosis uterine prolapse
10. Cite the major early symptom of endometrial
cancer and describe the relationship between

249
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250 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

22. Define the terms amenorrhea, hypomenor- 6. represents an inflammation of

rhea, oligomenorrhea, menorrhagia, metror- the vagina that is characterized by vaginal
rhagia, and menometrorrhagia discharge and burning, itching, redness, and
swelling of vaginal tissues.
23. Relate the alteration in estrogen and proges-
terone levels to the development of dysfunc- 7. The most common symptom of vaginal carci-
tional menstrual cycles noma is abnormal .
24. Differentiate between primary dysmenorrhea 8. During , the newly developed
and secondary dysmenorrhea squamous epithelial cells of the cervix are
vulnerable to development of dysplasia
25. Characterize the manifestations of the pre-
and genetic change if exposed to cancer-
menstrual syndrome, its possible causes, and
producing agents.
the methods of treatment
9. cancer is readily detected and, if
26. Describe changes in breast function that
detected early, is the most easily cured of all
occur with galactorrhea, mastitis, and ductal
the cancers of the female reproductive
ectasia
system.
27. Describe the manifestations of fibrocystic
10. Untreated may extend to in-
breast changes
clude the development of pelvic cellulitis, low
28. Cite the risk factors for breast cancer, the im- back pain, dyspareunia, cervical stenosis, dys-
portance of clinical breast examination, and menorrhea, and ascending infection of the
recommendations for mammography uterus or fallopian tubes.
29. Describe the methods used in the diagnosis 11. are the most common lesions of
and treatment of breast cancer the cervix.
30. Provide a definition of infertility 12. A preponderance of evidence suggests a
causal link between infection
31. List male and female factors that contribute
and cervical cancer.
to infertility
13. is the condition in which func-
32. Briefly describe methods used in the treat-
tional endometrial tissue is found in ectopic
ment of infertility
sites outside the uterus.
14. is the condition in which en-
dometrial glands and stroma are found
SECTION II: ASSESSING YOUR within the myometrium, interspersed be-
UNDERSTANDING tween the smooth muscle fibers.
15. and , which con-
Activity A Fill in the blanks. sists of dilating the cervix and scraping the
1. Diseases of the external genitalia are similar uterine cavity, is the definitive procedure for
to those that affect skin else- diagnosis of endometrial cancer because it
where in the body. provides a more thorough evaluation.

2. The is particularly susceptible to 16. Uterine are benign neoplasms of

skin infections because it is constantly being smooth muscle origin.
exposed to secretions and moisture. 17. is a polymicrobial infection of
3. A is a fluid-filled sac that results the upper reproductive tract associated with
from occlusion of the duct system in sexually transmitted and endogenous organ-
Bartholin’s gland. isms.

4. presents as thickened, gray- 18. occurs when a fertilized ovum

white plaques with an irregular surface. implants outside the uterine cavity, the most
common site being the fallopian tube.
5. The normal vaginal depends on
the delicate balance of hormones and bacter- 19. Disorders of the ovaries frequently cause
ial flora. and problems.

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CHAPTER 46 DISORDERS OF THE FEMALE REPRODUCTIVE SYSTEM 251

20. syndrome is characterized by Activity B Consider the following figure:

varying degrees of menstrual irregularity,
signs of hyperandrogenism, and infertility.
21. Most women with polycystic ovary syndrome
(PCOS) have elevated levels
with normal estrogen and follicle-stimulating
hormone (FSH) production.
22. tumors are common, most are
benign, but malignant tumors are the leading
cause of death from reproductive cancers.
23. The most significant risk factor for ovarian
cancer appears to be —the
length of time during a woman’s life when
her ovarian cycle is not suppressed by preg-
nancy, lactation, or oral contraceptive use.
24. The breast cancer susceptibility genes,
BRACA1 and BRCA2, which are
genes are incriminated in approximately 10%
of hereditary ovarian cancers despite being
identified as breast cancer genes.
In the figure above, locate and label all the com-
25. is the herniation of the rectum
mon locations of endometriosis within the pelvis
into the vagina.
and abdomen.
26. Uterine prolapse is the bulging of the uterus
into the vagina that occurs when the Activity C Match the key terms in Column A
ligaments are stretched. with their definitions in Column B.

27. Removal of the uterus through the vagina 1.

with appropriate repair of the vaginal wall Column A Column B
often is done when is accompa-
nied by cystocele or rectocele. 1. Papanicolaou a. Insertion of ra-
smear dioactive materials
28. Primary is the failure to men- into the body
struate by 15 years of age or by 13 years of age 2. Menorrhagia
b. Commonly called
if failure to menstruate is accompanied by ab- 3. Vulvodynia fibroids
sence of secondary sex characteristics.
4. Leiomyomas c. Unexplained
29. is the secretion of breast milk in vulvar pain
a nonlactating breast. 5. Cystocele
d. Herniation of the
30. is inflammation of the breast. 6. Curettage bladder into the
7. Atrophic vagina
31. are firm, rubbery, sharply de-
fined round masses in breast tissue. vaginitis e. Inflammation of
the vagina that
32. changes usually present as 8. Lichen
occurs after
nodular granular breast masses that are more sclerosus
menopause
prominent and painful during the luteal or 9. Brachytherapy f. Surgical procedure
progesterone-dominant portion of the men-
10. Cervicitis used to scrape out
strual cycle.
the surface of the
33. disease presents as an eczemoid endometrium
lesion of the nipple and areola. g. Inflammation of
34. is the inability to conceive a the cervix
child after 1 year of unprotected intercourse. h. Excessive men-
strual bleeding

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252 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

i. Vaginal cytology to 5. What is the mechanism of infection in pelvic

detect vaginal or inflammatory disease?
cervical cancer
j. Inflammatory dis-
ease of the vulva
2.
Column A Column B 6. Why should you be concerned about the fu-
ture of your patient with polycystic ovarian
1. Amenorrhea a. Frequent syndrome?
menstruation
2. Hypo-
menorrhea b. Infrequent
menstruation
3. Oligo-
c. Bleeding between
menorrhea
periods
4. Poly- 7. Describe the functional anatomy of normal
d. Absence of
menorrhea pelvic support.
menstruation
5. Menorrhagia e. Heavy bleeding
during and between
6. Metrorrhagia
menstrual periods
7. Meno- f. Scanty menstruation
metrorrhagia 8. Describe the alterations in a normal period and
g. Excessive men-
struation name the hormone thought to be responsible.

Activity D Briefly answer the following.

1. What measures should be taken to avoid vagi-
nal infections?
9. What is the genetic component of breast cancer?

2. What is the only approved vaccine for cervical

cancer and how does it work?

SECTION III: APPLYING YOUR

KNOWLEDGE
Activity E Consider the following scenario and
3. What is the normal method of detecting/diag- answer the questions.
nosis cervical cancer?
A 23-year-old woman is being seen in her physi-
cian’s office as a follow-up to an abnormal Pa-
panicolaou smear. The physician tells the patient
that she may have cervical cancer, and he wants
to do a colposcopy so he can diagnose and treat
4. What are the three most prominent theories of any lesions he may find. The patient gives her
the pathogenesis of endometriosis? consent.
1. While preparing the patient for the procedure,
she asks you for an explanation of the

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CHAPTER 46 DISORDERS OF THE FEMALE REPRODUCTIVE SYSTEM 253

colposcopy and the reason it is being done. c. Poor hygiene

How would you correctly respond? d. Vaginal deodorants
e. Tampon
4. The endocervix is covered with large-
branched mucous secreting glands. During
the menstrual cycle, they undergo functional
2. The colposcopy shows dysplastic lesions, and changes, and the amount and properties of
the physician wants to do a large loop electro- the mucus that they secret varies according to
surgical excision procedure (LEEP) of the the stage of the cycle. When one of these
transformation zone. The patient gives her glands gets blocked, what kind of cyst forms
consent, but wants to know what this proce- within the cervix?
dure is. How would you explain the procedure a. Bartholin cysts
to the patient?
b. Bulbouretheral cysts
c. Nabothian cysts
d. Metaplastic cysts
5. Endometriosis is the condition where en-
dometrial tissue is found growing outside of
the uterus in the pelvic cavity. What are risk
SECTION IV: PRACTICING factors for endometriosis?
FOR NCLEX a. Late menarche and regular periods with
longer cycles than 27 days
Activity F Answer the following questions.
b. Early menarche and lighter flow
1. Bartholin gland obstruction of the ductal sys- c. Increased menstrual pain and periods of
tem will cause a cyst. Sometimes the cyst be- shorter than 7 days
comes infected and an abscess occurs. What is
d. Periods longer than 7 days and increased
the surgical procedure to remove a Bartholin
menstrual pain
cyst or abscess when a wedge of vulvar skin is
removed along with the cyst wall? 6. Leiomyomas, or intrauterine fibroids, are
a. Marsupialization the most common form of pelvic tumor.
Approximately half the time leiomyomas are
b. Vulvectomy
asymptomatic. What are the symptoms of
c. Bartholectomy leiomyomas that are not asymptomatic?
d. Incision and drainage a. Anemia and urinary frequency
2. There are two types of vulvar cancer. One b. Diarrhea and rectal pressure
type is found in older women, and one type is c. Menorrhagia and urinary retention
found in younger women, generally younger
d. Abdominal distention and diarrhea
than 40 years of age. The type found in
younger women thought to be caused by 7. An 18-year-old woman presents at the clinic
which of the following? complaining new-onset breakthrough bleed-
a. Multiple sexual partners ing, even though she is on contraceptives.
What contraceptive use, along with new-
b. Human papillomavirus (HPV)
onset breakthrough bleeding, has been associ-
c. Nonsquamous cell lesions ated with pelvic inflammatory disease.
d. Lichen sclerotic lesions a. Intrauterine device
3. Vaginal infections can occur in young girls b. Depo-Provera
before menarche. These infections generally c. Spermicidal foam
have nonspecific causes. What are some of
d. Diaphragm
the causes of vaginal infections in premenar-
chal girls? Mark all that apply. 8. Ectopic pregnancies are true gynecologic
a. Presence of foreign bodies emergencies and are considered the leading
cause of maternal death in the first trimester.
b. Intestinal parasites

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254 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

What diagnostic test would you expect to have c. Acetaminophen

ordered for a suspected ectopic pregnancy? d. Metformic acid
a. Transvaginal ultrasound if pregnancy is 5
13. Mastitis is an inflammation of the breast that
weeks’ gestation
can occur at any time. What is the treatment
b. Serial -human chorionic gonadotropin for mastitis?
(hCG) with higher than normal hCG pro-
a. Opioid analgesics
duction
b. Nonsteroidal anti-inflammatory drugs
c. Ultrasonography followed by serial hCG tests
c. Application of heat or cold
d. Amniocentesis
d. Tylenol 3
9. Polycystic ovary syndrome is an endocrine dis-
order and a common cause of chronic anovula- 14. Fibrocystic changes in the breast are not un-
tion. In addition to the clinical manifestations common. How is the diagnosis of fibrocystic
of PCOS, long-term health problems, including changes made?
cardiovascular disease and diabetes, have been a. Physical examination and client history
linked to PCOS. What drug has emerged as an b. Galactography and biopsy
important part of PCOS treatment?
c. Mammography and galactography
a. Dehydroepiandrosterone
d. Ultrasonography and mammography
b. Methotrexate
15. Cancer of the breast is the most common can-
c. Mineralocorticoids
cer in women. Many breast cancers are found
d. Metformin by women themselves while doing breast self-
10. Ovarian cancer, once thought to be asympto- examination. When should postmenopausal
matic, has now been shown to produce non- women perform breast self-examination?
specific symptoms, which makes the diagnosis a. Any day of the month
of ovarian cancer difficult. What symptoms b. 2 days following menses
are believed to have a strong association to
c. On the first day of every month
ovarian cancer? Mark all that apply.
d. On the 15th of every month
a. Difficulty eating
b. Increased intestinal gas 16. The causes of infertility can be in either the
male or the female. Male tests for infertility
c. Bloating
require a specimen of ejaculate that is col-
d. Increased appetite lected when?
e. Abdominal or pelvic pain a. Any time
11. Uterine prolapse is a disorder of pelvic sup- b. After 3 days of abstinence
port and uterine position. It can range in c. After 3 consecutive days of intercourse
severity from a slight descent of the uterus
d. After 3 weeks of abstinence
into the vagina, all the way to the entire
uterus protruding through the vaginal open- 17. Couples who are being treated for infertility
ing. In women who want to have children or often choose to try in vitro fertilization (IVF).
in older women who are at significant risk if When using this technique, the eggs are in-
surgery is performed, what device is inserted seminated with sperm in a culture dish. After
to hold the uterus in place? a period of time, the ova are evaluated for
a. A pessary signs of fertilization. If signs of fertilization
are present, when are the fertilized eggs
b. A Colpexin sphere
placed in the woman’s uterus?
c. A vesicourethral suspenser
a. 12 to 24 hours after egg retrieval
d. A retroversion inducer
b. 36 to 48 hours after egg retrieval
12. In primary dysmenorrheal when contraception c. 48 to 72 hours after egg retrieval
is not desired, what is the treatment of choice?
d. 24 to 36 hours after egg retrieval
a. Aspirin
b. Ibuprofen

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47

CHAPTER
Sexually Transmitted
Infections

SECTION I: LEARNING SECTION II: ASSESSING YOUR

OBJECTIVES UNDERSTANDING
1. Define what is meant by a sexually transmit- Activity A Fill in the blanks.
ted infection (STI)
1. STIs can selectively infect the
2. List common portals of entry for STIs tissues of the external genitalia, primarily
cause vaginitis in women, or they can pro-
3. Name the organisms responsible for condylo-
duce both genitourinary and systemic
mata acuminata, genital herpes, molluscum
effects.
contagiosum, chancroid, granuloma in-
guinale, and lymphogranuloma venereum 2. STIs can be transmitted by an infected
mother to a , causing congenital
4. State the significance of being infected with
defects or death of the child.
high-risk strains of the human papillomavirus
3. are caused by the human papil-
5. Explain the pathogenesis of recurrent genital
lomavirus (HPV).
herpes infections
4. Genital warts typically present as soft, raised,
6. State the difference between wet-mount slide
fleshy lesions on the , including
and culture methods of diagnosis of STIs
the penis, vulva, scrotum, perineum, and
7. Compare the signs and symptoms of infec- perianal skin.
tions caused by Candida albicans, Trichomonas
5. is one of the most common
vaginalis, and bacterial vaginosis
causes of genital ulcers in patients in the
8. Compare the signs and symptoms of gonor- United States.
rhea in the male and female
6. Herpes simplex virus type-1 and herpes sim-
9. Describe the three stages of syphilis plex virus type-2 are viruses,
meaning that they grow in neurons and share
10. State the genital and nongenital complica-
the biologic property of latency.
tions that can occur with chlamydial infec-
tions, gonorrhea, and syphilis 7. Herpes simplex virus is responsi-
ble for greater than 90% of recurrent genital
11. State the treatment for chlamydial urogenital
herpes infections.
infections, gonorrhea, nonspecific urogenital
infections, and syphilis

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256 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

8. The initial symptoms of infec- 7. Chlamydia e. Large mononuclear

tions include tingling, itching, and pain in trachomatis cells filled with
the genital area, followed by eruption of intracytoplasmic
8. Lymphogra-
small pustules and vesicles. gram-negative rods
nuloma
9. is a common viral disease of the venereum f. Yeast infection
skin that gives rise to multiple umbilicated g. Spirochete responsi-
9. Donovan
papules. ble for syphilitic
bodies
infection
10. Candida albicans is the most commonly iden-
10. Döderlein h. Genital warts
tified organism in vaginal infec-
cytolysis
tions, but other Candida species, such as i. Obligate intracellular
Candida glabrata and Candida tropicalis may bacterial pathogen
also be present. that resembles a virus
but, as does bacteria,
11. can reside in the paraurethral
has RNA and DNA
glands of both sexes.
and is susceptible to
12. vaginosis is the most prevalent some antibiotics.
form of vaginal infection seen by health care j. In late stages, it is
professionals. associated with the
13. exist in two forms: elementary development of
bodies, which are the infectious particles ca- enlarged and ele-
pable of entering uninfected cells, and the phantoid external
initiator or reticulate bodies, which multiply genitalia
by binary fission to produce the inclusions
identified in stained cells. Activity C Briefly answer the following.

14. Untreated chlamydial infection results in 1. What are the risk factors for acquiring the
damage in female patients. human papillomavirus (HPV) and how is it
spread?
15. The is a pyogenic (i.e., pus-
forming) gram-negative diplococcus that
evokes inflammatory reactions characterized
by purulent exudates.
16. is spread by direct contact with
an infectious moist lesion, usually through 2. How do herpes simplex virus (HSV)-1 and HSV-
sexual intercourse. 2 spread, and where do they reside in the body?

Activity B Match the key terms in Column A

with their definitions in Column B.
Column A Column B
1. Granuloma a. Anaerobic proto- 3. What are the risk factors for developing a can-
inguinale zoan that can be didiasis infection?
transmitted sexually
2. Condylomata
cuminata b. Development of
large, tender, and
3. Trichomonas sometimes fluctuant
vaginalis inguinal lymph 4. What are the potential complications of tri-
4. Chancroid nodes called buboes chomoniasis in male and female patients?
c. Excess of lactobacilli
5. Treponema
pallidum d. Disease of the exter-
nal genitalia and
6. Candidiasis lymph nodes

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CHAPTER 47 SEXUALLY TRANSMITTED INFECTIONS 257

5. What are the sex-specific manifestations of a. 6 weeks to 8 months

gonorrhea? b. 6 weeks to 8 weeks
c. 6 months to 8 months
d. 6 days to 8 days
2. Primary genital herpes is a sexually transmit-
ted infection (STI) caused by either the herpes
6. What is the clinical course of syphilis? simplex virus type 1 (HSV-1) or the herpes
simplex virus type 2 (HSV-2). What are the
initial symptoms of primary genital herpes
infections? Mark all that apply.
a. Itching
b. Chancres
c. Genital pain
SECTION III: APPLYING YOUR d. Eczemalike lesions
KNOWLEDGE e. Small pustules

Activity D Consider the following scenario 3. There is no known cure for genital herpes and
and answer the questions. methods of treatment are often symptomatic.
Pharmacologic treatment of genital herpes in-
A 35-year-old man presents at the clinic com- cludes which drugs?
plaining of painful joints of the left leg and pain
a. Zidovudine
on urination. Also noted are mucocutaneous
lesions on the palms of his hands. b. Famciclovir
c. Nonsteroidal anti-inflammatory drugs
1. What would be important for you to note
while taking a nursing history? d. Topical corticosteroid compounds
4. Chancroid or soft chancre is a highly conta-
gious STI usually found in the Southeast
Asian and North African populations. What is
the recommended treatment for chancroid?
2. The patient is diagnosed with a chlamydial in- a. Tetracycline
fection complicated by Reiter syndrome. What b. Sulfamethoxazole
would be the expected treatment for this c. Erythromycin
patient? d. Acyclovir
5. A male patient presents at the clinic with flu-
like symptoms, weight loss of 10 pounds
without trying. On physical examination, he
is found to have splenomegaly and large, ten-
der, fluctuant inguinal lymph nodes. While
taking the nursing history, it is discovered
SECTION IV: PRACTICING that the patient prefers male sexual partners,
FOR NCLEX and 2 weeks ago he had small, painless
papules. What disease would the nurse sus-
Activity E Answer the following questions. pect the client has?
a. Genital herpes
1. After inoculation with human papilloma
virus (HPV), genital warts may begin to grow. b. Chancroid
They usually manifest as soft, raised fleshy le- c. Syphilis
sions on the external genitalia of either a d. Lymphogranuloma venereum (LGV)
male or female patient. What is the incuba-
tion period for HPV-induced genital warts?

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258 UNIT 11 DISORDERS OF GENITOURINARY AND REPRODUCTIVE FUNCTION

6. Candidiasis is a leading cause of vaginal infec- 9. Gonorrhea is an STI that affects both men
tions. Which antifungal agent is not available and women. When diagnosing gonorrhea,
without prescription to treat candidiasis? specimens should be collected from the ap-
a. Terconazole propriate site and inoculated onto the correct
medium. From what sites can specimens be
b. Clotrimazole
collected when diagnosing gonorrhea? Mark
c. Miconazole all that apply.
d. Butaconazole a. Oropharynx
7. Trichomoniasis is an STI that can occur in ei- b. Urethra
ther sex. Men carry the protozoan in the ure- c. Nasal passages
thra and prostate and remain asymptomatic.
d. Exocervix
This anerobic protozoan can cause a number
of complications. What is a risk factor for tri- e. Anal canal
chomoniasis in both men and women? 10. Tertiary syphilis is a delayed response of un-
a. Atypical pelvic inflammatory disease (PID) treated primary syphilis that can occur as long
b. Human immunodeficiency virus (HIV) as 20 years after the primary disease. When
transmission tertiary syphilis progresses to a symptomatic
stage, it can produce localized necrotic le-
c. Blockage of tubes and ducts
sions. What are these lesions called?
d. Ovarian and testicular cysts
a. Chancres
8. Bacterial vaginosis is the most common vagi- b. Chancroids
nal infection seen by health care providers.
c. Gummies
What is the predominant symptom of bacter-
ial vaginosis? d. Gummas
a. Thick, cottage cheese-like discharge with a
fishy odor
b. Painless chancres
c. Grayish white discharge with a fishy odor
d. Small, painless papules

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48

CHAPTER
Organization and Control
of Neural Function

SECTION I: LEARNING 11. Define the terms afferent, efferent, ganglia,

association neuron, cell column, and tract
OBJECTIVES
12. State the origin and destination of nerve
1. Distinguish between the functions of the fibers contained in the dorsal and ventral
neurons and supporting cells of the nervous roots
system
13. State the structures innervated by general so-
2. List the three parts of a neuron and describe matic afferent, special visceral afferent, gen-
their structure and function eral visceral afferent, special somatic afferent,
general visceral efferent, pharyngeal efferent,
3. Name the supporting cells in the central ner-
and general somatic efferent neurons
vous system and peripheral nervous system
and state their functions 14. Describe the longitudinal and transverse
structures of the spinal cord
4. Describe the energy requirements of nervous
tissue 15. Trace an afferent and efferent neuron from its
site in the periphery through its entrance into
5. Describe the three phases of an action poten-
or exit from the spinal cord
tial and relate the functional importance of
ion channels to the different phases 16. Explain the innervation and function of
spinal cord reflexes
6. State the difference between electrical and
chemical synapses 17. List the structures of the hindbrain, midbrain,
and forebrain and describe their functions
7. Describe the interaction of the presynaptic
and postsynaptic terminals 18. Name the cranial nerves and cite their loca-
tion and function
8. Characterize the role of excitatory and in-
hibitory postsynaptic potentials as they relate 19. Describe the characteristics of the CSF and
to spatial and temporal summation of mem- trace its passage through the ventricular
brane potentials system
9. Briefly describe how neurotransmitters are 20. Contrast and compare the blood-brain and
synthesized, stored, released, and inactivated CSF-brain barriers
10. Use the segmental approach to explain the 21. Compare the sensory and motor components
development of the nervous system and the of the autonomic nervous system with those
organization of the postembryonic nervous of the CNS
system

259
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260 UNIT 12 DISORDERS OF NEURAL FUNCTION

22. Compare the anatomic location and func- 10. The form the myelin in the
tions of the sympathetic and parasympathetic CNS.
nervous systems
11. is the major fuel source for the
23. Describe neurotransmitter synthesis, release, nervous system.
and degradation, and receptor function in the
12. Nerve signals are transmitted by ,
sympathetic and parasympathetic nervous
which are abrupt, pulsatile changes in the
systems
membrane potential.
13. The excitability of neurons can be affected
by conditions that alter the ,
SECTION II: ASSESSING YOUR moving it either closer to or further from
UNDERSTANDING the threshold potential.

Activity A Fill in the blanks. 14. Neurons communicate with each other
through structures known as .
1. The are the functional cells of
the nervous system. 15. synapses involve special presy-
naptic and postsynaptic membrane struc-
2. The supporting cells, such as in tures, separated by a synaptic cleft.
the PNS and the cells in the
CNS, protect the nervous system and provide 16. The secreted neurotransmitters diffuse into
metabolic support for the neurons. the and unite with receptors on
the postsynaptic membrane.
3. Neurons have three distinct parts: the cell
, and its cytoplasm-filled 17. In excitatory synapses, binding of the neuro-
processes, the and , transmitter to the receptor produces
which form the functional connections, or of the postsynaptic membrane,
, with other nerve cells, with re- whereas the binding of the neurotransmitter
ceptor cells, or with effector cells. to the receptor in an inhibitory synapse in-
duces of the postsynaptic mem-
4. are multiple, short-branched ex- brane by making the membrane more
tensions of the nerve cell body; they conduct permeable to potassium or chloride.
information toward the cell body and are the
main source of information for the neuron. 18. When the combination of a neurotransmitter
with a receptor site causes partial depolariza-
5. A bidirectional axonal transport system exists tion of the postsynaptic membrane, it is
to carry materials to the nerve terminal called an potential.
( direction) and back to the cell
body ( direction). 19. The process of involves the syn-
thesis, storage, and release of a neurotrans-
6. Supporting cells of the nervous system, the mitter; the reaction of the neurotransmitter
and cells of the with a receptor; and termination of the recep-
PNS and the several types of neuroglial cells tor action.
of the CNS, give the neurons protection and
metabolic support. 20. molecules react with presynap-
tic or postsynaptic receptors to alter the re-
7. cells secrete a basement mem- lease of or response to neurotransmitters.
brane that protects the cell body from the dif-
fusion of large molecules. 21. factors are required to maintain
the long-term survival of the postsynaptic cell
8. In some pathologic conditions, such as multi- and are secreted by axon terminals indepen-
ple sclerosis in the CNS and Guillain-Barré dent of action potentials.
syndrome in the PNS, the may
degenerate or be destroyed. 22. A functional system called the
operates in the lateral portions of the reticular
9. The increase nerve conduction formation of the medulla, pons, and espe-
by allowing the impulse to jump from node cially the midbrain.
to node through the extracellular fluid in a
process called .

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CHAPTER 48 ORGANIZATION AND CONTROL OF NEURAL FUNCTION 261

23. The spinal cord and the dorsal and ventral ture, touch, and proprioception to the super-
roots are covered by a connective tissue ficial and deep regions of the face.
sheath, the , which also contains
38. The makes continuous adjust-
the blood vessels that supply the white and
ments, resulting in smoothness of movement,
gray matter of the cord.
particularly during the delicate maneuvers.
24. The peripheral nerves that carry information
39. The plays a role in relaying criti-
to and from the spinal cord are called
cal information regarding motor activities to
.
and from selected areas of the motor cortex.
25. Each spinal cord segment communicates with
40. A is the ridge between two
its corresponding body segment through the
grooves, and the groove is called a
.
.
26. Spinal nerves do not go directly to skin and
41. The supply axial and proximal
muscle fibers; instead, they form complicated
unlearned and learned postures and move-
nerve networks called .
ments, which enhance and add gracefulness
27. A is a highly predictable rela- to UMN-controlled manipulative movements.
tionship between a stimulus and an elicited
42. The is necessary for somesthetic
motor response.
perception, especially concerning perception
28. The reflex is stimulated by a of “where” the stimulus is in space and in re-
damaging stimulus and quickly moves the lation to body parts.
body part away from the offending stimulus,
43. Inside the skull and vertebral column, the
usually by flexing a limb part.
brain and spinal cord are loosely suspended
29. Based on its embryonic development, the and protected by several connective tissue
brain is divided into three regions, the sheaths called the .
, the , and the
44. The provides a supporting and
.
protective fluid in which the brain and spinal
30. Damage to the nerve results in cord float.
weakness or paralysis of tongue muscles.
45. The ability to maintain homeostasis and per-
31. Sensory and motor components of the form the activities of daily living in an ever-
nerve innervate the pharynx, changing physical environment is largely
the gastrointestinal tract, the heart, the vested in the .
spleen, and the lungs.
46. The functions of the are con-
32. The sternocleidomastoid, a powerful head- cerned with conservation of energy, resource
turning muscle, and the trapezius muscle, replenishment and storage, and maintenance
which elevates the shoulders, are innervated of organ function during periods of minimal
by the . activity—the rest and digest response.
33. The dorsolateral contains the
Activity B Consider the following figures.
same components as the vagus nerve, but for
a more rostral segment of the gastrointestinal 1.
tract and the pharynx.
34. The special sensory afferent is
attached laterally at the junction of the
medulla oblongata and the pons, often called
the caudal pons.
35. The innervates the nasopharynx
and taste buds of the palate.
36. The nerve abducts the eye.
37. The is the main sensory nerve
conveying the modalities of pain, tempera-

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262 UNIT 12 DISORDERS OF NEURAL FUNCTION

1. In the figure above of the segments of the spinal

cord, please label the following structures:
• IA neuron
• segments
• ventral root
• dorsal root ganglion neuron
• spinal nerve
• dorsal root ganglion

2. Septum
pellucidum

Pineal
body
Interventricular
foramen Cerebral
Anterior aqueduct
commissure

Central canal

2. In the above figure of the brain, please label 6. Synaptic e. Chemical transmitter
the following structures: vesicles molecules
• spinal cord 7. Ependymal f. Small phagocytic cell
• medulla oblongata that is available for
8. Plexus cleaning up debris
• pons
• midbrain 9. Threshold after cellular damage,
• frontal lobe potential infection, or cell
• corpus callosum death
10. Oligoden-
• occipital lobe g. Membrane potential
drocytes
• third ventricle at which neurons or
• fourth ventricle other excitable tissues
• cerebellum are stimulated
h. Flow of electrically
Activity C Match the key terms in Column A charged ions toward
with their definitions in Column B. an equilibrium
1. i. Production of CNS
myelin
Column A Column B
j. Site of intermixing
1. Microglia a. Forms the lining of nerve branches
the neural tube cavity
2. Depolari- 2.
zation b. Phase during which
the polarity of the Column A Column B
3. Neurotrans- resting membrane po-
mitters 1. Afferent a. Neurons that com-
tential is reestablished
municate with the
4. Repolari- c. Membrane-bound 2. Bell’s palsy
central nervous
zation sacs that store neuro- 3. Efferent system and periph-
transmitters eral neural cells
5. Astrocytes 4. Proprioception
d. Form the blood–brain b. Nerves that con-
barrier 5. Ganglia duct impulses from

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CHAPTER 48 ORGANIZATION AND CONTROL OF NEURAL FUNCTION 263

6. Association the periphery of the 5. Describe the basic embryological development

neuron body to the brain or of the nervous system.
spinal cord.
7. Muscle
spindles c. Longitudinal columns
of neurons
8. Cell
d. Communication over
column
distances between
6. How are the cell columns organized in the
9. Tract neighboring and distal
dorsal and ventral horns of the spinal cord?
segment of neural tube
e. Carrying impulses from
the central nervous sys-
tem to an effector
f. Group of neural cell
bodies 7. What is the importance of cerebral spinal
g. Sense of body move- fluid?
ment and position
h. Stretch receptors dis-
tributed throughout
the belly of a muscle
i. Unilateral loss of facial 8. How does the blood–brain barrier affect drug/
nerve function toxin actions on the brain?

Activity D Briefly answer the following.

1. Describe the formation and attachment of
myelin to the axonal membrane.

SECTION III: APPLYING YOUR

KNOWLEDGE
2. Explain the fragileness of neural cells in regard
to metabolic requirements. Activity E Consider the following scenario and
answer the questions.
A woman in her fourth month of pregnancy
comes to the clinic to have an ultrasound done.
When the ultrasound is read, the physician tells
the woman that her fetus has a neural tube de-
3. How do neural cell bodies interpret the nu-
fect, and, when the infant is born, it will have a
merous incoming signals (action potentials) cystlike pouch on its lower back that contains
from other neurons? cerebrospinal fluid, meninges, and spinal
nerves.
1. The patient asks if there is a name for the de-
fect her child has. What is your correct re-
sponse to the patient’s question?
4. How are neurotransmitters inactivated in the
synaptic space following release?

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264 UNIT 12 DISORDERS OF NEURAL FUNCTION

2. The patient asks what this defect will mean for 5. Neuromodulators can produce slower and
her baby. What would be your correct response? longer-lasting changes in membrane ex-
citability by acting on postsynaptic receptors.
What do neuromodulators do?
a. Alter the release or response to neurotrans-
mitters
b. Alter the inhibitory response of postsynap-
tic electrical receptors
SECTION IV: PRACTICING c. Alter the metabolic function of Schwann
FOR NCLEX cells
d. Alter the Ligand-gate response to electrical
Activity F Answer the following questions. activity
1. There are two types of nervous tissue cells. 6. The basis for assessing the function of any pe-
One type is neurons, and the other type is the ripheral nerve lies in what?
supporting cells. What is the function of the a. Peripheral nerves contain only afferent
supporting cells? processes from the cell columns
a. Protect nervous system and provide meta- b. Peripheral nerves contain processes of
bolic support for the neurons more than one of the four afferent and
b. Transmit messages between parts of the pe- three efferent cell columns
ripheral nervous system (PNS) c. Peripheral nerves contain only efferent
c. Transmit messages between the central processes from the cell columns
nervous system and the PNS d. Peripheral nerves contain no processes
d. Provide metabolic support for the neurons from the seven cell columns
and the PNS
7. The spinal cord does not hang freely within
2. Ion channels in nervous system cells generate the spinal column. What is it supported by?
action potentials in the cells. What are the a. The pia mater and the posterior vertebra
ion channels guarded by?
b. The denticulate ligaments and the verte-
a. Schwann cells bral blood vessels
b. Voltage-dependent gates c. The pia mater and the denticulate ligaments
c. Ligand-gates d. The vertebral blood vessels and the poste-
d. Leyte cells rior vertebra
3. Neurons communicate through the use of 8. One of the spinal motor reflexes is the myotatic
synapses. These synapses may link neurons reflex. What does this reflex do for the body?
into functional circuits. What is the most a. Provides information to withdraw the
common type of synapse? body from noxious stimuli
a. Electrical synapse b. Provides information about nociceptive
b. Excitatory synapse stimuli
c. Chemical synapse c. Provides information about equilibrium
d. Inhibitory synapse d. Provides information about proprioception
4. Neurotransmitters are small molecules that 9. The cerebellum, separated from the cerebral
exert their actions through specific proteins, hemispheres by the tentorium cerebelli, lies
called receptors, embedded in the postsynap- in the posterior fossa of the cranium. What is
tic membrane. Where are neurotransmitters one of the functions of the cerebellum?
synthesized? a. Coordinates smooth and accurate move-
a. In the dendrite terminal ments of the body
b. In the presynaptic junction b. Conveys the senses of pain, temperature,
c. In the postsynaptic junction touch, and proprioception to the superfi-
cial and deep regions of the face
d. In the axon terminal

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CHAPTER 48 ORGANIZATION AND CONTROL OF NEURAL FUNCTION 265

c. Contains the pontine nuclei 12. The sympathetic and the parasympathetic
d. Contains the main motor pathways nervous systems are continuously at work in
between the forebrain and the pons. our bodies. This continual action gives a basal
activity to all parts of the body. What is this
10. The basal ganglia, part of the cerebral hemi- basal activity referred to as?
spheres, are damaged by diseases such as
a. Tension
Parkinson disease and Huntington chorea.
What does this result in? b. Relaxation
a. Uncontrollable tremors on movement c. Tone
b. Abnormal movement patterns d. Strength
c. Explosive, inappropriate speech 13. Dopamine is an intermediate compound
d. Inappropriate emotions made during the synthesis of norepinephrine.
It is the principal inhibitory transmitter of
11. The blood–brain barrier excludes most highly the internuncial neurons in the sympathetic
water-soluble drugs, but allows lipid-soluble ganglia. What other action does it have?
drugs to easily cross. What antibiotic is highly
a. Vasoconstricts renal and coronary blood
lipid soluble and readily enters the brain?
vessels when given intravenously (IV)
a. Ceftriaxone
b. Acts as a neuromoderator in the hindbrain
b. Penicillin
c. Acts as a neuromoderator in the forebrain
c. Chloramphenicol
d. Vasodilates renal and coronary blood
d. Cefadroxil vessels when given IV

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49
CHAPTER

Somatosensory Function,
Pain, and Headache

SECTION I: LEARNING ospinothalamic, and reticulospinal pathways,

including the role of chemical mediators and
OBJECTIVES factors that modulate pain transmission
1. Describe the four major classes of somatosen- 11. Describe the function of endogenous anal-
sory modalities gesic mechanisms as they relate to transmis-
sion of pain information
2. Describe the organization of the somatosen-
sory system in terms of first-, second-, and 12. Compare pain threshold and pain tolerance
third-order neurons
13. Differentiate acute pain from chronic pain in
3. Characterize the structure and function of the terms of mechanisms, manifestations, and
dorsal root ganglion neurons in terms of sen- treatment
sory receptors, conduction velocities, and
14. Describe the mechanisms of referred pain,
spinal cord projections
and list the common sites of referral for car-
4. Compare the discriminative pathway with diac and other types of visceral pain
the anterolateral pathway, and explain the
15. Describe three methods for assessing pain
clinical usefulness of this distinction
16. State the proposed mechanisms of pain relief
5. Compare the tactile, thermal, and position
associated with the use of heat, cold, transcu-
sense modalities in terms of receptors, ade-
taneous electrical nerve stimulation, and
quate stimuli, ascending pathways, and cen-
acupuncture and acupressure
tral integrative mechanisms
17. Cite the mechanisms whereby non-narcotic
6. Describe the role of clinical examination in
and narcotic analgesics, tricyclic antidepres-
assessing somatosensory function
sants, and antiseizure drugs relieve pain
7. Differentiate among the specificity, pattern,
18. Define allodynia, hypoesthesia, hyperesthe-
gate control, and neuromatrix theories of pain
sia, paresthesias, hyperpathia, analgesia, and
8. Characterize the response of nociceptors to hypoalgesia and hyperalgesia.
stimuli that produce pain
19. Describe the cause and characteristics and
9. State the difference between the A- and treatment of neuropathic pain, trigeminal
C-fiber neurons in the transmission of pain neuralgia, postherpetic neuralgia, and com-
information plex regional pain syndrome.
10. Trace the transmission of pain signals with 20. Cite possible mechanisms of phantom limb
reference to the neospinothalamic, pale- pain

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CHAPTER 49 SOMATOSENSORY FUNCTION, PAIN, AND HEADACHE 267

21. State the importance of distinguishing be- 7. The pathway is used for the
tween primary and secondary types of rapid transmission of sensory information,
headache such as discriminative touch.
22. Differentiate between the periodicity of oc- 8. The pathway provides for trans-
currence and manifestations of migraine mission of sensory information, such as pain,
headache, cluster headache, tension-type thermal sensations, crude touch, and pres-
headache, and headache due to temporo- sure that does not require discrete localiza-
mandibular joint syndrome tion of signal source or fine discrimination of
intensity.
23. Characterize the nonpharmacologic and
pharmacologic methods used in treatment of 9. Somatosensory experience can be divided
headache into , a term used for qualitative,
subjective distinctions between sensations,
24. Cite the most common cause of temporo-
such as touch, heat, and pain.
mandibular joint pain
10. The receptive endings of different afferent neu-
25. State how the pain response may differ in
rons can initiate to many forms
children and older adults
of energy at high energy levels, but they usu-
26. Explain how pain assessment may differ in ally are highly tuned to be differentially sensi-
children and older adults tive to low levels of a particular energy type.
27. Explain how pain treatment may differ in 11. The ability to discriminate the location of a
children and older adults somesthetic stimulus is called
and is based on the sensory field in a der-
matome innervated by an afferent neuron.
SECTION II: ASSESSING YOUR 12. The system, which relays sen-
UNDERSTANDING sory information regarding touch, pressure,
and vibration, is considered the basic so-
Activity A Fill in the blanks. matosensory system.

1. The system is designed to pro- 13. sensation is discriminated by

vide the central nervous system (CNS) with three types of receptors: cold receptors,
information related to deep and superficial warmth receptors, and pain receptors.
body structures as contrasted to special 14. Attention, motivation, past experience, and
senses, such sight and hearing. the meaning of the situation can influence
2. somatic afferent neurons have the individual’s reaction to .
branches with widespread distribution 15. The experience of pain depends on both
throughout the body and with many distinct stimulation and .
types of receptors that result in sensations
such as pain, touch, and temperature. 16. pain arises from direct injury or
dysfunction of the sensory axons of periph-
3. somatic afferent neurons sense eral or central nerves.
position and movement of the body.
17. The theory proposes that the
4. General afferent neurons have brain contains a widely distributed neural
receptors on various visceral structures that network that contains somatosensory, limbic,
sense fullness and discomfort. and thalamocortical components.
5. Somatosensory information from the face 18. stimuli are objectively defined
and cranial structures is transmitted by the as stimuli of such intensity that they cause or
sensory neurons, which func- are close to causing tissue damage.
tion in the same manner as the dorsal root
ganglion neurons. 19. Nociceptive stimulation that activates
can cause a response known as
6. The region of the body wall that is supplied neurogenic inflammation that produces vasodi-
by a single pair of dorsal root ganglia is called lation and an increased release of chemical
a . mediators to which nociceptors respond.

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268 UNIT 12 DISORDERS OF NEURAL FUNCTION

20. The faster-conducting fibers in the Activity B Consider the following figures.
tract are associated mainly with
the transmission of sharp-fast pain informa-
tion to the thalamus.
21. The tract is a slower-conducting,
multisynaptic tract concerned with the dif-
fuse, dull, aching, and unpleasant sensations
that commonly are associated with chronic
and visceral pain.
22. Through research, it was found that electrical
stimulation of the midbrain re-
gions produced a state of analgesia that lasted
for many hours.
23. Three families of endogenous opioid peptides
have been identified: the ,
, and .
24. Pain and tolerance affect an in- 1. In the figure above, label the flowing structures:
dividual’s response to a painful stimulus.
• receptor
25. pain arises from superficial • dorsal root ganglion
structures, such as the skin and subcutaneous • first order neuron
tissues. • second order neuron
26. pain originates in deep body • thalamus
structures, such as the periosteum, muscles, • somatosensory cortex
tendons, joints, and blood vessels. • third order neuron

27. The purpose of acute pain is to serve as a

system.
28. An drug is a medication that

Hip
Trunk
Head
Neck
Shoulder

Leg
Arm
Elbow m
Forea

acts on the nervous system to decrease or

Wri d

ot
Ha

eliminate pain without inducing loss of con- Fo

Lit g

st
n

r
Ri iddl

es
tle

sciousness.
n e

To
M dex mb

n
In hu

Ge
29. Primary describes pain sensitiv- E
T

Noye
ity that occurs directly in damaged tissues. s
Fac e
e
30. is the absence of pain on nox- Uppe
r lip
ious stimulation or the relief of pain without Lips
loss of consciousness.
Lower lip
31. is characterized by severe, brief, Teeth, gums, and jaw
often repetitive attacks of lightninglike or Tongue
throbbing pain.
Pharynx
32. headache is a type of primary Intra-
neurovascular headache that typically in- abdominal
cludes severe, unrelenting, unilateral pain lo-
cated, in order of decreasing frequency, in the
orbital, retro-orbital, temporal, supraorbital,
and infraorbital region.
2. Using the figure above, please answer the
33. The most common type of headache is following questions.
headache.
• Which area has the smallest receptor field?
34. A common cause of head pain is • Which area has the largest receptor field?
syndrome. • Which area has the highest acuity?

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CHAPTER 49 SOMATOSENSORY FUNCTION, PAIN, AND HEADACHE 269

Activity C Match the key terms in Column A 2.

with their definitions in Column B. Column A Column B
1. 1. Free nerve a. Stimulated by rapid
Column A Column B endings movements of the tis-
sues and adapts
1. Perception a. The perception of 2. Meissner
within a few hun-
tactual, propriocep- corpuscles
2. Somesthesia dredths of a second
tive, or gut sensa- 3. Merkel disks b.
3. Type A fibers tions Unmyelinated fibers
4. Pacinian entwined around most
4. Polymodal b. Transmit information of the length of the
about muscle length corpuscles
receptors hair follicle that detect
and tendon stretch 5. Hair follicle movement on the sur-
5. Type B fibers end-organs
c. Sensory threshold is face of the body
6. Hunting raised 6. Ruffini c. Are responsible for
reflex d. Convey cutaneous end-organs giving steady-state sig-
7. Primary pressure and touch nals that allow for
somato- sensation, cold sen- continuous determi-
sensory sation, mechanical nation of touch
cortex pain, and heat pain against the skin
e. Circulation to a d. Detect touch and pres-
8. Hyperpathia
cooled area under- sure
9. Type goes alternating e. Found in joint
C fibers periods of pallor capsules
caused by ischemia
10. Type A f. Elongated, encapsu-
and flushing caused
fibers lated nerve ending
by hyperemia
that is present in non-
f. Awareness of the hairy parts of the skin
stimuli, localization
and discrimination Activity D Briefly answer the following.
of their characteris-
1. How are sensory systems organized?
tics, and interpreta-
tion of their
meaning
g. Receives primary
sensory information
by way of direct pro- 2. What are the types of sensory information
jections from the that can be perceived by our sensory
thalamus receptors?
h. Convey warm-hot
sensation and me-
chanical and chemi-
cal as well as heat-
and cold-induced
pain sensation 3. How much information can be obtained from
i. Respond to mechan- a single pinprick to the bottom of your pa-
ical, thermal, and tient’s foot?
chemical stimuli
j. Transmit informa-
tion from cutaneous
and subcutaneous
mechanoreceptors

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270 UNIT 12 DISORDERS OF NEURAL FUNCTION

4. What is the gate control theory of pain? nursing home. The report from the accompany-
ing staff member is that she suffers from a physi-
ologic dementia and that 2 days ago she fell in
the bathroom. The patient denies pain, but has
been restless and agitated since the fall, and
today she will not use her right arm.
5. How can the phenomenon of referred pain be
1. The caregiver asks the nurse how the health-
explained?
care team is going to assess this client’s pain
since the client cannot give them any accurate
information. What is your best response?

6. In many sports injuries the athlete may be in-

structed to place heat on the injured area.
What is the effect on pain originating from
2. The patient is diagnosed with a fractured right
the injury?
ulna. She is taken to the OR, where the arm is
aligned and cast. When she is ready for release
back to the nursing home, the caregiver asks
what can be done for her discomfort. What in-
formation would you include at discharge?
7. What is phantom limb pain and what are
some of the theories postulated to explain its
presence?

SECTION IV: PRACTICING

8. What are the differences and similarities be- FOR NCLEX
tween migraine headaches with aura and mi-
graine headaches without aura? Activity F Answer the following questions.
1. Match the type of neuron with the informa-
tion it transmits and where it transmits it.
Information Trans-
Type of Neuron mitted and Site
9. What is known about the pathology of pain 1. Special somatic a. Sensations such
during a migrainous headache? afferent as pain, touch,
neurons and temperature
2. General somatic b. Transmit sen-
afferent sory informa-
neurons tion from the
periphery to the
3. General visceral CNS
afferent neurons
SECTION III: APPLYING YOUR c. Communicate
KNOWLEDGE 4. First-order with various
neurons reflex networks
Activity E Consider the following scenario and and sensory
5. Second-order
answer the questions. pathways in the
neurons
spinal cord and
An 82-year-old woman is brought to the emer- 6. Third-order travel directly to
gency department by ambulance from a local neurons the thalamus

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CHAPTER 49 SOMATOSENSORY FUNCTION, PAIN, AND HEADACHE 271

7. Dorsal root d. Transmits all d. Transmit information

ganglion somatosensory about muscle length and
neurons information from tendon stretch
the limbs and e. Sensory receptors that are
8. Trigeminal
trunk activated by noxious in-
sensory
neurons e. Sense position sults to peripheral tissues
and movement f. Carry the information
of the body from the spinal cord to
f. Somatosensory the thalamic level of
information from sensation and relay pre-
the face and cra- cise information regard-
nial structures ing spatial orientation
g. Sense fullness g. The cell body of the dor-
and discomfort sal root ganglion neuron,
h. Relay information its peripheral branch
from the thala- (which innervates a
mus to the cere- small area of periphery),
bral cortex and its central axon
(which projects to the
2. Match the term with the definition. CNS)
Term Definition h. Transmit information
from cutaneous and sub-
1. Discrimina- a. The region of the cutaneous mechanore-
tive touch body wall that is ceptors
supplied by a sin-
2. Sensory i. Convey cutaneous pres-
gle pair of dorsal
unit sure and touch sensation,
root ganglia
cold sensation, mechani-
3. Type A b. Stimulate auto- cal pain, and heat pain
fibers nomic nervous
j. The sense of shape and
4. Type A and system responses,
size of an object in the
A fibers such as a rise in
absence of visualization
heart rate and
5. Type B fibers blood pressure, di- k. Detect touch and pres-
lation of the sure
6. Dermatome
pupils, and the
7. Discrimi- pale, moist skin 3. A neurologic assessment of the somatosen-
native that results from sory function of the body is often necessary
pathway constriction of the for diagnostic information. How is this assess-
cutaneous blood ment done?
8. Stereognosis
vessels and activa- a. Testing the integrity of spinal segmental
9. Anterolateral tion of the sweat nerves
pathway glands b. Testing the integrity of cranial nerves
10. Free nerve c. Identifies the size c. Testing the integrity of peripheral nerves
endings and shape of ob-
d. Testing the integrity of the CNS
jects and their
11. Nociceptors
movement across 4. When testing nociceptive stimuli to elicit a
the skin, tempera- withdrawal reflex in the body, what stimuli
ture sensation, are commonly used?
sense of move- a. Weak electrical current
ment of the limbs
b. Pressure from a sharp object
and joints of the
body, and noci- c. Skin temperature damp cotton ball
ception, or pain d. Water heated to 5°C above skin temperature

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272 UNIT 12 DISORDERS OF NEURAL FUNCTION

5. One of the neurotransmitters between the g. Perceived at a site different

nociceptive neurons and the dorsal horn neu- from its point of origin, but
rons is a major excitatory neurotransmitter. innervated by the same
What is this neurotransmitter? spinal segment
a. Norepinephrine 8. It is often necessary to assess a patient’s pain.
b. Substance P What factors would you assess when assessing
c. Glutamate pain? Mark all that apply.
d. Dopamine a. Nature and severity of pain
b. Severity and spinal reflex involvement of
6. Which tract in the spinal cord conducts the
pain
diffuse, dull, aching sensations that are asso-
ciated with chronic and visceral pain? c. Location and radiation of pain
a. Multisynaptic tract d. Spinal reflex involvement and nature of pain
b. Neospinothalamic tract e. Spinal tract involvement and radiation of
pain
c. Anterolateral tract
d. Paleospinothalamic tract 9. When giving medicine for acute pain, health
care workers are reluctant to provide much
7. Match the type of pain with its description needed opioid pain medicine. What is your
Type of Pain Description of Pain major concern when providing opioid pain
relief?
1. Deep somatic a. Extends for long peri-
a. Fear of addiction
pain ods of time and gen-
erally represents low b. Fear of depressed respirations
2. Cutaneous
levels of underlying c. Fear of over-sedation
pain
pathology that does d. Fear of adverse reactions
3. Visceral not explain the pres-
pain ence and/or extent of 10. Chronic pain is difficult to treat. Cancer, a
the pain common cause of chronic pain, has been espe-
4. Referred cially addressed by the World Health Organiza-
pain b. The pain’s location,
tion (WHO). What has WHO created to assist
radiation, intensity,
5. Guarding clinicians in choosing appropriate analgesics?
and duration, as well
as those factors that a. An opioid ladder for pain control
6. Acute pain
aggravate or relieve it b. An analgesic ladder for pain control
7. Chronic provide essential di- c. Stepping stones for pain control
pain agnostic clues
d. A list of nonpharmacologic ways to control
c. Type of pain experi- pain
enced from a
sprained ankle 11. In describing the ideal analgesic, what factors
would be included? Mark all that apply.
d. A sharp pain with a
burning quality that a. Inexpensive
may be abrupt or b. Have minimal adverse effects
slow in onset. c. Effective
e. A protective reflex d. Addictive
rigidity; its purpose
e. Decrease the level of consciousness
is to protect the af-
fected body parts 12. Using surgery to relieve severe, intractable
f. Diffuse and poorly pain has been successful to a degree. For what
localized nature can surgery be used when a person is in pain?
with a tendency to a. Relief of severe peripheral contractures
be referred to other b. Cure inoperable cancer
locations
c. Block transmission of phantom limb pain
d. Cure severe myalgia

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CHAPTER 49 SOMATOSENSORY FUNCTION, PAIN, AND HEADACHE 273

13. When a peripheral nerve is sufficiently irri- 15. Phantom limb pain is a little understood pain
tated, it becomes hypersensitive to the nox- that develops after an amputation. Because it
ious stimuli, which results in increased is little understood, it is difficult to treat, even
painfulness or hyperalgesia. Health care pro- though the patient is experiencing severe
fessionals recognize both primary and sec- pain. What are the treatments for phantom
ondary forms of hyperalgesia. What is limb pain?
primary hyperalgesia? a. Sympathetic blocks and hypnosis
a. Pain that occurs in the tissue surrounding b. Relaxation training and transcutaneous
an injury. electrical nerve stimulation (TENS) on the
b. Pain sensitivity that lasts longer than efferents in the area
1 week c. Narcotic analgesics and relaxation training
c. Pain sensitivity that occurs in the viscera d. Biofeedback and nonsteroidal anti-
d. Pain sensitivity that occurs directly in inflammatory drugs (NSAIDs)
damaged tissues
16. Migraine headaches affect millions of people
14. Match the type of pain with its description. worldwide. What are first-line agents for the
treatment of migraine headaches?
Type of Pain Description
a. Ondansetron and morphine
1. Neuropathic a. Manifested by facial
b. Naproxen sodium and metoclopramide
pain tics or spasms and
characterized by c. Sumatriptan and Tramadol
2. Neuralgia
paroxysmal attacks of d. Caffeine and syrup of ipecac
3. Tic stabbing pain that
17. A severe type of headache that occurs more fre-
douloureux usually are limited to
quently in men than in women and is described
the unilateral sensory
4. Postherpetic as having unrelenting, unilateral pain located
distribution of one or
neuralgia most frequently in the orbit is called what?
more branches of the
trigeminal nerve, a. Migraine headache
most often the maxil- b. Tension headache
lary or mandibular di- c. Cluster headache
visions.
d. Chronic daily headache
b. Characterized by se-
vere, brief, often 18. When assessing pain in children, it is impor-
repetitive attacks of tant to use the correct pain rating scale. What
lightninglike or would be the appropriate pain rating scale
throbbing pain. with children who are 3 to 8 years of age?
c. Affected sensory gan- a. COMFORT pain scale
glia and the periph- b. FLACC pain scale
eral nerve to the skin c. CRIES pain scale
of the corresponding
d. FACES pain scale
dermatomes cause a
unilateral localized 19. Children feel pain just as much as adults do.
vesicular eruption What is the major principle in pain manage-
and hyperpathia (i.e., ment in the pediatric population?
abnormally exagger- a. Treat on individual basis and match anal-
ated subjective re- gesic agent with cause and level of pain
sponse to pain).
b. Always use nonpharmacologic pain treat-
d. Widespread pain that ment before using pharmacologic pain
is not otherwise ex- treatment
plainable, burning
c. Base treatment of pain on gender and age
pain, and attacks of
group
pain that occur with-
out seeming provo- d. Treat pediatric pain the way the parents
cation. wish

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50
CHAPTER

Disorders of
Motor Function

SECTION I: LEARNING 10. Define the term peripheral nervous system and
describe the characteristics of peripheral
OBJECTIVES nerves
1. Relate the functional hierarchy of motor 11. Trace the steps in regeneration of an injured
function to the performance of a complicated peripheral nerve
movement such as writing your name or
12. Compare the cause and manifestations of pe-
throwing a ball
ripheral mononeuropathies with polyneu-
2. Define the term motor unit and characterize its ropathies
mechanism of controlling skeletal muscle
13. Describe the manifestation of peripheral
movement
nerve root injury due to a ruptured interverte-
3. Describe the distribution of upper and lower bral disk
motor neurons in relation to the central ner-
14. Relate the functions of the cerebellum to pro-
vous system
duction of vestibulocerebellar ataxia, decom-
4. Differentiate between the functions of the position of movement, and cerebellar tremor
primary, premotor, and supplemental motor
15. Describe the functional organization of the
cortices
basal ganglia and communication pathways
5. Compare the effect of upper and lower motor with the thalamus and cerebral cortex
neuron lesions on the spinal cord stretch re-
16. State the possible mechanisms responsible for
flex function and muscle tone
the development of Parkinson disease and
6. Describe muscle atrophy and differentiate be- characterize the manifestations and treat-
tween disuse and degenerative atrophy ment of the disorder
7. Relate the molecular changes in muscle struc- 17. Relate the pathologic UMN and LMN changes
ture that occur in Duchenne muscular dystro- that occur in amyotrophic lateral sclerosis to
phy to the clinical manifestations of the the manifestations of the disease
disease
18. Explain the significance of demyelination
8. Describe the actions of Clostridium botulinum and plaque formation in multiple sclerosis
neurotoxins in terms of their pathologic and
19. Describe the manifestations of multiple
therapeutic potential
sclerosis
9. Relate the clinical manifestations of myasthe-
20. Relate the structures of the vertebral column
nia gravis to its cause
to mechanisms of spinal cord injury

274
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CHAPTER 50 DISORDERS OF MOTOR FUNCTION 275

21. Explain how loss of UMN function con- 11. Stretch reflexes tend to be hypoactive or ab-
tributes to the muscle spasms that occur after sent in cases of nerve damage or
recovery from spinal cord injury ventral horn injury involving the test area.
22. State the effects of spinal cord injury on ven- 12. Abnormalities in any part of the
tilation and communication, the autonomic pathway can produce muscle weakness.
nervous system, cardiovascular function,
13. Muscular usually results from
sensorimotor function, and bowel, bladder,
lower motor neuron (LMN) lesions as well as
and sexual function
diseases of the muscle themselves.
14. Any interruption of the myotatic or stretch
reflex circuitry by peripheral nerve injury,
SECTION II: ASSESSING YOUR pathology of the neuromuscular junction, in-
UNDERSTANDING jury to the spinal cord, or damage to the cor-
ticospinal system can results in disturbances
Activity A Fill in the blanks. of .
1. , whether it involves walking, 15. Hyperactive reflexes are suggestive of an
running, or precise finger movements, disorder.
requires movement and maintenance of
posture. 16. suggests the presence of an LMN
lesion.
2. The contains the neuronal cir-
cuits that mediate a variety of reflexes and au- 17. Disorders affecting the nerve cell body are
tomatic rhythmic movements. often referred to those affecting
the nerve axon as neuropathies,
3. Most reflexes are , meaning that and primary disorders affecting the muscle
they involve one or more interposed in- fibers as .
terneurons.
18. Muscular is a term applied to a
4. The medial descending systems of the brain number of genetic disorders that produce pro-
stem contribute to the control of gressive deterioration of skeletal muscles be-
by integrating visual, vestibular, cause of mixed muscle cell hypertrophy,
and somatosensory information. atrophy, and necrosis.
5. The is the highest level of motor 19. If the LMN dies or its axon is destroyed, the
function. skeletal muscle cell begins to have temporary
6. The primary cortex is located on spontaneous contractions, called .
the rostral surface and adjacent portions of 20. muscular dystrophy is inherited
the central sulcus. as a recessive single-gene defect on the X
7. The and provide chromosome and it is transmitted from the
feedback circuits that regulate cortical and mother to her male offspring.
brain stem motor areas. 21. The serves as a synapse between
8. Cerebellar are involved with the a motor neuron and a skeletal muscle fiber.
timing and coordination of movements that 22. Neurotoxins from the botulism organism
are in progress and with the learning of (Clostridium botulinum) produce paralysis by
motor skills. blocking release.
9. The , which are distributed 23. is a disorder of transmission at
throughout the belly of a muscle, relay infor- the neuromuscular junction that affects com-
mation about muscle length and rate of munication between the motor neuron and
stretch. the innervated muscle cell.
10. are found in muscle tendons 24. LMN diseases are progressive neurologic ill-
and transmit information about muscle tension nesses that selectively affect the anterior horn
or force of contraction at the junction of the cells of the and
muscle and the tendon that attaches to bone. motor neurons.

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276 UNIT 12 DISORDERS OF NEURAL FUNCTION

25. There are two main types of in- 37. The most common cause of is
jury based on the target of the insult: segmen- motor vehicle accidents, followed by falls,
tal demyelination involving the Schwann cell violence (primarily gunshot wounds), and
and axonal degeneration involving the neu- recreational sporting activities.
ronal cell body and/or its axon.
38. Sudden complete transection of the spinal
26. usually are caused by localized cord results in complete of
conditions, such as trauma, compression, or motor, sensory, reflex, and autonomic func-
infections, that affect a single spinal nerve, tion below the level of injury.
plexus, or peripheral nerve trunk.
39. is the impairment or loss of
27. involve demyelination or ax- motor or sensory function (or both) after
onal degeneration of multiple peripheral damage to neural structures in the cervical
nerves that leads to symmetric sensory, segments of the spinal cord.
motor, or mixed sensorimotor deficits.
40. refers to impairment or loss of
28. The signs and symptoms of a motor or sensory function (or both) in the
are localized to the area of the body inner- thoracic, lumbar, or sacral segments of the
vated by the nerve roots and include both spinal cord from damage of neural elements
motor and sensory manifestations. in the spinal canal.
29. Loss of function can result in 41. Vagal stimulation that causes a marked
total incoordination of these functions even bradycardia is called the
though its loss does not result in paralysis. response.
30. The are a group of deep, interre- 42. hypotension usually occurs in
lated subcortical nuclei that play an essential persons with injuries at T4 to T6 and above
role in control of movement. and is related to the interruption of descend-
ing control of sympathetic outflow to blood
31. Disorders of the basal ganglia comprise a
vessels in the extremities and abdomen.
complex group of motor disturbances charac-
terized by and other involun- 43. The high risk for in patients
tary movements, changes in posture and with acute SCI is owing to immobility, de-
muscle tone, and poverty and slowness of creased vasomotor tone below the level of in-
movement. jury, and hypercoagulability and stasis of
blood flow.
32. disease is a degenerative disor-
der of basal ganglia function that results in
Activity B Consider the following figure:
variable combinations of tremor, rigidity, and
bradykinesia.
33. The cardinal manifestations of Parkinson dis-
ease are tremor, rigidity, and or
slowness of movement.
34. affects motor neurons in three
locations: the anterior horn cells of the spinal
cord; the motor nuclei of the brain stem, par-
ticularly the hypoglossal nuclei; and the
UMNs of the cerebral cortex.
35. is characterized by inflamma-
tion and selective destruction of central ner-
vous system myelin.
In the figure above, locate and label the following
36. The pathophysiology of multiple sclerosis in-
areas of the brain:
volves the of nerve fibers in the
white matter of the brain, spinal cord, and
optic nerve.

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CHAPTER 50 DISORDERS OF MOTOR FUNCTION 277

• premotor cortex 6. Parkinsonism d. Rhythmic move-

• motor cortex ments of a particu-
7. Dysmetria
• Broca area lar body part
• vestibular cortex 8. Denervation e. Abnormal simulta-
• primary auditory cortex atrophy neous contractions
• primary visual cortex of agonist and an-
9. Constant
• somatosensory cortex tagonist muscles
conjugate
• frontal eye fields
readjustment f. Abnormal writhing
of eye movements
Activity C Match the key terms in Column A
position g. Inaccuracies of
with their definitions in Column B.
10. Tremor movements, leading
1. to a failure to reach
Column A Column B a specified target
h. Nystagmus
1. Clonus a. Increased muscle re-
sistance that varies i. Unsteadiness of the
2. Paralysis trunk
and commonly be-
3. Fascicu- comes worse at the j. Syndrome arising
lations extremities of the from the degenera-
range of motion tive changes in basal
4. Motor
b. Incomplete loss of ganglia function
homun-
culus strength
Activity D
c. Loss of movement
5. Spasticity 1. In the boxes below, put the following events
d. Rhythmic contrac-
6. Dysdiado- regarding synaptic transmission in order:
tion and alternate
chokinesia relaxation of a limb 1. Inactivation by acetylcholinesterase

7. Reflex e. Somatotopic array of 2. Action potential arrives at synaptic terminal

the body represent- 3. Depolarization of motor-end plate
8. Ataxia
ing motor areas 4. Release of acetylcholine into synapse
9. Proprio- f. The failure to accu- 5. Influx of Ca2
ception rately perform rapid
10. Paresis alternating move-
ments
g. Sense of body move- Activity E Briefly answer the following.
ment and position
1. Describe the basic hierarchy of the organiza-
h. A wide-based, un- tion of motor movement.
steady gait
i. Visible squirming
and twitching move-
ments of muscle
j. Involuntary motor
responses 2. What is the basic unit of motor control? How
does it vary between gross motor movement
2. and fine motor movements?
Column A Column B
1. Bradykinesia a. Muscle shrinkage
owing to loss of
2. Dystonia
neural stimulus
3. Chorea b. Involuntary jerk-
4. Truncal ataxia ing movement
c. Slowness of move-
5. Myoclonus
ments

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278 UNIT 12 DISORDERS OF NEURAL FUNCTION

3. What is a muscle spindle and how does it work? 11. What are the two pathologic types of spinal
chord injury?

4. What areas must be integrated for muscle

movement to be coordinated?
SECTION III: APPLYING YOUR
KNOWLEDGE
Activity F Consider the following scenario and
answer the questions.
5. Describe the molecular causation of Duchene
muscular dystrophy. A 27-year-old man is brought into the emergency
department after falling out of a tree stand while
deer hunting. He is awake and alert and states
that he cannot feel or move his legs. A magnetic
resonance image (MRI) indicates a subluxation of
the vertebrae with fractures above and below the
6. Compare segmental demyelination with ax- subluxation.
onal degeneration in relation to peripheral
1. The man’s wife arrives at the emergency de-
nerve injuries.
partment. She asks you what medicine is in
the intravenous medication and why her hus-
band is receiving it. What would you include
in your answer to her?

7. What is carpal tunnel syndrome?

2. The patient is transferred to a neurosurgic in-

tensive care unit. As the nurse caring for this
8. What are the clinical manifestations of client, what orders would you expect to receive?
Guillain-Barré syndrome?

9. What is the current theory of the pathogene- SECTION IV: PRACTICING

sis of Parkinson disease? FOR NCLEX
Activity G Answer the following questions.
1. The spinal cord contains the basic factors
necessary to coordinate function when a
10. What does amyotrophic lateral sclerosis movement is planned. It is the lowest level of
imply? function. What is the highest level of func-
tion in planning movement?
a. Frontal cortex
b. Cerebral cortex
c. Pons
d. Cerebellum

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CHAPTER 50 DISORDERS OF MOTOR FUNCTION 279

2. Match the neurons with their function/ a. Muscles of the upper arms
description. b. Large muscles of the legs
Neuron Function/Description c. Postural muscles of hip and shoulder
a. Motor neuron and d. Spinal and neck muscles
1. Motor
the group of muscle 6. Antibiotics, such as gentamicin, can produce
neurons
fibers it innervates in a disturbance in the body that is similar to
2. Motor unit a muscle botulism by preventing the release of acetyl-
3. Lower motor b. Control motor func- choline from nerve endings. In persons with
neurons tion preexisting neuromuscular transmission dis-
(LMNs) turbances, these drugs can be dangerous.
c. Project from the
4. Upper motor motor strip in the What disease falls into this category?
neurons cerebral cortex to a. Multiple sclerosis
(UMNs) the ventral horn and b. Duchenne muscular dystrophy
are fully contained
c. Becker muscular dystrophy
within the central
nervous system d. Myasthenia gravis
d. The motor neurons 7. In myasthenia gravis, periods of stress can
supplying a motor produce myasthenia crisis. When does myas-
unit are located in thenia crisis occur?
the ventral horn of a. When muscle weakness becomes suffi-
the spinal cord ciently severe to compromise ventilation
3. Reflexes are basically “hard-wired” into the b. When the patient is too weak to hold up
central nervous system. Anatomically, the his or her head
basis of a reflex is an afferent neuron that
c. When the patient is so weak he or she can-
synapses directly with an effector neuron that
not lift his or her arms
causes muscle movement. Sometimes the af-
ferent neuron synapses with what intermedi- d. When the patient can no longer walk
ary between the afferent and effector 8. Peripheral nerve disorders are not uncom-
neurons? mon. What is an example of a fairly common
a. Neurotransmitter mononeuropathy?
b. Interneuron a. Guillain-Barré syndrome
c. Intersegmental effectors b. Carpal tunnel syndrome
d. Suprasegmental effectors c. Myasthenia gravis
4. The signs and symptoms produced by disor- d. Phalen syndrome
ders of the motor system are useful in finding 9. Herniated disks occur when the nucleus pul-
the disorder. What signs and symptoms posus is compressed enough that it protrudes
would you assess when looking for a disorder through the annulus fibrosus putting pres-
of the motor system? Mark all that apply. sure on the nerve root. This type of injury oc-
a. Spinal reflex activity curs most often in the cervical and lumbar
b. Bulk region of the spine. What is an important
diagnostic test for a herniated disk in the
c. Motor coordination
lumbar region?
d. Muscle innervation
a. Hip flexion test
e. Tone
b. Computed tomography (CT) scan
5. Duchenne muscular dystrophy usually does c. Straight-leg test
not produce any signs or symptoms until
d. Electromyelography
between the ages of 2 and 3. What muscles
are usually first to be affected in Duchenne
muscular dystrophy?

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280 UNIT 12 DISORDERS OF NEURAL FUNCTION

10. Match the cerebellar pathway with its function. a. Decreased immunoglobulin G levels
Cerebellar b. Decreased total protein levels
Pathway Function c. Oligoclonal patterns
a. Maintains equilib- d. Decreased lymphocytes
1. Vestibulocere-
bellar pathway rium and posture 15. At what level of the cervical spine would an
2. Spinocerebellar b. Provides the cir- injury allow finger flexion?
pathway cuitry for coordi- a. C5
nating the
3. Cerebrocere- b. C6
movements of the
bellar c. C7
distal portions of
pathway
the limbs d. C8
c. Coordinates se- 16. A 14-year-old girl has been thrown from the
quential body and back of a pick-up truck. MRI shows broken
limb movements vertebrae at the C2 level. What is the main
11. The basal ganglia play a role in coordinated significance of an injury at this level of the
movements. Part of the basal ganglia system spinal column?
is the striatum which involves local choliner- a. Cannot breathe on own, needs ventilator
gic interneurons. What disease is thought to assistance
be related to the destruction of the choliner- b. Partial or full diaphragmatic function, ven-
gic interneurons? tilation is diminished because of the loss of
a. Parkinson syndrome intercostal muscle function, resulting in
b. Guillain-Barré syndrome shallow breaths and a weak cough
c. Myasthenia gravis c. Intercostal and abdominal musculature is
affected, the ability to take a deep breath
d. Huntington disease
and cough is less impaired
12. What disease results from the degeneration of d. Needs maintenance therapy to strengthen
the dopamine nigrostriatal system of the existing muscles for endurance and mobi-
basal ganglia? lization of secretions
a. Parkinson disease
17. Approximately 6 months after a spinal cord
b. Huntington disease injury, a 29-year-old man has an episode of
c. Guillain-Barré syndrome autonomic dysreflexia. What are the charac-
d. Myasthenia gravis teristics of autonomic dysreflexia? Mark all
that apply.
13. Amyotrophic lateral sclerosis (ALS) is consid-
a. Hypertension
ered a disease of the upper motor neurons.
What is the most common clinical presenta- b. Fever
tion of ALS? c. Skin pallor
a. Rapidly progressive weakness and atrophy d. Vasoconstriction
in distal muscles of both upper extremities e. Piloerector response
b. Slowly progressive weakness and atrophy
18. Bowel dysfunction is one of the most difficult
in distal muscles of one upper extremity
problems to handle after a spinal cord injury.
c. Rapidly progressive weakness and atrophy After a spinal cord injury, most people experi-
in distal muscles of both lower extremities ence constipation. Why does this occur?
d. Slowly progressive weakness and atrophy a. Innervation of the bowel is absent
in distal muscles of one lower extremity
b. Defecation reflex is lost
14. Although no laboratory test is diagnostic for c. Internal anal sphincter will not relax
multiple sclerosis (MS), some patients have al-
d. Peristaltic movements are not sufficiently
terations in their cerebrospinal fluid (CSF)
strong to move stool through the colon
that can be seen when a portion of the CSF is
removed during a spinal tap. What finding in
CSF is suggestive of MS?

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51

CHAPTER
Disorders of
Brain Function

SECTION I: LEARNING of pupillary changes, respiration, and motor

function as the effects of brain dysfunction
OBJECTIVES progress to involve structures in the dien-
cephalon, midbrain, pons, and medulla
1. Differentiate cerebral hypoxia from cerebral
ischemia and focal from global ischemia 12. State two criteria for the diagnosis of brain
death
2. Characterize the role of excitatory amino acids
as a common pathway for neurologic disorders 13. List the major vessels in the cerebral circula-
tion and state the contribution of the internal
3. State the determinants of intracranial pres-
carotid arteries, the vertebral arteries, and the
sure and describe compensatory mechanisms
circle of Willis to the cerebral circulation
used to prevent large changes in intracranial
pressure when there are changes in brain, 14. Describe the autoregulation of cerebral blood
blood, and cerebrospinal fluid volumes flow
4. Explain the causes of tentorial herniation of 15. Explain the substitution of “brain attack” for
the brain and its consequences stroke in terms of making a case for early di-
agnosis and treatment
5. Compare the causes of communicating and
noncommunicating hydrocephalus 16. Differentiate the pathologies of ischemic and
hemorrhagic stroke
6. Compare cytotoxic, vasogenic, and interstitial
cerebral edema 17. Explain the significance of transient ischemic
attacks, the ischemic penumbra, and water-
7. Differentiate primary and secondary brain in-
shed zones of infarction and how these con-
juries due to head trauma
ditions relate to ischemic stroke
8. Describe the mechanism of brain damage in
18. Cite the most common cause of subarachnoid
coup–contrecoup injuries
hemorrhage and state the complications asso-
9. List the constellation of symptoms involved ciated with subarachnoid hemorrhage
in the postconcussion syndrome
19. Describe the alterations in cerebral vascula-
10. Differentiate among the location, manifesta- ture that occur with arteriovenous malfor-
tions, and morbidity of epidural, subdural, mations
and intracerebral hematoma
20. Describe the patterns of motor deficits and
11. Define consciousness and trace the rostral-to- typical problems with speech and language
caudal progression of consciousness in terms that occur as a result of stroke

281
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282 UNIT 12 DISORDERS OF NEURAL FUNCTION

21. List the sequence of events that occur with by the penetrating arteries during an ischemic
meningitis event.
22. Describe the symptoms of encephalitis 7. In many neurologic disorders, various medi-
ators, including excitatory ,
23. List the major categories of brain tumors and
catecholamines, nitric oxide, free radicals,
interpret the meaning of benign and malig-
inflammatory cells, apoptosis, and intra-
nant as related to brain tumors
cellular can cause injury to
24. Describe the general manifestations of brain neurons.
tumors
8. Increased pressure is a common
25. List the methods used in diagnosis and treat- pathway for brain injury from different types
ment of brain tumors of insults and agents.
26. Explain the difference between a seizure and 9. Brain represents a displacement
epilepsy of brain tissue under the falx cerebri or
through the tentorial notch or incisura of the
27. State four or more causes of seizures other
tentorium cerebelli.
than epilepsy
10. Cerebral is an increase in tissue
28. Differentiate between the origin of seizure ac-
volume secondary to abnormal fluid accumu-
tivity in partial and generalized forms of
lation.
epilepsy and compare the manifestations of
simple partial seizures with those of complex 11. The functional manifestations of
partial seizures and major and minor motor edema include focal neurologic
seizures deficits, disturbances in consciousness, and
severe intracranial hypertension.
29. Characterize status epilepticus
12. edema involves an increase in
intracellular fluid.
SECTION II: ASSESSING YOUR 13. The effects of traumatic head injuries can be
UNDERSTANDING divided into two categories:
injuries, in which damage is caused by
Activity A Fill in the blanks. impact; and secondary injuries, in which
damage results from the subsequent brain
1. A number of regulatory mechanisms, includ- swelling, infection, or .
ing the blood–brain barrier and autoregula-
tory mechanisms that ensure its blood 14. usually are caused by head in-
supply, maintain the electrically jury in which the skull is fractured.
active cells. 15. A subdural hematoma develops in the area
2. Although the brain makes up only 2% of the between the dura and the arachnoid and usu-
body weight, it receives 15% of the resting ally is the result of a in the small
cardiac output and accounts for % bridging veins that connect veins on the sur-
of the oxygen consumption. face of the cortex to dural sinuses.

3. Because indicates decreased oxy- 16. is the state of awareness of self

gen levels in all brain tissue, it produces a and the environment and of being able to
generalized depressant effect on the brain. become oriented to new stimuli.

4. Cerebral ischemia can be , as in 17. Brain death is defined as the irreversible loss
stroke, or , as in cardiac arrest. of function of the , including the
brain stem.
5. Excessive influx of during
neural ischemia results in neuronal and inter- 18. The state is characterized by loss
stitial edema. of all cognitive functions and the unaware-
ness of self and surroundings.
6. refers to short serpiginous seg-
ments of necrosis that occur within and par- 19. Cerebral has been classically
allel to the cerebral cortex, in areas supplied defined as the ability of the brain to maintain

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CHAPTER 51 DISORDERS OF BRAIN FUNCTION 283

constant cerebral blood flow despite changes 33. The use of for brain tumors is
in systemic arterial pressure. somewhat limited by the blood–brain barrier.
20. At least three metabolic factors affect cerebral 34. A represents the abnormal be-
blood flow: , , and havior caused by an electrical discharge from
concentration. neurons in the cerebral cortex.
21. is the syndrome of acute focal 35. seizures usually involve only
neurologic deficit from a vascular disorder one hemisphere and are not accompanied by
that injures brain tissue. loss of consciousness or responsiveness.
22. strokes are caused by an inter- 36. seizures involve impairment of
ruption of blood flow in a cerebral vessel and consciousness and often arise from the tem-
strokes are caused by bleeding poral lobe.
into brain tissue.
37. Myoclonic seizures involve brief, involuntary
23. Transient ischemic attack (TIA) or induced by stimuli of cerebral
“ ” is equivalent to “brain origin.
angina” and reflects a temporary disturbance
38. seizures usually present with a
in focal cerebral blood flow, which reverses
person having a vague warning and experi-
before infarction occurs, analogous to
ence a sharp tonic contraction of the muscles
in relation to heart attack.
with extension of the extremities and imme-
24. are the most common cause of diate loss of consciousness.
ischemic strokes, usually occurring in athero-
39. Seizures that do not stop spontaneously or
sclerotic blood vessels.
occur in succession without recovery are
25. infarcts result from occlusion of called .
the smaller penetrating branches of large
cerebral arteries, commonly the middle cere- Activity B Consider the following figure.
bral and posterior cerebral arteries. Anterior

26. An stroke is caused by a moving

blood clot that travels from its origin to the
brain.
27. The most frequently fatal stroke is a sponta-
neous into the brain.
28. The specific manifestations of stroke or TIA
are determined by the that is af-
fected by the area of brain tissue that is sup-
plied by that vessel and by the adequacy of
the collateral circulation.
29. Aneurysmal subarachnoid hemorrhage repre-
sents bleeding into the subarachnoid space
caused by a ruptured .
30. malformations are a complex
tangle of abnormal arteries and veins linked
by one or more fistulas.
31. represents a generalized infec-
tion of the parenchyma of the brain or spinal
cord.
32. occurs with or without nausea, Posterior
may be projectile, and is a common symptom In the figure above, identify the subdural
of increased intracranial pressure (ICP) and hematoma, the epidural hematoma, and the
brain stem compression. intracerebral hematoma.

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284 UNIT 12 DISORDERS OF NEURAL FUNCTION

Activity C Match the key terms in Column A 8. Adhesions may impinge on the cranial
with their definitions in Column B. nerves or impair the outflow of CSF

Column A Column B
1. Vasogenic a. To attend to and react to
edema stimuli coming from the
contralateral side
2. Hypoxia
b. Inability to comprehend,
3. Tentorium integrate, and express
cerebelli language Glutamate
Glutamate
4. Hydro- c. Small cells intimately in-
cephalus volved in local circuitry
5. Aphasia d. Divides the cranial cavity
into anterior and poste-
6. Micro- rior fossae
neurons
e. Reduced or interrupted
7. Ischemia blood flow
8. Decorticate f. Occurs when integrity of
posturing the blood–brain barrier is
disrupted
9. Hemi-
g. Deprivation of oxygen
neglect
with maintained blood
10. Macro- flow
neurons h. Results from lesions of
the cerebral hemisphere
i. Large cells with long 2. Complete the flowchart above using the
axons that leave the following terms:
local network of inter-
communicating neurons • release of intracellular proteases, free radi-
to send action potentials cals, and fragmentation of nuclei
to other regions of the • calcium cascade
nervous system • opening calcium channels
j. Abnormal increase in
• N-methyl-D-aspartate (NMDA) receptor
cerebrospinal fluid (CSF) activation
volume in any part or all
Activity E Briefly answer the following.
of the ventricular system
Activity D
1. To what does “global ischemia” refer and
In the boxes below, put the pathologic process what is the result of global ischemia?
of bacterial meningitis in order:
1. Release endotoxins
2. Development of a cloudy, purulent exudate
in CSF
3. Endotoxins initiate inflammatory response 2. Explain what watershed infarcts are and why
4. Meninges thicken and adhesions form they occur.
5. Bacteria replicate and undergo lysis in CSF
6. Vascular congestion and infarction in the
surrounding tissues
7. Pathogens, neutrophils, and albumin to
move across the capillary wall into the CSF

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CHAPTER 51 DISORDERS OF BRAIN FUNCTION 285

3. What is the mechanism of toxicity of excito- SECTION III: APPLYING YOUR

toxic amino acids?
KNOWLEDGE
Activity F Consider the following scenario and
answer the questions.
A 78-year-old African American woman is
4. What is postconcussion syndrome? brought to the emergency department by ambu-
lance. She was found on the floor of her bedroom
by her daughter in a confused state, and she
could not move her left leg. A diagnosis of stroke
is suspected.

5. Compare the general manifestations of global 1. When taking the nursing history, for what risk
and focal brain injury. factors would you assess?

6. What are the two components of consciousness? 2. The diagnosis of ischemic stroke is confirmed.
What are the signs of altered consciousness? What orders would the nurse expect to receive
from the physician for acute ischemic stroke?

7. How are pupillary reflexes used to evaluate

levels of brain function?

SECTION IV: PRACTICING

FOR NCLEX
Activity G Answer the following questions.
8. What is the ischemic penumbra of an is-
1. Match the type of brain insult to its definition.
chemic stroke and how does it affect the de-
gree of irreversible damage? Type Definition
1. Hypoxic a. Excessive activity
2. Ischemic of the excitatory
neurotransmitters
3. Excitotoxic
and their receptor-
4. Increased mediated effects
9. Why do arteriovenous malformations predis-
intercranial
pose a patient to stroke? b. Displacement of
volume and
brain tissue under
pressure
the falx cerebri or
5. Brain through the tentor-
herniation ial notch or incisura
6. Cerebral of the tentorium
10. What are some of the possible causes of a edema cerebelli
seizure? 7. Hydro- c. Interferes with de-
cephalus livery of oxygen
and glucose as well
as the removal of
metabolic wastes

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286 UNIT 12 DISORDERS OF NEURAL FUNCTION

d. An abnormal increase dilated. The sulci on the

in cerebrospinal fluid surface of the brain be-
volume in any part or come effaced and shal-
all of the ventricular low, and the white
system matter is reduced in
e. Swelling of the brain volume.
f. Increase in intercra- g. Tissue perfusion becomes
nial tissue causing an inadequate, cellular
increase in intracra- hypoxia results, and neu-
nial pressure ronal death can occur.
g. Decreased oxygen lev- 3. Several types of brain injuries can occur.
els in all brain tissue What are the primary (or direct) brain in-
2. Match the type of brain insult to its effect on juries? Mark all that apply.
the brain a. Focal lesions of laceration
Type Effect on Brain b. Contusion
c. Hypoxic
1. Brain a. Can be focal or
herniation global, with only d. Diffuse axonal
2. Hypoxic one part of the e. Hemorrhage
brain being under-
3. Ischemic 4. Global and focal brain injuries manifest dif-
perfused or all of
4. Increased ferently. What is almost always a manifesta-
the brain being
intercranial tion of a global brain injury?
compromised
volume and a. Altered level of consciousness
b. Neuronal cell in-
pressure b. Change in behavior
jury and death
5. Excitotoxic c. Respiratory instability
c. Clouding of con-
6. Hydro- sciousness, bilater- d. Loss of eye movement reflexes
cephalus ally small pupils
5. You are the nurse caring for a 31-year-old
7. Cerebral (approximately 2
trauma victim admitted to the neurologic in-
edema mm in diameter)
tensive care unit (ICU). During your initial as-
with a full range of
sessment, you find that the patient is flexing
constriction, and
arms, wrists, and fingers. There is abduction
motor responses to
of the upper extremities with internal rota-
pain that are pur-
tion and plantar flexion of the lower extremi-
poseful or semipur-
ties. How would you describe this in your
poseful (localizing)
nursing notes?
and often asym-
metric a. Decerebrate posturing
d. Depends on the b. Decorticate posturing
brain’s compen- c. Extensor posturing
satory mechanisms d. Diencephalon posturing
and the extent of
the swelling 6. Brain death is the term used when irreversible
loss of function of the entire brain occurs. A
e. Generalized depres-
clinical examination must be done and repeated
sant effect on the
at least 6 hours later with the same findings for
brain
brain death to be declared. What is not assessed
f. Cerebral hemi- in the clinical examination for brain death?
spheres become en-
a. Blink reflex
larged, and the
ventricular system b. Responsiveness
beyond the point c. Electrocardiographic (ECG) findings
of obstruction is d. Respiratory effort

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CHAPTER 51 DISORDERS OF BRAIN FUNCTION 287

7. Much as with brain death, there are criteria 12. Match the type of seizure with its definition.
for the diagnosis of a persistent vegetative
Type of Seizure Definition
state, and the criteria have to have lasted for
more than 1 month. What are criteria for the 1. Unprovoked a. Motion takes the
diagnosis of persistent vegetative state? Mark 2. Complex form of automa-
all that apply. partial tisms such as lip
a. Bowel and bladder incontinence seizures smacking, mild
clonic motion (usu-
b. Ability to open the eyes 3. Generalized-
ally in the eyelids),
c. Lack of language comprehension onset
increased or de-
d. Lack of sufficient hypothalamic function 4. Absence creased postural
to maintain life seizures tone, and auto-
e. Variable preserved cranial nerve reflexes 5. Atonic nomic phenomena
6. Tonic-clonic b. These seizures also
8. The regulation of cerebral blood flow is ac-
are known as drop
complished through both autoregulation and
attacks
local regulation. This allows for the brain to
meet its metabolic needs. What is the low pa- c. Most common
rameter for blood pressure before cerebral major motor seizure
blood flow becomes severely compromised? d. Clinical signs,
a. 30 mm Hg symptoms, and sup-
porting electroen-
b. 40 mm Hg
cephalographic
c. 50 mm Hg (EEG) changes indi-
d. 60 mm Hg cate involvement of
both hemispheres
9. Intracranial aneurysms that rupture cause sub-
at onset
arachnoid hemorrhage in the patient. How is
the diagnosis of intracranial aneurysms and e. Begins in a localized
subarachnoid hemorrhage made? area of the brain
but may progress
a. Lumbar puncture
rapidly to involve
b. Magnetic resonance imaging (MRI) both hemispheres
c. Loss of cranial nerve reflexes f. No identifiable cause
d. Venography can be determined
10. When the suspected diagnosis is bacterial 13. For seizure disorders that do not respond to
meningitis, what assessment techniques can anticonvulsant medications, an option for sur-
assist in determining the presence of gical treatment exists. What is removed in the
meningeal irritation? most common surgery for seizure disorders?
a. Kernig sign and Chadwick sign a. Temporal neocortex
b. Brudzinski sign and Kernig sign b. Hippocampus
c. Brudzinski sign and Chadwick sign c. Entorhinal cortex
d. Chvostek sign and Guedel sign d. Amygdala

11. Manifestations of brain tumors are focal dis- 14. Generalized convulsive status epilepticus is a
turbances in brain function and increased in- medical emergency caused by a tonic-clonic
tracranial pressure (ICP). What causes the focal seizure that does not spontaneously end, or
disturbances manifested by brain tumors? recurs in succession without recovery. What
is the first-line drug of choice to treat status
a. Tumor infiltration and increased blood
epilepticus?
pressure
a. Intravenous (IV) diazepam
b. Brain compression and decreased ICP
b. Intramuscular (IM) lorazepam
c. Brain edema and disturbances in blood flow
c. IV cyclobenzaprine
d. Tumor infiltration and decreased ICP
d. IM cyproheptadine

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52
CHAPTER

Sleep and Sleep Disorders

SECTION I: LEARNING 10. Explain the physiologic mechanisms, con-

tributing factors, and manifestations of ob-
OBJECTIVES structive sleep apnea and describe the methods
used in diagnosis and treatment of the disorder
1. Cite the major brain structures that are in-
volved in sleep 11. Define the term parasomnias and relate it to
the manifestations of nightmare, sleep ter-
2. Describe the different stages of sleep in terms
rors, and sleep walking
of the electroencephalogram (EEG) tracing,
eye movements, motor movements, heart 12. Characterize normal sleep patterns of the in-
rate, blood pressure, and cerebral activity fant and small child and relate them to the
development of sleep disorders
3. Characterize the circadian rhythm as it relates
to sleep and wakefulness 13. Describe the normal changes in sleep stages
that occur with aging and relate them to
4. Describe the possible role of melatonin in reg-
sleep problems in the elderly
ulation of sleep
5. List the four categories of sleep disorders in-
cluded in the International Classification of SECTION II: ASSESSING YOUR
Sleep Disorders
UNDERSTANDING
6. Describe the methods used in diagnosis of
sleep disorders, including the sleep history, Activity A Fill in the blanks.
sleep diary, polysomnography, and wrist
1. is a time of mental activity and
actigraphy
energy expenditure; is a period
7. Characterize the non–24-hour sleep–wake of inactivity and restoration of mental and
syndrome experienced by visually impaired physical function.
individuals, sleep disorders associated with
2. Many hormones, such as growth hormone,
acute shifts in the sleep–wake cycle due to in-
are produced in a cyclic manner correlating
tercontinental travel and shift work, and ad-
with the sleep–wake cycle, suggesting that
vanced sleep phase and delayed sleep phase
and tissue may
circadian rhythm sleep disorders
occur during sleep.
8. Describe the causes, manifestations, diagno-
3. The of the midbrain, pons, and
sis, and treatment of acute and chronic in-
brain stem monitors and modulates the activ-
somnia
ity of various circuits controlling wakefulness.
9. Differentiate periodic limb movement disor-
4. The normal consists of brain
der and restless legs syndrome in terms of
waves of various frequencies rather than the
manifestations and treatment
combined activity and “cross-talk” among

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CHAPTER 52 SLEEP AND SLEEP DISORDERS 289

many hundreds of neurons responding to a 19. persons have more fragmented

given stimulus. sleep and shorter duration of stage 3 and 4
sleep.
5. sleep is a quiet type of sleep
characterized by a relatively inactive, yet fully
Activity B Consider the following figure.
regulating brain, and fully movable body.
6. sleep is associated with rapid
eye movements, loss of muscle movements,
and vivid dreaming.
7. It has been shown that adequate amounts of
sleep are necessary for normal
daytime functioning.
8. , a hormone produced by the
pineal gland, is thought to help regulate the
sleep–wake cycle and, possibly, circadian
rhythm.
9. A is fundamental to the process
of identifying the nature of a sleep disorder.
10. The are disorders that produce
either excessive sleepiness or difficulty initiat-
ing or maintaining sleep.
11. The non–24-hour sleep–wake syndrome con-
sists of a lack of between the in-
ternal sleep–wake rhythm and the external
24-hour day.
12. is caused by the sudden loss of
synchrony between a traveler’s intrinsic circa-
dian clock and the local time of the flight’s
destination.
13. People with have trouble stay-
In the figure above, label the structures of the
ing awake in the evening and have to curtail
mouth and throat; highlight those involved in
evening activities to avoid falling asleep.
obstructive sleep apnea.
14. has been defined as three or
• uvula
more of the following: difficulty initiating
• soft palate
sleep, difficulty maintaining sleep, waking up
• nasopharynx
too early, or sleep that is chronically non-
• oropharynx
restorative or poor in quality.
• laryngopharynx
15. Sleep refers to a set of rules and • tongue
information about personal and environmen- • epiglottis
tal activities that affect sleep.
Activity C Match the key terms in Column A
16. is characterized by episodes of
with their definitions in Column B.
repetitive movement of the large toe with flex-
ion of the ankle, knee, and hip during sleep. Column A Column B
17. Apnea is defined as cessation of airflow 1. Thalamo- a. A sudden recurrent
through the nose and mouth for cortical loop uncontrollable com-
or longer. pulsion to sleep
2. Narcolepsy
18. are vivid and terrifying noctur- b. Interrupted sleep
3. Periodic caused by disor-
nal episodes in which the dreamer is abruptly
breathing dered breathing
awakened from sleep.

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290 UNIT 12 DISORDERS OF NEURAL FUNCTION

4. Confusional c. EEG pattern that occurs 5. What are the components of a typical
arousals when a persons eyes polysomnography?
are open
5. Alpha
rhythm d. Measures muscle
motion
6. Actigraphy
e. Recollections of mental
7. Dreams activity that occurred
6. What are some of the common causes of
during sleep
8. Sleep apnea chronic insomnia?
f. Marked confusion,
9. Entrainment slow and inappropriate
10. Beta rhythm responses to questions,
and nonpurposeful
activities
g. EEG pattern that occurs 7. How does the National Institute of Health de-
when a person is awake fine restless leg syndrome (RLS)?
with eyes closed
h. Daily resetting of the
circadian clock
i. Differential patterns of
breathing associated 8. What is the pathologic mechanism of sleep
with non-REM sleep apnea?
j. Pathways between each
sensory area of the thal-
amus and the cortex

Activity D Briefly answer the following.

1. What is the sleep–wake cycle? Describe both
what it means to sleep and to be awake.
SECTION III: APPLYING YOUR
KNOWLEDGE
Activity E Consider the following scenario and
answer the questions.
2. What are the four stages of non-REM sleep and
what occurs during each stage? A 52-year-old man is being admitted for a sleep
study. He reports a history of severe snoring,
obesity for more than 10 years, falling asleep at
work, and waking frequently during the night.
His presumptive diagnosis is obstructive sleep
apnea.
3. What are the physiologic changes that are 1. As he is being prepared for the study, the pa-
seen during REM sleep? tient asks what obstructive sleep apnea is.
Your correct response would be what?

4. What are the categories of sleep disorders set

by the American Sleep Disorders Association?

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CHAPTER 52 SLEEP AND SLEEP DISORDERS 291

2. The patient asks how many episodes of apnea c. Symptoms that are worse in the afternoon
does it take to be diagnosed with obstructive d. Symptoms that become worse at rest
sleep apnea. Your correction response would
be what? 5. Match the type of dyssomnia with their
definition.
Type of
Dyssomnia Definition
1. Jet lag a. A lack of synchroniza-
3. The patient asks what his treatment would be tion between the in-
2. Change
if he is diagnosed with severe sleep apnea. You ternal sleep–wake
in sleep
would expect orders for what? rhythm and the exter-
phase
nal 24-hour day
disorder
b. Advanced or delayed
3. Shift sleep phase syndrome
work
c. Clash between shift
sleep
demands for wakeful-
disorder
ness as part of the
SECTION IV: PRACTICING 4. Non– work environment
FOR NCLEX 24-hour and the sleep setting
sleep–wake of the worker’s intrin-
Activity F Answer the following questions. syndrome sic circadian clock.
5. Insomnia d. Sudden loss of syn-
1. One of the stages of sleep is the rapid eye
chrony between a
movement, or REM, stage. What is it that the 6. Narcolepsy traveler’s intrinsic cir-
brain cannot do during REM sleep?
cadian clock and the
a. Acquire new sensory information local time of the
b. Regulate blood pressure flight’s destination.
c. Replay previous memories e. A syndrome character-
d. Arouse auditory and visual systems ized by abnormal sleep
tendencies, including
2. What hormone does the pineal gland synthe- excessive daytime
size and release under the direct control of sleepiness, disturbed
the suprachiasmatic nucleus (SCN)? nocturnal sleep, and
a. Growth hormone manifestations related
b. Melatonin to REM sleep, such as
cataplexy (brief peri-
c. Cortisol
ods of muscle weak-
d. Dehydroepiandrosterone (DHEA) ness), hypnagogic
3. The multiple sleep latency test (MSLT) is a di- hallucinations, and
agnostic sleep study used to evaluate daytime sleep paralysis.
sleepiness. What result of an MSLT would be f. Sleep that is chroni-
considered abnormal? cally nonrestorative or
a. 10 minutes poor in quality
b. 12 minutes 6. Sleepwalking can occur in both adults and
c. 4 minutes children. Typically, what does someone who
d. 5 minutes is sleepwalking do?
a. Refuse to respond to communication efforts
4. Restless leg syndrome (RLS) is a disorder that
of other people
has its peak onset in middle age. Diagnosis of
RLS is based on a history of what? b. Go outside
a. Compelling urge to rest legs c. Appear alert
b. Motor relaxation d. Fix something to eat

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292 UNIT 12 DISORDERS OF NEURAL FUNCTION

7. The onset of sleep terrors is usually between 9. In what disease is often seen more frequent
the ages of 2 and 4 years. What are the mani- periods of nighttime awakening and daytime
festations of sleep terrors? Mark all that apply. sleeping?
a. Dilated pupils a. Parkinson disease
b. Rapid breathing b. Huntington disease
c. Tachycardia c. Alzheimer disease
d. Screams on awakening d. Amyotrophic lateral sclerosis (ALS)
e. Refuses to go to sleep in own bed 10. Actigraphy can be used to diagnose sleep dis-
8. The prevalence of sleep disorders increases turbances. The actigraph is worn on the wrist
with age. Medication use is one reason for and is used most commonly with what?
this. What medication can have a stimulating a. A sleep diary
effect that interferes with sleep? b. CPAP
a. Vasoconstrictors c. Video tape of sleep
b. Antihypertensives d. Trial pharmacologic substances
c. Beta blockers
d. Vasodilators

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53

CHAPTER
Disorders of Thought,
Mood, and Memory

SECTION I: LEARNING 12. Cite the diagnostic criteria for schizophrenia

according to the DSM-IV-TR classification
OBJECTIVES
13. Describe the treatment for the positive and
1. Define the terms biologic psychiatry and psy- negative manifestations of schizophrenia
chosocial psychiatry and compare them in
14. Define the terms depression and mania
terms of their definitions of the origins of
mental disease 15. Describe the epidemiology of major depres-
sion and bipolar depression
2. Describe the changes in the treatment of
mental illness over the past three centuries 16. Describe the manifestations of major depres-
sion and bipolar depression
3. Explain the role that heredity plays in the epi-
demiology and development of mental illness 17. Cite the diagnostic criteria for depression ac-
cording to the DSM-IV-TR classification
4. Name the cerebral cortical structures and
structures from the primitive brain involved 18. Describe the treatment modalities for depres-
in thought and emotion sion
5. Describe the major functions of each brain 19. Define the terms panic disorder, generalized
structure in terms of thought processes, learn- anxiety disorder, social phobia, and obsessive-
ing, and emotion compulsive disorder
6. Describe the cortical pathways by which learn- 20. Describe the epidemiology of panic disorder,
ing and the development of memory occur generalized anxiety disorder, social phobia,
and obsessive-compulsive disorder
7. Define the terms synapse, synaptic
transmission, and neuromediators 21. Describe the manifestations of panic disorder,
generalized anxiety disorder, social phobia,
8. Name the major neuromediators in the
and obsessive-compulsive disorder and the
brain, their major location and source, and
underlying neuropathophysiology of each
possible involvement of each in the manifes-
tations of mental illness 22. Cite the diagnostic criteria for panic disorder,
generalized anxiety disorder, social phobia,
9. Define the term schizophrenia
and obsessive-compulsive disorder according
10. Describe the epidemiology of schizophrenia to the DSM-IV-TR classification
11. Describe the manifestations of schizophrenia, 23. Describe the treatment for panic disorder,
both positive and negative symptoms, and generalized anxiety disorder, social phobia,
their underlying neuropathophysiology and obsessive-compulsive disorder

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294 UNIT 12 DISORDERS OF NEURAL FUNCTION

24. Define substance dependence 4. The lobe is the largest lobe and
is often referred to as the chief administrator
25. Describe the epidemiology of addiction disor-
of the brain.
ders
5. A large part of the cerebral cortex forms
26. Describe the neurophysiologic alterations as-
areas that add perception and
sociated with substance dependence
meaning to incoming sensory information.
27. Cite the actions of medications used in the
6. The association area functions
treatment of substance dependence
in close connection with the motor cortex to
28. State the criteria for a diagnosis of dementia plan and execute complex motor movements.
29. Compare the causes associated with 7. Two disorders of information processing,
Alzheimer disease, vascular dementia, fron- and thoughts, are
totemporal dementia, Creutzfeldt-Jakob dis- common symptoms of many psychiatric dis-
ease, Wernicke-Korsakoff syndrome, and orders.
Huntington disease
8. hallucinations occur when a
30. Describe the changes in brain tissue that normal sensory input is blocked and, as a re-
occur with Alzheimer disease placement, stored images are experienced,
whereas hallucinations are pro-
31. Use the three stages of Alzheimer disease to
duced by abnormal neuronal discharges.
describe its progress
9. are characterized by a false be-
32. Cite the difference between Wernicke disease
lief and the persistent, unshakable acceptance
and the Korsakoff component of the
of the false belief.
Wernicke-Korsakoff syndrome
10. The treatment of many psychiatric disorders
is based on pharmacologic interventions that
alter or properties
SECTION II: ASSESSING of the brain.
YOUR UNDERSTANDING
11. alleviate depressive symptoms
Activity A Fill in the blanks. by increasing the activity of norepineph-
rine and serotonin at postsynaptic membrane
1. One view of psychiatric illness is that mental receptors.
disorders are due to anatomic, developmen-
tal, and functional disorders of the brain, and 12. is a chronic debilitating psy-
is called psychiatry. Another chotic disorder that affects thinking, feeling,
view is that mental disorders are due to im- perceiving, behaving, and experiencing the
paired psychological development, a conse- environment without the normal linkages to
quence of poor child rearing or that environment.
environmental stress, and is called 13. Mood disorders are disorders of
psychiatry. rather than disturbances of thought.
2. The introduction of as a treat- 14. is characterized by the same
ment for schizophrenia revolutionized psy- symptoms as major depression, but in a
chiatry because, although it did not cure milder form.
psychosis, it did control the symptoms of the
disease, increasing the potential for more tra- 15. is a hypothesized phenomenon
ditional therapies to work and allowing previ- in which a stressor creates an electrophysio-
ously institutionalized individuals to lead logic vulnerability to future stressful events
much more normal lives. by causing long-lasting changes in neuronal
function.
3. There is scientific evidence that anatomic and
biochemical in the brain play a 16. Dopamine activity has also been implicated
critical role in the behaviors observed in men- in mood disorders, with
tal illness. dopamine activity found in depression, and
dopamine activity in mania.

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CHAPTER 53 DISORDERS OF THOUGHT, MOOD, AND MEMORY 295

17. Substance refers to repeated use 28. disease is characterized by acute

of alcohol or other drugs resulting in func- weakness and paralysis of the extraocular
tional problems; substance muscles, nystagmus, ataxia, and confusion.
refers to the behaviors exhibited when an
29. disease is a hereditary disorder
individual is unable to control the use of
characterized by chronic progressive chorea,
drugs or alcohol and continues to use them
psychological changes, and dementia.
despite negative consequences.
30. Postmortem studies have shown a decrease of
18. problems that are associated
and in the basal
with normal aging tend to reflect a general-
ganglia of persons dying of Huntington
ized decrease in the efficiency by which infor-
disease.
mation is processed and retrieved.
19. The diagnosis of is based on as- Activity B Consider the following figures.
sessment of the presenting problem; history
about the person that is provided by an infor-
mant; complete physical and neurologic ex-
amination; evaluation of cognition,
behavioral, and functional status; and labora-
tory and imaging studies.
20. disease is characterized by corti-
cal atrophy and loss of neurons, particularly
in the parietal and temporal lobes.
21. The major microscopic features of Alzheimer
disease are the presence of ,
, and amyloid angiopathy.
A
22. A major component of the paired helical fila-
ments is an abnormally hyperphosphorylated
form of the protein , an axonal
microtubule-associated protein that enhances
microtubule assembly.
23. Death related to Alzheimer disease can occur
because of complications related to
.
24. The use of have been shown to
be effective in slowing the progression of
Alzheimer disease by potentiating the action
of available acetylcholine.
25. dementia is caused by brain
injury resulting from ischemic or hemor-
rhagic damage. B

26. Originally known as Pick disease, 1. In this figure, locate the following structures of
now refers to a syndrome that the brain that are linked to behavior:
includes primary progressive aphasia, corti-
• Amygdala
cobasal degeneration, progressive supranu-
• Mammillary body
clear palsy, and semantic dementias.
• Olfactory bulb
27. Creutzfeldt-Jakob disease is a rare rapidly de- • Frontal lobe
generative form of dementia believed to be • Parietal lobe
caused by an infective protein agent called a • Occipital lobe
. • Temporal lobe
• Central fissure

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296 UNIT 12 DISORDERS OF NEURAL FUNCTION

• Transverse fissure 7. Parietal familiar, as well as ap-

• Parietooccipital fissure lobe propriate interpreta-
• Cingulate gyrus tion of and response to
8. Neolo-
• Corpus callosum social contexts
gisms
• Anterior nucleus of thalamus f. Integration and pro-
• Fornix 9. Wernicke cessing of sensory (vi-
• Parahippocampus gyrus area sual, tactile, and
• Hippocampus auditory) input
10. Tangentia-
lity g. Sensory perceptions
with a compelling
Motor sense of reality
Somato-
sensory h. Responsible for lan-
guage comprehension
i. Receives visual infor-
mation
j. Severed the connec-
Auditory
tions between the pre-
Vision frontal areas of the
Broca brain and the remain-
area der of the brain
Limbic Wernicke
2.
association area
area Column A Column B

2. In this figure, label the corresponding area of 1. Mesolimbic a. Cognitive decline

the brain for the following functions: dopamine caused by any dis-
system order that perma-
• Behavior, emotions, motivation nently damages
• Word formation 2. Disorganized
large association
• Planning complex movements and elabora- schizophrenia
areas of the cerebral
tion of thoughts 3. Obsessive- hemispheres or sub-
• Spatial coordinates of body and surroundings compulsive cortical areas sub-
• Language comprehension and intelligence disorder serving memory
• Visual processing of words and learning
• Naming of objects 4. Dementia
b. Marked by racing
5. Anhedonia thoughts, high dis-
Activity C Match the key terms in Column A
with their definitions in Column B. 6. Dyskinesias tractibility, and
rapid and pressured
1. 7. Mania speech
Column A 8. Paranoid c. Major component
Column B
schizo- of neuritic plaque
1. Delusions
a. Using invented words phrenia d. Anxiety disorder
2. Prefrontal b. Abnormalities of characterized by re-
9. Amyloid
lobotomy thought current obsessions
precursor
3. Alogia c. Inability to stick to the protein and compulsions
original point e. Brain area that
4. Occipital 10. Anxiety
d. Tendency to speak adapts to habitual
lobe disorder
very little use of drugs
5. Temporal f. Inability to experi-
e. Integrates and inter-
lobe ence pleasure in
prets somatic, visual,
6. Halluci- and auditory informa- things that are ordi-
nations tion that is critical for narily pleasurable
recognition of the

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CHAPTER 53 DISORDERS OF THOUGHT, MOOD, AND MEMORY 297

g. Distortion in perform- 6. What are the symptoms of schizophrenia?

ing voluntary move- What is meant by positive and negative?
ments
h. Schizophrenia that
manifests with perse-
cutory or grandiose
delusions
7. What are the anatomic abnormalities associ-
i. Excessive worry that is
ated with schizophrenia?
not easily controlled
j. Disintegration of the
personality and a pre-
dominance of nega-
tive symptoms
8. What is meant by “major depressive disorder?”
Activity D Briefly answer the following.
1. What is known about the genetic potential of
mental illness?

9. There are several types of depression.

Each is categorized by its manifestations and
symptoms. What are the types and their
related manifestations?
2. What is the function of the hippocampus?

10. What is the biogenic amine theory of depres-

3. What can be said about how the brain physi-
sion?
ologically perceives thought and memory?

11. What are the manifestations of a panic at-

4. Which neurotransmitters have been impli-
tack? Why must it be considered, initially, as
cated in metal illness? a critical health problem?

5. What are the major types of antidepressants,

12. What is believed to be the cause of Alzheimer
and how do they work? disease?

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298 UNIT 12 DISORDERS OF NEURAL FUNCTION

SECTION III: APPLYING YOUR 4. What is the task of the prefrontal area of the
brain?
KNOWLEDGE
a. Control speech
Activity E Consider the following scenario b. Control hearing
and answer the question. c. Manage information
A 65-year-old woman has just been diagnosed d. Comprehend language
with Alzheimer disease. She calls the clinic and
5. Sensory input from the environment is re-
asks if she and her family can come in and have
ceived by what area of the brain?
someone talk to them about the disease. The nurse
sets aside time for this patient and her family. a. Hypothalamus
b. Broca’s area
1. In teaching this family about Alzheimer dis-
ease, what are the major points she should c. Amygdala
convey to them? d. Thalamus
6. Thought and memory pass across synapses in
the brain. What are the neural circuits trans-
mitted by new or reactivated pathways
called?
a. Memory traces
b. Information processing
SECTION IV: PRACTICING c. Information storage
FOR NCLEX d. Memory searches

Activity F Answer the following questions. 7. Hallucinations can be categorized in several

ways. What hallucinations are the products of
1. In the 1960s, the deinstitutionalization of the abnormal neuronal discharges?
mentally ill occurred along with a move to
a. Visual
community psychiatry. What was a cause of
this movement? b. Ictal
a. Psychopharmacology c. Emotional
b. Medicalizing of deviance d. Release
c. Feeling that a calming environment was 8. Hallucinations are abnormalities of percep-
crucial tion, whereas delusions are abnormalities of
d. Homelessness thought. What have delusions been associ-
ated with?
2. In the 1990s, studies were conducted on
a. Sensory overload
whether mental illness had a genetic basis.
What do the results of the studies show? b. Disorders of information management
a. Mental illness is a Mendelian trait c. Sensory deprivation
b. Mental illness is polygenic d. Disorders of speech
c. Mental illness is a recessive trait 9. The emergence of psychotropic medications
d. Mental illness is based solely on environ- gave us the ability to target specific actions in
ment the brain as treatment for mental illness.
Which psychotropic medication is a
3. What are the major neuromediators? Mark all monoamine oxidase inhibitor?
that apply.
a. Valium
a. Norepinephrine
b. Halcion
b. Gamma-aminobutyric acid
c. Paxil
c. Succinylcholine
d. Nardil
d. Serotonin
e. Dopamine

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CHAPTER 53 DISORDERS OF THOUGHT, MOOD, AND MEMORY 299

10. Schizophrenia is a complex disease that c. Thymus

strikes men and women equally. What is a d. Amygdala
common sign or symptom of schizophrenia
in its early stages? 15. Obsessive-compulsive disorder (OCD) is a dis-
order that remains under investigation as to
a. Enhancement of senses
its actual neurophysiology. What is OCD be-
b. Using invented words lieved to be a product of?
c. Visual hallucinations a. Dysfunction of the caudate nucleus
d. Catatonic behavior b. Overexcitement of the globus pallidus
11. Match the subclassification of depression or c. Hypersensitive reaction of the frontal cortex
dysthymia with its symptoms. d. Dysfunction of the amygdala
Subclassification Symptoms 16. Abuse and addiction are believed to have a
1. Catatonic a. Increased emphasis neurophysiologic basis. What does habitual
related to the baby use of drugs or alcohol do to the body?
2. Melancholic
b. Low self-esteem, a. Decrease serotonin reuptake
3. Atypical sleep and energy b. Increase dopamine transmission
4. Postpartum problems c. Alter gamma-aminobutyric acid pathways
c. Hypersomnia d. Reduce the brain’s ability to adapt
5. Dysthymia
d. Excessive mobility or
17. Wernicke-Korsakoff syndrome is a dementia
motoric immobility
that is associated with chronic alcoholism.
e. Insomnia with early It is caused by a deficiency in thiamine
morning awakening (vitamin B12). What is the most distinctive
12. Bipolar disorder, also called manic-depressive sign or symptom of this syndrome?
disorder, has a variety of subclassifications a. Loss of memory
based on the manic episodes of the disorder. b. Inability to interact with environment
What is the severity of manic symptoms c. Confabulation
called?
d. Isolationism
a. Mania
b. Cyclothymia 18. Huntington disease is a genetic disorder that
does not usually manifest itself until the pa-
c. Specifier
tient is in his or her 40s or 50s. What are the
d. Kindling most common early psychological changes
13. Anticonvulsive medications are used in the that occur with Huntington disease? Mark all
treatment of bipolar depression. What other that apply.
drug is used to treat bipolar disorder? a. Moodiness
a. Valium b. Impulsive behavior
b. Flexeril c. Personality changes
c. Lithium d. Mania
d. Restoril e. Heightened sensory awareness

14. Panic attacks may result from a “fear net-

work” that has become abnormally sensitive.
Where is this “fear network” centered?
a. Hippocampus
b. Prefrontal cortex

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54
CHAPTER

Disorders of
Visual Function

SECTION I: LEARNING 13. Describe changes in eye structure that occur

with near and farsighted vision
OBJECTIVES
14. Describe the changes in lens structure that
1. State the cause of eyelid weakness occur with cataract
2. Define the terms entropion and ectropion 15. Cite risk factors and visual changes associated
with cataract
3. Explain the differences between marginal ble-
pharitis, a hordeolum, and a chalazion as to 16. Describe the treatment of persons with
causes and manifestations cataracts
4. State the causes and treatment of dry eye 17. Relate the phagocytic function of the retinal
pigment epithelium to the development of
5. Compare symptoms associated with red eye
retinitis pigmentosa
caused by conjunctivitis, corneal irritation,
and acute glaucoma 18. Cite the manifestations and long-term visual
effects of papilledema
6. Describe the appearance of corneal edema
19. Describe the pathogenesis of background and
7. Characterize the manifestations, treatment,
proliferative diabetic retinopathies and their
and possible complications of bacterial, Acan-
mechanisms of visual impairment
thamoeba, and herpes keratitis
20. Relate the role of posterior vitreous detach-
8. Describe the structures of the uveal tract
ment to the development of retinal tears and
9. Describe tests used in assessing the pupillary detachment
reflex and cite the possible causes of abnor-
21. Explain the pathology and visual changes
mal pupillary reflexes
associated with macular degeneration
10. Describe the formation and outflow of aque-
22. Characterize what is meant by a visual field
ous humor from the eye and relate to the de-
defect
velopment of glaucoma
23. Explain the use of perimetry in the diagnosis
11. Compare open-angle and angle-closure glau-
of a visual field defect
coma in terms of pathology, symptomatol-
ogy, and diagnosis and treatment 24. Define the terms hemianopia, quadrantanopia,
heteronymous hemianopia, and homonymous
12. Explain why glaucoma leads to blindness
hemianopia and relate them to disorders of
the optic pathways

300
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CHAPTER 54 DISORDERS OF VISUAL FUNCTION 301

25. Describe visual defects associated with disor- 9. Symptoms of are a foreign body
ders of the visual cortex and visual associa- sensation, a scratching or burning sensation,
tion areas itching, and photophobia.
26. Describe the function and innervation of the 10. conjunctivitis is a severe, sight-
extraocular muscles threatening ocular infection.
27. Recognize the use of smooth pursuit, sac- 11. The is avascular and obtains its
cadic, and vergence conjugate gaze move- nutrient and oxygen supply by diffusion from
ments in self or others blood vessels of the adjacent sclera, from the
aqueous humor at its deep surface, and from
28. Explain the difference between paralytic and
tears.
nonparalytic strabismus
12. refers to inflammation of the
29. Define amblyopia and explain its pathogenesis
cornea caused by infections, misuse of con-
30. Explain the need for early diagnosis and tact lenses, hypersensitivity reactions, is-
treatment of eye movement disorders in chemia, trauma, defects in tearing, and
children interruption in sensory innervation, as occurs
with local anesthesia.
13. Herpes simplex virus with stro-
SECTION II: ASSESSING YOUR mal scarring is the most common cause of
UNDERSTANDING corneal ulceration and blindness in the
Western world.
Activity A Fill in the blanks.
14. Herpes zoster usually presents
1. The optic globe, commonly called the with malaise, fever, headache, and burning
, is a remarkably mobile, nearly and itching of the periorbital area.
spherical structure contained in a pyramid-
15. The is an adjustable diaphragm
shaped cavity of the skull called the orbit.
that permits changes in pupil size and in the
2. The outer layer of the eyeball consists of a light entering the eye.
tough, opaque, white, fibrous layer called the
16. Inflammation of the entire uveal tract, which
.
supports the lens and neural components of
3. The upper and lower eyelids, the the eye, is called .
, are modified folds of skin with
17. With diffuse damage to the forebrain involv-
associated muscle and cartilaginous plates
ing the thalamus and hypothalamus, the
that protect the eyeball.
are typically small but respond
4. Two striated muscles, the and to light.
the , provide for movement of
18. includes a group of conditions
the eyelids.
that produce an elevation in intraocular
5. is a common bilateral inflam- pressure.
mation of the anterior or posterior structures
19. In persons with glaucoma, temporary or per-
of eyelid margins.
manent impairment of vision results from
6. blepharitis is usually associated changes in the retina and optic
with dandruff of the scalp or brows. nerve and from corneal edema and opacifi-
cation.
7. The main symptoms of are irri-
tation, burning, redness, and itching of the 20. glaucoma is caused by a disorder
eyelid margins. in which the anterior chamber retains its fetal
configuration, with aberrant trabecular mesh-
8. blepharitis is inflammation of the
work extending to the root of the iris, or is
eyelids that involves the meibomian glands.
covered by a membrane.

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302 UNIT 13 DISORDERS OF SPECIAL SENSORY FUNCTION

21. Nonuniform curvature of the refractive 32. eye movements are sudden,
medium comparing the horizontal and verti- jerky conjugate movements that quickly
cal planes is called . change the fixation point.
22. is neurologically associated 33. refers to any abnormality of eye
with convergence of the eyes, pupillary coordination or alignment that results in loss
constriction, and results from thickening of of binocular vision.
the lens through contraction of the ciliary
34. describes a decrease in visual
muscle.
acuity resulting from abnormal visual devel-
23. A is a lens opacity that inter- opment in infancy or early childhood.
feres with the transmission of light to the
retina. Activity B Consider the following figures.
24. The function of the is to receive
visual images, partially analyze them, and 1.
transmit this modified information to the
brain.
25. The genetically person has
never experienced the full range of normal
color vision and is unaware of what he or she
is missing.
26. represents a group of hereditary
diseases that cause slow degenerative changes
in the retinal photoreceptors.
27. degeneration is characterized by
degenerative changes in the central portion
of the retina that results primarily in loss of
central vision.
28. are related inherited or acquired
mutations in the retinoblastoma (Rb) tumor 1. In this figure, locate and label the following
suppressor gene, located on the long arm of structures:
chromosome 13. • Conjunctiva
29. The refers to the area that is visi- • Cornea
ble during fixation of vision in one direction. • Lens
• Iris
30. Three pairs of extraocular muscles—the
• Meibomian gland
superior and , the medial and • Orbicularis oculi muscle
, and the superior and inferior • Inferior oblique muscle
—control the movement of each • Inferior rectus
eye. • Superior rectus
31. movements are those in which • Levator palpebrae superioris
the optical axes of the two eyes are kept paral- • Choroid
lel, sharing the same visual field. • Retina
• Superior tarsal plate
• Ciliary body
• Sclera
• Optic nerve

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CHAPTER 54 DISORDERS OF VISUAL FUNCTION 303

2. 3.

2. In this figure, which eye represents myopia? 3. In this figure, locate and label the following
Which eye represents hyperopia? Which eye muscles:
represents normal focal length? • Medial rectus
• Superior oblique
• Inferior rectus
• Levitator palpebrae
• Lateral rectus
• Temporalis
• Inferior oblique

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304 UNIT 13 DISORDERS OF SPECIAL SENSORY FUNCTION

Activity C Match the key terms in Column A 9. Direct f. Blindness in one eye
with their definitions in Column B. pupillary g. Paralysis of the ciliary
light reflex muscle, with loss of
1.
10. Papilledema accommodation
Column A Column B h. Leakage of fluid re-
1. Arcus senilis a. Caused by infection sults in edema of the
of the sebaceous optic papilla
2. Entropion
glands i. Rapid constriction of
3. Ophthalmia b. Infection of the the pupil exposed to
neonatorum lacrimal sac light
4. Hordeolum c. Chronic inflamma- j. Decrease in accom-
tory granuloma of a modation that occurs
5. Pink eye because of aging
meibomian gland
6. Chalazion d. Drooping of the
Activity D Briefly answer the following.
7. Ptosis eyelid
e. Extracellular lipid 1. Where are tears formed, and what purpose(s)
8. Dacryo- do they serve?
infiltration of the
cystitis
cornea
9. Ectropion f. Turning in of the lid
10. Sjögren margin
syndrome g. Conjunctivitis that
occurs in newborns 2. What is the most common cause of chronic
and is related to sex- bacterial conjunctivitis, and what are the
ually transmitted symptoms?
diseases
h. Diminished salivary
and lacrimal secre-
tions, resulting in
keratoconjunctivitis
sicca and xerostomia 3. How do the different levels of abrasional
i. Eversion of the lower trauma (less severe to more severe) affect the
lid margin cornea, and how fast to the abrasions heal?
j. Inflammation of the
conjunctiva
2.
Column A Column B
4. What is the mechanism of a primary herpes
1. Anopia a. The vitreous shrinks simplex virus optical epithelial infection?
and partly separates
2. Hyperopia
from the retinal
3. Cycloplegia surface
4. Scotoma b. Hole in the visual field
c. Anterior-posterior di-
5. Rhegmato- 5. What is the cause of acanthamoeba keratitis,
mension of the eye-
genous and what are the primary symptoms?
ball is too short
detachment
d. Anterior-posterior di-
6. Tonometry mension of the eye-
7. Presbyopia ball is too long
e. Measurement of in-
8. Myopia
traocular pressure

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CHAPTER 54 DISORDERS OF VISUAL FUNCTION 305

6. Explain how the pupil is able to change shape. 1. What diagnostic measures would the nurse
expect the doctor to order?

7. What is glaucoma? What is primary and

secondary glaucoma? 2. Retinoblastoma is confirmed, and a treatment
plan is being made. What are the treatment
options for retinoblastoma?

8. What is presbyopia, and how does it affect

vision?

SECTION IV: PRACTICING

FOR NCLEX

9. Retinal hemorrhage can occur at many layers. Activity F Answer the following questions.
What are the types of retinal bleeding, and 1. Causes of eyelid weakness include neurologic
where do they occur? causes. There can be damage to the cranial
nerves that innervate the eyelids, or there can
be damage to the central nuclei of the cranial
nerves. Where are the central nuclei of cranial
nerve (CN) III (oculomotor nerve) and CN VII
(facial nerve)?
10. Why is proliferative diabetic retinopathy a
a. Midbrain and caudal pons
major concern for all diabetic patients?
b. Faux cerebellum and amygdala
c. Hypothalamus and pyramid
d. Medulla oblongata and pineal body
2. Dacryocystitis is an infection in the lacrimal
11. What is the relationship between hyperten- sac. What symptoms indicate dacryocystitis?
sion and the development of a retinopathy? a. Purulent discharge
b. Swelling
c. Inflamed conjunctiva
d. Lack of tears
3. Ophthalmia neonatorum is a conjunctivitis
that develops in newborns. It is caused by the
agents that cause sexually transmitted dis-
SECTION III: APPLYING YOUR eases. When should ophthalmia neonatorum
KNOWLEDGE be suspected?
a. When a conjunctivitis develops 24 hours
Activity E Consider the following scenario and after birth
answer the questions.
b. When a conjunctivitis develops 12 hours
The mother of an 18-month-old girl brings her after birth
daughter to the clinic for a well-baby check. Dur- c. When a conjunctivitis develops 48 hours
ing the physical exam, the physician notices that after birth
the client has a white reflex in her left eye. He
d. When a conjunctivitis develops 36 hours
suspects retinoblastoma.
after birth

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306 UNIT 13 DISORDERS OF SPECIAL SENSORY FUNCTION

4. Keratitis can be caused by different infectious 4. Hyperopia distant target is anterior

agents. What is the treatment goal with her- to the retina
5. Astigma-
pes simplex virus keratitis? b. Paralysis of the ciliary
tism
a. Minimizing pain muscle, with loss of
b. Curing the disease accommodation
c. Eliminating viral replication within the c. Anterior-posterior di-
cornea mension of the eyeball
is too short; the image
d. Minimizing spread of virus to other parts
is theoretically focused
of the eye
posterior to (behind)
5. Corneal transplants are performed every day the retina
in hospitals around the world. The trans- d. Range of focus or ac-
planted corneas come from cadavers. Why do commodation is dimin-
corneal transplants have such a low rejection ished
rate? Mark all that apply.
e. Asymmetric bowing of
a. The cornea is very vascular. the cornea
b. Antigen-presenting cells are not present in
9. Age-related cataracts are characterized by
great numbers.
what?
c. The cornea secretes immunosuppressive
a. Everything looking grey
factors.
b. Visual distortion
d. The cornea has no lymphatics.
c. Narrowing visual field
e. Corneal cells secrete substances that pro-
tect against keratitis. d. Blind spots in visual field

6. Pharmacologic agents can affect dilation of 10. Vitreous humor occupies the posterior por-
the pupil and the papillary response. What tion of the eyeball. It is an amorphous bio-
types of drugs produce papillary constriction? logic gel. When liquefaction of the gel occurs,
as in aging, what can be seen during head
a. Sympathomimetic agents
movement?
b. Antihistamine agents
a. Blind spots
c. Cycloplegic agents
b. Meshlike structures
d. Miotic agents
c. Floaters
7. In open-angle glaucoma, there is an increased d. Red spots
pressure within the globe of the eye without
obstruction at the iridocorneal angle. Usually, 11. When conditions occur that impair retinal
this is caused by an abnormality in the tra- blood flow, such as hyperviscosity of the blood
becular meshwork, which controls the flow or or a sickle cell crisis, what can occur in the eye?
aqueous humor. Where is aqueous humor in a. Microaneurysms
a normal eye? b. Hypertensive retinopathy
a. Canal of Schlemm c. Microinfarcts
b. Ocular canal d. Neovascularization
c. Ductus lacrimalis
12. Age-related macular degeneration that is dry
d. Behind the pupil is characterized by what?
8. Match the terms with their definitions. a. Atrophy of the Bruch membrane
Term Definition b. Leakage of serous or hemorrhagic fluid
c. New blood vessels in the eye
1. Presbyopia a. Anterior-posterior di-
mension of the eyeball d. Formation of a choroidal neovascular
2. Cycloplegia membrane
is too long; the focus
3. Myopia point for an infinitely

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CHAPTER 54 DISORDERS OF VISUAL FUNCTION 307

13. Cortical blindness is the bilateral loss of the 15. Amblyopia, or lazy eye, occurs at a time when
primary visual cortex. What is retained in visual deprivation or abnormal binocular in-
cortical blindness? teractions occur in visual infancy. Whether
a. Red spots seen behind the eyelids amblyopia is reversible depends on what?
b. Pupillary reflexes a. Child has to be older than 5 years
c. Phytosis b. Maturity of the visual system at time of
onset
d. Myopia
c. Child has to have bilateral congenital
14. Adult strabismus is almost always of the para- cataracts
lytic variety. What is a cause of adult strabis-
d. Child has to be able to wear contact lenses
mus?
a. Huntington disease
b. Parkinson disease
c. Graves disease
d. Addison disease

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55
CHAPTER

Disorders of Hearing and

Vestibular Function

SECTION I: LEARNING 10. Characterize the causes of hearing loss in in-

fants and children and describe the need for
OBJECTIVES early diagnosis and treatment
1. List the structures of the external, middle, 11. Explain the function of the vestibular system
and inner ear and cite their function with respect to postural reflexes and main-
taining a stable visual field despite marked
2. Describe two common disorders of the outer
changes in head position
ear
12. Relate the function of the vestibular system
3. Relate the functions of the eustachian tube to
to nystagmus and vertigo
the development of middle ear problems, in-
cluding acute otitis media and otitis media 13. Differentiate the structures of peripheral and
with effusion central vestibular function
4. Describe anatomic variations as well as risk 14. Characterize the physiologic cause of motion
factors that make infants and young children sickness
more prone to develop acute otitis media
15. Compare the manifestations and pathologic
5. List three common symptoms of acute otitis processes associated with benign positional
media vertigo and Ménière disease
6. Describe the disease process associated with 16. Differentiate the manifestations of peripheral
otosclerosis and relate it to the progressive and central vestibular disorders
conductive hearing loss that occurs
7. Characterize tinnitus
8. Differentiate between conductive, sen-
SECTION II: ASSESSING YOUR
sorineural, and mixed hearing loss and cite UNDERSTANDING
the more common causes of each
Activity A Fill in the blanks.
9. Describe methods used in the diagnosis and
treatment of hearing loss 1. The external consists of the au-
ricle, which collects sound, and the external

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CHAPTER 55 DISORDERS OF HEARING AND VESTIBULAR FUNCTION 309

acoustic meatus or ear canal, which conducts 12. hearing loss occurs with disor-
sound to the tympanic membrane. ders that affect the inner ear, auditory nerve,
or auditory pathways of the brain.
2. Impacted usually produces no
symptoms unless it hardens and touches the 13. Deafness or some degree of hearing impair-
tympanic membrane or the canal becomes ir- ment is the most common serious complica-
ritated, resulting in symptoms of pain, itch- tion of in infants and children.
ing, and a sensation of fullness.
14. Acoustic neuromas are benign Schwann cell
3. is an inflammation of the exter- tumors affecting .
nal ear that can vary in severity from mild
15. The most common infectious cause of
allergic dermatitis to severe cellulitis.
congenital sensorineural hearing loss is
4. The tympanic cavity is a small, mucosa-lined .
cavity within the petrous portion of the
16. The system maintains and as-
bone.
sists recovery of stable body and head posi-
5. The tube, which connects the tion through control of postural reflexes, and
nasopharynx with the middle ear, is located it maintains a stable visual field despite
in a gap in the bone between the anterior and marked changes in head position.
medial walls of the middle ear.
17. Disorders of vestibular function are character-
6. The eustachian tube does not ized by a condition called , in
close or does not close completely. which an illusion of motion occurs.
7. refers to inflammation of the 18. is a form of normal physiologic
middle ear without reference to etiology or vertigo, caused by repeated rhythmic stimula-
pathogenesis. tion of the vestibular system, and encoun-
tered in car, air, or boat travel.
8. is characterized by acute onset
of otalgia (or pulling of the ears in an infant), 19. Benign vertigo is the most com-
fever, and hearing loss. mon cause of pathologic vertigo.
9. refers to the formation of new 20. Acute is characterized by an
spongy bone around the stapes and oval win- acute onset (usually hours) of vertigo, nausea,
dow, which results in progressive deafness. and vomiting lasting several days and not as-
sociated with auditory or other neurologic
10. The spiral canal of the , which is
manifestations.
shaped like a snail shell, begins at the
vestibule and winds around a central core of 21. disease is a disorder of the inner
spongy bone called the modiolus. ear due to distention of the endolymphatic
compartment of the inner ear, causing a triad
11. Persons with damage to of the
of hearing loss, vertigo, and tinnitus.
brain can speak intelligibly and read nor-
mally, but are unable to understand the 22. Abnormal nystagmus and vertigo can occur be-
meaning of major aspects of audible speech. cause of central nervous system lesions involv-
ing the and lower brain stem.

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310 UNIT 13 DISORDERS OF SPECIAL SENSORY FUNCTION

Activity B Consider the following figure.

Middle Inner
Cochlear
ear ear
portion
Vestibular
portion

Pharynx

In this figure, locate and label the following 6. Presbycusis d. Injury resulting from the
structures: inability to equalize mid-
7. Nystagmus
dle ear with ambient
• Auricle
8. Barotrauma pressures
• External acoustic meatus
• Malleus 9. Cholestea- e. Ringing of the ears, it
• Stapes tomas may also assume a hiss-
• Eustachian tube ing, roaring, buzzing, or
10. Frequency humming sound
• Cochlea
• Cranial nerve VIII f. Number of waves per
• Tympanic membrane unit time
• Incus g. Involuntary rhythmic
• Semicircular canals and oscillatory eye move-
ments that preserve eye
Activity C Match the key terms in Column A fixation on stable objects
with their definitions in Column B. in the visual field during
Column A Column B angular and rotational
movements of the head
1. Otitis media a. Degenerative hearing
h. Earwax
with effusion loss that occurs with
advancing age i. Examination that records
2. Cerumen eye movements in re-
b. Cystlike lesions of the
3. Tinnitus sponse to vestibular, vi-
middle ear
sual, cervical, rotational,
4. Streptococcus c. Most common cause and positional stimulation
pneumoniae of bacterial meningitis
j. Presence of fluid in the
that results in sen-
5. Electrony- middle ear without signs
sorineural hearing
stagmography and symptoms of acute
loss after the neonatal
ear infection
period

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CHAPTER 55 DISORDERS OF HEARING AND VESTIBULAR FUNCTION 311

Activity D Briefly answer the following. SECTION III: APPLYING YOUR

1. What is/are the function(s) of the eustachian KNOWLEDGE
tube?
Activity E Consider the following scenario and
answer the question.
You are the nurse preparing an educational event
for the local junior league, which has asked you
to speak on hearing loss and deafness. One of the
2. What are the complications associated with subjects that you will address is ototoxicity.
otitis media?
1. What drugs would you include when talking
about ototoxicity?

3. How does otosclerosis lead to progressive

deafness?

SECTION IV: PRACTICING

FOR NCLEX
4. What are the purported causes of subjective Activity F Answer the following questions.
tinnitus?
1. Otitis externa is an inflammation of the outer
ear. What fungi cause otitis externa?
a. Aspergillus
b. Pseudomonas aeruginosa
c. Staphylococcus aureus
5. What is the cause of hearing loss in conduc-
tive hearing loss? d. Escherichia coli
2. The eustachian tube connects the nasophar-
ynx and the middle ear. In infants and chil-
dren with abnormally patent tubes, what are
let into the eustachian tube when the infant
or child cries or blows their nose?
6. How does the vestibular system inform the
a. Air and cerumen
brain about head and body position?
b. Air and secretions
c. Secretions and saliva
d. Cerumen and saliva
3. Acute otitis media (AOM) is the disorder in
7. What is the test used to determine vestibular children for which antibiotics are most pre-
function in an unconscious patient? scribed. What are the risk factors for AOM?
Mark all that apply.
a. Ethnicity
b. Premature birth
c. Only child in household
d. Genetic syndromes
e. Female gender

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312 UNIT 13 DISORDERS OF SPECIAL SENSORY FUNCTION

4. Otosclerosis is a condition where spongy, 8. Tumors affecting cranial nerve VIII are
pathologic bone grows around the stapes and acoustic neuromas. What are these tumors of?
oval window. It can be treated either med- a. Inner ear
ically or surgically. What is the surgical treat-
b. Organ of Corti
ment for otosclerosis?
c. Schwann cells
a. Otosclerotomy
d. Labyrinth
b. Ovalectomy
c. Stapedectomy 9. It is important to differentiate between the
kinds of hearing loss so they can be appropri-
d. Amplification surgery
ately treated. What is used to test between
5. What separates the scala vestibule and the conductive and sensorineural hearing loss?
scala media? a. AudioScope
a. Corti membrane b. Audiometer
b. Tympani membrane c. Tone analysis
c. Modiolus membrane d. Tuning fork
d. Reissner membrane
10. Hearing loss in children can be either conduc-
6. Objective tinnitus is tinnitus that someone tive or sensorineural, as it is in adults. What is
else can hear. What does the tinnitus that is the major cause of sensorineural hearing loss
caused by vascular disorders sound like? in children?
a. Pulses a. Genetic causes
b. Rings b. Acute otitis media
c. Hums c. Paget disease
d. Roars d. Ototoxicity
7. Conductive hearing loss can occur for a vari- 11. Presbycusis is degenerative hearing loss asso-
ety of reasons, including foreign bodies in the ciated with aging. What is the first symptom
ear canal, damage to the ear drum, or disease. of this disorder?
What disease is associated with conductive a. Inability to localize sounds
hearing loss?
b. Reduction in ability to understand speech
a. Huntington disease
c. Inability to detect sound
b. Paget disease
d. Reduction in ability to identify sounds
c. Alzheimer disease
d. Parkinson disease

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56

CHAPTER
Structure and Function
of the Musculoskeletal
System

SECTION I: LEARNING SECTION II: ASSESSING YOUR

OBJECTIVES UNDERSTANDING
1. Describe locations and characteristics of com- Activity A Fill in the blanks.
pact and cancellous bone
1. The bones of the skeletal system serve
2. Describe the structure of a long bone as a framework for the attachment of
, , and .
3. Cite the characteristics and name at least one
location of elastic cartilage, hyaline cartilage, 2. The bones act as a storage reservoir for
and fibrocartilage , and the central cavity of some
bones contains the hematopoietic connective
4. Name and characterize the function of the
tissue in which cells are formed.
four types of bone cells
3. The skeletal system consists of the
5. State the function of parathyroid hormone,
and skeleton.
calcitonin, and vitamin D in terms of bone
formation and metabolism 4. bone has a densely packed calci-
fied intercellular matrix that makes it more
6. State the characteristics of tendons and liga-
rigid than cancellous bone.
ments
5. are classified by shape as long,
7. State the difference between synarthroses and
short, flat, and irregular.
synovial joints
6. Bones are covered, except at their articular
8. Describe the source of blood supply to a syn-
ends, by a membrane called the .
ovial joint
7. Bone occupies the medullary
9. Explain why pain is often experienced in all
cavities of the long bones throughout the
the joints of an extremity when only a single
skeleton and the cavities of cancellous bone
joint is affected by a disease process
in the vertebrae, ribs, sternum, and flat bones
10. Describe the structure and function of a bursa of the pelvis.
11. Explain the pathology associated with a torn
meniscus of the knee

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314 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

8. The enter the bone through a Activity B Consider the following figure.
nutrient foramen and supply the marrow
space and the internal one-half of the cortex.
9. Bone is tissue in which the in-
tercellular matrix has been impregnated with
inorganic salts so that it has
great tensile and compressible strength but is
light enough to be moved by coordinated
muscle contractions.
10. The undifferentiated cells are
found in the periosteum, endosteum, and
epiphyseal plate of growing bone.
A
11. are “bone-chewing” cells that
function in the resorption of bone, remov-
ing the mineral content and the organic
matrix.
12. cartilage is found in areas, such
as the ear, where some flexibility is impor-
tant.
13. is found in the intervertebral
disks, in areas where tendons are connected B C
to bone, and in the symphysis pubis.
14. cartilage forms the costal carti-
lages that join the ribs to the sternum and
vertebrae, many of the cartilages of the respi- In this figure, locate and label the following
ratory tract, the articular cartilages, and the structures:
epiphyseal plates. • Proximal epiphysis
15. inhibits the release of calcium • Medullary cavity
from bone into the extracellular fluid. • Periosteum
• Nutrient artery
16. , which attach skeletal muscles • Compact bone
to bone, are relatively inextensible because of • Spongy bone
their richness in collagen fibers. • Yellow marrow
17. are fibrous thickenings of the ar- • Diaphysis
ticular capsule that join one bone to its artic-
ulating mate. Activity C Match the key terms in Column A
with their definitions in Column B.
18. are joints that lack a joint cavity
and move little or not at all. Column A Column B

19. joints are freely movable joints. 1. Trabeculae a. Connect adjacent

haversian canals
20. The purpose of a sac is to pre- 2. Appendicular
skeleton b. Prebone that will be
vent friction on a tendon.
ossified

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CHAPTER 56 STRUCTURE AND FUNCTION OF THE MUSCULOSKELETAL SYSTEM 315

3. Osteoid c. Bones of the skull, • Reabsorption of calcium via 1,25-dihydroxy-

thorax, and vertebral vitamin D3
4. Lamellar
column • Synthesis of 1,25-dihydroxy-vitamin D3
bone
d. Mature bone found in • Release of calcium and phosphate
5. Haversian the adult skeleton • Reabsorption of calcium
canals • Urinary excretion of phosphate
e. Contains the blood ves-
6. Osteons sels and nerve supply
Activity E Briefly answer the following.
for the osteon
7. Volkmann
f. Bones of the upper and 1. What is the typical structure of a long bone?
canals
lower extremities, in-
8. Axial cluding the shoulder
skeleton and hip
9. Endosteum g. Membrane that lines the
spaces of spongy bone,
10. Chondro- 2. What are the two types of bone marrow, and
the marrow cavities, and
cytes what are their functions?
the haversian canals
h. Cells that form cartilage
i. Concentric lamellae of
bone matrix, surround-
ing a central canal
j. Lined with osteogenic 3. What is the make up of the intercellular
cells and filled with red matrix of bone tissue?
or yellow bone marrow
Activity D
1. In this flowchart, put the following in the
proper sequence:
4. What are the similarities and differences
Parathyroid
between bone and cartilage?
glands
Kidney

Bone
5. How does parathyroid hormone maintain
serum calcium levels?
Calcium
concentration
in extracellular
fluid

6. What is the action of vitamin D?

Intestine

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316 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

SECTION III: APPLYING YOUR 3. Lamellar bone is the bone tissue that is found
in the adult body. What is lamellar bone
KNOWLEDGE largely composed of?
Activity F Consider the following scenario and a. Hematopoietic cells
answer the questions. b. Spicules
A 62-year-old woman with multiple sclerosis c. Osteons
(MS) was referred to the orthopedic clinic by her d. Macrocrystalline cells
primary care physician due to pain on movement
4. Our bodies contain three types of cartilage:
in her upper arms. Because of the MS, the client’s
elastic cartilage, hyaline cartilage, and fibro-
legs were extremely weak, and the client had to
cartilage. Which of these types of cartilage is
lift herself out of a chair with her arms. After a
found in the symphysis pubis?
physical examination, the orthopedic physician
diagnosed her as having bilateral biceps ten- a. None
donitis. b. Elastic
1. The client asks what causes tendonitis. What c. Hyaline
would be the correct answer? d. Fibrocartilage
5. Parathyroid hormone functions to maintain
serum calcium levels. How does it fulfill this
function? Mark all that apply.
a. Initiates calcium release from bone
2. The client asks if all tendons are like the biceps b. Enhances intestinal absorption of calcium
tendons. What would be the correct answer? c. Activates conservation of calcium by the
kidney
d. Decreases intestinal absorption of calcium
e. Inhibits conservation of calcium by the
kidney
6. When vitamin D is metabolized, it breaks
down into various metabolites. 1,25(OH)2D3
SECTION IV: PRACTICING is the most potent of the vitamin D metabo-
FOR NCLEX lites. What is the function of this metabolite
of vitamin D?
Activity G Answer the following questions. a. Promotes actions of parathyroid hormone
1. The metaphysis is the part of the bone that on resorption of calcium and phosphate
fans out toward the epiphysis. What is the from bone
metaphysis composed of? b. Decreases intestinal absorption of calcium
a. Trabeculae c. Promotes absorption of calcium and phos-
b. Cancellous bone phate by bone
c. Red bone marrow d. Decreases absorption of phosphate and in-
creases absorption of calcium by bone
d. Endosteum
7. There are two types of joints in the human
2. We have both red and yellow bone marrow in
body. They are synarthroses and synovial
our bodies. What is yellow bone marrow
joints. Synarthroses joints are further broken
largely composed of?
down into three types of joint. What type of
a. Hematopoietic cells joint occurs when bones are connected by
b. Adipose cells hyaline cartilage?
c. Cancellous cells a. Synovial
d. Osteogenic cells b. Synchondroses
c. Syndesmoses
d. Diarthrodial

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CHAPTER 56 STRUCTURE AND FUNCTION OF THE MUSCULOSKELETAL SYSTEM 317

8. Rheumatic disorders attack the joints of the 10. Synovial membranes can form sacs called
body. Which joints are most frequently bursae. What is the function of bursae?
attacked by rheumatic disorders? a. Prevent friction on a tendon
a. Synchondroses b. Prevent injury to a joint
b. Articular c. Prevent friction on a ligament
c. Diarthrodial d. Cushion the joint
d. Synarthroses
9. Each joint capsule has tendons and liga-
ments? What are the tendons and ligaments
of the joint capsule sensitive to?
a. Position and elevating
b. Position and lowering
c. Position and turning
d. Position and movement

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57
CHAPTER

Disorders of
Musculoskeletal
Function: Trauma,
Infection, and Neoplasms

SECTION I: LEARNING hematogenous osteomyelitis, and osteomyelitis

due to vascular insufficiency in terms of etiolo-
OBJECTIVES gies, manifestations, and treatment
1. Describe the physical agents responsible for 12. Cite the characteristics of chronic os-
soft tissue trauma teomyelitis
2. Differentiate among the three types of soft 13. Describe the most common sites of tuberculo-
tissue injuries sis of the bone
3. Compare muscle strains and ligamentous 14. Define osteonecrosis
sprains
15. Cite four major causes of osteonecrosis
4. Describe the healing process of soft tissue in-
16. Characterize the blood supply of bone and
juries
relate it to the pathologic features of the
5. Differentiate open from closed fractures condition
6. List the signs and symptoms of a fracture 17. Describe the methods used in diagnosis and
treatment of the condition
7. Explain the measures used in treatment of
fractures 18. Differentiate between the properties of be-
nign and malignant bone tumors
8. Describe the fracture healing process
19. Contrast osteogenic sarcoma, Ewing sarcoma,
9. Differentiate the early complications of frac-
and chondrosarcoma in terms of the most
tures from later complications of fracture
common age groups and anatomic sites that
healing
are affected
10. Explain the implications of bone infection
20. List the primary sites of tumors that fre-
11. Differentiate among osteomyelitis due to quently metastasize to the bone
spread from a contaminated wound,

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CHAPTER 57 DISORDERS OF MUSCULOSKELETAL FUNCTION: TRAUMA, INFECTION, AND NEOPLASMS 319

21. State the three primary goals for treatment of 13. The signs and symptoms of a in-
metastatic bone disease clude pain, tenderness at the site of bone dis-
ruption, swelling, loss of function, deformity
of the affected part, and abnormal mobility.
SECTION II: ASSESSING YOUR 14. is another method for achieving
UNDERSTANDING immobility and maintaining alignment of the
bone ends and maintaining the reduction,
Activity A Fill in the blanks. particularly if the fracture is unstable or com-
minuted.
1. A broad spectrum of injuries re-
sult from numerous physical forces, including 15. are skin bullae and blisters rep-
blunt tissue trauma, disruption of tendons and resenting areas of epidermal necrosis with
ligaments, and fractures of bony structures. separation of epidermis from the underlying
dermis by edema fluid.
2. Unintentional are the number
one cause of nonfatal injuries in all age 16. Because of inactivity and restrictions in
groups. weight-bearing, the individual with a lower
extremity fracture is at risk for the develop-
3. injuries include contusions, ment of venous , which includes
hematomas, and lacerations. pulmonary embolism and deep venous
4. A is a stretching injury to a mus- thrombosis.
cle or a musculotendinous unit caused by me- 17. The syndrome refers to a con-
chanical overloading. stellation of clinical manifestations resulting
5. A usually is caused by abnormal from the presence of fat droplets in the small
or excessive movement of the joint. blood vessels of the lung or other organs after
a long bone fracture or other major trauma.
6. A involves the displacement or
separation of the bone ends of a joint with 18. osteomyelitis symptoms include
loss of articulation. pain, immobility, and muscle atrophy; joint
swelling, mild fever, and leukocytosis also
7. bodies are small pieces of bone may occur.
or cartilage within a joint space.
19. , or death of a segment of bone,
8. injuries and impingement disor- is a condition caused by the interruption of
ders can result from a number of causes, in- blood supply to the marrow, medullary bone,
cluding excessive use, a direct blow, or stretch or cortex.
injury, usually involving throwing or swing-
ing, as with baseball pitchers or tennis players. 20. Malignant bone tumors, such as ,
grow rapidly and can spread to other parts of
9. Meniscus injury commonly occurs as the re- the body through the bloodstream or lym-
sult of a injury from a sudden or phatics.
sharp pivot or a direct blow to the knee, as in
hockey, basketball, or football. 21. bone tumors usually are limited
to the confines of the bone, have well-
10. of the hip commonly result demarcated edges, and are surrounded by a
from the knee being struck while the hip and thin rim of sclerotic bone.
knee are in a flexed position.
22. A is a tumor composed of hya-
11. Grouped according to cause, fractures can line cartilage.
be divided into three major categories: frac-
tures caused by , fatigue or stress 23. , a malignant tumor of cartilage
fractures, and fractures. that can develop in the medullary cavity or
peripherally, is the second most common
12. A fracture occurs in bones that form of malignant bone tumor.
already are weakened by disease or tumors.

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320 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

Activity B Consider the following figure. h. A partial break in bone

continuity that resem-
bles that seen when a
Proximal
young sapling is broken
i. Area becomes ecchy-
Midshaft
motic (i.e., black and
blue) because of local
hemorrhage
j. C-shaped plates of fi-
Distal
brocartilage that are su-
perimposed between
the condyles of the
femur and tibia

Activity D
1. Put the following events of healing a bone
fracture into the proper order in the boxes
below.
a. Development of fibrin meshwork within the
hematoma
b. Replacement of callus with mature bone
c. Formation of fibro cartilaginous callus
In the figure above, label the type of fracture:
d. Remodeling of bone
• impacted
• butterfly
• comminuted
• transverse
Activity E Briefly answer the following.
• oblique
• segmental 1. What joints are most commonly involved in
• spiral sprain type injuries?

Activity C Match the key terms in Column A

with their definitions in Column B.
Column A Column B
1. Subluxation a. A partial dislocation 2. What is the normal healing process of a sprain?
b. Acute or chronic in- What are some of the greatest concerns?
2. Malunion
fection of the bone
3. Contusion
c. Bone fragments have
4. Compound broken through the
fracture skin
5. Menisci d. Injury in which the 3. What is the structure of the rotator cuff and
skin is torn or its con- how is it usually injured?
6. Hematoma tinuity is disrupted
7. Chondro- e. Healing of bone with
malacia deformity, angulation,
or rotation
8. Laceration
f. Large area of local he-
9. Greenstick morrhage
fracture
g. Softening of the artic-
10. Osteomyelitis ular cartilage

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CHAPTER 57 DISORDERS OF MUSCULOSKELETAL FUNCTION: TRAUMA, INFECTION, AND NEOPLASMS 321

4. When someone “breaks a hip” what is usually 2. The diagnosis of torn meniscus is confirmed.
occurring? What would the first-line treatment be for this
type of injury?

5. What is compartment syndrome and how

does it relate to bone tissue? 3. The client asks what will happen if his knee
does not heal right. The correct answer would
include what?

6. What are the manifestations of osteomyelitis?

SECTION IV: PRACTICING

FOR NCLEX
7. What is the pathogenesis of osteonecrosis?
Activity G Answer the following questions.
1. Where do overuse injuries commonly occur?
a. Knee
b. Wrist
8. What are the general characteristics of bone
c. Neck
tumors?
d. Fingers
2. Match the injury to its definition.
Injury Definition
1. Contusion a. The ligaments may be
9. What is metastatic bone disease?
incompletely torn or, as
2. Hematoma
in a severe sprain, com-
3. Laceration pletely torn or ruptured
4. Puncture b. An injury in which the
wounds skin is torn or its conti-
nuity is disrupted
SECTION III: APPLYING YOUR 5. Strain
c. A stretching injury
KNOWLEDGE 6. Sprain caused by mechanical
overloading
7. Dislocation
Activity F Consider the following scenario and d. Blood accumulates and
answer the questions. exerts pressure on
A 15-year-old boy is brought to the emergency nerve endings
department after an injury playing football. e. Displacement or sepa-
The doctor suspects an injury to the meniscus of ration of the bone ends
the knee. of a joint with loss of
articulation
1. As his nurse, what orders would you expect to
receive to confirm the suspected diagnosis? f. Provide the setting for
growth of anaerobic
bacteria
g. The skin overlying the
injury remains intact

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322 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

3. Shoulder and rotator cuff injuries usually 7. Match the complication with the definition.
occur from trauma or overuse. What orders
Complication
would be given for conservative treatment of
of Fracture Definition
an injured shoulder? Mark all that apply.
a. Anesthetic injections 1. Fracture blisters a. Areas of epider-
mal necrosis with
b. Physical therapy 2. Compartment
separation of epi-
c. Corticosteroid injections syndrome
dermis from the
d. Anti-inflammatory agents 3. Complex underlying der-
e. Pain medicine regional pain mis by edema
syndrome fluid
4. Hip injuries include dislocations and fractures
b. Reflex sympa-
of the hip. Why is hip dislocation considered
thetic dystrophy
a medical emergency?
c. A condition of
a. The dislocation causes great pain
increased pres-
b. Avascular necrosis can result from the dis- sure within a lim-
location ited space (e.g.,
c. The longer the hip is dislocated, the less abdominal and
chance of putting it back in place limb compart-
d. Dislocation interrupts the blood supply to ments) that com-
the femoral head promises the
circulation and
5. At times, fractures of long bones need en- function of the
hancement to promote healing. What can be tissues within the
done to induce bone formation and repair space
bone defects?
8. Fat emboli syndrome (FES) can occur after a
a. The use of steroids to induce bone growth
fracture of a long bone. What are the clinical
b. The use of growth factors to induce bone features of FES?
growth
a. Petechiae on soles of feet and palms of
c. The use of vibration therapy to induce hands
bone growth
b. Respiratory insufficiency
d. The use of physical therapy to induce bone
c. Encephalopathy
growth
d. Global neurologic deficits
6. Determining the extent of the injury when a
fracture occurs is important. It is also impor- 9. Osteomyelitis is an infection of the bone.
tant to obtain a thorough history. What is Chronic osteomyelitis is complicated by a
important to determine during the history piece of infected dead bone that has sepa-
taking? Mark all that apply. rated from the living bone. How long does
the initial intravenous (IV) antibiotic therapy
a. Anyone else in family susceptible to fractures
last for chronic osteomyelitis?
b. Recognition of symptoms
a. 4 weeks
c. Any treatment initiated
b. 8 weeks
d. Mechanism of injury
c. 12 weeks
e. What patient has eaten
d. 6 weeks

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CHAPTER 57 DISORDERS OF MUSCULOSKELETAL FUNCTION: TRAUMA, INFECTION, AND NEOPLASMS 323

10. Tuberculosis can spread from the lungs into a. Pain, worse during the day
the musculoskeletal system. What is the most b. Erythema in the overlaying skin
common site in the skeletal system for tuber-
c. Nighttime awakening
culosis to be found?
d. Soreness in nearest joint
a. Spine
b. Ankles 13. Metastatic bone disease is a frequent disor-
der. It occurs at a time when primary tumors
c. Shoulders
in the lungs, breasts, and prostate seed them-
d. Hips selves (metastasize) to the musculoskeletal
11. Osteonecrosis is a condition where part of a system. What are the primary goals of treat-
bone dies because of the interruption of its ment for metastatic bone disease? Mark all
blood supply. What is the most common that apply.
cause of osteonecrosis other than fracture? a. Prevent pathologic fractures
a. Vessel injury b. Cure the disease
b. Prior steroid therapy c. Promote survival with maximum function-
c. Radiation therapy ing
d. Embolism d. Prevent ischemia to the bone segment
e. Maintain mobility and pain control
12. Osteosarcoma is an aggressive malignancy of
the bone. What is the primary clinical feature
of osteosarcoma?

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58
CHAPTER

Disorders of
Musculoskeletal
Function: Developmental
and Metabolic Disorders

SECTION I: LEARNING 9. Differentiate between congenital, idiopathic,

and neuromuscular scoliosis
OBJECTIVES
10. Cite the origin of osteoclasts and osteoblasts
1. Describe the function of the epiphyseal and describe their functions in bone remodel-
growth plate in skeletal growth ing
2. Describe common torsional deformities that 11. Describe the function of the RANK
occur in infants and small children, proposed ligand/RANK receptor, and the osteoprote-
mechanisms of development, diagnostic gerin-blocking molecule in the regulation of
methods, and treatment bone remodeling
3. Define genu varum and genu valgum 12. Describe risk factors that contribute to the de-
velopment of osteoporosis and relate them to
4. List the problems that occur because of defec-
the prevention of the disorder
tive tissue synthesis in osteogenesis imperfecta
13. Describe the primary features of osteoporotic
5. Characterize the abnormalities associated
bone
with developmental dysplasia of the hip and
methods of diagnosis and treatment 14. Explain the methods used in the diagnosis of
osteoporosis
6. Describe the treatment for a newborn with
clubfoot 15. Describe the actions of medications used in
the treatment of osteoporosis
7. Define the term osteochondroses and describe the
pathology and symptomatology of Legg-Calvé- 16. Compare the pathogenesis and manifesta-
Perthes disease and Osgood-Schlatter disease tions of osteomalacia and rickets
8. Describe the pathology associated with a 17. Characterize the cause and manifestations of
slipped capital femoral epiphysis and explain Paget disease
why early treatment is important

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CHAPTER 58 DISORDERS OF MUSCULOSKELETAL FUNCTION: DEVELOPMENTAL AND METABOLIC DISORDERS 325

SECTION II: ASSESSING YOUR undergo cell division and differentiate into
osteoblasts.
UNDERSTANDING
12. is characterized by a reduction
Activity A Fill in the blanks. in bone mass greater than expected for age,
race, or sex that occurs because of a decrease
1. disorders may develop because
in bone formation, inadequate bone mineral-
of normal growth and developmental
ization, or excessive bone deossification.
processes due to hereditary or congenital in-
fluences. 13. is a metabolic bone disease char-
acterized by a loss of mineralized bone mass
2. The long bones of the skeleton, which grow
causing increased porosity of the skeleton
at a relatively rapid rate, are provided with a
and susceptibility to fractures.
specialized structure called the .
14. osteoporosis, which is caused by
3. The that accompanies joint lax-
an estrogen deficiency, is manifested by a loss
ity, coupled with the forces ex-
of cancellous bone and a predisposition to
erted on the limbs during growth, is
fractures of the vertebrae and distal radius.
responsible for a number of variants seen in
young children. 15. osteoporosis is associated with
many conditions, including endocrine disor-
4. disease is a developmental de-
ders, malabsorption disorders, malignancies,
formity of the medial half of proximal tibial
alcoholism, and certain medications.
epiphysis that results in a progressive varus
angulation below the knee. 16. is a generalized bone condition
in which there is inadequate mineralization
5. The most common anomaly of the toes or
of bone.
fingers is or the presence of an
extra digit on the hand or foot. 17. A form of osteomalacia called
occurs in persons with chronic renal failure.
6. Osteogenesis imperfecta is a hereditary dis-
ease characterized by defective synthesis of 18. Rickets is a metabolic bone disorder, charac-
. terized by a failure or delay in of
the cartilaginous growth plate in children
7. Developmental of the hip is an
whose epiphyses have not yet fused.
abnormality in hip development that leads to
a wide spectrum of hip problems in infants 19. Paget disease is characterized by focal areas of
and children, including hips that are unsta- excessive bone and disorganized
ble, malformed, subluxated, or dislocated. osteoid formation.
8. Maternal smoking is associated with the oc- 20. The bones most often affected in
currence of , and the risk in- disease are the femur, pelvis,
creases enormously when combined with a humerus, and tibia.
family history.
Activity B Match the key terms in Column A
9. The primary pathologic feature of Legg-Calvé-
with their definitions in Column B.
Perthes disease is an of the bone
and marrow involving the epiphyseal growth Column A Column B
center in the femoral head.
1. Pes planus a. Lateral deviation of
10. disease involves microfractures the spinal column
2. Genu varum
in the area where the patellar tendon inserts b. Outward bowing of
into the tibial tubercle, which is an extension 3. Osteomalacia the knees 1 inch
of the proximal tibial epiphysis. when the medial
4. Femoral
11. When appropriately stimulated by growth torsion malleoli of the ankles
factors, such as bone morphogenic proteins are touching
5. Scoliosis
(BMPs), fibroblast growth factor (FGF), c. Softening of the bones
platelet–derived growth factor (PDGF), 6. Femoral without loss of bone
insulin-like growth factor, and transforming anteversion tissue
growth factor-(TGF-),

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326 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

7. Syndactyly d. Expressed by os- 5. How do osteoclasts and osteoblasts achieve

teoblasts and their bone metabolism?
8. Internal
immature precursors
tibial torsion
and is necessary for
9. RANKL osteoclast differentia-
tion and function
10. Genu
valgum e. Abnormal variations
in hip rotation 6. What is the pathogenesis of osteoporosis?
f. Deformity in which
there is decreased
space between the
knees
g. Rotation of the tibia 7. What are the clinical manifestations of osteo-
that makes the feet porosis?
appear to turn inward
h. Flat footedness
i. Simple webbing of the
fingers or toes
j. 80 to 90 degrees of
internal rotation of
the hip in the prone SECTION III: APPLYING YOUR
position KNOWLEDGE
Activity C Briefly answer the following. Activity D Consider the following scenario
1. What factors have a negative impact on epi- and answer the questions.
physeal growth? You admit to your floor a 60-year-old man with
Paget disease. His symptoms include vertigo,
nerve palsies in the upper extremities, and men-
tal deterioration. He asks what drugs he will be
given while he is hospitalized.

2. What is toeing-in and toeing-out? 1. What drugs would the nurse include in her ex-
planation?

3. What are the clinical manifestations of osteo-

genesis imperfecta?
SECTION IV: PRACTICING
FOR NCLEX
Activity E Answer the following questions.

4. What are the different types of scoliosis? Ex- 1. Torsional deformities can be natural in in-
plain what is known about each type. fants. When a malalignment does not correct
itself, or is not corrected by the time the child
reaches the age of 10 to 12, a torsional defor-
mity or malalignment becomes problematic.
What is a problem that can occur with
femoral anteversion?

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CHAPTER 58 DISORDERS OF MUSCULOSKELETAL FUNCTION: DEVELOPMENTAL AND METABOLIC DISORDERS 327

a. Patellar subluxation 6. Osgood-Schlatter disease is a disease that

b. Toeing-in strikes children between the ages of 11 and
15. This disease involves microfractures,
c. Toeing-out
where the patellar tendon inserts into the tib-
d. Metatarsus adductus ial tubercle. What is Osgood-Schlatter disease
2. Genu varum and genu valgum, bowlegs and characterized by?
knock-knees, during infancy and toddler- a. Pain in the hip
hood, are common findings. They usually b. Thinning of the patellar tendon
correct themselves once the child becomes
c. Pain in knee at rest
weight-bearing on the lower extremities.
When it does not self-correct, what can genu d. Thickening of patellar tendon
valgum cause? 7. Scoliosis is an abnormal curvature of the
a. Gait awkwardness spine. Why is it first noticed?
b. Subluxation a. Because of the deformity it causes
c. Metatarsus adductus b. Because the child cannot stand straight
d. Radial torsion c. Because of the pain it causes
3. Osteogenesis imperfecta is the most common d. Because the child cannot walk straight
hereditary bone disease. What are the mani- 8. Osteoporosis is a disease caused by demineral-
festations of osteogenesis imperfecta? Mark ization of bone. What is the clinical method
all that apply. of choice for diagnosing osteoporosis?
a. Triangular appearance to face a. Serum calcium levels
b. Thick bones in lower extremities b. Dual-energy x-ray absorptiometry (DXA) of
c. Blue or gray sclera the spine and hip
d. Thick skin c. Magnetic resonance imaging (MRI) of the
e. Scoliosis chest cavity and femur
d. Body mass index (BMI)
4. Congenital clubfoot is usually corrected non-
surgically during the first few weeks of life. 9. Osteomalacia is a bone disease caused by one
Once the correction is made, how is it main- of two reasons: inadequate calcium absorp-
tained? tion or phosphate deficiency. In the elderly,
a. The Ponseti method of periodic stretching what is the least expensive and most effective
long-term treatment for osteomalacia?
b. Galeazzi splints worn for 6 months
a. Pharmacologic replacement of calcium and
c. Denis Browne splint worn for 3 months
vitamin D
d. Ortolani method of periodic stretching
b. Intravenous (IV) phosphorus
5. Legg-Calvé-Perthes disease is an osteonecrotic c. Vitamin D rich diet and exposure to mid-
disease of the proximal (capital) femoral epi- day sun
physis. What does treatment involve? Mark
d. Increased calcium and phosphorus in diet
all that apply.
a. Assistive devices 10. Adult rickets can result from several disorders.
It can also have a pharmacologic basis for its
b. Periods of rest
onset. Which medication can cause rickets in
c. Abduction braces an adult?
d. Weight-bearing braces a. Cephalosporins
e. Adduction braces b. Sulfur-based antibiotics
c. Sodium-sparing diuretics
d. Aluminum-sparing antacids

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59
CHAPTER

Disorders of the
Musculoskeletal Function:
Rheumatic Disorders

SECTION I: LEARNING 11. Compare rheumatoid arthritis and os-

teoarthritis in terms of joint involvement,
OBJECTIVES level of inflammation, and local and systemic
manifestations
1. Characterize the common characteristics of
the different systemic autoimmune 12. Describe the pathologic joint changes associ-
rheumatic disorders ated with osteoarthritis
2. Describe the pathologic changes that may be 13. Characterize the treatment of osteoarthritis
found in the joint of a person with rheuma-
14. Relate the metabolism and elimination of
toid arthritis
uric acid to the pathogenesis of crystal-
3. List the extra-articular manifestations of induced arthropathy
rheumatoid arthritis
15. State why asymptomatic hyperuricemia is a
4. Describe the immunologic process that occurs laboratory finding and not a disease
in systemic lupus erythematosus
16. Describe the clinical manifestations, diagnos-
5. List four major organ systems that may be in- tic measures, and methods used in the treat-
volved in systemic lupus erythematosus ment of gouty arthritis
6. Describe the manifestations of systemic sclerosis 17. List three types of juvenile arthritis and differ-
entiate among their major characteristics
7. Cite a definition of the seronegative spondy-
loarthropathies 18. Name one rheumatic disease that affects only
the elderly population
8. Cite the primary features of ankylosing
spondylitis
9. Describe how the site of inflammation differs
in spondyloarthropathies from that in
SECTION II: ASSESSING YOUR
rheumatoid arthritis UNDERSTANDING
10. Contrast and compare ankylosing spondyli- Activity A Fill in the blanks.
tis, reactive arthritis, and psoriatic arthritis in
terms of cause, pathogenesis, and clinical 1. The cause of remains uncertain,
manifestations but evidence points to a genetic predisposi-

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CHAPTER 59 DISORDERS OF THE MUSCULOSKELETAL FUNCTION: RHEUMATIC DISORDERS 329

tion and the development of joint inflamma- 13. Children with may present with
tion that is immunologically mediated. constitutional symptoms, including fever,
malaise, anorexia, and weight loss, just as do
2. It has been suggested that rheumatoid arthri-
adults.
tis is initiated in a genetically predisposed in-
dividual by the activation of a 14. Juvenile is an inflammatory my-
response to an immunologic trigger, such as a opathy primarily involving skin and muscle
microbial agent. and it is associated with a characteristic rash.
3. Systemic lupus erythematosus (SLE) is a 15. is the most common complaint
disease that can affect virtually of elderly persons.
any organ system, including the muscu-
16. is by far the most common form
loskeletal system.
of arthritis among the elderly.
4. Almost all persons with develop
17. is an inflammatory condition of
polyarthritis and Raynaud phenomenon, a
unknown origin characterized by aching and
vascular disorder characterized by reversible
morning stiffness in the cervical regions and
vasospasm of the arteries supplying the
shoulder and pelvic girdle areas.
fingers.
5. is a chronic, systemic inflam- Activity B Consider the following figure.
matory disease of the joints of the axial
skeleton manifested by pain and progressive
stiffening of the spine.
6. The reactive can be defined as
sterile inflammatory joint disorders that are
distant in time and place from the initial in-
citing infective process.
7. is considered a clinical manifes-
tation of reactive arthritis that may be accom-
panied by extra-articular symptoms such as
uveitis, bowel inflammation, and carditis.
8. Arthritis that is associated with an inflamma-
tory bowel disease usually is considered an
arthritis because the intestinal
disease is directly involved in the pathogenesis.
9. , the most prevalent form of
In the figure above, locate the following joint
arthritis, is a leading cause of disability and
changes seen in osteoarthritis.
pain in the elderly.
• joint space narrows
10. Popularly known as arthritis, os-
• erosion of cartilage and bone
teoarthritis (OA) is characterized by signifi-
• osteophyte development
cant changes in both the composition and
• bone cysts
mechanical properties of cartilage.
11. syndrome includes acute arthri- Activity C Match the key terms in Column A
tis with recurrent attacks of severe articular with their definitions in Column B.
and periarticular inflammation; tophi or the Column A Column B
accumulation of crystalline deposits in articu-
lar surfaces, bones, soft tissue, and cartilage; 1. Spondyloarthro- a. Autoimmune dis-
gouty nephropathy or renal impairment; and pathies ease of connective
uric acid kidney stones. tissue characterized
2. Reactive
by excessive colla-
12. , which is characterized by syn- arthritis
gen deposition
ovitis, can influence epiphyseal growth by 3. Systemic lapis b. Bone spurs
stimulating growth of the affected side. erythematosus

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330 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

4. Joint mice c. Multisystem inflamma- Activity E Briefly answer the following.

tory disorders that pri-
5. Scleroderma 1. What is the pathogenesis of rheumatoid
marily affect the axial
6. Osteophytes skeleton arthritis?

7. Ankylosing d. An inflammatory ero-

spondylitis sion of the sites where
tendons and ligaments
8. Baker cyst attach to bone
9. Polymyalgia e. Result from the presence 2. What causes the degradation of a joint in
rheumatica of a foreign substance rheumatoid arthritis?
in the joint tissue
10. Gout
f. Inflammatory condi-
tion marked by antinu-
clear antibodies
g. Enlargement of the
3. What are the musculoskeletal manifestations
bursa in the popliteal
area behind the knee of systemic lupus erythematosus (SLE)?
h. Disorder of the muscles
and joints, typically of
older persons, charac-
terized by pain and
stiffness, affecting both 4. What are the typical joint changes seen in os-
sides of the body, and teoarthritis?
involving the shoul-
ders, arms, neck, and
buttock areas
i. Uric acid crystals are
found in the joint cavity
j. Fragments of cartilage 5. What is the pathogenesis of primary and sec-
and bone often become ondary gout?
dislodged, creating free-
floating osteocartilagi-
nous bodies

Activity D
1. Put the following processes involved in
rheumatoid arthritis in proper sequence.
SECTION III: APPLYING YOUR
a. Inflammatory response
KNOWLEDGE
b. Recruitment of inflammatory cells
c. Destruction of articular cartilage Activity F Consider the following scenario and
d. Complement fixation answer the questions.
e. T cell-mediated response A 5-year-old girl is brought to the clinic by her
f. Release of enzymes and prostaglandins mother because she “just isn’t feeling well.”
While taking the history, you note a weight loss
g. RF antigen/IgG interaction
of 5 pounds during the past year and complaints
of malaise. The child’s growth chart shows she is
in the 20th percentile for height. During the
physical examination, the physician notes pain
in three joints, hepatosplenomegaly and lymph
adenopathy. The suspected diagnosis is juvenile

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CHAPTER 59 DISORDERS OF THE MUSCULOSKELETAL FUNCTION: RHEUMATIC DISORDERS 331

idiopathic arthritis (JIA). The mother asks you 3. Scleroderma is an autoimmune disease of con-
what JIA is. nective tissue that is characterized by harden-
ing of the skin. What diseases do most people
1. What information would you include in your
with scleroderma develop? Mark all that apply.
response?
a. Dumping syndrome
b. Chronic diarrhea
c. Polyarthritis
d. Raynaud phenomenon
2. What confirmative test would you expect to e. Chronic vasoconstriction
see ordered? 4. Polymyositis and dermatomyositis are
chronic inflammatory myopathies that com-
monly manifest systemically. What is the
treatment of choice for these myopathies?
a. Muscle relaxants
b. Corticosteroids
c. IgG
SECTION IV: PRACTICING d. Nonsteroidal anti-inflammatory drugs
FOR NCLEX (NSAIDS)
5. Ankylosing spondylitis is a disease that typi-
Activity G Answer the following questions.
cally manifests in late adolescence and early
1. Joint destruction in rheumatoid arthritis (RA) adulthood. What is characteristic of the pain
occurs by an obscure process. The cellular in ankylosing spondylitis?
changes, however, have been documented. a. Worse when active
Place the process in the correct order.
b. Worse when sitting
a. Vasodilation
c. Worse when resting or lying in bed
b. Joint swelling
d. Worse when standing
c. Neutrophils, macrophages and lympho-
cytes arrive 6. Reiter syndrome is a reactive arthropathy.
What disease is Reiter syndrome associated
d. Lysosomal enzymes released
with?
e. Immune complexes phagocytized
a. Pelvic inflammatory disease
f. Inflammatory response
b. Gonorrhea
g. Reactive hyperplasia of synovial cells and
c. Syphilis
subsynovial tissues
d. Human immunodeficiency virus (HIV)
h. Increased blood flow to joint
i. Destructive changes in joint cartilage 7. A seronegative inflammatory arthropathy is
psoriatic arthritis. What drug has been found
2. Systemic lupus erythematosus (SLE) has to be beneficial in controlling both the psori-
been called the great imitator because it can asis and the arthritis in these patients?
affect many different body systems. What
a. Etanercept
is one of the most commonly occurring
symptoms in the early stages of SLE? b. Acetaminophen
a. Arthritis c. Interferon B
b. Avascular necrosis d. Econazole
c. Rupture of the Achilles tendon 8. Osteoarthritis (OA) is the most common
d. Classic malar rash cause of arthritis and a significant cause of
disability in the elderly. What joint changes
occur in OA? Mark all that apply.

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332 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

a. Creation of spurs 10. Elderly patients need special consideration in

b. Loss of synovial fluid the treatment of the arthritic diseases. Non-
steroidal anti-inflammatory drugs (NSAIDs),
c. Loss of articular cartilage
a first-line group of drugs used in the general
d. Inflammation of cartilage population for arthritic diseases, may not be
e. Synovitis well tolerated by the elderly. What side
effects of NSAIDs might be seen in the
9. Gout, or gouty arthritis, cannot be diagnosed
elderly?
on the basis of hyperuricemia. What is the di-
agnostic criterion for gout? a. Malaise
a. Finding of tophaceous deposits b. Lethargy
b. Finding of monosodium urate crystals in c. Sleeplessness
the synovial fluid d. Mania
c. Finding of sodium urate crystals in the
tissues
d. Finding of urate crystal deposits in the syn-
ovial fluid

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60

CHAPTER
Structure and
Function of the Skin

SECTION I: LEARNING SECTION II: ASSESSING YOUR

OBJECTIVES UNDERSTANDING
1. Describe the protective functions of skin Activity A Fill in the blanks.
2. Characterize the changes in a keratinocyte 1. The skin, also called the , is one
from its inception in the basal lamina to its of the largest and most versatile organs of the
arrival on the outer surface of the skin body, accounting for approximately 16% of
the body’s weight.
3. List the four specialized cells of the epidermis
and describe their functions 2. Variations are found in the properties of the
skin, such as the of skin layers,
4. Describe the structure and function of the
the distribution of sweat glands, and the
dermis and subcutaneous layers of skin
number and size of hair follicles.
5. Describe the following skin appendages and
3. The covers the body, and it is
their functions: sebaceous gland, eccrine
specialized in areas to form the various skin ap-
gland, apocrine gland, nails, and hair
pendages: hair, nails, and glandular structures.
6. Characterize the skin in terms of sensory and
4. The top or surface layer of the skin, the
immune functions
, consists of dead, keratinized
7. Describe the following skin rashes and le- cells.
sions: macule, patch, papule, plaque, nodule,
5. produce keratin, a complex pro-
tumor, wheal, vesicle, bulla, and pustule
tein that that forms the surface of the skin, is
8. Describe the characteristics and causes of blis- also the structural protein of the hair, and nails.
ters, calluses, and corns
6. are pigment-synthesizing cells
9. Cite two physiologic explanations for that are located at or in the basal layer.
pruritus
7. Exposure to the sun’s ultraviolet rays in-
10. Describe the causes and treatment of dry creases the production of ,
skin causing tanning to occur.
11. State common variations found in dark skin 8. cells are potent antigen-
presenting cells.

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334 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

9. The is involved in skin disorders 15. Hair is a structure that is pushed

that cause bullae or blister formation. upward from the hair follicle.
10. The dermis supports the and 16. The nails are hardened plates,
serves as its primary source of nutrition. called fingernails and toenails, which protect
the fingers and toes and enhance dexterity.
11. The receptors for touch, pressure, heat, cold,
and pain are widely distributed in the 17. A is a vesicle or fluid-filled papule.
.
18. A is a hyperkeratotic plaque of
12. The layer of the dermis is sup- skin caused by chronic pressure or friction.
plied with free nerve endings that serve as no-
19. are small, well-circumscribed,
ciceptors and thermoreceptors.
conical, keratinous thickenings of the skin.
13. sweat glands are simple tubular
20. Dry skin, also called , may be a
structures that originate in the dermis and
natural occurrence, as in the drying of skin
open directly to the skin surface.
associated with aging, or it may be sympto-
14. sweat glands open through a matic of underlying systemic disease or skin
hair follicle and are found primarily in the ax- disorder such as contract dermatitis.
illae and groin.
Activity B Consider the following figures.

1. In the figure above, locate and label the follow-

ing structures:
• nerve ending • dermis
• sebaceous gland • sweat gland
• blood vessel • papillae
• arrector pili muscle • epidermis

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CHAPTER 60 STRUCTURE AND FUNCTION OF THE SKIN 335

f. Inner layer of skin

g. Mechanoreceptors
h. Immune cells
i. Transformation from
viable cells to the dead
cells of the stratum
corneum
j. Provide sensory informa-
tion

Activity D Briefly answer the following.

1. What are the vital functions of the skin?

2. What are the layers of the epidermis?

2. In the figure above, locate and label the follow-
ing structures:
• epidermis
• hair papilla
• dermis
• hair shaft 3. How is it that a person with albinism cannot
• arrector pili synthesize melanin?
• sebaceous gland
• keratinized cells
• hair follicle
• dermal blood vessels

Activity C Match the key terms in Column A 4. What is the relationship between melanin and
with their definitions in Column B. different colors of skin?

Column A Column B
1. Keratinocytes a. Consists of collagen
fibers and ground sub-
2. Merkel cells
stance
3. Keratinization b. 5. Describe the structure and function of seba-
Responsible for skin
ceous glands.
4. Epidermis color, tanning, and
protecting against ul-
5. Papillary traviolet radiation
dermis
c. Outer layer of skin
6. Langerhans’ d. Produce a fibrous pro-
cells tein called keratin, 6. How does an itch differ from pain?
7. Dermis which is essential to
the protective function
8. Ruffini
e. Complex meshwork
corpuscles
of three-dimensional
9. Melanin collagen bundles in-
terconnected with
10. Reticular
large elastic fibers and
dermis
ground substance

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336 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

SECTION III: APPLYING YOUR c. Lamina lucida

KNOWLEDGE d. Type IV collagen
4. The pars reticularis is characterized by what?
Activity E Consider the following scenario and
a. Dendritic cells
answer the questions.
b. Its color
You are the nurse preparing an educational event
c. Three-dimensional collagen bundles
for the local chapter of the Parent-Teacher Asso-
ciation (PTA). You have been asked to speak on d. Its immunologic function
skin disorders. 5. Why is the subcutaneous tissue considered
1. What information would you include about part of the skin? Mark all that apply.
dark-skinned people? a. Eccrine glands extend to this layer
b. The keratinocytes are formed in the subcu-
taneous tissue
c. Skin diseases can involve the subcutaneous
tissue
d. The Merkel cells are formed in the subcuta-
neous tissue
SECTION IV: PRACTICING e. Deep hair follicles can be found in the sub-
FOR NCLEX cutaneous tissue
6. Sebaceous glands excrete a mixture that lubri-
Activity F Answer the following questions. cates the hair and skin. What is this mixture
1. Among the skin’s known protective functions called?
is that it serves as an immunologic barrier. a. Sweat
What cells detect foreign antigens? b. Chalasia
a. Langerhans’ cells c. Cerumen
b. Merkel cells d. Sebum
c. Keratinocytes
7. Fingernails and toenails, unlike hair, grow
d. Melanocytes continuously. The nail plate itself is nearly
2. Match the cells of the epidermis with their transparent and acts as a window for viewing
description or function. what?
a. The amount of oxygen in the blood
Cell Description or Function
b. The color of the blood in the subcutaneous
1. Keratino- a. Thought to be neu- tissue
cytes roendocrine cells
c. The health of the nail plate
2. Melanocytes b. Pigment-synthesiz-
d. The color of the stratum corneum
ing cells
3. Merkel cells 8. When a degeneration of the epidermal cells
c. Replaces lost skin
4. Langerhans cells occurs, layers of the skin separate because of a
cells disruption of the intercellular junctions.
d. Immunologic cells
When this occurs what is formed?
3. The basement membrane separates the ep- a. Lichenifications
ithelium from the underlying connective tis-
b. Vesicles
sue. It is a major site of what is found in skin
disease? c. Petechiae
a. Melanocytes d. Pressure ulcer
b. Complement deposition

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CHAPTER 60 STRUCTURE AND FUNCTION OF THE SKIN 337

9. Pruritus, or the itch sensation, is a byproduct 10. The first-line treatment for dry skin is a mois-
of almost all skin disorders. However, we can turizing agent. How do these agents work?
itch without having a skin disorder. Itch then a. Decreasing pruritus
can be local or central in our bodies. Where is
b. Penetrating the lipid barrier of the skin
it postulated that a central “itch center” exists?
c. Increasing transepidermal water loss
a. Pons
d. Repairing the skin barrier
b. Medulla oblongata
c. Somatosensory cortex
d. Sensory area of the cerebrum

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61
CHAPTER

Disorders of Skin
Integrity and Function

SECTION I: LEARNING 11. Use knowledge of the life cycles of Pediculus

humanus corporis and Pediculus humanus capi-
OBJECTIVES tis to explain the lesions associated with
body, head, and pubic lice
1. Describe common pigmentary disorders of
the skin 12. Describe the three types of ultraviolet radia-
tion and relate them to sunburn, aging skin
2. Relate the behavior of fungi to the produc-
changes, and the development of skin cancer
tion of superficial skin lesions associated with
tinea or ringworm 13. Describe the manifestations and treatment of
sunburn
3. State the cause and describe the appearance
of impetigo and ecthyma 14. State the properties of an effective sunscreen
4. Compare the viral causes, manifestations, and 15. Compare the tissue involvement in first, sec-
treatments of verrucae, herpes simplex, and ond-degree full-thickness, and third-degree
herpes zoster lesions burns
5. Compare acne vulgaris, acne conglobata, and 16. State how the rule of nine is used in deter-
rosacea in terms of appearance and location mining the body surface area involved in a
of lesions burn
6. Describe the pathogenesis of acne vulgaris 17. Cite the determinants for grading burn sever-
and relate it to measures used in treating the ity using the American Burn Association clas-
disorder sification of burns
7. Differentiate allergic and contact dermatitis 18. Describe the systemic complications of burns
and atopic and nummular eczema
19. Describe the major considerations in treat-
8. Describe the differences and similarities be- ment of burn injury
tween erythema multiforme minor, Stevens-
20. Cite two causes of pressure ulcers
Johnson syndrome, and toxic epidermal
necrolysis 21. Explain how shearing forces contribute to is-
chemic skin damage
9. Define the term papulosquamous and use the
term to describe the lesions associated with 22. List four measures that contribute to the pre-
psoriasis, pityriasis rosea, and lichen planus vention of pressure ulcers
10. Relate the life cycle of Sarcoptes scabiei to the 23. Describe the origin of nevi and state their re-
skin lesions seen in scabies lationship to skin cancers

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CHAPTER 61 DISORDERS OF SKIN INTEGRITY AND FUNCTION 339

24. Compare the appearance and outcome of small vesicle or pustule or as a large bulla on
basal cell carcinoma, squamous cell carci- the face or elsewhere on the body.
noma, and malignant melanoma
8. is a deeper infection affecting
25. Differentiate a hemangioma of infancy from the dermis and subcutaneous tissues.
a port-wine stain in terms of appearance and
9. and occur on the
outcome
soles of the feet and palms of the hands, re-
26. Describe the manifestations and probable spectively.
causes of diaper dermatitis, prickly heat, and
10. Herpes is an acute, localized
cradle cap
vesicular eruption distributed over a der-
27. Describe the distinguishing features of rashes matomal segment of the skin.
associated with the following infectious
11. is a disorder of the piloseba-
childhood diseases: roseola infantum, rube-
ceous unit.
ola, rubella, and varicella
12. consists of a mixture of free
28. Characterize the physiologic changes of aging
fatty acids, triglycerides, diglycerides, mono-
skin
glycerides, sterol esters, wax esters, and squa-
29. Describe the appearance of skin tags, ker- lene.
atoses, lentigines, and vascular lesions that
13. Noninflammatory acne lesions consist of
are commonly seen in the elderly
; are plugs of mate-
rial that accumulate in sebaceous glands that
open to the skin surface and are
SECTION II: ASSESSING YOUR pale, slightly elevated papules with no visible
UNDERSTANDING orifice.
14. acne lesions consist of papules,
Activity A Fill in the blanks. pustules, nodules, and, in severe cases, cysts.
1. skin disorders include pigmen- 15. Hypersensitivity are usually
tary skin disorders, infectious processes, acne, characterized by epidermal edema with sepa-
rosacea, papulosquamous dermatoses, allergic ration of epidermal cells; they include irritant
disorders and drug reactions, and arthropod contact dermatitis, allergy contact dermatitis,
infestations. atopic and nummular eczema, urticaria, and
2. An absence of production re- drug-induced skin eruptions.
sults in vitiligo or albinism. 16. dermatitis results from a cell-
3. is a genetic disorder in which mediated, type IV hypersensitivity response
there is complete or partial congenital ab- brought about by sensitization to an allergen.
sence of pigment in the skin, hair, and eyes, 17. The lesions of eczema are coin-
which is found in all races. shaped papulovesicular patches mainly in-
4. are free-living, saprophytic volving the arms and legs.
plantlike organisms; certain strains of which 18. Acute immunologic is com-
are considered part of the normal skin flora. monly the result of an IgE-mediated immune
5. is a yeastlike fungus that is a reaction that usually occurs within 1 hour of
normal inhabitant of the gastrointestinal exposure to an antigen.
tract, mouth, and vagina. 19. drugs are usually responsible for
6. Primary infections are superfi- localized contact dermatitis types of rashes,
cial skin infections, such as impetigo or ec- whereas drugs cause generalized
thyma. skin lesions.

7. is common, superficial bacterial 20. dermatoses are a group of skin

infections caused by staphylococci or group A disorders characterized by scaling papules and
-hemolytic streptococci that appears as a plaques.

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340 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

21. is a relatively common chronic, 34. are the second most frequently
pruritic disease that involves inflammation occurring malignant tumors of the outer epi-
and papular eruption of the skin and mucous dermis.
membranes.
35. Pigmented represent abnormal
22. Lichen simplex chronicus is a localized migration or proliferation of melanocytes
lichenoid, pruritic dermatitis resulting from seen in infants.
rubbing and scratching.
36. of infancy are generally benign
23. A mite, Sarcoptes scabiei, which burrows into vascular tumors produced by proliferation of
the epidermis, causes . the endothelial cells.
24. commonly referred to as sun- 37. represent slow-growing capillary
burn rays are responsible for nearly all the malformations that grow proportionately
skin effects of sunlight, including with the child and persist throughout life.
photoaging—the wrinkles, pigmentary
38. is a form of contact dermatitis
changes, dryness, and loss of skin tone that
that is caused by an interaction with several
occurs with, and is enhanced by, exposure to
factors, including prolonged contact of the
sunlight.
skin with a mixture of urine and feces.
25. Some drugs are classified as
39. results from constant macera-
drugs because they produce an exaggerated
tion of the skin because of prolonged expo-
response to ultraviolet light when the drug is
sure to a warm, humid environment.
taken in combination with sun exposure.
40. is a greasy crust or scale forma-
26. is caused by excessive exposure
tion on the scalp that is usually attributed to
of the epidermal and dermal layers of the skin
infrequent and inadequate washing of the
to ultraviolet radiation, resulting in an ery-
scalp.
thematous inflammatory reaction.
27. are typically classified according Activity B Match the key terms in Column A
to the depth of involvement as first-degree, with their definitions in Column B.
second-degree, and third-degree
1.
28. victims often are confronted
Column A Column B
with hemodynamic instability, impaired res-
piratory function, hypermetabolic response, 1. Herpes a. Pain that persists
major organ dysfunction, and sepsis. simplex virus longer than 1 to
3 months after the
29. Pressure ulcers are lesions of the 2. Vitiligo resolution of her-
skin and underlying structures caused by un- pes zoster rash
3. Postherpetic
relieved pressure that impairs the flow of
neuralgia b. Responsible for
blood and lymph.
cold sore
4. Sermatophytid
30. Another form of nevi, the , is im- c. Superficial mycoses
portant because of its capacity to transform to 5. Melasma
d. Warts that are
malignant melanoma.
6. Ecthyma common benign
31. Malignant melanoma is a malignant tumor of papillomas caused
7. Verrucae
the . by DNA-contain-
8. Dermatophytoses ing human papil-
32. Severe, blistering sunburns in early childhood
lomaviruses
and intermittent intense sun exposures con- 9. Tinea capitis
tribute to increased susceptibility to e. Sudden appearance
10. Shingles of white patches
in young and middle-aged
adults. on the skin
f. Darkened macules
33. , which is a neoplasm of the
on the face
nonkeratinizing cells of the basal layer of the
epidermis, is the most common skin cancer
in white-skinned people.

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CHAPTER 61 DISORDERS OF SKIN INTEGRITY AND FUNCTION 341

g. Allergic reaction Activity C Briefly answer the following.

during an acute
episode of a fungal 1. What is the cause and symptomology of
infection albinism?
h. Ulcerative form of
impetigo
i. Caused by infection
of herpes zoster
j. Ringworm of the 2. What is the mechanism of skin irritation with
scalp a fungal infection?
2.
Column A Column B
1. Pediculosis a. Comedones form pri-
marily on the face and
2. Acne 3. What are the types of tinea capitis and what
neck and, to a lesser
vulgaris are the mechanisms of irritation?
extent, on the back,
3. Psoriasis chest, and shoulders.
4. Acne b. Disorder characterized
conglobata the development of
edematous wheals ac-
5. Decubitus companied by intense 4. What is the port of entry for cellulitis infec-
ulcers itching tions? What are the most common symptoms?
6. Rosacea c. Thickening of the skin
associated with rosacea
7. Urticaria
d. Bed sore
8. Nevi
e. Comedones, papules,
9. Rhino- pustules, nodules, ab-
5. Herpes simplex virus (HSV)-1 virus will have
phyma scesses, cysts, and scars
episodic recurrences. What is the mechanism
occur on the back, but-
10. Hyper- of recurrence? What are the signs and symp-
tocks, and chest.
keratosis toms of recurrence?
f. Mole
g. Erythema (flushing
and redness) on the
central face and across
the cheeks, nose, or
forehead 6. What are the factors believed to contribute to
h. Infestation with lice the development of acne?
i. Increased epidermal
cell turnover with
marked epidermal
thickening
j. Chronic inflammatory 7. What is atopic dermatitis and how does it af-
skin disease character- fect adults differently than infants?
ized by circumscribed
red, thickened plaques
with an overlying
silvery-white scale

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342 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

8. What is thought to be the cause of psoriasis? 1. The mother asks why her son must be sent to
another hospital. You explain that the patient
is at high risk for complications from his
burns. To what does the massive loss of skin
tissue predispose him?

9. What is scabies and why does it itch?

2. The parents ask what specific complication

can occur because of the burns their son has.
10. What is the hypothesized mechanism of skin Your correct response would include what?
damage brought about by UVB rays?

11. What are the steps recommended to protect a

patient from UV exposure? SECTION IV: PRACTICING
FOR NCLEX
Activity E Answer the following questions.
1. Match the skin disorder with its description.
12. Why are severe burns an immediate medical Skin Disorder Description
emergency?
1. Vitiligo a. Darkened macules on
the face
2. Albinism
b. Sudden appearance
3. Melasma of white patches on
the skin
13. Describe the two main types of basal cell car- c. A genetic disorder in
cinoma which complete or
partial congenital
absence of pigment
in the skin, hair, and
eyes is found, which
occurs in all races.
2. Human bodies have, as endemic organisms,
SECTION III: APPLYING YOUR both yeast (Candida albicans) and molds.
What is used as a confirmatory diagnostic test
KNOWLEDGE is used when a fungus invades the skin?
Activity D Consider the following scenario a. Potassium hydroxide (KOH) preparations
and answer the questions. b. The Forest light

A 17-year-old with second- and third-degree c. Tinea preparations

burns on his trunk, arms, and neck is brought to d. Sodium chloride (NaCl) preparations
the emergency department (ED). In the ED, he is
being stabilized for shipment to the nearest burn
unit.

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CHAPTER 61 DISORDERS OF SKIN INTEGRITY AND FUNCTION 343

3. Match the bacterial or viral skin infection 8. In severe Stevens-Johnson syndrome and
with its preferred treatment. toxic epidermal necrolysis, hospitalization is
requiree. When large areas of the skin are lost
Skin Infection Preferred Treatment
what IV medication may speed-up the heal-
1. Impetigo a. Systemic antibi- ing process?
2. Ecthyma otics a. Immunoglobulin
b. Bactroban or sys- b. Broad-spectrum antibiotics
3. Cellulitis
temic antibiotics c. Diflucan
4. Verrucae c. Acyclovir d. Corticosteroids
5. Herpes simplex d. Oral acyclovir 9. What disease has primary lesions that have a
virus (HSV-1) e. Penciclovir cream silvery scale over thick red plaques?
6. Herpes simplex f. Oral and intra- a. Pityriasis rosea
virus (HSV-2) venous (IV) anti- b. Psoriasis vulgaris
biotics
7. Herpes zoster c. Lichen planus
g. A keratolytic agent
d. Lichen simplex chronicus
4. Acne vulgaris is typically an infection in the
10. What skin disease manifests with lesions on
adolescent population. What topical agent
the skin and oral lesions that look like milky
used in the treatment of acne is both an an-
white lacework?
tibacterial and a comedolytic?
a. Eczema
a. Alcohol
b. Psoriasis
b. Benzoyl peroxide
c. Lichen planus
c. Bactroban
d. Pityriasis rosea
d. Resorcinol
11. Scabies infections are caused by mites that
5. Rosacea is a chronic inflammatory process
burrow under the skin. They are usually easily
that occurs in middle-aged and older adults.
treated by bathing with a mite-killing agent
What are common manifestations of rosacea?
and leaving it on for 12 hours. When scabies
Mark all that apply.
are resistant to the mite-killing agent what
a. Swelling of the eyelid oral drug is prescribed?
b. Heat sensitivity a. Clindomycin
c. Burning eyes b. Interferon B
d. Telangiectasia c. Potassium hydroxide
e. Erythema d. Ivermectin
6. Allergic contact dermatitis is a common in- 12. Pressure ulcers can occur quickly in the
flammation of the skin. It produces lesions in elderly and in those who are immobile. What
the affected areas. What do these lesions look is a method for preventing pressure ulcers?
like? a. Preventing dehydration
a. Papules
b. Frequent position changes
b. Papulosquamous pustules
c. Use of water-based skin moisturizers
c. Vesicles
d. Infrequent changing of incontinent patients
d. Ulcers
13. Nevi are benign tumors of the skin. One type
7. Atopic dermatitis, or eczema, occurs at all of nevi is important because of its capacity to
ages and in all races. What happens in black- transform to malignant melanoma. What
skinned people who have eczema? type of nevus is this?
a. Hyperpigmentation of skin a. Nevocellular
b. Papules cover the area affected b. Compound nevi
c. Erythema is a prominent symptom c. Dysplastic
d. Loss of pigmentation from lichenified skin d. Dermal

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344 UNIT 14 DISORDERS OF MUSCULOSKELETAL AND INTEGUMENTARY FUNCTION

14. Malignant melanomas are metastatic tumors 17. Hemangiomas of infancy are small, red le-
of the skin. In the past decades, the incidence sions that are noticed shortly after birth and
of malignant melanoma has grown. This is re- grow rapidly. What is the treatment of choice
lated to more exposure to UV light, such as for hemangiomas of infancy?
tanning salons. What are risk factors for de- a. Surgical excision
veloping malignant melanoma?
b. Laser surgery
a. Freckles across the bridge of the nose
c. No treatment
b. Blistering sunburns after age 20
d. Chemotherapy
c. Palmar nevi
18. Rubella, or 3-day measles, is a childhood dis-
d. Presence of actinic keratoses
ease caused by a togavirus. Because rubella
15. Basal cell carcinoma is the most common can be easily transmitted and, because it is
skin cancer in white-skinned people. Al- dangerous to the fetus if contracted by preg-
though the treatment goal that is most im- nant women early in their gestational period,
portant is elimination of the lesion, it is also immunization is required. What type of vac-
important to maintain the function and cos- cine is the rubella vaccine?
metic effect. What treatment is used for basal a. Attenuated virus vaccine
cell carcinoma?
b. Antibody/antigen vaccine
a. Curettage with electrodesiccation
c. Dead virus vaccine
b. Systemic chemotherapy
d. Live virus vaccine
c. Topical chemotherapy
19. Lentigines are skin lesions common in the el-
d. Simple radiographic radiation
derly. A type of lentigine is tan to brown in
16. Squamous cell carcinoma in light-skinned color with benign spots. Lentigines are re-
people is a red scaling, keratotic, slightly ele- moved because they are considered precur-
vated lesion with an irregular border, usually sors to skin cancer. How are lentigines
with a shallow chronic ulcer. How do the removed?
lesions appear in black-skinned people? a. Cryotherapy
a. Keratotic lesions with rolling, irregular b. Chemotherapy
borders
c. Bleaching agents
b. Hyperpigmented nodules
d. Curettage
c. Hypopigmented nodules
d. Lichenous plaques with silvery scales

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Answers

CHAPTER 1 CONCEPTS OF HEALTH conditions are often self-limiting. Chronic dis-

ease states, however, run a continuous course
AND DISEASE and present with aggravations and remissions.
3. Congenital conditions are present at birth and
SECTION II: ASSESSING YOUR result from genetic disturbances, environmen-
UNDERSTANDING tal effects, or a combination of genetic and en-
Activity A vironmental causes. Acquired defects,
1. altered health conversely, are brought about by conditions
2. health following birth.
3. disease 4. Syndromes are the collection of signs, symp-
4. risk factors toms, and manifestations of the disease. Se-
5. Congenital defects quelae are injuries that come as a secondary
6. acquired result of the disease.
7. diagnosis 5. The importance of risk factors lies in their pro-
8. Subclinical disease, Clinical disease viding a window into developing disease. It is
9. Epidemiology possible to avoid risky behavior and therefore
10. Prevalence, incidence lower the chances of developing the disease.
Risk factors are determined from studying a
Activity B
controlled population where most of the
1. b 2. g 3. f 4. c 5. e habits and practices are similar. Some of the
6. h 7. d 8. a 9. i 10. j most prominent studies are the Framingham
Activity C Study (coronary heart disease), the Nurses’
Health Study (breast cancer), and the Nun’s
1. Study (Alzheimer disease).
Etiology Pathogenesis Morphology

Clinical Course Clinical Manifestations SECTION III: APPLYING YOUR

KNOWLEDGE
Prognosis Activity E
1. Epidemiology
Activity D Incidence and prevalence of diseases
1. Pathophysiology is the study of the disease Morbidity and mortality statistics
process and the body’s response to disease. Natural history of a disease and its risk factors
Physiology is the study of normal bodily Prognosis
process, and pathology is the study of the dis- Prevention
ease manifestations. Pathophysiology can be 2. The nurse should explain that evidence-based
viewed as a combination of physiology and practice and evidence-based practice guide-
pathology. lines are mechanisms that use the current best
2. The clinical course of a disease describes the scientific findings (evidence) to make deci-
evolution of the disease process. In acute con- sions about the health care of individuals.
ditions, the disease is usually rapid in onset They are based on the expertise of the individ-
and quite severe. Consequently, though, acute ual practitioner integrated with the evidence
345
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346 ANSWERS

gathered from a systematic review of credible dated by The Joint Commission (as well as
research studies. Practice guidelines may take the laws of most states in the case of written
the form of algorithms, which are step-by-step orders by the doctor) and used in every
methods for solving a problem, written direc- health care institution in the United States.
tives, or a combination thereof. 5. a. Rationale: Secondary prevention detects
disease early in its course when it is still
SECTION IV: PRACTICING FOR NCLEX asymptomatic and treatment measures can
effect a cure or stop the disease from pro-
Activity F
gressing. Most secondary prevention is
1. a. Rationale: Most disease states do not have a undertaken in clinical settings. Tertiary
single cause but instead stem from a number prevention goes beyond treating the present-
of factors. Some disease states are compli- ing problem. Tertiary prevention programs
cated and hard to diagnose, such as multiple are located within health care systems and
sclerosis, whereas some are simple, straight- involve the services of a number of different
forward, and easy to diagnose, such as a bro- types of health care professionals. Primary
ken leg. prevention is often accomplished outside the
2. d. Rationale: Epidemiology is the study of pat- health care system at the community level.
terns of disease, such as the spread of a dis- 6. c. Rationale: A syndrome is a compilation of
ease in an epidemic. It has also emerged as a signs and symptoms (e.g., chronic fatigue
science to study the risk factors in multifacto- syndrome) that are characteristic of a specific
rial diseases, such as heart disease and cancer. disease state. Complications are possible ad-
Scientology is a religion. Morphology refers verse extensions of a disease or outcomes
to the fundamental structure or form of cells from treatment. Sequelae are lesions or im-
or tissues. Histology deals with the study of pairments that follow or are caused by a dis-
the cells and extracellular matrix of body tis- ease. There is no name for a group of disease
sues. states that all have the same cause.
3. c. Rationale: Morbidity and mortality statistics 7. c. Rationale: The natural history of a disease
provide information about the functional ef- refers to the way the disease will run its
fects (morbidity) and death-producing (mor- course and the expected outcome of the dis-
tality) characteristics of a disease. ease process if medical intervention is not un-
Morbidity statistics do address the effects a dertaken. Prognosis is the term used to
disease has on a person’s life and the long- designate the probable outcome and prospect
term consequences of the disease state, but of recovery from a disease. Morbidity de-
morbidity and mortality statistics taken to- scribes the effects an illness has on a person’s
gether have a broader scope. Neither morbid- life. It is concerned with the incidence of
ity nor mortality statistics address recovery disease as well as its persistence and long-
rates from a disease or treatment modalities term consequences. Conditions suspected of
for a disease. Although mortality does address contributing to the development of a disease
the causes of death in a given population, are called risk factors.
morbidity does not address the impact the 8. d. Rationale: The pathogenesis of a disease is
disease state has on the family. the mechanism by which an etiologic factor
4. a, b, c. Rationale: Clinical practice guidelines causes the disease. Etiology is what sets the
are systematically developed statements in- disease process in motion, or what causes the
tended to inform practitioners and clients in disease. Risk factors are multiple factors that
making decisions about health care for spe- predispose to a particular disease.
cific clinical circumstances. They should re- 9. d. Rationale: A black eye is usually indicative
view and weigh various outcomes, both of an unfortunate accident and could be a
positive and negative, and make recommen- sign that a caregiver would see. However, a
dations. Guidelines are different from system- green thumb is a mythical ability usually as-
atic reviews. They can take the form of signed to a good gardener. The other choices
algorithms, which are step-by-step methods are either subjective symptoms (reported by
for solving a problem, written directives for the patient) or objective signs (observed by
care, or a combination thereof. Nothing takes the caregiver) of disease states.
the place of either written orders by the doc- 10. b, c. Rationale: Standardization relies on the use
tor or the nursing care plan. These are man- of written standards, reference measurement

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ANSWERS 347

procedures, and reference materials. In vitro 3. Surfactant reduces surface tension by inter-
diagnostic devices and laboratory equipment rupting hydrogen bonds in the fluid that coats
are regulated by the U.S. Food and Drug Ad- the interior surface of the alveoli. This pre-
ministration (FDA) and are, of themselves, vents the alveoli from collapsing and allows
standardized. Standardization does not need them to inflate.
FDA approval. However, new reagents, test 4. The most common risk factors include sleep-
kits, and clinical laboratory instruments must ing in the prone position, prematurity and low
meet standardization guidelines mandated by birth weight, African American or Native
law and obtain FDA approval before they can American race, and exposure to environmen-
be marketed in the United States. tal cigarette smoke, as well as young age of the
mother, lack of or inadequate prenatal care,
and smoking or substance use during
CHAPTER 2 CONCEPTS OF ALTERED pregnancy.
HEALTH IN CHILDREN 5. Organic failure to thrive is the result of a phys-
iologic cause that prevents the infant from ob-
SECTION II: ASSESSING YOUR taining or using nutrients. An example of
UNDERSTANDING organic failure to thrive is inadequate growth
Activity A of an infant with deficient energy reserve be-
cause of a congenital defect that makes feed-
1. growth and development
ing difficult. Failure of any organ system can
2. growth, morphogenesis, differentiate
cause an organic failure to thrive.
3. Apgar score
6. Jaundice and hyperbilirubinemia are consid-
4. injuries during birth
ered pathologic if their time and pattern of
5. respiratory distress syndrome
appearance and duration vary significantly
6. Colic
from that of physiologic jaundice. The great-
7. 3–3.5 kg, 6 cm
est risk associated with hyperbilirubinemia is
8. decreases
the development of bilirubin encephalopathy,
9. lesions
a neurologic syndrome resulting from deposi-
10. obesity
tion of unconjugated bilirubin in the basal
Activity B ganglia.
1. Small for gestational age
2. Appropriate for gestational age SECTION III: APPLYING YOUR
Activity C KNOWLEDGE
1. h 2. i 3. c 4. j 5. f Activity E
6. a 7. b 8. e 9. g 10. d 1. Primary teeth are lost and replaced by perma-
Activity D nent teeth at this stage. There is a high inci-
1. Gestational age is divided into prenatal and dence of dental caries during late childhood
postnatal assessment. Prenatal assessment of that is related to inadequate dental care and a
gestational age mostly includes careful men- high amount of dietary sugar. Children in the
strual history, physical milestones during early part of this stage may not be as effective
pregnancy such as uterine size, detection of at brushing their teeth and may require adult
fetal heart rate, and fetal movements. Ad- assistance, but may be reluctant to accept
vanced prenatal tests for maturity include ul- parental help.
trasound and amniotic fluid studies. 2. Many chronic health problems are first diag-
Postnatal assessment of gestational age is nosed during middle to late childhood. Spe-
done by examination of external physical cific learning disabilities can also be identified
and neuromuscular characteristics alone or in at this time. Infections with bacterial and
combination using the Dubowitz or Ballard fungal agents are a common problem in
methods. childhood.
2. Due to the force put on the infant during the 3. The major task is the development of indus-
birth process and the movement of the fetus try or accomplishment. Failure to meet this
through the pelvic outlet, the clavicle will task results in a sense of inferiority or in-
often fracture. This is more common in large competence, which can impede further
for gestational age infants. progress.

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348 ANSWERS

pancreas does not produce enough insulin for

SECTION IV: PRACTICING FOR NCLEX
the body’s requirements, the infant is diag-
Activity F nosed as insulin-dependent diabetic and
1. b. Rationale: A standard is established for the would be hyperglycemic.
height, weight, and age of children by sam- 6. d. Rationale: Allergic reactions cause asthma,
pling a specific population. Statistics from which frequently manifests for the first time
that sample are used to account for variations during middle childhood. Cerebral palsy is a
(called standard deviations) from the “norm” disease process with which the child is usu-
or “average” of the population sampled. Sta- ally born. Nephrotic syndrome occurs most
tistically, a child who falls within 1 standard commonly in children younger than 3 years,
deviation of the norm (or mean for that pop- whereas pneumonia can occur anytime across
ulation) is the same in height and weight as the life span.
68% of other 2-year-old children. A child who 7. a. Rationale: The anterior fontanel is open and
is the same height and weight as 75% of palpable until about 18 months to 2 years of
other 2-year-old children would fall within 2 age; the smaller fontanels are replaced by
standard deviations of the norm. A child who bone by the end of the first year. The bones of
is considered small and underweight would the child’s skull are solidified by 2 years of
fall 3 standard deviations below the mean, age, not 3 years of age.
and a toddler who is tall and overweight 8. b. Rationale: Because of the immaturity of the
would fall 3 standard deviations above the immune system in children of this age, they
norm, or mean. are at risk for communicable diseases such as
2. d. Rationale: There are two main periods of chickenpox, the common cold, influenza,
fetal development. The first is the embryonic and intestinal tract infections. Diaper rash
period, which begins during the second week and croup are not communicable diseases,
after fertilization and ends during the eighth and a urinary tract infection is not transmit-
week after fertilization. The other answers de- ted from one child to another.
scribe blocks of time in the early stage of 9. c. Rationale: Women are routinely tested for
pregnancy. GBS prior to delivery. If they test positive for
3. a. Rationale: An infant is considered term GBS infection, they are treated with antibi-
when born between the beginning of the otics during the intrapartal period to help
38th week and completion of the 41st week. prevent transmission of the bacteria to the
A child born at 36 or 37 weeks would be con- newborn. After delivery, infants are treated
sidered preterm. Weight is not a measure- prophylactically with antibiotics, unless they
ment used to decide whether an infant is test positive for GBS themselves. Then they
term. are given a full course of IV antibiotics to pre-
4. a. Rationale: Psychosomatic disorders may vent sepsis.
manifest during adolescence. Common 10. c. Rationale: An increased risk of SIDS is asso-
health problems experienced by adolescents ciated with sleeping in the prone position
that may be psychosomatic in origin in- and smoking or substance use during preg-
clude headache, stomachache, and insom- nancy. Other risk factors include being Native
nia. Dental caries occur frequently in American or African American; the Asian race
middle to late childhood, and leg and skele- is not associated with an increased risk of
tal pain are not common complaints of ado- SIDS. Exposure to environmental cigarette
lescence. smoke is also a risk factor; however, placing
5. c. Rationale: It is believed that infants who are the infant on its back to sleep is recom-
considered small for gestational age have de- mended to decrease the incidence of SIDS,
pleted hepatic glycogen stores. Brown fat is and breast-feeding has not been identified as
found near the heart and blood vessels that a risk for SIDS.
supply the kidneys and brain and is believed 11. a, b, c, d. Rationale: Complications that may
to play a role in maintaining the temperature occur when an infant is large for gestational
of these organs during the environmental age include asphyxia during birth and me-
change that occurs at birth. If the pancreas chanical difficulties that cause trauma during
produces too much insulin for the infant’s the birth process. They are also at risk for hy-
body requirement, then the infant is usually poglycemia and polycythemia due to their in-
large for gestational age. When an infant’s creased size.

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ANSWERS 349

12. a, b, c. Rationale: The information to include whereas disease is the loss of function due to a
in an educational event for women having pathological process.
their first babies is information about gesta- 3. The somatic mutation theory of aging states
tional age and what it means. It should also that the longevity and function of cells in vari-
include information about intrauterine ous tissues of the body are determined by a
growth retardation, which can occur at any double-stranded DNA molecule and its specific
time during the pregnancy. An infant who is repair enzymes. DNA undergoes continuous
small for gestational age weighs less than 90% change in response to both exogenous agents
of all other infants. and intrinsic processes. Aging may result from
13. height. Rationale: Sex hormones not only ini- conditions that produce mutations in DNA or
tiate the growth spurt, but also stop it by deficits in DNA repair mechanisms.
causing bone maturity, which means that the 4. There is a reduction in muscle size and
skeleton ceases to grow. strength that is related to a loss of muscle
fibers and a reduction in the size of the exist-
ing fibers. There is a decline in high-speed per-
CHAPTER 3 CONCEPTS OF ALTERED formance and reaction time because of a
HEALTH IN OLDER ADULTS decrease in type II muscle fibers. Impairments
in the nervous system can also cause move-
SECTION II: ASSESSING YOUR ments to slow. However, type I muscle fibers,
UNDERSTANDING which offer endurance, are believed to remain
Activity A consistent with age.
5. Alterations in vision and hearing impairment
1. 65 to 74, 75 to 84, 85
impair sensory input, increasing the risk for
2. intrinsic
falls. Input from the skeletal muscles is also in-
3. Stochastic
tegrated to help control balance. As the neu-
4. telomerase
ronal signaling degrades the ability to send
5. oxidative free radical
and interpret, sensory data input decreases,
6. Collagen
which increases the likelihood of falling.
7. vertebral column
6. Dementia is a general decrease in cognitive
8. systolic
abilities without a known pathology.
9. elastic recoil
Alzheimer disease is associated with discrete
10. Presbycusis
changes in the cellular structure and enzyme
11. Xerostomia
activity of neurons.
12. achlorhydria
13. glomerular filtration
14. Katz SECTION III: APPLYING YOUR
15. inhibit KNOWLEDGE
16. depressed Activity D
17. stroke 1. The nurse should respond that an unstable
18. Dementia gait is only one of the reasons a person falls.
19. Delirium The daughter should see that her father gets
20. total body water his vision and hearing checked. Age- and dis-
Activity B ease-related alterations in vision and hearing
1. b 2. e 3. d 4. c 5. g can contribute to an elderly person falling.
6. h 7. i 8. a 9. f 10. j Medications can also cause elderly people to
fall, so the daughter should know what med-
Activity C
ications her father is taking and their side ef-
1. The slow steady oxidation of the structures of fects. She should check the environment her
the epithelial lining of the arterioles results in father lives in and remove any objects he
cellular injury. The constant assault results in could trip on, such as scatter rugs or electrical
adaptation, scarring, and overall thickening of cords that cross an area used as a walkway. She
the blood vessel. This reduces the compliance should also make sure his shoes fit properly.
and results in increased systolic pressure. 2. The nurse should assess for depression because
2. The changes seen in aging are the result of a these are common signs of depression in
slow steady decrease in physiological activity, elderly patients. Depression is often seen in

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350 ANSWERS

older people, especially if they have suffered cal changes in the body that occur with
many losses related to aging, such as the death aging.
of friends, diminished hearing or vision, de- 6. d. Rationale: Serum creatinine, a byproduct of
creased mobility, or illness or injury. muscle metabolism, is often used as a measure
of GFR. The decline in GFR that occurs with
SECTION IV: PRACTICING FOR NCLEX aging is not accompanied by an equivalent
increase in serum creatinine levels because
Activity E
the production of creatinine is reduced as
1. a. Rationale: Skin disorders are common muscle mass declines with age. Serum creati-
among the older adult population and can nine levels do not increase with age and nei-
include skin cancers, keratoses (i.e., warty le- ther does the GFR. Although GFR decreases
sions), xerosis (i.e., excessive dryness), der- with age, serum creatinine levels do not.
matitis, and pruritus (i.e., generalized 7. a. Rationale: Urge incontinence is an irrita-
itching). The term xenobiotic refers to a tive, not an obstructive symptom of BPH. The
chemical compound foreign to a given bio- other irritative symptoms include urinary fre-
logical system, and xenomas are tumors that quency, nocturia, and urinary urgency. The
develop on skin infested with certain para- obstructive symptoms of BPH include hesi-
sites. tancy in initiation of stream, a diminished
2. d. Rationale: As a person ages, there are force of urine stream, urinary retention, and
changes in cardiac function in the body. postvoid dribbling.
There is an increase, not a decrease, in sys- 8. d. Rationale: According to the American Psy-
temic vascular resistance and left ventricular chiatric Association’s Diagnostic and Statistical
afterload, as well as a decrease in the maxi- Manual of Mental Disorders (DSM-IV-TR), the
mal heart rate and maximal cardiac output. criteria for the diagnosis and treatment of a
The heart becomes less responsive to major depression include at least five of the
-adrenergic stimulation and circulating following symptoms during the same 2-week
catecholamines. period, with at least one of the symptoms
3. a. Rationale: Speech discrimination, or the being depressed mood or anhedonia (i.e., loss
ability to distinguish among words that are of interest or pleasure): depressed or irritable
near-homonyms or to distinguish words spo- mood; loss of interest or pleasure in usual ac-
ken by several different speakers, is often im- tivities; appetite and weight changes; sleep
paired. Elderly people who are hearing disturbance; psychomotor agitation or retar-
impaired do not repeat themselves because of dation; fatigue and loss of energy; feelings of
a hearing loss nor do they speak slower or worthlessness, self-reproach, or excessive
softer then their peers who are not hearing guilt; diminished ability to think or concen-
impaired. They also do not shout unnecessar- trate; and suicidal ideation, plan, or attempt.
ily due to a hearing impairment. 9. b. Rationale: Currently, the diagnosis of
4. b. Rationale: Smell is a protective mechanism, Alzheimer disease is one of exclusion. That is,
and persons who cannot smell may be at risk no specific diagnostic tests can confirm or
for exposure to environmental hazards. For rule out the diagnosis. The Mini-Mental State
example, people who cannot smell smoke Examination, developed in 1975, is a screen-
would be at particular risk if a fire broke out. ing tool that gives a brief, quick picture of a
Taking the wrong medication would be more person’s cognitive ability. It is not meant to
apt to occur due to visual problems. Living in be used as the sole diagnostic tool to confirm
unhealthy and unclean conditions is not or rule out dementia in any patient.
caused by a decline in the ability to either A complete metabolic panel run on a pa-
taste or smell. An elderly person who has lost tient’s blood can confirm the presence of
some of their ability to taste or smell may be hyperlipidemia, which is believed to be a
at risk for eating raw food that has spoiled possible indication of vascular dementia.
but not at risk for eating food that is not Although auscultation of bruits in the carotid
cooked properly. arteries indicates a decrease in blood flow to the
5. d. Rationale: Dementia affects memory, lan- brain because of a narrowing of the carotids, it
guage, visuospatial ability, and cognition is not diagnostic of dementia in any form.
(i.e., abstraction, calculation, judgment, 10. b. Rationale: One of the many concerns
problem solving). It does not affect the physi- surrounding the medication of the elderly

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ANSWERS 351

population is polypharmacy because it in- sic factor can cause malabsorption of vitamin
creases the risk of drug interactions and ad- B12. Vitamin B12 is essential in the maturation
verse drug reactions. Being prescribed of red blood cells and, without it, pernicious
multiple drugs has also been found to de- anemia, a macrocytic anemia, can occur. A
crease the patient’s compliance with drug reg- lack of vitamin B12 can also affect the central
imens. Psychotropic drugs administered to nervous system, causing peripheral neu-
older adults with dementia may cause an in- ropathies. It is a lack of intrinsic factor that
crease in any confusion they are experiencing. causes the lack of vitamin B12 in the body,
Nonsteroidal anti-inflammatory medications not the other way around, and a lack of vita-
given to an older adult with hypertension can min B12 can cause ataxia, which is an im-
cause an increase in blood pressure. Beta- paired ability to coordinate movement, not
blocking agents administered to an individual an improvement in coordination.
with chronic obstructive pulmonary disease 14. a, b, d. Rationale: Depression can be a symp-
may induce bronchoconstriction. tom of a medical condition, such as pancre-
11. 1-d, 2-b, 3-a, 4-c. Rationale: Medications are atic cancer, hypothyroidism or
an important and potentially correctable hyperthyroidism, pneumonia and other in-
cause of instability and falls. Centrally acting fections, congestive heart failure, dementia,
medications, such as sedatives and hypnotics, and stroke. Hypocholesteremia does not have
have been associated with an increase in the depression as a symptom.
risk of falling and injury. Diuretics can cause 15. b, c, d. Rationale: A decrease in bladder capac-
volume depletion, electrolyte disturbances, ity, in bladder and sphincter tone, and in the
and fatigue, predisposing a person to falls. ability to inhibit detrusor (i.e., bladder mus-
Antihypertensive drugs can cause fatigue, or- cle) contractions, combined with the nervous
thostatic hypotension, and impaired alert- system’s increased variability to interpret
ness, contributing to the risk of falls. bladder signals, can cause incontinence. Im-
12. c. Rationale: Because of the serious implica- paired mobility and a slower reaction time
tions of medication use in the elderly, strate- can also aggravate incontinence. Of particu-
gies to enhance therapeutic effects and lar importance is the role of pharmaceuticals,
prevent harm need to be used. Careful evalu- such as long-acting sedatives and hypnotics,
ation of the need for the medication by the psychotropics, and diuretics, as a cause of
health care provider is the first step. Once de- transient urinary incontinence. Aging causes
cided, analysis of the individual’s current a decrease in the ability to inhibit the detru-
medication regimen and disease states is nec- sor contractions rather than increasing the
essary to prevent drug–drug interactions, patient’s ability to inhibit the contractions.
drug–disease interactions, and adverse re-
sponses. Dosing should be at the low end,
and frequency of drug administration should
CHAPTER 4 CELL AND TISSUE
be kept to a minimum to simplify the routine CHARACTERISTICS
and enhance compliance. Timing the dose to
a specific activity of daily living (e.g., “take SECTION II: ASSESSING YOUR
with breakfast”) can also improve compli- UNDERSTANDING
ance, as can special packaging devices such as Activity A
pill boxes and blister packs. The cost of med-
1. Protoplasm
ications is another important factor for older
2. eukaryotic, prokaryotic
adults living on reduced, fixed incomes.
3. DNA, RNA, proteins
Choosing less expensive products of equal ef-
4. protein
ficacy can increase compliance. The impor-
5. Rough
tance of educating the individual about the
6. Golgi
medication cannot be overemphasized.
7. Lysosomes
Health care professionals need to provide ver-
8. peroxides
bal and written information on the principles
9. respiration, ATP
of medication use and on the specific medica-
10. microtubules
tions being used.
11. microfilaments
13. a, c. Rationale: Atrophy of the gastric mucosa
12. peripheral
and a decrease in the ability to secrete intrin-

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352 ANSWERS

13. epithelial, connective, muscle, neuronal 3. Individual cells produce extracellular matrix
14. ion proteins that form a basement membrane
15. muscle, neural where cells can form anchors. Cells will then
Activity B form connections between each other via cell
junctions (tight, gap, desmosome, hemidesmo-
1.
some). This interaction between cytoskeletal
1. b 2. h 3. f 4. j 5. d
elements, the basement membrane, and cellu-
6. a 7. e 8. g 9. i 10. c
lar adhesion is the basis for tissue formation.
2. 4. First messengers can be neurotransmitters,
1. j 2. f 3. b 4. g 5. d protein hormones and growth factors,
6. e 7. h 8. i 9. c 10. a steroids, and/or other chemical messengers.
Activity C
They will bind to receptors either on the cell
membrane (hydrophilic first messengers) or in
the cytoplasm (hydrophobic first messengers).
7 4 1 5 6 2 3 The activation of a receptor via first messen-
ger results in the activation of a second mes-
senger. Cell surface receptors are
Activity D transmembrane proteins that will activate an
Hydrophilic polar head
array of second messengers (cAMP, G pro-
teins, and tyrosine kinases) that will have di-
rect effects on membrane potential or a host
Extracellular
Cholesterol
molecule
Pore fluid of other cellular functions. Activation of an
Carbohydrate
Hydrophobic Glycoprotein intracellular receptor involves the activation
fatty acid chain
Glycolipid of a transcription factor that will directly in-
fluence the expression of a gene product. The
Phospholipids: gene product will then have an effect on cel-
polar head
(hydrophilic) lular function.
Fatty acid tails
(hydrophobic)
5. Endocytosis is the process of bringing in large
Cytosol
Channel protein
Peripheral molecules or substances to a cell. Receptor-
protein
Filaments of
cytoskeleton Transmembrane Integral mediated endocytosis is triggered by a specific
proteins
Cholesterol protein
ligand. The inflammatory system contains cells
(macrophages, neutrophils) that will endocy-
tose dead cell material, bacteria, or foreign ma-
Activity E
terial. This process is known as phagocytosis.
1. The three protein complexes are (a) cyclins, (b) Exocytosis is the release of large quantities of
cyclin-dependent kinases, and (c) anaphase- material, such as the exocytosis of a neuro-
promoting complex. The central components transmitter.
of the cell cycle control system are the cyclin-
dependent kinases (CDKs), whose activity de-
SECTION III: APPLYING YOUR
pends on their association with the regulatory
KNOWLEDGE
units called cyclins. The anaphase-promoting
complex allows for progression through the Activity F
cell cycle via destruction of previous CDK 1. In our bodies, fat is stored in tissue called adi-
complexes. Each molecule functions under pose tissue. Adipose tissue is a special form of
variable concentrations. connective tissue that helps connect different
2. In ischemia and hypoxia (an anoxia), the cells types of tissue in our body to each other. Adi-
do not receive enough oxygen. As a result, the pose cells have big empty spaces in them so
electron transport chain cannot pass electrons they can store large quantities of triglycerides
from complex to complex. Proton pumping and are the largest storage spaces of energy in
slows or is halted, and the proton gradient de- the body. The subcutaneous fat we store helps
creases, resulting in a decreased production, or shape our body. It also helps insulate our body
a complete lack, of ATP. With no ATP, the cell because fat is a poor conductor of heat.
cannot maintain normal functioning (e.g., Adipose tissue exists in two forms: uniloc-
membrane potential, transport) and begins to ular and multilocular. Unilocular (white) adi-
malfunction. pose tissue is composed of cells in which the

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ANSWERS 353

fat is contained in a single, large droplet in the cross into the cell nucleus itself, where they
cytoplasm. Multilocular (brown) adipose tissue influence DNA activity. Ion-channel–linked
is composed of cells that contain multiple receptors transiently open or close ion chan-
droplets of fat and numerous mitochondria. nels. Thyroid and steroid hormones act
We have deposits of brown fat when we within the cell nucleus to increase transcrip-
are born, but they decrease over time. White tion of mRNA to alter cell function.
fat is the kind we have most of, and it is what 7. c. Rationale: Each of the two pyruvate mole-
we add to our body when we gain weight. cules formed in the cytoplasm from one mol-
ecule of glucose yields another molecule of
SECTION IV: PRACTICING FOR NCLEX ATP, which is a special carrier for cellular en-
ergy. FAD (flavin adenine dinucleotide) is a
Activity G
coenzyme of protein metabolism that accepts
1. a. Rationale: Rough ER is studded with ribo- electrons and is reduced. NADH  H is an
somes attached to specific binding sites on the end product of glycolysis. The electron trans-
membrane. Proteins produced by the rough port chain oxidizes NADH  H and FADH2
ER are usually destined for incorporation into and donates the electrons to oxygen, which
cell membranes and lysosomal enzymes or for is reduced to water.
exportation from the cell. The rough ER segre- 8. d. Rationale: Active transport is what occurs
gates (rather than combines) these proteins when cells use energy to move ions against
from other components of the cytoplasm and an electrical or chemical gradient. Passive
modifies their structure for a specific function. transport is another term for diffusion. There
Rough ER does not transport anything is no such thing as neutral transport. Co-
through the cell membrane. Rough ER is stud- transport is when the sodium ion and the
ded with ribosomes; it does not destroy them. solute are transported in the same direction
2. b. Rationale: Recently, data suggest that the 9. a. Rationale: Four categories of tissue exist: (a)
Golgi apparatus has yet another function: It epithelium, (b) connective (supportive), (c)
can receive proteins and other substances muscle, and (d) nerve. Binding, connecting,
from the cell surface by a retrograde transport and exothelial tissue are not categories of
mechanism. Golgi bodies do not produce tissue.
bile. They produce secretory, not excretory, 10. b. Rationale: These glands are ductless and
granules, and they produce large carbohy- produce secretions (i.e., hormones) that
drate molecules rather than small ones. move directly into the bloodstream. Exocrine
3. c. Rationale: Although GM2 ganglioside accu- glands retain their connection with the sur-
mulates in many tissues, such as the heart, face epithelium from which they originated.
liver, and spleen, its accumulation in the ner- This connection takes the form of epithe-
vous system and retina of the eye causes the lium-lined tubular ducts through which the
most damage. secretions pass to reach the surface. Exocyto-
4. d. Rationale: They do not make energy, but sis occurs when part of the cell membrane
they extract it from organic compounds. Pro- ruptures to release particles that are too large
teasomes are small organelles composed of to pass through the cell membrane. These
protein complexes that are believed to be cells are ductless, but do not necessarily se-
present in both the cytoplasm and the nu- crete their contents into the bloodstream.
cleus. They are not formed by mitochondria. 11. c. Rationale: Thin and thick filaments are the
Mitochondria contain their own DNA and ri- two types of muscle fibers that are responsible
bosomes and are self-replicating. for muscle contraction. The thin filaments are
5. a. Rationale: The cell membrane is often called composed primarily of actin, whereas the
the plasma membrane. The nuclear mem- thick filaments are composed of myosin. Dur-
brane is another type of membrane within the ing muscle contraction, the thick myosin and
cell. The cell membrane provides receptors for thin actin filaments slide over each other,
hormones and other biologically active sub- causing shortening of the muscle fiber, al-
stances; it is not a receptor membrane. A main though the length of the individual thick and
structural component of the membrane is its thin filaments remains unchanged. When ac-
lipid bilayer. It is not a bilayer membrane. tivated by ATP, the cross-bridges swivel in a
6. b. Rationale: At the membrane of the cell nu- fixed arc, much like the oars of a boat, as they
cleus, both thyroid and steroid hormones become attached to the actin filament.

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354 ANSWERS

During contraction, each cross-bridge under- 9. Pathological, nonphysiologic

goes its own cycle of movement, forming a 10. Metaplasia
bridge attachment and releasing it, and mov- 11. irritation, inflammation
ing to another site where the same sequence 12. dysplasia
of movement occurs. This pulls the thin and 13. cancer
thick filaments past each other. The calcium- 14. accumulations
calmodulin complex is in smooth muscle. It 15. Free
binds to and activates the myosin-containing 16. Hypoxia
thick filaments, which interact with actin. 17. swelling, fatty
12. cytoplasm. Rationale: When seen under a 18. Necrosis
light microscope, three major components of 19. calcium
the cell become evident: the nucleus, the cy- 20. coagulation
toplasm, and the cell membrane. Activity B
13. jaundice. Rationale: When bilirubin collects
within the cells, they take on a yellowish
color, which is called jaundice. Nucleus
14. a, c, d. Rationale: The human body has sev-
eral means of transmitting information be- Basement
tween cells. These mechanisms include direct Normal cells—Physiologic membrane
communication between adjacent cells
through gap junctions, autocrine and
paracrine signaling, and endocrine or synap-
tic signaling. There is no such thing as ex-
Atrophy—Pathologic
press communication between cells.
15. b, c, d. Rationale: Nondividing cells, such as
neurons and skeletal and cardiac muscle cells,
have left the cell cycle and are not capable of
mitotic division in postnatal life. The cells
that produce mucous are capable of mitotic
division. Smooth muscle is often called invol- Hypertrophy—Both
untary muscle because it contracts sponta-
neously or through activity of the autonomic
nervous system.
16. involuntary. Rationale: Three types of muscle
tissue exist: skeletal, cardiac, and smooth.
Smooth muscle is often called involuntary Hyperplasia—Both
muscle because it contracts without the per-
son willing it to contract.

CHAPTER 5 CELLULAR
ADAPTATION, INJURY,
AND DEATH
Metaplasia—Both
SECTION II: ASSESSING YOUR
UNDERSTANDING
Activity A
1. size, number, type
2. housekeeping, differentiation
3. size
4. atrophy
5. increase
6. physiologic
7. hyperplasia Dysplasia—Pathologic
8. compensatory
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ANSWERS 355

Activity C dependent and results from injury. The execu-

tion phase of both pathways is initiated by
1. e 2. b 3. d 4. g 5. a
proteolytic enzymes called caspases.
6. c 7. f 8. i 9. h 10. j

Activity D SECTION III: APPLYING YOUR

1. The pathogenesis of dystrophic calcification KNOWLEDGE
involves the intracellular and/or extracellular Activity E
formation of crystalline calcium phosphate. 1. Chemotherapy is a general term that can tech-
The components of the calcium deposits are nically refer to chemical (drug) therapy for any
derived from the bodies of dead or dying cells kind of illness. However, in practice, this term
as well as from the circulation and interstitial usually refers to the pharmacologic treatment
fluid. As tissues die, the calcium crystallizes of cancer. It is important to remember that all
and deposits form. rapidly dividing cells (both normal and cancer
2. The five categories of cellular injury are (a) in- cells) are affected by chemotherapy drugs,
jury from physical agents, (b) radiation injury, such as the rapidly dividing normal cells
(c) chemical injury, (d) injury from biologic found in mucous membranes, hair follicles,
agents, and (e) injury from nutritional imbal- and the components of bone marrow. Anti-
ances. neoplastic drugs, or chemotherapy drugs, are
3. The toxicity of lead is related to its multiple very toxic drugs. They act on the tumor cells
biochemical effects. It has the ability to inacti- because tumor cells divide and produce more
vate enzymes, compete with calcium for incor- tumor cells so rapidly, and while tumor cells
poration into bone, and interfere with nerve are dividing, they are very vulnerable to the
transmission and brain development. Lead ex- destructive actions of the chemotherapy
posure in children has been demonstrated to drugs. Some of the normal cells surrounding
result in neurobehavioral and cognitive the tumor are also damaged or destroyed be-
deficits. cause they are vulnerable while they are divid-
4. The three major mechanisms of cellular dam- ing to produce new, healthy cells.
age are free radical formation, hypoxia and
ATP depletion, and disruption of intracellular
calcium homeostasis. Multiple pathologies,
SECTION IV: PRACTICING FOR NCLEX
whether mechanical, chemical, biological, or Activity F
blunt force, will result in a combination of 1. a. Rationale: There are numerous molecular
these mechanisms being activated. mechanisms mediating cellular adaptation,
5. Oxidative stress leads to the oxidation of cell including factors produced by other cells or
components, activation of signal transduction by the cells themselves. These mechanisms
pathways, and changes in gene and protein depend largely on signals transmitted by
expression. DNA modification and damage chemical messengers that exert their effects
can occur because of oxidative stress. In addi- by altering gene function. In general, the
tion, mitochondrial DNA as a target of oxida- genes expressed in all cells fall into two cate-
tion and subsequent cause of mitochondrial gories: “housekeeping” genes that are neces-
dysfunction may be the cause of diseases. sary for normal function of a cell, and genes
6. As oxygen concentrations fall, oxidative me- that determine the differentiating characteris-
tabolism slows down. To make ATP, the cell tics of a particular cell type. In many adaptive
reverts to anaerobic metabolism. With a de- cellular responses, the expression of the differ-
crease in ATP, the ion distribution is altered entiation genes is altered, whereas that of the
and cells will swell. The product of anaerobic housekeeping genes remains unaffected.
metabolism is lactic acid, and as lactic acid ac- Thus, a cell is able to change size or form
cumulates, the pH falls. Low pH will change without compromising its normal function.
protein conformation, resulting in total loss of Once the stimulus for adaptation is removed,
enzyme function. the effect on expression of the differentiating
7. Two basic pathways for apoptosis are the ex- genes is removed and the cell resumes its pre-
trinsic pathway, which is death receptor de- vious state of specialized function.
pendent and is under cellular control, and the 2. b. Rationale: Compensatory hypertrophy is
intrinsic pathway, which is death receptor in- the enlargement of a remaining organ or

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356 ANSWERS

tissue after a portion has been surgically re- skin to toughen and become leathery feeling,
moved or rendered inactive. The body does but not in patches of pink-pigmented skin.
not enlarge its major organs during times of Vitiligo is a benign acquired skin disease of
malnutrition. Gene expression, not actin unknown cause, consisting of irregular
expression, stimulates the body to increase patches of various sizes totally lacking in pig-
the muscle mass of the heart. Hypertrophy ment and often having hyperpigmented bor-
is not a progressive decrease in the size of ders. It can appear in the skin of any race and
anything. is not scaly. Photosensitivity is a sign of xero-
3. c. Rationale: Metastatic calcification occurs in derma pigmentosum, but this disease in-
normal tissues as the result of increased creases, not decreases, the person’s risk of
serum calcium levels (hypercalcemia). Almost skin cancer.
any condition that increases the serum cal- 7. b, c. Rationale: Lightning and high-voltage
cium level can lead to calcification in inap- wires that carry several thousand volts pro-
propriate sites such as the lung, renal tubules, duce the most severe damage. In electrical in-
and blood vessels. The major causes of hyper- juries, the body acts as a conductor of the
calcemia are hyperparathyroidism, either pri- electrical current.
mary or secondary to phosphate retention in 8. d. Rationale: Injury from freezing probably
renal failure; increased mobilization of cal- results from a combination of ice crystal for-
cium from bone as in Paget disease, cancer mation and vasoconstriction. The decreased
with metastatic bone lesions, or immobiliza- blood flow leads to capillary stasis and arte-
tion; and vitamin D intoxication. Diabetes riolar and capillary thrombosis. Edema re-
mellitus and hypoparathyroidism do not sults from increased capillary permeability.
cause hypercalcemia; therefore, they cannot Exposure to low-intensity heat (43ºC–46ºC),
be a cause of metastatic calcification. such as occurs with partial-thickness burns
4. d. Rationale: The main source of methyl mer- and severe heat stroke, causes cell injury by
cury exposure is from consumption of long- inducing vascular injury. The process of
lived fish, such as tuna and swordfish. warming tissue that has been frozen or par-
Although there is mercury in amalgam fill- tially frozen causes pain. If the pain is bad
ings, the amount of mercury vapor given off enough, then medication is given to control
by the fillings is very small. Most thermome- the pain. Health team members are always
ters today are made without mercury. The concerned about giving pain medication to
same holds true for most blood pressure ma- someone who might be an addict. Asking
chines. whether this is the first time this person has
Lead in paint is a concern, not mercury. had an injury induced by the cold is appro-
5. a. Rationale: Children are exposed to lead priate when taking a health history. How-
through ingestion of peeling lead paint, by ever, pointing out that “it is obvious you are
breathing dust from lead paint (e.g., during a homeless person” is not an appropriate re-
remodeling), or from playing in contami- mark for the nurse to make. Also not appro-
nated soil. The lead danger to potters is from priate is wondering when it will happen
the ceramic glaze before it is fired. You do not again.
have to keep children away from everything 9. a. Rationale: Destructive changes occur in
ceramic. Newsprint contains lead, but you are small blood vessels such as the capillaries and
not exposed to a significant amount of lead venules. Acute reversible necrosis is repre-
when you read the newspaper. You have to sented by such disorders as radiation cystitis,
work directly with ore to be exposed to toxic dermatitis, and diarrhea from enteritis. More
levels of lead. Walking through part of a persistent damage can be attributed to acute
mine on a field trip is not a contributing fac- necrosis of tissue cells that are not capable of
tor to lead poisoning. regeneration and chronic ischemia. Neither
6. b. Rationale: In a genetic disorder called xero- hunger nor muscle spasms are signs of radia-
derma pigmentosum, an enzyme needed to tion injury.
repair sunlight-induced DNA damage is lack- 10. b. Rationale: Gram-negative bacilli release en-
ing. This autosomal recessive disorder is char- dotoxins that cause cell injury and increased
acterized by extreme photosensitivity and a capillary permeability. Certain bacteria excrete
2,000-fold increased risk of skin cancer in elaborate exotoxins that interfere with cellular
sun-exposed skin. Exposure to sun causes the production of ATP. Gram-negative bacilli do

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ANSWERS 357

not disrupt a cell’s ability to replicate. Many agents in that they are able to replicate and
gram-negative bacilli cause harm to cells. continue to produce injury. Among the nutri-
11. atrophy. Rationale: When confronted with a tional factors that contribute to cell injury
decrease in work demands or adverse envi- are excesses and deficiencies of nutrients, vit-
ronmental conditions, most cells are able to amins, and minerals.
revert to a smaller size and a lower and more 14. a, b, c, d. Rationale: Many drugs—alcohol,
efficient level of functioning that is compati- prescription drugs, over-the-counter drugs,
ble with survival. This decrease in cell size is and street drugs—are capable of directly or
called atrophy. indirectly damaging tissues. Ethyl alcohol
12. 1-a, 2-d, 3-b, 4-c. Rationale: Pigments are col- can harm the gastric mucosa, liver, develop-
ored substances that may accumulate in cells. ing fetus, and other organs. Antineoplastic
They can be endogenous (i.e., arising from (anticancer) and immunosuppressant drugs
within the body) or exogenous (i.e., arising can directly injure cells. Other drugs produce
from outside the body). Icterus, also called metabolic end products that are toxic to cells.
jaundice, is characterized by a yellow discol- Acetaminophen, a commonly used over-the-
oration of tissue due to the retention of counter analgesic drug, is detoxified in the
bilirubin, an endogenous bile pigment. This liver, where small amounts of the drug are
condition may result from increased bilirubin converted to a highly toxic metabolite.
production from red blood cell destruction,
obstruction of bile passage into the intestine,
or toxic diseases that affect the liver’s ability
to remove bilirubin from the blood. Lipofus-
CHAPTER 6 GENETIC CONTROL OF
cin is a yellow-brown pigment that results CELL FUNCTION AND INHERITANCE
from the accumulation of the indigestible
residues produced during normal turnover of SECTION II: ASSESSING YOUR
cell structures. The accumulation of lipofus- UNDERSTANDING
cin increases with age and is sometimes re- Activity A
ferred to as the wear-and-tear pigment. It is
1. deoxyribonucleic
more common in heart, nerve, and liver cells
2. Ribonucleic
than other tissues and is seen more often in
3. proteome
conditions associated with atrophy of an
4. purine, pyrimidine
organ. One of the most common exogenous
5. complementary
pigments is carbon in the form of coal dust.
6. 23
In coal miners or persons exposed to heavily
7. chromatin, chromosomes
polluted environments, the accumulation of
8. triplet
carbon dust blackens the lung tissue and may
9. mutations
cause serious lung disease. The formation of a
10. haplotype
blue lead line along the margins of the gum is
11. transcription
one of the diagnostic features of lead poison-
12. exons
ing. Melanin a black or dark brown pigment
13. translation
that occurs naturally in the hair, skin, and
14. chaperones
iris and choroid of the eye.
15. expression
13. 1-b, 2-c, 3-a, 4-d. Rationale: Cell injury can be
16. hedgehog
caused by a number of agents, including
17. fibroblast
physical agents, chemical agents, biologic
18. phenotype
agents, and nutritional factors. Among the
19. locus, alleles
physical agents that generate cell injury are
20. pedigree
mechanical forces that produce tissue
trauma, extremes of temperature, electricity, Activity B
radiation, and nutritional disorders. Chemi- 1.
cal agents can cause cell injury through sev- 1. a 2. c 3. b 4. e 5. j
eral mechanisms: They can block enzymatic 6. f 7. d 8. h 9. g 10. i
pathways, cause coagulation of tissues, or dis-
rupt the osmotic or ionic balance of the cell. 2.
Biologic agents differ from other injurious 1. d 2. a 3. c 4. b 5. e

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358 ANSWERS

Activity C SECTION III: APPLYING YOUR

1. KNOWLEDGE
Activity E
A C G F B
DNA fingerprinting is a technique for comparing
the nucleotide sequences of fragments of DNA
D E H I from different sources. The fragments are ob-
tained by treating the DNA with various enzymes
that break DNA strands at specific sites. There is a
Activity D chance of 1 in 30 billion that two persons who
1. Mendel discovered the basic pattern of inheri- are not monozygotic twins would have identical
tance by conducting carefully planned experi- DNA fingerprints. Because genetic variations are
ments with garden peas. Experimenting with so distinctive, DNA fingerprinting (analysis of
phenotypic traits in peas, Mendel proposed DNA sequence differences) can be used to deter-
that inherited traits are transmitted from par- mine family relationships or help identify per-
ents to offspring by means of independently sons involved in criminal acts.
inherited factors, now known as genes, and
that these factors are transmitted as recessive SECTION IV: PRACTICING FOR NCLEX
and dominant traits from parents to their off-
Activity F
spring.
2. Genetic maps use linkage studies to estimate 1. a. Rationale: The term proteome is a relatively
the distances between chromosomal land- new term, created to define the complete set
marks. They are similar to a road map. Physi- of proteins encoded by a genome. A chromo-
cal maps are similar to a surveyor’s map. They some is any of the threadlike structures in the
make use of cytogenetic and molecular tech- nucleus of a cell that function in the trans-
niques to determine the physical locations of mission of genetic information. The terms
genes on chromosomes. protogene and nucleotomics are not real
3. While in metaphase I, chromosomes are words.
paired and condensed. Over time, an inter- 2. b. Rationale: The two strands of the helix sep-
change of chromatid segments can occur. This arate, and a complementary molecule is du-
process is called crossing over. Crossing over plicated next to each original strand. Two
allows for new combinations of genes result- strands become four strands. During cell divi-
ing in an increase in genetic variability. This is sion, the newly duplicated double-stranded
a very beneficial process. molecules are separated and placed in each
4. There are 22 pairs of somatic chromosomes. daughter cell by the mechanics of mitosis. As
Half of each pair is received from the female, a result, each daughter cell again contains the
and the other half is from the male. We then meaningful strand and the complementary
have two sex chromosomes, an X from our strand joined together as a double helix.
mother and, in the case of females, an X 3. c. Rationale: Of the 23 pairs of human chro-
from the father for a total of two Xs. Males mosomes, 22 are called autosomes and are
only have one X chromosome from their alike in both males and females. The double
mother and one Y chromosome from their helix is the shape of the DNA molecule. Ribo-
father. somes are areas in a cell that synthesize pro-
5. Gene activator and repressor sites within teins. Haploid have only one complete set of
DNA commonly monitor levels of the syn- nonhomologous chromosomes.
thesized product and regulate gene tran- 4. d. Rationale: Rarely, accidental errors in du-
scription through a negative feedback plication of DNA occur. These errors are
mechanism. Expression is also regulated at called mutations. Ribosomes are areas in a
the transcription level by transcription fac- cell that synthesize proteins. Several repair
tors that directly affect protein structure and mechanisms exist, and each depends on
function specific enzymes called endonucleases that

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ANSWERS 359

recognize local distortions of the DNA helix, guanine, adenine, cytosine, and thymine
cleave the abnormal chain, and remove the (uracil is substituted for thymine in RNA)—
distorted region. Four bases—guanine, ade- make up the alphabet of the genetic code. A
nine, cytosine, and thymine (uracil is substi- sequence of three of these bases forms the
tuted for thymine in RNA)—make up the fundamental triplet code used in transmit-
alphabet of the genetic code. A sequence of ting the genetic information needed for pro-
three of these bases forms the fundamental tein synthesis. This triplet code is called a
triplet code used in transmitting the genetic codon. Alternate forms of a gene at the same
information needed for protein synthesis. locus are called alleles.
This triplet code is called a codon. 9. a. Rationale: Banding patterns are analyzed to
5. a. Rationale: Polygenic inheritance involves determine whether they match. Four bases—
multiple genes at different loci, with each guanine, adenine, cytosine, and thymine
gene exerting a small additive effect in deter- (uracil is substituted for thymine in RNA)—
mining a trait. Multifactorial inheritance is make up the alphabet of the genetic code. A
similar to polygenic inheritance in that mul- sequence of three of these bases forms the
tiple alleles at different loci affect the out- fundamental triplet code used in transmit-
come; the difference is that multifactorial ting the genetic information needed for pro-
inheritance includes environmental effects tein synthesis. The small variation in gene
on the genes. Monofactorial inheritance is sequence (termed a haplotype) is believed to
nonexistent, as is collaborative inheritance. account for the individual differences in
6. b. Rationale: When the deletion is inherited physical traits, behaviors, and disease suscep-
from the mother, the infant presents with tibility. Chromosomes contain all genetic
Angelman (“happy puppet”) syndrome. content of the genome.
Turner syndrome is a chromosomal anomaly 10. b. Rationale: Cloned DNA sequences are usu-
seen in about 1 in 3000 live female births, ally the compounds used in gene therapy.
characterized by the absence of one X chro- Messenger RNA carries the instructions for
mosome. Down syndrome is a congenital protein synthesis. Sterically stable liposomes
condition characterized by varying degrees of are stable liposomes with long circulation
mental retardation and multiple defects. It is times. Sites in the DNA sequence where indi-
the most common chromosomal abnormality viduals differ at a single DNA base are called
of a generalized syndrome and is caused by single nucleotide polymorphisms (SNPs, pro-
the presence of an extra chromosome 21 in nounced “snips”).
the G group. Fragile X syndrome is a repro- 11. haplotype. Rationale: As the Human
ductive disorder characterized by a nearly Genome Project progressed, it became evi-
broken X chromosome, which has a tip hang- dent that the human genome sequence is
ing by a flimsy thread. It is the most common almost exactly (99.9%) the same in all peo-
inherited cause of mental retardation. ple. It is the small variation (0.01%) in gene
7. c. Rationale: A recessive trait is one that is ex- sequence (termed a haplotype) that is be-
pressed only when two homozygous people lieved to account for the individual differ-
have a child. A dominant trait is one ex- ences in physical traits, behaviors, and
pressed in either a homozygous or a heterozy- disease susceptibility.
gous pairing. A single-gene trait and a 12. b, c, d. Rationale: RNA is a single-stranded
penetrant trait do not exist. However, single- rather than a double-stranded molecule. Sec-
gene inheritance does exist. ond, the sugar in each nucleotide of RNA is
8. d. Rationale: The establishment of the Inter- ribose, not deoxyribose. Third, the pyrimi-
national HapMap Project was to map the dine base thymine in DNA is replaced by
haplotypes of the many closely related single uracil in RNA. All cells are supposed to have
nucleotide polymorphisms in the human 23 pairs of chromosomes.
genome and to develop methods for applying 13. insulin. Rationale: Recombinant DNA tech-
the technology of these projects to the diag- nology has also made it possible to produce
nosis and treatment of disease. Four bases— proteins that have therapeutic properties.

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360 ANSWERS

One of the first products to be produced was Activity B Labeling

human insulin.
14. a, b, c. Rationale: A karyotype is a photo- 1.
graph of a person’s chromosomes. It is pre-
pared by special laboratory techniques in
which body cells are cultured, fixed, and then
stained to display identifiable banding pat- A Deletion
terns. A centromere is the constricted region
of a chromosome that joins the two chro- Lost
matids to each other and attaches to spindle
fibers in mitosis and meiosis. Human chro-
mosomes are classified as one of three types,
depending on the position of their cen- Balanced
B translocation
tromere. Two types of genes, complementary
genes, in which each gene is mutually depen-
dent on the other; and collaborative genes, in
which two different genes influencing the
same trait interact, play a part in multifactor-
ial inheritance. Inversion
C
15. 1-c, 2-a, 3-b, 4-e, 5-d. Rationale: The genotype
of a person is the genetic information stored
in the base sequence triplet code. The pheno- Pericentric Paracentric
type refers to the recognizable traits, physical
or biochemical, associated with a specific
genotype. Pharmacogenetics is the variability Robertsonian
D Lost translocation
of drug response due to inherited characteris-
tics in individuals. Somatic cell hybridization
involves the fusion of human somatic cells
with those of a different species (typically,
the mouse) to yield a cell containing the
chromosomes of both species. Penetrance Isochromosomal
E translocation
represents the ability of a gene to express its
function. Seventy-five percent penetrance
means 75% of persons of a particular geno-
type present with a recognizable phenotype.

CHAPTER 7 GENETIC AND F Ring formation

CONGENITAL DISORDERS
Fragments
SECTION II: ASSESSING YOUR
UNDERSTANDING
Activity A 2. The figure represents a simple pedigree for in-
heritance of an autosomal dominant trait. The
1. Congenital
colored circle or square represents an affected
2. DNA, chromosomal
parent with a mutant gene. An affected parent
3. codominant
with an autosomal dominant trait has a 50%
4. mutation
chance of passing the mutant gene on to each
5. inherited, spontaneous
child regardless of sex.
6. carrier
7. Marfan
8. recessive
9. 60
10. structure, abnormal
11. Translocation

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ANSWERS 361

Activity C other agents harmful to the fetus, the harmful

effects of alcohol are not restricted to the sen-
1. h 2. c 3. e 4. a 5. g
sitive period of early gestation but extend
6. b 7. j 8. d 9. i 10. f
throughout pregnancy. Alcohol consumption
Activity D during pregnancy can cause fetal alcohol syn-
drome in the baby.
1. Conditions are inherited as dominant or reces-
2. Alcohol has widely variable effects on fetal de-
sive on one of the autosomal chromosomes or
velopment, ranging from minor abnormalities
one of the sex chromosomes. If the trait is
to fetal alcohol syndrome. There may be pre-
dominant, the patient will inherit the condi-
natal or postnatal growth retardation; central
tion. For a recessive trait to be expressed, both
nervous system involvement, including neuro-
parents must carry the mutation. If the muta-
logic abnormalities, developmental delays, be-
tion is on the Y chromosome, all male chil-
havioral dysfunction, intellectual impairment,
dren will be affected; if it is on the X
and skull and brain malformation; and a char-
chromosome, about half the offspring may po-
acteristic set of facial features that include
tentially be affected.
small eye openings, a thin upper lip, and an
2. Multifactorial congenital malformations in-
elongated, flattened midface and philtrum
volve a single organ or tissue derived from the
(i.e., the groove in the middle of the upper
same embryonic developmental field. Second,
lip). Each defect can vary in severity, probably
the risk of recurrence in future pregnancies is
reflecting the timing of alcohol consumption
increased for the same or a similar defect.
in terms of the period of fetal development,
Third, the risk increases with increasing inci-
amount of alcohol consumed, and hereditary
dence of the defect among relatives.
and environmental influences.
3. Structural changes in chromosomes usually re-
sult from breakage in one or more of the chro-
mosomes, followed by rearrangement or SECTION IV: PRACTICING FOR NCLEX
deletion of the chromosome parts. Among the Activity F
factors believed to cause chromosome break- 1. a. Rationale: If the members of a gene pair are
age are exposure to radiation sources, such as identical (i.e., code the exact same gene prod-
x-rays; influence of certain chemicals; extreme uct), then the person is homozygous, and if
changes in the cellular environment; and viral the two members are different, then the per-
infections. son is heterozygous. The phenotype is the ob-
4. Alterations in sex chromosomes are better tol- servable expression of a genotype in terms of
erated than alterations of autosomal chromo- morphologic, biochemical, or molecular
somes because of (a) the inactivation of all but traits. Although gene expression usually fol-
one X chromosome and (b) the modest lows a dominant or recessive pattern, it is
amount of genetic material that is carried on possible for both alleles (members) of a gene
the Y chromosome. pair to be fully expressed in the heterozygote,
5. Ova contain the majority of the mitochondria, a condition called codominance. A gene mu-
whereas spermatozoa have very few, if any, so tation is a biochemical event such as nu-
the embryo will inherit most, if not all, of the cleotide change, deletion, or insertion that
mitochondria from the mother. The neural produces a new allele. The terms phenotypic,
and muscular tissues are most affected by codominant, and mutant are not used to de-
mtDNA mutations due to their great depen- scribe a person when referring to the expres-
dence on oxidative phosphorylation. These sion of a gene pair.
tissues will have numerous mitochondria and 2. b. Rationale: In more than 90% of persons
suffer from their malfunction. with neurofibromatosis type 1, cutaneous
and subcutaneous neurofibromas develop in
SECTION III: APPLYING YOUR late childhood or adolescence. The cutaneous
KNOWLEDGE neurofibromas, which vary in number from a
Activity E few to many hundred, manifest as soft, pe-
dunculated lesions that project from the skin.
1. Alcohol passes freely across the placental bar-
Marfan syndrome affects several organ sys-
rier so concentrations of alcohol in the fetus
tems, including the ocular system (eyes),
are at least as high as in the mother. Unlike
the cardiovascular system (heart and blood

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362 ANSWERS

vessels), and the skeletal system (bones and which is often referred to as the period of
joints). Down syndrome is a congenital con- organogenesis, extends from day 15 to day 60
dition characterized by varying degrees of after conception. There are no periods of sus-
mental retardation and multiple defects. ceptibility, fetal anomalies, or hormonal im-
Klinefelter syndrome is a condition that oc- balance.
curs in men who have an extra X chromo- 7. c. Rationale: Teratogenic agents have been
some in most of their cells. The syndrome divided into three groups: radiation, drugs
can affect different stages of physical, lan- and chemical substances, and infectious
guage, and social development. The most agents. The period of organogenesis, the
common symptom is infertility. third trimester, and the second trimester are
3. c. Rationale: Cleft lip with or without cleft not teratogenic substances. They are time
palate is one of the most common birth de- periods during the pregnancy. Teratogenic
fects. This process is under the control of substances are not classified as outside, in-
many genes, and the disturbances in gene ex- side, or internal. Although drugs and chemi-
pression (hereditary or environmental) at this cal substances are a class of teratogenic
time may result in cleft lip with or without agents, smoking is included in that class as a
cleft palate. The defect may also be caused by teratogenic agent. It is not a class unto itself.
teratogens (e.g., rubella, anticonvulsant Bacteria and viruses are considered infec-
drugs) and is often encountered in children tious agents and are therefore teratogenic
with chromosomal abnormalities. agents.
4. d. Rationale: Occasionally, mitotic errors in 8. d. Rationale: The acronym TORCH stands for
early development give rise to two or more Toxoplasmosis, Other, Rubella (i.e., German
cell lines characterized by distinctive kary- measles), Cytomegalovirus, and Herpes,
otypes, a condition referred to as mosaicism. which are the agents most frequently impli-
A gene mutation is a biochemical event, such cated in fetal anomalies. Common clinical
as nucleotide change, deletion, or insertion, and pathological manifestations include
that produces a new allele. Referring to some- growth retardation and abnormalities of the
one as a “mutant” is a derogatory expression. brain (microcephaly, hydrocephalus), eye,
Monosomy refers to the presence of only one ear, liver, hematopoietic system (anemia,
member of a chromosome pair; it is not a thrombocytopenia), lungs (pneumonitis),
term used to denote a person. Having an ab- and heart (myocarditis, congenital heart dis-
normal number of chromosomes is referred orders).
to as aneuploidy; it is not a term used to de- 9. a. Rationale: The birth of a defective child is a
note a person. traumatic event in any parent’s life. Usually,
5. a. Rationale: The risk of having a child with two issues must be resolved. The first deals
Down syndrome increases with maternal age; with the immediate and future care of the af-
it is 1 in 1250 at 25 years of age, 1 in 400 at fected child, and the second with the possi-
35 years, and 1 in 100 at 45 years of age. The bility of future children in the family having
reason for the correlation between maternal a similar defect.
age and nondisjunction is unknown, but is 10. b. Rationale: The purpose of prenatal screen-
believed to reflect some aspect of aging of the ing and diagnosis is not just to detect fetal
oocyte. Although males continue to produce abnormalities. Rather, it is meant to provide
sperm throughout their reproductive life, fe- parents with information needed to make an
males are born with all the oocytes they ever informed choice about having a child with
will have. These oocytes may change as a re- an abnormality; to provide reassurance and
sult of the aging process. With increasing age, reduce anxiety among high-risk groups; and
there is a greater chance of a woman having to allow parents at risk for having a child
been exposed to damaging environmental with a specific defect, who might otherwise
agents such as drugs, chemicals, and radia- forgo having a child, to begin a pregnancy
tion. There is no correlation with maternal with the assurance that knowledge about
age and the other syndromes. the presence or absence of the disorder in
6. b. Rationale: The embryo’s development is the fetus can be confirmed by testing. It is
most easily disturbed during the period when not the object of genetic counseling and pre-
differentiation and development of the or- natal screening to provide information on
gans are taking place. This time interval, where to terminate a pregnancy if that is

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ANSWERS 363

what the parents choose to do. Prenatal 14. a, d. Rationale: The physiologic status of the
screening cannot be used to rule out all pos- mother—her hormone balance, her general
sible fetal abnormalities. It is limited to de- state of health, her nutritional status, and
termining whether the fetus has (or the drugs she takes—undoubtedly influ-
probably has) designated conditions indi- ences the development of the unborn child.
cated by late maternal age, family history, or Other agents, such as radiation, can cause
well-defined risk factors. chromosomal and genetic defects and pro-
11. 1-a, 2-b, 3-c, 4-d, 5-e. Rationale: A single mu- duce developmental disorders. Neither
tant gene may be expressed in many different weather nor air pollution has been linked
parts of the body. Marfan syndrome, for ex- with fetal abnormalities or developmental
ample, is a defect in connective tissue that disorders.
has widespread effects involving skeletal, eye, 15. a. Rationale: In 1983, the U.S. Food and Drug
and cardiovascular structures. In autosomal Administration established a system for clas-
dominant disorders, a single mutant allele sifying drugs according to probable risks to
from an affected parent is transmitted to an the fetus. According to this system, drugs are
offspring regardless of sex. In many condi- put into five categories: A, B, C, D, and X.
tions, the age of onset is delayed, and the Drugs in category A are the least dangerous,
signs and symptoms of the disorder do not and categories B, C, and D are increasingly
appear until later in life, as in Huntington’s more dangerous. Those in category X are con-
chorea. traindicated during pregnancy because of
Tay-Sachs is inherited as an autosomal re- proven teratogenicity.
cessive trait. Fragile X syndrome is a single-
gene disorder in which the mutation is
characterized by a long repeating sequence of
CHAPTER 8 NEOPLASIA
three nucleotides within the fragile X gene.
SECTION II: ASSESSING YOUR
12. a, b, c. Rationale: First, multifactorial con-
UNDERSTANDING
genital malformations tend to involve a
single organ or tissue derived from the Activity A
same embryonic developmental field. Sec- 1. differentiation, growth
ond, the risk of recurrence in future preg- 2. proliferation
nancies is for the same or a similar defect. 3. Differentiation
This means that parents of a child with a 4. cyclins
cleft palate defect have an increased risk of 5. phosphorylate
having another child with a cleft palate, 6. progenitor
but not with spina bifida. Third, the in- 7. Stem
creased risk (compared with the general 8. Embryonic
population) among first-degree relatives of 9. neoplasm
the affected person is 2% to 7%, and among 10. Benign
second-degree relatives, it is approximately 11. differentiated
one-half that amount. The risk increases 12. -oma
with increasing incidence of the defect 13. polyp
among relatives. Disorders of multifactorial 14. carcinoma
inheritance can be expressed during fetal 15. solid tumors, hematologic
life and be present at birth, or they may be 16. anaplasia
expressed later in life. 17. growth factors
13. Phenylketonuria. Rationale: Phenylke- 18. cadherin-catenin-actin
tonuria is a rare metabolic disorder that af- 19. protooncogenes, suppressor
fects approximately 1 in every 15,000 20. Human T-cell leukemia virus type 1
infants in the United States. The disorder, 21. 30
which is inherited as a recessive trait, is 22. anorexia-cachexia
caused by a deficiency of the liver enzyme 23. ulceration, necrosis
phenylalanine hydroxylase. As a result of 24. Anemia
this deficiency, toxic levels of the amino 25. biopsy
acid phenylalanine accumulate in the blood 26. Radiation
and other tissues. 27. Chemotherapy

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364 ANSWERS

Activity B 2. Both benign and malignant tumors have lost

the ability to suppress growth. As a result, the
tumor cells continue to proliferate. Benign
Carcinogenic Normal
tumors are composed of well-differentiated
agent cell cells and are confined to the area of tissue ori-
gin. In contrast, malignant tumors are com-
DNA repair posed of less differentiated cells that will
(DNA repair genes) reenter circulation and establish secondary
tumors in another region of the body.
DNA damage
3. The five factors used to describe benign and
malignant neoplasm are (a) cell characteris-
Failure of DNA
tics, (b) rate of growth, (c) manner of growth,
repair
(d) capacity to invade and metastasize to
• Activation of growth-promoting oncogenes other parts of the body, and (e) potential for
• Inactivation of tumor suppressor genes causing death.
• Alterations in genes that control apoptosis
4. Metastasis occurs via lymph channels and
blood vessels. When metastasis occurs by way
of the lymphatic channels, the tumor cells
lodge first in the initial lymph node that re-
Unregulated cell
differentiation and growth
ceives drainage from the tumor site. If they
survive, cancer cells may spread from more
distant lymph nodes to the thoracic duct,
and then gain access to the blood vascula-
Malignant
ture. With hematologic spread, the blood-
neoplasm borne cancer cells may enter the venous flow
that drains the site of the primary neoplasm.
Cancer cells may also enter tumor-associated
blood vessels that either infiltrate the tumor
or are found at the periphery of the tumor.
Activity C
5. Cancer cells express abnormal cell surface
1. proteins. Normally, the immune system rec-
1. b 2. a 3. e 4. j 5. f ognizes these abnormal proteins and destroys
6. c 7. d 8. h 9. g 10. i the cancerous cell. With a compromised im-
mune system, these abnormalities are missed
2. and allowed to persist in the body.
1. d 2. f 3. e 4. h 5. b 6. Chemicals will cause cellular transformation
6. a 7. i 8. j 9. c 10. g either directly (direct reacting agents) or indi-
rectly, only becoming activated via a meta-
Activity D bolic process (initiators).
1. 7. Hypermetabolism is the result of the rapidly
growing tumor and the increased expression of
uncoupling proteins. The first reason is that
B A D C
the tumor uses large quantities of glucose via
glycolysis, therefore producing high levels of
Activity E
lactic acid. The lactic acid undergoes the en-
1. In terms of cell proliferation, the cells may be ergy-requiring process of gluconeogenesis in
divided into three groups: (a) the well- order to convert it back to glucose. This process
differentiated neurons and cells of skeletal and uses large amounts of glucose and wastes large
cardiac muscle that rarely divide and repro- amounts of adenosine triphosphate (ATP). The
duce; (b) the progenitor or parent cell that con- second reason is the presence of uncoupling
tinues to divide and reproduce, such as blood proteins. The uncoupling proteins uncouple
cells, skin cells, and liver cells; and (c) the un- oxidative phosphorylation, thereby reducing
differentiated stem cells that can be triggered the amount of ATP produced.
to enter the cell cycle and produce large num- 8. Paraneoplastic syndromes are characterized
bers of progenitor cells when the need arises. by manifestations in sites that are not directly

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ANSWERS 365

affected by the disease. Most commonly, not understand the educational material he
manifestations are caused by the elaboration has been given. For unknown reasons, benign
of hormones by cancer cells and others from tumors have lost the ability to suppress the
the production of circulating factors that pro- genetic program for cell proliferation but
duce hematopoietic, neurologic, and derma- have retained the program for normal cell
tologic syndromes. differentiation. They do not have the capac-
9. Blood tests for tumor markers, cytologic stud- ity to infiltrate, invade, or metastasize to dis-
ies and tissue biopsy, endoscopic examina- tant sites.
tions, ultrasound, x-ray studies, magnetic 2. b. Rationale: Metastasis occurs by way of the
resonance imaging, computed tomography, lymph channels (i.e., lymphatic spread) and
and positron emission tomography. the blood vessels (i.e., hematogenic spread).
10. The clinical staging of cancer is intended to In many types of cancer, the first evidence of
group patients according to the extent of disseminated disease is the presence of tumor
their disease. Grading of tumors involves the cells in the lymph nodes that drain the
microscopic examination of cancer cells to tumor area. When metastasis occurs by way
determine their level of differentiation and of the lymphatic channels, the tumor cells
the number of mitoses. Cancers are classified lodge first in the initial lymph node that re-
as grades I, II, III, and IV, with increasing ceives drainage from the tumor site. Once in
anaplasia or lack of differentiation. The two this lymph node, the cells may die because of
basic methods for classifying cancers are grad- the lack of a proper environment, grow into a
ing according to the histologic or cellular discernible mass, or remain dormant for un-
characteristics of the tumor and staging ac- known reasons. If they survive and grow, the
cording to the clinical spread of the disease. cancer cells may spread from more distant
lymph nodes to the thoracic duct, and then
SECTION III: APPLYING YOUR gain access to the blood vasculature. Because
KNOWLEDGE cancer cells have the ability to shed them-
selves from the original tumor, they are often
Activity F
found floating in the body fluids around the
1. “To make it better for you, the doctor is going tumor. Cancer cells neither are moved from
to put a tube just under your skin that the one place to another by transporter cells, nor
nurses can put your medication in so they do they form a chain to grow to a new place
won’t have to stick you in the hands and arms in the body to form a new tumor.
so many times. You will still get stuck by a 3. c. Rationale: Cancer occurs because of interac-
needle but it will not be as painful as trying to tions among multiple risk factors or repeated
start IVs in your arms.” exposure to a single carcinogenic (cancer-pro-
2. Because Joe’s cancer is found in his blood and ducing) agent. Among the traditional risk fac-
bone marrow, surgery cannot be used to cure it. tors that have been linked to cancer are
Chemotherapy is the primary treatment for heredity, hormonal factors, immunologic
most hematologic and some solid tumors. mechanisms, and environmental agents,
Chemotherapy is a systemic treatment that en- such as chemicals, radiation, and cancer-
ables drugs to reach the site of the tumor as well causing viruses. More recently, there has been
as other distant sites. Cancer chemotherapeutic interest in obesity and type 2 diabetes melli-
drugs exert their effects through several mecha- tus as risk factors for a number of cancers.
nisms. At the cellular level, they exert their Body type, age, and color of skin have not
lethal action by targeting processes that prevent been identified as risk factors for cancer.
cell growth and replication. These mechanisms 4. d. Rationale: Familial adenomatous polyposis
include disrupting the production of essential of the colon also follows an autosomal domi-
enzymes; inhibiting DNA, RNA, and protein nant inheritance pattern. It is caused by mu-
synthesis; and preventing cell reproduction. tation of another tumor suppressor gene, the
APC gene. In people who inherit this gene,
SECTION IV: PRACTICING FOR NCLEX hundreds of adenomatous polyps may de-
Activity G velop, some of which inevitably become
malignant. Retinoblastoma is inheritable
1. a. Rationale: Asking whether his tumor will
through an autosomal dominant gene,
make him die shows that the patient does but only about 40% of retinoblastomas are

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366 ANSWERS

inherited. Osteosarcoma and acute lympho- and protein. It does not result from cancer
cytic leukemia are not inheritable through an therapy during childhood.
autosomal dominant process. Hyperinsulinemia is associated with syn-
5. a. Rationale: Most known dietary carcinogens drome X, which is a condition characterized
occur either naturally in plants (e.g., aflatox- by hypertension with obesity, type 2 diabetes
ins) or are produced during food preparation. mellitus, hypertriglyceridemia, increased pe-
Among the most potent of the procarcino- ripheral insulin resistance, hyperinsulinemia,
gens are the polycyclic aromatic hydrocar- and elevated catecholamine levels.
bons. These are of particular interest because 9. a. Rationale: Chemotherapy is more widely
they are produced from animal fat in the used in the treatment of children with cancer
process of charcoal-broiling meats and are than in adults because children tend to better
present in smoked meats and fish. Polycyclic tolerate the acute adverse effects, and in gen-
aromatic hydrocarbons are also produced in eral, pediatric tumors are more responsive to
the combustion of tobacco and are present in chemotherapy than adult cancers. Children
cigarette smoke. Initiators is another term for are very adaptable and tolerate more forms of
procarcinogens. Diethylstilbestrol was a drug cancer treatment than do adults. Children do
that was widely used in the United States complain about the nausea and vomiting
from the mid-1940s to 1970 to prevent mis- chemotherapy can cause, just like adults. And
carriages. they do not like losing their hair, just like
6. b. Rationale: Lung cancers, breast cancers, and adults.
lymphomas account for about 75% of malig- 10. b. Rationale: The combination of select cyto-
nant pleural effusions. Complaints of abdom- toxic drugs with radiation has demonstrated
inal discomfort, swelling and a feeling of a radiosensitizing effect on tumor cells by al-
heaviness, and an increase in abdominal tering the cell cycle distribution, increasing
girth, which reflect the presence of peritoneal DNA damage, and decreasing DNA repair.
effusions or ascites, are the most common Some radiosensitizers are 5-fluorouracil,
presenting symptoms in ovarian cancer, oc- capecitabine, paclitaxel, gemcitabine, and cis-
curring in up to 65% of women with the dis- platin. Doxorubicin is an antitumor antibi-
ease. otic, vincristine is a vinca alkaloid, and
7. c. Rationale: Tumor markers are antigens ex- docetaxel is a taxane.
pressed on the surface of tumor cells or sub- 11. neoplasm. Rationale: An abnormal mass of
stances released from normal cells in tissue in which the growth exceeds and is un-
response to the presence of tumor. The serum coordinated with that of the normal tissues is
markers that have proven most useful in clin- called a neoplasm. Unlike normal cellular
ical practice are the human chorionic go- adaptive processes such as hypertrophy and
nadotropin, CA 125, prostate-specific hyperplasia, neoplasms do not obey the laws
antigen, alpha-fetoprotein, carcinoembryonic of normal cell growth. They serve no useful
antigen, and CD blood cell antigens. Deoxyri- purpose, do not occur in response to an ap-
bonucleic acid is DNA, which is not a serum propriate stimulus, and continue to grow at
tumor marker. Cyclin-dependent kinases the expense of the host.
(CDKs) come from a family of proteins called 12. a, c, e. Rationale: Malignant neoplasms are
cyclins, which control entry and progression less well differentiated and have the ability to
of cells through the cell cycle. Cyclins act by break loose, enter the circulatory or lym-
complexing with (and thereby activating) phatic systems, and form secondary malig-
proteins called CDKs. They are not serum nant tumors at other sites. They frequently
tumor markers. cause suffering and death if untreated or un-
8. d. Rationale: Growth hormone deficiency in controlled. Malignant neoplasms form sec-
adults is associated with increased prevalence ondary tumors at sites other than the original
of dyslipidemia, insulin resistance, and car- tumor site. They are not passed out of the
diovascular mortality. Hypocalcemia is a defi- body as waste through the alimentary canal.
ciency of calcium in the serum that may be 13. b, c, e. Rationale: Cancer cells differ from nor-
caused by hypoparathyroidism, vitamin D mal cells by being immortal with an unlim-
deficiency, kidney failure, acute pancreatitis, ited life span. Cancer cells often lose cell
or inadequate amounts of plasma magnesium density–dependent inhibition, which is the

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ANSWERS 367

cessation of growth after cells reach a particu- Activity B

lar density. This is sometimes referred to as
contact inhibition because cells often stop
growing when they come into contact with
each other. Another characteristic of cancer
cells is the ability to proliferate even in the
Immune system
absence of growth factors. Most cancer cells (cytokines)
exhibit a characteristic called genetic instabil- Hypothalamus
CRF
ity, which is often considered to be a hall-
mark of cancer.
14. 1-b, 2-d, 3-c, 4-a. Rationale: Cancers for which Brain stem
Adrenal
current screening or early detection has led to gland Locus
Ceruleus
improvement in outcomes include those of Cortisol Pituitary
ACTH
the breast (breast self-examination, mam-
Autonomic
mography), cervix (Pap smear), colon and nervous system
rectum (rectal exam, fecal occult blood test, manifestations

flexible sigmoidoscopy, colonoscopy),

prostate (prostate-specific antigen testing,
transrectal ultrasonography), and malignant
melanoma (self-examination). Activity C
15. a, b, d. Rationale: With improvement in treat- 1. d 2. j 3. g 4. c 5. f
ment methods, the number of children who 6. e 7. a 8. h 9. i 10. b
survive childhood cancer is continuing to in-
Activity D
crease. As these children approach adult-
hood, there is continued concern that the 1. Negative feedback mechanisms are the pri-
lifesaving therapy they received during child- mary mechanisms used to maintain home-
hood may produce late effects, such as im- ostasis. The negative feedback mechanism
paired growth, cognitive dysfunction, controls blood glucose levels—an increase in
hormonal dysfunction, cardiomyopathy, pul- blood glucose stimulates an increase in in-
monary fibrosis, and risk for second malig- sulin—which enhances the removal of glu-
nancies. Liver failure is not viewed as a late cose from the blood. When glucose has been
effect of childhood cancer therapy. taken up by cells and blood glucose levels
fall, insulin secretion is inhibited, and
glucagon and other counter-regulatory mech-
CHAPTER 9 STRESS AND anisms stimulate the release of glucose from
ADAPTATION the liver, which causes the blood glucose to
return to normal.
SECTION II: ASSESSING YOUR 2. The stages of general adaptation syndrome
UNDERSTANDING are the alarm stage, the resistance stage, and
Activity A the exhaustion stage. The alarm stage is char-
acterized by a generalized stimulation of the
1. homeostasis, physiologic sympathetic nervous system and the hypo-
2. Homeostasis thalamic-pituitary-adrenocortical axis, result-
3. negative ing in the release of catecholamines and
4. stress cortisol. During the resistance stage, the body
5. disease selects the most effective and economic
6. hypothalamic-pituitary-adrenocortical, channels of defense. During this stage, the in-
adrenomedullary, sympathetic creased cortisol levels present during the first
7. adapting stage drop because they are no longer
8. coping strategy needed. If the stressor is prolonged or over-
9. Sleep whelms the ability of the body to defend it-
10. Alcohol self, the exhaustion stage ensues, during
which resources are depleted and signs of
“wear and tear” or systemic damage appear.

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368 ANSWERS

3. The results of the coordinated release of these History of life-threatening event

neurohormones include the mobilization of Client’s coping strategies
energy, a sharpened focus and awareness, in- 2. Nursing interventions include the following:
creased cerebral blood flow and glucose uti- Teaching the family about PTSD
lization, enhanced cardiovascular and Using a family-centered approach to care
respiratory functioning, redistribution of Assuring the client of confidentiality
blood flow to the brain and muscles, modula- Validating client’s feelings about the trauma
tion of the immune response, inhibition of Allowing the client to tell the story of the
reproductive function, and decrease in ap- trauma
petite. Assessing the client’s ability to meet primary
4. Many organs are functioning at much less needs
than maximum capacity, giving the organ a Identifying other stressors that might affect
safety margin. The safety margin for adapta- the client’s ability to cope
tion of most body systems is considerably
greater than that needed for normal activi- SECTION IV: PRACTICING FOR NCLEX
ties. The red blood cells carry more oxygen
Activity F
than the tissues can use, the liver and fat cells
store excess nutrients, and bone tissue stores 1. a. Rationale: The body’s control systems regu-
calcium in excess of that needed for normal late cellular function, control life processes,
neuromuscular function. Many of the body and integrate functions of the different organ
organs, such as the lungs, kidneys, and systems. Homeostatic control systems do not
adrenals, are paired to provide anatomical re- feed cells when they are under stress, do not
serve as well. Both organs are not needed to act on invading organisms, and do not shut
ensure the continued existence and mainte- down the body at death.
nance of the internal environment. As the 2. b. Rationale: A homeostatic control system
body expends greater amounts of energy, consists of a collection of interconnected
athletes are able to tap into these reserves. components that function to keep a physical
5. Physiological symptoms arise from exagger- or chemical parameter of the body relatively
ated sympathetic nervous system activation constant. An organ system is a group of or-
in response to the traumatic event. Persons gans that function together to accomplish
with chronic post-traumatic stress disorder necessary functions in the body; for example,
(PTSD) have been shown to have increased the cardiovascular system provides blood to
levels of norepinephrine and increased activ- all the body’s components. Biochemical mes-
ity of (2-adrenergic receptors. The increases sengers are in the brain; they are not control
in catecholamines, in tandem with increased systems. Neuroendocrine systems are control
thyroid levels in persons with PTSD, are be- systems that help regulate the body’s re-
lieved to explain some of the intrusive and sponse to stress. Neurovascular systems do
somatic symptoms of the disorder. In the not aid in the control of homeostasis in the
central nervous system, reactivity of the body.
amygdala and hippocampus and decreased 3. c. Rationale: Selye contended that many ail-
reactivity of the anterior cingulate and or- ments, such as various emotional distur-
bitofrontal areas are believed to also con- bances, mildly annoying headaches,
tribute to PTSD. insomnia, upset stomach, gastric and duode-
nal ulcers, certain types of rheumatic disor-
ders, and cardiovascular and kidney diseases,
SECTION III: APPLYING YOUR
appear to be initiated or encouraged by the
KNOWLEDGE
“body itself because of its faulty adaptive re-
Activity E actions to potentially injurious agents.” Psy-
1. When eliciting the history of the present ill- chotic disorders are not caused by stress.
ness, the nurse should inquire about the fol- Osteogenesis refers to the origin of bone tis-
lowing: sue; this is not due to stress. Sarcomas are a
Primary health problems type of cancer. There is no such thing as os-
History of substance abuse teogenesis sarcomas. Infections in the head
Sleep patterns and neck are caused by bacterial or viral in-
Onset of symptoms vaders of the body; they are not due to stress.

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ANSWERS 369

4. d. Rationale: The results of the coordinated re- 9. d. Rationale: In persons with limited coping
lease of these neurohormones include the abilities, either because of physical or mental
mobilization of energy, sharpened focus and health, the acute stress response may be
awareness, increased cerebral blood flow and detrimental. This is true of persons with pre-
glucose utilization, enhanced cardiovascular existing heart disease in whom the over-
and respiratory functioning, redistribution of whelming sympathetic behaviors associated
blood flow to the brain and muscles, modula- with the stress response can lead to arrhyth-
tion of the immune response, inhibition of mias. The acute stress response is not neces-
reproductive function, and decrease in ap- sarily going to be detrimental to the client
petite. who has undergone the resection of a brain
5. a. Rationale: Diseases of the cardiovascular, tumor, the client who is schizophrenic and
gastrointestinal, immune, and neurologic sys- off medication, or the client who has a bro-
tems, as well as depression, chronic alco- ken femur.
holism and drug abuse, eating disorders, 10. a. Rationale: PTSD is an example of chronic
accidents, and suicide, have all been linked to activation of the stress response as the result
the chronic and excessive activation of the of experiencing a severe trauma. In this disor-
stress response. der, memory of the traumatic event seems to
6. b. Rationale: The response to physiologic dis- be enhanced. Flashbacks of the event are ac-
turbances that threaten the integrity of the companied by intense activation of the neu-
internal environment is specific to the threat; roendocrine system. Chronic renal
the body usually does not raise the body tem- insufficiency, schizophrenia, and post deliv-
perature when an increase in heart rate is ery depression in a new mother are not the
needed. In contrast, the response to psycho- result of chronic activation of the stress re-
logical disturbances is not regulated with the sponse following a severe trauma.
same degree of specificity and feedback con- 11. multicellular. Rationale: A multicellular or-
trol; instead, the effect may be inappropriate ganism is able to survive only as long as the
and sustained. No systems in the body are composition of the internal environment is
regulated by a positive feedback system. In compatible with the survival needs of the in-
cardiovascular physiology, the baroreflex or dividual cells.
baroreceptor reflex is one of the body’s 12. eustress. Rationale: Selye suggested that mild,
homeostatic mechanisms for maintaining brief, and controllable periods of stress could
blood pressure. It has nothing to do with the be perceived as positive stimuli to emotional
body’s response to a psychological threat. and intellectual growth and development.
7. c. Rationale: The ability of body systems to These periods of stress are called eustress.
increase their function given the need to 13. b, d. Rationale: The treatment of stress should
adapt is known as the physiologic reserve. be directed toward helping people avoid cop-
Many of the body organs, such as the lungs, ing behaviors that impose a risk to their
kidneys, and adrenals, are paired to provide health and providing them with alternative
anatomic reserve as well. Both organs are not stress-reducing strategies. Nonpharmacologic
needed to ensure the continued existence methods used for stress reduction are relax-
and maintenance of the internal environ- ation techniques, guided imagery, music
ment. Genetic endowment, physiologic re- therapy, massage, and biofeedback.
serve, and health status are all coping 14. 1-b. Rationale: Corticotropin-releasing factor
mechanisms, but they do not affect the is a small peptide hormone found in both the
body’s need to survive when one organ out of hypothalamus and extrahypothalamic struc-
a pair is missing. tures, such as the limbic system and the brain
8. c. Rationale: The configuration of significant stem. It is both an important endocrine regula-
others that constitutes the social network tor of pituitary and adrenal activity and a neu-
functions to mobilize the resources of the rotransmitter involved in autonomic nervous
person; these friends, colleagues, and family system activity, metabolism, and behavior.
members share the person’s tasks and provide 2-d. Rationale: The sympathetic nervous
monetary support, materials and tools, and system manifestation of the stress reaction has
guidance in improving problem-solving capa- been called the fight-or-flight response. This is
bilities. Social networks cannot protect the the most rapid of the stress responses and rep-
person from other internal stressors. resents the basic survival response of our

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370 ANSWERS

primitive ancestors when confronted with the 10. 15

perils of the wilderness and its inhabitants. 11. PFAPA
3-c. Rationale: The term allostasis has 12. Aspirin and NSAIDs, prostaglandin E2
been used by some investigators to describe 13. elderly
the physiological changes in the neuroen- 14. Hyperthermia
docrine, autonomic, and immune systems 15. heat index
that occur in response to either real or per- 16. salt, water
ceived challenges to homeostasis. The persis- 17. hypothermia
tence and/or accumulation of these allostatic 18. anesthetic, hypothermia
changes (e.g., immunosuppression, activa- 19. heart rate, cardiac output
tion of the sympathetic nervous and renin- Activity B
angiotensin-aldosterone systems) has been
called an “allostatic load,” and this concept ˚F ˚C
has been used to measure the cumulative ef- 114 Upper limits
fects of stress on humans. of survival?
44 Temperature
4-a. Rationale: The hallmark of the stress 110 Heatstroke regulation
response, as first described by Selye, is the en- 42 Brain lesions seriously
impaired
docrine–immune interactions (i.e., increased 106
corticosteroid production and atrophy of the 40 Febrile disease Temperature
thymus) that are known to suppress the im- 102 and regulation
38 hard exercise efficient in
mune response. In concert, these two compo- Usual range
98 febrile disease,
nents of the stress system, through endocrine of normal health, and work
36
and neurotransmitter pathways, produce the
physical and behavioral changes designed to 94
34
adapt to acute stress.
15. a, b, c. Rationale: The most significant argu- 90 32 Temperature
regulation
ments for interaction between the neuroen-
impaired
docrine and immune systems derive from 86 30
evidence that the immune and neuroen-
docrine systems share common signal path- 82 28
ways (i.e., messenger molecules and Temperature
26 regulation
receptors), that hormones and neuropeptides 78
lost
can alter the function of immune cells, and 24
that the immune system and its mediators 74
can modulate neuroendocrine function.
These systems do not need each other to
function. Activity C
1. g 2. e 3. f 4. d 5. a
CHAPTER 10 ALTERATIONS IN 6. b 7. i 8. c 9. j 10. h
TEMPERATURE REGULATION Activity D

SECTION II: ASSESSING YOUR B D C A

UNDERSTANDING
Activity A Activity E
1. 36.0–37.5 1. Most of the body’s heat is produced by the
2. hypothalamus deeper core tissues (i.e., muscles and vis-
3. Metabolism cera), which are insulated from the envi-
4. pilomotor ronment and protected against heat loss by
5. fever an outer shell of subcutaneous tissues and
6. cyclic adenosine monophosphate skin
7. Kupffer 2. During the first or prodromal period, there
8. neurogenic fever are nonspecific complaints such as mild
9. intermittent fever headache and fatigue, general malaise, and

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ANSWERS 371

aches and pains. During the chill, there is the allowing rewarming to occur at the person’s
uncomfortable sensation of being chilled and own pace. Active external rewarming involves
the onset of generalized shaking. Vasoconstric- immersing the person in warm water, using
tion and piloerection usually precede the forced air warming systems, or placing heating
onset of shivering. At this point, the skin is pads or hot water bottles on the surface of the
pale and covered with goose flesh. There is a body, including the extremities. Active core re-
feeling of being cold and an urge to put on warming can be done by instilling warmed flu-
more clothing or covering and to curl up in a ids into the gastrointestinal tract; peritoneal
position that conserves body heat. When the dialysis; extracorporeal blood warming, in
shivering has caused the body temperature to which blood is removed from the body and
reach the new set-point of the temperature passed through a heat exchanger and then re-
control center, the shivering ceases, and a sen- turned to the body; or inhalation of an oxygen
sation of warmth develops. At this point, the mixture warmed to 42ºC to 46ºC.
third stage or flush begins, during which cuta-
neous vasodilation occurs and the skin be- SECTION III: APPLYING YOUR
comes warm and flushed. The fourth, or KNOWLEDGE
defervescence, stage of the febrile response is
Activity F
marked by the initiation of sweating.
3. Infants and young children have decreased 1. Rationale: When obtaining the history of the
immunologic function and are more com- present illness, the nurse should inquire about
monly infected with virulent organisms. In ad- the following:
dition, the mechanisms for controlling • Onset of illness
temperature are not as well developed in in- • Any known exposure to infectious or com-
fants as they are in older children and adults. municable disease
4. Muscle exertion continued for long periods in • Immunization history for pneumonia and flu
warm weather can result in excessive heat • History of having pneumonia or flu
loads. Elderly persons and those with cardio- • Fever
vascular disease are at increased risk for hyper- • Sore throat
thermia due to inactive cooling responses. • Lethargy
Drugs that increase muscle tone and metabo- • Malaise
lism or reduce heat loss will impair thermoreg- • Poor appetite
ulation. Infants and small children who are • Vomiting
left in a closed car for even short periods in • Diarrhea
hot weather are potential victims of hyper- • Cough
thermia. • Shortness of breath
5. Drugs can interfere with heat dissipation; they • Chest pain or joint pain
can alter temperature regulation by the hypo- • Smoking
thalamic centers, act as direct pyrogens, injure 2. Rationale: The nurse should perform the fol-
tissues directly, or induce an immune re- lowing physical examinations:
sponse. • Measure temperature, respiratory rate, pulse,
6. Malnutrition decreases the fuel available for and blood pressure
heat generation, and loss of body fat decreases • Assess the mouth and throat for erythema
tissue insulation. Alcohol and sedative drugs or lesions
dull mental awareness to cold and impair • Auscultate the lungs and heart for any ad-
judgment to seek shelter or put on additional ventitious sounds
clothing. Alcohol also inhibits shivering. Per- • Percuss the lung fields to assess for tenderness
sons with cardiovascular disease, cerebrovascu- • Observe the patient’s affect and energy level
lar disease, spinal cord injury, and • Observe whether there is any discharge from
hypothyroidism are also predisposed to hy- the nose, or a cough or respiratory difficulty
pothermia. Elderly and inactive persons living • Assess O2 saturation and capillary refill
in inadequately heated quarters are particu- • Assess hydration status by inspecting oral
larly vulnerable to hypothermia. mucosa and eyes
7. Passive external rewarming is done by removing • Palpate the skin to assess temperature, mois-
the person from the cold environment, cover- ture, texture, and turgor
ing with a blanket, supplying warm fluids, and

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372 ANSWERS

• Palpate the lymph nodes and note any that and usually a brief cry. The Bainbridge reflex
are swollen and tender is a cardiac reflex in which stimulation of
• Observe the teeth stretch receptors in the wall of the left
atrium causes an increased pulse rate. The
SECTION IV: PRACTICING FOR NCLEX oculocephalic reflex is a test of the integrity
of brain stem function that involves moving
Activity G
the patient’s head quickly and noting
1. a. Rationale: Temperature-sensitive ion chan- whether the eyes lag behind the head move-
nels, identified as a subset of the transient re- ment and then slowly assume the midline
ceptor potential family (thermoTRPs) present position.
in peripheral and central sensory neurons, 6. b. Rationale: FUO is defined as a temperature
are activated by innocuous (warm and cool) elevation of 38.3ºC (101ºF) or higher that is
and noxious (hot and cold) stimuli. Strong present for 3 weeks or longer. Among the
and weak and unpleasant and pleasant are causes of FUO are malignancies (i.e., lym-
not types of stimuli that influence the regula- phomas, metastases to the liver and central
tion of body temperature. Hot and cold are nervous system); infections such as HIV or tu-
considered noxious stimuli. berculosis, or abscessed infections; and drug
2. b. Rationale: Hyperthermia occurs when the fever. Disseminated intravascular coagulation
set-point of the body is unchanged, but the and pulmonary and femoral artery emboli do
mechanisms that control body temperature not cause FUO.
are ineffective in maintaining body tempera- 7. c. Rationale: Familial Mediterranean fever, an
ture within a normal range during situations autosomal recessive disease, is characterized
when heat production outpaces the ability of by an early age of onset (20 years) of acute
the body to dissipate that heat. A body tem- episodic bouts of peritonitis and high fever
perature of either 37.6°C or 39.5°C is consid- with an average duration of less than 2 days.
ered a fever, the same as when the set-point In some cases, pleuritis, pericarditis, and
of the body is raised. arthritis are present.
3. c. Rationale: Exogenous pyrogens, such as 8. d. Rationale: Aspirin can cause Reye syn-
bacterial products, bacterial toxins, or whole drome in children; therefore, the Centers
microorganisms, induce host cells to produce for Disease Control and Prevention, U.S.
fever-producing mediators called endogenous Food and Drug Administration, and Ameri-
pyrogens. “Outer” and “set-point” pyrogens can Academy of Pediatrics Committee on
do not exist. Infectious Diseases advise against the use of
4. d. Rationale: A fever that has its origin in the aspirin and other salicylates in children
central nervous system is sometimes referred with influenza or chickenpox. Münch-
to as a neurogenic fever. Neurogenic fevers hausen syndrome is an unusual psychiatric
are characterized by a high temperature that condition characterized by habitual pleas
is resistant to antipyretic therapy and is not for treatment and hospitalization for a
associated with sweating. symptomatic but imaginary acute illness.
Temperatures that go up and down for no ap- Guillain-Barré syndrome is an idiopathic,
parent reason and variable temperatures are peripheral polyneuritis that occurs 1 to 3
not neurogenic fevers. weeks after a mild episode of fever associ-
5. a. Rationale: The diving reflex triggers apnea ated with a viral infection or with immu-
and circulatory shunting to establish a heart- nization. Angelman syndrome is an
brain circulation. In children, the diving re- autosomal recessive syndrome characterized
flex along with the rapid cooling process by jerky puppetlike movements, frequent
may account for the surprisingly high sur- laughter, mental and motor retardation, a
vival rate after submersion. The diving reflex peculiar open-mouthed facial expression,
is greatly diminished in adults. The Moro re- and seizures.
flex is a normal mass reflex in a young infant 9. a. Rationale: Infants with fever may not nec-
(up to 3 to 4 months of age) elicited by a essarily appear ill. In infants younger than 3
sudden loud noise, consisting of flexion of months, a mild elevation in temperature (i.e.,
the legs, an embracing posture of the arms, rectal temperature of 38ºC [100.4F]) can

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ANSWERS 373

indicate serious infection that requires imme- CHAPTER 11 ACTIVITY TOLERANCE

diate medical attention. Signs of toxicity in-
clude lethargy, poor feeding, hypoventilation, AND FATIGUE
poor tissue oxygenation, and cyanosis.
10. b. Rationale: Heat stroke is a severe, life- SECTION II: ASSESSING YOUR
threatening failure of thermoregulatory UNDERSTANDING
mechanisms resulting in an excessive rise in Activity A
body temperature—a core temperature
1. Physical activity
greater than 40ºC (104ºF). The resulting local
2. Aerobic
and systemic inflammatory responses may re-
3. resistance
.
sult in acute respiratory distress syndrome,
4. VO2max
acute renal failure, disseminated intravascular
5. cardiac output
clotting, multiorgan dysfunction, and rhab-
6. Frank-Starling
domyolysis. Hyperthermia is also known to
7. Muscle strength
cause edema and microhemorrhages in the
8. Fast-twitch
brain. Rhabdomyoma is a tumor of striated
9. atrophy
muscle.
10. creatine kinase
11. b, c, d. Rationale: Drugs can interfere with
11. gastrointestinal tract
(not cause) heat dissipation; they can alter
12. glutamine
temperature regulation by the hypothalamic
13. stress-related
centers, act as direct pyrogens, injure tissues
14. decline
directly, or induce an immune response.
15. intolerance
12. pilomotor. Rationale: Contraction of the pilo-
16. fatigue
motor muscles of the skin aids in heat conser-
17. Acute
vation by reducing the surface area available
18. bed rest
for heat loss.
19. deep vein thrombosis
13. d. Rationale: The physiologic behaviors that
20. cardiac output, pneumonia, kidney stones
occur during the development of fever can be
divided into four successive stages: a pro- Activity B
drome; a chill, during which the temperature 1. j 2. g 3. e 4. b 5. c
rises; a flush; and defervescence. 6. a 7. f 8. d 9. i 10. h
14. a, b, c. Rationale: The methods of fever treat- Activity C
ment focus on modifications of the external
environment intended to increase heat trans- 1. The physiologic and psychological benefits of
fer from the internal to the external environ- exercise are cardiopulmonary fitness; increased
ment, support of the hypermetabolic state muscle strength, flexibility, and endurance;
that accompanies fever, protection of vulner- availability of energy substrates to meet the in-
able body organs and systems, and treatment creased energy demands imposed by increased
of the infection or condition causing the physical activity; and motivation and mental
fever. endurance.
15. a, b, c, d. Rationale: Malignant hyperthermia 2. Increases in blood flow increase shear stress
is an autosomal dominant metabolic disorder and result in several beneficial functions, such
in which heat generated by uncontrolled as the production of vasodilators, antioxidants,
skeletal muscle contraction can produce se- and anticoagulants. This contributes to im-
vere and potentially fatal hyperthermia. The proved endothelial cell function, which results
syndrome is most frequently associated with in vasodilation, inhibition of platelet activa-
the halogenated anesthetic agents and the tion, and increased fibrinolysis, thus leading to
depolarizing muscle relaxant succinylcholine. improved patency of the vasculature and
There are also various nonoperative precipi- maintenance of blood flow and vessel patency.
tating factors, including trauma, exercise, en- Adaptation to exercise also induces angiogene-
vironmental heat stress, and infection. The sis, with an increased growth of vessels to sup-
condition is particularly dangerous in a port blood flow to the exercising muscle.
young person who has a large muscle mass to 3. In terms of skeletal muscle function, there is
generate heat. a decrease in muscle mass and strength, flexi-
bility and range of joint movement, and

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374 ANSWERS

muscle endurance. There is a decrease in size address the person’s physical and psychosocial
of the individual muscles that occurs with needs. The goals of care for the immobilized
aging, particularly beyond 60 years of age. person include structuring a safe environment
Muscle strength and mass reportedly decline in which the person is not at risk for complica-
30% to 50% between ages 30 and 80 years, tions; providing diversional activities to offset
with loss of muscle mass accounting for most problems with sensory deprivation; and pre-
of the decrease observed in muscle strength. venting complications of bed rest by imple-
Muscle mass loss is subordinate to an age-re- menting an interdisciplinary plan of care that
lated denervation of type II fibers, which re- includes repositioning schedules, prophylactic
moves the trophic effect on the fibers, interventions to prevent deep vein thrombo-
leading to atrophy. Type I fiber collaterals ex- sis, and consultation with various disciplines
pand to some of the denervated type II fiber to provide a comprehensive approach to care
areas in an attempt to lessen muscle fiber and treatment.
loss. This leads to an increase in type I motor 2. The concerns of his caregiver are as follows:
neuron units at the expense of type II fibers, • Cardiovascular changes, including venous
resulting in a reduction in muscle mass and stasis, a redistribution of blood volume, and
muscle strength. deep vein thrombosis
4. Acute fatigue and chronic fatigue are the result • Water and sodium diuresis; the loss of water
of a decrease in the ability to generate muscle and sodium results in an increase in hemat-
contractions. Acute fatigue is rapid in onset ocrit, hemoglobin, and red cell mass owing
and resolves with rest. In contrast to acute fa- to the loss of plasma volume
tigue, chronic fatigue has an insidious onset, is • Postural intolerance
typically perceived as being unusually intense • Changes in lung volumes and the mechan-
relative to the amount of activity performed, ics of breathing that can contribute to respi-
lasts longer than 1 month, has a cumulative ratory complications, such as atelectasis,
effect, and is not relieved by cessation of activ- accumulation of secretions, hypoxemia, and
ity. pneumonia
5. The pathogenesis of CFS include infections, • Prolonged bed rest affects the renal system
psychological disorders, a dysfunction in the by altering the composition of body fluids
hypothalamic-pituitary-adrenal axis, or an al- and predisposing to the development of
teration in the autonomic nervous system. kidney stones; bed rest may also predis-
Despite much research and the development pose to urinary tract infections and uri-
of several theories, the underlying patho- nary incontinence because of positional
physiology of CFS remains elusive. Many peo- changes and difficulty in emptying the
ple with CFS attribute the onset of their bladder
disease to an influenzalike infection. Symp- • Loss of strength; muscles atrophy, change
toms are changing and variable among pa- shape and appearance, and shorten when
tients. As a result, there are no biologic immobilized
markers for CFS. • Metabolic and endocrine changes
6. The mechanism of orthostatic intolerance fol- • Gastrointestinal responses, including loss of
lowing bed rest involves multiple factors, in- appetite, slowed rate of absorption, and dis-
cluding a decrease in vascular volume, a taste for food combine to contribute to nu-
decline in skeletal muscle pump function, re- tritional hypoproteinemia
duced sympathetic innervation of the resis- • Pressure sores
tance vessels, and resetting of the • Psychosocial changes, including depression
baroreceptors that control blood pressure. and social isolation

SECTION III: APPLYING YOUR

KNOWLEDGE SECTION IV: PRACTICING FOR NCLEX
Activity D Activity E
1. A holistic approach should be taken when car- 1. d. Rationale: Skeletal muscle consists of two
ing for persons who are immobile or require distinct types of muscle fibers based on differ-
prolonged periods of bed rest. Interventions ences in their size, speed, contractile proper-
and treatment should include actions that ties, endurance, and metabolic

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ANSWERS 375

characteristics: red (dark) slow-twitch (type I) decrease cardiac output. There is a natural de-
and white (light) fast-twitch (type II) muscle crease in muscle strength in the elderly, not a
fibers. Periods of sustained inactivity, such as decrease in the peripheral blood vessels. Even
prolonged immobility or bed rest, primarily with a decrease in peripheral blood vessels, it
affect slow-twitch fibers, which quickly de- would not cause a decreased cardiac output.
condition. 6. c. Rationale: This type of fatigue is common
2. c. Rationale: Persons with congestive heart among persons with forced immobility, mus-
failure (CHF) typically experience symptoms culoskeletal disorders such as arthritis, neuro-
of breathlessness, exertional fatigue, and ex- muscular disorders such as multiple sclerosis,
ercise intolerance, resulting in atrophy of and wasting syndromes such as HIV/AIDS.
skeletal muscles. When these individuals en- 7. d. Rationale: The deconditioning responses to
gage in exercise, there is a shift toward using the inactivity of immobility and bed rest af-
fast-twitch muscle fibers. This causes an early fect all body systems. One of the important
dependence on anaerobic metabolism and factors to keep in mind is the rapidity with
excessive intramuscular acidification that which the changes occur and the length of
leads to increased fatigability. The increased time required to overcome these effects.
reliance on anaerobic metabolism and subse- 8. a. Rationale: Muscle atrophy and disuse not
quent vasoconstrictor response can also lead only contribute to wasting and weakening of
to an increase in afterload work for an al- muscle tissue, but also play a role in the de-
ready compromised left ventricle. velopment of joint contractures. A contrac-
3. d. Rationale: Because of the effects of exercise ture is the abnormal shortening of muscle
training on vascular function and angiogene- tissue and connective tissue, rendering the
sis, it has been proposed as a mechanism for muscle highly resistant to stretch.
improving blood flow and decreasing exer- 9. b. Rationale: To be classified as CFS, the fa-
cise-related leg pain (claudication) in persons tigue must be clinically evaluated, cause se-
with peripheral vascular disease(PVD). The vere mental and physical exhaustion, and
vastus lateralis is the large muscle on the lat- result in a significant reduction in the indi-
eral thigh. Weight training will strengthen vidual’s premorbid activity level. In addition,
this muscle, but is not recommended for peo- there must be evidence of the concurrent oc-
ple with PVD. Isometric exercise does not in- currence of four of the following symptoms:
crease the endurance of the heart. Aerobic sore throat, tender cervical or axillary lymph
exercise does not decrease respiratory stress. nodes, muscle pain, multijoint pain without
4. a. Rationale: With sufficient training, the swelling or redness, headaches, unrefreshing
body adapts by increasing the rate of sweat sleep, and postexertional malaise lasting
production. As temperature regulation im- more than 24 hours. The fatigue and concur-
proves with training, the trained person be- rent symptoms must be of 6 months’ dura-
gins to sweat sooner, often within 1 to 2 tion or longer.
minutes of the start of exercise. Sweat pro- 10. c. Rationale: The immune system is also sub-
duction begins even before the core tempera- ject to physiologic changes associated with
ture rises, and a cooling effect is initiated bed rest or immobility. Research demon-
soon after the start of exercise; the sweat pro- strates that there is an increase in inter-
duced is more dilute than that produced by a leukin (IL)-1, IL-6, and tumor necrosis
nontrained person. Sweat normally contains factor-alpha production. An increase in
large amounts of sodium chloride; produc- these mediators has been associated with hy-
tion of a dilute sweat allows evaporative cool- perinflammatory reactions and tissue injury
ing to take place while sodium chloride is or wasting.
conserved. 11. resistance. Rationale: In isometric, or resis-
5. b. Rationale: Maximal heart rate decreases 6 to tance, exercise, sustained muscle contraction
10 beats/minute/decade, and it is this de- is generated against an immovable load with
crease in heart rate that is believed to con- no change in length of the involved muscle
tribute to a decreased cardiac output. group or joint movement.
Although there is a natural decrease in lung 12. c. Rationale: The role of the respiratory system
capacity as a person ages, it does not con- during exercise is to increase the rate of oxy-
tribute to decreased cardiac output. The resis- gen and carbon dioxide exchange. This takes
tance of major blood vessels does not place through a series of physiologic

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376 ANSWERS

responses. With exercise, the respiratory rate Activity B

increases four- to fivefold, tidal volume in-
creases five- to sevenfold, and minute ventila-
tion (respiratory rate  tidal volume)
increases up to 20 to 30 times its resting
value. With the increase in cardiac output, a
greater volume of blood under slightly in-
creased pressure is delivered to the pul-
monary vessels in the lungs. This results in Plasma
(55% of
the opening of more pulmonary capillary whole blood)
beds, producing better alveolar perfusion and
more efficient exchange of oxygen and car-
Buffy coat leukocytes
bon dioxide.
and platelets
13. ergometry. Rationale: Ergometry is a proce- (<1% of
dure for determining physical performance Formed
whole blood)
elements
capacity.
14. a, b, c, e. Rationale: After a period of bed rest Erythrocytes
and assumption of the supine position, the (45% of
whole blood)
cardiovascular system exhibits changes that
reflect the loss of gravitational and exercise
stimuli. These changes include (a) a redistrib-
ution and change in blood volume, (b) in-
creased cardiac workload, (c) orthostatic
hypotension, and (d) venous stasis with the Activity C
potential for development of deep venous 1. f 2. b 3. c 4. g 5. a
thrombosis. 6. h 7. d 8. e 9. i 10. j
15. Wolff’s. Rationale: According to Wolff’s law, Activity D
the density of bone is directly proportional to
the stress placed on it.
C D E B A

CHAPTER 12 BLOOD CELLS AND Activity E

THE HEMATOPOIETIC SYSTEM 1. The lifelong potential for proliferation and
self-renewal of stem cells makes them an indis-
SECTION II: ASSESSING YOUR
pensable and lifesaving source of reserve cells
UNDERSTANDING
for the entire hematopoietic system. Several
Activity A levels of differentiation lead to the develop-
1. hematocrit ment of committed unipotential cells, which
2. 90%, 6.5%, 2% are the progenitors for each blood cell type.
3. liver They serve as an unending reserve of cells.
4. Albumin 2. When a person trains at high elevations, the
5. cells partial pressure of O2 is low, resulting in sys-
6. hemoglobin temic hypoxia. The body responds by releas-
7. Carbonic anhydrase ing erythropoietin, which stimulates red blood
8. granulocytes cell production. After some time, the body will
9. Neutrophils return to normal oxygenation. When the per-
10. eosinophils son then returns to lower elevations to race or
11. immune train, the body has a greater oxygen-carrying
12. thymus capacity and can perform at a higher level.
13. monocytes, macrophages
14. megakaryocytes
15. constant

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ANSWERS 377

cancer cells, and they participate in the in-

SECTION III: APPLYING YOUR
flammatory response and wound healing.
KNOWLEDGE
3. c. Rationale: Pluripotent stem cells with their
Activity F lifelong potential for proliferation and self-re-
1. The nurse can tell Sally that growth factors newal are an indispensable and lifesaving
help make her new bone marrow grow faster. source of reserve cells for the entire
The rationale behind this answer is that hematopoietic system. Several levels of differ-
growth factors are used to increase peripheral entiation lead to the development of com-
stem cells for transplantation and to accelerate mitted unipotential cells, which are the
cell proliferation after bone marrow engraft- progenitors for each blood cell type. These
ment. cells are referred to as colony-forming units.
4. d. Rationale: Sources of the stem cells include
SECTION IV: PRACTICING FOR NCLEX bone marrow, peripheral blood, and umbili-
cal cord blood. All replenish the recipient
Activity G
with a normal population of pluripotent
1. a. Rationale: There are three types of globu- stem cells. Immature embryonic cells do not
lins: the alpha globulins that transport biliru- necessarily contain stem cells. Immature
bin and steroids, the beta globulins that neural cells are not stem cells. Yellow bone
transport iron and copper, and the gamma marrow does not make blood cells, so it
globulins that constitute the antibodies of would not contain stem cells.
the immune system. Alpha globulins trans- 5. a. Rationale: Cytokines, such as the inter-
port bilirubin and steroids. Beta globulins leukins, interferons, and tumor necrosis fac-
transport iron and copper. Autoantibodies tor, support the proliferation of stem cells
are immunoglobulins that recognize an anti- and the development of lymphocytes, and
gen on that person’s own tissue. act synergistically to aid the multiple func-
2. b. Rationale: The erythrocytes, or red blood tions of the colony-stimulating factors. B-cell
cells, are the most numerous of the formed growth factor, T-cell growth factor, colony-
elements. They are small, biconcave disks stimulating factors, and transforming growth
with a large surface area and can easily de- factor are all cytokines that stimulate the
form to move through the small capillaries growth and production of new blood cells.
of the circulatory system. They contain the 6. b. Rationale: The erythrocyte sedimentation
oxygen-carrying protein, hemoglobin, which rate is a screening test for monitoring the
functions in the transport of oxygen. The fluctuations in the clinical course of a disease.
neutrophils are primarily responsible for In anticoagulated blood, red blood cells ag-
maintaining normal host defenses against in- gregate and sediment to the bottom of a tube.
vading bacteria and fungi, cell debris, and a The rate of fall of the aggregates is accelerated
variety of foreign substances. Eosinophils in the presence of fibrinogen and other
constitute 1% to 3% of the total number of plasma proteins that are often increased in
white blood cells and increase in number inflammatory diseases.
during allergic reactions and parasitic infec- 7. c. Rationale: Usually, the posterior iliac crest is
tions. In allergic reactions, it is believed that used in all persons older than 12 to 18
they release enzymes or chemical mediators months of age. Other sites include the ante-
that detoxify the agents associated with aller- rior iliac crest, sternum, and spinous
gic reactions. In parasitic infections, the processes T10 through L4. The sternum is not
eosinophils use surface markers to attach commonly used in children because the cav-
themselves to the parasite and then release ity is too shallow, and there is danger of me-
hydrolytic enzymes that kill it. The leuko- diastinal and cardiac perforation.
cytes, or white blood cells, constitute only 8. d. Rationale: Under normal conditions, the
1% of the total blood volume. They originate numbers and total mass for each type of
in the bone marrow and circulate throughout circulating blood cell remain relatively con-
the lymphoid tissues of the body. Leukocytes stant. The blood cells are produced in differ-
are crucial to our defense against disease. ent numbers according to needs and
They are responsible for the immune re- regulatory factors. This regulation of blood
sponse that protects against disease-causing cells is believed to be at least partially con-
microorganisms; they identify and destroy trolled by hormonelike growth factors called

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378 ANSWERS

cytokines. The immune system does not reg- Rationale: Albumin is the most abundant and
ulate the number of each type of blood cell. comprises approximately 54% of the plasma
The hematopoietic system is the system in proteins. It does not pass through the pores
which the blood cells are made, but it does in the capillary wall to enter the interstitial
not regulate the number of each type of cell. fluid, and, therefore, contributes to the
Pluripotent stem cells are the precursors to plasma osmotic pressure and maintenance of
every type of cell. blood volume. Albumin also serves as a car-
9. a. Rationale: Peripheral blood stem cells are rier for certain substances and acts as a blood
harvested from the blood after the adminis- buffer. The globulins comprise approximately
tration of a cytokine growth factor that in- 38% of plasma proteins. There are three types
creases the quantity and migration of the of globulins: the alpha globulins that transport
cells from the bone marrow. HLA is the ab- bilirubin and steroids, the beta globulins that
breviation for human leukocyte antigen and transport iron and copper, and the gamma
is what is matched in umbilical cord blood. It globulins that constitute the antibodies of the
does not increase either the quantity or the immune system. Fibrinogen comprises ap-
migration of peripheral blood stem cells. proximately 7% of the plasma proteins and is
Platelets are a rich source of growth factors, a key factor in blood clotting. The remaining
but they do not, by themselves, increase ei- 1% of the circulating proteins is comprised
ther the quantity or the migration of periph- of hormones, enzymes, complement, and
eral blood stem cells. There is a human carriers for lipids.
growth hormone but not a human growth 13. Abbreviation Definition
factor.
10. b. Rationale: The genes for most hematopoi- Hgb Measurement of hemoglobin
etic growth factors have been cloned, and
Hct Measurement of hematocrit
their recombinant proteins have been gen-
erated for use in a wide range of clinical MCV Mean corpuscular volume
problems. They are used to treat bone mar-
MCHC Mean corpuscular hemoglobin
row failure caused by chemotherapy or concentration
aplastic anemia, the anemia of kidney fail-
ure and cancer, hematopoietic neoplasms, MCH Mean cell hemoglobin
infectious diseases such as AIDS, and con-
genital and myeloproliferative disorders. Rationale: Measurement of hemoglobin,
Autoimmune disorders, Parkinson disease, hematocrit, mean corpuscular volume
and Huntington disease are not anemic dis- (MCV), mean corpuscular hemoglobin con-
orders, so the recombinant proteins have centration (MCHC), and mean cell hemoglo-
not been used in the treatment of these dis- bin (MCH) is usually included in the CBC.
14. a, b. Rationale: Blood is made up of plasma,
eases.
11. heat. Rationale: Because water has a high ca-
plasma proteins, fixed elements or blood
pacity to hold heat, plasma can absorb and cells, and substances such as hormones, en-
distribute much of the heat that is generated zymes, electrolytes, and byproducts of cellu-
in the body. lar waste. Ascites is an accumulation of
12.
intraperitoneal fluid containing large
Protein Percent Purpose amounts of protein and electrolytes. Bile is a
Albumin 54 Contributes to the secretion of the liver that is stored in the
plasma osmotic pres- gallbladder.
sure and mainte- 15. a, c, d. Rationale: Bone marrow and periph-
nance of blood eral blood transplants may be derived from
volume; buffer the patient (autologous) or from a histocom-
Globulins 38 Transporters and patible donor (allogeneic). A heterologous
antibodies donor has incompatible tissue types.

Fibrinogen 7 Key factor in blood

clotting

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ANSWERS 379

CHAPTER 13 DISORDERS OF 2.

HEMOSTASIS Intrinsic pathway Extrinsic pathway

(Endothelial injury) (Tissue injury)

SECTION II: ASSESSING YOUR Trauma

Burns Trauma
UNDERSTANDING Gram-negative sepsis Obstetric complications
Hypoxia Complications of cancer
Activity A Acidosis
Shock
1. hemostasis Vasculitis

2. nucleus
Thrombin
3. actin, myosin generation
4. growth factors Platelet
Intravascular
5. ADP, TXA2 fibrin deposition Plasminogen consumption
activation
6. coagulation cascade
7. liver Plasmin
Thrombocytopenia

8. disseminated intravascular coagulation generation

Thrombosis
9. Hypercoagulability Clotting factor
Fibrinolysis degradation
10. Smoking
11. thrombocytosis Hemolytic Tissue Fibrin degradation
Bleeding
anemia ischemia products
12. protein C (inhibit thrombin
13. coagulation and platelet aggregation)

14. Bleeding
15. thrombocytopenia
16. Platelet
17. Immune
18. Thrombocytopathia
19. X-linked Activity C
20. clotting factors
1. c 2. g 3. i 4. e 5. a
21. scurvy
6. f 7. j 8. h 9. d 10. b
22. disseminated intravascular coagulation
Activity D
Activity B
1.
E D C A B
Intrinsic system
(blood or vessel injury)

XII XIIa
Activity E
1. The five stages of hemostasis are (a) vessel
XI XIa spasm, which constricts the vessel and reduces
Extrinsic system blood flow; (b) formation of the platelet plug,
IXa (tissue factor)
IX
Ca++ which initiates platelet contact with suben-
VIIa VII
VIII Ca++ dothelial tissue; c) blood coagulation via fibrin
Thrombin
polymerization; (d) clot retraction in order to
VIIIa squeeze out serum; and (e) clot dissolution by
Xa
fibrinolysis by plasminogen.
X X
Ca++ 2. Platelets are attracted to a damaged vessel wall,
become activated, and change from smooth
Prothrombin Thrombin disks to spiny spheres, exposing glycoprotein
Ca++
Fibrinogen Fibrin (monomer) receptors on their surfaces. Platelet adhesion
requires a protein molecule called von Wille-
brand factor, which is produced by the en-
Fibrin (polymer)
dothelial cells of blood vessels and circulates
in the blood as a carrier protein for coagula-
tion factor VIII. Adhesion to the vessel suben-
dothelial layer occurs when the platelet

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380 ANSWERS

receptor binds to von Willebrand factor at the • Ways to be active without injuring
injury site, linking the platelet to exposed col- themselves.
lagen fibers. • How to cope with the disorder.
3. The intrinsic pathway, which is a relatively • Referrals to a genetic counselor.
slow process, begins in the circulation with the • Local support groups.
activation of factor XII, which is activated as
The nurse also provides home care.
blood comes in contact with collagen in the in-
jured vessel wall. The extrinsic pathway, which
is a much faster process, begins with trauma to SECTION IV: PRACTICING FOR NCLEX
the blood vessel or surrounding tissues and the Activity G
release of tissue factor, an adhesive lipoprotein 1. a. Rationale: Platelet adhesion requires a pro-
released from the subendothelial cells. The ter- tein molecule called von Willebrand factor.
minal steps in both pathways are the same: the This factor is produced by the endothelial
activation of factor X and the conversion of cells of blood vessels and circulates in the
prothrombin to thrombin. blood as a carrier protein for coagulation fac-
4. These drugs act as haptens and induce tor VIII. The release of growth factors results
antigen-antibody response and formation of in the proliferation and growth of vascular
immune complexes that cause platelet de- endothelial cells, smooth muscle cells, and fi-
struction by complement-mediated lysis. In broblasts, and is important in vessel repair.
persons with drug-associated thrombocytope- Ionized calcium contributes to vasoconstric-
nia, there is a rapid fall in the platelet count tion. Platelet factor 4 is a heparin-binding
within 2 to 3 days of resuming a drug or 7 or chemokine.
more days (i.e., the time needed to mount an 2. b. Rationale: The coagulation process results
immune response) after starting a drug for the from the activation of what has traditionally
first time. been designated the intrinsic or the extrinsic
5. Activation through the extrinsic pathway oc- pathways. The intrinsic pathway, which is a
curs with liberation of tissue factors, associated relatively slow process, begins in the circula-
with obstetric complications, trauma, bacterial tion with the activation of factor XII. The ex-
sepsis, and cancers. The intrinsic pathway may trinsic pathway, which is a much faster
be activated through extensive endothelial process, begins with trauma to the blood ves-
damage with activation of factor XII. Dissemi- sel or surrounding tissues and the release of
nated intravascular coagulation begins with tissue factor, an adhesive lipoprotein released
massive activation of the coagulation se- from the subendothelial cells. The terminal
quence as a result of unregulated generation of steps in both pathways are the same: the acti-
thrombin, resulting in systemic formation of vation of factor X and the conversion of pro-
fibrin. In addition, levels of all major anticoag- thrombin to thrombin. All other answers do
ulants are reduced. The microthrombi that re- not exist in the formation of clots.
sult cause vessel occlusion and tissue ischemia. 3. a. Rationale: The anticoagulant drugs war-
Multiple organ failure may ensue. Clot forma- farin and heparin are used to prevent throm-
tion consumes all available coagulation pro- boembolic disorders, such as deep vein
teins and platelets, and severe hemorrhage thrombosis and pulmonary embolism. War-
results. farin acts by decreasing prothrombin and
other procoagulation factors. It alters vitamin
SECTION III: APPLYING YOUR K in a manner that reduces its ability to partic-
KNOWLEDGE ipate in synthesis of the vitamin K–dependent
Activity F coagulation factors in the liver.
4. b. Rationale: Heparin binds to antithrombin
1. Prevent bleeding and make the environment
III, causing a conformational change that in-
as safe as possible.
creases the ability of antithrombin III to inac-
2. When teaching families and clients about he-
tivate thrombin, factor Xa, and other clotting
mophilia, the nurse would include informa-
factors. By promoting the inactivation of
tion on
clotting factors, heparin ultimately sup-
• Measures for controlling bleeding. presses the formation of fibrin. Heparin does
• Limiting local joint damage. not bind to factors X and Xa. Heparin does
not inactivate factor VIII.

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ANSWERS 381

5. b. Rationale: Platelets, through the action of 11. c. Rationale: Hemostasis is divided into five
their actin and myosin filaments, also con- stages: (a) vessel spasm, (b) formation of the
tribute to clot retraction. Clot retraction platelet plug, (c) blood coagulation or devel-
therefore requires large numbers of platelets, opment of an insoluble fibrin clot, (d) clot re-
and failure of clot retraction is indicative of a traction, and (e) clot dissolution.
low platelet count. Factor Xa is necessary fac- 12. intravascular
tor in blood coagulation. It does not cause 13. Heparin
failure of clot retraction. 14. a, b, c, e. Rationale: Platelets that adhere to
6. c. Rationale: The common underlying causes the vessel wall release growth factors that
of secondary thrombocytosis include tissue cause proliferation of smooth muscle and
damage due to surgery, infection, cancer, and thereby contribute to the development of
chronic inflammatory conditions such as atherosclerosis. Smoking, elevated levels of
rheumatoid arthritis and Crohn disease. blood lipids and cholesterol, hemodynamic
Lyme disease, caused by a tick bite, does not stress, diabetes mellitus, and immune mecha-
cause thrombocytosis. Hirschsprung disease nisms may cause vessel damage, platelet ad-
and megacolon are the same thing, and they herence, and, eventually, thrombosis.
are not inflammatory conditions. 15. a, c, e. Rationale: In disseminated intravascu-
7. a. Rationale: A reduction in platelet number, lar coagulation, microemboli may obstruct
also referred to as thrombocytopenia, is an im- blood vessels and cause tissue hypoxia and
portant cause of generalized bleeding. necrotic damage to organ structures, such as
Thrombocytopenia usually refers to a de- the kidneys, heart, lungs, and brain. As a re-
crease in the number of circulating platelets sult, common clinical signs may be due to
to a level less than 100,000/µL. The greater renal, circulatory, or respiratory failure; acute
the decrease in the platelet count, the greater bleeding ulcers; or convulsions and coma. A
the risk of bleeding. Thrombocytopenia can form of hemolytic anemia may develop when
result from a decrease in platelet production, red blood cells are damaged as they pass
increased sequestration of platelets in the through vessels partially blocked by thrombus.
spleen, or decreased platelet survival.
8. b. Rationale: Hemophilia A is an X-linked re-
cessive disorder that primarily affects males.
CHAPTER 14 DISORDERS OF RED
Approximately 90% of persons with hemo- BLOOD CELLS
philia produce insufficient quantities of fac-
tor VIII. The prevention of trauma is SECTION II: ASSESSING YOUR
important in persons with hemophilia. UNDERSTANDING
9. c. Rationale: In persons with bleeding disor- Activity A
ders caused by vascular defects, the platelet
1. biconcave, cell membrane
count and results of other tests for coagula-
2. iron
tion factors are normal. A shift to the left in-
3. nucleus
dicates an infectious or inflammatory
4. 4
process, not a clotting disorder. A lack of iron
5. glycolytic
indicates iron-deficiency anemia, not a clot-
6. methemoglobin
ting disorder. A normal hematocrit indicates
7. red blood cell count
a normal number of packed red blood cells,
8. hematocrit
not a clotting disorder.
9. mean corpuscular hemoglobin concentration
10. a. Rationale: Disseminated intravascular coag-
10. Anemia
ulation is a paradox in the hemostatic se-
11. hypoxia
quence and is characterized by widespread
12. Hemolytic
coagulation and bleeding in the vascular
13. sickle cell, thalassemias
compartment. It is not a primary disease but
14. Spherocytosis
occurs as a complication of a wide variety of
15. -thalassemias, -thalassemias
conditions, including disease or injury such
16. G6PD
as septicemia, acute hypotension, poisonous
17. Iron-deficiency
snakebites, neoplasms, obstetric emergencies,
18. chronic blood loss
severe trauma, extensive surgery, and hemor-
19. Megaloblastic
rhage.

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382 ANSWERS

20. Pernicious and defective RBCs, and then ingest and de-
21. Aplastic anemia stroy them in a series of enzymatic reactions.
22. Polycythemia During these reactions, the amino acids from
23. oxygen the globulin chains and iron from the heme
24. conjugate units are salvaged and reused. The bulk of the
25. anemia heme unit is converted to bilirubin, which is
Activity B insoluble in plasma and attaches to plasma
proteins for transport. Bilirubin is removed
from the blood by the liver and conjugated
with glucuronide to render it water soluble so
Spleen
that it can be excreted in the bile.
3. The three categories of anemic effects are (a)
manifestations of impaired oxygen transport
and the resulting compensatory mechanisms,
Hemoglobin
(b) reduction in red blood cell indices and he-
moglobin levels, and (c) signs and symptoms
Heme Globin associated with the pathologic process that is
causing the anemia.
Iron Amino acids 4. Premature destruction of the cells due to the
(reutilized) rigid nondeformable membrane occurs in the
Free, unconjugated
spleen, causing hemolysis and anemia due to a
bilirubin
decrease in red blood cell numbers. Vessel oc-
Liver
clusion, a complex process involving an inter-
action among the sickle cells, endothelial cells,
Reused by bone
leukocytes, platelets, and other plasma pro-
marrow or stored in teins, will interrupt blood flow. The adherence
spleen and liver of sickle cells to the vessel endothelium causes
endothelial activation with liberation of in-
Conjugated bilirubin flammatory mediators and substances that in-
Bone crease platelet activation and promote blood
marrow Secreted in bile; coagulation.
excreted in feces 5. Exposure to high doses of radiation, chemi-
or urine
cals, and toxins that suppress cellular activity
directly or through immune mechanisms are
the standard cancer treatments. Chemother-
Activity C apy and irradiation commonly result in bone
marrow depression, which causes anemia,
1. e 2. a 3. f 4. c 5. i
thrombocytopenia, and neutropenia. Identi-
6. j 7. b 8. d 9. h 10. g
fied toxic agents, including benzene, the an-
Activity D tibiotic chloramphenicol, and the alkylating
1. The hemoglobin molecule is composed of two agents and antimetabolites used in the treat-
pairs of structurally different  and  polypep- ment of cancer, will decrease bone marrow of
tide chains. Each polypeptide chain consists of stem cells, thus affecting the production of red
a globin (protein) portion and heme unit, blood cells.
which surrounds an atom of iron that binds 6. Viscosity rises exponentially with the hemat-
oxygen. Thus, each molecule of hemoglobin ocrit and interferes with cardiac output and
can carry four molecules of oxygen. The bind- blood flow. Hypertension is common, and
ing that occurs is cooperative, or allosteric. there may be complaints of headache, dizzi-
When one oxygen molecule binds, it makes it ness, inability to concentrate, and some diffi-
easier for the next to bind. The process also culty with hearing and vision because of
works in reverse. decreased cerebral blood flow. Venous stasis
2. A group of large phagocytic cells found in the gives rise to a plethoric appearance or dusky
spleen, liver, bone marrow, and lymph nodes redness, even cyanosis, particularly of the lips,
facilitates the destruction of red blood cells fingernails, and mucous membranes. Because
(RBCs). These phagocytic cells recognize old of the increased concentration of blood cells,

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ANSWERS 383

the person may experience itching and pain in

SECTION IV: PRACTICING FOR NCLEX
the fingers or toes, and the hypermetabolism
may induce night sweats and weight loss. Activity F
7. Hyperbilirubinemia in the neonate is treated 1. a. Rationale: When red blood cells (RBCs) age
with phototherapy or exchange transfusion. and are destroyed in the spleen, the iron
Phototherapy is more commonly used to treat from their hemoglobin is released into the
jaundiced infants and reduce the risk of ker- circulation and returned to the bone marrow
nicterus. Exposure to fluorescent light in the for incorporation into new RBCs or to the
blue range of the visible spectrum (420- to liver and other tissues for storage. Iron is not
470-nm wavelength) reduces bilirubin levels. bound to RBCs in the liver. Iron does not
Bilirubin in the skin absorbs the light energy bind with oxygen in the lung without first
and is converted to a structural isomer that is being incorporated into an RBC. Iron is
more water soluble and can be excreted in the stored in tissues of the body, but not for
stool and urine. Hyperbilirubinemia in the strength, only for its oxygen-binding capac-
neonate is treated with phototherapy or ex- ity.
change transfusion. Phototherapy is more 2. d. Rationale: The plasma-insoluble form of
commonly used to treat jaundiced infants and bilirubin is referred to as unconjugated biliru-
reduce the risk of kernicterus. Exposure to flu- bin, and the water-soluble form as conju-
orescent light in the blue range of the visible gated bilirubin. Serum levels of conjugated
spectrum (420- to 470-nm wavelength) re- and unconjugated bilirubin can be measured
duces bilirubin levels. Bilirubin in the skin ab- in the laboratory and are reported as direct
sorbs the light energy and is converted to a and indirect, respectively.
structural isomer that is more water soluble 3. a. Rationale: Hyperbilirubinemia, an increased
and can be excreted in the stool and urine. level of serum bilirubin, is a common cause
of jaundice in the neonate. A benign, self-
SECTION III: APPLYING YOUR limited condition, it is most often related to
KNOWLEDGE the developmental state of the neonate.
Rarely, cases of hyperbilirubinemia are patho-
Activity E logic and may lead to kernicterus and serious
1. During a blood transfusion, the nurse and Mrs. brain damage.
McFee will watch for the following symptoms: 4. b. Rationale: It takes about 5 days for the
progeny of stem cells to fully differentiate, an
• Sensation of heat along the vein while the
event marked by increased reticulocytes in
transfusion is going in
the blood. If the bleeding is controlled and
• Urticaria
sufficient, iron stores are available. The red
• Headache
blood cell concentration returns to normal
• Pain in the low back
within 3 to 4 weeks.
• Chills
5. c. Rationale: Chronic blood loss does not af-
• Fever
fect blood volume, but instead leads to iron-
• Chest pain
deficiency anemia when iron stores are
• Abdominal cramps
depleted. It is commonly caused by gastroin-
• Nausea
testinal bleeding and menstrual disorders. Be-
• Vomiting
cause of compensatory mechanisms, patients
• Tachycardia
are commonly asymptomatic until the hemo-
• Hypotension
globin level is less than 8 g/dL. The red blood
• Dyspnea
cells (RBCs) that are produced have too little
The most feared and lethal transfusion reac- hemoglobin, giving rise to microcytic
tion is the destruction of donor red blood cells hypochromic anemia. Macrocytic anemia is
by reaction with antibody in the recipient’s when the RBCs are larger than normal. Hy-
serum. This immediate hemolytic reaction is perchromic means the cells are a darker color
usually caused by ABO incompatibility. red then they should be.
2. Most transfusion reactions result from admin- 6. d. Rationale: Hemolytic anemia is character-
istrative errors or misidentification, and care ized by the premature destruction of red
should be taken to correctly identify the recip- blood cells (RBCs), the retention in the body
ient and the transfusion source. of iron and the other products of hemoglobin

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384 ANSWERS

destruction, and an increase in erythro- 12. a, b, d. Rationale: Factors associated with sick-
poiesis. Almost all types of hemolytic anemia ling and vessel occlusion include cold, stress,
are distinguished by normocytic and nor- physical exertion, infection, and illnesses that
mochromic RBCs. cause hypoxia, dehydration, or acidosis.
7. d. Rationale: In hemolytic anemia, intravascu- 13. 1-c, 2-a, 3-b. Rationale: Red blood cell (RBC)
lar hemolysis is less common than extravas- indices are used to differentiate types of ane-
cular hemolysis and occurs as a result of mias by size or color of RBCs. The mean cor-
complement fixation in transfusion reac- puscular volume (MCV) reflects the volume
tions, mechanical injury, or toxic factors. It is or size of the RBCs. The MCV falls in micro-
characterized by hemoglobinemia, hemoglo- cytic (small cell) anemia and rises in macro-
binuria, jaundice, and hemosiderinuria. cytic (large cell) anemia. Some anemias are
Spherocytosis is the most common inherited normocytic (i.e., cells are of normal size or
disorder of the red blood cell membrane and MCV). The mean corpuscular hemoglobin
is not associated with hemolytic anemia. concentration is the concentration of hemo-
8. b. Rationale: Therapy for aplastic anemia in the globin in each cell.
young and severely affected includes stem cell 14. a, b. Rationale: In anemia, the oxygen-carrying
replacement by bone marrow or peripheral capacity of hemoglobin is reduced, causing
blood transplantation. Histocompatible donors tissue hypoxia. Tissue hypoxia can give rise
supply the stem cells to replace the patient’s to fatigue, weakness, dyspnea, and sometimes
destroyed marrow cells. A liver transplant will angina. Hypoxia of brain tissue results in
not produce new blood cells for the body. headache, faintness, and dim vision. The re-
Spleen transplants are not done and would not distribution of the blood from cutaneous tis-
produce new blood cells for the body. sues or a lack of hemoglobin causes pallor of
9. a. Rationale: Chronic renal failure almost al- the skin, mucous membranes, conjunctiva,
ways results in anemia, primarily because of a and nail beds. Tachycardia and palpitations
deficiency of erythropoietin. Unidentified may occur as the body tries to compensate
uremic toxins and retained nitrogen also in- with an increase in cardiac output Ruddy skin
terfere with the actions of erythropoietin, and bradycardia are not signs or symptoms of
and red blood cell production and survival. anemia.
Hemolysis and blood loss associated with he- 15. a, b, e. Rationale: Primary polycythemia, or
modialysis and bleeding tendencies also con- polycythemia vera, is a neoplastic disease of
tribute to the anemia of renal failure. the pluripotent cells of the bone marrow
Fibrinogen is essential for blood clotting, not characterized by an absolute increase in total
oxygen transportation. red blood cell mass accompanied by elevated
10. c. Rationale: Erythroblastosis fetalis, or he- white blood cell and platelet counts. It is
molytic disease of the newborn, occurs in Rh- most commonly seen in men with a median
positive infants of Rh-negative mothers who age of 62 years, but may occur at any age. In
have been sensitized. The Rh-negative addition, early findings include splenomegaly
mother usually becomes sensitized during the and depletion of iron stores. Hypertension is
first few days after delivery, when fetal Rh- common, and there may be complaints of
positive red blood cells from the placental headache, dizziness, inability to concentrate,
site are released into the maternal circulation. and some difficulty with hearing and vision
Because the antibodies take several weeks to because of decreased cerebral blood flow. Ve-
develop, the first Rh-positive infant of an Rh- nous stasis gives rise to a plethoric appear-
negative mother is usually not affected. There ance or dusky redness, even cyanosis,
is no such thing as microcytic or macrocytic particularly of the lips, fingernails, and
disease of the newborn, or is there a he- mucous membranes.
molytic iron-deficiency anemia. 16. transfusion. Rationale: Persons who are ho-
11. vitamin B12. Rationale: Pernicious anemia is be- mozygous for the trait (thalassemia major)
lieved to result from immunologically medi- have severe, transfusion-dependent anemia
ated, possibly autoimmune, destruction of the that is evident at 6 to 9 months of age when
gastric mucosa. The resultant chronic atrophic the hemoglobin switches from HbF to HbA. If
gastritis is marked by loss of parietal cells and transfusion therapy is not started early in life,
production of antibodies that interfere with severe growth retardation occurs in children
binding of vitamin B12 to intrinsic factor. with the disorder.

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ANSWERS 385

CHAPTER 15 DISORDERS OF underlying oropharyngeal lymphoid tissue,

and, more specifically, to B lymphocytes, all of
WHITE BLOOD CELLS AND which have receptors for EBV. Infection of the
LYMPHOID TISSUES B cells may take one of two forms—it may kill
the infected B cell, or it may become incorpo-
SECTION II: ASSESSING YOUR rated into its genome. The B cells that harbor
UNDERSTANDING the EBV genome proliferate in the circulation
and produce the well-known heterophil anti-
Activity A
bodies that are used for the diagnosis of
1. granulocytes infectious mononucleosis. The resultant de-
2. thymus struction of B cells and production of large T
3. plasma cells result in enlarged lymph nodes, particu-
4. natural killer larly in the cervical, axillary, and groin areas.
5. myeloid, lymphoid Hepatitis and splenomegaly are common man-
6. thymus, spleen ifestations of the disease and are believed to
7. CD4 , CD8 be immune mediated.
8. aplastic 3. The manifestations of non-Hodgkin lym-
9. alloantibodies phoma depend on lymphoma type and the
10. neutropenia stage of the disease. Persons with indolent or
11. Infectious mononucleosis slow-growing lymphomas usually present with
12. Leukemias painless lymphadenopathy due to increased
13. Lymphomas cell filtering, which may be isolated or wide-
14. B- spread. The indolent lymphomas are usually
15. nodular, lymphocyte disseminated at the time of diagnosis, and
16. Hodgkin lymphoma bone marrow involvement is frequent. Many
17. leukemias low-grade lymphomas eventually transform
18. lymphocytic into more aggressive forms of lymphoma/
19. leukemia leukemia. Persons with intermediate or more
20. Acute leukemias aggressive forms of lymphoma usually present
21. lymphocytic, monocytic with symptoms such as fever, drenching night
22. Chronic leukemias sweats, or weight loss. Frequently, there is in-
23. B lymphocytes creased susceptibility to bacterial, viral, and
24. lymphocytosis fungal infections, as well as a poor humoral
25. Philadelphia antibody response.
26. Plasma cell dyscrasias 4. First, it usually arises in a single node or chain
27. bone of nodes, whereas non-Hodgkin lymphoma
28. M protein frequently originates at extranodal sites and
spreads to anatomically contiguous nodes.
Activity B
Second, Hodgkin lymphoma is characterized
1. e 2. d 3. b 4. a 5. f by the presence of large, atypical, mononu-
6. h 7. i 8. c 9. g 10. j clear tumor cells called Reed-Sternberg cells.
The cells, which frequently constitute less
Activity C
than 1% of the total cell population, are a di-
1. Neutrophils migrate to sites of infection, agnostic hallmark of the disease.
where they engulf, digest, and destroy mi- 5. The incidence of leukemia among persons
croorganisms. Thus, a decrease in the number who have been exposed to high levels of radia-
of neutrophils places a person at risk for infec- tion is unusually high. An increased incidence
tion. The risk for and severity of neutropenia- of leukemia is also associated with exposure to
associated infection are directly proportional benzene and the use of antitumor drugs.
to the absolute neutrophil count and duration Leukemia may occur as a second cancer after
of the neutropenia (defined as a circulating aggressive chemotherapy for other cancers.
neutrophil count of less than 1500 /mL) The existence of a genetic predisposition to
2. The Epstein-Barr virus (EBV) initially pene- develop acute leukemia is suggested by the in-
trates the nasopharyngeal, oropharyngeal, and creased leukemia incidence among a number
salivary epithelial cells. It then spreads to the of congenital disorders. In individuals with

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386 ANSWERS

Down syndrome, the incidence of acute nounced during this period, and
leukemia is ten times that of the general popu- splenomegaly may increase significantly.
lation. Also, there are numerous reports of Isolated infiltrates of leukemic cells can in-
multiple cases of acute leukemia occurring volve the skin, lymph nodes, bones, and
within the same family. central nervous system.
6. Both are characterized by an abrupt onset of 8. The cause of multiple myeloma is unknown.
symptoms, including fatigue resulting from Risk factors are believed to include chronic im-
anemia; low-grade fever, night sweats, and mune stimulation, autoimmune disorders, ex-
weight loss due to the rapid proliferation and posure to ionizing radiation, and occupational
hypermetabolism of the leukemic cells; exposure to pesticides or herbicides. Myeloma
bleeding because of a decreased platelet has been associated with exposure to Agent
count; and bone pain and tenderness due to Orange during the Vietnam War. A number of
bone marrow expansion. Infection results viruses have been associated with the patho-
from neutropenia. Generalized lympha- genesis of myeloma. There is a 4.5-fold in-
denopathy, splenomegaly, and he- crease in the likelihood of developing
patomegaly caused by infiltration of myeloma for persons with HIV.
leukemic cells occur in all acute leukemias
but are more common in acute lymphocytic
leukemia (ALL). In addition to the common SECTION III: APPLYING YOUR
manifestations of acute leukemia, infiltration KNOWLEDGE
of malignant cells in the skin, gums, and Activity D
other soft tissue is particularly common in 1. The causes of leukemia are really unknown.
the monocytic form of acute myelogenous We do know that the event or events causing
leukemia (AML). The leukemic cells may also the leukemias exert their effects through dis-
cross the blood-brain barrier and establish ruption or dysregulation of genes that nor-
sanctuary in the central nervous system mally regulate blood cell development, blood
(CNS). CNS involvement is more common in cell stability, or both.
ALL than AML and is more common in chil- 2. Treatment of acute lymphocytic leukemia
dren than adults. Signs and symptoms of consists of a number of chemotherapeutic
CNS involvement include cranial nerve agents designed to achieve remission fol-
palsies, headache, nausea, vomiting, pa- lowed by high doses of chemotherapy given
pilledema, and, occasionally, seizures and to patients who have achieved remission
coma. Leukostasis and blood clotting are with their induction therapy. This part of
seen in severe cases. Lucy’s treatment is designed to reduce the
7. The early chronic stage is marked by leuko- number of cancer cells in her body even
cytosis, anemia, and thrombocytopenia. more once remission has been achieved.
Splenomegaly and hepatomegaly are often Then, in an attempt to cure her, she will re-
present. The accelerated phase of chronic ceive lower doses of chemotherapy over a
myelogenous leukemia (CML) is character- long period of time.
ized by enlargement of the spleen, resulting
in a feeling of abdominal fullness and dis-
comfort. An increase in basophil count and SECTION IV: PRACTICING FOR NCLEX
more immature cells in the blood or bone Activity E
marrow confirm transformation to the accel-
1. a. Rationale: A small population of cells called
erated phase. Symptoms such as low-grade
fever, night sweats, bone pain, and weight pluripotent stem cells are capable of provid-
loss develop because of rapid proliferation ing progenitor cells, or parent cells, for
and hypermetabolism of the leukemic cells. myelopoiesis and lymphopoiesis, processes
Bleeding and easy bruising may arise from by which myeloid and lymphoid blood cells
dysfunctional platelets. The terminal blast are made. Unipotent cells are the progenitors
crisis phase of CML represents evolution to for each of the blood cell types and come
acute leukemia and is characterized by an in- from pluripotent stem cells. Multipotential
creasing number of myeloid precursors, es- progenitor cells act as parent cells for multi-
ple types of blood cells. Myeloproliferative
pecially blast cells, in the blood.
cells do not exist.
Constitutional symptoms become more pro-

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2. b. Rationale: The portion of the cortex be- malaria infection are common. Neither her-
tween the medullary and superficial cortex is pes zoster nor streptococcal infections are
called the paracortex. The region contains associated with endemic Burkitt lym-
most of the T cells in the lymph nodes. phoma.
The B-cell–dependent cortex consists of two 8. a. Rationale: Although acute lymphoblastic
types of follicles: immunologically inactive leukemia and acute myelogenous leukemia
follicles, called primary follicles, and active are distinct disorders, they typically present
follicles that contain germinal centers called with similar clinical features. Both are charac-
secondary follicles. There is no primary cor- terized by an abrupt onset of symptoms, in-
tex in the lymph nodes. cluding fatigue resulting from anemia;
3. d. Rationale: Severe congenital neutropenia, low-grade fever, night sweats, and weight loss
or Kostmann syndrome, is characterized by due to the rapid proliferation and hyperme-
an arrest in myeloid maturation at the tabolism of the leukemic cells; bleeding be-
promyelocyte stage of development, resulting cause of a decreased platelet count; and bone
in an absolute neutrophil count of less than pain and tenderness due to bone marrow
200 cells/L. The disorder is characterized by expansion. Polycythemia is an increase in the
severe bacterial infections. Kostmann syn- erythrocytes in the blood. It is not an
drome is not characterized by bone marrow indication of leukemia.
disorders, viral infections, or autoimmune 9. b. Rationale: Diagnosis of multiple myeloma is
disorders. based on clinical manifestations, blood tests,
4. a. Rationale: The incidence of drug-induced and bone marrow examination. The classic
neutropenia has increased significantly over triad of bone marrow plasmacytosis (more
the past few decades and is attributed primar- than 10% plasma cells), lytic bone lesions, and
ily to a wider use of drugs in general and, either the serum M-protein spike or the pres-
more specifically, to the use of chemothera- ence of Bence-Jones proteins in the urine is de-
peutic drugs in the treatment of cancer. finitive for a diagnosis of multiple myeloma.
5. b. Rationale: Hepatitis and splenomegaly are Oligoclonal bands are indicative of multiple
common manifestations of infectious sclerosis, and BCR-ABL fusion protein is found
mononucleosis and are believed to be im- in chronic myelogenous leukemia.
mune mediated. Hepatitis is characterized by 10. c. Rationale: Hypogammaglobulinemia is com-
hepatomegaly, nausea, anorexia, and jaun- mon in chronic lymphocytic leukemia, espe-
dice. Although discomforting, it is usually a cially in persons with advanced disease. An
benign condition that resolves without caus- increased susceptibility to infection reflects an
ing permanent liver damage. The spleen may inability to produce specific antibodies and
be enlarged two to three times its normal abnormal activation of complement. The most
size, and rupture of the spleen is an infre- common infectious organisms are those that
quent complication. Cranial nerve palsies, require opsonization for bacterial killing, such
not peripheral nerve palsies, can occur. as Streptococcus pneumoniae, Staphylococcus au-
Lymph nodes do not rupture. Severe bacterial reus, and Haemophilus influenzae. Acne rosacea,
infections are complications of Kostmann Pseudomonas aeruginosa, and Escherichia coli are
syndrome. not infectious agents common in clients with
6. c. Rationale: Non-Hodgkin lymphomas chronic lymphocytic leukemia.
(NHLs) represent the cancer with the second 11. lyse
fastest rate of increase in the United States 12. c. Rationale: The alimentary canal, respiratory
and the most commonly occurring hemato- passages, and genitourinary systems are
logic cancer. Neoplasms of immature B cells guarded by accumulations of lymphatic tis-
include lymphoblastic leukemia/lymphoma sue that are not enclosed in a capsule. This
(i.e., acute lymphocytic leukemia). They are form of lymphatic tissue is called diffuse lym-
not classed as NHLs. Mantle cell lymphoma is phatic tissue or MALT because of its associa-
one of the mature B-cell lymphomas. tion with mucous membranes. Lymphocytes
7. d. Rationale: Endemic Burkitt lymphoma is are found in the subepithelial of these tissues.
the most common childhood cancer (peak Lymphomas can arise from MALT as well as
ages 3–7 years) in Central Africa, often be- lymph node tissue. The cardiovascular system
ginning in the jaw. It occurs in regions of and the central nervous system do not have
Africa where both Epstein-Barr virus and MALT.

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388 ANSWERS

13. b, c, d. Rationale: The existence of a genetic Activity B

predisposition to develop acute leukemia is
suggested by the increased leukemia inci- Death
dence among a number of congenital disor-
Critical threshold
ders, including Down syndrome,
neurofibromatosis, and Fanconi anemia.

replication of pathogens
Neither Cushing syndrome nor Prader-Willi

Severity of illness
syndrome are genetic disorders. Chronic disease

14. a, c, e. Rationale: Massive necrosis of malig-

nant cells can occur during the initial phase
of treatment. This phenomenon, known as
Clinical
tumor lysis syndrome, can lead to life-threat- threshold
ening metabolic disorders, including hyper- Subclinical disease
kalemia, hyperphosphatemia, hyperuricemia, Incubation Acute Convalescent
hypomagnesemia, hypocalcemia, and acido- Prodromal
sis, with the potential for causing acute renal
Infection Resolution
failure.
15. radiation. Rationale: As the cure rate for
Hodgkin lymphoma has risen and longer-term
follow-up data became available, the impor- Activity C
tance of the late effects of treatment, includ- 1.
ing secondary malignancies, has become more 1. b 2. f 3. d 4. g 5. a
apparent. Because these malignancies have 6. e 7. c 8. h 9. i 10. j
mainly been attributed to radiation therapy,
studies are being conducted to determine the 2.
lowest effective radiation dose. 1. f 2. a 3. j 4. e 5. c
6. d 7. b 8. h 9. g 10. i
CHAPTER 16 MECHANISMS OF Activity D
INFECTIOUS DISEASE 1.
SECTION II: ASSESSING YOUR
D E A C F B
UNDERSTANDING
Activity A
1. commensalism Activity E
2. infection 1. Viruses are incapable of replication outside a
3. parasitic living cell. They must penetrate a susceptible
4. opportunistic living cell and use the biosynthetic machinery
5. transmissible neurodegenerative of the cell to produce viral progeny. Not every
6. Viruses viral agent causes lysis and death of the host
7. prokaryotes cell during the course of replication. Some
8. Staining viruses enter the host cell and insert their
9. spirochetes genome into the host cell chromosome, where
10. mycoplasmas it remains in a latent, nonreplicating state for
11. fungal long periods without causing disease. Under
12. yeasts, molds the appropriate stimulation, the virus under-
13. feces goes active replication and produces symp-
14. prodromal stage toms of disease months to years later.
15. acute stage 2. The portal of entry refers to the process by
16. convalescent period which a pathogen enters the body, gains ac-
17. -itis cess to susceptible tissues, and causes disease.
18. -emia Among the potential modes of transmission
19. Virulence are penetration, direct contact, ingestion, and
20. exotoxins inhalation. In terms of pathophysiology,
symptoms are the outward expression of the

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ANSWERS 389

struggle between invading organisms and the zalcitabine, nevirapine, efavirenz, and delavir-
retaliatory inflammation and immune re- dine.
sponses of the host.
3. The course of any infectious disease can be di- SECTION IV: PRACTICING FOR NCLEX
vided into several distinguishable stages after
Activity G
the point of time in which the potential
pathogen enters the host. These stages are the 1. a. Rationale: A parasitic relationship is one in
incubation period, the prodromal stage, the which only the infecting organism benefits
acute stage, the convalescent stage, and the from the relationship and the host either
resolution stage. The stages are based on the gains nothing from the relationship or sus-
progression and intensity of the host’s symp- tains injury from the interaction. If the host
toms over time. The duration of each phase sustains injury or pathologic damage in re-
and the pattern of the overall illness can be sponse to a parasitic infection, the process is
specific for different pathogens, thereby aiding called an infectious disease. Mutual and com-
in the diagnosis of an infectious disease. mensal relationships do not harm the human
4. The goal of treatment for an infectious disease body. Communicable diseases can be passed
is complete removal of the pathogen from the from one human to another; they are not
host and the restoration of normal physiologic parasitic.
function to damaged tissues. When an infec- 2. b. Rationale: The Rickettsiaceae are acciden-
tious process gains the upper hand and thera- tally transmitted to humans through the bite
peutic intervention is essential, the choice of of the arthropod (i.e., vector) and produce a
treatment may be medicinal using antimicro- number of potentially lethal diseases, includ-
bial agents; immunologic with antibody prepa- ing Rocky Mountain spotted fever and epi-
rations, vaccines, or substances that stimulate demic typhus. Viruses, Chlamydiaceae, and
and improve the host’s immune function; or Anaplasmataceae do not cause either epidemic
surgical by removing infected tissues. typhus or Rocky Mountain spotted fever.
5. Potential agents of bioterrorism have been cat- 3. c. Rationale: SARS was recognized in the
egorized into three levels (A, B, C) based on Guangdong province in southern China be-
risk of use, transmissibility, invasiveness, and ginning in November 2002. The illness was
mortality rate. The agents considered to be in highly transmissible, as evidenced by the first
the highest biothreat level—plague, tularemia, recognized occurrence in Taiwan. Four days
smallpox, and hemorrhagic fever—are cate- after returning to Taiwan from work in the
gory A. The category B agents include agents Guangdong province, a businessman devel-
of food- and waterborne disease, agents of oped a febrile illness and was admitted to a
zoonotic infections, and viral encephalitides. local hospital. Within 1 month, a large noso-
Category C agents are defined as emerging comial outbreak of SARS was documented to
pathogens and potential risks for the future, have affected ~3000 people in Taipei City,
even though many of these organisms are Taiwan. Since the SARS outbreak began in
causes of ancient diseases such as tuberculosis China and crossed continental borders for
and tickborne fever viruses. the first time, it was classified as not only an
epidemic but also a pandemic. Regional and
endemic mean the same thing, a specific area
SECTION III: APPLYING YOUR
where the disease occurs. Nosocomial is an
KNOWLEDGE
infection acquired in a health care facility.
Activity F 4. d. Rationale: Symptomatology refers to the
1. An antibiotic is considered bactericidal if it collection of signs and symptoms expressed
causes irreversible and lethal damage to the by the host during the disease course. This is
bacterial pathogen and bacteriostatic if its in- also known as the clinical picture or disease
hibitory effects on bacterial growth are re- presentation. The virulence of the disease is
versed when the agent is eliminated. its power to produce the disease. The source
2. The drugs used to treat HIV infections are not of the disease is the place where it came from.
antibiotics or antiviral agents. They are classi- The diagnosis of the disease is the naming of
fied as antiretroviral agents. These drugs are the disease process in the body.
acyclovir, ganciclovir, vidarabine, ribavirin, zi- 5. a. Rationale: The diagnosis of an infectious
dovudine, lamivudine, didanosine, stavudine, disease requires two criteria: the recovery of a

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390 ANSWERS

probable pathogen or evidence of its presence burger meat or unpasteurized fruit juices con-
from the infected sites of a diseased host, and taminated with this organism produces hem-
accurate documentation of clinical signs and orrhagic colitis and a sometimes fatal illness
symptoms compatible with an infectious called hemolytic uremic syndrome, character-
process. Culture and sensitivity are the grow- ized by vascular endothelial damage, acute
ing of microorganisms outside the body and renal failure, and thrombocytopenia.
the testing to see what kills it. Identifying a E. coli does not cause nephritic syndrome, he-
microorganism by microscopic appearance molytic thrombocytopenia, or neuroleptic
and Gram stain reaction are not the criteria malignant syndrome.
for diagnosis. Serology, an indirect means of 11. prions. Rationale: Prions, protein particles
identifying infectious agents by measuring that lack any kind of a demonstrable
serum antibodies in the diseased host, and genome, have been found to cause patho-
the quantification of those antibodies, an an- logic processes in humans. The various prion-
tibody titer, are not criteria for diagnosis. associated diseases produce very similar
6. b. Rationale: Potential agents of bioterrorism symptomatology and pathology in the host
have been categorized into three levels (A, B, and are collectively called transmissible
C) based on risk of use, transmissibility, inva- neurodegenerative diseases.
siveness, and mortality rate. 12. Congenital. Rationale: When an infectious
7. c. Rationale: Aided by a global market and the disease is transmitted from mother to child
ease of international travel, the past 5 years during gestation or birth, it is classified as a
have witnessed the importation or emergence congenital infection.
of a host of novel infectious diseases. During 13. 1-c, 2-a, 3-d, 4-b
the late summer and early fall of 1999, West 14. a, c, d, e. Rationale: Virulence factors are
Nile virus (WNV) was identified as the cause substances or products generated by infec-
of an epidemic involving 56 patients in the tious agents that enhance their ability to
New York City area. This outbreak, which led cause disease. Although the number and type
to seven deaths (primarily in the elderly), of microbial products that fit this description
marked the first time that WNV had been rec- are numerous, they can generally be grouped
ognized in the Western hemisphere since its into four categories: toxins, adhesion factors,
discovery in Uganda nearly 60 years earlier. evasive factors, and invasive factors. Prodro-
Coxsackie diseases, caused by the Coxsackie mal means occurring first or prior to a spe-
virus; respiratory syncytial disease, better cific event. It is not a virulence factor.
known as RSV; and hand, foot, and mouth 15. a, d, e. Rationale: A number of factors pro-
disease are not considered global diseases. duced by microorganisms enhance virulence
8. d. Rationale: The course of any infectious dis- by evading various components of the host’s
ease can be divided into several distinguish- immune system. Extracellular polysaccharides,
able stages after the point of time in which including capsules, slime, and mucous layers,
the potential pathogen enters the host. These discourage engulfment and killing of
stages are the incubation period, the prodro- pathogens by the host’s phagocytic white
mal stage, the acute stage, the convalescent blood cells. Phospholipases and collagenases
stage, and the resolution stage. There are no are enzymes that are invasive virulence factors.
postacute, subacute, or postdromal stages to a
disease.
9. a. Rationale: An abscess is a localized pocket
CHAPTER 17 INNATE AND
of infection composed of devitalized tissue, ADAPTIVE IMMUNITY
microorganisms, and the host’s phagocytic
white blood cells: in essence, a stalemate in SECTION II: ASSESSING YOUR
the infectious process. A pimple is a small UNDERSTANDING
papule or pustule. A lesion is a pathologic Activity A
change in body tissue. Acne is a disease of the 1. immune system
skin. 2. allergies, autoimmune
10. c. Rationale: Other exotoxins that have 3. innate
gained notoriety include the Shiga toxins 4. Adaptive
produced by E. coli O157:H7 and other select 5. antigens
strains. The ingestion of undercooked ham-

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6. Humoral Activity C
7. Cell-mediated
1.
8. macrophages
1. c 2. j 3. f 4. h 5. e
9. neutrophils, macrophages
6. d 7. a 8. b 9. i 10. g
10. Neutrophils
11. macrophage
2.
12. B, T
1. g 2. d 3. f 4. e 5. a
13. Natural killer cells
6. b 7. c 8. h 9. j 10. i
14. Dendritic
15. Chemokines Activity D
16. colony-stimulating factors
1. Although cells of both innate and adaptive im-
17. epithelial
mune systems communicate critical informa-
18. pathogens
tion by cell-to-cell contact, many interactions
19. Opsonization
and effector responses depend on the secretion
20. Antigens
of short-acting soluble molecules called cy-
21. immunoglobulins
tokines. One type of cytokine, chemokines, di-
22. Humoral
rect leukocyte movement and migration, and
23. CD4 helper T cell (TH)
another group of cytokines, the colony-stimu-
24. Regulatory
lating factors, promote the proliferation and
25. bone marrow, thymus
differentiation of bone marrow progenitor
26. spleen
cells. Chemokines give the cells of the immune
system the ability to act systemically as one.
Activity B
2. The innate immune system consists of the
The figure is a schematic model of an epithelial barriers, phagocytic cells (mainly
immunoglobulin G molecule showing the neutrophils and macrophages), natural killer
constant and variable regions of the light and cells, and several plasma proteins, including
dark chains. Each immunoglobulin is composed those of the complement system. These
of two identical light (L) chains and two identical mechanisms are present in the body before
heavy (H) chains to form a Y-shaped molecule. an encounter with an infectious agent and
The two forked ends of the immunoglobulin are rapidly activated by microbes before the
molecule bind antigen and are called Fab development of adaptive immunity. The acti-
(i.e., antigen-binding) fragments, and the tail of vation and regulation of inflammation is also
the molecule, which is called the Fc fragment, a major job of innate immunity.
determines the biologic properties that 3. These phagocytic cells were recruited during
are characteristic of a particular class of an inflammatory response to recognize and
immunoglobulins. The amino acid sequence of kill infectious invaders. The early responding
the heavy and light chains shows constant (C) innate immune cell is the neutrophil, fol-
regions and variable (V) regions. The constant lowed shortly by the more efficient, multi-
regions have sequences of amino acids that vary functional macrophage. They are activated to
little among the antibodies of a particular class of engulf and digest microbes that attach to
immunoglobulin. The constant regions allow their cell membrane. Once the cell is acti-
separation of immunoglobulins into classes (e.g., vated and the microbe is ingested, the cell
IgM, IgG) and allow each class of antibody to generates digestive enzymes, toxic oxygen,
interact with certain effectors cells and and nitrogen intermediates (i.e., hydrogen
molecules. The variable regions contain the peroxide or nitric oxide) through metabolic
antigen-binding sites of the molecule. The pathways. The phagocytic killing of microor-
wide variation in the amino acid sequence of ganisms helps contain infectious agents.
the variable regions seen from antibody to 4. There are three pathways for recognizing mi-
antibody allows this region to recognize its croorganisms that result in activation of the
complementary epitope. A unique amino acid complement system: the classical, the lectin,
sequence in this region determines a distinctive and the alternative pathway. The reactions of
three-dimensional pocket that is complementary the complement systems are divided into
to the antigen, allowing recognition and three phases: (a) initiation or activation, (b)
binding. amplification of inflammation, and (c) mem-
brane attack response.

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392 ANSWERS

5. The MHC molecules involved in self-recogni- circulating antibodies. Passive immunity is

tion and cell-to-cell communication fall into immunity transferred from another source.
two classes: class I and class II. Class I MHC An infant receives passive immunity natu-
molecules are cell surface glycoproteins that rally from the transfer of antibodies from its
interact with the antigen receptor-foreign mother in utero and through a mother’s
peptide complex and the CD8 molecule on T breast milk.
cytotoxic lymphocytes. MHC-I molecules are
found on nearly all nucleated cells in the SECTION III: APPLYING YOUR
body and thereby are capable of alerting the KNOWLEDGE
immune system of any cell changes due to
Activity E
viruses, intracellular bacteria, or cancer.
6. Macrophages are key members of the 1. The nurse will be sure to mention the follow-
mononuclear phagocytic system that engulf ing key points:
and digest microbes and other foreign sub- • Every baby is born with passive immunity.
stances. The monocytes migrate from the • The baby receives antibodies from the
blood to various tissues, where they mature mother through placenta and colostrum.
into the major tissue phagocyte, the • Passive immunity lasts up to 6 months.
macrophages. As the general scavenger cells • Passive immunity is replaced by immunity
of the body, the macrophage can be fixed in a received from immunizations.
tissue or can be free to migrate from an organ
to lymphoid tissues. The tissue macrophages SECTION IV: PRACTICING FOR NCLEX
are scattered in connective tissue or clustered
Activity F
in organs such as the lung (i.e., alveolar
macrophages), liver (i.e., Kupffer cells), 1. a. Rationale: The major components of innate
spleen, lymph nodes, peritoneum, central immunity are the skin and mucous mem-
nervous system (i.e., microglial cells), and branes; phagocytic cells (mainly neutrophils
other areas. Macrophages are activated to en- and macrophages); specialized lymphocytes
gulf and break down complex antigens into called natural killer (NK) cells; and several
peptide fragments for association with class II plasma proteins, including the proteins of the
MHC molecules. Macrophages can then pre- complement system. Adaptive, humoral, and
sent these complexes to the helper T cell so cell-mediated immunity do not use NK cells.
that self–nonself recognition and activation 2. b. Rationale: The actions of cytokines are
of the immune response can occur. often pleiotropic and redundant. Cytokines
7. The immunoglobulins have been divided are not described as rapid and self-limiting,
into five classes: IgG, IgA, IgM, IgD, and IgE. cell specific and targeted, or dendritic and
morphologic.
I. IgG—protects against bacteria, toxins, and
3. c. Rationale: The T lymphocytes (T cells) are
viruses in body fluids and activates the
generated from stem cells in the bone mar-
complement system
row. They complete their maturation in the
II. IgA—serves as a primary defense against
thymus and function in the peripheral tissues
local infections in mucosal tissues
to produce cell-mediated immunity and aid
III. IgM—is first circulating immunoglobulin
in antibody production.
to appear in response to an antigen
4. d. Rationale: Activation of macrophages en-
IV. IgD—serves as an antigen receptor for ini-
sures enhanced phagocytic, metabolic, and
tiating the differentiation of B cells
enzymatic potential, resulting in more effi-
V. IgE—is involved in inflammation, allergic
cient destruction of infected cells. This type
responses, and combating parasitic infec-
of defense is important against intracellular
tions
pathogens such as Mycobacterium species and
8. Active immunity is acquired through immu-
Listeria monocytogenes. Contact dermatitis due
nization or actually having a disease. It is ac-
to a poison ivy reaction or sensitivity to dyes
tive because it depends on a response to the
is an example of delayed or cell-mediated hy-
antigen by the person’s immune system. Due
persensitivity caused by hapten-carrier com-
to memory, the immune system is usually
plexes. Blood transfusions do not cause
able to react within hours to subsequent ex-
hypersensitivity reactions by hapten-carrier
posure to the same agent because of the pres-
complexes.
ence of memory B and T lymphocytes and

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ANSWERS 393

5. a. Rationale: Passive immunity can also be ar- Osteoporosis is the abnormal loss of bone tis-
tificially provided by the transfer of antibod- sue and density. Osteogenesis imperfecta is a
ies produced by other people or animals. genetic disease causing multiple bone frac-
Some protection against infectious disease tures in a newborn. Hydronephrosis is a con-
can be provided by the injection of hyperim- dition of the kidney causing distension of the
mune serum, which contains high concentra- pelvis and calyces due to an obstruction in
tions of antibodies for a specific disease, or the ureter that does not enable urine to pass.
immune serum or gamma-globulin, which 11. Antigens
contains a pool of antibodies from many in- 12. 1-d, 2-e, 3-a, 4-c, 5-b
dividuals providing protection against nu- 13. epithelial
merous infectious agents. Immunizations and 14. b, c. Rationale: Although cells of both innate
allergy shots are examples of active immu- and adaptive immune systems communicate
nity. Exposure to poison ivy can be the cause critical information about the invading mi-
of a hypersensitivity reaction; it is not immu- crobe or pathogen by cell-to-cell contact,
nity. many interactions and effector responses de-
6. b. Rationale: Self-regulation is an essential pend on the secretion of chemical mediators
property of the immune system. An inade- (cytokines, chemokines, and colony-stimulat-
quate immune response may lead to immun- ing factors). Virulence factors define how
odeficiency, but an inappropriate or excessive much power an organism has to produce dis-
response may lead to conditions varying ease. Coxiella are organisms that cause Q
from allergic reactions to autoimmune dis- fever.
eases. All answers are autoimmune diseases 15. b, e. Rationale: The T and B lymphocytes are
except for Huntington disease. the only cells in the body capable of specifi-
7. c. Rationale: The term tolerance is used to de- cally recognizing different antigenic determi-
fine the ability of the immune system to be nants of microbial agents and other
nonreactive to self-antigens while producing pathogens and therefore responsible for two
immunity to foreign agents. All other re- defining characteristics of adaptive immu-
sponses have nothing to do with the recogni- nity, specificity and memory. Phagocytes,
tion of and tolerance to self-antigens. dendritic cells, and natural killer cells all
8. d. Rationale: Cord blood does not normally participate in innate immunity.
contain IgM or IgA. If present, these antibod-
ies are of fetal origin and represent exposure
to intrauterine infection.
CHAPTER 18 INFLAMMATION,
9. a. Rationale: Aging is characterized by a de- TISSUE REPAIR, AND WOUND
clining ability to adapt to environmental HEALING
stresses. One of the factors believed to con-
tribute to this problem is a decline in im- SECTION II: ASSESSING YOUR
mune responsiveness. This includes changes UNDERSTANDING
in cell-mediated and humoral immune re- Activity A
sponses. Elderly persons tend to be more sus-
ceptible to infections, have more evidence of 1. Inflammation
autoimmune and immune complex disorders 2. rubor, tumor, calor, dolor
than younger persons, and have a higher in- 3. systemic
cidence of cancer. None of the other answers 4. Acute, chronic
are true or acceptable. 5. vascular, cellular
10. b. Rationale: Among the functions of the in- 6. leukocytosis
nate immune system is the induction of a 7. Monocyte/macrophages
complex cascade of events known as the in- 8. Vascular
flammatory response. Recent evidence sug- 9. leukocytes
gests that inflammation plays a key role in 10. cell-to-cell
the pathogenesis of a number of disorders, 11. cell migration
such as atherosclerosis and coronary artery 12. chemokines
disease, bronchial asthma, type 2 diabetes 13. metabolic burst
mellitus, rheumatoid arthritis, multiple scle- 14. coagulation, complement
rosis, and systemic lupus erythematosus. 15. dilation, permeability

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394 ANSWERS

16. eicosanoid to histamine release. The tumor, or swelling, is

17. prostaglandins due to an increased permeability of blood ves-
18. cyclooxygenase sels due to histamine and other long-term va-
19. omega-3 fatty acids soactive mediators. The calor, or heat, is the
20. Complement result of increased perfusion of the tissues at
21. kinin, smooth muscle, pain the wound site. Dolor, or pain, is due to
22. tumor necrosis factor- bradykinin, prostaglandins, and histamine ef-
23. superoxide, hydrogen peroxide, hydroxyl fects on sensory nerve endings.
24. endothelial cell damage 2. Acute inflammation is the early (almost imme-
25. exudates diate) reaction of local tissues and their blood
26. penetrate deeply, spread rapidly vessels to injury. It typically occurs before
27. CRP (C-reactive protein) adaptive immunity becomes established and is
28. parenchymal, stromal aimed primarily at removing the injurious
29. Labile cells agent and limiting the extent of tissue damage.
30. stabile Acute inflammation can be triggered by a vari-
31. Granulation ety of stimuli, including infections, immune
32. collagen, fibroblast reactions, blunt and penetrating trauma, phys-
33. premature infant ical or chemical agents, and tissue necrosis
from any cause. In contrast to acute inflamma-
Activity B tion, chronic inflammation is self-perpetuating
1. The figure depicts the cyclooxygenase and and may last for weeks, months, or even years.
lipoxygenase pathways and sites where the It may develop as the result of a recurrent or
corticosteroids and nonsteroidal anti- progressive acute inflammatory process or
inflammatory drugs (NSAIDs) exert their action. from low-grade, smoldering responses that fail
Inflammation is essential to the first to evoke an acute response.
phase of wound healing, and immune mecha- 3. The first pattern is an immediate transient re-
nisms prevent infections that impair wound sponse, which occurs with minor injury. It de-
healing. Among the conditions that impair in- velops rapidly after injury and is usually
flammation and immune function is adminis- reversible and of short duration. Typically, this
tration of corticosteroid drugs. Release of type of leakage affects venules 20 to 60 mm in
arachidonic acid by phospholipases initiates a diameter, leaving capillaries and arterioles un-
series of complex reactions that lead to the affected. The second pattern is an immediate
production of inflammatory mediators. The sustained response, which occurs with more
cyclooxygenase pathway culminates in the serious types of injury and continues for sev-
synthesis of prostaglandins, and the lipoxyge- eral days. It affects all levels of the microcircu-
nase pathway culminates in the synthesis of lation and is usually due to direct damage of
the leukotrienes. Aspirin and the NSAIDs re- the endothelium by injurious stimuli. The
duce inflammation by inactivating the first en- third pattern is a delayed hemodynamic re-
zyme in the cyclooxygenase pathway for sponse in which the increased permeability
prostaglandin synthesis. begins after a delay of 2 to 12 hours, lasts for
several hours or even days, and involves
Activity C venules as well as capillaries. A delayed re-
1. c 2. a 3. i 4. f 5. j sponse often accompanies radiation types of
6. g 7. b 8. h 9. d 10. e injuries.
4. Phagocytosis involves three distinct steps: (a)
Activity D recognition and adherence, (b) engulfment,
and (c) intracellular killing. Phagocytosis is
B D A C initiated by recognition and binding of parti-
cles by specific receptors on the surface of
phagocytic cells. Microbes can be bound di-
Activity E rectly to the membrane of the phagocytic cells
1. These signs are rubor (redness), tumor by several types of pattern recognition recep-
(swelling), calor (heat), and dolor (pain). The tors or indirectly by receptors that recognize
rubor is the result of increased blood flow due microbes coated with carbohydrate-binding
lectins, antibody, and/or complement.

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Endocytosis is accomplished through cytoplas- 8. Depending on the extent of tissue loss, wound
mic extensions that surround and enclose the closure and healing occur by primary or sec-
particle in a membrane-bound phagocytic ondary intention. Small or “clean” wounds
vesicle. Intracellular killing of pathogens is ac- (e.g., a surgical incision) are an example of
complished through several mechanisms, in- healing by primary intention. Larger wounds
cluding toxic oxygen and nitrogen products, that have a greater loss of tissue and contami-
lysozymes, proteases, and defensins. nation heal by secondary intention. Healing
5. Mediators can be classified by function: (a) by secondary intention is slower than healing
those with vasoactive and smooth muscle– by primary intention and results in the forma-
constricting properties such as histamine, tion of larger amounts of scar tissue.
arachidonic acid metabolites, and platelet-acti-
vating factor; (b) plasma proteases that acti- SECTION III: APPLYING YOUR
vate members of the complement system, KNOWLEDGE
coagulation factors of the clotting cascade,
Activity F
and vasoactive peptides of the kinin system;
(c) chemotactic factors such as complement 1. After an injury, the body initiates what is called
fragments and chemokines; and (4) reactive the inflammatory response. This means that
molecules and cytokines liberated from leuko- the body sends cells and fluids that are specific
cytes, which when released into the extracellu- to destroying infectious organisms and healing
lar environment can affect the surrounding the injury to the site of the wound. What you
tissue and cells. are seeing on the bandages is a serous exudate
6. The types of chronic inflammation are non- from the plasma in the circulatory system that
specific and granulomatous. Nonspecific has responded to the burn injury.
chronic inflammation involves a diffuse accu- 2. The body’s response to an injury activates
mulation of macrophages and lymphocytes at many different types and kinds of cells. This
the site of injury. Ongoing chemotaxis causes response is called the acute phase response,
macrophages to infiltrate the inflamed site, and some of the cells that are released during
where they accumulate owing to prolonged this response act on the central nervous sys-
survival and immobilization. These mecha- tem. Their actions can cause outward manifes-
nisms lead to fibroblast proliferation, with tations of their work, such as anorexia,
subsequent scar formation that in many cases somnolence, and malaise.
replaces the normal connective tissue or the
functional parenchymal tissues of the in- SECTION IV: PRACTICING FOR NCLEX
volved structures. A granulomatous lesion is a Activity G
small, 1- to 2-mm lesion in which there is a
1. a. Rationale: The classic description of inflam-
mass of epithelioid cells surrounded by lym-
phocytes. Granulomatous inflammation is mation has been handed down through the
associated with foreign bodies and with ages. In the first century AD, the Roman
microorganisms that are poorly digested and physician Celsus described the local reaction
usually not easily controlled by other inflam- of injury in terms now known as the cardinal
matory mechanisms. signs of inflammation. These signs are rubor
(redness), tumor (swelling), calor (heat), and
7. The acute phase response includes changes in
dolor (pain). In the second century AD, the
the concentrations of plasma proteins, skeletal
Greek physician Galen added a fifth cardinal
muscle catabolism, negative nitrogen balance,
sign, functio laesa (loss of function).
elevated erythrocyte sedimentation rate, and
Altered level of consciousness is not a car-
increased numbers of leukocytes. These re-
dinal sign of inflammation. Sepsis and fever
sponses are generated by the release of cy-
are systemic signs of infection.
tokines that affect the thermoregulatory
2. b, c, e. Rationale: Eosinophils, basophils, and
center in the hypothalamus to produce fever.
mast cells produce lipid mediators and cy-
The metabolic changes provide amino acids
tokines that induce inflammation. They are
that can be used in the immune response and
particularly important in inflammation associ-
for tissue repair. In general, the acute phase re-
sponse serves to coordinate the various ated with immediate hypersensitivity reactions
changes in body activity to enable an optimal and allergic disorders. Neutrophils and
host response. macrophages are white blood cells that

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396 ANSWERS

respond to inflammation and destroy invading fibroblasts and deposition of collagen fibers.
bacteria. They do not induce inflammation. All wounds are contaminated at the time of
3. b. Rationale: Chronic inflammation involves injury. Although body defenses can handle
the proliferation of fibroblasts instead of exu- the invasion of microorganisms at the time of
dates. As a result, the risk of scarring and de- wounding, badly contaminated wounds can
formity is usually greater than in acute overwhelm host defenses. Trauma and exist-
inflammation. Chronic inflammation is not ing impairment of host defenses can also
the persistent destruction of healthy tissue. contribute to the development of wound
Typically, agents that cause chronic inflam- infections.
mation do not penetrate deeply or spread 9. c. Rationale: Histamine causes dilation of
rapidly. Acute inflammation, not chronic, is arterioles and increases the permeability of
the result of allergic reactions. venules. It acts at the level of the microcircu-
4. b, d, e. Rationale: Wound healing is com- lation by binding to histamine 1 receptors on
monly divided into three phases: (a) the in- endothelial cells and is considered the princi-
flammatory phase, (b) the proliferative phase, pal mediator of the immediate transient
and (c) the maturational or remodeling phase of increased vascular permeability in
phase. There is no activation or nutritional the acute inflammatory response. Arachi-
phase in wound healing. donic acid is a 20-carbon unsaturated fatty
5. c. Rationale: An increase in tissue oxygen ten- acid found in phospholipids of cell mem-
sion by hyperbaric oxygen enhances wound branes. Release of arachidonic acid by phos-
healing by a number of mechanisms, includ- pholipases initiates a series of complex
ing the increased killing of bacteria by neu- reactions that lead to the production of the
trophils, impaired growth of anaerobic eicosanoid family of inflammatory mediators
bacteria, and promotion of angiogenesis and (prostaglandins, leukotrienes, and related
fibroblast activity. Eosinophil activity is not metabolites). Fibroblasts and cytokines are
affected by hyperbaric treatment of wounds. not the principal mediator of the transient
6. b. Rationale: Animal and human bites are par- phase of an acute inflammatory response.
ticularly troublesome in terms of infection. 10. a. Rationale: The most prominent systemic
The animal inflicting the bite, the location of manifestations of inflammation include the
the bite, and the type of injury are all impor- acute phase response, alterations in white
tant determinants of whether the wound be- blood cell count (leukocytosis or leukopenia),
comes infected. Approximately 28% to 80% of and fever. A widening pulse pressure is not
all cat bites become infected. Dog bites, for indicative of systemic inflammation, and
unclear reasons, become infected only approx- thrombocytopenia is a hematologic disorder,
imately 3% to 18% of the time. Bites inflicted not an indication of systemic inflammation.
by children are usually superficial and seldom
become infected, whereas bites inflicted by
adults have a much higher rate of infection.
CHAPTER 19 DISORDERS OF THE
7. c. Rationale: The child has a greater capacity for IMMUNE RESPONSE
repair than the adult but may lack the reserves
needed to ensure proper healing. This lack of SECTION II: ASSESSING YOUR
reserves is evidenced by an easily upset elec- UNDERSTANDING
trolyte balance, sudden elevation or lowering Activity A
of temperature, and rapid spread of infection.
1. immune
The neonate and small child may have an im-
2. Immunodeficiency
mature immune system with no antigenic ex-
3. innate
perience with organisms that contaminate
4. adaptive
wounds. The younger the child, the more
5. humoral, cellular
likely that the immune system is not fully de-
6. X
veloped. The skin of a neonate or a small child
7. pyogenic
is not as fragile as the skin of an elderly person.
8. maternal
8. c. Rationale: Infection impairs all dimensions
9. antibody
of wound healing. It prolongs the inflamma-
10. kidney
tory phase, impairs the formation of granula-
11. malignancies
tion tissue, and inhibits proliferation of

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12. CD4 helper, CD8 cytotoxic Activity C

13. T lymphocytes
1. e 2. h 3. l 4. a 5. f
14. combined immunodeficiency
6. m 7. d 8. k 9. i 10. c
15. severe combined immunodeficiency
11. n 12. j 13. g 14. B 15. o
16. boys
17. complement Activity D
18. secondary
19. degranulation 3 5 1 4 2
20. respiratory burst
21. Hypersensitivity
Activity E
22. allergic reactions
23. Anaphylaxis 1. A primary deficiency or immunodeficiency is
24. atopic congenital or inherited. Secondary immunod-
25. rhinitis eficiency is acquired.
26. type II 2. During the first few months of life, infants are
27. ADCC protected from infection by IgG antibodies
28. Type III that have been transferred from the maternal
29. Serum circulation during fetal life. An infant’s level of
30. Arthus reaction maternal IgG gradually declines over a period
31. type IV reactions of approximately 6 months. Concomitant
32. contact dermatitis with the loss of maternal antibody, the in-
33. transplantation fant’s immature humoral immune system
34. autologous, syngeneic, allogeneic begins to function, and between the ages of
35. Graft-versus-host-disease 1 and 2 years, the child’s antibody production
36. Autoimmune reaches adult levels. Once the level of mater-
37. self-tolerance nal antibodies drops, the infant is susceptible
38. autoantibodies to infection.
3. Type I hypersensitivity reactions begin with
Activity B mast cell or basophil sensitization. During the
sensitization or priming stage, allergen-specific
IgE antibodies attach to receptors on the sur-
Bone marrow face of mast cells and basophils. With subse-
quent exposure, the sensitizing allergen binds
to the cell-associated IgE and triggers a series
of events that ultimately lead to degranulation
Pre-T cells of the sensitized mast cells or basophils, caus-
ing release of their preformed mediators. Mast
cells are also the source of lipid-derived mem-
brane products (e.g., prostaglandins,
Thymus
leukotrienes) and cytokines that participate in
the continued response to the allergen.
Self-antigen 4. In direct cell-mediated cytotoxicity, CD8 cy-
not expressed
in thymus
tolytic T lymphocytes (CTLs) directly kill the
antigen-presenting target cells. In viral infec-
tions, CTL responses can lead to tissue injury
Self-reactive clones Nonreactive clones Self-reactive clones by killing infected target cells even if the virus
itself has no cytotoxic effects. Because CTLs
Apoptosis
Failure of Activation-
cannot distinguish between cytopathic and
antigens to induced noncytopathic viruses, they kill virtually all
activate apoptosis
Development of
lymphocyte infected cells regardless of whether the infec-
central tolerance
A Induction of normal tion is harmful. Delayed-type hypersensitivity
immune function with
self versus nonself Clonal anergy reactions occur in response to soluble pro-
B recognition tein antigens and primarily involve antigen-
presenting cells such as macrophages and
Induction of peripheral tolerance
C CD4 helper T cells of the TH1 type. During

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398 ANSWERS

the reaction, TH1 cells are activated and secrete from the maternal circulation during fetal
an array of cytokines that recruit and activate life. IgA, IgM, IgD, and IgE do not normally
monocytes, lymphocytes, fibroblasts, and cross the placenta.
other inflammatory cells. These T-cell– 2. a, b, c, d. Rationale: Medications that cause re-
mediated responses require the synthesis of versible secondary hypogammaglobulinemia
effector molecules and take 24 to 72 hours to include the disease-modifying antirheumatic
develop, which is why they are called delayed- drugs; corticosteroid agents; and the
type hypersensitivity disorders. antiepileptic drugs, phenytoin and carba-
5. Severe combined immunodeficiency (SCID) is mazepine. Interferon-beta 1a drugs are used
the result of genetic mutations that lead to in the treatment of autoimmune disorders.
absence of all T- and B-cell function and, in 3. a. Rationale: In general, persons with cell-me-
some cases, a lack of natural killer cells. Af- diated immunodeficiency disorders have in-
fected infants have a disease course that re- fections or other clinical problems that are
sembles AIDS, with failure to thrive, chronic more severe than antibody disorders. Chil-
diarrhea, and opportunistic infections. Sur- dren with defects in this branch of the im-
vival beyond the first year of life is rare with- mune response rarely survive beyond infancy
out prompt immune reconstitution through or childhood, unless immunologic reconsti-
bone marrow or hematopoietic stem cell trans- tution is achieved through bone marrow
plantation. Early diagnosis is critical because transplantation. In DiGeorge syndrome, chil-
the chances of successful treatment are highest dren who survive the immediate neonatal pe-
in infants who have not experienced severe riod may have recurrent or chronic infections
opportunistic infections. There is also hope because of impaired T-cell immunity.
that gene therapy will someday be available, Children may also have an absence of im-
for some, if not all, forms of SCID. munoglobulin production, caused by a lack
of helper T-cell function. X-linked immunod-
SECTION III: APPLYING YOUR eficiency with hyper-IgM, the X-linked im-
KNOWLEDGE munodeficiency of hyper-IgM, also known as
the hyper-IgM syndrome, is characterized by
Activity F
low IgG and IgA levels with normal or, more
1. The correct response would include informa- frequently, high IgM concentrations. X-
tion about the antinuclear antibodies test. The linked agammaglobulinemia is a primary
basis for most serologic assays is the demon- humeral immunodeficiency disorder. Y-
stration of antibodies directed against tissue linked agammaglobulinemia does not exist.
antigens or cellular components. For example, 4. b. Rationale: Disorders that affect both B and
a child with chronic or acute history of fever, T lymphocytes, with resultant defects in both
arthritis, and a macular rash along with high humoral and cell-mediated immunity, fall
levels of antinuclear antibody has a probable under the broad classification of combined
diagnosis of systemic lupus erythematous. The immunodeficiency syndrome. A single muta-
detection of autoantibodies in the laboratory tion in any one of the many genes that influ-
is usually accomplished by one of three meth- ence lymphocyte development or response,
ods: indirect fluorescent antibody assays, en- including lymphocyte receptors, cytokines,
zyme-linked immunosorbent assay, or particle or major histocompatibility antigens, could
agglutination of some kind. lead to combined immunodeficiency.
2. Medications used in the treatment of systemic 5. c. Rationale: Ataxia-telangiectasia is a com-
lupus erythematous include corticosteroids plex syndrome of neurologic, immunologic,
(prednisone) and immunosuppressive endocrinologic, hepatic, and cutaneous ab-
(cytotoxic) agents (azathioprine, cyclophos- normalities. Pierre-Robin syndrome, Angel-
phamide, methotrexate). man syndrome, and Adair-Dighton syndrome
are not immunologic deficiencies.
SECTION IV: PRACTICING FOR NCLEX 6. a. Rationale: Disorders caused by immune re-
Activity G sponses are collectively referred to as hyper-
sensitivity reactions. Antigens cause allergic
1. c. Rationale: During the first few months of
reactions. Mediator response action and aller-
life, infants are protected from infection by gen stimulating reaction have nothing to do
IgG antibodies that have been transferred with hypersensitivity reactions.

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ANSWERS 399

7. b. Rationale: Anaphylaxis is a systemic life- 6. percutaneous inoculation; needle stick

threatening hypersensitivity reaction charac- 7. CD4 T lymphocytes, macrophages, dendritic
terized by widespread edema, vascular shock 8. antibody-producing B lymphocytes, cell-me-
secondary to vasodilation, and difficulty diated
breathing. It is not called an antigen reaction 9. interrupt
or an Arthus reaction. 10. CD4 T
8. c. Rationale: Serum sickness is a systemic im- 11. Opportunistic
mune complex disorder that is triggered by 12. bacterial pneumonia, tuberculosis
the deposition of insoluble antigen-antibody 13. Wasting
(IgM, IgG, and, occasionally, IgA) complexes 14. lipodystrophy
in blood vessels, joints, heart, and kidney tis- 15. low-risk; risk-free
sue. This is not anti-immune disease, systemic 16. antibody
lupus erythematosus, or antigen-antibody 17. western blot
sickness. 18. DNA
9. d. Rationale: Cornstarch powder is applied to 19. decrease, eradicate
the gloves during the manufacturing process 20. depression, anxiety
to prevent stickiness and give the gloves a 21. Polymerase chain reaction testing
smooth feel. The cornstarch glove powder
has an important role in the allergic re- Activity B
sponse. Latex proteins are readily absorbed by 1. h 2. e 3. i 4. c 5. a
glove powder and become airborne during re- 6. f 7. b 8. d 9. g
moval of the gloves. Baking powder is not
used inside gloves. Pieces of latex that be- Activity C :
come airborne and latex proteins that attach The steps of viral replication are as follows:
to clothing are not significant contributors to 1. Binding of the virus to the CD4 T cell
the incidence of latex allergy. 2. Attachment and uncoating of the virus,
10. antidonor. Rationale: When preformed anti- allowing the genetic material to enter the
donor antibodies are present, rejection occurs host cell
immediately after transplantation. 3. DNA synthesis via reverse transcriptase
11. a, b, d. Rationale: Because autoimmunity 4. Integration into the host DNA
does not develop in all persons with genetic 5. Transcription of viral DNA into mRNA
predisposition, it appears that other factors 6. Translation of mRNA into a protein
such as a “trigger event” interact to precipi- 7. Cleavage of protein product into separate pro-
tate the altered immune state. The event or teins for new viruses
events that trigger the development of an au- 8. Assemblage of new HIV
toimmune response are unknown. It has
been suggested that the “trigger” may be a Activity D
virus or other microorganism, a chemical 1. HIV replication involves the killing of the
substance, or a self-antigen from a body tis- CD4 T cell and the release of copies of HIV
sue that has been hidden from the immune into the bloodstream. These virions invade
system during development. other CD4 T cells, allowing the infection to
progress. Every day, millions of infected CD4
CHAPTER 20 ACQUIRED T cells are destroyed, releasing billions of viral
particles into the bloodstream; nearly all CD4
IMMUNODEFICIENCY SYNDROME T cells are replaced; and nearly all viral parti-
cles are destroyed. As the years progress, the
SECTION II: ASSESSING YOUR CD4 cell count gradually decreases through
UNDERSTANDING this process, and the number of viruses de-
Activity A tected in the blood of persons infected with
1. HIV, immunosuppression, opportunistic HIV increases, resulting in decreased activa-
2. retrovirus tion of B and T cells.
3. sexual, blood-to-blood, perinatally 2. The three phases are the primary infection
4. Sexual phase, chronic asymptomatic or latency
5. blood phase, and overt AIDS phase. In the primary

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400 ANSWERS

infection phase, the signs and symptoms (e.g., • Tests for opportunistic infections
fever, malaise, fatigue) usually appear 1 to 4 • Complete blood count
weeks after exposure to HIV and last 7 to 10 • Sedimentation rate
days. After several weeks, the immune system • Culture and sensitivity tests
acts to control viral replication and reduces • U.S. Department of Health and Human
the viral load to a stable level. In the chronic Services Guidelines for the treatment of
asymptomatic phase, which lasts about 10 HIV/AIDS
years, the patient is symptom free. Slowly, the • HAART
CD4 cell count drops from 1000 cells/_L to • Antiviral drugs and what they are used for
200 cells/L. In the overt AIDS phase, CD4 • Treatment of opportunistic infections
counts are below 200 cells/L. The risk of op- as/when they occur
portunistic infections and death increases • Support for psychosocial issues
significantly. 2. The evaluation will include a complete his-
3. The goal of HAART is sustained suppression of tory, physical evaluation, and baseline labo-
HIV replication, resulting in an undetectable ratory tests, and a plan of care will be devel-
viral load and an increasing CD4 cell count. oped based on symptoms, viral load, and cell
In general, antiviral therapies are prescribed to count. Routine follow-up care of a stable,
slow the progression to AIDS and improve the asymptomatic HIV-infected patient should
overall survival time of persons with HIV in- include a history and physical examination
fection. along with CD4 cell count and viral load
4. Reverse transcriptase inhibitors inhibit HIV testing every 3 to 4 months. Persons who
replication by acting on the enzyme reverse are symptomatic may need to be seen more
transcriptase by either blocking elongation or frequently.
copying. Protease inhibitors bind to the pro-
tease enzyme and inhibit its action, prevent- SECTION IV: PRACTICING FOR NCLEX
ing the cleavage of the polyprotein chain into
Activity F
individual proteins, which would be used to
construct the new virus. Entry inhibitors pre- 1. b, c, d. Rationale: HIV is transmitted from
vent HIV from entering or fusing with the one person to another through sexual con-
CD4 cell, thus blocking HIV from inserting tact, blood-to-blood contact, or perinatally.
its genetic information into the CD4 T cell. It is not transmitted through casual contact.
Integrase inhibitors block the integration step Several studies involving more than 1,000
of the viral cycle, thus preventing the ability uninfected, nonsexual household contacts
of HIV’s genome to integrate into the host’s with persons with HIV infection (including
genome. siblings, parents, and children) have shown
5. Infected women may transmit the virus to no evidence of casual transmission. HIV is
their offspring in utero, during labor and de- not spread by mosquitoes or other insect
livery, or through breast milk. The risk of vectors.
transmission is increased if the mother has 2. b, h, a, e, f, g, c, d. Rationale: Replication of
advanced HIV disease, prolonged time from HIV occurs in eight steps. The first step in-
rupture of membranes to delivery, if the volves the binding of the virus to the CD4
mother breast-feeds the child, or if there is in- T cell. The second step allows for the inter-
creased exposure of the fetus to maternal nalization of the virus. The third step con-
blood. sists of DNA synthesis. The fourth step is
called integration. The fifth step involves
transcription of the double-stranded viral
SECTION III: APPLYING YOUR
DNA to form a single-stranded messenger
KNOWLEDGE
RNA (mRNA) with the instructions for build-
Activity E ing new viruses. The sixth step includes
1. The nurse should include the following: translation of mRNA. The seventh step is
• Information on lab tests that will need to be called cleavage. Finally, during the eighth
done: step, the proteins and viral RNA are assem-
• Viral load testing every 3–4 months bled into new HIV viruses and released from
• CD4 cell count every 3–4 months the CD4 T cell.

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ANSWERS 401

3. a. Rationale: The typical course of HIV is de- 8. b. Rationale: The HIV antibody test procedure
fined by three phases, which usually occur consists of screening with an enzyme im-
over a period of 8 to 12 years. The three munoassay (EIA), also known as enzyme-
phases are the primary infection phase, linked immunoabsorbent assay (ELISA),
chronic asymptomatic or latency phase, and followed by a confirmatory test, the western
overt AIDS phase. There is no identified blot assay, which is performed if the EIA is
conversion phase. positive. The complete metabolic panel can-
4. b. Rationale: Opportunistic infections in- not diagnose HIV/AIDS. The diagnostic test
volve common organisms that normally do for HIV/AIDS is the ELISA, not the ALEA. The
not produce infection unless there is im- confirmatory test for HIV/AIDS is not the
paired immune function. Although a person eastern blot test.
with AIDS may live for many years after the 9. c. Rationale: Because different drugs act on
first serious illness, as the immune system different stages of the replication cycle, opti-
fails, these opportunistic illnesses become mal treatment includes a combination of at
progressively more severe and difficult to least two to three drugs, often referred to as
treat. HAART. The goal of HAART is sustained sup-
5. c. Rationale: The most common causes of res- pression of HIV replication, resulting in an
piratory disease in persons with HIV infec- undetectable viral load and an increasing
tion are bacterial pneumonia, Pneumocystis CD4 cell count. The other treatments are
carinii pneumonia (PCP), and pulmonary tu- not used in the treatment of HIV/AIDS.
berculosis. The best predictor of PCP is a 10. a. Rationale: In 1997, wasting became an
CD4 cell count below 200 cell/L, and it is AIDS-defining illness. The syndrome is com-
at this point that prophylaxis with trimetho- mon in persons with HIV infection or AIDS.
prim-sulfamethoxazole (or an alternative Wasting is characterized by involuntary
agent in the case of adverse reactions to sulfa weight loss of at least 10% of baseline body
compounds) is strongly recommended. weight in the presence of diarrhea, more than
Trimethobenzamide, triamterene, and trim- two stools per day, or chronic weakness and
ipramine are drugs that are not used as pro- fever. This diagnosis is made when no other
phylactics against opportunistic respiratory opportunistic infections or neoplasms can be
infections in people with HIV/AIDS. identified as causing these symptoms. Beal
6. a, c, e. Rationale: More than 50% of people syndrome and WAGAR syndrome are not
with skin lesions also have gastrointestinal le- identified with HIV/AIDS. AIDS is not a rec-
sions. Gastrointestinal tract Kaposi sarcoma is ognized syndrome.
often asymptomatic, but can cause pain, 11. a, b, c. Rationale: These reactions may be in-
bleeding, or obstruction. Rectal burning and fluenced by inadequate information, fear of
diarrhea are not symptoms of Kaposi sarcoma contagion, shame, prejudices, and condem-
of the gastrointestinal tract. nation of risk behaviors. Acknowledging a di-
7. c. Rationale: Because there is no cure for HIV agnosis of HIV or AIDS may be the first
or AIDS, adopting riskfree or low-risk behav- indication to family and colleagues of an oth-
ior is the best protection against the disease. erwise hidden lifestyle (i.e., homosexuality,
Abstinence or a long-term, mutually monoga- drug use). This increases the strain on rela-
mous sexual relationship between two unin- tionships with important support persons.
fected partners is the best way to avoid HIV Shock is a common reaction people have
infection and other sexually transmitted dis- when they are diagnosed with HIV, often fol-
eases. Correct and consistent use of latex con- lowed by anger at themselves or others and
doms can provide protection from HIV by denial or guilt. In addition to the fear and
not allowing contact with semen or vaginal grief associated with death, the person with
secretions during intercourse. Natural or HIV or AIDS may also experience uncertainty
lambskin condoms do not provide the same and may feel helpless, hopeless, stigmatized,
protection from HIV as latex because of the and out of control. Acceptance of the lifestyle
larger pores in the material. Only water-based may also have occurred prior to the diagnosis
lubricants should be used with condoms be- of HIV/AIDS.
cause petroleum (oil-based) products weaken 12. b. Rationale: The risk of transmission is in-
the structure of the latex. creased if the mother has advanced HIV

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402 ANSWERS

disease, as evidenced by low CD4 cell Activity B

counts, high levels of HIV in the blood (high
1.
viral load), prolonged time from rupture of
External
membranes to delivery, or breast-feeds the jugular vein Internal
child, or if there is increased exposure of the Subclavian vein jugular vein

fetus to maternal blood.

Superior
vena cava
Aortic arch
CHAPTER 21 STRUCTURE AND
FUNCTION OF THE
CARDIOVASCULAR SYSTEM Right
atrium
Left atrium

SECTION II: ASSESSING YOUR Left coronary

UNDERSTANDING artery

Activity A
Left
1. oxygen, waste, hormones Pericardium
ventricle

2. pulmonary, systemic Right

Right coronary ventricle
3. pulmonary Pleura Posterior
artery
4. systemic
5. low
Left
6. atria, ventricles Right ventricle ventricle
7. same Interventricular
septum
8. volume, pressure
9. hemodynamics Anterior

10. large
11. Viscosity 2.
12. Turbulent
Superior vena cava
13. thicker
14. distensibility
15. aortic, pulmonic
Right pulmonary
16. precedes artery
Left pulmonary
artery
17. elastic Pulmonic valve

18. Diastole Pulmonary veins

19. stroke volume Pulmonary Left atrium
veins Aortic valve
20. ejection
Mitral valve
21. cardiac output Right atrium
Tricuspid valve Chordae
22. cardiac reserve tendineae
23. Frank-Starling Left
ventricle
24. heart rate Right ventricle Papillary
25. tunica adventitia, tunica media, tunica intima muscles
Inferior vena cava
26. arterial pressure pulse
27. decreases Papillary muscles

28. central venous pressure

29. Valves Descending
aorta
30. Autoregulation
31. hyperemia Activity C
32. anastomotic
1. d 2. b 3. j 4. c 5. i
33. microcirculation
6. h 7. e 8. f 9. a 10. g
34. capillary pores
35. colloidal osmotic Activity D
36. medulla oblongata
1. The most important factors governing the flow
37. sympathetic, parasympathetic
of blood in the cardiovascular system are pres-
38. Cushing reflex
sure, resistance, and flow. Blood flow (F) through
a vessel or series of blood vessels is determined

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by the pressure difference ( P) between the two SECTION III: APPLYING YOUR
ends of a vessel (the inlet and the outlet) and the KNOWLEDGE
resistance (R) that blood must overcome as it
moves through the vessel (F P/R). Activity E
2. This is because, even though each individual 1. You would give this client nitroglycerin and
capillary is very small, the total cross-sectional calcium channel blocking drugs to reverse the
area of the systemic capillaries greatly exceeds spasm of the artery.
the cross-sectional area of other parts of the
circulation. Because of this large surface area, SECTION IV: PRACTICING FOR NCLEX
the slower movement of blood allows ample Activity F
time for exchange of nutrients, gases, and
metabolites between the tissues and the 1. a. Rationale: The total blood volume is a func-
blood. tion of age and body weight, ranging from 85
3. The anatomic arrangement of the actin and to 90 mL/kg in the neonate and from 70 to
myosin filaments in the myocardial muscle 75 mL/kg in the adult.
fibers is such that the tension or force of 2. b. Rationale: The blood vessels and the blood
contraction is dependent on the degree to vessel itself constitute resistance to flow. A
which the muscle fibers are stretched just be- helpful equation for understanding the rela-
fore the ventricles begin to contract. The tionship between resistance, blood vessel di-
maximum force of contraction and cardiac ameter (radius), and blood viscosity factors
output is achieved when venous return pro- that affect blood flow was derived by the
duces an increase in left ventricular end dias- French physician Poiseuille more than a cen-
tolic filling (i.e., preload) such that the tury ago. The other laws do not address resis-
muscle fibers are stretched about two and tance to flow.
one-half times their normal resting length. 3. b. Rationale: Compliance refers to the total
When the muscle fibers are stretched to this quantity of blood that can be stored in a given
degree, there is optimal overlap of the actin portion of the circulation for each millimeter
and myosin filaments needed for maximal rise in pressure. Compliance reflects the disten-
contraction. sibility of the blood vessel. Wall tension,
4. Sympathetic innervation via -adrenergic re- laminar blood flow, and resistance are not
ceptors is excitatory in that they produce vaso- major factors in the distensibility of the blood
constriction; -adrenergic receptors are vessel.
inhibitory in that they produce vasodilation. 4. c. Rationale: The Cushing reflex is a special
Smooth muscle contraction and relaxation type of central nervous system (CNS) reflex
also occur in response to local tissue factors, resulting from an increase in intracranial pres-
such as lack of oxygen, increased hydrogen sure (ICP). When the ICP rises to levels that
ion concentrations, and excess carbon diox- equal intraarterial pressure, blood vessels to
ide. Nitric oxide acts locally to produce the vasomotor center become compressed,
smooth muscle relaxation and regulate blood initiating the CNS ischemic response. The
flow. purpose of this reflex is to produce a rise in
5. The factors that travel in the bloodstream that arterial pressure to levels above ICP so that
will regulate blood flow are as follows: the blood flow to the vasomotor center can be
reestablished. If the ICP rises to the point that
• Norepinephrine—potent vasoconstrictor the blood supply to the vasomotor center be-
• Epinephrine—mild vasoconstriction or dila- comes inadequate, vasoconstrictor tone is
tion, depending on the receptor type found lost, and the blood pressure begins to fall. The
in target tissue elevation in blood pressure associated with
• Angiotensin II—powerful vasoconstrictor the Cushing reflex is usually of short duration
• Histamine—powerful vasodilator and can and should be considered a protective homeo-
increase permeability static mechanism. The brain and other cere-
• Serotonin—vasoconstrictor bral structures are located within the rigid
• Bradykinin—vasodilator confines of the skull, with no room for expan-
• Prostaglandins—vasodilator or vasoconstric- sion, and any increase in ICP tends to com-
tor, depending on type of prostaglandin press the blood vessels that supply the brain.

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404 ANSWERS

5. c. Rationale: In clinical practice, the measure- into the right and left thoracic ducts. The
ment of the cardiac forms of troponin T and thoracic ducts empty into the circulation at
troponin I are used in the diagnosis of my- the junctions of the subclavian and internal
ocardial infarction. Troponin C is not diag- jugular veins. The lymphatic system only
nostic of a myocardial infarction. Troponin A joins the vascular system in one place, so no
is not one of the troponin complexes. other answer is accurate.
6. d. Rationale: Approximately 60% of the stroke 13. b. Rationale: The medullary cardiovascular
volume is ejected during the first quarter of neurons are grouped into three distinct pools
systole, and the remaining 40% is ejected that lead to sympathetic innervation of the
during the next two quarters of systole. Little heart and blood vessels and parasympathetic
blood is ejected from the heart during the last innervation of the heart. The first two, which
quarter of systole, although the ventricle re- control sympathetic-mediated acceleration of
mains contracted. heart rate and blood vessel tone, are called the
7. a. Rationale: With peripheral arterial disease, vasomotor center. The third, which controls
there is a delay in the transmission of the re- parasympathetic-mediated slowing of heart
flected wave so that the pulse decreases rather rate, is called the cardioinhibitory center.
than increases in amplitude.
8. b. Rationale: The efficiency of the heart as a
pump is often measured in terms of cardiac
CHAPTER 22 DISORDERS OF
output (CO), or the amount of blood the BLOOD FLOW IN THE SYSTEMIC
heart pumps each minute. The CO is the CIRCULATION
product of the stroke volume (SV) and the
heart rate (HR), and can be expressed by the SECTION II: ASSESSING YOUR
equation: CO SV  HR. AV stands for atri- UNDERSTANDING
oventricular, and EF stands for ejection frac-
tion. Neither is part of the equation for CO. Activity A
9. b, c, d, e. Rationale: The heart’s ability to in- 1. blood vessels
crease its output according to body needs 2. endothelium
mainly depends on four factors: the preload, 3. vasoconstriction, dilation
or ventricular filling; the afterload, or 4. ischemia
resistance to ejection of blood from the heart; 5. Infarction
cardiac contractility; and the heart rate. Car- 6. cholesterol
diac reserve does not add to the heart’s ability 7. cholesterol, triglyceride
to increase its output. 8. lipoproteins
10. d. Rationale: The fact that nitric oxide is re- 9. lipolytic
leased into the vessel lumen (to inactivate 10. small intestine, liver
platelets) and away from the lumen (to relax 11. Chylomicrons
smooth muscle) suggests that it protects 12. bad cholesterol
against both thrombosis and vasoconstric- 13. low-density lipoprotein receptors, scavenger
tion. Nitroglycerin, which is used in treat- 14. atherosclerosis
ment of angina, produces its effects by 15. good cholesterol
releasing nitric oxide in vascular smooth 16. coronary heart disease
muscle of the target tissues. None of the 17. genetic
other answers are released by nitroglycerin. 18. secondary
11. a. Rationale: The osmotic pressure caused by 19. lower, elevate
the plasma proteins in the blood tends to 20. Atherosclerosis
pull fluid from the interstitial spaces back 21. hypercholesterolemia
into the capillary. This pressure is termed col- 22. Cigarette smoking
loidal osmotic pressure to differentiate the os- 23. inflammation
motic effects of the plasma proteins, which 24. C-reactive protein
are suspended colloids, from the osmotic ef- 25. Homocysteine
fects of substances such as sodium and glu- 26. free radicals
cose, which are dissolved crystalloids. 27. vasculitides
12. c. Rationale: The lymph capillaries drain into 28. embolus
larger lymph vessels that ultimately empty 29. Thromboangiitis obliterans

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ANSWERS 405

30. Raynaud phenomenon 2. High-calorie diets increase the production of

31. aneurysm very low-density lipoprotein (VLDL) with
32. asymptomatic, rupture triglyceride elevation and high conversion of
33. hemorrhage VLDL to low-density lipoprotein (LDL). Excess
34. valves ingestion of cholesterol may reduce the forma-
35. deep vein thrombosis tion of LDL receptors and thereby decrease LDL
36. Venous insufficiency removal. Diets that are high in triglycerides and
37. stasis of blood, increased blood coagulability, saturated fats increase cholesterol synthesis and
vessel wall injury suppress LDL receptor activity. In diabetes mel-
litus and the metabolic syndrome, typical dys-
Activity B lipidemia is seen with elevation of triglycerides,
LUMEN low high-density lipoprotein, and minimal or
CAP Macrophage
Smooth muscle cells modest elevation of LDL.
3. Lipid-lowering drugs work in several ways, in-
Endothelial cell
cluding decreasing cholesterol production, de-
Lymphocytes
creasing cholesterol absorption from the
SHOULDER intestine, or removing cholesterol from the
bloodstream. Drugs that act directly to de-
NECROTIC
CORE crease cholesterol levels also have the benefi-
Lipid-laden
cial effect of further lowering cholesterol levels
macrophage by stimulating the production of additional
ELASTIC MEDIA low-density lipoprotein receptors.
4. The seven signs and symptoms of acute arter-
ial occlusion are (a) pistol shot (acute onset),
(b) pallor, (c) polar (cold), (d) pulselessness,
(e) pain, (f) paresthesia, and (g) paralysis.
Activity C 5. Ischemia due to vasospasm causes changes in
skin color that progress from pallor to
1. h 2. i 3. g 4. j 5. d
cyanosis, a sensation of cold, and changes in
6. a 7. f 8. c 9. e 10. b
sensory perception, such as numbness and tin-
Activity D
gling. After the ischemic episode, there is a pe-
Following is the sequence of events of atheroscle- riod of hyperemia with intense redness,
rotic pathogenesis: throbbing, and paresthesias. In severe, pro-
1. Endothelial injury gressive cases usually associated with Raynaud
2. Foam cell formation phenomenon, trophic changes may develop.
3. Development of fatty streak The nails may become brittle, and the skin
4. Formation of fibrofatty plaque over the tips of the affected fingers may
5. Complicated lesion thicken. Ulceration and superficial gangrene of
the fingers, although infrequent, may occur.
Activity E 6. During muscle contraction, which is similar to
1. Once believed to be nothing more than a lin- systole, valves in the communicating channels
ing for blood vessels, it is now known that the close to prevent backward flow of blood into
endothelium is a versatile, multifunctional tis- the superficial system, as blood in the deep
sue that plays an active role in controlling vas- veins is moved forward by the action of the
cular function. As a semipermeable contracting muscles. During muscle relax-
membrane, the endothelium controls the ation, which is similar to diastole, the commu-
transfer of molecules across the vascular wall. nicating valves open, allowing blood from the
The endothelium also plays a role in the con- superficial veins to move into the deep veins.
trol of platelet adhesion and blood clotting,
modulation of blood flow and vascular resis- SECTION III: APPLYING YOUR
tance, metabolism of hormones, regulation of KNOWLEDGE
immune and inflammatory reactions, and Activity F
elaboration of factors that influence the
growth of other cell types, particularly vascu- 1. The nurse would expect to receive the follow-
lar smooth muscle cells. ing orders from the physician: CT and MRI

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406 ANSWERS

scans, aortic angiography, and trans- calorie intake and diabetes mellitus. It does
esophageal echocardiography not have a genetic basis.
2. The priority nursing action is to give medica- 4. b. Rationale: The cause or causes of athero-
tion to lower the blood pressure. A large-bore sclerosis have not been determined with cer-
IV would be started, and IV sodium nitroprus- tainty. Epidemiologic studies have, however,
side would be given along with a -adrenergic identified predisposing risk factors, which in-
blocking drug. clude a major risk factor of hypercholes-
terolemia. Other risk factors include
SECTION IV: PRACTICING FOR NCLEX increasing age, family history of premature
coronary heart disease, and male gender.
Activity G
5. c. Rationale: Temporal arteritis (i.e., giant cell
1. 1-f, 2-e, 3-b, 4-a, 5-d, 6-c. Rationale: Distur- arteritis), the most common of the vasculi-
bances in blood flow can result from tides, is a focal inflammatory condition of
pathologic changes in the vessel wall (i.e., medium-size and large arteries. It predomi-
atherosclerosis, vasculitis), acute vessel nantly affects branches of arteries originating
obstruction due to thrombus or embolus, from the aortic arch, including the superficial
vasospasm (i.e., Raynaud phenomenon), or temporal, vertebral, ophthalmic, and poste-
abnormal vessel dilation (i.e., arterial rior ciliary arteries. Neither polyarteritis no-
aneurysms or varicose veins). dosa nor Raynaud disease are the most
2. a, d. Rationale: There are two sites of lipopro- common of the vasculitides. Varicose veins
tein synthesis: the small intestine and the are not vasculitides.
liver. The chylomicrons, which are the largest 6. c. Rationale: Acute arterial occlusion is a sud-
of the lipoprotein molecules, are synthesized den event that interrupts arterial flow to the
in the wall of the small intestine. The liver affected tissues or organ. Most acute arterial
synthesizes and releases very low-density occlusions are the result of an embolus or a
lipoprotein and high-density lipoprotein. The thrombus. Other answers are not appropriate
large intestine and the pancreas play no part for the nurse to give the client.
in synthesizing lipoprotein. 7. a, d. Rationale: Raynaud disease or phenome-
3. a. Rationale: Many types of primary hyper- non is a functional disorder caused by
cholesterolemia have a genetic basis. There intense vasospasm of the arteries and arteri-
may be a defective synthesis of the apopro- oles in the fingers and, less often, the toes.
teins, a lack of receptors, defective receptors, There are two types of Raynaud disease: pri-
or defects in the handling of cholesterol in mary and secondary. The secondary type,
the cell that are genetically determined. For called Raynaud phenomenon, is associated
example, the low-density lipoprotein (LDL) with other disease states or known causes of
receptor is deficient or defective in the ge- vasospasm. Raynaud phenomenon is associ-
netic disorder known as familial hypercholes- ated with previous vessel injury, such as frost-
terolemia (type 2A). This autosomal bite, occupational trauma associated with the
dominant type of hyperlipoproteinemia re- use of heavy vibrating tools, collagen dis-
sults from a mutation in the gene specifying eases, neurologic disorders, and chronic arter-
the receptor for LDL. Although heterozygotes ial occlusive disorders. The initial diagnosis is
commonly have an elevated cholesterol level based on history of vasospastic attacks sup-
from birth, they do not develop symptoms ported by other evidence of the disorder.
until adult life, when they often develop xan- Treatment measures are directed toward elim-
thomas (i.e., cholesterol deposits) along the inating factors that cause vasospasm and pro-
tendons and atherosclerosis appears. Myocar- tecting the digits from trauma during an
dial infarction (MI) before 40 years of age is ischemic episode. Abstinence from smoking
common. Homozygotes are much more se- and protection from cold are priorities. The
verely affected; they have cutaneous xan- presenting symptoms of this patient do not
thomas in childhood and may experience MI support a diagnosis of, or treatment for, arter-
by as early as 1 to 2 years of age. Homozy- ial thrombosis or peripheral artery disease.
gotic cutaneous xanthoma and adult onset 8. c, d. Rationale: Abdominal aortic aneurysms
hypercholesterolemia (type 1A) are not can involve any part of the vessel circumfer-
known diseases. Causes of secondary hyper- ence (saccular) or extend to involve the entire
lipoproteinemia include obesity with high- circumference (fusiform). Berry aneurysms

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ANSWERS 407

typically occur in the circle of Willis. Dissect- 18. calcium channel receptor-blocking
ing aneurysms are false aneurysms and typi- 19. systole
cally occur in the thoracic aorta. Aneurysms 20. secondary
can occur at the bifurcation of a blood vessel 21. oral contraceptive
but are not termed “bifurcating aneurysms.” 22. Malignant
9. b. Rationale: Sclerotherapy, which is often 23. Preeclampsia-eclampsia
used in the treatment of small residual vari- 24. orthostatic hypotension.
cosities, involves the injection of a sclerosing 25. Antihypertensive, psychotropic
agent into the collapsed superficial veins to
produce fibrosis of the vessel lumen. Surgical Activity B
treatment consists of removing the varicosi- 1. Mechanisms of blood pressure regulation. The
ties and the incompetent perforating veins, solid lines represent the mechanisms for renal
but it is limited to persons with patent deep and baroreceptor control of blood pressure
venous channels. Sclerotherapy produces through changes in cardiac output and pe-
fibrosis of the vessel lumen. There is no ripheral vascular resistance. The dashed lines
fibrotherapy for varicose veins. There is no represent the stimulus for regulation of blood
Trendelenburg therapy for varicose veins. pressure by the baroreceptors and the kidneys.
There is a Trendelenburg test that is diagnos- 2.
tic for primary or secondary varicose veins.
10. d. Rationale: In 1846, Virchow described the
triad that has come to be associated with ve- Blood pressure returns to normal
nous thrombosis: stasis of blood, increased
blood coagulability, and vessel wall injury. In- Increased Increased
flammation is a symptom of venous thrombo- venous return cardiac output
sis, not a risk factor. Decreased venous blood
flow can occur because of venous thrombosis; Increased Vasoconstriction
if the thrombus does not completely obstruct heart rate
the vein, it is not a risk factor. Hypocoagula-
bility would not cause a thrombus to form.
Baroreceptors

CHAPTER 23 DISORDERS OF BLOOD

PRESSURE REGULATION Compression
of veins
SECTION II: ASSESSING YOUR
UNDERSTANDING
Drop in
Activity A blood pressure
1. Arterial
2. systolic, diastolic Decreased cardiac
3. pulse pressure Activation of
output
4. mean arterial pressure skeletal muscle
5. cardiac output, peripheral vascular resistance pumps Decreased venous
6. vessel constriction, fluid retention return to the heart
7. equilibrium
8. kidneys, sodium, water Pooling of blood
9. Primary, secondary in lower body
10. 140 mm Hg, 90 mm Hg
11. constitutional
12. left ventricle
13. nephrosclerosis
14. ischemic, hemorrhage
15. 140/90 mm Hg
16. Diuretics
17. 1-adrenergic Assumption of the upright position

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408 ANSWERS

Activity C to angiotensin II by angiotensin-converting

enzyme, which is found on epithelial cells. An-
1. i. 2. h 3. d 4. j 5. a
giotensin II is a potent vasoconstrictor; it stim-
6. b 7. e 8. g 9. f 10. c
ulates the release of ADH and aldosterone.
Activity D ADH will increase water retention in the kid-
ney, and aldosterone will increase Na reten-
1. Decrease in blood pressure
tion, which will facilitate water resorption.
2. Stimulation of juxtaglomerular apparatus
This effectively increases peripheral resistance
3. Release of renin
and increases vascular volume.
4. Conversion of angiotensinogen to angiotensin I
4. Among the aging processes that contribute to
5. Conversion of angiotensin I to angiotensin II
an increase in blood pressure is stiffening of
by angiotensin-converting enzyme
the large arteries, particularly the aorta. With
6. Increased vascular resistance, release of aldos-
aging, the elastin fibers in the walls of the ar-
terone
teries are gradually replaced by collagen fibers
7. Na retention, stimulation of ADH release
that render the vessels stiffer and less com-
8. Water retention
pliant. Decreased baroreceptor sensitivity,
Activity E increased peripheral vascular resistance, and
decreased renal blood flow also contribute.
1. Short-term regulation is accomplished through
the cardiovascular center of the autonomic
nervous system, baroreceptors, and chemore- SECTION III: APPLYING YOUR
ceptors. The cardiovascular center transmits KNOWLEDGE
parasympathetic impulses to the heart through Activity F
the vagus nerve and sympathetic impulses to 1. The following assessments need to be made in
the heart and blood vessels through the spinal further evaluating this patient: (a) history to
cord and peripheral sympathetic nerves. The elicit symptoms, especially dizziness and his-
baroreceptors are pressure-sensitive receptors tory of syncope and falls; medical conditions
located in the walls of blood vessels and the such as diabetes mellitus; use of prescription
heart. They respond to changes in the stretch and over-the-counter drugs; and symptoms of
of the vessel wall by sending impulses to car- autonomic nervous system dysfunction (i.e.,
diovascular centers in the brain stem to effect erectile or bladder dysfunction); (b) physical
appropriate changes in heart rate and vascular examination to document blood pressure in
smooth muscle tone. The arterial chemorecep- both arms and the heart rate while in supine,
tors are chemosensitive cells that monitor the sitting, and standing positions, noting espe-
oxygen, carbon dioxide, and hydrogen ion cially the occurrence of symptoms; and
content of the blood. (c) noninvasive, 24-hour ambulatory blood
2. Most acute kidney disorders result in decreased pressure monitoring
urine formation, retention of salt and water, 2. Treatment of orthostatic hypotension is usually
and hypertension. Renovascular hypertension directed toward alleviating the cause or, if this
refers to hypertension caused by reduced renal is not possible, toward helping people learn
blood flow and activation of the renin- ways to cope with the disorder and prevent falls
angiotensin-aldosterone mechanism. The re- and injuries. Medications that predispose to
duced renal blood flow that occurs with postural hypotension should be avoided. Cor-
renovascular disease causes the affected kidney recting the fluid deficit and trying a different
to release excessive amounts of renin, increas- antihypertensive medication are examples of
ing circulating levels of angiotensin II. An- measures designed to correct the cause.
giotensin II, in turn, acts as a vasoconstrictor to 3. We would teach your father to do things such
increase peripheral vascular resistance and as a as sitting on the edge of the bed for a few min-
stimulus for increased aldosterone levels and utes and moving his legs before getting up;
sodium retention by the kidney. avoiding alcohol and vigorous exercise in a
3. Decreases in blood pressure are sensed by the warm environment; using diuretics in modera-
juxtaglomerular apparatus, which releases tion; and exerting himself only to the point
renin. Renin, an enzyme, will react with its where he is ready to sweat or lose body fluids.
substrate angiotensinogen in circulation to It might also be necessary for him to learn to
form angiotensin I. Angiotensin I is converted wear tight-fitting elastic support hose or an

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ANSWERS 409

abdominal support garment to help prevent measures should be to obtain a partial reduc-
pooling of blood in the lower extremities and tion in blood pressure to a safer, less critical
abdomen. level, rather than to normotensive levels.
5. b. Rationale: Cerebral vasoconstriction is prob-
SECTION IV: PRACTICING FOR NCLEX ably an exaggerated homeostatic response de-
signed to protect the brain from excesses of
Activity G
blood pressure and flow. The regulatory
1. c. Rationale: At normal heart rates, mean arter- mechanisms are often insufficient to protect
ial pressure can be estimated by adding one- the capillaries, and cerebral edema frequently
third of the pulse pressure to the diastolic develops. As it advances, papilledema (i.e.,
pressure (i.e., diastolic blood pressure pulse swelling of the optic nerve at its point of en-
pressure/3). trance into the eye) ensues, giving evidence
2. a, b, e. Rationale: The constitutional risk fac- of the effects of pressure on the optic nerve
tors include a family history of hypertension, and retinal vessels. The patient may have
race, and age-related increases in blood pres- headache, restlessness, confusion, stupor,
sure. Another factor that is believed to con- motor and sensory deficits, and visual distur-
tribute to hypertension is insulin resistance bances. In severe cases, convulsions and coma
and the resultant hyperinsulinemia that oc- follow. Lethargy, nervousness, and hyper-
curs in metabolic abnormalities such as type reflexia are not signs or symptoms of cerebral
2 diabetes. Lifestyle factors can contribute to edema in malignant hypertension.
the development of hypertension by interact- 6. c. Rationale: Liver damage, when it occurs,
ing with other risk factors. These lifestyle fac- may range from mild hepatocellular necrosis
tors include high salt intake, excessive calorie with elevation of liver enzymes to the more
intake and obesity, excessive alcohol con- ominous Hemolysis, Elevated Liver function
sumption, and low intake of potassium. Al- tests, and Low Platelet count (HELLP) syn-
though stress can raise blood pressure drome that is associated with significant ma-
acutely, there is less evidence linking it to ternal mortality.
chronic elevations in blood pressure. Smok- 7. d. Rationale: Hypertension in infants is associ-
ing and a diet high in saturated fats and cho- ated most commonly with high umbilical
lesterol, although not identified as primary catheterization and renal artery obstruction
risk factors for hypertension, are independent caused by thrombosis. Cerebral vascular
risk factors for coronary heart disease and bleeds, coarctation of the aorta, and
should be avoided. pheochromocytoma can raise blood pressure;
3. d. Rationale: Like adrenal medullary cells, however, they are not the most common
the tumor cells of a pheochromocytoma cause of hypertension in an infant.
produce and secrete the catecholamines, epi- 8. a. Rationale: Among the aging processes that
nephrine and norepinephrine. The hyper- contribute to an increase in blood pressure are
tension that develops is a result of the a stiffening of the large arteries, particularly
massive release of these catecholamines. the aorta; decreased baroreceptor sensitivity;
Their release may be paroxysmal rather than increased peripheral vascular resistance; and
continuous, causing periodic episodes of decreased renal blood flow.
headache, excessive sweating, and palpita- 9. b. Rationale: Pseudohypertension should be
tions. Headache is the most common symp- suspected in older persons with hypertension
tom and can be quite severe. Nervousness, in whom the radial or brachial artery remains
tremor, facial pallor, weakness, fatigue, and palpable but pulseless at higher cuff pressures.
weight loss occur less frequently. Marked The presenting parameters of the patient are
variability in blood pressure between not compatible with essential, orthostatic, or
episodes is typical. secondary hypertension.
4. a. Rationale: Because chronic hypertension is 10. c. Rationale: The renin-angiotensin-aldos-
associated with autoregulatory changes in terone system plays a central role in blood
coronary artery, cerebral artery, and kidney pressure regulation. Angiotensin II has two
blood flow, care should be taken to avoid ex- major functions in the rennin-angiotensin-
cessively rapid decreases in blood pressure, aldosterone system and acts as both a short-
which can lead to hypoperfusion and ischemic and a long-term regulation of blood pressure.
injury. Therefore, the goal of initial treatment It is a strong vasoconstrictor, especially of the

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410 ANSWERS

arterioles regulating blood pressure in the 35. regurgitation

short term. However, its second major action, 36. prolapse
the stimulation of aldosterone secretion from 37. stenosis
the adrenal gland, is the end of the renin- 38. regurgitation
angiotensin-aldosterone loop. The aldosterone 39. fetal heart
that is secreted notifies the kidneys to stop 40. blood, cyanosis, pulmonary
production or rennin (the negative feedback 41. acyanotic
in the loop) and contributes to the long-term 42. ventricular septal
regulation of blood pressure by increasing salt 43. Kawasaki
and water retention by the kidney.
Activity B

CHAPTER 24 DISORDERS OF
Right
CARDIAC FUNCTION Superior
vena
Left Superior
pulmonary pulmonary vena
veins veins
cava Aortic cava
arch Aortic valve Left
atrium Coronary
SECTION II: ASSESSING YOUR sinus Inferior
vena
Circumflex branch
UNDERSTANDING of left coronary cava
Right artery
Activity A atrium Anterior descending Right
atrium
branch of left
coronary artery
1. pericardium
Right
2. frictional coronary Left circumflex
branch Right
artery
3. pericarditis Right
ventricle
ventricle Left Posterior descending
4. effusion ventricle branch of right
coronary artery
5. tamponade
6. constrictive Activity C
7. atherosclerosis
8. metabolic activity, autoregulatory 1.
9. increased activity 1. i 2. h 3. c 4. d 5. a
10. 12-lead ECG 6. f 7. g 8. b 9. e 10. j
11. Echocardiography 2.
12. Atherosclerosis 1. g 2. e 3. b 4. h 5. a
13. stable, unstable 6. f 7. c 8. j 9. i 10. d
14. chronic ischemic heart disease, acute coro-
nary syndrome Activity D
15. T-wave inversion, ST-segment elevation, de-
Coronary heart disease
velopment of an abnormal Q wave
16. resting membrane potential
17. troponin assays Chronic ischemic heart disease Acute coronary syndrome
18. Acute ST-segment
19. 20 to 40
Stable Variant Silent No ST-segment ST-segment
20. ventricular remodeling angina angina myocardial elevation elevation
21. vagal ischemia
22. nitroglycerin
Unstable Non-ST-segment Q-wave
23. Atherectomy angina elevation AMI AMI
24. papillary muscle
25. Stable angina
Activity E
26. exertion, emotional
27. genetic 1. The pericardial cavity has little reserve vol-
28. mixed ume, so small additions of fluid increase the
29. hypertrophic cardiomyopathy pericardial pressure. Right heart filling pres-
30. Dilated sures are lower than the left, and increases in
31. Polyarthritis pericardial fluid pressure will result in de-
32. neurologic creased right-side filling.
33. valves 2. Myocardial oxygen supply is determined by
34. stenosis the coronary arteries, capillary inflow, and
ability of hemoglobin to transport and

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ANSWERS 411

deliver oxygen to the heart muscle. Impor- 7. The term reperfusion refers to reestablish-
tant factors in the transport and delivery of ment of blood flow through use of fibri-
oxygen include the fraction of inspired oxy- nolytic therapy, percutaneous coronary
gen in the blood and the number of red intervention, or coronary artery bypass graft-
blood cells with normal functioning hemo- ing. Early reperfusion (within 15–20 min-
globin. There are three major determinants of utes) after onset of ischemia can prevent
myocardial oxygen demand (MVO2): the necrosis and improve myocardial perfusion
heart rate, myocardial contractility, and in the infarct zone. Reperfusion after a
myocardial wall stress or tension. The heart longer interval can salvage some of the my-
rate is the most important factor in myocar- ocardial cells that would have died owing to
dial oxygen demand for two reasons: (a) as longer periods of ischemia. It may also pre-
the heart rate increases, myocardial oxygen vent microvascular injury that occurs over a
consumption or demand also increases; and longer period.
(b) subendocardial coronary blood flow is re- 8. Cardiomyopathy is a heterogeneous group of
duced because of the decreased diastolic fill- diseases of the myocardium associated with
ing time with increased heart rates. mechanical and/or electrical dysfunction that
3. On rupture, lipid core provides a stimulus usually exhibit inappropriate ventricular hy-
for platelet aggregation and thrombus forma- pertrophy or dilatation and are due to a vari-
tion. Both smooth muscle and foam cells in ety of causes that frequently are genetic.
the lipid core contribute to the expression of Cardiomyopathies are either confined to the
tissue factor in unstable plaques. Once ex- heart or part of generalized systemic disor-
posed to blood, tissue factor initiates the ders, often leading to cardiovascular death or
extrinsic coagulation pathway, resulting in progressive heart failure–related disability.
the local generation of thrombin and deposi- 9. Rheumatic heart disease is a complication of
tion of fibrin. immune-mediated response to group A strep-
4. Biomarkers for acute coronary syndrome in- tococcal throat infection. The acute stage of
clude cardiac-specific troponin I and troponin rheumatic fever includes history of an initiat-
T, myoglobin, and creatine kinase MB. As the ing streptococcal infection and subsequent
myocardial cells become necrotic, their intra- involvement of the connective tissue ele-
cellular enzymes begin to diffuse into the sur- ments of the heart, blood vessels, joints, and
rounding interstitium and then into the blood. subcutaneous tissues. The recurrent phase
5. The pathophysiology is divided into three usually involves extension of the cardiac
phases: development of the unstable plaque effects of the disease. The chronic phase of
that ruptures, the acute ischemic event, and rheumatic fever is characterized by perma-
the long-term risk of recurrent events that re- nent deformity of the heart valves.
main after the acute event. Inflammation 10. Blood typically shunts across the ductus from
plays a prominent role in plaque instability, the higher pressure left side to the lower pres-
with inflammatory cells releasing cytokines sure right side. A murmur is typically de-
that cause the fibrous cap to become thinner tected within days or weeks of birth. The
and more vulnerable to rupture. The acute murmur is loudest at the second left inter-
ischemic event can be caused by an increase costal space, continuous through systole and
in myocardial oxygen demand precipitated by diastole, and has a characteristic machinery
tachycardia or hypertension, or, more com- sound. A widened pulse pressure is common
monly, by a decrease in oxygen supply related due to the continuous runoff of aortic blood
to a reduction in coronary lumen diameter into the pulmonary artery.
due to platelet-rich thrombi or vessel spasm. 11. Tetralogy of Fallot consists of four associated
6. The extent of the infarct depends on the loca- defects: (a) a ventricular septal defect involv-
tion and extent of occlusion, amount of heart ing the membranous septum and the anterior
tissue supplied by the vessel, duration of the portion of the muscular septum; (b) dex-
occlusion, metabolic needs of the affected tis- troposition or shifting to the right of the
sue, extent of collateral circulation, and other aorta; (c) obstruction or narrowing of the pul-
factors such as heart rate, blood pressure, and monary outflow channel, including pul-
cardiac rhythm. An infarct may involve the monic valve stenosis, a decrease in the size of
endocardium, myocardium, epicardium, or a the pulmonary trunk, or both; and (d) hyper-
combination of these. trophy of the right ventricle because of the

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412 ANSWERS

increased work required to pump blood volume with respiration. None of the other
through the obstructed pulmonary channels. answers occur in cardiac tamponade.
3. c. Rationale: Kussmaul’s sign is an inspiratory
SECTION III: APPLYING YOUR distention of the jugular veins caused by the
KNOWLEDGE inability of the right atrium, encased in its
Activity F rigid pericardium, to accommodate the in-
1. Classic symptoms of a STEMI include: crease in venous return that occurs with in-
• Abrupt onset and pain as the significant spiration. None of the other physiologic signs
symptom. occur in constrictive pericarditis.
• Pain that is typically severe, crushing, and 4. a, c, e. Rationale: The major determinants of
usually substernal. plaque vulnerability to disruption include the
• Pain that radiates to the left arm, neck, or jaw. size of the lipid-rich core, the stability and
• Pain that is not relieved by rest or nitroglyc- thickness of its fibrous cap, the presence of
erin. inflammation, and lack of smooth muscle
• Gastrointestinal distress, including nausea cells. A decrease in blood pressure and coro-
and vomiting. nary blood flow are not determinants of
• Fatigue and weakness, especially of the arms plaque vulnerability to rupture.
and legs. 5. d. Rationale: The troponin assays have high
• Tachycardia, anxiety, restlessness, and feel- specificity for myocardial tissue and have be-
ings of impending doom. come the primary biomarker for the diagno-
• Pale, cool, moist skin. sis of myocardial infarction (MI). The
2. The emergency department goals of manage- troponin complex, which is part of the actin
ment for a patient with a STEMI are: filament, consists of three subunits (i.e., TnC,
• Identification of persons who are candidates TnT, TnI) that regulate calcium-mediated
for reperfusion therapy. actin-myosin contractile process in striated
• Evaluation of the person’s chief complaint, muscle. TnI and TnT, which are present in
typically chest pain, along with other associ- cardiac muscle, begin to rise within 3 hours
ated symptoms to differentiate acute coro- after the onset of MI and may remain ele-
nary syndrome from other diagnoses. vated for 7 to 10 days after the event. This is
• Institution of a monitor: a 12-lead ECG especially adventitious in the late diagnosis
should be obtained and read by a physician of MI. The other blood work may be ordered,
within 10 minutes of arrival to the emer- but not to confirm the diagnosis of MI.
gency department. 6. b, d. Rationale: Unstable angina (UA)/non–ST-
• Administration of oxygen, aspirin, nitrates, segment elevation myocardial infarction
pain medications, antiplatelet and anticoag- (NSTEMI) is classified as either low or inter-
ulant therapy, -adrenergic blocking agents, mediate risk of acute MI, the diagnosis of
and an angiotensin-converting enzyme in- which is based on the clinical history, ECG
hibitor. pattern, and serum biomarkers. The other an-
• Administration of immediate reperfusion swers are not diagnostic of UA/NSTEMI.
therapy with a thrombolytic agent or percu- 7. a. Rationale: The principal biochemical conse-
taneous coronary intervention for persons quence of MI is the conversion from aerobic
with ECG evidence of infarction. to anaerobic metabolism with inadequate
production of energy to sustain normal
SECTION IV: PRACTICING FOR NCLEX myocardial function. As a result, a striking
loss of contractile function occurs within 60
Activity G
seconds of onset. None of the other answers
1. a. Rationale: The pain is typically worse with occur.
deep breathing, coughing, swallowing, and 8. b. Rationale: Although a number of analgesic
positional changes because of changes in ve- agents have been used to treat the pain of
nous return and cardiac filling. All other an- STEMI, morphine is usually the drug of
swers make the pain worse. choice. It is indicated if chest pain is unre-
2. b. Rationale: A key diagnostic finding is pul- lieved with oxygen and nitrates. The reduc-
sus paradoxus, or an exaggeration of the nor- tion in anxiety that accompanies the
mal variation in the systemic arterial pulse administration of morphine contributes to

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ANSWERS 413

a decrease in restlessness and autonomic comfort, anxiety, and fatigue, often respond
nervous system activity, with a subsequent to therapy with the -adrenergic blocking
decrease in the metabolic demands of the drugs. None of the other types of drugs are
heart. Morphine does not cause a feeling of used in the treatment of mitral valve pro-
depression to the patient. lapse to relieve symptoms or prevent com-
9. c. Rationale: If blood flow can be restored plications.
within the 20- to 40-minute time frame, 17. b. Rationale: Heart failure manifests itself as
loss of cell viability does not occur or is tachypnea or dyspnea at rest or on exertion.
minimal. For the infant, this most commonly occurs
10. d. Rationale: Angina pectoris is usually precip- during feeding. The other answers are incor-
itated by situations that increase the work de- rect.
mands of the heart, such as physical exertion, 18. c. Rationale: The degree of obstruction may be
exposure to cold, and emotional stress. The dynamic and can increase during periods of
pain is typically described as a constricting, stress, causing hypercyanotic attacks (“tet
squeezing, or suffocating sensation. It is usu- spells”). None of the other answers occur in as-
ally steady, increasing in intensity only at the sociation with tetralogy of Fallot or tet spells.
onset and end of the attack. Changing posi-
tions abruptly does not cause an attack of
angina pectoris.
CHAPTER 25 DISORDERS
11. a. Rationale: Serum biochemical markers for OF CARDIAC CONDUCTION
myocardial infarction are normal in patients AND RHYTHM
with chronic stable angina. All other an-
swers are tests used in the diagnosis of SECTION II: ASSESSING YOUR
angina. UNDERSTANDING
12. Hypertrophic cardiomyopathy—genetic
Left ventricular noncompaction—genetic Activity A
Myocarditis—acquired 1. pacemaker
Dilated cardiomyopathy—mixed 2. interrupts
Peripartum cardiomyopathy—acquired 3. circumflex
13. b. Rationale: Alcoholic cardiomyopathy is the 4. Purkinje system
single most common identifiable cause of 5. Depolarization
DCM in the United States and Europe. The 6. Repolarization
other answers are incorrect. 7. absolute refractory period
14. c. Rationale: The intracardiac vegetative le- 8. ECG
sions also have local and distant systemic ef- 9. frontal or vertical, horizontal
fects. The loose organization of these lesions 10. lead specific
permits the organisms and fragments of the 11. rhythm, impulse conduction
lesions to form emboli and travel in the 12. automaticity
bloodstream, causing cerebral, systemic, or 13. reentry
pulmonary emboli. Prevention of the valves 14. paroxysmal supraventricular tachycardias
of the heart from either opening or closing 15. sinus rhythm
completely is not a systemic effect of the le- 16. Premature atrial contractions
sions. Fragmentation of the lesions does not 17. bundle of His
make them larger. 18. sawtooth
15. d. Rationale: It is believed that antibodies di- 19. Atrial fibrillation
rected against the M protein of certain strains 20. torsade de pointes
of streptococci cross-react with glycoprotein 21. premature ventricular contraction
antigens in the heart, joint, and other tissues 22. Ventral tachycardia
to produce an autoimmune response through 23. quivers
a phenomenon called molecular mimicry. 24. Heart block
None of the other answers are correct. 25. First
16. a. Rationale: Persons with palpitations and 26. Ischemic
mild tachyarrhythmias or increased adrener- 27. Catecholaminergic polymorphic
gic symptoms, as well as those with chest dis- 28. pacemaker, cardioversion, defibrillation

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414 ANSWERS

Activity B ity, contributing to the rapid outward move-

ment of K and reestablishment of the resting
R
membrane potential. Phase 4 represents the
resting membrane potential. Phase 4 corre-
Delay in
AV node
sponds to diastole.
2. There are several forms of reentry: anatomic,
functional, and reflective. Anatomic reentry
T consists of an excitation wave that travels in a
P
U set pathway. Functional reentry depends on
Baseline the local differences in conduction velocity.
Q Reflection is another form of reentry that can
occur in parallel pathways of myocardial tissue
Depolarization S Repolarization
of atria
or the Purkinje network.
of ventricles
Depolarization
3. Anticoagulant medications may be used to pre-
of ventricles vent embolic stroke, and medications may be
used to control the ventricular rate in persons
Activity C with persistent atrial fibrillation. Cardioversion
1. e 2. l 3. i 4. a 5. g may be considered when pulmonary edema or
6. k 7. j 8. c 9. h 10. m unstable cardiac status is present.
11. b 12. d 13. f 4. Long QT syndrome can be caused by various
agents and conditions that reduce the magni-
tude of outward repolarizing potassium cur-
Activity D
rents, enhance the magnitude of the inward
1. Sinoatrial node depolarization depolarizing sodium and calcium currents, or
2. Atrioventricular node depolarization both. Thus, there is delayed repolarization of
3. Bundle of His the ventricles with development of early depo-
4. Bundle branches larizing afterpotentials that initiate the ar-
5. Purkinje fibers rhythmia.
5. The exercise stress test elicits the body’s re-
Activity E sponse to measured increases in acute exercise.
1. The point at which the Na channels open is This technique provides information about
called the depolarization threshold. When the changes in heart rate, blood pressure, respira-
cell has reached this threshold, a rapid influx tion, and perceived level of exercise. It is useful
of Na occurs. This rapid influx of Na pro- in determining exercise-induced alterations in
duces a rapid, positively directed change in hemodynamic response and ECG ischemic-
the transmembrane potential, resulting in the type ST segment changes, and can detect and
electrical spike and overshoot during phase 0 classify disturbances in cardiac rhythm and
of the action potential. The rapid depolariza- conduction associated with exercise. These
tion that comprises phase 0 is responsible for changes are indicative of a poorer prognosis in
the QRS complex on the ECG. Depolarization persons with known coronary disease and re-
of a cardiac cell causes adjacent cells to depo- cent myocardial infarction.
larize, stimulating a wave of depolarization 6. Antiarrhythmic drugs act by modifying disor-
across the heart, cell by cell. Phase 1 occurs at dered formation and conduction of impulses
the peak of the action potential and signifies that induce cardiac muscle contraction. Class I
inactivation of the fast Na channels with an medications block fast sodium channels, thus
abrupt decrease in sodium permeability. Phase slowing depolarization. Class II drugs are -
2 represents the plateau of the action poten- adrenergic blocking drugs that act by blunting
tial. K permeability is low. An influx of Ca the effect of sympathetic nervous system stimu-
into the cell contributes to the phase 2 lation on the heart, thereby inhibiting calcium
plateau. The phase 2 plateau coincides with channel opening, and thus decreasing rate and
the ST segment of the ECG. During the phase contractility. Class III drugs act by inhibiting
3 repolarization period, the slow Ca chan- the potassium current and repolarization,
nels close, and the influx of Ca and Na thereby extending the action potential and
ceases. There is a sharp rise in K permeabil- refractory period. Class IV drugs act by blocking

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ANSWERS 415

the slow calcium channels, reducing the force rate are not variables in treatment of atrial
of myocardial contractility, and thereby de- fibrillation.
creasing myocardial oxygen demand. 5. d. Rationale: The long QT syndrome (LQTS) is
characterized by prolongation of the QT in-
SECTION III: APPLYING YOUR terval that may result in a characteristic type
KNOWLEDGE of polymorphic ventricular tachycardia called
Activity F torsade de pointes and sudden cardiac death.
Torsade de pointes (twisting or rotating
1. The drugs of choice for atrial fibrillation are
around a point) is a specific type of ventricular
anticoagulant medications and medications
tachycardia. The term refers to the polarity
such as digitalis and beta blockers used to con-
of the QRS complex, which swings from
trol the ventricular rate of the heart.
positive to negative and vice versa. The
2. The treatment used to convert atrial fibrilla-
QRS abnormality is characterized by large
tion to sinus rhythm is cardioversion. Compli-
bizarre polymorphic multiformed QRS com-
cations of this treatment include an increased
plexes that vary, often from beat to beat, in
risk of thromboembolism.
amplitude and direction, as well as in rota-
tion of the complexes around the isoelectric
SECTION IV: PRACTICING FOR NCLEX
line. Medications linked to LQTS include
Activity G digitalis, antiarrhythmic agents (e.g., amio-
1. a. Rationale: Persons with acute coronary darone, procainamide, quinidine), verapamil
syndrome are at risk for developing exten- (calcium channel blocker), haloperidol
sion of an infarcted area, ongoing myocar- (antipsychotic agent), and erythromycin
dial ischemia, and life-threatening (antibiotic).
arrhythmias. Research has revealed that 80% 6. a. Rationale: A distinguishing feature of
to 90% of ECG-detected ischemic events are second-degree atrioventricular block is that
clinically silent. Thus, ECG monitoring is conducted P waves relate to QRS complexes
more sensitive than a patient’s report of with recurring PR intervals; that is, the
symptoms for identifying transient ongoing association of P waves with QRS complexes
myocardial ischemia. Other answers are in- is not random. The other answers are not
correct. correct.
2. b. Rationale: Today, it is accepted that a more 7. d. Rationale: The disorder typically mani-
optimal rhythm is respiratory sinus arrhyth- fests in adulthood with very incomplete
mia. Respiratory sinus arrhythmia is a car- penetrance, and a high percentage of muta-
diac rhythm characterized by gradual tion carriers are asymptomatic. Cardiac
lengthening and shortening of RR intervals. events typically occur during sleep or rest.
This variation in cardiac cycles is related to Cardiac events during exercise, on arising
intrathoracic pressure changes that occur in the morning, and just before bedtime
with respiration and resultant alterations in at night are not indicative of Brugada syn-
autonomic control of the sinoatrial node. drome.
The other answers do not cause the variation 8. a, d. Rationale: Holter monitoring is use
in cardiac cycles related to respiratory sinus ful for documenting arrhythmias, conduc-
arrhythmia. tion abnormalities, and ST segment
3. c. Rationale: Sick sinus syndrome is a term changes.
that describes a number of forms of cardiac 9. a. Rationale: This technique provides infor-
impulse formation and intraatrial and atri- mation about changes in heart rate, blood
oventricular conduction abnormalities. In pressure, respiration, and perceived level of
children, the syndrome is most commonly exercise. It is useful in determining exer-
associated with congenital heart defects, cise-induced alterations in hemodynamic
particularly following corrective cardiac response and ECG ischemic-type ST seg-
surgery. ment changes, and can detect and classify
4. a, b, c. Rationale: The treatment of atrial fib- disturbances in cardiac rhythm and con-
rillation depends on its cause, recency of duction associated with exercise. Exercise
onset, and persistence of the arrhythmia. stress tests do not determine any of the
The size of the pulse deficit and the atrial other answers.

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416 ANSWERS

10. 16. side

Drug Use Class
17. peripheral edema
18. hepatic
Procainamide Supraventricular and Class IA 19. Left ventricular failure
ventricular arrhythmias 20. left
Atenolol Supraventricular Class II 21. High-output failure
arrhythmias and 22. Low-output failure
tachyarrhythmias 23. C-reactive protein
24. myocardial hypertrophy
Amiodarone Treatment of serious Class III 25. acute heart failure
ventricular arrhythmias
26. Paroxysmal nocturnal
Diltiazem Slowing the sinoatrial Class IV 27. Acute pulmonary edema
node pacemaker and 28. brain
inhibiting conduction in 29. right
the atrioventricular node 30. oxygenation
Lidocaine Treating ventricular Class IB 31. ventricular
arrhythmias only 32. brain natriuretic peptide
33. left ventricular
34. Circulatory shock
35. myocardial infarction
11. b. Rationale: Ablation therapy is used for 36. Hypovolemic
treating recurrent, life-threatening supraven- 37. Vasodilatory
tricular and ventricular tachyarrhythmias. 38. neurogenic shock
Ablative therapy may be performed by 39. immune
catheter or surgical techniques. It involves 40. Structural
localized destruction, isolation, or excision 41. Aging
of cardiac tissue that is considered to be
arrhythmogenic. Ablation therapy does not Activity B
involve open heart surgery. It neither excises 1.
ischemic cardiac tissue nor reestablishes 1. j 2. f 3. d 4. i 5. c
conductivity in areas of mild infarct. 6. b 7. e 8. a 9. g 10. h

CHAPTER 26 HEART FAILURE AND 2.

1. g 2. c 3. a 4. d 5. b
CIRCULATORY SHOCK 6. f 7. h 8. e
3.
SECTION II: ASSESSING YOUR 1. c 2. e 3. b 4. d 5. a
UNDERSTANDING
Activity A Activity C
1. Heart failure
2. coronary artery disease, hypertension, valvular
3. large
4. Cardiac output
5. sympathetic, parasympathetic
6. stroke volume
Right heart failure Left heart failure
7. Ejection fraction
8. decrease
Congestion of peripheral tissues Decreased cardiac output Pulmonary congestion
9. normal
10. compensatory mechanisms
Dependent Liver congestion Activity Impaired gas Pulmonary
11. Frank-Starling edema intolerance exchange edema
and ascites and signs of
12. contractile, volume overload, pressure overload decreased
tissue
GI tract Signs related
13. diastolic congestion to impaired liver perfusion
function
Cyanosis
and signs of
Orthopnea
hypoxia
14. compress, increase, delay
Anorexia, GI distress, Cough with Paroxysmal
15. tachycardia weight loss
frothy sputum nocturnal dyspnea

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ANSWERS 417

Activity D • Myocardial hypertrophy and remodeling:

cardiomyocyte hypertrophy and increased
1. A number of factors determine cardiac con-
inotropy, but demands more oxygen and in-
tractility by altering the systolic Ca++ levels.
creases metabolic needs
Catecholamines increase Ca++ entry into the
5. The signs and symptoms include shortness of
cell by phosphorylation of the Ca++ channels
breath and other respiratory manifestations,
via a cAMP-dependent protein kinase. Another
fatigue and limited exercise tolerance, fluid re-
mechanism that can modulate inotropy is the
tention and edema, cachexia and malnutri-
Na+/Ca+ exchange pump and the ATPase-de-
tion, and cyanosis. Persons with severe heart
pendent Ca++ pump on the myocardial cell
failure may exhibit diaphoresis and tachycar-
membrane. These pumps transport Ca++ out of
dia. These signs are the result of decreased tis-
the cell, thereby preventing the cell from be-
sue perfusion and resultant hypoxia.
coming overloaded with Ca++. If Ca++ extrusion
6. Diuretics promote the excretion of fluid and
is inhibited, the rise in intracellular Ca++ can
help sustain cardiac output and tissue perfu-
increase inotropy.
sion by reducing preload and allowing the
2. With both systolic and diastolic ventricular
heart to operate at a more optimal part of the
dysfunction, compensatory mechanisms are
Frank-Starling curve.
usually able to maintain adequate resting car-
7. In severe shock, cellular metabolic processes are
diac function until the later stages of heart
essentially anaerobic due to the decreased avail-
failure. Therefore, cardiac function measured
ability of oxygen. Excess amounts of lactic acid
at rest is a poor clinical indicator of the extent
accumulate in the cellular and extracellular
of cardiac impairment because cardiac output
compartments, limited amounts of ATP are
may be relatively normal at rest.
produced, and normal cell function cannot be
3. With diastolic dysfunction, blood is unable to
maintained. The sodium-potassium membrane
move freely into the left ventricle, causing an
pump is impaired, resulting in cellular edema
increase in intraventricular pressure at any
and an increase in the permeability of cell mem-
given volume. The elevated pressures are
branes. Mitochondrial activity becomes severely
transferred backward from the left ventricle
depressed, and lysosomal membranes may rup-
into the atria and pulmonary venous system,
ture, resulting in the release of enzymes that
causing a decrease in lung compliance that in-
cause further intracellular destruction. This is
creases the work of breathing and evokes
followed by cell death and the release of intra-
symptoms of dyspnea. Cardiac output is de-
cellular contents into the extracellular spaces.
creased because of a decrease in the volume
The destruction of the cell membrane activates
(preload) available for adequate cardiac out-
the arachidonic acid cascade, release of inflam-
put. Inadequate cardiac output during exercise
matory mediators, and production of oxygen
may lead to fatigue of the legs and the acces-
free radicals that extend cellular damage.
sory muscles of respiration.
8. The five major complications of severe shock
4. The many compensatory mechanisms of the
are (a) pulmonary injury, (b) acute renal fail-
cardiovascular system work in the following
ure, (c) gastrointestinal ulceration, (d) dissemi-
ways; however, they only serve to make heart
nated intravascular coagulation, and (e)
failure worse:
multiple organ dysfunction syndrome.
• Frank-Starling mechanism: increases in-
otropy, but eventually increases metabolic
demand of cardiac tissue
SECTION III: APPLYING YOUR
• Activation of the sympathetic nervous sys-
KNOWLEDGE
tem: increases inotropy, but increases wall Activity E
tension and metabolic demand 1. The diagnostic tests the nurse would expect to
• Renin-angiotensin-aldosterone mechanism: be ordered for this child would be echocardio-
increases blood volume and maintains car- graph, chest x-rays, and laboratory studies for
diac output, but eventually increases wall anemia and electrolyte imbalances.
tension 2. Drugs used in the treatment of heart failure in
• Natriuretic peptides: inhibits sympathetic infants and children include inotropic agents
and renal compensation and decreases work such as digitalis, diuretics, and vasodilating
of heart, but inactivation results in de- agents. Medication dosages are based on the
creased cardiac output child’s weight and renal function.

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418 ANSWERS

tissues. Medications are usually administered

SECTION IV: PRACTICING FOR NCLEX
intravenously. In hypovolemic shock, the goal
Activity F of treatment is to restore vascular volume. This
1. 1-f, 2-a, 3-c, 4-b, 5-e, 6-d can be accomplished through intravenous ad-
2. a, c. Rationale: The signs and symptoms of ministration of fluids and blood. The crystal-
heart failure include shortness of breath and loids (e.g., isotonic saline, Ringer’s lactate) are
other respiratory manifestations, fatigue and readily available and effective, at least tem-
limited exercise tolerance, fluid retention and porarily. Plasma volume expanders (e.g., pen-
edema, cachexia and malnutrition, and tastarch, colloidal albumin) have a high
cyanosis. Persons with severe heart failure molecular weight, do not necessitate blood
may exhibit diaphoresis and tachycardia. A typing, and remain in the vascular space for
ruddy complexion, bradycardia, and a longer periods than the crystalloids, such as
chronic productive cough are not signs or dextrose and saline. Blood or blood products
symptoms of heart failure. (packed or frozen red cells) are administered
3. a, b, d, e. Rationale: Shock is not a specific dis- based on hematocrit and hemodynamic find-
ease but a syndrome that can occur in the ings. Fluids and blood are best administered
course of many life-threatening traumatic based on volume indicators such as central ve-
conditions or disease states. It can be caused nous pressure and urine output. Vasoactive
by an alteration in cardiac function (cardio- medications are agents capable of constricting
genic shock), a decrease in blood volume (hy- or dilating blood vessels. Considerable contro-
povolemic shock), excessive vasodilation versy exists about the advantages or disadvan-
with maldistribution of blood flow (distribu- tages related to the use of these drugs.
tive shock), or obstruction of blood flow Generally, vasoconstrictor agents are not used
through the circulatory system (obstructive as a primary form of therapy in hypovolemic
shock). Excessive vasoconstriction and hyper- shock and may be detrimental. These agents
volemia are not causes of shock. are given only when volume deficits have been
4. a, c, e. Rationale: Signs and symptoms of car- corrected, yet hypotension persists.
diogenic shock include indications of hypo- 6. a. Rationale: In contrast to other shock states
perfusion with hypotension, although a due to the loss of blood volume or impaired
preshock state of hypoperfusion may occur cardiac function, the heart rate in neurogenic
with a normal blood pressure. The lips, nail shock is often slower than normal, and the
beds, and skin may become cyanotic because skin is dry and warm. This type of distribu-
of stagnation of blood flow and increased ex- tive shock is rare and usually transitory. The
traction of oxygen from the hemoglobin as it other answers are not correct.
passes through the capillary bed. Mean arterial 7. b. Rationale: Anaphylaxis is a clinical syn-
and systolic blood pressures decrease due to drome that represents the most severe form
poor stroke volume, and there is a narrow of systemic allergic reaction. Anaphylactic
pulse pressure and near-normal diastolic blood shock results from an immune-mediated re-
pressure due to arterial vasoconstriction. action in which vasodilator substances such
Urine output decreases due to lower renal as histamine are released into the blood. The
perfusion pressures and the increased release vascular response in anaphylaxis is often ac-
of aldosterone. Elevation of preload is re- companied by life-threatening laryngeal
flected in a rise in central venous pressure and edema and bronchospasm, circulatory col-
pulmonary capillary wedge pressure. Neuro- lapse, contraction of gastrointestinal and
logic changes, such as alterations in cognition uterine smooth muscle, and urticaria (hives)
or consciousness, may occur due to low car- or angioedema.
diac output and poor cerebral perfusion. The 8. a. Rationale: Although activated neutrophils
other physiologic occurrences are not signs or kill microorganisms, they also injure the en-
symptoms of shock. dothelium by releasing mediators that in-
5. c. Rationale: The treatment of hypovolemic crease vascular permeability. In addition,
shock is directed toward correcting or control- activated endothelial cells release nitric
ling the underlying cause and improving tis- oxide, a potent vasodilator that acts as a key
sue perfusion. Ongoing loss of blood must be mediator of septic shock.
corrected, such as in surgery. Oxygen is ad- 9. b. Rationale: The primary physiologic result
ministered to increase oxygen delivery to the of obstructive shock is elevated right heart

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ANSWERS 419

pressure due to impaired right ventricular 29. blood

function. The other answers are not correct. 30. Hemoglobin
10. c. Rationale: The degree of renal damage in 31. cooperatively
shock is related to the severity and duration 32. pH, carbon dioxide, temperature
of shock. None of the other answers relate to 33. dissolved carbon dioxide, hemoglobin, bicar-
the damage to the renal system in shock. bonate
11. c. Rationale: Major risk factors for the devel- 34. pneumotaxic, apneustic
opment of MODS are severe trauma, sepsis, 35. chemoreceptors, lung
prolonged periods of hypotension, hepatic 36. carbon dioxide
dysfunction, infarcted bowel, advanced age, 37. Dyspnea
and alcohol abuse. Respiratory dysfunction is Activity B
not a major risk factor in MODS.
12. b. Rationale: Structural (congenital) heart de-
Trachea
fects are the most common cause of heart
failure in children. The other answers are not
correct.
Left primary
bronchus

CHAPTER 27 STRUCTURE AND Secondary

bronchi
FUNCTION OF THE RESPIRATORY
SYSTEM Segmental
bronchi

SECTION II: ASSESSING YOUR UNDER-

STANDING
Terminal
Activity A bronchioles

1. gas exchange
2. conducting, respiratory
3. conducting Activity C
4. warmed, filtered, moistened 1. f 2. g 3. h 4. b 5. i
5. mucus 6. a 7. c 8. j 9. d 10. e
6. glottis Activity D
7. hyaline aScSbSgSfSeSd
8. hilum
9. pulmonary lobule Activity E
10. alveoli 1. The pleural membrane lines the thoracic cav-
11. pulmonary ity and encases the lungs. The outer parietal
12. lymphatic layer lines the pulmonary cavities and adheres
13. parasympathetic to the thoracic wall, the mediastinum, and the
14. sympathetic diaphragm. The inner visceral pleura closely
15. partial pressure covers the lung and is adherent to its surfaces.
16. pressure difference It is continuous with the parietal pleura at the
17. intrapleural hilum of the lung, where the major bronchus
18. Valsalva and pulmonary vessels enter and leave the
19. compliance lung. A thin film of serous fluid separates the
20. tidal volume two pleural layers, allowing the two layers to
21. inspiratory reserve volume (IRV), expiratory glide over each other and yet hold together, so
reserve volume (ERV) there is no separation between the lungs and
22. inspiratory capacity the chest wall.
23. vital capacity 2. During inspiration, the size of the chest cavity
24. minute volume increases, the intrathoracic pressure becomes
25. Pulmonary, alveolar more negative, and air is drawn into the lungs.
26. collapse The diaphragm is the principal muscle of in-
27. Dead space spiration. When the diaphragm contracts, the
28. mismatching abdominal contents are forced downward, and

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420 ANSWERS

the chest expands from top to bottom. The ex-

SECTION III: APPLYING YOUR
ternal intercostal muscles, which also aid in
KNOWLEDGE
inspiration, connect to the adjacent ribs and
slope downward and forward. When they con- Activity F
tract, they raise the ribs and rotate them
1. When the oxygen levels in the body drop
slightly so that the sternum is pushed forward;
below a specific set-point, the small blood
this enlarges the chest from side to side and
vessels in the lungs go into a vasoconstrictive
from front to back. The scalene muscles ele-
state; they squeeze down so very little blood
vate the first two ribs, and the sternocleido-
can go through them. This means that no
mastoid muscles raise the sternum to increase
oxygen is exchanged at this point either. This
the size of the chest cavity. Expiration is
vasoconstriction can occur in a limited part of
largely passive. It occurs as the elastic compo-
the lung, or it can occur throughout the lung.
nents of the chest wall and lung structures
This is called generalized hypoxia.
that were stretched during inspiration recoil,
2. Arterial blood gas and pulmonary function
causing air to leave the lungs as the intratho-
tests would be ordered.
racic pressure increases. When needed, the ab-
dominal and the internal intercostal muscles
can be used to increase expiratory effort. SECTION IV: PRACTICING FOR NCLEX
3. Pulmonary surfactant forms a monolayer with Activity G
its hydrophilic surface binding to liquid film
on the surface of the alveoli and its hydropho- 1. a, c. Rationale: The lungs are the functional
bic surface facing outward toward the gases in structures of the respiratory system. In addi-
the alveolar air. This monolayer interrupts the tion to their gas exchange function, they in-
surface tension that develops at the air–liquid activate vasoactive substances such as
interface in the alveoli, keeping them from bradykinin and convert angiotensin I to an-
collapsing and allowing equal inflation. giotensin II. They also serve as a reservoir for
blood storage. Heparin-producing cells are
4. Gas diffusion in the lung is described by the particularly abundant in the capillaries of the
Fick’s law of diffusion. The Fick’s law states lung, where small clots may be trapped. The
that the volume of a gas diffusing across the other functions do not occur in the lungs.
membrane per unit time is directly propor- 2. a. Rationale: The bronchial blood vessels are
tional to the partial pressure difference of the the only ones that can undergo angiogenesis
gas (P1 – P2), the surface area (SA) of the mem- (formation of new vessels) and develop col-
brane, and the diffusion coefficient (D), and is lateral circulation when vessels in the pul-
inversely proportional to the thickness (T) of monary circulation are obstructed, as in
the membrane. pulmonary embolism. The development of
5. Arterial blood is commonly used for measur- new blood vessels helps keep lung tissue alive
ing blood gases. Venous blood is not used be- until the pulmonary circulation can be re-
cause venous levels of oxygen and carbon stored. The blood in the bronchiole blood
dioxide reflect the metabolic demands of the vessels is unoxygenated, so they neither carry
tissues rather than the gas exchange function oxygen-rich blood to the lung tissues nor par-
of the lungs. ticipate in gas exchange. Bronchiole blood
6. Coughing is a neurally mediated reflex that vessels drain blood into the bronchial veins.
protects the lungs from accumulation of secre- 3. 1-b, 2-d, 3-c, 4-a
tions and from entry of irritating and destruc- 4. b. Rationale: Specifically, lung compliance (C)
tive substances. It is one of the primary defense describes the change in lung volume ( V)
mechanisms of the respiratory tract. The cough that can be accomplished with a given
reflex is initiated by receptors located in the change in respiratory pressure ( P); thus,
tracheobronchial wall; these receptors are ex- C V/ P. This equation has nothing to do
tremely sensitive to irritating substances and to with surface tension, airway resistance, or
the presence of excess secretions. Afferent im- change in peak expiratory flow.
pulses from these receptors are transmitted 5. c. Rationale: The work of breathing is deter-
through the vagus to the medullary center, mined by the amount of effort required to
which integrates the cough response. move air through the conducting airways and

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ANSWERS 421

by the ease of lung expansion, or compliance. son can consciously alter the depth and
Expansion of the lungs is difficult for persons rate of respiration. Fever, pain, and emotion
with stiff and noncompliant lungs; they usu- exert their influence through lower brain
ally find it easier to breathe if they keep their centers.
tidal volume low and breathe at a more rapid 11. d-c-e-a-b. Rationale: Coughing itself requires
rate (e.g., 300  20 6,000 mL) to achieve the rapid inspiration of a large volume of air
their minute volume and meet their oxygen (usually about 2.5 L), followed by rapid clo-
needs. In contrast, persons with obstructive sure of the glottis and forceful contraction
airway disease usually find it less difficult to of the abdominal and expiratory muscles. As
inflate their lungs but expend more energy in these muscles contract, intrathoracic pres-
moving air through the airways. As a result, sures are elevated to levels of 100 mm Hg or
these persons take deeper breaths and breathe more. The rapid opening of the glottis at
at a slower rate (e.g., 600  10 6,000 mL) this point leads to an explosive expulsion
to achieve their oxygen needs. People with of air.
chronic obstructive pulmonary disease do 12. d. Rationale: Dyspnea is observed in at least
not have hyperpneic breathing under normal three major cardiopulmonary disease states:
conditions. primary lung diseases, such as pneumonia,
6. c. Rationale: The distribution of ventilation asthma, and emphysema; heart disease that
between the apex and base of the lung varies is characterized by pulmonary congestion;
with body position and the effects of gravity and neuromuscular disorders, such as myas-
on intrapleural pressure. Intrapleural pressure thenia gravis and muscular dystrophy, that
impacts the distribution of ventilation, not affect the respiratory muscles. Dyspnea is
intrathoracic or alveolar pressures. not an identified component of multiple
7. d. Rationale: Generalized hypoxia occurs at sclerosis.
high altitudes and in persons with chronic
hypoxia due to lung disease and causes vaso-
constriction throughout the lung. Prolonged CHAPTER 28 RESPIRATORY TRACT
hypoxia can lead to pulmonary hyperten- INFECTIONS, NEOPLASMS, AND
sion and increased workload on the right
heart.
CHILDHOOD DISORDERS
8. a. Rationale: Physiologic shunting of blood
SECTION II: ASSESSING YOUR
usually results from destructive lung disease
UNDERSTANDING
that impairs ventilation or from heart failure
that interferes with movement of blood Activity A
through sections of the lungs. Obstructive
1. Viruses
lung disease, pulmonary hypertension, and
2. bronchial, obstruct, bacterial
regional hypoxia usually do not cause the
3. upper
physiologic shunting of blood.
4. rhinoviruses
9. b. Rationale: In the clinical setting, blood gas
5. Antihistamines
measurements are used to determine the par-
6. Rhinitis, paranasal
tial pressure of oxygen and carbon dioxide in
7. oxygen
the blood. Arterial blood is commonly used
8. hemagglutinin, neuraminidase
for measuring blood gases. Venous blood is
9. upper, viral, bacterial
not used because venous levels of oxygen and
10. vaccination
carbon dioxide reflect the metabolic demands
11. reassortment
of the tissues rather than the gas exchange
12. pneumonia
function of the lungs. The other answers are
13. Lobar pneumonia, bronchopneumonia
not correct.
14. nosocomial
10. a, c, e. Rationale: The automatic and volun-
15. immunocompromised
tary components of respiration are regulated
16. Legionnaire
by afferent impulses that are transmitted to
17. mycoplasma
the respiratory center from a number of
18. Tuberculosis
sources. Afferent input from higher brain
19. waxy
centers is evidenced by the fact that a per-

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422 ANSWERS

20. Primary Activity D

21. tuberculin skin, x-rays
22. Histoplasmosis Inhalation of
23. Fungal tubercle bacillus
24. smoking
25. 80%
26. Lung cancers
27. small cell lung cancers (SCLCs)
28. non–small cell lung cancers (NSCLCs)
29. Croup
30. 25th to 28th
Primary Secondary
Activity B tuberculosis tuberculosis

Cell-mediated Development of
hypersensitivity cell-mediated Reinfection
response immunity

Granulomatous
Frontal sinus inflammatory
Positive skin
test
response

Ethmoid sinuses
Progressive
Ghon
Maxillary sinus or disseminated
complex
tuberculosis

Healed dormant Reactivated

lesion tuberculosis

Activity E
Frontal sinus
1. The fingers are the greatest source of spread,
Sphenoidal and the nasal mucosa and conjunctival sur-
sinus face of the eyes are the most common portals
Superior turbinate
of entry of the virus. The most highly conta-
Middle turbinate gious period is during the first 3 days after
the onset of symptoms, and the incubation
Inferior turbinate
period is approximately 5 days. Cold viruses
have been found to survive for more than
5 hours on the skin and hard surfaces, such as
plastic countertops. Aerosol spread of colds,
through coughing and sneezing, is much less
important than the spread by fingers picking
Activity C up the virus from contaminated surfaces and
carrying it to the nasal membranes and eyes.
1. i 2. c 3. a 4. b 5. d
2. Contagion results from the ability of the in-
6. j 7. e 8. f 9. g 10. h
fluenza A virus to develop new HA and NA
subtypes against which the population is not
protected. An antigenic shift, which involves
a major genetic rearrangement in either anti-
gen, may lead to epidemic or pandemic infec-
tion. Lesser changes, called antigenic drift,
find the population partially protected by
cross-reacting antibodies.

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ANSWERS 423

3. Viral pneumonia occurs as a complication of 7. Inhaled droplet nuclei pass down the
influenza. It typically develops within 1 day bronchial tree without settling on the epithe-
after onset of influenza and is characterized lium and are deposited in the alveoli. Soon
by rapid progression of fever, tachypnea, after entering the lung, the bacilli are phago-
tachycardia, cyanosis, and hypotension. The cytosed by alveolar macrophages, but resist
clinical course of influenza pneumonia pro- killing, because cell wall lipids of the My-
gresses rapidly. It can cause hypoxemia and cobacterium tuberculosis block fusion of phago-
death within a few days of onset. Survivors somes and lysosomes. Although the
often develop diffuse pulmonary fibrosis. macrophages that first ingest M. tuberculosis
4. The lung below the main bronchi is normally cannot kill the organisms, they initiate a cell-
sterile, despite frequent entry of microor- mediated immune response that eventually
ganisms into the air passages by inhalation contains the infection. As the tubercle bacilli
during ventilation or aspiration of nasopha- multiply, the infected macrophages degrade
ryngeal secretions. Bacterial pneumonia re- the mycobacteria and present their antigens
sults due to loss of the cough reflex, damage to T lymphocytes. The sensitized T lympho-
to the ciliated endothelium that lines the res- cytes, in turn, stimulate the macrophages to
piratory tract, or impaired immune defenses. increase their concentration of lytic enzymes
Bacterial adherence also plays a role in colo- and ability to kill the mycobacteria. When re-
nization of the lower airways. The epithelial leased, these lytic enzymes also damage lung
cells of critically and chronically ill persons tissue. The development of a population of
are more receptive to binding microorgan- activated T lymphocytes and related develop-
isms that cause pneumonia. Other clinical ment of activated macrophages capable of in-
risk factors favoring colonization of the tra- gesting and destroying the bacilli constitutes
cheobronchial tree include antibiotic therapy the cell-mediated immune response.
that alters the normal bacterial flora, dia- 8. Lung cancer is classified as squamous cell
betes, smoking, chronic bronchitis, and viral lung carcinoma, adenocarcinoma, small cell
infection. carcinoma, and large cell carcinoma.
5. During the first stage, alveoli become filled 9. The manifestations of lung cancer can be di-
with protein-rich edema fluid containing nu- vided into three categories: (a) those due to
merous organisms. Marked capillary conges- involvement of the lung and adjacent struc-
tion follows, leading to massive outpouring of tures; (b) the effects of local spread and
polymorphonuclear leukocytes and red blood metastasis; and (c) nonmetastatic paraneo-
cells. Because the first consistency of the plastic manifestations involving endocrine,
affected lung resembles that of the liver, this neurologic, and connective tissue function.
stage is referred to as the “red hepatization” 10. Pulmonary immaturity, together with surfac-
stage. The next stage involves the arrival of tant deficiency, lead to alveolar collapse. The
macrophages that phagocytose the frag- type II alveolar cells that produce surfactant
mented polymorphonuclear cells, red blood do not begin to mature until approximately
cells, and other cellular debris. During this the 25th to 28th weeks of gestation, and con-
stage, which is termed the “gray hepatization” sequently, many premature infants are born
stage, the congestion has diminished, but the with poorly functioning type II alveolar cells
lung is still firm. The alveolar exudate is then and have difficulty producing sufficient
removed, and the lung returns to normal. amounts of surfactant. Without surfactant,
6. Mycobacterium tuberculosis hominis is an air- the large alveoli remain inflated, whereas the
borne infection spread by minute, invisible small alveoli become difficult to inflate, re-
particles called droplet nuclei that are har- sulting in respiratory distress syndrome.
bored in the respiratory secretions of persons
with active tuberculosis. Coughing, sneezing, SECTION III: APPLYING YOUR
and talking all create respiratory droplets; KNOWLEDGE
these droplets evaporate, leaving the organ-
isms, which remain suspended in the air and Activity F
are circulated by air currents. Thus, living 1. Diagnostic tests for squamous cell cancer of
under crowded and confined conditions in- the lung include chest radiography, bron-
creases the risk for spread of the disease. choscopy, cytologic studies (Papanicolaou

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424 ANSWERS

test) of the sputum or bronchial washings, per- 4. a, c, d. Rationale: Community-acquired pneu-

cutaneous needle biopsy of lung tissue, scalene monia may be further categorized according
lymph node biopsy, CT scans, MRI studies, ul- risk of mortality and need for hospitalization
trasonography to locate lesions and evaluate based on age, presence of coexisting disease,
the extent of the disease, and positron emis- and severity of illness using physical exami-
sion tomography, a noninvasive alternative nation findings and laboratory and radiologic
for identifying metastatic lesions in the medi- findings. The other answers are not categories
astinum or distant sites. used to classify community-acquired pneu-
2. Treatments used for squamous cell (non–small monia.
cell lung cancer [NSCLC]) cancer of the lung 5. d. Rationale: Neutropenia and impaired gran-
include surgery—for the removal of small, lo- ulocyte function, as occurs in persons with
calized NSCLC tumors; radiation therapy—a leukemia, chemotherapy, and bone marrow
definitive or main treatment modality for palli- depression, predispose to infections caused
ation of symptoms; and chemotherapy—often by Staphylococcus aureus, Aspergillus, gram-
using a combination of drugs. A combination negative bacilli, and candida. The other or-
of these treatments can also be used. ganisms can cause pneumonia, but they are
not usually seen in people with neutropenia
SECTION IV: PRACTICING FOR NCLEX and impaired granulocyte function.
6. a. Rationale: Elderly persons are less likely to
Activity G
experience marked elevations in temperature;
1. c. Rationale: Decongestant drugs (i.e., sympa- in these persons, the only sign of pneumonia
thomimetic agents) are available in over-the- may be a loss of appetite and deterioration in
counter nasal sprays, drops, and oral cold mental status. Pleuritic pain, a sharp pain
medications. These drugs constrict the blood that is more severe with respiratory move-
vessels in the swollen nasal mucosa and re- ments, is common.
duce nasal swelling. Rebound nasal swelling 7. b. Rationale: The pathogenesis of tuberculosis
can occur with indiscriminate use of nasal in a previously unexposed immunocompe-
drops and sprays. Oral preparations contain- tent person is centered on the development
ing decongestants may cause systemic vaso- of a cell-mediated immune response that
constriction and elevation of blood pressure confers resistance to the organism and de-
when given in doses large enough to relieve velopment of tissue hypersensitivity to the
nasal congestion. They should be avoided by tubercular antigens. The destructive nature
persons with hypertension, heart disease, of the disease, such as caseating necrosis
hyperthyroidism, diabetes mellitus, or other and cavitation, results from the hypersensi-
health problems. tivity immune response rather than the de-
2. b. Rationale: One distinguishing feature of an structive capabilities of the tubercle bacillus.
influenza viral infection is the rapid onset, Tuberculosis does not have rapidly progress-
sometimes in as little as 1 to 2 minutes, of ing pulmonary lesions, nor does it have
profound malaise. None of the other answers purulent necrosis or purulent pulmonary
are distinguishing characteristics of an in- lesions.
fluenza viral infection. 8. c. Rationale: The oral antifungal drugs itra-
3. c. Rationale: Recently, a highly pathogenic in- conazole and fluconazole are used for treat-
fluenza A subtype H5N1 was found in poultry ment of less severe forms of infection.
in East and Southeast Asian countries. Al- Intravenous amphotericin B is used in the
though the H5N1 strain is highly contagious treatment of persons with progressive disease.
from one bird to another, the transmission Long-term treatment is often required. Bacil-
from human to human is relatively ineffi- lus Calmette-Guérin is an attenuated strain of
cient and not sustained. The result is only live tubercle vaccine. Rifampin is an oral drug
rare cases of person-to-person transmission. used in the treatment of tuberculosis.
Most cases occur after exposure to infected 9. d. Rationale: The non–small cell lung cancers
poultry or surfaces contaminated with poul- (NSCLCs) include squamous cell carcinomas,
try droppings. Because infection in humans is adenocarcinomas, and large cell carcinomas.
associated with high mortality, there exists As with the small cell lung cancers (SCLCs),
considerable concern that the H5N1 strain these cancers have the capacity to synthesize
might mutate and initiate a pandemic. bioactive products and produce paraneoplas-

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ANSWERS 425

tic syndromes. NSCLCs do not neutralize 28. Pulmonary hypertension

bioactive syndromes. In addition, they nei- 29. hypoxemia
ther synthesize ACTH nor produce panneo- 30. Respiratory failure
plastic syndromes.
Activity B
10. a. Rationale: The infant with bronchopul-
monary dysplasia (BPD) often demonstrates a
barrel chest, tachycardia, rapid and shallow
Smoking Attraction of
breathing, chest retractions, cough, and poor inflammatory cells
weight gain. Other signs and symptoms listed
are not signs and symptoms of BPD.
Release of elastase
11. Epiglottitis: Upper airway
Acute bronchiolitis: Lower airway
Asthma: Lower airway
Spasmodic croup: Upper airway 1
Laryngotracheobronchitis: Upper airway
12. b. Rationale: The child with bronchiolitis is at
risk for respiratory failure resulting from im- 1 1
paired gas exchange. The other answers are
not applicable.
Macrophages
and neutrophils Destruction of
CHAPTER 29 DISORDERS OF elastic fibers in lung

VENTILATION AND GAS EXCHANGE

Emphysema
SECTION II: ASSESSING
YOUR UNDERSTANDING
Activity A Activity C

1. carbon dioxide (CO2), oxygen (O2) 1.

2. Ventilation 1. d 2. b 3. i 4. a 5. j
3. oxygenation, removal of CO2 6. e 7. f 8. g 9. h 10. c
4. Hypoxemia
2.
5. hypoxia
1. e 2. b 3. g 4. i 5. d
6. ventilation, vasoconstriction, red blood
6. j 7. a 8. h 9. f 10. c
7. Hypercapnia
8. pH, acidosis
Activity D
9. Pleural effusion
10. Hemothorax 1.
11. inflated E B C A F D
12. expiratory
13. asthma
Activity E
14. T lymphocyte
15. Chronic obstructive 1. The mechanisms that result in hypoxemia are
16. inflammation, fibrosis hypoventilation, impaired diffusion of gases,
17. Emphysema, proteases inadequate circulation of blood through the
18. 1-antitrypsin pulmonary capillaries, and mismatching of
19. hypersecretion of mucus ventilation and perfusion.
20. pink puffers 2. The clinical manifestations of atelectasis in-
21. blue bloaters clude tachypnea, tachycardia, dyspnea,
22. Bronchiectasis cyanosis, signs of hypoxemia, diminished
23. Cystic fibrosis chest expansion, absence of breath sounds,
24. interstitial and intercostal retractions. Both chest expan-
25. collagen, elastic sion and breath sounds are decreased on the
26. embolism affected area. There may be intercostal retrac-
27. pulmonary embolism tion over the involved area during inspiration.

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426 ANSWERS

3. The symptoms of the acute response are heart failure may develop when there is
caused by the release of chemical mediators massive vasoconstriction because of a large
from the presensitized mast cells. Mediator re- embolus.
lease results in the infiltration of inflammatory 7. Pathologic lung changes include diffuse
cells, opening of the mucosal intercellular epithelial cell injury with increased perme-
junctions, and increased access of antigen to ability of the alveolar-capillary membrane,
submucosal mast cells. There is bronchospasm which permits fluid, plasma proteins, and
caused by direct stimulation of parasympa- blood cells to move out of the vascular com-
thetic receptors, mucosal edema caused by in- partment into the interstitium and alveoli of
creased vascular permeability, and increased the lung. Diffuse alveolar cell damage leads to
mucus secretions. The late phase response in- accumulation of fluid, surfactant inactivation,
volves inflammation and increased airway re- and formation of a hyaline membrane. The
sponsiveness that prolong the asthma attack. work of breathing becomes greatly increased
An initial trigger in the late phase response as the lung stiffens and becomes more diffi-
causes the release of inflammatory mediators cult to inflate. There is increased intrapul-
from mast cells, macrophages, and epithelial monary shunting of blood, impaired gas
cells. These substances induce the migration exchange, and hypoxemia despite high sup-
and activation of other inflammatory cells, plemental oxygen therapy. Gas exchange is
which then produce epithelial injury and further compromised by alveolar collapse re-
edema, changes in mucociliary function, and sulting from abnormalities in surfactant pro-
reduced clearance of respiratory tract secre- duction. When injury to the alveolar
tions, and increased airway responsiveness. epithelium is severe, disorganized epithelial
4. The two processes that are critical to the repair may lead to fibrosis.
pathogenesis of bronchiectasis are airway ob-
struction and chronic persistent infection, SECTION III: APPLYING
causing damage to the bronchial walls, leading YOUR KNOWLEDGE
to weakening and dilation.
5. Cystic fibrosis is caused by mutations in a sin- Activity F
gle gene on the long arm of chromosome 7 1. Diagnostic tests that the nurse would expect
that encodes for the cystic fibrosis transmem- to be ordered to confirm the diagnosis of
brane regulator (CFTR), which functions as a asthma include spirometry, inhalation chal-
chloride channel in epithelial cell membranes. lenge tests, and laboratory findings.
Mutations in the CFTR gene render the epithe- 2. “A plan of care will be developed with the
lial membrane relatively impermeable to the input of both you and your daughter to en-

chloride ion. The impaired transport of Cl ul- courage independence as it relates to the con-
timately leads to a series of secondary events, trol of her symptoms, along with measures
including increased absorption of Na and directed at helping her develop and maintain
water from the airways into the blood. This a positive self-concept.”
lowers the water content of the mucociliary
blanket coating the respiratory epithelium,
SECTION IV: PRACTICING FOR NCLEX
causing it to become more viscid. The result-
ing dehydration of the mucous layer leads to Activity G
defective mucociliary function and accumula-
1.
tion of viscid secretions that obstruct the air-
ways and predispose to recurrent pulmonary Mechanism Outcome
infections. The obstruction develops from the Decreased oxygen in air Hypoxemia
thick mucus, and recurrent infections damage
lung tissue, leading to the development of Inadequate circulation through Decreased PO2
bronchiectasis. pulmonary capillaries
6. Obstruction of pulmonary blood flow causes Hypoventilation Decreased PO2
reflex bronchoconstriction in the affected
area of the lung, wasted ventilation and im- Disease in respiratory system Hypoxemia
paired gas exchange, and loss of alveolar sur- Mismatched ventilation and perfusion Decreased PO2
factant. Pulmonary hypertension and right
Dysfunction of neurologic system Hypoxemia

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ANSWERS 427

Rationale: Hypoxemia can result from an in- Children between 3 and 5 years of age may
adequate amount of O2 in the air, disease of begin using a metered-dose inhaler with a
the respiratory system, dysfunction of the spacer and holding chamber. The other an-
neurologic system, or alterations in circula- swers are not correct.
tory function. The mechanisms, whereby res- 8. b. Rationale: The term chronic obstructive
piratory disorders lead to a significant pulmonary disease encompasses two types
reduction in PO2, are hypoventilation, im- of obstructive airway disease: emphysema,
paired diffusion of gases, inadequate circula- with enlargement of air spaces and destruc-
tion of blood through the pulmonary tion of lung tissue; and chronic obstructive
capillaries, and mismatching of ventilation bronchitis, with increased mucus produc-
and perfusion. tion, obstruction of small airways, and a
2. a, b, c, e. Rationale: Hypercapnia refers to an chronic productive cough. Persons with
increase in CO2 levels. In the clinical set- COPD often have overlapping features of
ting, four factors contribute to hypercapnia: both disorders. Asthma and chronic bron-
alterations in CO2 production, disturbance chitis have not been identified as compo-
in the gas exchange function of the lungs, nents of COPD.
abnormalities in respiratory function of the 9. c. Rationale: In the past, bronchiectasis often
chest wall and respiratory muscles, and followed a necrotizing bacterial pneumonia
changes in neural control of respiration. A that frequently complicated measles, pertus-
decrease in CO2 production does not cause sis, or influenza. Chickenpox has never been
hypercapnia. linked to bronchiectasis.
3. b. Rationale: One of the complications of un- 10. d. Rationale: In addition to airway obstruc-
treated moderate or large hemothorax is fi- tion, the basic genetic defect that occurs
brothorax—the fusion of the pleural surfaces with CF predisposes to chronic infection
by fibrin, hyalin, and connective tissue—and, with a surprisingly small number of organ-
in some cases, calcification of the fibrous tis- isms, the most common being Pseudomonas
sue, which restricts lung expansion. Calcifica- aeruginosa, Burkholderia cepacia, Staphylococ-
tion of the lung tissue does not occur because cus aureus, and Haemophilus influenzae. The
of a hemothorax. Neither does pleuritis or an other disease-causing organisms are not
atelectasis. linked to CF.
4. d. Rationale: Persons with talc lung are also 11. a, b, e. Rationale: Important etiologic determi-
highly susceptible to the occurrence of pneu- nants in the development of the pneumoco-
mothorax. Talc lung may result from inhala- nioses are the size of the dust particle, its
tion of talc particles, but is more commonly chemical nature and ability to incite lung de-
an occurrence of injected or inhaled talc struction, and the concentration of dust and
powder that is used as a filler with heroin, the length of exposure to it. The density and
methamphetamine, or codeine. Hemothorax, biologic nature of the dust particles are not
chylothorax, or fibrothorax is not a complica- linked to their ability to cause pneumoco-
tion of talc lung. nioses.
5. a, b, c. Rationale: Treatment of pleuritis 12. a. Rationale: Drugs can cause a variety of both
consists of treating the underlying disease acute and chronic alterations in lung function.
and inflammation. Analgesics and nons- For example, some of the cytotoxic drugs (e.g.,
teroidal anti-inflammatory drugs (e.g., bleomycin, busulfan, methotrexate, cyclophos-
indomethacin) may be used for pleural phamide) used in treatment of cancer cause
pain. Although these agents reduce inflam- pulmonary damage as a result of direct toxicity
mation, they may not entirely relieve the of the drug and by stimulating the influx of in-
discomfort associated with deep breathing flammatory cells into the alveoli. Amiodarone,
and coughing. a drug used to treat resistant cardiac arrhyth-
6. c. Rationale: If the collapsed area is large, the mias, is preferentially sequestered in the lung
mediastinum and trachea shift to the affected and causes significant pneumonitis in 5% to
side. In compression atelectasis, the medi- 15% of persons receiving it. Inderal does not
astinum shifts away from the affected lung. cause a direct toxicity in the lungs.
None of the other answers are correct. 13. b. Rationale: Chest pain, dyspnea, and in-
7. a. Rationale: For children younger than 2 creased respiratory rate are the most frequent
years, nebulizer therapy is usually preferred.

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428 ANSWERS

signs and symptoms of pulmonary embolism. CHAPTER 30 STRUCTURE AND

Pulmonary infarction often causes pleuritic
pain that changes with respiration; it is more FUNCTION OF THE KIDNEY
severe on inspiration and less severe on expi-
ration. Neither mediastinal and tracheal SECTION II: ASSESSING
shifts nor pericardial pain are signs of a pul- YOUR UNDERSTANDING
monary infarction. Activity A
14. b. Rationale: Continued exposure of the pul-
monary vessels to hypoxemia is a common 1. kidneys
cause of pulmonary hypertension. Unlike 2. hilus
blood vessels in the systemic circulation, 3. Nephrons
most of which dilate in response to hypox- 4. cortex
emia and hypercapnia, the pulmonary ves- 5. renal pyramids
sels constrict. None of the other answers are 6. aorta
correct. 7. glomeruli
15. c. Rationale: Management of cor pulmonale 8. glomerulus
focuses on the treatment of the lung disease 9. Peritubular capillaries
and heart failure. Low-flow oxygen therapy 10. filtrate
may be used to reduce the pulmonary hyper- 11. glomerular filtration rate
tension and polycythemia associated with se- 12. concentration, basolateral
vere hypoxemia caused by chronic lung 13. Cotransport
disease. Low-flow oxygen used in treating cor 14. proximal
pulmonale does not stimulate the body to 15. renal threshold
breathe, it does not act in an inhibitory way 16. loop of Henle
on the respiratory center in the brain, nor 17. Na-K-2Cl
does it reduce the formation of pulmonary 18. distal convoluted
emboli. 19. antidiuretic hormone
16. b, d, e. Rationale: Clinically, acute lung 20. sympathetic
injury/ARDS is marked by a rapid onset, usu- 21. clearance
ally within 12 to 18 hours of the initiating 22. Aldosterone
event, of respiratory distress, an increase in 23. sodium
respiratory rate, and signs of respiratory fail- 24. bicarbonate, hydrogen
ure. Chest radiography shows diffuse bilateral 25. Urea
infiltrates of the lung tissue in the absence of 26. erythropoietin
cardiac dysfunction. Marked hypoxemia oc- 27. Proteinuria
curs that is refractory to treatment with sup- 28. specific gravity
plemental oxygen therapy, which results in a 29. Creatinine
decrease in the PF ratio. Many persons with 30. Blood urea nitrogen
ARDS have a systemic response that results in
multiple organ failure, particularly the renal, Activity B
gastrointestinal, cardiovascular, and central
1. e 2. d 3. i 4. a 5. j
nervous systems. The other answers are not
6. g 7. b 8. h 9. f 10. c
clinical signs of ARDS.
17. d. Rationale: Many of the adverse conse-
quences of hypercapnia are the result of res- Activity C
piratory acidosis. Direct effects of acidosis 1. Decreased glomerular filtration rate→juxta-
include depression of cardiac contractility, glomerular release of renin→ conversion of
decreased respiratory muscle contractility, angiotensinogen to angiotensin I by renin→
and arterial vasodilation. Raised levels of conversion of angiotensin I to angiotensin II
PCO2 greatly increase cerebral blood flow, by angiotensin-converting enzyme→ an-
which may result in headache, increased giotensin II stimulates release of antidiuretic
cerebral spinal fluid pressure, and sometimes hormone and aldosterone→ sodium and water
papilledema. retention

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ANSWERS 429

Activity D reabsorption indirectly by stimulating aldos-

terone secretion from the adrenal gland and
1. The glomerular capillary membrane is com- directly by increasing sodium reabsorption by
posed of three layers: the capillary endothelial the proximal tubule cells. The increase in
layer, the basement membrane, and the sodium will result in an increase in water re-
single-celled capsular epithelial layer. The en- tention, which will increase blood volume
dothelial layer contains many small perfora- and, in turn, increase GFR.
tions called fenestrations. The epithelial layer 4. The actions of atrial natriuretic peptide (ANP)
that covers the glomerulus is continuous with include vasodilation of the afferent and effer-
the epithelium that lines Bowman’s capsule. ent arterioles, which results in an increase in
The cells of the epithelial layer have unusual renal blood flow and glomerular filtration rate.
octopuslike structures that possess a large ANP inhibits aldosterone secretion by the
number of extensions, or foot processes. These adrenal gland and sodium reabsorption from
foot processes form slit pores through which the collecting tubules through its action on al-
the glomerular filtrate passes. The basement dosterone and through direct action on the
membrane consists of a homogeneous acellu- tubular cells. It also inhibits ADH release from
lar meshwork of collagen fibers, glycoproteins, the posterior pituitary gland, thereby increas-
and mucopolysaccharides. The spaces between ing excretion of water by the kidneys. ANP
the fibers that make up the basement mem- also has vasodilator properties.
brane represent the pores of a filter and deter- 5. The kidneys function as an endocrine organ in
mine the size-dependent permeability barrier that they produce chemical mediators that
of the glomerulus. travel through the blood to distant sites where
2. The basic mechanisms of transport across the they exert their actions. The kidneys partici-
tubular epithelial cell membrane include ac- pate in control of blood pressure by way of the
tive and passive transport mechanisms. Water renin-angiotensin mechanism, in calcium me-
and urea are passively absorbed along concen- tabolism by activating vitamin D, and in regu-
tration gradients. Sodium, K, chloride, calcium, lating red blood cell production through the
and phosphate ions, as well as urate, glucose, synthesis of erythropoietin.
and amino acids, are reabsorbed using primary 6. By blocking the reabsorption of these solutes,
or secondary active transport mechanisms to diuretics create an osmotic pressure gradient
move across the tubular membrane. Some within the nephron that prevents the passive
substances, such as hydrogen, potassium, and reabsorption of water. Thus, diuretics cause
urate ions, are secreted into the tubular water and sodium to be retained within the
fluids. nephron, thereby promoting the excretion of
3. The juxtaglomerular complex is a feedback both. The increase in urine flow that a di-
control system that links changes in the uretic produces is related to the amount of
glomerular filtration rate (GFR) with renal sodium and chloride reabsorption that it
blood flow. It is located at the site where the blocks.
distal tubule extends back to the glomerulus,
and then passes between the afferent and ef-
ferent arteriole. The distal tubular site that is SECTION III: APPLYING
nearest the glomerulus is characterized by YOUR KNOWLEDGE
densely nucleated cells called the macula
Activity E
densa. In the adjacent afferent arteriole, the
smooth muscle cells of the media are modified 1. Tests that the nurse would expect to be or-
as special secretory cells called juxtaglomerular dered to either confirm or deny the diagnosis
cells. These cells contain granules of inactive include urine-specific gravity, urinalysis with
renin, an enzyme that functions in the con- culture and sensitivity, urine osmolality,
version of angiotensinogen to angiotensin. glomerular filtration rate, blood urea nitrogen,
Renin functions by means of angiotensin II to and serum electrolytes.
produce vasoconstriction of the efferent arteri- 2. A simple flat-plate x-ray will show the kidneys,
ole as a means of preventing serious decreases ureters, and any radiopaque stones that may
in GFR. Angiotensin II also increases sodium be in the kidney, ureters, or pelvis.

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430 ANSWERS

8. b. Rationale: With diminished renal function,

SECTION IV: PRACTICING FOR NCLEX
there is a loss of renal concentrating ability,
Activity F and the urine-specific gravity may fall to lev-
els of 1.006 to 1.010 (usual range is
1. a. Rationale: The plasma level at which the
1.010–1.025 with normal fluid intake). These
substance appears in the urine is called the
low levels are particularly significant if they
renal threshold. Renal clearance, renal filtra-
occur during periods that follow a decrease in
tion rate, and renal transport level are not the
water intake (e.g., during the first urine speci-
right answers.
men on arising in the morning). The other
2. b. Rationale: With ingestion of a high-protein
answers are incorrect.
diet, renal blood flow increases 20% to 30%
9. d. Rationale: Creatinine is freely filtered in the
within 1 to 2 hours. Although the exact
glomeruli, is not reabsorbed from the tubules
mechanism for this increase is uncertain, it is
into the blood, and is only minimally secreted
believed to be related to the fact that amino
into the tubules from the blood; therefore, its
acids and sodium are absorbed together in
blood values depend closely on the glomeru-
the proximal tubule (secondary active trans-
lar filtration rate (GFR). A normal serum crea-
port). The same mechanism is believed to ex-
tinine level usually indicates normal renal
plain the large increases in renal blood flow
function. In addition to its use in calculating
and glomerular filtration rate that occur with
the GFR, the serum creatinine level is used in
high blood glucose levels in persons with un-
estimating the functional capacity of the kid-
controlled diabetes mellitus.
neys. If the value doubles, the GFR—and renal
3. Renal clearance is the volume of plasma that is
function—has probably fallen to one-half its
completely cleared each minute of any sub-
normal state. A rise in the serum creatinine
stance that finds its way into the urine. It is de-
level to three times its normal value suggests
termined by the ability of the substance to be
that there is a 75% loss of renal function. A
filtered in the glomeruli and the capacity of
blood urea nitrogen level, 24-hour urine test,
the renal tubules to reabsorb or secrete the sub-
and urine test of first void in the morning do
stance. Every substance has its own clearance
not tell you about serum creatinine levels.
rate, the units of which are always volume of
10. a. Rationale: Cystoscopy provides a means for
plasma per unit time. It can be determined by
direct visualization of the urethra, bladder,
measuring the amount of a substance that is ex-
and ureteral orifices. It relies on the use of a
creted in the urine (i.e., urine concentration 
cystoscope, an instrument with a lighted
urine flow rate in milliliters per minute) and
lens. None of the other tests provides direct
dividing by its plasma concentration.
visualization of the bladder, urethra, and
4. c. Rationale: Small doses of aspirin compete
ureteral orifices.
with uric acid for secretion into the tubular
fluid and reduce uric acid secretion, and large
doses compete with uric acid for reabsorption CHAPTER 31 DISORDERS OF THE
and increase uric acid excretion in the urine.
5. d. Rationale: Alkaline or acid diuresis may be FLUID AND ELECTROLYTE BALANCE
used to increase elimination of drugs in the
urine, particularly in situations of drug over- SECTION II: ASSESSING YOUR
dose. The other answers are incorrect UNDERSTANDING
6. a. Rationale: Persons with end-stage kidney Activity A
disease are often anemic because of an inabil-
ity of the kidneys to produce erythropoietin. 1. intracellular fluid compartment
This anemia is usually managed by the ad- 2. extracellular fluid compartment
ministration of a recombinant erythropoietin 3. Electrolytes
(epoetin alfa) that is produced through DNA 4. nonelectrolytes
technology to stimulate erythropoiesis. 5. Diffusion
7. b. Rationale: The increase in urine flow that a 6. Osmosis
diuretic produces is related to the amount of 7. Osmolarity, osmolality
sodium and chloride reabsorption that it 8. Na
blocks. The other answers are not correct. 9. osmolar gap

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ANSWERS 431

10. Osmotically active Activity C

11. Na/K-ATPase
12. Capillary filtration 1.
13. lymphatic system 1. c 2. g 3. e 4. b 5. j
14. Edema 6. f 7. a 8. h 9. d 10. i
15. plasma proteins 2.
16. Pitting 1. d 2. h 3. b 4. a 5. c
17. Third-space fluids 6. j 7. e 8. g 9. i 10. f
18. insensible water losses Activity D
19. kidney
20. effective circulating volume
21. angiotensin II, aldosterone Decreased serum
calcium
22. Thirst, antidiuretic hormone
23. Psychogenic polydipsia
24. Diabetes insipidus
25. hyponatremia, hypernatremia
26. hypovolemia Parathyroid
27. Third-space losses glands
28. isotonic
29. Hyponatremia Parathyroid
30. Normovolemic hypotonic hormone
Activated
31. antidiuretic hormone vitamin D
32. Hypernatremia
33. water Bone
34. Na-K exchange mechanism
35. resting membrane potential Release of
36. hyperkalemia calcium
Kidney
37. hypokalemia
38. renal failure Intestine
39. excess Increased calcium
40. Vitamin D absorption
41. Magnesium
42. hypocalcemia Decreased calcium
elimination and increased
43. hypophosphatemia phosphate elimination
44. calcium
45. Magnesium
Activity B Increased
//Insert FIGURE serum
31-12.//
calcium
Feedback

Activity E
Blood volume
Serum osmolality 1. The extracellular fluid (ECF), including blood
plasma and interstitial fluids, contains large
amounts of sodium and chloride; moderate
Secretion of amounts of bicarbonate; and only small quan-
Thirst
ADH tities of potassium, magnesium, calcium, and
phosphorus. In contrast to the ECF, the intra-
Water ingestion Reabsorption of cellular fluid contains almost no calcium;
water by the kidney
small amounts of sodium, chloride, bicarbon-
ate, and phosphorus; moderate amounts of
Extracellular magnesium; and large amounts of potassium.
water volume
Feedback

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432 ANSWERS

2. The forces that control the movement of action potential, returning the membrane po-
water between the capillary and interstitial tential to its normal resting value. Hy-
spaces are (a) capillary filtration pressure, pokalemia reduces the permeability of the
which pushes water out of the capillary and cell membrane to potassium and thus pro-
into the interstitial spaces; (b) capillary col- duces a decrease in potassium efflux that pro-
loidal osmotic pressure, which pulls water longs the rate of repolarization and lengthens
back into the capillary; (c) interstitial hydro- the relative refractory period. The U wave
static pressure, which opposes the movement may normally be present on the ECG but
of water out of the capillary; and (d) tissue should be of lower amplitude than the T
colloidal osmotic pressure, which pulls water wave. With hypo-kalemia, the amplitude of
out of the capillary and into the interstitial the T wave decreases as the U-wave amplitude
spaces. increases.
3. Mechanisms that contribute to edema forma- 8. Systemic effects of hypercalcemia are (a)
tion include factors that increase the capillary changes in neural excitability, (b) alterations
filtration pressure, decrease the capillary col- in smooth and cardiac muscle function, and
loidal osmotic pressure, increase capillary per- (c) exposure of the kidneys to high concentra-
meability, or produce obstruction to lymph tions of calcium.
flow.
4. The major regulator of sodium and water bal- SECTION III: APPLYING YOUR
ance is the maintenance of the effective circu- KNOWLEDGE
lating volume, which can be described as that
portion of the extracellular fluid that fills the Activity F
vascular compartment and is “effectively” per- 1. “When a patient has burns over a large area of
fusing the tissues. A low effective circulating her body, there is a loss of protein in the
volume results in feedback mechanisms that plasma of the body. There is also injury to the
produce an increase in renal and sodium and capillaries in the burned area. Large amounts
water retention, as well as a high circulating of albumin are moved out of the blood and are
volume in feedback mechanisms that de- lost in the urine. We are working hard to in-
creases sodium and water retention. fuse fluid that the body needs with our IV so-
5. The three types of polydipsia include (a) symp- lutions.”
tomatic or true thirst, (b) inappropriate or false 2. The nurse knows that the diagnosis of fluid
thirst that occurs despite normal levels of volume deficit is based on these factors:
body water and serum osmolality, and • History of conditions that predispose to
(c) compulsive water drinking. sodium and water losses
6. There may be a decrease in blood urea nitro- • Weight loss
gen and hematocrit because of dilution due to • Intake and output
expansion of the plasma volume. An increase • Heart rate
in vascular volume may be evidenced by dis- • Blood pressure
tended neck veins, slow-emptying peripheral • Testing for venous refill
veins, a full and bounding pulse, and an in- • Capillary refill time
crease in central venous pressure. When excess
fluid accumulates in the lungs (i.e., pulmonary
SECTION IV: PRACTICING FOR NCLEX
edema), there are complaints of shortness of
breath and difficult breathing, respiratory Activity G
crackles, and a productive cough. Ascites and
1. a, b, d, e. Rationale: The physiologic mecha-
pleural effusion may occur with severe fluid
nisms that contribute to edema formation in-
volume excess.
clude factors that (a) increase the capillary
7. These changes include prolongation of the PR
filtration pressure, (b) decrease the capillary
interval, depression of the ST segment, flatten-
colloidal osmotic pressure, (c) increase capil-
ing of the T wave, and appearance of a pro-
lary permeability, or (d) produce obstruction
minent U wave. Normally, potassium leaves
to lymph flow.
the cell during the repolarization phase of the

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ANSWERS 433

2. 1-d, 2-e, 3-a, 4-c, 5-b hypophosphatemia occurs. The other condi-
3. a. Rationale: The major regulator of sodium tions are not caused by hypophosphatemia.
and water balance is the maintenance of the 10. a. Rationale: Severe hypermagnesemia (12
effective circulating volume. The other an- mg/dL) is associated with muscle and respira-
swers are not regulated by the effective circu- tory paralysis, complete heart block, and car-
lating volume. diac arrest.
4. b. Rationale: Psychogenic polydipsia may be
compounded by antipsychotic medications
that increase ADH levels and interfere with
CHAPTER 32 DISORDERS OF
water excretion by the kidneys. Cigarette ACID-BASE BALANCE
smoking, which is common among persons
with psychiatric disorders, also stimulates SECTION II: ASSESSING YOUR
ADH secretion. UNDERSTANDING
5. c. Rationale: Other acquired causes of Activity A
nephrogenic DI are drugs such as lithium
and electrolyte disorders such as potassium 1. 7.35, 7.45
depletion or chronic hypercalcemia. The 2. pH
other answers are not acquired causes of 3. metabolic
nephrogenic DI. 4. volatile, nonvolatile
6. c. Rationale: When this occurs, water moves 5. H2CO3
into the brain cells, causing cerebral edema 6. dietary proteins
and potentially severe neurologic impair- 7. Henderson-Hasselbalch equation
ment. The other cells are not correct. 8. buffer system
7. a. Rationale: Changes in nerve and muscle ex- 9. bone
citability are particularly important in the 10. bicarbonate
heart, where alterations in plasma potassium 11. Albumin, plasma globulins
can produce serious cardiac arrhythmias and 12. H , HCO3–
conduction defects. The other answers are 13. ammonia
not correct. 14. Hypokalemia
8. b. Rationale: The small, but vital, amount of 15. Aldosterone
extracellular fluid, calcium, phosphorus, and 16. variability
magnesium is directly or indirectly regulated 17. anion gap
by vitamin D and parathyroid hormone. The 18. acidosis, alkalosis
other answers are not correct. 19. Compensatory mechanisms
9. d. Rationale: The NPT2 gene is also inhibited 20. Metabolic acidosis
by the recently identified hormone phospha- 21. lactic
tonin. When this hormone is overproduced, 22. ketoacids
as in tumor-induced osteomalacia, marked 23. salicylates

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434 ANSWERS

24. alcohol dehydrogenase 28. hypoventilation, hypoxemia

25. Chronic kidney 29. acidosis
26. HCO3 30. vasodilation
27. Metabolic alkalosis 31. alkalosis

Activity B

7.4

6.9 7.9

24 1.2
pH = 6.1 + log10 (ratio HCO3-: H2CO3)
HCO3- H2CO3
(mEq/L) (mEq/L)

A Ratio: HCO3-: H2CO3 = 20:1

normal, ph 7.4

7.4 7.4
7.7
6.9 7.9 6.9 7.9

12 0.6

HCO3- 1.2 24 H2CO3

(mEq/L) (mEq/L)
H2CO3 HCO3-
(mEq/L) (mEq/L)

B Ratio: HCO3-: H2CO3 = 10:1 D Ratio: HCO3-: H2CO3 = 40:1

metabolic acidosis respiratory alkalosis

7.4 7.4

6.9 7.9 6.9 7.9

12 0.6 12 0.6

HCO3- H2CO3 HCO3- H2CO3

(mEq/L) (mEq/L) (mEq/L) (mEq/L)

C Ratio: HCO3-: H2CO3 = 20:1 E Ratio: HCO3-: H2CO3 = 20:1

metabolic acidosis with respiratory alkalosis
respiratory compensation with renal compensation

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ANSWERS 435

Activity C ation in the PCO2, reflecting an increase or de-

crease in alveolar ventilation. Respiratory acidosis
1. e 2. a 3. i 4. h 5. c is characterized by a decrease in pH, reflecting a
6. b 7. d 8. j 9. f 10. g decrease in ventilation and an increase in PCO2.
Respiratory alkalosis involves an increase in pH,
Activity D
resulting from an increase in alveolar ventilation
1. Carbon dioxide is transported in the body (a) as and a decrease in PCO2.
a dissolved gas; (b) as bicarbonate (HCO3–); and 6. The manifestations of metabolic acidosis fall
(c) as carbaminohemoglobin, bound to amino into three categories. The first category is signs
acids. and symptoms of the disorder causing the aci-
2. Excess H ions can be exchanged for Na and K dosis or the primary condition. The second is
on the bone surface and dissolution of bone changes in body function related to recruit-
minerals with release of compounds, such as ment of compensatory mechanisms that con-
sodium bicarbonate (NaHCO3) and calcium tribute to the manifestations. In situations of
carbonate (CaCO3), into the extracellular fluid acute metabolic acidosis, the respiratory system
can be used for buffering excess acids. It has compensates for a decrease in pH by increasing
been estimated that as much as 40% of buffer- ventilation to reduce PCO2; this is accom-
ing of an acute acid load takes place in bone. plished through deep and rapid respirations.
The role of bone buffers is even greater in the There may be complaints of difficult breathing
presence of chronic acidosis. The consequences or dyspnea with exertion; with severe acidosis,
of bone buffering include demineralization of dyspnea may be present even at rest. The third
bone and predisposition to development of is alterations in cardiovascular, neurologic, and
kidney stones due to increased urinary excre- musculoskeletal function resulting from the de-
tion of calcium. Persons with chronic kidney creased pH and its effect on protein structure.
disease are at particular risk for reduction in 7. The signs and symptoms of respiratory alkalo-
bone calcium due to acid retention. sis are associated with hyperexcitability of the
3. The transcompartmental exchange of H and nervous system and a decrease in cerebral
potassium ions (K) provides an important blood flow. Alkalosis increases protein binding
system for regulation of acid-base balance. of extracellular calcium. This reduces ionized
Both ions are positively charged, and both calcium levels, causing an increase in neuro-
ions move freely between the intracellular muscular excitability. A decrease in the CO2
fluid (ICF) and extracellular fluid (ECF) com- content of the blood causes constriction of
partments. When excess H is present in the cerebral blood vessels. Because CO2 crosses the
ECF, it moves into the ICF in exchange for K blood-brain barrier rather quickly, the mani-
and when excess K is present in the ECF, it festations of acute respiratory alkalosis are usu-
moves into the ICF in exchange for H. Thus, ally of sudden onset. The person often
alterations in potassium levels can affect acid- experiences lightheadedness, dizziness, tin-
base balance, and changes in acid-base balance gling, and numbness of the fingers and toes.
can influence potassium levels. These manifestations may be accompanied by
4. The kidneys play two major roles in regulating sweating, palpitations, panic, air hunger, and
acid-base balance. The first is accomplished dyspnea. Because CO2 provides the stimulus
through the reabsorption of the HCO3 that is for short-term regulation of respiration, short
filtered in the glomerulus so this important periods of apnea may occur in persons with
buffer is not lost in the urine. The second is acute episodes of hyperventilation.
through the excretion of H from fixed acids
that result from protein and lipid metabolism.
5. There are two types of acid-base disorders: meta- SECTION III: APPLYING YOUR
bolic and respiratory. Metabolic disorders produce KNOWLEDGE
an alteration in the plasma HCO3 concentration
Activity E
and result from the addition or loss of nonvolatile
acid or alkali to or from the extracellular fluids. A 1. This patient’s laboratory values indicate meta-
reduction in pH due to a decrease in HCO3 is bolic acidosis.
called metabolic acidosis, and an elevation in pH 2. A blood glucose level would be important to
due to increased HCO3 levels is called metabolic rule out diabetes mellitus as a cause of the
alkalosis. Respiratory disorders involve an alter- metabolic acidosis.

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436 ANSWERS

are not signs or symptoms of respiratory

SECTION IV: PRACTICING FOR NCLEX
acidosis.
Activity F 10. a. Rationale: One of the most common causes
of respiratory alkalosis is hyperventilation
1. a. Rationale: The H2CO3 content of the blood
syndrome, which is characterized by recur-
can be calculated by multiplying the partial
ring episodes of overbreathing, often associ-
pressure of CO2 (PCO2) by its solubility coeffi-
ated with anxiety.
cient, which is 0.03.
2. a, c, e. Rationale: The pH of body fluids is reg-
ulated by three major mechanisms: (a) chem- CHAPTER 33 DISORDERS
ical buffer systems of the body fluids, which
immediately combine with excess acids or
OF RENAL FUNCTION
bases to prevent large changes in pH; (b) the
SECTION II: ASSESSING YOUR
lungs, which control the elimination of CO2;
UNDERSTANDING
and (c) the kidneys, which eliminate H and
both reabsorb and generate HCO3–. None of Activity A
the other answers are correct.
1. shape, position
3. c. Rationale: The renal mechanisms for regu-
2. agenesis
lating acid-base balance cannot adjust the pH
3. Potter syndrome
within minutes as respiratory mechanisms
4. hypoplasia
can, but they continue to function for days,
5. dysplasia
until the pH has returned to normal or near-
6. multicystic
normal range. It is the respiratory system that
7. Polycystic
responds within minutes to return the body’s
8. autosomal dominant
pH near to its normal limits. The rest of the
9. destructive
answers are wrong.
10. Stagnation
4. d. Rationale: The total base excess or deficit,
11. Hydronephrosis
also referred to as the whole blood buffer
12. distention
base, measures the level of all buffer systems
13. calculi
of the blood—hemoglobin, protein, phos-
14. nidus
phate, and HCO3–. For clinical purposes, base
15. calcium
excess or deficit can be viewed as a measure-
16. pain
ment of bicarbonate excess or deficit.
17. second
5. a. Rationale: Metabolic disorders produce an al-
18. Escherichia coli
teration in the plasma HCO3 concentration
19. urethra
and result from the addition or loss of non-
20. more
volatile acid or alkali to or from the extracellu-
21. anatomic, functional
lar fluids. None of the other answers are correct.
22. Catheter
6. b. Rationale: Often, compensatory mecha-
23. cystitis
nisms are interim measures that permit sur-
24. Glomerulonephritis
vival while the body attempts to correct the
25. nephritic, nephrotic
primary disorder. All other answers are wrong.
26. Acute nephritic
7. c. Rationale: The anion gap is often useful in
27. deposition
determining the cause of the metabolic aci-
28. hypercellularity
dosis. None of the other tests are used to de-
29. Goodpasture
termine the cause of metabolic acidosis.
30. Nephrotic
8. d. Rationale: A fall in pH to less than 7.0 to
31. Membranous
7.10 can reduce cardiac contractility and pre-
32. Buerger
dispose to potentially fatal cardiac dysrhyth-
33. basement membrane
mias. No other answer is correct.
34. Renal tubular acidosis
9. a, b, c. Rationale: Elevated levels of CO2 pro-
35. HCO3
duce vasodilation of cerebral blood vessels,
36. Acute pyelonephritis
causing headache, blurred vision, irritabil-
37. Wilms tumor
ity, muscle twitching, and psychological
38. hematuria, mass
disturbances. Seizures and psychotic breaks

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ANSWERS 437

Activity B Activity E
1. The destructive effects of urinary obstruction
on kidney structures are determined by the de-
gree (i.e., partial vs. complete, unilateral vs. bi-
lateral) and the duration of the obstruction.
The two most damaging effects of urinary ob-
struction are stasis of urine, which predisposes
to infection and stone formation, and progres-
sive dilation of the renal collecting ducts and
Kidney renal tubular structures, which causes destruc-
stone tion and atrophy of renal tissue.
Pregnancy 2. Kidney stone formation requires supersatu-
or tumor rated urine and an environment that allows
Scar the stone to grow. The risk for stone formation
Uretero-
tissue is increased when the urine is supersaturated
vesical with stone components (e.g., calcium salts,
junction uric acid, magnesium ammonium phosphate,
stricture cystine). Supersaturation depends on urinary
pH, solute concentration, ionic strength, and
Neurogenic complexation. The greater the concentration
bladder of two ions, the more likely they are to precip-
Bladder itate. Complexation influences the availability
outflow of specific ions.
obstruction
3. The risk factors for urinary tract infection are
Activity C higher:
• In persons with urinary obstruction and reflux
1. c 2. a 3. f 4. g 5. e • In persons with neurogenic disorders that
6. i 7. d 8. h 9. b 10. j impair bladder emptying
• In women who are sexually active
Activity D
• In postmenopausal women
• In men with diseases of the prostate
• In elderly persons
• In persons who have undergone catheteriza-
tion
• In women with diabetes
4. The host defenses of the bladder include the
Glomerular damage
washout phenomenon, in which bacteria are
removed from the bladder and urethra during
voiding; the protective mucin layer that lines
the bladder and protects against bacterial inva-
Increased permeability to proteins
Proteinuria ( 3.5 g/24 h)
sion; and local immune responses. In the
ureters, peristaltic movements facilitate the
movement of urine from the renal pelvis
Hypoproteinemia
through the ureters and into the bladder. Im-
mune mechanisms, particularly secretory im-
munoglobulin A, appear to provide an
Decreased plasma Compensatory synthesis
important antibacterial defense. Phagocytic
oncotic pressure of proteins by liver blood cells further assist in the removal of bac-
teria from the urinary tract. In women, the
Edema Hyperlipidemia
normal flora of the periurethral area, which
consists of organisms such as lactobacillus,
provides defense against the colonization of

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438 ANSWERS

uropathic bacteria. In men, the prostatic fluid 2. To prevent further contamination by the in-
has antimicrobial properties that protect the dwelling catheter, the nurse would maintain a
urethra from colonization. closed drainage system, pay careful attention
5. The cellular changes that occur with glomeru- to perineal hygiene, and practice careful hand-
lar disease include increases in glomerular washing.
and/or inflammatory cell number, basement
membrane thickening, and changes in noncel- SECTION IV: PRACTICING FOR NCLEX
lular glomerular components.
6. The development of glomerulonephritis fol- Activity G
lows a streptococcal infection by approxi- 1. a, b, c, e. Rationale: Bilateral renal dysplasia
mately 7 to 12 days—the time needed for the causes oligohydramnios and the resultant
production of antibodies. The primary infec- Potter facies, pulmonary hypoplasia, and
tion usually involves the pharynx. Oliguria, renal failure. Multicystic kidneys are a disor-
which develops as the glomerular filtration der, not the result of a congenital problem.
rate decreases, is one of the first symptoms. 2. 1-b, 2-a, 3-d, 4-c
Proteinuria and hematuria follow because of 3. a. Rationale: Urinary tract obstruction encour-
increased glomerular capillary wall perme- ages the growth of microorganisms and
ability. The red blood cells are degraded by should be suspected in persons with recurrent
materials in the urine, and cola-colored urine UTIs. The other answers can cause lower
may be the first sign of the disorder. Sodium UTIs, but an obstruction would be considered
and water retention gives rise to edema (par- because of the frequency of the infections.
ticularly of the face and hands) and hyper- 4. b. Rationale: Phosphate levels are increased in
tension. alkaline urine and magnesium, always pres-
7. Widespread thickening of the glomerular cap- ent in the urine, and combine to form stru-
illary basement membrane occurs in almost all vite stones. These stones can increase in size
persons with diabetes and can occur without until they fill an entire renal pelvis. Because
evidence of proteinuria. This is followed by a of their shape, they are often called staghorn
diffuse increase in mesangial matrix, with stones. The other minerals can form stones,
mild proliferation of mesangial cells. As the but not staghorn stones.
disease progresses, the mesangial cells impinge 5. c. Rationale: Most uncomplicated lower UTIs
on the capillary lumen, reducing the surface are caused by Escherichia coli. The other or-
area for glomerular filtration. ganisms can cause UTIs, but are not the most
8. Drug-related nephropathies involve functional common cause of infection.
or structural changes in the kidneys that occur 6. b, c, d. Rationale: Toddlers often present with
after exposure to a drug. Because of their large abdominal pain, vomiting, diarrhea, abnor-
blood flow and high filtration pressure, the mal voiding patterns, foul-smelling urine,
kidneys are exposed to any substance that is in fever, and poor growth. Toddlers do not typi-
the blood. The kidneys are also active in the cally have frequency in voiding, nor do they
metabolic transformation of drugs and there- complain of burning when they urinate.
fore are exposed to a number of toxic metabo- 7. d. Rationale: Group A -hemolytic strepto-
lites. Drugs and toxic substances can damage cocci has the ability to seed from one area of
the kidneys by causing a decrease in renal the body to another. One area it seeds to is
blood flow, obstructing urine flow, directly the kidney, where it causes acute postinfec-
damaging tubulointerstitial structures, or pro- tious glomerulonephritis. Other organisms
ducing hypersensitivity reactions. can cause acute postinfectious glomeru-
lonephritis, but they are not the most com-
SECTION III: APPLYING YOUR mon cause of the disease.
KNOWLEDGE 8. a. Rationale: The lesions of diabetic nephropa-
thy most commonly involve the glomeruli
Activity F
and are associated with three glomerular syn-
1. The nurse would expect the following orders: dromes: nonnephrotic proteinuria, nephrotic
urine analysis, urine culture and sensitivity, syndrome, and chronic renal failure. The
and broad-spectrum antibiotic given intra- other answers are not commonly associated
venously. with diabetic nephropathy.

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ANSWERS 439

9. b. Rationale: The most common causative Activity B

agents of acute pyelonephritis are gram-
negative bacteria, including Escherichia coli
Prerenal
and Proteus, Klebsiella, Enterobacter, and Intrinsic (marked decrease
Pseudomonas. The other answers are not con- (damage to in renal blood flow)
sidered a common causative agent of acute structures
pyelonephritis. within the
kidney)
10. c. Rationale: The tolerance to drugs varies
with age and depends on renal function,
state of hydration, blood pressure, and pH
of the urine. None of the other answers are
correct.
11. d. Rationale: The common presenting signs of
Postrenal
a Wilms’ tumor are a large asymptomatic ab- (obstruction of
dominal mass and hypertension. The tumor urine outflow
is often discovered inadvertently, and it is from the kidney)
not uncommon for the mother to discover it
while bathing the child. Some children may
present with abdominal pain, vomiting, or
both. Hypotension, oliguria, and diarrhea are Activity C
not common presenting signs of a Wilms
tumor. 1. b 2. j 3. d 4. g 5. a
6. e 7. h 8. i 9. f 10. c

CHAPTER 34 ACUTE RENAL FAILURE Activity D

AND CHRONIC KIDNEY DISEASE 1. Acute tubular necrosis (ATN) is characterized
by the destruction of tubular epithelial cells
SECTION II: ASSESSING YOUR with acute suppression of renal function. ATN
UNDERSTANDING can be caused by a variety of conditions, in-
Activity A cluding acute tubular damage due to ischemia,
sepsis, nephrotoxic effects of drugs, tubular
1. Acute renal failure obstruction, and toxins from a massive infec-
2. prerenal, intrinsic, postrenal tion. Tubular epithelial cells are particularly
3. Prerenal sensitive to ischemia and are vulnerable to
4. tubular epithelial toxins. The tubular injury that occurs in ATN
5. blood urea nitrogen is frequently reversible.
6. Postrenal 2. The onset or initiating phase, which lasts
7. cause hours or days, is the time from the onset of
8. chronic kidney disease the precipitating event until tubular injury oc-
9. 120 to 130 curs. The maintenance phase of acute tubular
10. creatinine necrosis is characterized by a marked decrease
11. tubulointerstitial, albumin in the glomerular filtration rate, causing sud-
12. uremic den retention of endogenous metabolites,
13. dehydration, overload such as urea, potassium, sulfate, and creati-
14. sodium nine, that are normally cleared by the kidneys.
15. bone Fluid retention gives rise to edema, water in-
16. osteodystrophy toxication, and pulmonary congestion. If the
17. Hypertension period of oliguria is prolonged, hypertension
18. uremia frequently develops and, with it, signs of ure-
19. atrophy, demyelination mia. The recovery phase is the period during
20. glomerular filtration rate which repair of renal tissue takes place. Its
onset is usually heralded by a gradual increase
in urine output and a fall in serum creatinine,

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440 ANSWERS

indicating that the nephrons have recovered to Congestive heart failure and pulmonary
the point at which urine excretion is possible. edema tend to occur in the late stages of kid-
3. Glomerular filtration rate (GFR) is used to clas- ney failure. Coexisting conditions that have
sify chronic kidney disease (CKD) into five been identified as contributing to the burden
stages, beginning with kidney damage with of cardiovascular disease include hyperten-
normal or elevated GFR and progressing to sion, anemia, diabetes mellitus, dyslipidemia,
CKD and, potentially, kidney failure. and coagulopathies. Anemia, in particular, has
4. As kidney structures are destroyed, the remain- been correlated with the presence of left ven-
ing nephrons undergo structural and functional tricular hypertrophy.
hypertrophy, each increasing its function as a
means of compensating for those that have SECTION III: APPLYING YOUR
been lost. In the process, each remaining KNOWLEDGE
nephron must filter more solute particles from
Activity E
the blood. It is only when the few remaining
nephrons are destroyed that the manifestations 1. The nurse would include the following in dis-
of kidney failure become evident. charge teaching to the child and his family:
5. The manifestations of chronic kidney disease description of the disease process; prognosis;
include an accumulation of nitrogenous manifestations of the disease, including physi-
wastes; alterations in water, electrolyte, and cal growth and developmental delays; medica-
acid-base balance; mineral and skeletal disor- tion regimen, including side effects; and
ders; anemia and coagulation disorders; hyper- dietary restrictions, including protein, caloric,
tension and alterations in cardiovascular sodium, and fluid restrictions.
function; gastrointestinal disorders; neurologic 2. Chronic kidney disease is a progressive disor-
complications; disorders of skin integrity; and der that can be slowed by adherence to dietary
disorders of immunologic function. The point restrictions and medication regimen. The dis-
at which these disorders make their appear- order usually progresses to the point where the
ance and the severity of the manifestations are child needs hemodialysis or peritoneal dialysis,
determined largely by the extent of renal func- or a kidney transplant. All forms of renal re-
tion that is present and the coexisting disease placement therapy are considered safe in the
conditions. pediatric population, and renal transplantation
6. The anemia of chronic kidney disease is due to is considered the best treatment for a child.
several factors, including chronic blood loss,
hemolysis, bone marrow suppression due to SECTION IV: PRACTICING FOR NCLEX
retained uremic factors, and decreased red
Activity F
blood cell (RBC) production due to impaired
production of erythropoietin and iron defi- 1. a. Rationale: The most common indicator of
ciency. The kidneys are the primary site for acute renal failure is azotemia, an accumula-
the production of the hormone erythropoi- tion of nitrogenous wastes (urea nitrogen,
etin, which controls RBC production. In renal uric acid, and creatinine) in the blood and a
failure, erythropoietin production is usually decrease in the glomerular filtration rate. The
insufficient to stimulate adequate RBC produc- other answers are not common indicators of
tion by the bone marrow. acute renal failure.
7. People with chronic kidney disease tend to 2. a, c, d. Rationale: Ischemic ATN occurs most
have an increased prevalence of left ventricu- frequently in persons who have major
lar dysfunction, with both depressed left ven- surgery, severe hypovolemia, overwhelming
tricular ejection fraction, as in systolic sepsis, trauma, and burns. Hypervolemia and
dysfunction, and impaired ventricular filling, hypertension are not considered contributing
as in diastolic failure. Multiple factors lead to factors to ischemic ATN.
development of left ventricular dysfunction, 3. b. Rationale: In clinical practice, GFR is usu-
including extracellular fluid overload, shunt- ally estimated using the serum creatinine
ing of blood through an arteriovenous fistula concentration. The other answers are not
for dialysis, and anemia. Coupled with the hy- used to estimate the GFR.
pertension that is often present, they cause in- 4. c. Rationale: The number one hematologic
creased myocardial work and oxygen demand, disorder that accompanies CKD is anemia.
with eventual development of heart failure. The other answers are incorrect.

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ANSWERS 441

5. a, b, c. Rationale: Uremic pericarditis resem- 4. ureters

bles viral pericarditis in its presentation. This 5. epithelial lining
includes all potential complications, up to 6. external sphincter
and including cardiac tamponade. The pre- 7. parasympathetic, sympathetic
senting signs include mild to severe chest 8. sacral, pelvic nerve
pain with respiratory accentuation and a 9. pons
pericardial friction rub. Fever is variable in 10. Cortical
the absence of infection and is more com- 11. 2-adrenergic
mon in dialysis than uremic pericarditis. 12. 1 receptors
Shortness of breath and thromboangiitis are 13. obstruction, incontinence
not indicative of uremic pericarditis. 14. prostate gland
6. d. Rationale: Restless leg syndrome is a mani- 15. store, empty
festation of peripheral nerve involvement 16. micturition reflex
and can be seen in as many as two-thirds of 17. stroke
patients on dialysis. The other answers are 18. Atony
not correct. 19. Stress incontinence
7. a. Rationale: Many persons with chronic kid- 20. neurogenic, myogenic
ney disease fail to mount a fever with infec- 21. transitional
tion, making the diagnosis more difficult. All 22. hematuria
of the other answers occur.
8. a, b, c. Rationale: The cause of sexual dysfunc- Activity B
tion in men and women with CKD is unclear. Epithelium when Epithelium when
The cause is probably multifactorial and may bladder is empty bladder is full
result from high levels of uremic toxins, neu-
ropathy, altered endocrine function, psycho-
logical factors, and medications (e.g.,
antihypertensive drugs). The other answers
do not apply in this situation.
Detrusor
9. b. Rationale: Access to the vascular system is muscle
accomplished through an external arteriove-
nous shunt (i.e., tubing implanted into an Ureters
artery and a vein) or, more commonly,
through an internal arteriovenous fistula (i.e.,
anastomosis of a vein to an artery, usually in
the forearm). The other answers are incorrect.
10. c. Rationale: At least 50% of the protein in- Trigone
take for clients with CKD should consist of
Internal sphincter
proteins of high biologic value, such as those
in eggs, lean meat, and milk, which are rich External sphincter
in essential amino acids. The other sources of
protein contribute to high levels of nitrogen.
Activity C
1. i 2. f 3. a 4. d 5. j
CHAPTER 35 DISORDERS OF 6. g 7. b 8. e 9. h 10. c
THE BLADDER AND LOWER
URINARY TRACT Activity D
1. The bladder is composed of four layers: (a) is an
SECTION II: ASSESSING YOUR outer serosal layer, which covers the upper sur-
UNDERSTANDING face and is continuous with the peritoneum;
Activity A (b) a network of smooth muscle fibers called
the detrusor muscle; (c) a submucosal layer of
1. bladder loose connective tissue; and (d) an inner mu-
2. retroperitoneally, symphysis cosal lining of transitional epithelium.
3. prostate

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442 ANSWERS

2. The pelvic nerve carries sensory fibers from the The inner smooth surface of the bladder is re-
stretch receptors in the bladder wall; the pu- placed with coarsely woven structures called
dendal nerve carries sensory fibers from the trabeculae. Small pockets of mucosal tissue
external sphincter and pelvic muscles; and the commonly develop between the trabecular
hypogastric nerve carries sensory fibers from ridges. These pockets form diverticula, making
the trigone area. the patent more susceptible to secondary infec-
3. As bladder filling occurs, ascending spinal affer- tions. Along with hypertrophy of the bladder
ents relay this information to the micturition wall, there is hypertrophy of the trigone area
center, which also receives important descend- and the interureteric ridge, which is located be-
ing information from the forebrain concerning tween the two ureters. This causes backpressure
behavioral cues for bladder emptying and urine on the ureters, the development of hy-
storage. Descending pathways from the pontine droureters, and, eventually, kidney damage.
micturition center produce coordinated inhibi- 7. The angle between the bladder and the poste-
tion or relaxation of the external sphincter. rior proximal urethra normally is 90 to 100 de-
Cortical brain centers enable inhibition of the grees, with at least one-third of the bladder
micturition center in the pons and conscious base contributing to the angle when not void-
control of urination. Neural influences from the ing. During the first stage of voiding, this
subcortical centers in the basal ganglia modu- angle is lost as the bladder descends. In
late the contractile response. They modify and women, diminution of muscle tone associated
delay the detrusor contractile response during with childbirth can cause weakness of the
filling, and then modulate the expulsive activity pelvic floor muscles and result in stress incon-
of the bladder to facilitate complete emptying. tinence by obliterating the critical posterior
4. The detrusor muscle of the bladder fundus and urethrovesical angle. In these women, loss of
bladder neck contract down on the urine, the the posterior urethrovesical angle, descent and
ureteral orifices are forced shut, the bladder neck funneling of the bladder neck, and backward
is widened and shortened as it is pulled up by and downward rotation of the bladder occur,
the globular muscles in the bladder fundus, the so that the bladder and urethra are already in
resistance of the internal sphincter in the blad- an anatomic position for the first stage of
der neck is decreased, and the external sphincter voiding. Any activity that causes downward
relaxes as urine moves out of the bladder. pressure on the bladder is sufficient to allow
5. The necessary factors that every child must the urine to escape involuntarily.
possess in order to attain conscious control of 8. The neurogenic theory for overactive bladder
bladder function are (a) normal bladder postulates that the central nervous system
growth, (b) myelination of the ascending affer- (CNS) functions as an on–off switching circuit
ents that signal awareness of bladder filling, for voluntary control of bladder function.
(c) development of cortical control and de- Therefore, damage to the CNS inhibitory path-
scending communication with the sacral mic- ways may trigger bladder overactivity owing to
turition center, (d) ability to consciously tighten uncontrolled voiding reflexes. Neurogenic
the external sphincter to prevent incontinence, causes of overactive bladder include stroke,
(e) and motivation of the child to stay dry. Parkinson disease, and multiple sclerosis.
6. During the early stage of obstruction, the blad- 9. The overall capacity of the bladder is reduced,
der begins to hypertrophy and becomes hyper- as is the urethral closing pressure. Detrusor
sensitive to afferent stimuli arising from stretch muscle function also tends to decline with
receptors in the bladder wall. The ability to sup- aging; thus, there is a trend toward a reduction
press urination is diminished, and bladder con- in the strength of bladder contraction and im-
traction can become so strong that it virtually pairment in emptying that leads to larger
produces bladder spasm. There is further hyper- postvoid residual volumes.
trophy of the bladder muscle, the thickness of
the bladder wall may double, and the pressure SECTION III: APPLYING YOUR
generated by detrusor contraction will increase KNOWLEDGE
to overcome resistance from the obstruction. As
Activity E
the force needed to expel urine from the blad-
der increases, compensatory mechanisms may 1. “In people who have multiple sclerosis, the
become ineffective, causing muscle fatigue be- demyelination of the nerves can cause an
fore complete emptying can be accomplished. interruption in the messages from the brain

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ANSWERS 443

and the spinal cord reaching the bladder. This tract infections, medications that alter blad-
causes a condition known as a neurogenic der function or perception of bladder filling
bladder.” and the need to urinate, diuretics and condi-
2. The nurse would expect the client to be given tions that increase bladder filling, stool im-
an antimuscarinic drug, such as oxybutynin, paction, restricted mobility, and confusional
tolterodine, or propantheline, to decrease detru- states. The other answers are not associated
sor muscle tone and increase bladder capacity. with transient urinary incontinence.
9. b. Rationale: Habit training with regularly
SECTION IV: PRACTICING FOR NCLEX scheduled toileting—usually every 2 to 4
hours—is often effective. The other answers
Activity F
are incorrect.
1. a, c, e. Rationale: Disruption of pontine con- 10. c. Rationale: The intervesicular administration
trol of micturition, as in spinal cord injury, of bacillus Calmette-Guérin vaccine, made
results in uninhibited spinal reflex–controlled from a strain of Mycobacterium bovis that was
contraction of the bladder without relaxation formerly used to protect against tuberculosis,
of the external sphincter, a condition known causes a significant reduction in the rate of re-
as detrusor-sphincter dyssynergia. The other lapse and prolongs relapsefree interval in per-
answers are not true. sons with cancer in situ. The other drugs are
2. a. Rationale: As the child grows, the bladder used to treat bladder cancer, but not cancer
gradually enlarges, with an increase in capac- in situ.
ity, in ounces, that approximates the age of the
child plus 2. The other answers are not true. CHAPTER 36 STRUCTURE
3. b. Rationale: Sphincter electromyelogram al-
lows the activity of the striated (voluntary) AND FUNCTION OF THE
muscles of the perineal area to be studied. Cys- GASTROINTESTINAL SYSTEM
tometry measures the ability of the bladder to
store urine as well as the pressure of the blad- SECTION II: ASSESSING YOUR
der during filling and emptying. Uroflowme- UNDERSTANDING
try measures the flow rate during urination.
Activity A
4. b. Rationale: During the early stage of obstruc-
tion, the bladder begins to hypertrophy and 1. gastrointestinal system
becomes hypersensitive to afferent stimuli aris- 2. pharyngoesophageal
ing from stretch receptors in the bladder wall. 3. gastroesophageal
The ability to suppress urination is diminished, 4. stomach
and bladder contraction can become so strong 5. duodenum, jejunum, ileum
that it virtually produces bladder spasm. There 6. jejunum
is urgency, sometimes to the point of inconti- 7. epithelial, mucus
nence, and frequency during the day and at 8. Serous
night. The other answers are wrong. 9. mesentery
5. c. Rationale: The most common causes of 10. pacemaker
spastic bladder dysfunction are spinal cord le- 11. enteric
sions such as spinal cord injury, herniated in- 12. Mechanoreceptors, chemoreceptors
tervertebral disk, vascular lesions, tumors, 13. vagovagal
and myelitis. The other answers are wrong. 14. oral, pharyngeal, esophageal
6. d. Rationale: With acute overdistention of the 15. small intestine
bladder, usually no more than 1000 mL of 16. Defecation
urine is removed from the bladder at one 17. hormones
time. The other answers are incorrect. 18. gastrin
7. a. Rationale: In women, the angle between the 19. Ghrelin
bladder and the posterior proximal urethra 20. Cholecystokinin
(i.e., urethrovesical junction) is important to 21. parietal, vitamin B12
continence. This angle normally is 90 to 100 22. pepsinogen
degrees. The other answers are incorrect. 23. gastrin
8. b, c, e. Rationale: Among the transient causes 24. Brunner glands
of urinary incontinence are recurrent urinary 25. bacteria

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444 ANSWERS

26. indigestible dietary residue

27. Digestion
28. Absorption 32. Anorexia
29. enterocytes 33. Nausea
30. brush border enzymes 34. Vomiting
31. lipase

Activity B
1.

Mesentery
Muscularis externa

Epithelium
Longitudinal Circular
muscle muscle Lamina propria Mucosa
Muscularis
mucosa

Serosa
(mesothelium)
Serosa
(connective
tissue)
Submucosa

Activity C
2.
1. c 2. e 3. b 4. f 5. g
Enterocyte being extruded 6. i 7. h 8. d 9. a 10. j
from a villus
Activity D

Enterocyte 1. The upper part—the mouth, esophagus, and

stomach—acts as an intake source and recepta-
cle through which food passes and in which ini-
tial digestive processes take place. The middle
portion—the duodenum, jejunum, and ileum—
Vein
is the place where most digestive and absorptive
Lacteal processes occur. The lower segment—the
Artery cecum, colon, and rectum—serves as a storage
channel for the efficient elimination of waste.
2. The emptying of the stomach is regulated by
hormonal and neural mechanisms. The hor-
Crypt of
mones cholecystokinin and glucose-dependent
Lieberkü
i hn
insulinotropic polypeptide, which are believed
in part to control gastric emptying, are released
in response to the pH and the osmolar and fatty
acid composition of the chyme. Afferent recep-
tor fibers synapse with the neurons in the intra-
mural plexus or trigger intrinsic reflexes by
means of vagal or sympathetic pathways that
participate in extrinsic reflexes.

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ANSWERS 445

3. With segmentation waves, slow contractions out of the cell and into blood from the basolat-
of the circular muscle layer occlude the lumen eral membrane. At the luminal side of the mem-
and drive the contents forward and backward. brane, H is secreted into the stomach via the
Most of the contractions that produce seg- H/K-ATPase transporter, and chloride follows
mentation waves are local events involving H into the stomach by diffusing through Cl–
only 1 to 4 cm of intestine at a time. They channels in the luminal membrane.
function mainly to mix the chyme with the 7. Digestion of starch begins in the mouth with
digestive enzymes from the pancreas and to the action of amylase. Pancreatic secretions
ensure adequate exposure of all parts of the also contain an amylase. Amylase breaks down
chyme to the mucosal surface of the intestine, starch into several disaccharides, including
where absorption takes place. Peristaltic move- maltose, isomaltose, and -dextrins. The brush
ments are rhythmic propulsive movements de- border enzymes convert the disaccharides into
signed to propel the chyme along the small monosaccharides that can be absorbed.
intestine toward the large intestine. 8. Protein digestion begins in the stomach with
4. The incretin effect is the increase in insulin re- the action of pepsin. Proteins are broken down
lease after an oral glucose load. The two hor- further by pancreatic enzymes, such as
mones that account for about 90% of the trypsin, chymotrypsin, carboxypeptidase, and
incretin effect are GLP-1, which is released elastase. The pancreatic enzymes are secreted
from L cells in the distal small bowel, and GIP, as precursor molecules. Trypsinogen, which
which is released by K cells in the upper gut lacks enzymatic activity, is activated by an en-
(mainly, the jejunum). Because increased levels zyme located on the brush border cells of the
of GLP-1 and GIP can lower blood glucose lev- duodenal enterocytes. Activated trypsin acti-
els by augmenting insulin release in a glucose- vates additional trypsinogen molecules and
dependent manner (i.e., at low blood glucose other pancreatic precursor proteolytic en-
levels no further insulin is secreted, minimiz- zymes. The amino acids are liberated on the
ing the risk of hypoglycemia), these hormones surface of the mucosal surface of the intestine
have been targeted as possible antidiabetic by brush border enzymes that degrade pro-
drugs. Moreover, GLP-1 can exert other meta- teins into peptides that are one, two, or three
bolically beneficial effects, including suppress- amino acids long. Similar to glucose, many
ing glucagon release, slowing gastric emptying, amino acids are transported across the mu-
augmenting net glucose clearance, and de- cosal membrane in a sodium-linked process
creasing appetite and body weight. that uses ATP as an energy source. Some
5. The first is protection and lubrication. Saliva is amino acids are absorbed by facilitated diffu-
rich in mucus, which protects the oral mucosa sion processes that do not require sodium.
and coats the food as it passes through the
mouth, pharynx, and esophagus. The sublin- SECTION III: APPLYING YOUR
gual and buccal glands produce only mucus- KNOWLEDGE
type secretions. The second function of saliva
is its protective antimicrobial action. The saliva Activity E
cleans the mouth and contains the enzyme 1. The gastrointestinal (GI) tract is the largest en-
lysozyme, which has an antibacterial action. docrine gland in the body. Many nerves make
Third, saliva contains ptyalin and amylase, the GI tract work. The stomach begins diges-
which initiate the digestion of dietary starches. tion by kneading and churning the food we
6. The cellular mechanism for hydrochloric acid eat. Food then progresses to the small intes-
(HCL) secretion by the parietal cells in the stom- tine, where most of the food is digested and
ach involves the hydrogen (H)/potassium (K)- absorbed. Our food then goes into the large in-
adenosine triphosphatase (ATPase) transporter testine, where it is compacted into the feces
and chloride (Cl–) channels located on their lu- that we expel from our bodies.
minal membrane. During the process of HCL se-
cretion, carbon dioxide (CO2) produced by
aerobic metabolism combines with water (H2O), SECTION IV: PRACTICING FOR NCLEX
catalyzed by carbonic anhydrase, to form car-
Activity F
bonic acid (H2CO3), which dissociates into H
and bicarbonate (HCO3–). The H is secreted 1. a. Rationale: At the end of the pyloric chan-
with Cl– into the stomach, and the HCO3– moves nel, the circular layer smooth muscle

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446 ANSWERS

thickens to form the pyloric sphincter. This intestinal tract. The other answers are not as-
muscle serves as a valve that controls the rate sociated with nausea.
of stomach emptying and prevents the regur- 10. d. Rationale: Serotonin is believed to be in-
gitation of intestinal contents back into the volved in the nausea and emesis associated
stomach. There is no cardiac sphincter in the with cancer chemotherapy and radiation ther-
gastrointestinal tract. The antrum is a portion apy. Serotonin antagonists (e.g., granisetron,
of the stomach that is the wider, upper por- ondansetron) are effective in treating the nau-
tion of the pyloric region. The cardiac orifice sea and vomiting associated with these stim-
is the opening between the esophagus and uli. The other answers are incorrect.
the stomach.
2. b. Rationale: It is in the jejunum and ileum
that food is digested and absorbed. The other
CHAPTER 37 DISORDERS OF
answers are incorrect. GASTROINTESTINAL FUNCTION
3. c. Rationale: No contraction can occur with-
out an action potential, and an action poten- SECTION II: ASSESSING YOUR
tial cannot occur unless the slow wave brings UNDERSTANDING
the membrane potential to threshold. The Activity A
other answers are incorrect.
4. d. Rationale: The external sphincter is con- 1. esophagus
trolled by nerve fibers in the pudendal nerve, 2. Congenital
which is part of the somatic nervous system 3. Dysphagia
and therefore under voluntary control. The 4. Hiatal hernia
other answers are incorrect. 5. gastroesophageal reflux disease
5. a. Rationale: Ghrelin is a newly discovered pep- 6. bronchial asthma
tide hormone produced by endocrine cells in 7. Reflux esophagitis
the mucosal layer of the fundus of the stom- 8. infant
ach. It displays potent growth hormone– 9. alcohol, tobacco
releasing activity and has a stimulatory effect 10. impermeable
on food intake and digestive function, while 11. prostaglandins
reducing energy expenditure. The isolation of 12. Gastritis
this hormone has led to new insights into the 13. Acute gastritis
gut-brain regulation of growth hormone se- 14. Chronic gastritis
cretion and energy balance. The other hor- 15. autoantibodies
mones are secreted elsewhere in the 16. Peptic ulcer
gastrointestinal tract. 17. hemorrhage, obstruction
6. a, b, c, d. Rationale: Saliva has three functions. 18. bleeding ulcers
The first is protection and lubrication. Saliva is 19. Histamine
rich in mucus, which protects the oral mucosa 20. stress ulcers
and coats the food as it passes through the 21. carcinoma
mouth, pharynx, and esophagus. The second 22. Irritable bowel syndrome
function of saliva is its protective antimicro- 23. Crohn, ulcerative colitis
bial action. Third, saliva contains ptyalin and 24. Crohn
amylase, which initiate the digestion of di- 25. colon, rectum
etary starches. The other answer is incorrect. 26. Nutritional
7. b. Rationale: The major metabolic function of 27. Lieberkühn
colonic microflora is the fermentation of 28. Cancer
undigestible dietary residue and endogenous 29. bacterial enterocolitis
mucus produced by the epithelial cells. The 30. Diverticulosis
other answers are not their main function. 31. Diverticulitis
8. c. Rationale: Absorption is accomplished by 32. appendicitis
active transport and diffusion. The other an- 33. diarrhea
swers are incorrect. 34. noninflammatory diarrhea
9. d. Rationale: A common cause of nausea is 35. Chronic
distention of the duodenum or upper small 36. Inflammatory diarrhea

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ANSWERS 447

37. Constipation tric mucosal surface and provides protection

38. Fecal impaction from the proteolytic (protein-digesting) actions
39. cephalocaudal of pepsin. It also forms an unstirred layer that
40. Paralytic traps bicarbonate, forming an alkaline interface
41. serous membrane between the luminal contents of the stomach
42. gluten and its mucosal surface. The water-soluble
43. Colonoscopy mucus is washed from the mucosal surface and
mixes with the luminal contents; its viscid na-
Activity B ture makes it a lubricant that prevents me-
chanical damage to the mucosal surface.
1.
3. A peptic ulcer can affect one or all layers of the
1. g 2. f 3. a 4. e 5. j
stomach or duodenum. The ulcer may pene-
6. h 7. d 8. i 9. c 10. b
trate only the mucosal surface, or it may ex-
2.
tend into the smooth muscle layers.
1. c 2. g 3. a 4. b 5. e
Occasionally, an ulcer penetrates the outer
6. j 7. d 8. f 9. i 10. h
wall of the stomach or duodenum. Sponta-
neous remissions and exacerbations are com-
Activity C
mon. Healing of the muscularis layer involves
1. Gastroesophageal reflux disease is believed to replacement with scar tissue. Although the
be associated with a weak or incompetent mucosal layers that cover the scarred muscle
lower esophageal sphincter that allows reflux layer regenerate, the regeneration is often less
to occur, the irritant effects of the refluxate, than perfect, which contributes to repeated
and decreased clearance of the refluxed acid episodes of ulceration.
from the esophagus after it has occurred. In 4. Chronic infection with Helicobacter pylori ap-
most cases, reflux occurs during transient re- pears to serve as a cofactor in some types of
laxation of the esophagus. Gastric distension gastric carcinomas. The bacterial infection
and meals high in fat increase the frequency causes gastritis, followed by atrophy, intestinal
of relaxation. Delayed gastric emptying may metaplasia, and carcinoma. This sequence of
also contribute to reflux by increasing gastric cellular events depends on both the presence
volume and pressure with greater chance for of the bacterial proteins and the host immune
reflux. Esophageal mucosal injury is related to response, the latter being influenced by the
the destructive nature of the refluxate and the host genetic background. However, the vast
amount of time it is in contact with mucosa. majority of people with H. pylori will not de-
Acidic gastric fluids (pH 4.0) are particularly velop gastric cancer, and not all H. pylori infec-
damaging. tions increase the risk of gastric cancer,
2. Several factors contribute to the protection of suggesting that other factors must be involved.
the gastric mucosa, including an impermeable 5. The condition is believed to result from
epithelial cell surface covering, mechanisms deregulation of intestinal motor and sensory
for the selective transport of hydrogen and functions modulated by the central nervous
bicarbonate ions, and the characteristics of system. Irritable bowel syndrome is character-
gastric mucus. The gastric epithelial cells are ized by persistent or recurrent symptoms of
connected by tight junctions that prevent abdominal pain; altered bowel function; and
acid penetration, and they are covered with varying complaints of flatulence, bloatedness,
an impermeable hydrophobic lipid layer that nausea and anorexia, constipation or diar-
prevents diffusion of ionized water-soluble rhea, and anxiety or depression. A hallmark
molecules. The secretion of hydrochloric acid of irritable bowel syndrome is abdominal
by the parietal cells of the stomach is accompa- pain that is relieved by defecation and associ-
nied by secretion of bicarbonate ions (HCO3). ated with a change in consistency or fre-
For every hydrogen ion (H) that is secreted, a quency of stools. Abdominal pain is usually
HCO3 is produced, and as long as HCO3 pro- intermittent, cramping, and in the lower ab-
duction is equal to H secretion, mucosal in- domen.
jury does not occur. Water-insoluble mucus 6. According to the currently accepted hypothesis,
forms a thin, stable gel that adheres to the gas- this normal state of homeostasis is disrupted in

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448 ANSWERS

inflammatory bowel disease, leading to unregu- 9. The cause of colon cancer is unknown, but at-
lated and exaggerated immune responses tention has focused on dietary fat intake, re-
against bacteria in the normal intestinal flora of fined sugar intake, fiber intake, and the
genetically susceptible individuals. Thus, as in adequacy of such protective micronutrients as
many other autoimmune disorders, the patho- vitamins A, C, and E in the diet. It has been
genesis of Crohn disease and ulcerative colitis hypothesized that a high level of fat in the
involves a failure of immune regulation, ge- diet increases the synthesis of bile acids in the
netic predisposition, and an environmental liver, which may be converted to potential car-
trigger, especially microbial flora. cinogens by the bacterial flora in the colon.
7. In a manner similar to the small intestine, Bacterial organisms in particular are suspected
bands of circular muscle constrict the large of converting bile acids to carcinogens; their
intestine. As the circular muscle contracts at proliferation is enhanced by a high dietary
each of these points (approximately every level of refined sugars. Dietary fiber is believed
2.5 cm), the lumen of the bowel becomes con- to increase stool bulk, and thereby dilute and
stricted, so that it is almost occluded. The remove potential carcinogens. Refined diets
combined contraction of the circular muscle often contain reduced amounts of vitamins A,
and the lack of a continuous longitudinal C, and E, which may act as oxygen free radical
muscle layer cause the intestine to bulge out- scavengers.
ward into pouches called haustra. Diverticula
develop between the longitudinal muscle SECTION III: APPLYING YOUR
bands of the haustra, in the area where the KNOWLEDGE
blood vessels pierce the circular muscle layer
to bring blood to the mucosal layer. An in- Activity D
crease in intraluminal pressure in the haustra 1. “The doctor wants to give you the chemother-
provides the force for creating these hernia- apy medicine to try to reduce the size of your
tions. The increase in pressure is believed to be tumor so the surgery will not be as extensive
related to the volume of the colonic contents. as it would be if the surgery were done today.”
The scantier the contents, the more vigorous 2. “Even though your cancer has already spread,
are the contractions and the greater is the removing the tumor in your esophagus will
pressure in the haustra. make you more comfortable and, hopefully,
8. The pathophysiology of constipation can be allow you to live longer than you would with-
classified into three broad categories: normal out the surgery.”
transit constipation, slow transit constipation,
and disorders of defecatory or rectal evacua-
SECTION IV: PRACTICING FOR NCLEX
tion. Normal transit constipation (or func-
tional constipation) is characterized by Activity E
perceived difficulty in defecation, and usually
1. a. Rationale: The newborn infant with EA/tra-
responds to increased fluid and fiber intake.
cheoesophageal fistulae typically has frothing
Slow transit constipation, which is character-
and bubbling at the mouth and nose, episodes
ized by infrequent bowel movements, is often
of coughing, cyanosis, and respiratory distress.
caused by alterations in intestinal innervation.
The other answers are not associated with EA
Hirschsprung disease is an extreme form of
as signs and symptoms of the defect.
slow transit constipation, in which the gan-
2. b. Rationale: Esophageal acid clearance can be
glion cells in the distal bowel are absent due to
retarded in cases of severe erosive esophagitis
a defect that occurred during embryonic devel-
where gastroesophageal reflux and a large hi-
opment; the bowel narrows at the area that
atal hernia coexist. The other answers are in-
lacks ganglionic cells. Although most persons
correct.
with this disorder present in infancy or early
3. c. Rationale: Tilting of the head to one side
childhood, some with a relatively short seg-
and arching of the back may be noted in
ment of involved colon do not have symp-
children with severe reflux. Early satiety is
toms until later in life. Defecatory disorders
another indication of gastroesophageal
are most commonly due to dysfunction of the
reflux, but not coupled with consolable cry-
pelvic floor or anal sphincter.
ing. The other answers are not correct.

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ANSWERS 449

4. a, c, e. Rationale: The stomach lining is usu- 9. c. Rationale: A characteristic feature of Crohn

ally impermeable to the acid it secretes, a disease is the sharply demarcated, granulo-
property that allows the stomach to contain matous lesions that are surrounded by nor-
acid and pepsin without having its wall di- mal-appearing mucosal tissue. When the
gested. Several factors contribute to the pro- lesions are multiple, they are often referred to
tection of the gastric mucosa, including an as skip lesions because they are interspersed
impermeable epithelial cell surface covering, between what appear to be normal segments
mechanisms for the selective transport of hy- of the bowel.
drogen and bicarbonate ions, and the charac- 10. d. Rationale: Rotavirus infection typically be-
teristics of gastric mucus. These mechanisms gins after an incubation period of less than
are collectively referred to as the gastric mu- 24 hours, with mild to moderate fever and
cosal barrier. The other answers are incorrect. vomiting, followed by onset of frequent wa-
5. d. Rationale: Helicobacter pylori gastritis can be tery, stools. The fever and vomiting usually
a chronic infection that can lead to gastric at- disappear on about the second day, but the
rophy, peptic ulcer, and is associated with in- diarrhea continues for 5 to 7 days. Dehydra-
creased risk of gastric adenocarcinoma and tion may develop rapidly, particularly in in-
low-grade B-cell gastric lymphoma mucosa- fants. The other answers are incorrect.
associated lymphoid tissue (MALToma). The 11. a. Rationale: One of the most common com-
other answers are incorrect. plaints of diverticulitis is pain in the lower
6. a. Rationale: Diagnostic procedures for peptic left quadrant, accompanied by nausea and
ulcer include history taking, laboratory tests, vomiting, tenderness in the lower left quad-
radiologic imaging, and endoscopic examina- rant, a slight fever, and an elevated white
tion. The other answers are not expected or- blood cell count. Both B and D describe a sus-
ders for a suspected peptic ulcer. pected appendicitis, and C describes symp-
7. a, c. Rationale: Diagnosis of gastric cancer is toms of a peptic ulcer.
accomplished by means of a variety of tech- 12. b, c, d. Rationale: Noninflammatory diarrhea
niques, including barium x-ray studies, en- is associated with large-volume watery and
doscopic studies with biopsy, and cytologic nonbloody stools, periumbilical cramps,
studies (e.g., Papanicolaou [Pap] smear) of bloating, nausea, and/or vomiting. The other
gastric secretions. Cytologic studies can answers are incorrect.
prove particularly useful as routine screen- 13. b. Rationale: One of the most important man-
ing tests for persons with atrophic gastritis ifestations of peritonitis is the translocation
or gastric polyps. CT and endoscopic ultra- of extracellular fluid into the peritoneal cav-
sonography are often used to delineate the ity (through weeping or serous fluid from the
spread of a diagnosed stomach cancer. Pap inflamed peritoneum) and into the bowel be-
smears are done on gastric secretions, but cause of bowel obstruction. The other an-
not by the nurse. A lower gastrointestinal swers are incorrect.
study would be of no value in diagnosing 14. c. Rationale: The primary treatment of celiac
this client. A tech does not do an endo- disease consists of removal of gluten and re-
scopic ultrasound. lated proteins from the diet. No other answer
8. b. Rationale: A hallmark of irritable bowel syn- is correct.
drome is abdominal pain that is relieved by 15. d. Rationale: To reduce the likelihood of false-
defecation and associated with a change in positive tests, persons are instructed to avoid
consistency or frequency of stools. Nausea, al- nonsteroidal antiinflammatory drugs such as
tered bowel function, and diarrhea are also ibuprofen and aspirin for 7 days prior to test-
symptoms of irritable bowel syndrome, but ing, to avoid vitamin C in excess of 250 mg
not combined with abdominal pain that is from either supplements or citrus fruits for
unrelieved by defecation. A bowel impaction 3 days before testing, and to avoid red meats
is not a symptom of irritable bowel syndrome. for 3 days before testing. The other answers
are incorrect.

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450 ANSWERS

CHAPTER 38 DISORDERS OF 17. toxic metabolites

18. Cholestatic
HEPATOBILIARY AND EXOCRINE 19. Hepatitis
PANCREAS FUNCTION 20. injection drug, blood transfusions, high-risk
sexual behavior
SECTION II: ASSESSING YOUR 21. Autoimmune
UNDERSTANDING 22. Intrahepatic
23. Secondary
Activity A 24. fatty
1. accessory 25. Cirrhosis
2. artery, portal vein 26. Portal hypertension
3. hepatic portal vein 27. increased, dilatation
4. bile 28. Ascites
5. albumin 29. Spontaneous bacterial peritonitis
6. cholesterol, bile 30. hepatorenal
7. fat 31. encephalopathy
8. triglycerides 32. liver cancer
9. emulsifying, micelles 33. gallbladder
10. Cholestasis 34. Cholecystokinin
11. bile 35. cholesterol, bilirubin
12. Hemolytic 36. cholecystitis
13. Conjugation 37. exocrine
14. Phase 1 reactions 38. pancreatitis
15. CYP gene 39. Chronic pancreatitis
16. Phase 2 reactions 40. cigarette smoking

Activity B

Diaphragm

Liver

Gallbladder Spleen

Cystic duct Hepatic duct

Common
bile duct
Ampulla of Vater
Tail of the
pancreas
Sphincter of Oddi
Duodenum Pancreatic duct

Head of the pancreas

Activity C
1. 2.
1. c 2. f 3. h 4. b 5. e 1. d 2. c 3. e 4. a 5. b
6. g 7. a 8. d 9. i 10. j

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ANSWERS 451

Activity D
1.
Amino acids Glycerol Lactic acid

Gluconeogenesis

Glucose Glycogen

Triglycerides

Bloodstream

2.

Portal hypertension

Increased pressure in Portosystemic

peritoneal capillaries shunting of blood Splenomegaly

Ascites Development of Shunting of ammonia Anemia Leukopenia

collateral channels and toxins from the
intestine into the
general circulation
Caput Esophageal Thrombocytopenia
medusae varices
Hepatic
Hemorrhoids encephalopathy Bleeding

Activity E
effects begin with increased pressure in the
large bile ducts. Genetic disorders involving
1. The liver is one of the most versatile and ac- the transport of bile into the canaliculi can
tive organs in the body. It produces bile; me- also result in cholestasis.
tabolizes hormones and drugs; synthesizes 3. The four major causes of jaundice are exces-
proteins, glucose, and clotting factors; stores sive destruction of red blood cells, impaired
vitamins and minerals; changes ammonia uptake of bilirubin by the liver cells, de-
produced by deamination of amino acids to creased conjugation of bilirubin, and obstruc-
urea; and converts fatty acids to ketones. The tion of bile flow in the canaliculi of the
liver degrades excess nutrients and converts hepatic lobules or in the intrahepatic or
them into substances essential to the body. In extrahepatic bile ducts. From an anatomic
its capacity for metabolizing drugs and hor- standpoint, jaundice can be categorized as
mones, the liver serves as an excretory organ. prehepatic, intrahepatic, and posthepatic.
2. A number of mechanisms are implicated in 4. Elevated serum enzyme tests usually indicate
the pathogenesis of cholestasis. Primary bil- liver injury earlier than other indicators of
iary cirrhosis and primary sclerosing cholan- liver function. The key enzymes are alanine
gitis are caused by disorders of the small aminotransferase (ALT) and aspartate amino-
intrahepatic canaliculi and bile ducts. In the transferase (AST), which are present in liver
case of extrahepatic obstruction caused by cells. ALT is liver specific, whereas AST is
conditions such as cholelithiasis, common derived from organs other than the liver. In
duct strictures, or obstructing neoplasms, the most cases of liver damage, there are parallel

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452 ANSWERS

rises in ALT and AST. The most dramatic rise hypertension and its complications, obstruc-
is seen in cases of acute hepatocellular injury. tion of biliary channels and exposure to the
5. The clinical course of viral hepatitis involves destructive effects of bile stasis, and loss of
a number of syndromes, including asympto- liver cells, leading to liver failure.
matic infection with only serologic evidence 9. An increase in capillary pressure due to portal
of disease, acute hepatitis, the carrier state hypertension and obstruction of venous flow
without clinically apparent disease or with through the liver, salt and water retention by
chronic hepatitis, and chronic hepatitis with the kidney, and decreased colloidal osmotic
or without progression to cirrhosis, with pressure due to impaired synthesis of albu-
rapid onset of liver failure. Not all hepato- min by the liver. Diminished blood volume
toxic viruses provoke each clinical syndrome. (i.e., underfill theory) and excessive blood
6. The metabolic end products of alcohol me- volume (i.e., overfill theory) have been used
tabolism (e.g., acetaldehyde, free radicals) are to explain the increased salt and water reten-
responsible for a variety of metabolic alter- tion by the kidney.
ations that can cause liver injury. Acetalde- 10. With the gradual obstruction of venous blood
hyde, for example, has multiple toxic effects flow in the liver, the pressure in the portal
on liver cells and liver function. The metabo- vein increases, and large collateral channels
lism of alcohol leads to chemical attack on develop between the portal and systemic veins
certain membranes of the liver. Acetaldehyde that supply the lower rectum. The dilation of
is known to impede the mitochondrial elec- the collaterals between the inferior and inter-
tron transport system, which is responsible nal iliac veins may give rise to hemorrhoids.
for oxidative metabolism and generation of
ATP; as a result, the hydrogen ions that are SECTION III: APPLYING YOUR
generated in the mitochondria are shunted KNOWLEDGE
into lipid synthesis and ketogenesis. Binding
of acetaldehyde to other molecules impairs Activity F
the detoxification of free radicals and synthe- 1. The nurse would expect serum aminotrans-
sis of proteins. Acetaldehyde also promotes ferase, liver biopsy, complete blood count, and
collagen synthesis and fibrogenesis. complete metabolic panel to be ordered.
7. Fatty liver is characterized by the accumula- 2. Interferons, nucleotide and nucleotide analog
tion of fat in hepatocytes, a condition called antiretroviral agents, and pegylated interferon
steatosis. The liver becomes yellow, enlarges -2a might be ordered for this patient.
owing to excessive fat accumulation, and is
characterized by inflammation and necrosis
of liver cells. Alcoholic hepatitis is the inter- SECTION IV: PRACTICING FOR NCLEX
mediate stage between fatty changes and cir-
Activity G
rhosis. It is often seen after an abrupt increase
in alcohol intake and is common in “spree” 1. a. Rationale: Kupffer cells are reticuloendothe-
drinkers. Alcoholic cirrhosis is the result of lial cells that are capable of removing and
repeated bouts of drinking-related liver injury phagocytizing old and defective blood cells,
and designates the onset of end-stage alco- bacteria, and other foreign material from the
holic liver disease. The gross appearance of portal blood as it flows through the sinusoid.
the early cirrhotic liver is one of fine, uni- Langerhans cells are stellate dendritic cells
form nodules on its surface. found mostly in the stratum spinosum of the
8. Cirrhosis is characterized by diffuse fibrosis epidermis. Epstein’s cells do not exist. David-
and conversion of normal liver architecture off cells are large granular epithelial cells
into nodules containing proliferating hepato- found in intestinal glands.
cytes encircled by fibrosis. The formation of 2. b. Rationale: The morphologic features of
nodules represents a balance between regen- cholestasis depend on the underlying cause.
erative activity and constrictive scarring. The Common to all types of obstructive and he-
fibrous tissue that replaces normally function- patocellular cholestasis is the accumulation
ing liver tissue forms constrictive bands that of bile pigment in the liver. The other an-
disrupt flow in the vascular channels and bil- swers are incorrect.
iary duct systems of the liver. The disruption 3. c. Rationale: Usually, only a small amount of
of vascular channels predisposes to portal bilirubin is found in the blood; the normal

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ANSWERS 453

level of total serum bilirubin is 0.1 to 1.2 5. voluntary physical activity

mg/dL. The other answers are incorrect. 6. adipose
4. d. Rationale: Because of the greater activity of 7. Leptin
the drug-metabolizing enzymes in the central 8. recommended dietary allowance
zones of the liver, these agents typically cause 9. Percent daily value
centrilobular necrosis. The other answers are 10. Proteins
incorrect. 11. nitrogen
5. a. Rationale: The earliest symptoms are unex- 12. elevate, lower
plained pruritus or itching, weight loss, and 13. increase, decrease
fatigue, followed by dark urine and pale 14. carbohydrates
stools. The other answers are not indicative 15. Vitamins
of primary biliary cirrhosis. 16. Minerals
6. b. Rationale: When the capacity of the liver to 17. Fiber
export triglyceride is saturated, excess fatty 18. hypothalamus
acids contribute to the formation of fatty liver. 19. glucose
7. c. Rationale: Because of the many limitations 20. Anthropometric
in sodium restriction, the use of diuretics has 21. body mass index
become the mainstay of treatment for ascites. 22. circumference
A paracentesis may be done if the diuretics do 23. Obesity
not correct the problem. A thoracentesis 24. fat distribution
would never be done for ascites. DDAVP is 25. Weight cycling
given to decrease urine output, not increase it. 26. increased
8. d. Rationale: Diagnostic methods include ul- 27. Bariatric surgery
trasound, CT scans, and MRI. Liver biopsy 28. pediatric
may be used to confirm the diagnosis. The 29. Malnutrition, starvation
serum -fetoprotein can be indicative of liver 30. starvation
cancer, but it is not confirmatory. An en- 31. marasmus
doscopy is of no value. An ultrasound of the 32. recurrent
liver is not confirmatory for liver cancer.
9. a. Rationale: Gallbladder sludge (thickened gall- Activity B
bladder mucoprotein with tiny trapped choles-
1.
terol crystals) is believed to be a precursor of
1. f 2. d 3. b 4. h 5. i
gallstones. The other answers are incorrect.
6. c 7. a 8. g 9. j 10. e
10. b. Rationale: Serum amylase and lipase are the
2.
laboratory markers most commonly used to
1. f 2. c 3. b 4. a 5. g
establish a diagnosis of acute pancreatitis,
6. d 7. e
whereas cholesterol and triglycerides are not
used as such.
Activity C
11. c. Rationale: In pancreatic cancer, the most
significant and reproducible environmental 1. There are two types of adipose tissue: white fat
risk factor is cigarette smoking. The other an- and brown fat. White fat is the prevalent form.
swers are incorrect. At body temperature, the lipid content of fat
cells exists as an oil of triglycerides. Triglyc-
erides have the highest caloric content of all
CHAPTER 39 ALTERATIONS OF nutrients and are an efficient form of energy
NUTRITIONAL STATUS storage. Fat cells synthesize triglycerides from
dietary fats and carbohydrates. When calorie
SECTION II: ASSESSING YOUR intake is restricted for any reason, fat cell
UNDERSTANDING triglycerides are broken down, and the resul-
tant fatty acids and glycerol are released as en-
Activity A
ergy sources. Brown fat differs from white fat
1. Nutritional status in terms of its thermogenic capacity or ability
2. Metabolism to produce heat. Brown fat, the site of diet-
3. ATP induced thermogenesis and nonshivering
4. basal metabolic rate thermogenesis, is found primarily in early

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454 ANSWERS

neonatal life in humans and in animals that 5. The criteria to diagnose bulimia nervosa are
hibernate. In humans, brown fat decreases (a) recurrent binge eating (at least two times
with age, but is still detectable in the sixth per week for 3 months); (b) inappropriate
decade. This small amount of brown fat has a compensatory behaviors such as self-induced
minimal effect on energy expenditure. vomiting, abuse of laxatives or diuretics, fast-
2. Bioimpedance is performed by attaching elec- ing, or excessive exercise that follow the binge
trodes at the wrist and ankle that send a harm- eating episode; (c) self-evaluation that is un-
less current through the body. The flow of the duly influenced by body shape and weight;
current is affected by the amount of water in and (d) a determination that the eating disor-
the body. Because fatfree tissue contains virtu- der does not occur exclusively during episodes
ally all water and conducting electrolytes, of anorexia nervosa.
measurements of the resistance (i.e., imped- 6. Binge eating is characterized by recurrent
ance) to current flow can be used to estimate episodes of binge eating at least 2 days per
the percentage of body fat present. week for 6 months and at least three of the fol-
3. Nongenetic causes of obesity are family eating lowing: (a) eating rapidly; (b) eating until be-
patterns, inactivity because of labor-saving de- coming uncomfortably full; (c) eating large
vices and time spent on the computer and amounts when not hungry; (d) eating alone
watching television, reliance on the automo- because of embarrassment; and (e) disgust,
bile for transportation, easy access to food, en- depression, or guilt because of eating episodes.
ergy density of food, increased consumption
of sugar-sweetened beverages, and increasing SECTION III: APPLYING YOUR
portion sizes. The obese may be greatly influ- KNOWLEDGE
enced by the availability of food, the flavor of
Activity D
food, time of day, and other cues. The compo-
sition of the diet may also be a causal factor, 1. Questions include the following:
and the percentage of dietary fat independent •Do you consider yourself a perfectionist?
of total calorie intake may play a part in the •Do you do things compulsively?
development of obesity. Psychological factors •Is there a family history of obesity?
include using food as a reward, comfort, or •Is anyone in your family overweight?
means of getting attention. Eating may be a •Does anyone in your family have an anxiety
way to cope with tension, anxiety, and mental disorder?
fatigue. Some persons may overeat and use • Does anyone in your family have a history
obesity as a means of avoiding emotionally of depression?
threatening situations. 2. Criteria include the following:
4. The causes of anorexia appear to be multifac- • Refusal to maintain a minimally normal
torial, with determinants that include genetic body weight for age and height
influence; personality traits of perfectionism • An intense fear of gaining weight or becom-
and compulsiveness; anxiety disorders; family ing fat
history of depression and obesity; and peer, fa- • A disturbance in the way one’s body size,
milial, and cultural pressures with respect to weight, and shape is perceived
appearance. The DSM-IV-TR diagnostic criteria • Amenorrhea (in girls and women after
for anorexia nervosa are (a) a refusal to main- menarche)
tain a minimally normal body weight for age
and height (e.g., at least 85% of minimal ex- SECTION IV: PRACTICING FOR NCLEX
pected weight or BMI 17.5); (b) an intense
Activity E
fear of gaining weight or becoming fat; (c) a
disturbance in the way one’s body size, 1. 1-e, 2-c, 3-b, 4-d, 5-a
weight, and shape is perceived; and (d) amen- 2. a, c, e. Rationale: The factors secreted by adi-
orrhea (in girls and women after menarche). pose tissue are termed adipokines and in-
Other psychiatric disorders often coexist with clude leptin, certain cytokines (e.g., tumor
anorexia nervosa, including major depression necrosis factor-), growth factors, and
or dysthymia and obsessive-compulsive disor- adiponectin (important in insulin resistance).
der. Alcohol and substance abuse may also be 3. a. Rationale: An estimated average require-
present, more often among those with ment is the intake that meets the estimated
binging-purging type of anorexia nervosa. nutrient need of half of the persons in a

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ANSWERS 455

specific group. The adequate intake (AI) is set CHAPTER 40 MECHANISMS

when there is not enough scientific evidence
to estimate an average requirement. The rec- OF ENDOCRINE CONTROLS
ommended dietary allowance (RDA) defines
the intakes that meet the nutrient needs of SECTION II: ASSESSING YOUR
almost all healthy persons in a specific age UNDERSTANDING
and gender group. The dietary reference in- Activity A
take includes a set of at least four nutrient-
based reference values—the estimated 1. hormones
average requirement, the AI, the RDA, and 2. nervous, immune
the tolerable upper intake level. 3. paracrine
4. b. Rationale: The Food and Nutrition Board 4. autocrine
has set an acceptable macronutrient distribu- 5. free, bound
tion range for fat of no less than 20% to pre- 6. high-affinity receptors
vent the fall of HDL cholesterol associated 7. receptors
with very low-fat diets. The other answers are 8. Lipid-soluble
incorrect. 9. hypothalamus
5. c. Rationale: Centers in the hypothalamus 10. master gland
also control the secretion of several hor- 11. metabolites, hormone levels
mones (e.g., thyroid and adrenocortical hor-
mones) that regulate energy balance and Activity B
metabolism. Cholecystokinin and glucagon- 1. c 2. a 3. e 4. d 5. b
like peptide-1 are intestinal hormones. Ghre- 6. f 7. g
lin is secreted mostly in the stomach.
6. d. Rationale: The body mass index (BMI) uses Activity C
height and weight to determine healthy
weight. It is calculated by dividing the weight CNS input Other
input
in kilograms by the height in meters squared
(BMI weight [kg]/height [m2]). The other
answers are incorrect. Hypothalamus
7. a. Rationale: The obesity type is determined
by dividing the waist by the hip circumfer-
ence. The other answers are incorrect. Releasing hormone
8. b. Rationale: Compared with women, men
tend to experience less pressure to engage in
behaviors such as self-induced vomiting or
Pituitary
laxative use when overeating, less of a subjec-
tive sense of loss of control when binge eating,
and a greater tendency to use compulsive ex-
ercise rather than purging for weight control. Tropic hormone
9. b. Rationale: Pediatricians are now beginning
to see hypertension, dyslipidemia, type 2 dia-
betes, and psychosocial stigma in obese chil- Peripheral gland
dren and adolescents. The other answers are
not correct.
10. c. Rationale: The hospitalized patient often
Hormone
finds eating a healthful diet difficult and
commonly has restrictions on food and water
intake in preparation for tests and surgery.
Target
Pain, medications, special diets, and stress
can decrease appetite. Even when the patient
is well enough to eat, being alone in a room
where unpleasant treatments may be given is Effect
not conducive to eating. The other answers
are not correct.

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456 ANSWERS

Activity D 4. The intracellular signal system is termed the sec-

ond messenger, and the hormone is considered
1. Hormones are generally thought of as chemi- the first messenger. The most widely distributed
cal messengers transported in body fluids. second messenger is cyclic adenosine
They are highly specialized organic mole- monophosphate. Adenylate cyclase is function-
cules produced by endocrine organs that ally coupled to various cell surface receptors by
exert their action on specific target cells. the regulatory actions of G proteins. The second
Hormones do not initiate reactions but func- major cell surface receptor involving the binding
tion as modulators of cellular and systemic of a hormone or neurotransmitter to a surface
responses. Most hormones are present in receptor acts directly to open an ion channel in
body fluids at all times, but in greater or the cell membrane. The influx of ions, then,
lesser amounts depending on the needs of serves as an intracellular signal to convey the
the body. hormonal message to the interior of the cell.
2. Hormones are divided into three categories: 5. Hormones produced by the anterior pituitary
(a) amines and amino acids; (b) peptides, control body growth and metabolism (GH),
polypeptides, proteins, and glycoproteins; and function of the thyroid gland (TSH), glucocorti-
(c) steroids. The first category, the amines, in- coid hormone levels (ACTH), function of the
cludes norepinephrine and epinephrine, gonads (FSH and LH), and breast growth and
which are derived from a single amino acid, milk production (prolactin). Melanocyte-stimu-
and the thyroid hormones, which are derived lating hormone, which is involved in the con-
from two iodinated tyrosine amino acid trol of pigmentation of the skin, is produced by
residues. The second category, the peptides, the pars intermedia of the pituitary gland.
polypeptides, proteins, and glycoproteins, can 6. The level of hormones in the body is regulated
be as small as to only contain three amino by negative feedback mechanisms. Sensors de-
acids, and as large and complex as to consist of tect a change in the hormone level and adjust
approximately 200 amino acids. The third cat- hormone secretion so that body levels are
egory consists of the steroid hormones, which maintained within an appropriate range.
are derivatives of cholesterol. When the sensors detect a decrease in hor-
3. The response of a target cell to a hormone mone levels, they initiate changes that cause
varies with the number of receptors present an increase in hormone production; when
and with the affinity of these receptors for hormone levels rise above the set-point of the
hormone binding. The number of hormone system, the sensors cause hormone production
receptors on a cell may be altered for any of and release to decrease the level.
several reasons. Antibodies may destroy or
block the receptor proteins. Increased or de-
creased hormone levels often induce changes
SECTION III: APPLYING YOUR
in the activity of the genes that regulate recep-
KNOWLEDGE
tor synthesis. For example, decreased hormone Activity E
levels often produce an increase in receptor
1. The nurse would expect a dual electron x-ray
numbers by means of a process called up-
absorptiometry to be ordered because she
regulation; this increases the sensitivity of the
knows that this test is used routinely for the
body to existing hormone levels. Likewise, sus-
diagnosis and monitoring of osteoporosis and
tained levels of excess hormone often bring
metabolic bone diseases.
about a decrease in receptor numbers by
2. The nurse would expect an assessment of in-
down-regulation, producing a decrease in hor-
sulin function through a blood glucose level.
mone sensitivity.

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ANSWERS 457

samples and the fact that blood sampling is

SECTION IV: PRACTICING FOR NCLEX
not required. The other answers are not true.
Activity F 9. a. Rationale: A suppression test may be useful
to confirm this situation. The other answers
1. a. Rationale: Neurotransmitters such as epi-
are incorrect.
nephrine can act as neurotransmitters or
10. b. Rationale: Isotopic imaging includes radio-
as hormones. The other answers are not
active scanning of the thyroid. The other
correct.
answers are all examples of nonisotopic
2. b. Rationale: When hormones act locally on
imaging.
cells other than those that produced the hor-
mone, the action is called paracrine. Hor-
mones can also exert an autocrine action on CHAPTER 41 DISORDERS OF
the cells from which they were produced. The ENDOCRINE CONTROL OF GROWTH
other terms are incorrect.
3. c. Rationale: Hormones that are synthesized AND METABOLISM
by non–vesicle-mediated pathways include
the glucocorticoids, androgens, estrogens, and SECTION II: ASSESSING YOUR
mineralocorticoids—all steroids derived from UNDERSTANDING
cholesterol. The other answers are incorrect. Activity A
4. d. Rationale: Unbound adrenal and gonadal
steroid hormones are conjugated in the liver, 1. hypofunction, hyperfunction
which renders them inactive, and then ex- 2. Congenital
creted in the bile or urine. Adrenal and go- 3. growth
nadal steroid hormones are not excreted in 4. insulin-like growth factors
the feces, cell metabolites, or lungs. 5. Growth hormone
5. a. Rationale: The hypothalamus and pituitary 6. Constitutional short stature
(i.e., hypophysis) form a unit that exerts con- 7. Constitutional tall stature
trol over many functions of several endocrine 8. gigantism
glands as well as a wide range of other physio- 9. acromegaly
logic functions. These two structures are con- 10. overstimulation
nected by blood flow in the hypophyseal 11. Precocious
portal system, which begins in the hypothala- 12. Thyroid
mus and drains into the anterior pituitary 13. metabolism, protein
gland, and by the nerve axons that connect 14. metabolism
the supraoptic and paraventricular nuclei of 15. immunoassay
the hypothalamus with the posterior pituitary 16. preventable mental retardation
gland. The other answers are not correct. 17. Myxedema
6. b. Rationale: The level of many of the hormones 18. Thyrotoxicosis
in the body is regulated by negative feedback 19. Graves
mechanisms. The other answers are incorrect. 20. oxygen, metabolic
7. c. Rationale: Real progress in measuring 21. Thyroid storm
plasma hormone levels came more than 40 22. adrenal cortex
years ago with the use of competitive binding 23. Aldosterone
and the development of radioimmunoassay 24. glucocorticoid
methods. The other answers are incorrect. 25. Cortisol
8. d. Rationale: The advantages of a urine test in- 26. Addison
clude the relative ease of obtaining urine 27. Cushing syndrome

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458 ANSWERS

Activity B

Hypothalamus

Anterior
pituitary

Growth-promoting actions Anti-insulin effects

Growth hormone

Liver

IGF-1

Adipose Carbohydrate
Increased protein synthesis tissue metabolism

Bone and Body Decreased

Muscle Increased lipolysis
cartilage organs glucose use
Increased FFA use

Increased Increased Increased

linear size and Decrease in Increased blood
lean muscle
growth function adiposity glucose
mass

Activity C 3. Growth hormone (GH) is necessary for growth

and contributes to the regulation of metabolic
1. i 2. j 3. d 4. e 5. b functions. All aspects of cartilage growth are
6. g 7. f 8. c 9. a 10. h stimulated by GH; one of the most striking ef-
fects of GH is on linear bone growth, resulting
Activity D from its action on the epiphyseal growth
1. Primary defects in endocrine function origi- plates of long bones. The width of bone in-
nate in the target gland responsible for pro- creases because of enhanced periosteal growth;
ducing the hormone. In secondary disorders of visceral and endocrine organs, skeletal and
endocrine function, the target gland is essen- cardiac muscle, skin, and connective tissue all
tially normal, but its function is altered by de- undergo increased growth in response to GH.
fective levels of stimulating hormones or In many instances, the increased growth of
releasing factors from the pituitary system. A visceral and endocrine organs is accompanied
tertiary disorder results from hypothalamic by enhanced functional capacity.
dysfunction. 4. Growth hormone (GH) secretion is stimulated
2. Hormones directly affected by hypopitu- by hypoglycemia, fasting, starvation, in-
itarism are ACTH, thyroid-stimulating hor- creased blood levels of amino acids (particu-
mone, growth hormone, the gonadotrophic larly arginine), and stress conditions such as
hormones, and prolactin. Hypopituitarism is trauma, excitement, emotional stress, and
characterized by a decreased secretion of pitu- heavy exercise. GH is inhibited by increased
itary hormones, which affects many of the glucose levels, free fatty acid release, cortisol,
other endocrine systems by understimulation. and obesity. Impairment of secretion, leading

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ANSWERS 459

to growth retardation, is common in children 8. The major manifestations of Cushing syn-

with severe emotional deprivation. drome represent an exaggeration of the many
5. The secretion of thyroid hormone is regulated actions of cortisol. Altered fat metabolism
by the hypothalamic-pituitary-thyroid feed- causes a peculiar deposition of fat character-
back system. In this system, thyrotropin- ized by a protruding abdomen; subclavicular
releasing hormone (TRH) controls the release fat pads or “buffalo hump” on the back; and a
of thyroid-stimulating hormone (TSH) from round, plethoric “moon face.” There is muscle
the anterior pituitary gland. TSH increases the weakness, and the extremities are thin because
overall activity of the thyroid gland by in- of protein breakdown and muscle wasting.
creasing thyroglobulin breakdown and the re-
lease of thyroid hormone from follicles into SECTION III: APPLYING YOUR
the bloodstream, activating the iodide pump KNOWLEDGE
(by increasing Na/I symporter [NIS] activity),
increasing the oxidation of iodide and the Activity E
coupling of iodide to tyrosine, and increasing 1. “We are testing the baby for a disorder called
the number and size of the follicle cells. In- congenital hypothyroidism. This means that
creased levels of thyroid hormone act in the the baby’s thyroid gland is not functioning nor-
feedback inhibition of TRH or TSH. mally and is not producing thyroid hormone.”
6. The manifestations of the disorder are related 2. “Thyroid hormone is necessary for the brain
largely to two factors: the hypometabolic state to grow and develop. If the baby’s thyroid
resulting from thyroid hormone deficiency, gland is not working correctly, the doctor will
and myxedematous involvement of body tis- order thyroid medicine for the baby. As long
sues. The hypometabolic state associated with as the baby receives the medication as the doc-
hypothyroidism is characterized by a gradual tor orders, the baby’s brain will grow and de-
onset of weakness and fatigue, a tendency to velop just as it is supposed to.”
gain weight despite a loss of appetite, and cold
intolerance. As the condition progresses, the
SECTION IV: PRACTICING FOR NCLEX
skin becomes dry and rough and acquires a
pale yellowish cast, which primarily results Activity F
from carotene deposition, and the hair be-
1. a. Rationale: When further information re-
comes coarse and brittle. There can be loss of
garding pituitary function is required, com-
the lateral one- third of the eyebrows. Gas-
bined hypothalamic-pituitary function tests
trointestinal motility is decreased, producing
are undertaken (although these are per-
constipation, flatulence, and abdominal dis-
formed less often today). These tests consist
tention. Nervous system involvement is mani-
mainly of hormone stimulation tests (e.g.,
fested in mental dullness, lethargy, and
rapid ACTH stimulation test) or suppression
impaired memory.
tests (e.g., growth hormone suppression test).
7. Addison disease is a relatively rare disorder in
The other answers are incorrect.
which all layers of the adrenal cortex are de-
2. b. Rationale: The secretion of GH fluctuates
stroyed. Autoimmune destruction is the most
over a 24-hour period, with peak levels occur-
common cause. Because of a lack of glucocorti-
ring 1 to 4 hours after onset of sleep. The
coids, the person with Addison disease has
other answers are incorrect.
poor tolerance to stress. Hyperpigmentation
3. a, b, c. Rationale: In addition to its effects on
results from elevated levels of ACTH. The skin
growth, GH facilitates the rate of protein syn-
looks bronzed or suntanned in exposed and
thesis by all cells of the body, enhances fatty
unexposed areas, and the normal creases and
acid mobilization and increases the use of
pressure points tend to become especially
fatty acids for fuel, and maintains or in-
dark. The gums and oral mucous membranes
creases blood glucose levels by decreasing the
may become bluish-black. Mineralocorticoid
use of glucose for fuel. GH has an initial ef-
deficiency causes increased urinary losses of
fect of increasing insulin levels. GH does not
sodium, chloride, and water, along with de-
decrease the production of ACTH.
creased excretion of potassium. The result is
4. b. Rationale: When the production of exces-
hyponatremia, loss of extracellular fluid, de-
sive growth hormone occurs after the epiphy-
creased cardiac output, and hyperkalemia.
ses of the long bones have closed, as in the

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460 ANSWERS

adult, the person cannot grow taller, but the subclavicular fat pads or “buffalo hump” on
soft tissues continue to grow. Enlargement of the back; and a round, plethoric “moon
the small bones of the hands and feet and of face.” There is muscle weakness, and the ex-
the membranous bones of the face and skull tremities are thin because of protein break-
results in a pronounced enlargement of the down and muscle wasting. The other answers
hands and feet, a broad and bulbous nose, a are incorrect.
protruding lower jaw, and a slanting fore-
head. The other answers are incorrect.
5. c. Rationale: Persons with precocious puberty
CHAPTER 42 DIABETES MELLITUS
are usually tall for their age as children, but AND THE METABOLIC SYNDROME
short as adults because of the early closure of
the epiphyses. The other answers are incor- SECTION II: ASSESSING YOUR
rect. UNDERSTANDING
6. d. Rationale: The assessment of thyroid au- Activity A
toantibodies (e.g., antithyroid peroxidase an-
tibodies in Hashimoto thyroiditis) is 1. glucose
important in the diagnostic work-up and 2. brain
consequent follow-up of thyroid patients. 3. hypoglycemia
7. a. Rationale: As a result of myxedematous fluid 4. glycogen
accumulation, the face takes on a characteris- 5. glycogenolysis
tic puffy look, especially around the eyes. The 6. gluconeogenesis
tongue is enlarged, and the voice is hoarse 7. 9, 4
and husky. The other answers are incorrect. 8. proteins
8. a, c, e. Rationale: Thyroid storm is manifested 9. fatty acids, proteins
by a very high fever, extreme cardiovascular 10. glucose transporter
effects (i.e., tachycardia, congestive failure, 11. GLUT-4
angina), and severe central nervous system 12. Glucagon
effects (i.e., agitation, restlessness, delirium). 13. glycogenolysis, gluconeogenesis
The mortality rate is high. Very low fever and 14. insulin
bradycardia are not manifestations of a thy- 15. Diabetes
roid storm. 16. 100 mg/dL, 140 mg/dL
9. b. Rationale: Chronic suppression causes atro- 17. Type 1
phy of the adrenal gland, and the abrupt 18. idiopathic
withdrawal of drugs can cause acute adrenal 19. Type 2
insufficiency. The other answers are incorrect. 20. resistance
10. c. Rationale: In female infants, an increase in 21. obesity, physical inactivity
androgens is responsible for creating the viril- 22. obesity
ization syndrome of ambiguous genitalia 23. Gestational
with an enlarged clitoris, fused labia, and 24. fasting
urogenital sinus. The other answers are 25. casual, 200
incorrect. 26. glycated hemoglobin
11. d. Rationale: Hydrocortisone is usually the 27. insulin
drug of choice. The other answers are not 28. ketoacidosis
drugs; they are naturally occurring steroids. 29. hyperosmolar hyperglycemic
12. a, b, c, e. Rationale: If Addison disease is the 30. Advanced glycation end products
underlying problem, exposure to even a 31. diabetic nephropathy
minor illness or stress can precipitate nausea, 32. Diabetic retinopathy
vomiting, muscular weakness, hypotension, 33. macrovascular disease
dehydration, and vascular collapse.
13. a. Rationale: The major manifestations of Activity B
Cushing syndrome represent an exaggeration 1. d 2. c 3. f 4. e 5. h
of the many actions of cortisol. Altered fat 6. a 7. j 8. i 9. b 10. g
metabolism causes a peculiar deposition of 11. k
fat characterized by a protruding abdomen;

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ANSWERS 461

Activity C evidence has focused on the inherited major

histocompatibility (MHC) complex genes on
in insulin glucagon and gluconeogenesis chromosome 6. In addition to the MHC sus-
ceptibility genes for type 1 diabetes on chro-
mosome 6, an insulin gene regulating beta
cell replication and function has been identi-
blood glucose fied on chromosome 11.
5. The metabolic abnormalities that lead to type
2 diabetes include (1) insulin resistance, (2)
insulin release deranged secretion of insulin by the pancre-
glucagon atic beta cells, and (3) increased glucose pro-
from beta cells
duction by the liver
6. Specific causes of beta cell dysfunction in-
removal of
clude (1) an initial decrease in the beta cell
glucose from blood
hepatic glucose mass related to genetic or prenatal factors, (2)
production increased apoptosis and/or decreased beta cell
regeneration, (3) beta cell exhaustion caused
by long-standing insulin resistance, (4) gluco-
blood glucose toxicity, (5) lipotoxicity, and (6) amyloid de-
position, as well as other conditions that
Activity D have the potential to reduce beta cell mass.
7. The manifestations of metabolic syndrome
1. The actions of insulin are threefold: (1) it pro- include obesity, high levels of plasma triglyc-
motes glucose uptake by target cells and pro- erides and low levels of high-density lipopro-
vides for glucose storage as glycogen; (2) it teins (HDL), hypertension, systemic
prevents fat and glycogen breakdown; and inflammation, abnormal fibrinolysis, abnor-
(3) it inhibits gluconeogenesis and increases mal function of the vascular endothelium,
protein synthesis and macrovascular disease.
2. The release of insulin from the pancreatic 8. Insulin resistance and increased glucose pro-
beta cells is regulated by blood glucose levels, duction has several consequences: first, exces-
increasing as blood glucose levels rise and de- sive and chronic elevation of FFAs can cause
creasing when blood glucose levels decline. beta cell dysfunction (lipotoxicity); second,
Blood glucose enters the beta cell by means FFAs act at the level of the peripheral tissues
of the glucose transporter; it is phosphory- to cause insulin resistance and glucose under-
lated by an enzyme called glucokinase and utilization by inhibiting glucose uptake and
metabolized to form the adenosine triphos- glycogen storage; and, third, the accumula-
phate (ATP) needed to close the potassium tion of FFAs and triglycerides reduce hepatic
channels and depolarize the cell. Depolariza- insulin sensitivity, leading to increased he-
tion, in turn, results in opening of the cal- patic glucose production and hyperglycemia,
cium channels and insulin secretion. especially fasting plasma glucose levels. Thus,
3. The absolute lack of insulin in people with an increase in FFAs that occurs in obese indi-
type 1 diabetes mellitus means that they are viduals with a genetic predisposition to type
particularly susceptible to the development 2 diabetes may eventually lead to beta cell
of ketoacidosis. One of the actions of insulin dysfunction, increased insulin resistance, and
is the inhibition of lipolysis and release of greater hepatic glucose production.
free fatty acids (FFAs) from fat cells. In the ab- 9. The most commonly identified signs and
sence of insulin, ketosis develops when these symptoms of diabetes are referred to as the
fatty acids are released from fat cells and con- three polys: (1) polyuria (i.e., excessive urina-
verted to ketones in the liver. tion); (2) polydipsia (i.e., excessive thirst);
4. Type 1A diabetes is thought to be an autoim- and (3) polyphagia (i.e., excessive hunger).
mune disorder resulting from (1) a genetic These three symptoms are closely related to
predisposition; (2) an environmental trigger- the hyperglycemia and glycosuria of diabetes.
ing event, such as an infection; and (3) a T 10. Weight loss despite normal or increased ap-
lymphocyte-mediated hypersensitivity reac- petite is a common occurrence in people with
tion against some beta cell antigen. Much uncontrolled type 1 diabetes. First, loss of

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462 ANSWERS

body fluids results from osmotic diuresis. 15. Various glomerular changes may occur in
Second, body tissue is lost because the lack people with diabetic nephropathy, including
of insulin forces the body to use its fat capillary basement membrane thickening,
stores and cellular proteins as sources of diffuse glomerular sclerosis, and nodular
energy. glomerulosclerosis. Changes in the capillary
11. The technique of continuous subcutaneous basement membrane take the form of thick-
insulin infusion involves the insertion of a ening of basement membranes along the
small needle or plastic catheter into the sub- length of the glomeruli. Diffuse glomeru-
cutaneous tissue of the abdomen. Tubing losclerosis consists of thickening of the base-
from the catheter is connected to a syringe ment membrane and the mesangial matrix.
set into a small infusion pump worn on a Nodular glomerulosclerosis, Kimmelstiel-
belt or in a jacket pocket. The computer- Wilson disease, is a form of glomerulosclero-
operated pump then delivers one or more set sis that involves the development of nodular
basal amounts of insulin. In addition to the lesions in the glomerular capillaries of the
basal amount delivered by the pump, a bolus kidneys, causing impaired blood flow with
amount of insulin can be delivered when progressive loss of kidney function and, even-
needed (e.g., before a meal) by pushing a tually, renal failure. Changes in the basement
button. membrane in diffuse glomerulosclerosis and
12. The three major metabolic derangements in Kimmelstiel-Wilson syndrome allow plasma
DKA are hyperglycemia, ketosis, and meta- proteins to escape in the urine, causing pro-
bolic acidosis. Hyperglycemia leads to os- teinuria and the development of hypopro-
motic diuresis, dehydration, and a critical teinemia, edema, and others signs of
loss of electrolytes. Serum potassium levels impaired kidney function.
may be normal or elevated, despite total
potassium depletion resulting from pro-
tracted polyuria and vomiting. Metabolic aci- SECTION III: APPLYING YOUR
dosis is caused by the excess ketoacids that KNOWLEDGE
require buffering by bicarbonate ions; this Activity E
leads to a marked decrease in serum bicar-
bonate levels. 1. Type 1A diabetes mellitus is thought to be a
13. The chronic complications of diabetes in- chronic autoimmune disease that has a ge-
clude disorders of the microvasculature (i.e., netic predisposition. Type 1A diabetes mellitus
neuropathies, nephropathies, and is characterized by a total lack of insulin, an el-
retinopathies); macrovascular complications evation of blood glucose, and a breakdown of
(i.e., coronary artery, cerebral vascular, and body fats and proteins. Type 1A diabetics are
peripheral vascular diseases), and foot ulcers. susceptible to the development of ketoacido-
In the sorbitol pathway, glucose is trans- sis. Type 1A diabetics require daily injections
formed first to sorbitol and then to fructose. of exogenous insulin to control blood glucose
Although glucose is converted readily to sor- levels and prevent ketosis.
bitol, the rate at which sorbitol can be con- 2. Presently, there is no cure for diabetes melli-
verted to fructose and then metabolized is tus. Research is being conducted into ways of
limited. Sorbitol is osmotically active, and it preventing the disease, but none has yet been
has been hypothesized that the presence of found.
excess intracellular amounts may alter cell
function in those tissues that use this SECTION IV: PRACTICING FOR NCLEX
pathway.
Activity F
14. The peripheral neuropathies associated with
chronic diabetes mellitus include thickening of 1. b. Rationale: Each islet is composed of beta
the walls of the nutrient vessels that supply the cells that secrete insulin and amylin, alpha
nerve, leading to the assumption that vessel is- cells that secrete glucagon, and delta cells
chemia plays a major role in the development that secrete somatostatin. In addition, at least
of neural changes. In addition, a segmental de- one other type of cell, the PP cell, is present
myelinization process affects the Schwann cell. in small numbers in the islets and secrets a
This demyelinization process is accompanied hormone of uncertain function called pan-
by a slowing of nerve conduction. creatic polypeptide.

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ANSWERS 463

2. a, b, c, e. Rationale: These hormones, along 8. c. Rationale: The most commonly identified

with glucagon, are sometimes called counter- signs and symptoms of diabetes are referred
regulatory hormones because they counteract to as the three polys: (1) polyuria (i.e., exces-
the storage functions of insulin in regulating sive urination), (2) polydipsia (i.e., excessive
blood glucose levels during periods of fasting, thirst), and (3) polyphagia (i.e., excessive
exercise, and other situations that either limit hunger). Pheochromocytoma and poly-
glucose intake or deplete glucose stores. Min- cythemia are not hallmark signs of diabetes
eralocorticoids are not considered counter- mellitus.
regulatory hormones. 9. 1-d, 2-c, 3-e, 4-b, 5-f, 6-a
3. c. Rationale: In predisposed persons, the pro- 10. d. Rationale: The definitive diagnosis of DKA
longed elevation of glucocorticoid hor- consists of hyperglycemia (blood glucose lev-
mones can lead to hyperglycemia and the els 250 mg/dL), low bicarbonate (15
development of diabetes mellitus and star- mEq/L), and low pH (7.3), with ketonemia
vation. These hormones stimulate gluco- (positive at 1:2 dilution) and moderate ke-
neogenesis by the liver, sometimes tonuria. The other answers are not diagnostic
producing a 6- to 10-fold increase in hepatic for DKA.
glucose production. A prolonged increase in 11. a. Rationale: Alcohol decreases liver gluco-
glucocorticoid hormones does not cause he- neogenesis, and people with diabetes need to
patomegaly, portal hypertension, or adrenal be cautioned about its potential for causing
hyperplasia. hypoglycemia, especially if alcohol is con-
4. a. Rationale: Type 1A diabetes is thought to sumed in large amounts or on an empty
be an autoimmune disorder resulting from a stomach.
genetic predisposition (i.e., diabetogenic 12. b. Rationale: The signs and symptoms of hy-
genes); an environmental triggering event, poglycemia can be divided into two cate-
such as an infection; and a T lymphocyte- gories: (1) those caused by altered cerebral
mediated hypersensitivity reaction against function and (2) those related to activation
some beta cell antigen. The other answers are of the autonomic nervous system. Because
incorrect. the brain relies on blood glucose as its main
5. a, c, d. Rationale: The metabolic abnormalities energy source, hypoglycemia produces be-
that lead to type 2 diabetes include (1) in- haviors related to altered cerebral function.
sulin resistance, (2) deranged secretion of Headache, difficulty in problem-solving, dis-
insulin by the pancreatic beta cells, and turbed or altered behavior, coma, and
(3) increased glucose production by the liver. seizures can occur. Muscle spasms are not
The other answers are incorrect. one of the signs or symptoms of hypo-
6. a. Rationale: Secondary diabetes can occur glycemia.
with pancreatic disease or the removal of 13. c. Rationale: The Somogyi effect describes a
pancreatic tissue and with endocrine dis- cycle of insulin-induced posthypoglycemic
eases, such as acromegaly, Cushing syn- episodes. In 1924, Joslin and associates no-
drome, or pheochromocytoma. Endocrine ticed that hypoglycemia was associated with
disorders that produce hyperglycemia do so alternate episodes of hyperglycemia. The
by increasing the hepatic production of glu- other answers are not correct.
cose or decreasing the cellular use of glu- 14. d. Rationale: The loss of feeling, touch, and
cose. Dwarfism, hepatomegaly, and position sense increases the risk of falling.
pancreatic hyperplasia do not cause sec- Impairment of temperature and pain sensa-
ondary diabetes. tion increases the risk of serious burns and
7. b. Rationale: Diagnosis and careful medical injuries to the feet. Denervation of the
management are essential because women small muscles of the foot result in clawing
with GDM are at higher risk for complica- of the toes and displacement of the sub-
tions of pregnancy, mortality, and fetal ab- metatarsal fat pad anteriorly. These
normalities. Fetal abnormalities include changes, together with joint and connec-
macrosomia (i.e., large body size), hypo- tive tissue changes, alter the biomechanics
glycemia, hypocalcemia, polycythemia, and of the foot, increasing plantar pressure and
hyperbilirubinemia. Microsomia and hyper- predisposing to development of foot
calcemia are not fetal abnormalities associ- trauma and ulcers. The other answers are
ated with GDM. incorrect.

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464 ANSWERS

15. a. Rationale: Diabetic nephropathy is the lead- Activity B

ing cause of chronic kidney disease, account-
ing for 40% of new cases. Also, diabetes is the 1.
Urinary bladder opening
leading cause of acquired blindness in the Surface of Seminal vesicle
United States. The liver and pancreas are not urinary bladder
organs that diabetes attacks. Ampulla

16. a. Rationale: Multiple risk factors for macrovas-

cular disease, including obesity, hyperten-
Ejaculatory duct
sion, hyperglycemia, hyperinsulinemia, Prostatic
Prostate gland
hyperlipidemia, altered platelet function, en- Spongy urethra
urethra Membranous
dothelial dysfunction, systemic inflammation urethra
(as evidenced by increased C-reactive protein
[CRP]), and elevated fibrinogen levels, fre-
Penis
quently are found in people with diabetes. Ductus deferens
Hypotension, hypoinsulinemia, and de-
Epididymis
creased fibrinogen levels are not risk factors
Urethra
for macrovascular disease in diabetics. Testis

17. b. Rationale: Foot problems have been re-

ported as the most common complication Seminiferous
leading to hospitalization among people with tubules

diabetes.
18. c. Rationale: Pyelonephritis and urinary tract 2.
infections are relatively common in persons Deep penile fascia
with diabetes, and it has been suggested that
these infections may bear some relation to
Corpus cavernosum
the presence of a neurogenic bladder or
nephrosclerotic changes in the kidneys. Uri- Central artery
nary retention and urinary incontinence can
both be the result of a neurogenic bladder.
Nephrotic syndrome is not thought to be re- Corpus spongiosum
lated to a neurogenic bladder in diabetics.
Urethra

CHAPTER 43 STRUCTURE Activity C

AND FUNCTION OF THE MALE 1. j 2. i 3. e 4. d 5. c
GENITOURINARY SYSTEM 6. a 7. b 8. f 9. g 10. h

SECTION II: ASSESSING YOUR Activity D

UNDERSTANDING 1. At approximately 10 or 11 years of age, the
Activity A adenohypophysis, or anterior pituitary, under
the control of the hypothalamus begins to se-
1. genitourinary crete the gonadotropins that stimulate testicu-
2. antimüllerian hormone lar function and cause the interstitial cells of
3. Testosterone Leydig to begin producing testosterone. Ap-
4. inguinal canal proximately the same time, hormonal stimula-
5. accessory organs tion induces mitotic activity of the germ cells
6. prostate that develop in sperm. After cell maturation
7. Spermatogenesis has begun, the testes begin to enlarge rapidly
8. Testosterone as the individual tubules grow. Full maturity
9. protein synthesis and spermatogenesis usually are attained by
10. andropause 15 or 16 years of age.

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ANSWERS 465

2. In the first stage of spermatogenesis, small and tests will be needed to determine what is
unspecialized diploid germinal cells located causing this condition before treatment is
immediately adjacent to the tubular wall, determined.
called the spermatogonia, undergo rapid mi-
totic division and provide a continuous source SECTION IV: PRACTICING FOR NCLEX
of new germinal cells. As these cells multiply,
the more mature spermatogonia divide into Activity F
two daughter cells, which grow and become 1. a. Rationale: Two systems maintain the tem-
the primary spermatocytes—the precursors of perature of the testes at a level consistent
sperm. Over several weeks, large primary sper- with sperm production. One is the pampini-
matocytes divide by a process called meiosis to form plexus of testicular veins that surround
form two smaller secondary spermatocytes. the testicular artery. This plexus absorbs heat
The spermatid elongates into a spermatozoon, from the arterial blood, cooling it as it enters
or mature sperm cell, with a head and tail. the testes. The other is the cremaster muscle,
3. Among the undesired or harmful effects of which responds to decreases in testicular tem-
supraphysiologic doses of androgens are acne, perature by moving the testes closer to the
decreased testicular size, and azoospermia. body. The testicular artery and the tunica
These effects may persist for months after use vaginalis are not used by the body to main-
of the agents has ceased. Because testosterone tain optimal temperature in the testes for
can be aromatized to estradiol in the periph- sperm production. The cremaster is a muscle,
eral tissues, androgens can also produce gy- not a vein.
necomastia. 2. b. Rationale: Spermatozoa can be stored in the
4. Erection involves the shunting of blood into genital ducts for as long as 42 days and still
the corpus cavernosum. It is controlled by the maintain their fertility. The other answers are
sympathetic, parasympathetic, and nonadren- incorrect.
ergic–noncholinergic systems. Nitric oxide is 3. c. Rationale: Because sperm mobilization oc-
the released locally as a mediator that pro- curs at a pH of 6.0 to 6.5, the alkaline nature
duces relaxation of vascular smooth muscle. In of the prostatic secretions is essential for suc-
the flaccid state, sympathetic discharge cessful fertilization of the ovum. The other
through -adrenergic receptors maintains con- answers are incorrect.
traction of the arteries that supply the penis 4. a, c. Rationale: The cylindrical body or shaft
and vascular sinuses of the corpora cavernosa of the penis is composed of three masses of
and corpus spongiosum. Parasympathetic erectile tissue held together by fibrous strands
stimulation produces erection by inhibiting and covered with a thin layer of skin. The
sympathetic neurons that cause detumescence two lateral masses of tissue are called the cor-
and by stimulating the release of nitric oxide pora cavernosa. The third, ventral mass is
to effect a rapid relaxation of the smooth called the corpus spongiosum. All other an-
muscle in the sinusoidal spaces of the corpus swers are incorrect.
cavernosum. 5. d. Rationale: The outer layer of the seminifer-
ous tubules is made up of connective tissue
SECTION III: APPLYING YOUR and smooth muscle; the inner lining is com-
KNOWLEDGE posed of Sertoli cells, which are embedded
with sperm in various stages of development.
Activity E
The other answers are incorrect.
1. Serum testosterone level, drawn at its peak, 6. a. Rationale: The function of the male repro-
which is around 8 AM. If the initial total testos- ductive system is under the negative feedback
terone level is low, the diagnosis of hypogo- control of the hypothalamus and the anterior
nadism should be confirmed with either a pituitary gonadotropic hormones, FSH and
repeat measure of total testosterone or a mea- LH. Testosterone, AMG, and GH are not part
sure of free (bioavailable) testosterone. Other of the negative feedback loop that regulates
tests include serum LH and FSH levels and the male reproductive system.
seminal fluid analysis (SFA) 7. a, b, d. Rationale: Among the undesired or
2. Secondary hypogonadism is related to either harmful effects of supraphysiologic doses of
the pituitary gland or the hypothalamus. More androgens are acne, decreased testicular size,

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466 ANSWERS

and azoospermia. These effects may persist Activity B

for months after use of the agents have
A
ceased. Because testosterone can be aroma-
tized to estradiol in the peripheral tissues, an-
drogens can also produce gynecomastia Deep dorsal vein
(breast enlargement). Dorsal artery Cavernous
8. b. Rationale: Plasminogen activator, which Dorsal nerve nerve
converts plasminogen to plasmin, functions (somatic) (autonomic)
in the final detachment of mature spermato-
zoa from Sertoli cells. Prostate secretions,
testosterone, and androgen-binding protein
do not release mature spermatozoa from the Circumflex
Sertoli cells. artery and vein
9. c. Rationale: Erectile dysfunction can be B Circumflex vein Subtunical
caused by disease or dysfunction of the brain, venular plexus
spinal cord, cavernous or pudendal nerves, or
terminal nerve endings or receptors. The
other answers do not cause erectile dysfunc- Deep dorsal vein
tion. Tunica albuginea
10. d. Rationale: The term andropause has been Corpora cavernosa
used to describe an ill-defined collection of Sinusoidal spaces
symptoms in aging men, typically those older Cavernous artery
than 50 years, who have a relative or absolute
hypogonadism associated with aging. The Activity C
other answers are incorrect. 1. a 2. c 3. h 4. d 5. b
6. e 7. f 8. j 9. g 10. i
CHAPTER 44 DISORDERS OF THE
Activity D
MALE GENITOURINARY SYSTEM
1. Neurogenic disorders, such as Parkinson dis-
SECTION II: ASSESSING YOUR ease, stroke, and cerebral trauma, often con-
UNDERSTANDING tribute to erectile dysfunction by decreasing
libido or preventing the initiation of erection.
Activity A In spinal cord injury, the extent of neural im-
1. Hypospadias, epispadias pairment depends on the level, location, and
2. Peyronie disease extent of the lesion. Hormonal causes of erec-
3. Peyronie tile dysfunction include a decrease in andro-
4. parasympathetic, sympathetic gen levels owing to both primary and
5. nitric oxide, arterial secondary hypogonadism. Common risk
6. Erectile dysfunction factors for generalized penile arterial insuffi-
7. cardiovascular, metabolic ciency include hypertension, hyperlipidemia,
8. Priapism cigarette smoking, diabetes mellitus, and
9. penile cancer pelvic irradiation.
10. cryptorchidism 2. Sildenafil (Viagra) is a selective inhibitor of
11. motility phosphodiesterase type 5 (PDE-5), the enzyme
12. Epididymitis that inactivates cyclic guanosine monophos-
13. Prostatitis phate (cGMP). This acts by facilitating corpo-
14. acute bacterial prostatitis real smooth muscle relaxation in response to
15. prostate sexual stimulation.
16. chronic bacterial prostatitis 3. Testicular torsion is a twisting of the spermatic
17. extraprostatic cord that suspends the testis. Extravaginal tor-
18. prostate-specific antigen sion, which occurs almost exclusively in

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ANSWERS 467

neonates, is the less common form. It occurs untreated cases, the level of PSA correlates
when the testicle and the fascial tunicae that with the volume and stage of disease.
surround it rotate around the spermatic cord
at a level well above the tunica vaginalis. The
SECTION III: APPLYING YOUR
torsion probably occurs during fetal or
KNOWLEDGE
neonatal descent of the testes before the tu-
nica adheres to the scrotal wall. Intravaginal Activity E
torsion is considerably more common than
1. The cause of penile cancer is not known, al-
extravaginal torsion. It occurs when the testis
though several risk factors are thought to be
rotates on the long axis in the tunica vagi-
linked to this cancer.
nalis. In most cases, congenital abnormalities
2. Research data has shown that the most impor-
of the tunica vaginalis or spermatic cord
tant prognostic indicator is the status of your
exist. The tunica vaginalis normally sur-
lymph nodes. The more lymph nodes that are
rounds the testes and epididymis, allowing
involved, the more advanced your cancer has
the testicle to rotate freely in the tunica. Pa-
become. It is important that you ask your
tients usually present in severe distress within
physician what your prognosis is.
hours of onset and often have nausea, vomit-
ing, and tachycardia. The affected testis is
large and tender, with pain radiating to the SECTION IV: PRACTICING FOR NCLEX
inguinal area.
Activity F
4. The clinical staging for testicular cancer is as
follows: stage I, tumor confined to testes, epi- 1. a, c, e. Rationale: Factors that influence the
didymis, or spermatic cord; stage II, tumor timing of surgical repair include anesthetic
spread to retroperitoneal lymph nodes below risk, penile size, and the psychological ef-
the diaphragm; and stage III, metastases out- fects of the surgery on the child. In mild
side the retroperitoneal nodes or above the di- cases, the surgery is done for cosmetic rea-
aphragm. sons only. In more severe cases, repair be-
5. The anatomic location of the prostate at the comes essential for normal sexual
bladder neck contributes to the pathophysiol- functioning and to prevent the psychologi-
ogy and symptomatology of benign prostatic cal sequelae of having malformed genitalia.
hyperplasia (BPH). The two prostatic compo- Testicular involvement and presence of an
nents to the obstructive properties of BPH and abdominal hernia have no bearing on the
development of lower urinary tract symptoms timing of the surgery.
are dynamic and static. The static component 2. a. Rationale: Peyronie disease involves a local-
of BPH is related to an increase in prostatic ized and progressive fibrosis of unknown ori-
size; it gives rise to symptoms such as a weak gin that affects the tunica albuginea (i.e., the
urinary stream, postvoid dribbling, frequency tough, fibrous sheath that surrounds the cor-
of urination, and nocturia. The dynamic com- pora cavernosa) of the penis The disorder is
ponent of BPH is related to prostatic smooth characterized initially by an inflammatory
muscle tone. 1-Adrenergic receptors are the process that results in dense fibrous plaque
main receptors for the smooth muscle compo- formation. The plaque usually is on the dor-
nent of the prostate. sal midline of the shaft, causing upward bow-
6. The diagnosis of prostate cancer is based on ing of the shaft during erection. The other
history and physical examination and con- answers are incorrect.
firmed through biopsy methods. Transrectal 3. b. Rationale: Priapism can occur at any age, in
ultrasonography is used to guide a biopsy nee- the newborn as well as other age groups.
dle and document the exact location of the Sickle cell disease or neoplasms are the most
biopsied tissue. Radiologic examination of the common cause in boys between 5 and 10
bones of the skull, ribs, spine, and pelvis can years of age. Hemophilia and hypospadias are
be used to reveal metastases. Prostatic-specific not linked to priapism in any age group.
antigen (PSA) levels are important in the stag- 4. c. Rationale: The treatment goals for the boys
ing and management of prostatic cancer. In with cryptorchidism include measures to

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468 ANSWERS

enhance future fertility potential, placement CHAPTER 45 CONCEPTS OF

of the gonad in a favorable place for cancer
detection, and improved cosmetic appear- HEALTH AND DISEASE
ance. The other answers are incorrect.
5. d. Rationale: Hydroceles are palpated as cystic SECTION II: ASSESSING YOUR
masses that may attain massive proportions. UNDERSTANDING
With sufficient fluid, the mass may be mistaken
Activity A
for a solid tumor. Transillumination of the
scrotum (i.e., shining a light through the scro- 1. mons pubis
tum to visualize its internal structures) or ultra- 2. labia majora
sonography can help to determine whether the 3. labia minora
mass is solid or cystic and whether the testicle 4. clitoris
is normal. The other answers are incorrect. 5. vagina
6. a. Rationale: The most common acute scrotal 6. uterus
disorder in the pediatric population is testicu- 7. broad, round, uterosacral,
lar torsion. The other answers are incorrect. transverse
7. b. Rationale: Sexually transmitted acute epi- 8. myometrium
didymitis occurs mainly in young men with- 9. endometrium
out underlying genitourinary disease and is 10. fallopian tube
most commonly caused by Chlamydia tra- 11. estrogen, progesterone
chomatis and Neisseria gonorrhoeae. Candida 12. follicle-stimulating hormone (FSH),
albicans and Escherichia coli are not the most luteinizing hormone (LH)
common causes of epidiymitis in young men 13. sex
without underlying genitourinary disease. 14. fat tissue
8. a, b, c. Rationale: Signs of metastatic spread 15. anti-inflammatory
include swelling of the lower extremities, 16. progesterone
back pain, neck mass, cough, hemoptysis, or 17. endometrium
dizziness. Gynecomastia (breast enlargement) 18. oocyte
may result from human chorionic go- 19. corpus albicans, menstruation
nadotropin (hCG)-producing tumors and 20. human chorionic gonadotropin
occurs in about 5% of men with germ cell 21. endometrium
tumors. The other answers are not signs of 22. ferning
metastatic spread of a testicular cancer. 23. Menopause
9. c. Rationale: The manifestations of acute bac- 24. urogenital atrophy
terial prostatitis include fever and chills, 25. osteoporosis, cardiovascular
malaise, myalgia, arthralgia, frequent and ur- 26. breasts
gent urination, dysuria, and urethral dis- 27. Estrogen
charge. Dull, aching pain often is present in 28. Progesterone
the perineum, rectum, or sacrococcygeal re-
gion. The other answers are incorrect.
10. d. Rationale: The incidence of benign prostatic
hyperplasia increases with advanced age and is
highest in African Americans and lowest in na-
tive Japanese. The other answers are incorrect.

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ANSWERS 469

Activity B
1.

Ovary

Fallopian tube

Uterus

Urinary bladder
Cervix
Pubic symphysis
Urethra
Clitoris
Vagina
Anus

Vaginal orifice

2.

Suspensory ligament of ovary Frequent site of implantation Ovarian

Site of fertilization
ligament
Fundus Uterine
tube

Fimbriae
Ovary Path of oocyte
Broad Ruptured
ligament ovarian
follicle
Round ligament
Uterosacral of uterus
ligament

Cardinal
ligament

Path of sperm

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470 ANSWERS

Activity C to the growth of axillary and pubic hair, and

alter the distribution of body fat to produce
1. f 2. j 3. c 4. h 5. a the typical female body contours, including
6. g 7. i 8. b 9. d 10. e the accumulation of body fat around the hips
and breasts. Larger quantities of estrogen stim-
Activity D ulate pigmentation of the skin in the nipple,
1. Vaginal tissue usually is moist, with a pH areolar, and genital regions.
maintained within the bacteriostatic range of 5. Over the past four to five decades, hormone
3.8 to 4.2. Glycogen is fermented to lactic acid therapy (HT) became increasingly prescribed
by the lactobacilli (i.e., Döderlein’s bacilli) that for postmenopausal women. Initially, HT was
are part of the normal vaginal flora, account- used only for symptom management and later
ing for the mildly acid pH of vaginal fluid. for prevention of osteoporosis. During the
2. Evidence indicates that a certain minimal 1990s, HT evolved to the status of replacement
body weight (48 kg) and fat content for a vital hormone lost because of an en-
(16%–24%) are necessary for menarche to docrine organ failure (menopause). It was rou-
occur and for the menstrual cycle to be main- tinely offered to all postmenopausal women
tained. This is supported by the observation of based on mounting evidence of preventive
amenorrhea in women with anorexia nervosa, benefits in numerous areas. During this time,
chronic disease, and malnutrition and in those data from observational studies demonstrated
who are long-distance runners. In women a 50% reduction in coronary artery disease
with anorexia nervosa, gonadotropin and (CAD) mortality rates in women using HT.
estradiol secretion, including LH release Other demonstrated advantages of HT in-
and responsiveness to the hypothalamic cluded a reduced risk of Alzheimer disease,
gonadotropin-releasing hormone (GnRH), can decreased risk of colon cancer, less tooth loss,
revert to prepubertal levels. and lower incidence of macular degeneration.
3. Estrogens have additional cardioprotective ac- Unopposed estrogen can lead to the develop-
tions, including direct antiatherosclerotic ef- ment of endometrial hyperplasia which, in
fects on the arterial wall (augmentation of some cases, can increase a woman’s risk for en-
vasodilating and antiplatelet aggregation fac- dometrial cancer. The Women’s Health Initia-
tors such as nitric oxide and prostacyclin), va- tive study to investigate the potential effects of
sodilation through endothelium-independent HT was stopped after 5.2 years of data analysis
mechanisms, antioxidant activity, reduced lev- when it was found that the risk of breast can-
els of angiotensin-converting enzyme and cer crossed the predetermined safety boundary
renin, reduction of homocysteine levels, im- and it was determined that the risks of HT
proved peripheral glucose metabolism with outweighed its benefits. In addition to breast
subsequent decreased circulating insulin lev- cancer risk, CAD, stroke, and venous throm-
els, and direct effects on cardiac function. boembolic disease were all increased. On the
4. Estrogens are necessary for normal female positive side, a reduction was noted in colorec-
physical maturation. In concert with other tal cancer and hip fractures among the women
hormones, estrogens provide for the reproduc- using HT.
tive processes of ovulation, implantation of 6. During lactation, milk is secreted by alveolar
the products of conception, pregnancy, partu- cells, which are under the influence of the
rition, and lactation by stimulating the devel- anterior pituitary hormone prolactin. Milk
opment and maintaining the growth of the ejection from the ductile system occurs in
accessory organs. In the absence of androgens, response to the release of oxytocin from the
estrogens stimulate the intrauterine develop- posterior pituitary. The suckling of the infant
ment of the vagina, uterus, and uterine tubes provides the stimulus for milk ejection. Suck-
from the embryonic müllerian system. They ling produces feedback to the hypothalamus,
also stimulate the stromal development and stimulating the release of oxytocin from the
ductal growth of the breasts at puberty. Estro- posterior pituitary. Oxytocin causes contrac-
gens are responsible for the accelerated puber- tion of the myoepithelial cells lining the alve-
tal skeletal growth phase and for closure of the oli and ejection of milk into the ductal
epiphyses of the long bones; they contribute system.

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ANSWERS 471

8. a, b, d. Rationale: Problems that can arise as a

SECTION III: APPLYING
result of urogenital atrophy include vaginal
YOUR KNOWLEDGE
dryness, urinary stress incontinence, urgency,
Activity E nocturia, vaginitis, and urinary tract infec-
1. Several studies have been conducted to either tion. URI, an upper respiratory infection, has
confirm or refute the use of HT in post- nothing to do with menopause and urinary
menopausal women. Evidence-based practice retention is not a problem that arises from
now shows that HT can increase the risk of menopause.
cardiovascular events, as well as increase the 9. d. Rationale: The small bumps or projections
risk of breast cancer. on the areolar surface known as Mont-
2. No research data show that HT can reverse the gomery’s tubercles are sebaceous glands that
normal signs of aging in the female body. keep the nipple area soft and elastic. The
other answers are incorrect.
10. a. Rationale: Milk ejection from the ductile
SECTION IV: PRACTICING FOR NCLEX
system occurs in response to the release of
Activity F oxytocin from the posterior pituitary. The
other answers are incorrect.
1. a. Rationale: The area between labia minora is
called the vestibule. Located in the vestibule
are the urethral and vaginal openings and CHAPTER 46 DISORDERS OF THE
Bartholin’s lubricating glands. The other an-
swers are incorrect.
FEMALE REPRODUCTIVE SYSTEM
2. b. Rationale: The glycogen is fermented to lac-
SECTION II: ASSESSING YOUR
tic acid by the lactobacilli (i.e., Döderlein’s
UNDERSTANDING
bacilli), which are part of the normal vaginal
flora, accounting for the mildly acid pH of Activity A
vaginal fluid. The other answers are incorrect. 1. hair-bearing
3. c. Rationale: Anteriorly, the perimetrium is re- 2. vulva
flected over the bladder wall, forming the 3. Bartholin gland cyst
vesicouterine pouch; posteriorly, it extends 4. Chronic dermatitis
to form the cul-de-sac, or pouch of Douglas. 5. ecology
The other answers are incorrect. 6. Vaginitis
4. d. Rationale: The end of the fallopian tube 7. bleeding
nearest the ovary forms a funnel-like opening 8. metaplasia
with fringed, fingerlike projections called 9. Cervical
fimbriae, which pick up the ovum after its 10. cervicitis
release into the peritoneal cavity after ovula- 11. Polyps
tion. The other answers are incorrect. 12. Human papillomavirus (HPV)
5. a. Rationale: After ovulation, the follicle be- 13. Endometriosis
comes luteinized; as the corpus luteum, it 14. Adenomyosis
produces estrogen and progesterone to sup- 15. Dilatation, curettage
port the endometrium until conception 16. leiomyomas
occurs or the cycle begins again. The other 17. Pelvic inflammatory disease (PID)
answers are incorrect. 18. Ectopic pregnancy
6. b. Rationale: Although the mechanism is un- 19. menstrual, fertility
certain, progesterone increases basal body 20. Polycystic ovary
temperature and is responsible for the in- 21. luteinizing hormone (LH)
crease in body temperature that occurs with 22. Ovarian
ovulation. The other answers are effects of 23. ovulatory age
estrogen. 24. tumor suppressor
7. c. Rationale: High levels of estrogen exert a 25. Rectocele
negative feedback effect on FSH, inhibiting 26. cardinal
multiple follicular development and causing 27. uterine prolapse
an increase in LH levels. The other answers 28. amenorrhea
are incorrect. 29. Galactorrhea

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472 ANSWERS

30. Mastitis 33. Paget

31. Fibroadenomas 34. Infertility
32. Fibrocystic

Activity B

Umbilicus

Ovary

Small bowel

Colon
Fallopian tube

Uterine serosa
Rectovaginal septum
and uterosacral
Peritoneum ligaments

Bladder

Uterovesical fold

Activity C dergarments that can withstand hot water and

bleach (a fungicide) may be preferable for
1.
women to prevent such infections.
1. i 2. h 3. c 4. b 5. d
2. A quadrivalent vaccine (Gardisil) to prevent in-
6. f 7. e 8. j 9. a 10. g
fection with the HPV subtypes 6, 11, 16, and
2.
18 was licensed by the US Food and Drug Ad-
1. d 2. f 3. b 4. a 5. g
ministration (FDA) in June 2006. The vaccine
6. c 7. e
targets the two strains of HPV (HPV 16 and
18), which are responsible for 70% of cervical
Activity D
cancer, and the two most common benign
1. The prevention and treatment of vaginal infec- strains (HPV 6 and 11), which account for up
tions depend on proper health habits and ac- to 90% of genital warts. The vaccine is targeted
curate diagnosis and treatment of ongoing for females between the ages of 9 to 26 years,
infections. Measures to prevent infection in- optimally before initiating sexual activity.
clude those that keep the genital area clean Clinical studies provided to the FDA have con-
and dry, maintenance of normal vaginal flora firmed that the vaccine appears safe and effec-
and healthy vaginal mucosa, and avoidance of tive in inducing long-term immunity to HPV.
contact with organisms known to cause vagi- 3. Diagnosis of cervical cancer requires patho-
nal infections. Perfumed products, such as fem- logic confirmation. Papanicolaou smear results
inine deodorant sprays, douches, bath demonstrating squamous intraepithelial lesion
powders, soaps, and even toilet paper, can be (SIL) often require further evaluation by col-
irritating and may alter the normal vaginal poscopy during which a biopsy sample may be
flora. Tight clothing prevents the dissipation of obtained from suspect areas and examined mi-
body heat and evaporation of skin moisture croscopically. An alternate diagnostic tool in
and promotes favorable conditions for irrita- areas where colposcopy is not readily available
tion and the growth of pathogens. Cotton un- is a noninvasive photographic technique, in

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ANSWERS 473

which a cervicography camera is used to pho- tubes, and ovaries in the pelvis. The vagina is
tograph the cervix. The projected cervicogram encased in the semirigid structure of the
(a slide made from the film) is then sent for strong supporting fascia. The muscular floor
expert evaluation. In one study, the cer- of the pelvis is a strong, slinglike structure
vicogram was found to give a greater yield of that supports the uterus, vagina, urinary blad-
cervical intraepithelial neoplasia (CIN) than der, and rectum.
Papanicolaou smear alone in patients with 8. Dysfunctional menstrual cycles are related to
previous abnormal Papanicolaou smears. alterations in the hormones that support
4. The first theory, the regurgitation/implanta- normal cyclic endometrial changes. Estrogen
tion theory suggests that menstrual blood con- deprivation causes retrogression of a previ-
taining fragments of endometrium is forced ously built-up endometrium and bleeding.
upward through the fallopian tubes into the Such bleeding often is irregular in amount
peritoneal cavity. Retrograde menstruation is and duration, with the flow varying with the
not an uncommon phenomenon, and it is un- time and degree of estrogen stimulation and
known why endometrial cells implant and with the degree of estrogen withdrawal. A
grow in some women but not in others. A sec- lack of progesterone can cause abnormal
ond theory, the metaplastic theory, proposes menstrual bleeding; in its absence, estrogen
that dormant, immature cellular elements, induces development of a much thicker en-
spread over a wide area during embryonic de- dometrial layer with a richer blood supply.
velopment, persist into adult life and then dif- The absence of progesterone results from the
ferentiate into endometrial tissue. A third failure of any of the developing ovarian folli-
theory, the vascular/lymphatic theory, sug- cles to mature to the point of ovulation, with
gests that the endometrial tissue may metasta- the subsequent formation of the corpus lu-
size through the lymphatics or vascular teum and production and secretion of prog-
system. Genetic and immune factors also have esterone.
been studied as contributing factors to the de- 9. Approximately 5% to 10% of all breast cancers
velopment of endometriosis. are hereditary, with genetic mutations causing
5. The organisms ascend through the endocervi- up to 80% of breast cancers in women under
cal canal to the endometrial cavity, and then age 50. Two breast cancer susceptibility
to the tubes and ovaries. The endocervical genes—BRCA1 on chromosome 17 and BRCA2
canal is slightly dilated during menstruation, on chromosome 13—may account for most in-
allowing bacteria to gain entrance to the herited forms of breast cancer. BRCA1 is
uterus and other pelvic structures. After enter- known to be involved in tumor suppression.
ing the upper reproductive tract, the organ- A woman with known mutations in BRCA1
isms multiply rapidly in the favorable has a lifetime risk of 60% to 85% for breast
environment of the sloughing endometrium cancer and an increased risk of ovarian can-
and ascend to the fallopian tube. cer. BRCA2 is another susceptibility gene that
6. There is also concern that women with PCOS carries an elevated cancer risk similar to that
who are anovulatory do not produce signifi- with BRCA1
cant amounts of progesterone. This, in turn,
may subject the uterine lining to an unop- SECTION III: APPLYING YOUR
posed estrogen environment, which is a KNOWLEDGE
significant risk factor for development of Activity E
endometrial cancer. Although an association
with breast cancer and ovarian cancer has 1. A colposcopy is the examination of the
been reported, PCOS has not been conclu- vagina and cervix with an optical magnifying
sively shown to be an independent risk factor instrument. It is usually done after a Papani-
for either malignancy. colaou smear shows abnormal cells.
7. The uterus and the pelvic structures are main- 2. A LEEP uses a thin, rigid, wire loop that is
tained in proper position by the uterosacral, attached to a generator. It blends high-
round, broad, and cardinal ligaments. The two frequency, low-voltage current for cutting
cardinal ligaments maintain the cervix in its with a higher voltage current for coagulation.
normal position. The uterosacral ligaments The wire loop allows the physician to remove
hold the uterus in a forward position and the the entire transformation zone of the cervix.
broad ligaments suspend the uterus, fallopian This removes the entire lesion and provides a

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474 ANSWERS

specimen for further histologic evaluation. tion (Depo-Provera) has been associated with
The procedure is done under local anesthesia pelvic inflammatory disease (PID). The other
in the physician’s office at a lower cost than a forms of contraception have not been associ-
cone biopsy, which is done in the hospital or ated with PID.
out-patient surgery clinic. 8. c. Rationale: Diagnostic tests for ectopic preg-
nancy include a urine pregnancy test, ultra-
SECTION IV: PRACTICING FOR NCLEX sonography, and -human chorionic
gonadotropin (hCG), the hormone produced
Activity F
by placental cells) levels. Serial - hCG tests
1. a. Rationale: Surgical treatment of a Bartholin may detect lower-than-normal hCG produc-
cyst that has abscessed or blocks the entroitis tion. Transvaginal ultrasound studies after
is called marsupialization, a procedure that in- 5 weeks’ gestation may demonstrate an
volves removal of a wedge of vulvar skin and empty uterine cavity or presence of the gesta-
the cyst wall. The other answers are incorrect. tional sac outside the uterus. In a comparison
2. b. Rationale: One-third to one-half of vulvar of various protocols for diagnosing ectopic
intraepithelial neoplasm (VIN) cases appear to pregnancy, ultrasound followed by serial
be caused by the cancer-promoting potential hCG levels was found to yield the best re-
of certain strains (subtypes 16 and 18) of HPV sults. The other answers are incorrect.
that are sexually transmitted and are associ- 9. d. Rationale: Metformin, an insulin-sensitizing
ated with the type of vulvar cancer found in drug, used with or without ovulation-induc-
younger women. The other answers are not ing medications, is emerging as an important
thought to be associated with vulvar cancer component of polycystic ovary syndrome
in younger women. (PCOS) treatment. Dehydroepiandrosterone
3. a, b, c. Rationale: In premenarchal girls, most (DHEAS) is often found in the blood of
vaginal infections have nonspecific causes, women with PCOS; Methotrexate is used in
such as poor hygiene, intestinal parasites, or ectopic pregnancies; Spironalactone, an an-
the presence of foreign bodies. Vaginal de- timineralocorticoid, is used in treating PCOS,
odorants and tampons are not associated not mineralocorticoids.
with vaginal infections in premenarchal girls. 10. a, c, e. Rationale: Symptoms believed to have
4. c. Rationale: Blockage of the mucosal glands a strong correlation with ovarian cancer in-
results in trapping of mucus in the deeper clude abdominal or pelvic pain, increased ab-
glands leading to the formation of dilated dominal size or bloating, and difficulty eating
cysts within the cervix, called nabothian or feeling full quickly after ingesting food.
cysts. The other answers are incorrect. Increased intestinal gas and an increased
5. d. Rationale: Risk factors for endometriosis appetite are not highly correlated with ovar-
may include early menarche; regular periods ian cancer.
with shorter cycles (27 days), longer dura- 11. a. Rationale: A pessary can be inserted to hold
tion (7 days), or heavier flow; increased the uterus in place and it may stave off surgi-
menstrual pain; and other first-degree rela- cal intervention in women who want to have
tives with the condition. Late menarche, children or in older women for whom the
light flow, and periods shorter than 7 days surgery may pose a significant health risk.
are not risk factors for endometriosis. The other answers are incorrect.
6. a. Rationale: Leiomyomas are asymptomatic 12. b. Rationale: Although analgesic agents, such
approximately half of the time and may be as aspirin and acetaminophen, may relieve
discovered during a routine pelvic examina- minor uterine cramping or low back pain,
tion, or they may cause menorrhagia (exces- prostaglandin synthetase inhibitors (e.g.,
sive menstrual bleeding), anemia, urinary ibuprofen, naproxen, mefenamic acid, in-
frequency, rectal pressure/constipation, ab- domethacin) are more specific for dysmenor-
dominal distention, and, infrequently, pain. rhea and the treatment of choice, if
Diarrhea and urinary retention are not symp- contraception is not desired. Metformic acid
toms of leiomyomas. is incorrect.
7. b. Rationale: New-onset breakthrough bleed- 13. c. Rationale: Treatment for mastitis symptoms
ing in women who are on oral contraceptives include application of heat or cold, excision,
or medroxyprogesterone contraceptive injec- aspiration, mild analgesics, antibiotics, and a

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ANSWERS 475

supportive brassiere or breast binder. The Activity C

other answers are incorrect.
14. d. Rationale: Diagnosis of fibrocystic changes 1. Risk factors for acquiring the human papillo-
is made by physical examination, mammog- mavirus (HPV) include young age (25 years),
raphy, ultrasonography, and biopsy (i.e., as- early age of first intercourse (16 years), in-
piration or tissue sample). Patient history and creasing numbers of sex partners, and having
galactography are not used to diagnose fibro- a male partner with multiple sex partners.
cystic changes in the breast. HPV infection can occur with any type of vagi-
15. a. Rationale: Postmenopausal women and nal or anal penetration and is common in
women who have had a hysterectomy can men having sex with men and women having
perform the examination any day of the sex with women. Oral–genital and manual–
month. The other answers are incorrect. genital contact are less likely means of spread-
16. b. Rationale: The specimen is best collected by ing this infection.
masturbation into a sterile container after 2. Herpes simplex virus (HSV) is transmitted by
3 days of abstinence. The other answers are contact with infectious lesions or secretions.
incorrect. Herpes simplex virus type-1 is transmitted by
17. c. Rationale: Between 12 and 24 hours after oral secretions, and infections frequently
insemination, the ova are evaluated for signs occur in childhood. Herpes simplex virus type-
of fertilization. If signs are present, the ova 1 can be spread to the genital area by au-
are returned to the incubator, and 48 to 72 toinoculation after poor handwashing or
hours after egg retrieval, the fertilized eggs through oral–genital contact. Herpes simplex
are placed into the woman’s uterus by means virus type-2 usually is transmitted by sexual
of a transcervical catheter. The other answers contact but can be passed to an infant during
are incorrect. childbirth if the virus is actively being shed
from the genital tract. In genital herpes, the
virus ascends through the peripheral nerves to
CHAPTER 47 SEXUALLY the sacral dorsal root ganglia. The virus can re-
TRANSMITTED INFECTIONS main dormant in the dorsal root ganglia, or it
can reactivate, in which case the viral particles
SECTION II: ASSESSING YOUR are transported back down the nerve root to
UNDERSTANDING the skin, where they multiply and cause a le-
sion to develop.
Activity A
3. Reported risk factors for the overgrowth of Can-
1. mucocutaneous dida albicans include recent antibiotic therapy,
2. fetus or newborn which suppresses the normal protective bacter-
3. Genital warts ial flora; high hormone levels owing to preg-
4. external genitalia nancy or the use of oral contraceptives, which
5. Genital herpes cause an increase in vaginal glycogen stores;
6. neurotropic and uncontrolled diabetes mellitus or human
7. type-2 immunodeficiency virus (HIV) infection, be-
8. primary genital herpes cause they compromise the immune system.
9. Molluscum contagiosum 4. Trichomoniasis is a risk factor for HIV trans-
10. yeast mission and infectivity in both men and
11. Trichomonads women. In women, it increases the risk of
12. Bacterial tubal infertility and atypical pelvic inflamma-
13. Chlamydiae tory disease, and it is associated with adverse
14. fallopian tube outcomes, such as premature birth in pregnant
15. gonococcus women. Trichomonads attach easily to mucous
16. Syphilis membrane. They can serve as vectors for the
spread of other organisms, carrying pathogens
Activity B attached to their surface into the fallopian
tubes. In men, it is a common cause of non-
1. j 2. h 3. a 4. d 5. g
gonococcal urethritis and is a risk factor for in-
6. f 7. i 8. b 9. e 10. c
fertility, altering sperm motility and viability.

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476 ANSWERS

It has also been associated with chronic prosta- urethral itching, meatal erythema and tender-
titis. ness, urethral discharge, history of sexual rela-
5. Men are more likely to be symptomatic than tions with someone being treated for a
women. In men, the initial symptoms include chlamydial infection, and history of recent
urethral pain and a creamy yellow, sometimes conjunctivitis
bloody, discharge. The disorder may become 2. The expected treatment for chlamydial infec-
chronic and affect the prostate, epididymis, tion includes pharmacologic treatment with
and periurethral glands. Rectal infections are either azithromycin or doxycycline, simulta-
common in homosexual men. In women, rec- neous treatment of both sexual partners, and
ognizable symptoms include unusual genital or abstinence from sexual activity to facilitate
urinary discharge, dysuria, dyspareunia, pelvic cure.
pain or tenderness, unusual vaginal bleeding
(including bleeding after intercourse), fever,
SECTION IV: PRACTICING FOR NCLEX
and proctitis. Symptoms can occur or increase
during or immediately after menses because Activity E
the bacterium is an intracellular diplococcus
1. a. Rationale: The incubation period for HPV-
that thrives in menstrual blood but cannot sur-
induced genital warts ranges from 6 weeks to
vive long outside the human body. There may
8 months, with a mean of 2 to 3 months. The
be infections of the uterus and development of
other answers are incorrect.
acute or chronic infection of the fallopian
2. a, c, e. Rationale: The initial symptoms of pri-
tubes, with ultimate scarring and sterility.
mary genital herpes infections include tin-
6. The clinical disease is divided into three
gling, itching, and pain in the genital area,
stages: primary, secondary, and tertiary. Pri-
followed by eruption of small pustules and
mary syphilis is characterized by the appear-
vesicles. Chancres and eczemalike lesions are
ance of a chancre at the site of exposure. These
not indicative of genital herpes.
lesions usually are painless and located at the
3. b. Rationale: The antiviral drugs acyclovir,
site of sexual contact. The timing of the sec-
valacyclovir, and famciclovir have become
ond stage of syphilis varies even more than
the cornerstone for the treatment of genital
that of the first, lasting from 1 week to 6
herpes. The other drugs are not used in the
months. The symptoms of a rash, fever, sore
treatment of genital herpes.
throat, stomatitis, nausea, loss of appetite, and
4. c. Rationale: Chancroid organisms have
inflamed eyes may come and go for a year but
shown resistance to treatment with sul-
usually last for 3 to 6 months. Secondary man-
famethoxazole alone and to tetracycline. The
ifestations can include alopecia and genital
Centers for Disease Control and Prevention
condylomata latum. Condylomata latum are
(CDC) recommends treatment with
elevated, red-brown lesions that can ulcerate
azithromycin, erythromycin, or ceftriaxone.
and produce a foul discharge. They are 2 to
The other answers are incorrect.
3 cm in diameter, contain many spirochetes,
5. d. Rationale: An important characteristic of
and are highly infectious. Tertiary syphilis is a
Lymphogranuloma venereum (LGV) is the early
delayed response of the untreated disease. It
(1 to 4 weeks later) development of large, ten-
can occur as long as 20 years after the initial
der, and sometimes fluctuant inguinal lymph
infection. When syphilis does progress to the
nodes called buboes.
symptomatic tertiary stage, it commonly takes
6. a. Rationale: Antifungal agents, such as clotri-
one of three forms: development of localized
mazole, miconazole, butaconazole, and ter-
destructive lesions called gummas, develop-
conazole, in various forms, are effective in
ment of cardiovascular lesions, or develop-
treating candidiasis. These drugs, with the ex-
ment of central nervous system lesions.
ception of terconazole, are available without
prescription for use by women who have had a
SECTION III: APPLYING YOUR
previously confirmed diagnosis of candidiasis.
KNOWLEDGE
7. b. Rationale: Trichomoniasis can cause a num-
Activity D ber of complications. It is a risk factor for HIV
transmission and infectivity in both men and
1. While taking the nursing history, you would
women. In women, it increases the risk of
find it important to note the following:

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ANSWERS 477

tubal infertility and atypical pelvic inflamma- 16. synaptic cleft

tory disease, and it is associated with adverse 17. depolarization, hyperpolarization
outcomes, such as premature birth, in preg- 18. excitatory postsynaptic
nant women. The other answers are incorrect. 19. neurotransmission
8. c. Rationale: The predominant symptom of 20. Neuromodulator
bacterial vaginosis is a thin, grayish-white 21. Neurotrophic
discharge that has a foul, fishy odor. The 22. reticular activating system
other answers are incorrect. 23. pia mater
9. a, b, e. Rationale: A specimen should be col- 24. spinal nerves
lected from the appropriate site (i.e., endo- 25. paired segmental spinal nerves
cervix, urethra, anal canal, or oropharynx), 26. plexuses
inoculated onto a suitable medium, and 27. reflex
transported under appropriate conditions. 28. withdrawal
The nasal passages and the exocervix are not 29. hindbrain, midbrain, forebrain
sites that would be used for the collection of 30. hypoglossal
Neisseria gonorrhoeae. 31. vagus
10. d. Rationale: The syphilitic gumma is a pecu- 32. spinal accessory nerve
liar, rubbery, necrotic lesion that is caused by 33. glossopharyngeal nerve
noninflammatory tissue necrosis. Gummas 34. vestibulocochlear nerve
can occur singly or multiply and vary in size 35. facial nerve
from microscopic lesions to large, tumorous 36. abducens
masses. They most commonly are found in 37. trigeminal nerve
the liver, testes, and bone. Chancres occur in 38. cerebellum
primary syphilis. Chancroid is a sexually 39. thalamus
transmitted infection (STI). Gummies are 40. gyrus, sulcus
candy. 41. basal ganglia
42. primary somatosensory cortex
43. meninges
CHAPTER 48 ORGANIZATION AND 44. CSF
CONTROL OF NEURAL FUNCTION 45. autonomic nervous system.
46. parasympathetic nervous system
SECTION II: ASSESSING YOUR
UNDERSTANDING Activity B
Activity A 1.
Segments
1. neurons
2. Schwann cells, neuroglial
3. body, dendrites, axons, synapses
Dorsal
4. Dendrites root
5. anterograde, retrograde
6. Schwann, satellite
7. Satellite
8. myelin
9. nodes of Ranvier, saltatory conduction Dorsal root
10. oligodendrocytes ganglion
neuron
11. Glucose
12. action potentials IA neuron Ventral Spinal
root nerve
13. resting membrane potential
14. synapses Dorsal root
ganglion
15. Chemical

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478 ANSWERS

2.
Corpus
callosum
Septum
pellucidum
Third
Frontal ventricle
lobe
Occipital
lobe
Pineal
body
Interventricular
foramen Cerebral
Anterior aqueduct
commissure
Fourth
Midbrain ventricle
Pons Cerebellum
Medulla Central canal
oblongata
Spinal cord

Activity C metabolism. An interruption in the blood or

oxygen supply to the brain rapidly leads to
1. clinically observable signs and symptoms.
1. f 2. h 3. e 4. b 5. d Without oxygen, brain cells continue to func-
6. c 7. a 8. j 9. g 10. i tion for approximately 10 seconds. Uncon-
2. sciousness occurs almost simultaneously with
1. b 2. i 3. e 4. g 5. f cardiac arrest, and the death of brain cells
6. a 7. h 8. c 9. d begins within 4 to 6 minutes.
3. The local currents resulting from an excitatory
Activity D postsynaptic potential (EPSP) (sometimes
1. Myelin formation is essentially the same in called a generator potential) are usually insuf-
both the peripheral nervous system (PNS) and ficient to reach threshold and cause depolar-
central nervous system (CNS); both contain ization of the axon’s initial segment. However,
myelin basic protein and both involve the if several EPSPs occur simultaneously, the area
winding of plasma membranes around the of depolarization can become sufficiently large
nerve fiber. During the wrapping of myelin, and the currents at the initial segment can be-
the cytoplasm between two adjacent inner come sufficiently strong to exceed the thresh-
leaflets of the plasma membrane is expelled. old potential and initiate an action potential.
The two adjacent inner leaflets and any re- This summation of depolarized areas is called
maining cytoplasm appear as a dark line called “spatial summation.” EPSPs also can summate
the “major dense line.” Likewise, during the and cause an action potential if they occur in
wrapping of the plasma membranes to form rapid succession. This temporal aspect of the
myelin, adjacent outer plasma membrane occurrence of two or more EPSPs is called
leaflets become opposed, creating the interpe- “temporal summation.” Inhibitory postsynap-
riod or minor dense line. Linking proteins, tic potentials (IPSPs) also can undergo spatial
proteolipid protein (PLP) found only in the and temporal summation with each other and
CNS and myelin protein zero (MPZ) found with EPSPs, reducing the effectiveness of the
only in the PNS, help stabilize adjacent plasma latter by a roughly algebraic summation. If the
membranes of the myelin sheath. sum of EPSPs and IPSPs keeps the depolariza-
2. Nervous tissue has a high rate of metabolism. tion at the initial segment below threshold
Although the brain comprises only 2% of the levels, no action potential occurs.
body’s weight, it receives approximately 15% 4. (1) They can be broken down into inactive
of the resting cardiac output and consumes substances by enzymes; (2) they can be taken
20% of its oxygen. Despite its substantial en- back up into the presynaptic neuron in a
ergy requirements, the brain cannot store oxy- process called “reuptake”; or (3) they can dif-
gen or effectively engage in anaerobic fuse away into the intercellular fluid until its

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ANSWERS 479

concentration is too low to influence postsy- maintaining the stable chemical environment
naptic excitability. of the brain. Only water, carbon dioxide, and
5. The nervous system appears very early in em- oxygen enter the brain with relative ease; the
bryonic development. At the beginning of transport of other substances between the brain
week 3, the ectoderm begins to invaginate and and the blood is slower and more controlled.
migrates between the two layers, forming a 8. The blood–brain barrier prevents many drugs
third layer called the “mesoderm.” Mesoderm from entering the brain. Most highly water-
along the entire midline of the embryo forms soluble compounds are excluded from the
a specialized rod of embryonic tissue called the brain, especially molecules with high ionic
“notochord.” The notochord and adjacent charge, such as many of the catecholamines.
mesoderm provide the necessary induction In contrast, many lipid-soluble molecules
signal for the overlying ectoderm to differenti- cross the lipid layers of the blood–brain barrier
ate and form a thickened structure called the with ease. Some drugs, such as the antibiotic
“neural plate.” Within the neural plate an chloramphenicol, are highly lipid soluble and
axial groove develops and sinks into the un- therefore enter the brain readily. Other med-
derlying mesoderm, allowing its walls to fuse ications have a low solubility in lipids and
across the top and form an ectodermal tube enter the brain slowly or not at all. Alcohol,
called the “neural tube.” As the neural tube nicotine, and heroin are very lipid soluble and
closes, ectodermal cells called “neural crest rapidly enter the brain. Some substances that
cells” migrate away from the dorsal surface of enter the capillary endothelium are converted
the neural tube to become the progenitors of by metabolic processes to a chemical form
the neurons and supporting cells of the pe- incapable of moving into the brain.
ripheral nervous system. During development,
the more rostral portions of the embryonic
SECTION III: APPLYING YOUR KNOWLEDGE
neural tube—approximately 10 segments—
undergo extensive modification and enlarge- Activity E
ment to form the brain.
1. Your baby has a meningomyeloceles.
6. Four columns of afferent (sensory) neurons in
2. Most children with meningomyeloceles have
the dorsal root ganglia directly innervate four
clinical dysfunction in both the motor and
corresponding columns of IA neurons in the
sensory nerves of the lower extremities. Dys-
dorsal horn. These columns are categorized as
function usually extends to bowel and bladder
special and general afferents: special somatic
control. The extent of the dysfunction cannot
afferent, general somatic afferent, special vis-
be assessed until the infant is born and can be
ceral afferent, and general visceral afferent.
better assessed.
The ventral horn contains three longitudinal
cell columns: general visceral efferent, pharyn-
geal efferent, and general somatic efferent. SECTION IV: PRACTICING FOR NCLEX
Each of these cell columns contains OA and
Activity F
efferent neurons. The OA neurons coordinate
and integrate the function of the efferent 1. a. Rationale: The supporting cells, such as
motor neurons cells of its column. Schwann cells in the peripheral nervous sys-
7. Maintenance of a chemically stable environ- tem and the neuroglial cells in the central
ment is essential to the function of the brain. nervous system, protect the nervous system
In most regions of the body, extracellular fluid and provide metabolic support for the neu-
undergoes small fluctuations in pH and con- rons. The other answers are incorrect.
centrations of hormones, amino acids, and 2. b. Rationale: These membrane channels are
potassium ions during routine daily activities guarded by voltage-dependent gates that open
such as eating and exercising. If the brain were and close with changes in the membrane po-
to undergo such fluctuations, the result would tential. The other answers are incorrect.
be uncontrolled neural activity, because some 3. c. Rationale: The most common type of
substances, such as amino acids, act as neuro- synapse is the chemical synapse. The other
transmitters, and ions, such as potassium, in- answers are incorrect.
fluence the threshold for neural firing. Two 4. d. Rationale: Neurotransmitters are synthe-
barriers, the blood–brain barrier and the sized in the cytoplasm of the axon terminal.
CSF–brain barrier, provide the means for The other answers are incorrect.

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480 ANSWERS

5. a. Rationale: Neuromodulator molecules react The effect of this continual or basal (baseline)
with presynaptic or postsynaptic receptors to activity is referred to as “tone.”
alter the release of or response to neurotrans- 13. d. Rationale: Dopamine, which is an interme-
mitters. The other answers are incorrect. diate compound in the synthesis of norepi-
6. b. Rationale: With rare exceptions, peripheral nephrine, also acts as a neurotransmitter. It is
nerves, including the cranial nerves, contain the principal inhibitory transmitter of inter-
afferent and efferent processes of more than nuncial neurons in the sympathetic ganglia.
one of the four afferent and three efferent cell It also has vasodilator effects on renal,
columns. This provides the basis for assessing splanchnic, and coronary blood vessels when
the function of the any peripheral nerve. The given intravenously and is sometimes used in
other answers are incorrect. the treatment of shock.
7. c. Rationale: On the lateral sides of the spinal
cord, extensions of the pia mater, the dentic-
ulate ligaments, attach the sides of the spinal
CHAPTER 49 SOMATOSENSORY
cord to the bony walls of the spinal canal. FUNCTION, PAIN, AND HEADACHE
Thus, the cord is suspended by both the den-
ticulate ligaments and the segmental nerves. SECTION II: ASSESSING YOUR
The posterior vertebra and vertebral blood UNDERSTANDING
vessels do not support the spinal cord. Activity A
8. d. Rationale: The myotatic or stretch reflex
controls muscle tone and helps maintain pos- 1. somatosensory
ture. Specialized sensory nerve terminals in 2. General
skeletal muscles and tendons relay informa- 3. Special
tion on muscle stretch and joint tension to 4. visceral
the central nervous system. This information, 5. trigeminal
which drives postural reflex mechanisms, 6. dermatome
also is relayed to the thalamus and the sen- 7. discriminative
sory cortex and is experienced as propriocep- 8. anterolateral
tion, the sense of body movement and 9. modalities
position. 10. action potentials
9. a. Rationale: The cerebellum compares what is 11. acuity
actually happening with what is intended to 12. tactile
happen. It then transmits the appropriate 13. Thermal
corrective signals back to the motor system, in- 14. pain
structing it to increase or decrease the activity 15. sensory, perception
of the participating muscle groups so that 16. Neuropathic
smooth and accurate movements can be per- 17. neuromatrix
formed. Answer B describes the trigeminal 18. Nociceptive
nerve which exits the brainstem. Answer C de- 19. C fibers
scribes the pons. Answer D describes midbrain. 20. neospinothalamic
10. b. Rationale: Parkinson disease, Huntington 21. paleospinothalamic
chorea, and some forms of cerebral palsy, 22. periaqueductal gray
among other dysfunctions involving the 23. enkephalins, endorphins, dynorphins
basal ganglia, result in a frequent or continu- 24. threshold
ous release of abnormal postural or axial and 25. Cutaneous
proximal movement patterns. If damage to 26. Deep somatic
the basal ganglia is localized to one side, the 27. warning
movements occur on the opposite side of the 28. analgesic
body. The other answers are incorrect. 29. hyperalgesia
11. c. Rationale: Some drugs, such as the antibi- 30. Analgesia
otic chloramphenicol, are highly lipid soluble 31. Neuralgia
and therefore enter the brain readily. The 32. Cluster
other answers are incorrect. 33. tension-type
12. c. Rationale: The sympathetic and parasympa- 34. temporomandibular joint (TMJ)
thetic nervous systems are continually active.

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ANSWERS 481

Activity B identify the size and shape of objects and their

movement across the skin; temperature sensa-
1. tion; sense of movement of the limbs and
Somatosensory
joints of the body; and nociception, or pain.
cortex
3. A pinpoint pressed against the skin of the sole
Third-
of the foot that results in a withdrawal reflex
order and a complaint of skin pain confirms the
functional integrity of the afferent terminals
in the skin, the entire pathway through the
Thalamus peripheral nerves of the foot, leg, and thigh
to the sacral (S1) dorsal root ganglion, and
Dorsal root through the dorsal root into the spinal cord
ganglion Second- segment. It confirms that the somatosensory
Receptor order input association cells receiving this informa-
tion are functioning and that the reflex cir-
cuitry of the cord segments (L5 to S2) is
First- functioning. In addition, the lower motor neu-
order
rons of the L4 to S1 ventral horn can be con-
sidered operational, and their axons through
the ventral roots, the mixed peripheral nerve,
and the motor neuron to the muscles produc-
2. • lips ing the withdrawal response can be considered
• trunk/back intact and functional. The communication be-
• lips tween the lower motor neuron and the muscle
cells is functional, and these muscles have
Activity C normal responsiveness and strength. Observa-
1. tion of a normal withdrawal reflex rules out
1. f 2. a 3. d 4. i 5. j peripheral nerve disease, disorders of the dor-
6. e 7. g 8. c 9. h 10. b sal root and ganglion, diseases of the my-
2. oneural junction, and severe muscle diseases.
1. d 2. f 3. c 4. a 5. b Normal reflex function also indicates that
6. e many major descending central nervous sys-
tem tract systems are functioning within nor-
Activity D mal limits. If the person is able to report the
pinprick sensation and accurately identify its
1. Sensory systems are organized in a serial suc- location, many ascending systems through
cession of neurons consisting of first-order, much of the spinal cord and brain also are
second-order, and third-order neurons. First- functioning normally, as are basic intellect
order neurons transmit sensory information and speech mechanisms.
from the periphery to the central nervous 4. According to the gate control theory, the
system. Second-order neurons communicate internuncial neurons involved in the gating
with various reflex networks and sensory path- mechanism are activated by large-diameter,
ways in the spinal cord and travel directly to faster-propagating fibers that carry tactile
the thalamus. Third-order neurons relay infor- information. The simultaneous firing of the
mation from the thalamus to the cerebral cor- large-diameter touch fibers has the potential
tex. This organizing framework corresponds for blocking the transmission of impulses from
with the three primary levels of neural integra- the small-diameter myelinated and unmyeli-
tion in the somatosensory system: the sensory nated pain fibers. Pain therapists have long
units, which contain the sensory receptors; known that pain intensity can be temporarily
the ascending pathways; and the central pro- reduced during active tactile stimulation.
cessing centers in the thalamus and cerebral 5. Referred pain is pain that is perceived at a site
cortex. different from its point of origin, but inner-
2. These somatosensory receptors monitor four vated by the same spinal segment. It is hy-
major types or modalities of sensation: pothesized that visceral and somatic afferent
discriminative touch, which is required to neurons converge on the same dorsal horn

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482 ANSWERS

projection neurons. For this reason, it can be disturbances commonly occur and consist of
difficult for the brain to identify the original visual hallucinations, such as stars, sparks, and
source of pain. Pain that originates in the ab- flashes of light. Migraine with aura has similar
dominal or thoracic viscera is diffuse, poorly symptoms, but with the addition of reversible
localized, and often perceived at a site far re- visual symptoms including positive features
moved from the affected area. (e.g., flickering lights spots, or lines) and/or
6. Heat dilates blood vessels and increases local negative features (loss of vision); fully re-
blood flow; it also can influence the transmis- versible sensory symptoms including positive
sion of pain impulses and increase collagen features (feeling or pins or needles) or negative
extensibility. An increase in local circulation features (numbness); and fully reversible
can reduce the level of nociceptive stimulation speech disturbance.
by reducing local ischemia caused by muscle 9. Activation of the trigeminal sensory fibers can
spasm or tension, increase the removal of lead to the release of neuropeptides, causing
metabolites and inflammatory mediators that painful neurogenic inflammation within the
act as nociceptive stimuli, and help to reduce meningeal vasculature characterized by
swelling and relieve pressure on local nocicep- plasma protein extravasation, vasodilation,
tive endings. It also may trigger the release of and mast cell degranulation. Another possible
endogenous opioids. Heat also alters the vis- mechanism implicates neurogenic vasodila-
cosity of collagen fibers in ligaments, tendons, tion of meningeal blood vessels as a key com-
and joint structures so that they are more eas- ponent of the inflammatory processes that
ily extended and can be stretched further be- occur during migraine. Activation of trigemi-
fore the nociceptive endings are stimulated. nal sensory fibers evokes a neurogenic dural
7. Phantom limb pain often begins as sensations vasodilation mediated by calcitonin gene-
of tingling, heat and cold, or heaviness, fol- related peptide. It also has been observed that
lowed by burning, cramping, or shooting pain. calcitonin gene-related peptide level is ele-
It may disappear spontaneously or persist for vated during migraine.
many years. Several theories have been pro-
posed as to the causes of phantom pain. One SECTION III: APPLYING YOUR KNOWLEDGE
theory is that the end of a regenerating nerve
becomes trapped in the scar tissue of the am- Activity E
putation site. It is known that when a periph- 1. It is difficult to assess pain and discomfort in
eral nerve is cut, the scar tissue that forms someone suffering with dementia. In our facil-
becomes a barrier to regenerating outgrowth ity we use The Assessment for Discomfort in De-
of the axon. The growing axon often becomes mentia Protocol as it has been shown to
trapped in the scar tissue, forming a tangled improve pain management in this population.
growth of small-diameter axons, including pri- 2. Acetaminophen is the drug of choice to man-
mary nociceptive afferents and sympathetic age this patient’s discomfort. You can also
efferents. It has been proposed that these affer- place ice on the cast at the point of fracture
ents show increased sensitivity to innocuous for 20 minutes, each hour, to help reduce the
mechanical stimuli and to sympathetic activ- discomfort.
ity and circulating catecholamines. A related
theory moves the source of phantom limb
SECTION IV: PRACTICING FOR NCLEX
pain to the spinal cord, suggesting that the
pain is caused by the spontaneous firing Activity F
of spinal cord neurons that have lost their
1. 1-e, 2-a, 3-g, 4-b, 5-c, 6-h, 7-d, 8-f
normal sensory input from the body. In one
2. 1-c, 2-g, 3-i, 4-d, 5-h, 6-a, 7-f, 8-j, 9-b, 10-k,
hypothesis, the pain is caused by changes in
11-e
the flow of signals through somatosensory
3. a. Rationale: Clinically, neurologic assessment
areas of the brain.
of somatosensory function can be done by
8. Migraine without aura is a pulsatile, throb-
testing the integrity of spinal segmental
bing, unilateral headache that typically lasts 1
nerves. The other answers are incorrect.
to 2 days and is aggravated by routine physical
4. b. Rationale: Stimuli used include pressure
activity. The headache is accompanied by nau-
from a sharp object, strong electric current
sea and vomiting, which often is disabling,
to the skin, or application of heat or cold of
and sensitivity to light and sound. Visual

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ANSWERS 483

approximately 10ºC above or below normal tions of acetaminophen, acetylsalicylic acid,

skin temperature. The other answers are caffeine, and nonsteroidal anti-inflammatory
incorrect. drugs (NSAIDs) (e.g., naproxen sodium,
5. c. Rationale: The amino acid glutamate is a ibuprofen), serotonin (5-HT1) receptor ago-
major excitatory neurotransmitter released nists (e.g., sumatriptan, naratriptan, rizatrip-
from the central nerve endings of the nocicep- tan, zolmitriptan), ergotamine derivatives
tive neurons. The other answers are incorrect. (e.g., dihydroergotamine), and antiemetic
6. d. Rationale: The paleospinothalamic tract is a medications (e.g., ondansetron, metoclo-
slower-conducting, multisynaptic tract con- pramide). Morphine, tramadol, and syrup of
cerned with the diffuse, dull, aching, and ipecac are not first-line drugs in the treat-
unpleasant sensations that commonly are as- ment of migraine.
sociated with chronic and visceral pain. The 17. c. Rationale: Cluster headache is a type of pri-
other answers are incorrect. mary neurovascular headache that typically
7. 1-c, 2-d, 3-f, 4-g, 5-e, 6-b, 7-a includes severe, unrelenting, unilateral pain
8. a, c. Rationale: Assessment includes such located, in order of decreasing frequency, in
things as the nature, severity, location, and the orbital, retro-orbital, temporal, supraor-
radiation of the pain. Spinal reflex involve- bital, and infraorbital region. The other
ment and spinal tract involvement are not answers are incorrect.
assessed when assessing pain. 18. d. Rationale: With children 3 to 8 years of age,
9. a. Rationale: Part of the reluctance of health scales with faces of actual children or cartoon
care workers to provide adequate relief for faces can be used to obtain a report of pain.
acute pain has been fear of addiction. How- The other pain rating scales are inappropriate
ever, addiction to opioid medications is in this age group.
thought to be virtually nonexistent when 19. a. Rationale: The overriding principle in all
these drugs are prescribed for acute pain. The pediatric pain management is to treat each
other answers are not the major concern. child’s pain on an individual basis and to
10. b. Rationale: The World Health Organization match the analgesic agent with the cause
has created an analgesic ladder for cancer and the level of pain. The other answers are
pain that assists clinicians in choosing the incorrect.
appropriate analgesic. The other answers are
incorrect.
11. a, b, c. Rationale: The ideal analgesic would be
CHAPTER 50 DISORDERS
effective, nonaddictive, and inexpensive. In OF MOTOR FUNCTION
addition, it would produce minimal adverse
effects and not affect the person’s level of SECTION II: ASSESSING YOUR
consciousness. UNDERSTANDING
12. c. Rationale: Surgery for severe, intractable pain Activity A
of peripheral or central origin has met with
some success. It can be used to remove the 1. Motor function
cause or block the transmission of intractable 2. spinal cord
pain from phantom limb pain, severe neural- 3. polysynaptic
gia, inoperable cancer of certain types, and 4. posture
causalgia. The other answers are incorrect. 5. cortex
13. d. Rationale: Primary hyperalgesia describes 6. motor
pain sensitivity that occurs directly in dam- 7. cerebellum, basal ganglia
aged tissues. The other answers are incorrect. 8. circuits
14. 1-d, 2-b, 3-a, 4-c 9. muscle spindles
15. a. Rationale: Treatment of phantom limb pain 10. Golgi tendon organs
is accomplished by the use of sympathetic 11. peripheral
blocks, transcutaneous electrical nerve stimu- 12. motor
lation (TENS) of the large myelinated affer- 13. atrophy
ents innervating the area, hypnosis, and 14. muscle tone
relaxation training. 15. Upper motor neuron (UMN)
16. b. Rationale: Based on clinical trials, first-line 16. Hyporeflexia
agents include acetylsalicylic acid, combina-

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484 ANSWERS

17. lower motor neuron disorders, peripheral, Activity D

myopathies
18. dystrophy 1.
19. fibrillations 2 5 4 3 1
20. Duchenne
21. neuromuscular junction
22. acetylcholine Activity E
23. Myasthenia gravis 1. The lowest level of the hierarchy occurs at
24. spinal cord, cranial nerve the spinal cord, which contains the basic re-
25. peripheral nerve flex circuitry needed to coordinate the func-
26. Mononeuropathies tion of the motor units involved in the
27. Polyneuropathies planned movement. Above the spinal cord is
28. herniated disk the brain stem, and above the brain stem is
29. cerebellar the cerebellum and basal ganglia, structures
30. basal ganglia that modulate the actions of the brain stem
31. tremor systems. Overseeing these supraspinal struc-
32. Parkinson tures are the motor centers in the cerebral
33. bradykinesia cortex. The highest level of function, which
34. Amyotrophic lateral sclerosis occurs at the level of the frontal cortex, is
35. Multiple sclerosis (MS) concerned with the purpose and planning of
36. demyelination the motor movement. The efficiency of
37. spinal cord injury (SCI) movement depends on input from sensory
38. loss systems that operate in parallel with the
39. Tetraplegia motor systems.
40. Paraplegia 2. The motor neuron and the group of muscle
41. vasovagal fibers it innervates in a muscle is called a
42. Orthostatic “motor unit.” When the motor neuron devel-
43. deep venous thrombosis ops an action potential, all of the muscle
fibers in the motor unit it innervates develop
Activity B action potentials, causing them to contract
Premotor simultaneously. Thus, a motor neuron and
cortex Motor Somatosensory the muscle fibers it innervates function as a
(8) (6) cortex cortex single unit—the basic unit of motor control.
Frontal
(4) (3,1,2) Each motor neuron undergoes multiple
eye fields
(part of branching, making it possible for a single
area 8) motor neuron to innervate a few to thousands
of muscle fibers. In general, large muscles—
those containing hundreds or thousands of
muscle fibers and providing gross motor
movement—have large motor units (LMUs).
This sharply contrasts with those that control
the hand, tongue, and eye movements, for
Broca
Primary
which the motor units are small and permit
area
Primary very precise control.
(45,44) visual
Vestibular auditory 3. The muscle spindles consist of a group of
cortex
cortex cortex (17) specialized miniature skeletal muscle fibers
(44)
called intrafusal fibers that are encased in a
Activity C connective tissue capsule and attached to the
1. extrafusal fibers of a skeletal muscle. In the
1. d 2. c 3. i 4. e 5. a center of the receptor area, a large sensory
6. f 7. j 8. h 9. g 10. b neuron spirals around the intrafusal fiber
2. forming the so-called primary or annulospiral
1. c 2. e 3. f 4. i 5. b ending. The intrafusal muscle fibers function
6. j 7. g 8. a 9. h 10. d as stretch receptors. When a skeletal muscle is

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ANSWERS 485

stretched, the spindle and its intrafusal fibers affects some Schwann cells while sparing oth-
are stretched, resulting in increased firing of ers. Axonal degeneration is caused by pri-
their afferent nerve fibers. Segmental mary injury to a neuronal cell body or its
branches make connections, along with other axon. Damage to the axon may be caused by
branches, that pass directly to the anterior either a focal event occurring at some point
gray matter of the spinal cord and establish along the length of the nerve (e.g., trauma or
monosynaptic contact with each of the lower ischemia) or a more generalized abnormality
motor neurons (LMNs) that have motor units affecting the neuronal cell body (neuropa-
in the muscle containing the spindle recep- thy).
tor. This produces an opposing muscle con- 7. Carpal tunnel syndrome can be caused by a
traction. Another segmental branch of the variety of conditions that produce a reduc-
same afferent neuron innervates an internun- tion in the capacity of the carpal tunnel (i.e.,
cial neuron that is inhibitory to motor units bony or ligament changes) or an increase in
of antagonistic muscle groups. This disynap- the volume of the tunnel contents (i.e., in-
tic inhibitory pathway is the basis for the rec- flammation of the tendons, synovial
iprocal activity of agonist and antagonist swelling, or tumors). Carpal tunnel syndrome
muscles (i.e., when an agonist muscle is is an example of a compression-type
stretched, the antagonists relax). mononeuropathy that is relatively common.
4. Coordination of muscle movement requires It is caused by compression of the median
that four areas of the nervous system function nerve as it travels with the flexor tendons
in an integrated manner—the motor system through a canal made by the carpal bones
for muscle strength, the cerebellar system for and transverse carpal ligament
rhythmic movement and steady posture, the 8. Guillain-Barré syndrome is an acute immune-
vestibular system for posture and balance, and mediated polyneuropathy that is character-
the sensory system for position sense. ized by rapidly progressive limb weakness
5. Duchenne muscular dystrophy (DMD) is and loss of tendon reflexes. The disorder is
caused by mutations in a gene located on the marked by progressive ascending muscle
short arm of the X chromosome that codes weakness of the limbs, producing a symmet-
for a protein called dystrophin. Dystrophin is ric flaccid paralysis. Symptoms of paresthesia
a large cytoplasmic protein located on the and numbness often accompany the loss of
inner surface of the sarcolemma or muscle motor function. Paralysis may progress to
fiber membrane. The dystrophin molecules involve the respiratory muscles. Autonomic
are concentrated over the Z-bands of the nervous system involvement that causes pos-
muscle, where they form a strong link be- tural hypotension, arrhythmias, facial flush-
tween the actin filaments of the intracellular ing, abnormalities of sweating, and urinary
contractile apparatus and the extracellular retention is common. Pain is another com-
connective tissue matrix. Abnormalities in mon feature.
the dystrophin-associated protein complex 9. The primary brain abnormality found in all
compromise sarcolemma integrity, particu- persons with Parkinson disease is degenera-
larly with sustained contractions. This disrup- tion of the nigrostriatal dopamine neurons.
tion in integrity may be responsible for the On microscopic examination, there is loss of
observed increased fragility of dystrophic pigmented substantia nigra neurons. Some
muscle, excessive influx of calcium ions, and residual nerve cells are atrophic, and a few
release of soluble muscle enzymes, such as contain Lewy bodies, which are visualized as
creatine kinase into the serum. The degenera- spherical, eosinophilic cytoplasmic inclu-
tive process in DMD consists of a relentless sions. Although the cause of Parkinson dis-
necrosis of muscle fibers, accompanied by a ease is still unknown, it is widely believed
continuous process of repair and regenera- that most cases are caused by an interaction
tion, and progressive fibrosis. of environmental and genetic factors. Over
6. Segmental demyelination occurs when there the past several decades, several pathologic
is a disorder of the Schwann cell (as in Guillain- processes (e.g., oxidative stress, apoptosis, and
Barré syndrome) or damage to the myelin mitochondrial disorders) that might lead to
sheath (e.g., sensory neuropathies), without a degeneration have been identified. One theory
primary abnormality of the axon. It typically is that the auto-oxidation of catecholamines,

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486 ANSWERS

such as dopamine, during melanin synthesis

SECTION IV: PRACTICING FOR NCLEX
injures neurons in the substantia nigra.
Increasing evidence suggests that the devel- Activity G
opment of Parkinson disease may be related
1. a. Rationale: The highest level of function,
to oxidative metabolites of this process and
which occurs at the level of the frontal cor-
the inability of neurons to render these prod-
tex, is concerned with the purpose and plan-
ucts harmless.
ning of the motor movement. The other
10. The death of lower motor neurons leads to
answers are incorrect.
denervation, with subsequent shrinkage of
2. 1-b, 2-a, 3-d, 4-c
musculature and muscle fiber atrophy. It is
3. b. Rationale: The anatomic basis of a reflex
this fiber atrophy, called amyotrophy, which
consists of an afferent neuron, which synapses
appears in the name of the disease. The loss of
either directly with an effector neuron that
nerve fibers in lateral columns of the white
innervates a muscle or with an interneuron
matter of the spinal cord, along with fibrillary
that synapses with an effector neuron.
gliosis, imparts a firmness or sclerosis to this
4. a, b, c, e. Rationale: These signs and symp-
central nervous system (CNS) tissue; the term
toms include changes in muscle characteris-
lateral sclerosis designates these changes.
tics (strength, bulk, and tone), spinal reflex
11. The primary neurologic injury occurs at the
activity, and motor coordination. Muscle in-
time of mechanical injury and is irreversible.
nervation is incorrect.
It is characterized by small hemorrhages in
5. c. Rationale: The postural muscles of hip and
the gray matter of the cord, followed by ede-
shoulder are usually the first to be affected.
matous changes in the white matter that lead
The other answers are incorrect.
to necrosis of neural tissue. This type of
6. d. Rationale: The aminoglycoside antibiotics
pathology results from the forces of compres-
(e.g., gentamicin) can produce a clinical dis-
sion, stretch, and shear associated with frac-
turbance similar to botulism by preventing
ture or compression of the spinal vertebrae,
the release of acetylcholine from nerve end-
dislocation of vertebrae, and contusions
ings. These drugs are particularly dangerous
owing to jarring of the cord in the spinal
in persons with preexisting disturbances of
canal. Secondary injuries follow the primary
neuromuscular transmission, such as myas-
injury and promote the spread of injury.
thenia gravis. The other answers are incorrect.
Although there is considerable debate about
7. a. Rationale: Myasthenia crisis occurs when
the pathogenesis of secondary injuries, the
muscle weakness becomes sufficiently severe
tissue destruction that occurs ends in progres-
to compromise ventilation to the extent that
sive neurologic damage. After a spinal cord
ventilatory support and airway protection are
injury, several pathologic mechanisms come
needed. The other answers are incorrect.
into play, including vascular damage, neu-
8. b. Rationale: Carpal tunnel syndrome is an
ronal injury that leads to loss of reflexes
example of a compression-type mononeu-
below the level of injury, and release of
ropathy that is relatively common. The
vasoactive agents and cellular enzymes.
other answers are not mononeuropathies.
9. c. Rationale: The straight-leg test is an impor-
SECTION III: APPLYING YOUR KNOWLEDGE
tant diagnostic maneuver for a herniated disk
Activity F in the lumbar area. The other answers are
incorrect.
1. “The medicine that we are giving your hus-
10. 1-a, 2-b, 3-c
band is methylprednisolone, a short-acting
11. d. Rationale: The function of the striatum also
corticosteroid. In a case of spinal cord injury,
involves local cholinergic interneurons and
the drug is thought to enhance the generation
their destruction is thought to be related to
of impulses down the spinal cord and improve
the choreiform movements of Huntington
the blood flow around the site of the injury.”
disease, another basal ganglia-related syn-
2. • Bed rest with log rolling only
drome. The other answers do not involve the
• Continuous pulse oximetry
cholinergic interneurons of the striatum.
• Vital signs hourly until stable
12. a. Rationale: In Parkinson disease, also
• Methylprednisolone intravenously (IV)
known as idiopathic parkinsonism, dopamine
• Monitor for gastric bleeding; venous
depletion results from degeneration of the
thrombosis and steroid myopathy

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ANSWERS 487

dopamine nigrostriatal system. The other 12. Cytotoxic

answers are incorrect. 13. primary, cerebral hypoxia
13. b. Rationale: The most common clinical pre- 14. Epidural hematomas
sentation is slowly progressive weakness and 15. tear
atrophy in distal muscles of one upper ex- 16. Consciousness
tremity. The other answers do not describe 17. brain
the clinical presentation of amyotrophic 18. vegetative
lateral sclerosis (ALS). 19. autoregulation
14. c. Rationale: A large percentage of patients 20. carbon dioxide, hydrogen ion, oxygen
with multiple sclerosis (MS) have elevated im- 21. Stroke
munoglobulin G (IgG) levels, and some have 22. Ischemic, hemorrhagic
oligoclonal patterns (i.e., discrete electro- 23. ministroke, angina
phoretic bands) even with normal IgG levels. 24. Thrombi
15. d. Rationale: A functional C7 injury allows 25. Lacunar
full elbow flexion and extension, wrist plan- 26. embolic
tar flexion, and some finger control. At the 27. hemorrhage
C8 level, finger flexion is added. The other 28. cerebral artery
answers are incorrect. 29. cerebral aneurysm
16. a. Rationale: Cord injuries involving C1 to C3 30. Arteriovenous
result in a lack of respiratory effort, and af- 31. Encephalitis
fected patients require assisted ventilation. 32. Vomiting
The other answers involve injuries further 33. chemotherapy
down the spinal column. 34. seizure
17. a, c, e. Rationale: Autonomic dysreflexia is char- 35. Simple partial
acterized by vasospasm, hypertension ranging 36. Complex partial
from mild (20 mm Hg above baseline) to severe 37. muscle contractions
(as high as 240/120 mm Hg or higher), skin pal- 38. Tonic-clonic
lor, and gooseflesh associated with the piloerec- 39. status epilepticus
tor response. Fever and vasoconstriction are not
manifestations of autonomic dysreflexia. Activity B
18. b. Rationale: Although the enteric nervous Anterior
system innervation of the bowel remains in- Epidural Subdural
tact, without the defecation reflex, peristaltic hematoma hematoma
movements are ineffective in evacuating
stool. The other answers are incorrect.

CHAPTER 51 DISORDERS OF
THE BRAIN FUNCTION
SECTION II: ASSESSING YOUR
UNDERSTANDING
Activity A
1. brain’s
2. 20
3. hypoxia
4. focal, global
5. sodium
6. Laminar necrosis
7. amino acids, proteases
8. intracranial
9. herniation
10. edema Intracerebral
hematoma
11. vasogenic Posterior

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488 ANSWERS

Activity C flow is restored, if ischemic thresholds for

injury were exceeded, then permanent cell
1. f 2. g 3. d 4. j 5. b death ensues.
6. c 7. e 8. h 9. a 10. i 2. Watershed infarcts are concentrated in
anatomically vulnerable border zones be-
Activity D
tween the overlapping territories supplied
1. by the major cerebral arteries, notably the
middle, anterior, and posterior cerebral ar-
5 1 3 7 teries. The overlapping territory at the distal
ends of these vessels forms extremely vul-
8 4 6 2 nerable areas in terms of global ischemia,
called “watershed zones.” During events
2. such as severe hypotension, these distal ter-
ritories undergo a profound lowering of
Glutamate
Glutamate blood flow, predisposing to focal ischemia
and infarction of brain tissues. Therefore,
global ischemia can result in focal infarcts
NMDA receptor
that occur in the border zones between
major vascular territories.
Opening calcium channels 3. During prolonged ischemia, the glutamate
transport mechanisms become immobilized,
causing extracellular glutamate to accumu-
Calcium cascade late. Additionally, intracellular glutamate is
released from the damaged cells. This gluta-
mate excess then drives the uncontrolled
Release of intracellular enzymes opening of N-methyl-D-aspartate (NMDA)
Protein breakdown receptor-operated channels producing an
Free radical formation
increase in intracellular calcium. Excess in-
Lipid peroxidation
Fragmentation of DNA tracellular calcium leads to a series of cal-
Nuclear breakdown cium-mediated processes called the calcium
cascade, including the release of intracellular
enzymes that cause protein breakdown, free
radical formation, lipid peroxidation, frag-
Activity E
mentation of DNA, mitochondrial injury,
1. Global ischemia occurs at a time when blood nuclear breakdown, and eventually cell
flow is inadequate to meet the metabolic death.
needs of the entire brain. The result is a spec- 4. Although recovery usually takes place within
trum of neurologic disorders reflecting global 24 hours, mild symptoms, such as headache,
brain dysfunction. Unconsciousness occurs irritability, insomnia, and poor concentration
within seconds of severe global ischemia, and memory, may persist for months. The
such as that resulting from complete cessa- memory loss usually includes an interval of
tion of blood flow, as in cardiac arrest, or time preceding the accident (retrograde am-
with marked decrease in blood flow, as in se- nesia) and following the injury (anterograde
rious cardiac arrhythmias. If cerebral circula- amnesia).
tion is restored immediately, consciousness is 5. Global brain injury, whether caused by
regained quickly. However, if blood flow is head trauma, stroke, or other pathologies, is
not promptly restored, severe pathologic manifested by alterations in sensory, motor,
changes take place. Energy sources, glucose, and cognitive function and by changes in
and glycogen, are exhausted in 2 to 4 min- the level of consciousness. In contrast to
utes, and cellular adenosine triphosphate focal injury, which causes focal neurologic
(ATP) stores are depleted in 4 to 5 minutes. deficits without altered consciousness,
When ischemia is sufficiently severe or pro- global injury nearly always results in
longed, infarction or death of all the cellular altered levels of consciousness ranging from
elements of the brain occurs. Even if blood inattention to stupor or coma. Severe injury

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ANSWERS 489

that seriously compromises brain function 10. Seizures can be caused by alterations in cell
can result in brain death. membrane permeability or distribution of
6. (1) Arousal and wakefulness, and (2) content ions across the neuronal cell membranes. An-
and cognition. The content and cognition other cause may be decreased inhibition of
aspects of consciousness are determined by a cortical or thalamic neuronal activity or struc-
functioning cerebral cortex. Arousal and tural changes that alter the excitability of
wakefulness requires the concurrent func- neurons. Neurotransmitter imbalances, such
tioning of both cerebral hemispheres and an as an acetylcholine excess or -aminobutyric
intact RAS in the brainstem. The earliest acid (GABA, an inhibitory neurotransmitter)
signs of diminution in level of consciousness deficiency, have been proposed as causes.
are inattention, mild confusion, disorienta- Certain epilepsy syndromes have been linked
tion, and blunted responsiveness. With fur- to specific genetic mutations causing ion
ther deterioration, the delirious person channel defects.
becomes markedly inattentive and variably
lethargic or agitated. The person may be-
come obtunded and respond only to vigor- SECTION III: APPLYING YOUR
ous or noxious stimuli. KNOWLEDGE
7. A bilateral loss of the pupillary light response Activity F
is indicative of lesions of the brain stem. A
unilateral loss of the pupillary light response 1.
may be caused by a lesion of the optic or ocu- Family history of stroke
lomotor pathways. The oculocephalic reflex • history of hypertension
(doll’s-head eye movement) can be used to • history of smoking
determine whether the brain stem centers for • history of diabetes mellitus
eye movement are intact and the oculovesti- • history of sickle cell disease
bular may be used to elicit nystagmus. • history of hyperlipidemia
8. During the evolution of a stroke, there usu- • history of atrial fibrillation
ally is a central core of dead or dying cells, • weight
surrounded by an ischemic band or area of • alcohol and drug use
minimally perfused cells called the “penum- • hormone replacement therapy
bra.” Brain cells of the penumbra receive • oral contraceptive use
marginal blood flow, and their metabolic ac- • activity level
tivities are impaired; although the area un- 2. Administration of tissue-type plasminogen ac-
dergoes an “electrical failure,” the structural tivator (tPA) to be given within 3 hours of
integrity of the brain cells is maintained. onset
Whether the cells of the penumbra continue • Administration of neuroprotective drugs
to survive depends on the successful timely • Hypothermia treatment
return of adequate circulation, the volume of
toxic products released by the neighboring
SECTION IV: PRACTICING FOR NCLEX
dying cells, the degree of cerebral edema, and
alterations in local blood flow. If the toxic Activity G
products result in additional death of cells in
1. 1-g, 2-c, 3-a, 4-f, 5-b, 6-e, 7-d
the penumbra, the core of dead or dying tis-
2. 1-e, 2-a, 3-b. 4-g, 5-c, 6-d, 7-f
sue enlarges, and the volume of surrounding
3. a, b, d, e. Rationale: The direct brain injuries
ischemic tissue increases.
include diffuse axonal injury and the focal le-
9. First, blood is shunted from the high-pressure
sions of laceration, contusion, and hemor-
arterial system to the low-pressure venous sys-
rhage. Hypoxic brain injury is considered a
tem without the buffering advantage of the
secondary type of injury.
capillary network. The draining venous chan-
4. a. Rationale: In contrast to focal injury, which
nels are exposed to high levels of pressure, pre-
causes focal neurologic deficits without al-
disposing them to rupture and hemorrhage.
tered consciousness, global injury nearly al-
Second, the elevated arterial and venous pres-
ways results in altered levels of consciousness
sures divert blood away from the surrounding
ranging from inattention to stupor or coma.
tissue, impairing tissue perfusion.

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490 ANSWERS

The other answers are manifestations of dif- 11. c. Rationale: Intracranial tumors give rise to
ferent types of brain injury, not a global focal disturbances in brain function and in-
injury. creased intracranial pressure (ICP). Focal
5. b. Rationale: Decorticate (flexion) posturing is disturbances occur because of brain compres-
characterized by flexion of the arms, wrists, sion, tumor infiltration, disturbances in
and fingers, with abduction of the upper ex- blood flow, and brain edema. Blood pressure,
tremities, internal rotation, and plantar flex- either increased or decreased, is not a mani-
ion of the lower extremities. Decerebrate and festation of a brain tumor.
extensor posturing are the same thing and 12. 1-f, 2-e, 3-d, 4-a, 5-b, 6-c
are incorrect. Diencephalon posturing does 13. d. Rationale: The most common surgery con-
not exist, so it is incorrect. sists of removal of the amygdala and an ante-
6. c. Rationale: Clinical examination must dis- rior part of the hippocampus and entorhinal
close at least the absence of responsiveness, cortex, as well as a small part of the temporal
brain stem reflexes, and respiratory effort. pole, leaving the lateral temporal neocortex
Brain death is a clinical diagnosis, and a re- intact. Only a portion of the hippocampus
peat evaluation at least 6 hours later is recom- and entorhinal cortex, and temporal pole are
mended. An ECG is not assessed in an removed.
examination for brain death. 14. a. Rationale: Treatment consists of appropri-
7. a, c, e. Rationale: The criteria for diagnosis of ate life-support measures. Medications are
vegetative state include the absence of aware- given to control seizure activity. Intra-
ness of self and environment and an inability venously (IV) administered diazepam or lo-
to interact with others; the absence of sus- razepam is considered first-line therapy for
tained or reproducible voluntary behavioral the condition. Lorazepam is not given intra-
responses; lack of language comprehension; muscularly (IM) in status epilepticus. Cy-
sufficiently preserved hypothalamic and brain clobenzaprine and cyproheptadine are not
stem function to maintain life; bowel and used to treat status epilepticus.
bladder incontinence; and variably preserved
cranial nerve (e.g., pupillary, gag) and spinal
cord reflexes. People in a persistent vegetative
CHAPTER 52 SLEEP AND
state can open their eyes and have sufficient SLEEP DISORDERS
hypothalamic function to maintain life.
8. d. Rationale: If blood pressure falls below SECTION II: ASSESSING YOUR
60 mm Hg, cerebral blood flow becomes se- UNDERSTANDING
verely compromised and, if it rises above the Activity A
upper limit of autoregulation, blood flow in-
creases rapidly and overstretches the cerebral 1. Wakefulness, sleep
vessels. The other answers are incorrect. 2. growth, repair
9. a. Rationale: The diagnosis of subarachnoid he- 3. reticular formation
morrhage and intracranial aneurysms is made 4. Electroencephalogram (EEG)
by clinical presentation, computed tomo- 5. Non-REM
graphic (CT) scan, lumbar puncture, and an- 6. REM
giography. Magnetic resonance imaging (MRI) 7. REM
is not necessary for the diagnosis of subarach- 8. Melatonin
noid hemorrhage and intracranial aneurysm. 9. sleep history
Loss of cranial nerve reflexes is not diagnostic 10. dyssomnias
of subarachnoid hemorrhage and intracranial 11. synchronization
aneurysm and neither is venography. 12. Jet lag
10. b. Rationale: Two assessment techniques can 13. advanced sleep phase syndrome
help determine whether meningeal irritation 14. Insomnia
is present. Kernig’s sign is resistance to exten- 15. hygiene
sion of the knee while the person is lying 16. Periodic limb movement disorder
with the hip flexed at a right angle. Brudzin- 17. 10 seconds
ski sign is elicited when flexion of the neck 18. Nightmares
induces flexion of the hip and knee. The 19. Elderly
other answers are incorrect.

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ANSWERS 491

Activity B 2. Stage 1 consists of low-voltage, mixed-frequency

EEG activity. It occurs at sleep onset and is a
brief transitional stage between wakefulness
Uvula
and true sleep. Stage 1 serves as a transitional
Soft stage for repeated sleep cycles throughout the
palate
night. Stage 2 is a deeper sleep during which
EEG activity is interrupted by sleep spindles
Nasopharynx consisting of bursts of high frequency (12–14
Hz) waves. Stages 3 and 4 represent deep
Oropharynx Tongue sleep and are dominated by high-voltage, low
frequency waves. Stage 3 usually lasts only a
Epiglottis
few minutes and is transitional to stage 4,
Laryngopharynx
which lasts for approximately 20–40 minutes.
During deep sleep, the muscles of the body
relax and posture is adjusted intermittently.
Heart rate and blood pressure decrease and
gastrointestinal activity is slowed. An incre-
mentally larger stimulus is required for arousal
from slow-wave sleep.
3. External sensory input is inhibited in REM
sleep, whereas internal sensory circuits such as
those of the auditory and visual systems are
aroused. During this time, the brain can replay
previous memories but cannot acquire new
Soft palate Tongue
sensory information. At the same time, motor
systems that control body movements are in-
hibited. There is a loss of muscle movement
Uvula and muscle tone. There also are changes in au-
Epiglottis tonomic nervous system–controlled functions
during REM sleep—blood pressure, heart rate,
Activity C and respirations increase and fluctuate and
temperature regulation is lost. Cerebral blood
1. j 2. a 3. i 4. f 5. g flow and metabolic rate decrease. Sleep-related
6. d 7. e 8. b 9. h 10. c penile erection occurs during this stage of sleep.
4. (1) Dyssomnias, which are disorders of initiat-
Activity D ing and maintaining sleep and disorders of ex-
1. The sleep–wake cycle normally consists of a cessive sleepiness; (2) parasomnias, which are
synchronous pattern of wakefulness and sleep. not responsible for disturbing the sleep–wake
Wakefulness is a state of being aware of the cycle but are undesirable phenomena that
environment—of receiving and responding to occur primarily during sleep; (3) sleep disor-
information arriving from all the senses, plac- ders associated with other medical or psychi-
ing that information into memory, and recall- atric disorders; and (4) proposed sleep
ing and integrating present experiences with disorders, such as pregnancy-induced sleep
previously stored memories. During wakeful- disruptions.
ness, both the thalamocortical loop and brain 5. A typical sleep study, or polysomnography, in-
stem centers are active. A full repertoire of volves use of the EEG, electro-oculogram
motor movements is made possible by corti- (EOG), electromyogram (EMG), electrocardio-
cospinal circuits that travel through the brain gram (ECG), breathing movements, and pulse
stem. Sleep represents a period of diminished oximetry. The EOG records eye movements.
consciousness from which a person can be Because the eye is like a small battery with the
aroused by sensory or other stimuli. It occurs retina negative to the cornea, an electrode
in stages during which the brain remains ac- placed on the skin near the eye records
tive, but does not effectively process sensory changes in voltage as the eye rotates in its
information. socket. The EMG records the electrical activity
from muscle movement. It is recorded from

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492 ANSWERS

the surface of the skin. It typically is recorded critical feature of obstructive sleep apnea is
from under the chin because muscles in this sleep-related collapse of the upper airway at
area of the body show very dramatic changes the level of the pharynx and is most pro-
associated with the sleep cycle. The ECG is nounced during REM sleep.
used to measure the heart rate and detect car- 2. You correctly respond that the average num-
diac dysrhythmias. The pulse oximeter (ear or ber of apnea-hypopnea periods per hour is
finger) measures arterial oxygen saturation. called the apnea-hypopnea index (AHI). An
6. Chronic insomnia often is related to medical AHI of 5 or greater in combination with re-
or psychiatric disorders. Factors such as pain, ports of excessive daytime sleepiness is indica-
immobility, and hormonal changes associated tive of sleep apnea.
with pregnancy or menopause also can cause 3. Continuous positive airway pressure (CPAP)
insomnia. Interrupted sleep can accompany
other sleep disorders, such as restless legs syn- SECTION IV: PRACTICING FOR NCLEX
drome and sleep apnea. Many health prob-
Activity F
lems worsen during the night. Heart failure,
respiratory disease, and gastroesophageal re- 1. a. Rationale: During REM sleep, the brain can
flux can cause frequent awakening during the replay previous memories, but cannot acquire
night. Mood and anxiety disorders are the new sensory information. The other answers
most frequent cause of insomnia in persons are incorrect.
with psychiatric diagnoses. A number of drugs 2. b. Rationale: The pineal gland synthesizes and
can lead to poor-quality sleep. Drugs com- releases melatonin at night, a rhythm that is
monly related to insomnia are caffeine, nico- under the direct control of the suprachias-
tine, stimulating antidepressants, alcohol, and matic nucleus (SCN). The other answers are
recreational drugs. Although alcohol initially incorrect.
may induce sleep, it often causes disrupted 3. c. Rationale: The multiple sleep latency test
and fragmented sleep. Sleep also is disrupted (MSLT) is used to evaluate daytime sleepi-
in persons undergoing alcohol or sleep med- ness. This test usually is completed the morn-
ication withdrawal. ing after a diagnostic sleep study. An average
7. The National Institute of Health defines RLS as adult requires 10 or more minutes to fall
(1) an urge to move the limbs with or without asleep. An MSLT result of less than 5 minutes
sensations, (2) worsening at rest; (3) improv- is considered abnormal.
ing with activity; and (4) worsening in the 4. d. Rationale: Diagnosis of RLS is based on a
evening or night. history of (1) a compelling urge to move the
8. A critical pathophysiologic feature of obstruc- legs, usually associated with paresthesias;
tive sleep apnea is sleep-related collapse of the (2) motor restlessness, as seen by activities
upper airway at the level of the pharynx. All such as pacing, tossing and turning in bed, or
skeletal muscles, except the diaphragm, un- rubbing the legs; (3) symptoms that become
dergo a decrease in tone during sleep. This loss worse at rest and are relieved by activity; and
of muscle tone is most pronounced during REM (4) symptoms that are worse in the evening
sleep. The loss of muscle tone in the upper air- or at night.
ways predisposes to airway obstruction as the 5. 1-d, 2-b, 3-c, 4-a, 5-f, 6-e
negative airway pressure produced by contrac- 6. a. Rationale: During a typical episode, the
tion of the diaphragm brings the vocal cords to- sleepwalker appears dazed and relatively un-
gether, collapses the pharyngeal wall, and sucks responsive to the communication efforts of
the tongue back into the throat. others. The other answers are incorrect.
7. a, b, c. Rationale: In a typical episode, the
SECTION III: APPLYING YOUR child sits up abruptly in bed, appears fright-
KNOWLEDGE ened, and demonstrates signs of extreme
anxiety, including dilated pupils, excessive
Activity E
perspiration, rapid breathing, and tachycar-
1. Apnea is defined as cessation of airflow dia. Children with sleep terrors typically do
through the nose and mouth for 10 seconds or not scream on awakening or refuse to sleep
longer. The apneic periods typically last for in their own bed.
15–120 seconds, and some persons may have 8. b. Rationale: Many medications have stimu-
as many as 100 apneic periods per night. A lating effects and interfere with sleep. These

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ANSWERS 493

include some of the antidepressants, decon- Activity B

gestants, bronchodilators, corticosteroids,
and some antihypertensives. The other med- 1.
ications are not linked to sleep disturbances. Central fissure
(Rolando)
9. c. Rationale: Persons with Alzheimer disease
often have increased periods of nighttime Parietal lobe
Frontal lobe
awakening and daytime napping. The other
diseases are not associated with increased Parieto-occipital
fissure
periods of nighttime awakening and daytime
sleeping.
10. a. Rationale: The actigraph is a compact
Occipital
device that is worn on the wrist and is used lobe
most often in conjunction with a sleep diary.
The other answers are not correct.
(Sylvius)

CHAPTER 53 DISORDERS OF Transverse

Temporal lobe
THOUGHT, MOOD, AND MEMORY A fissure

SECTION II: ASSESSING YOUR Corpus callosum

UNDERSTANDING Cingulate
Anterior nucleus
gyrus
of thalamus
Activity A Prefrontal
lobe Fornix
1. biologic, psychosocial
2. chlorpromazine
3. alterations
4. frontal
5. association
6. prefrontal
Olfactory
7. hallucinations, delusional bulb
8. Release, ictal
9. Delusions Mammilary body
Parahippocampus
10. neurotransmitter, receptor Amygdala Temporal lobe gyrus
11. Antidepressants B Hippocampus
12. Schizophrenia
13. emotion
14. Dysthymia 2.
15. Kindling
16. decreased, increased
17. abuse, dependence
Motor
18. Memory Somato- Spatial
19. dementia Planning complex sensory coordinates
20. Alzheimer movements and of body and
elaboration of surroundings
21. neuritic (senile) plaques, neurofibrillary thoughts
tangles Word Visual
formation Language
22. tau comprehension, processing
Auditory intelligence of words
23. chronic debilitation Behavior,
24. cholinesterase inhibitors emotions, Naming of
motivation Vision
25. Vascular Broca objects
26. frontotemporal dementia area
27. prion Limbic Wernicke
28. Wernicke association area
29. Huntington area
30. gamma-aminobutyric acid (GABA), GABA
receptors

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494 ANSWERS

Activity C then integrating memories with sensory

input for decision making.
1. 4. The substances generally agreed to be neuro-
1. b 2. j 3. d 4. i 5. e transmitters and that are implicated in men-
6. g 7. f 8. a 9. h 10. c tal illness include acetylcholine, the biogenic
2. amines (dopamine, epinephrine, norepineph-
1. e 2. j 3. d 4. a 5. f rine, and serotonin), and amino acids
6. g 7. b 8. h 9. c 10. i (gamma-aminobutyric acid, glutamate,
glycine, and aspartate).
Activity D
5. Monoamine oxidase inhibitors increase the
1. Studies of twins have shown a 45% concor- concentration of serotonin and norepineph-
dance for schizophrenia among monozygotic rine by reducing the degradation of these
twins, compared with 15% for dizygotic neurotransmitters by monoamine oxidase.
twins or other siblings. With bipolar depres- The tricyclic antidepressants block the reup-
sion, there is an 80% concordance in take of serotonin and norepinephrine by the
monozygotic twins, compared with 10% for presynaptic membrane, whereas the sero-
siblings. In monozygotic twins living apart, tonin reuptake inhibitors inhibit the reup-
the concordance rate for affective disorders is take of serotonin. The atypical
40% to 60%. Even the concordance rates antidepressants affect serotonergic and nora-
among siblings for these two disorders are drenergic neurotransmission.
suggestive of a genetic influence because 6. The psychopathology of schizophrenia can
schizophrenia has approximately a 1% inci- be organized into positive and negative
dence and depression a 5% incidence among symptoms. Positive symptoms are those that
the general population. Although the evi- reflect the presence of abnormal behaviors
dence for a genetic basis for mental illness is and include incomprehensible speech, delu-
compelling, the fact that the concordance sions, hallucinations, and grossly disorga-
among monozygotic twins is not 100% indi- nized or catatonic behavior. Alterations in
cates that other factors may be involved in speech patterns can include using invented
the development of a mental illness. words, derailment, tangentiality, incoher-
2. The hippocampus, along with its adjacent ence, or word salad. Frequently, persons with
temporal and parietal lobe structures, has nu- schizophrenia lose the ability to appropri-
merous indirect connections with many por- ately sort and interpret incoming stimuli,
tions of the cerebral cortex and other parts of which impairs the ability to respond to the
the limbic system. The hippocampus plays a environment. An enhancement or a blunting
major role in the encoding, consolidation, of the senses is very common in the early
and retrieval of memories. Almost all types of stages of schizophrenia. The negative symp-
sensory information activate some part of the toms of schizophrenia reflect the absence of
hippocampus. In turn, the hippocampus dis- normal social and interpersonal behaviors
tributes information to the anterior thala- and include alogia, avolition, apathy, affec-
mus, hypothalamus, and other parts of the tive flattening, inappropriate affect, and an-
limbic system. The hippocampus also groups hedonia. Some persons with schizophrenia
and schematizes input in preparation for have a blunted response to pain.
memory encoding. It plays a significant role 7. There is an enlargement of the lateral and
in converting short-term memory to long- third ventricles; a reduction of frontal, tempo-
term memory. ral, and whole brain volumes; and diminished
3. Perception is the final stage of information neuronal content in both the thalamus and
processing. It is the conscious awareness of hippocampus. At the cellular anatomic level,
sensory stimuli and results in behavioral re- there is an increased density of dopamine re-
sponses to that sensation. Information from ceptor sites, particularly in the basal ganglia.
the senses is received by the thalamus, and 8. Major depressive disorder is characterized by
then projected to the somatosensory cortex depressed mood, anhedonia, feelings of
and prefrontal association area. The pre- worthlessness or excessive guilt, decreased
frontal association area keeps track of where concentration, psychomotor agitation or retar-
information has been stored in long-term dation, insomnia or hypersomnia, decreased
memory, and is responsible for retrieving and libido, and change.

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ANSWERS 495

9. Depression has various subclassifications dis-

SECTION III: APPLYING YOUR
tinguished by symptom patterns. Depression
KNOWLEDGE
with melancholic features is characterized by
depression that is worse in the morning, in- Activity E
somnia with early morning awakening,
1. The nurse should convey the following major
anorexia with significant weight loss, psy-
points about Alzheimer disease to this family:
chomotor retardation or agitation, excessive
• Alzheimer disease is a physiologic dementia
or inappropriate guilt, loss of interest in ac-
that is progressive and occurs most often in
tivity, inability to respond to pleasurable
middle or late life.
stimuli, and a complete loss of capacity for
• The pathophysiologic aspects of Alzheimer
joy. The symptoms of atypical depression are
disease involve neuropathologic and neuro-
opposite that of melancholic depression; it is
transmitter changes. It is characterized by
characterized by a depression that becomes
cortical atrophy and loss of neurons, partic-
worse as the day progresses, overeating, and
ularly in the parietal and temporal lobes.
hypersomnia. Depression with psychotic fea-
• It is likely that Alzheimer disease is caused
tures involves the presence of delusions or
by several factors that interact differently in
hallucinations that may or may not be mood
different persons.
congruent. The classification of depression
• Alzheimer-type dementia follows an insidi-
with catatonic features is applied when
ous and progressive course, with an average
symptoms include excessive mobility or mo-
survival of 8 to 10 years after diagnosis.
toric immobility, extreme negativism, repeti-
• The hallmark symptoms are loss of short-
tive speech, and peculiar voluntary
term memory and a denial of such memory
movements.
loss, with eventual disorientation, impaired
10. The biogenic amine hypothesis suggests that
abstract thinking, apraxia, and changes in
decreased levels of these neurotransmitters in
personality and affect.
the synaptic cleft, due either to decreased
• In the initial stage, clients with Alzheimer
presynaptic release or decreased postsynaptic
disease forget where things are placed, get
sensitivity, is the underlying pathology in de-
lost easily, and have trouble remembering
pression. The hypothesis is derived from the
appointments and performing novel tasks.
fact that drugs that depleted brain serotonin
• In the moderate stage, which may last sev-
and norepinephrine caused depression, and
eral years, there is a more global impairment
drugs that increased brain levels of norepi-
of cognitive functioning. During this stage,
nephrine and serotonin decreased depression.
there are changes in higher cortical func-
11. Persons with panic disorder typically have at-
tioning needed for language, spatial rela-
tacks characterized by neurologic symptoms
tionships, and problem solving.
(dizziness or lightheadedness, paresthesias,
• Severe Alzheimer disease is characterized by
fainting), cardiac symptoms (tachycardia,
a loss of ability to respond to the environ-
chest pain and palpitations), respiratory
ment. Individuals in this stage require total
symptoms (shortness of breath, feeling of
care and spend most of their time bedridden.
smothering or choking), sweating, nausea or
• There is no curative treatment for Alzheimer
abdominal distress, and psychological symp-
dementia. Drugs are used primarily to slow
toms (feelings of impending doom, fear of
the progression and to control depression,
dying, a sense of unreality). Panic attacks
agitation, or sleep disorders. Two major
must be distinguished from acute cardiac
goals of care are maintaining the person’s
disease.
socialization and providing support for the
12. Although age is the greatest risk, additional
family.
factors have been identified as adding to the
• It is important for the nurse to provide in-
risks for developing Alzheimer disease. These
formation for support groups in the area.
include head trauma, inflammatory factors,
and oxidative stress. Education has been
identified as a protective factor; with sugges- SECTION IV: PRACTICING FOR NCLEX
tions that education can increase synaptic
Activity F
density. Other studies have looked at exercise
as a possible protective factor in maintaining 1. a. Rationale: This antipsychiatry attitude, cou-
hippocampal health. pled with the advent of psychopharmacology,

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496 ANSWERS

laid the foundations for the deinstitutional- [Parnate]) increase the concentration of sero-
ization of the mentally ill and the move to tonin and norepinephrine by reducing the
community psychiatry. The other answers are degradation of these neurotransmitters by
incorrect. monoamine oxidase. Valium is a sedative and
2. b. Rationale: It is highly likely that mental ill- antianxiety agent. Halcion is a hypnotic
nesses are polygenic and multifactorial rather agent. Paxil is a serotonin reuptake inhibitor.
than simply inherited through transmission 10. a. Rationale: An enhancement or a blunting of
of a classic disordered dominant or recessive the senses is very common in the early stages
Mendelian trait. of schizophrenia. Sounds may be experienced
3. a, b, d, e. Rationale: The substances generally as louder and more intrusive; colors may be
agreed to be neurotransmitters and that are brighter and sharper. The other answers are
implicated in mental illness include acetyl- later signs or symptoms of schizophrenia.
choline, the biogenic amines (dopamine, epi- 11. 1-d, 2-e, 3-c, 4-a, 5-b
nephrine, norepinephrine, and serotonin), 12. b. Rationale: The severity of manic symptoms
and amino acids (gamma-aminobutyric acid, runs the gamut from a condition called cy-
glutamate, glycine, and aspartate). Succinyl- clothymia, in which mood fluctuates be-
choline is a depolarizing neuromuscular tween mild elation and depression to severe
blocker. delusional mania. Mania is the overall term
4. c. Rationale: It is the function of the pre- for mood fluctuations between mild elation
frontal areas to keep track of many bits of in- and depression. Specifier has nothing to do
formation simultaneously and then to recall with bipolar disorder. Kindling is a hypothe-
this information as needed for subsequent sized phenomenon in which a stressor creates
intellectual tasks. The other answers are an electrophysiologic vulnerability to future
incorrect. stressful events by causing long-lasting
5. d. Rationale: Information from the senses is changes in neuronal function.
received by the thalamus, and then pro- 13. c. Rationale: Lithium and several anticonvul-
jected to the somatosensory cortex and pre- sant agents are used in the treatment of bipo-
frontal association area. The hypothalamus lar depression. Valium is a sedative and
oversees temperature, sleep-rest, etc. Broca’s antianxiety agent. Flexeril is a muscle relax-
area forms words. The amygdale processes ant. Restoril is a hypnotic agent.
emotion. 14. d. Rationale: Neurophysiologic studies suggest
6. a. Rationale: During the process, new or reac- that the attacks may result from an abnor-
tivated pathways transmit neural circuits, mally sensitive “fear network” that is centered
sometimes called memory traces, through the in the amygdala and involves interactions
brain. The other answers are incorrect. with the hippocampus and prefrontal cortex.
7. b. Rationale: Ictal hallucinations are produced The thymus has nothing to do with the “fear
by abnormal neuronal discharges. Visual hal- network.”
lucinations are not from abnormal neuronal 15. a. Rationale: Although the neurophysiology of
discharges. Emotional hallucinations are un- OCD remains under investigation, the gen-
known. Release hallucinations occur at times eral anatomic model suggests dysfunction of
when a normal sensory input is blocked and, prefrontal cortex and structures of the basal
as a replacement, stored images are experi- ganglia, particularly the caudate nucleus and
enced. globus pallidus. The frontal cortex and the
8. c. Rationale: Interestingly, delusions have amygdale are not believed to be involved in
been associated with conditions that produce the neurophysiology of OCD.
sensory deprivation, such as hearing loss. The 16. b. Rationale: Habitual use of drugs, including
other answers have not been associated with alcohol, is believed to induce adaptations in
delusions. brain systems that alter the normal dopamine
9. d. Rationale: Monoamine oxidase inhibitors pathways and increase dopamine transmis-
(e.g., phenelzine [Nardil], tranylcypromine sion. The other answers are incorrect.

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ANSWERS 497

17. c. Rationale: Confabulation (i.e., recitation of 9. conjunctivitis

imaginary experiences to fill in gaps in mem- 10. Hyperacute
ory) is probably the most distinctive feature 11. cornea
of the disease. 12. Keratitis
18. a, b, c. Rationale: Depression and personality 13. keratitis
changes are the most common early psycho- 14. ophthalmicus
logical manifestations. Memory loss is often 15. iris
accompanied by impulsive behavior, moodi- 16. uveitis
ness, antisocial behavior, and a tendency to- 17. pupils
ward emotional outbursts. Mania and 18. Glaucoma
heightened sensory awareness are not com- 19. degenerative
ponents of Huntington disease. 20. Congenital
21. astigmatism
22. Accommodation
CHAPTER 54 DISORDERS 23. cataract
OF VISUAL FUNCTION 24. retina
25. color-blind
SECTION II: ASSESSING YOUR 26. Retinitis pigmentosa
UNDERSTANDING 27. Macular
Activity A
28. Retinoblastomas
29. visual field
1. eyeball 30. inferior recti, lateral recti, obliques
2. sclera 31. Conjugate
3. palpebrae 32. Saccadic
4. levator palpebrae superioris, orbicularis oculi 33. Strabismus
5. Blepharitis 34. Amblyopia
6. Seborrheic
7. anterior blepharitis Activity B
8. Posterior
1.

Retina
Choroid
Sclera
Superior
rectus
Bulbar and
Levator palpebral
palpebrae conjunctiva
superioris
Cornea

Lens
Superior tarsal
plate
Iris
Optic Meibomian
nerve gland in
tarsal plate
Inferior
rectus
Orbicularis
Inferior oculi muscle
oblique
muscle
Ciliary body

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498 ANSWERS

2. 3.

Inferior oblique

Temporalis
muscle
Lateral
Medial rectus
rectus

Superior
oblique
A
Inferior
Normal focal length rectus Superior rectus
Stump of
levator palpebrae
Optic nerve

Levator palpebrae
superioris
Superior
Medial oblique
rectus
B Superior
Hyperopia rectus

C Inferior
Myopia rectus Lateral
Inferior
rectus
oblique

Activity C surface by abolishing minute surface irregu-

larities. Tears also wet and protect the deli-
1. cate surface of the cornea and conjunctiva.
1. e 2. f 3. g 4. a 5. j They flush and remove irritating substances
6. c 7. d 8. b 9. i 10. h and microorganisms, and provide the cornea
2. with necessary nutrient substances. Tears also
1. f 2. c 3. g 4. b 5. a contain lysozymes and immunoglobulins A,
6. e 7. j 8. d 9. i 10. h G, and E, which synergistically act to protect
against infection.
Activity D 2. Chronic bacterial conjunctivitis is most com-
1. The lacrimal system includes the major monly caused by Staphylococcus species,
lacrimal gland; it produces the tears; the although other bacteria may be involved. It is
puncta; canaliculi; the tear sac, which collect often associated with blepharitis and bacter-
the tears; and the nasolacrimal duct, which ial colonization of eyelid margins. The symp-
empties the tears into the nasal cavity. Tears toms of chronic bacterial conjunctivitis vary
contain approximately 98% water; 1.5% and can include itching, burning, foreign
sodium chloride; and small amounts of body sensation, and morning eyelash crust-
potassium, albumin, and glucose. The func- ing. Other symptoms include flaky debris and
tion of tears is to provide a smooth optical erythema along the lid margins, eyelash loss,

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ANSWERS 499

and eye redness. Some people with chronic outflow. Primary glaucoma occurs without
bacterial conjunctivitis also have recurrent evidence of preexisting ocular or systemic
styes and chalazia of the lid margins. disease. Secondary glaucoma can result from
3. Trauma that causes abrasions of the cornea can inflammatory processes that affect the eye,
be extremely painful, but, if minor, the abra- from tumors, or from blood cells of trauma-
sions usually heal in a few days. The epithelial produced hemorrhage that obstruct the out-
layer can regenerate, and small defects heal flow of aqueous humor.
without scarring. If the stroma is damaged, 8. The term presbyopia refers to decrease in
healing occurs more slowly, and the danger accommodation that occurs because of aging.
of infection is increased. Injuries to Bowman The lens consists of transparent fibers
membrane and the stromal layer heal with scar arranged in concentric layers, of which the
formation and permanent opacification. Opac- external layers are the newest and softest. No
ities of the cornea impair the transmission of loss of lens fibers occurs with aging; instead,
light. A minor scar can severely distort vision additional fibers are added to the outermost
because it disturbs the refractive surface. portion of the lens. As the lens ages, it thick-
4. Primary epithelial infections are the optical ens, and its fibers become less elastic, so that
counterpart of labial herpes with similar the range of focus or accommodation is
immunologic and pathologic features as well diminished to the point where reading
as a similar time course. During childhood, glasses become necessary for near vision.
mild primary herpes simplex virus infection 9. Hemorrhage can be preretinal, intraretinal, or
may go unnoticed. After the initial primary subretinal. Preretinal hemorrhages occur be-
infection, the virus may persist in a quiescent tween the retina and the vitreous. These hem-
or latent state that remains in the trigeminal orrhages are usually large because the blood
ganglion and possibly in the cornea without vessels are only loosely restricted; they may be
causing signs of infection. associated with a subarachnoid or subdural
5. Acanthamoeba keratitis is a rare but serious hemorrhage and are usually regarded as a seri-
and sight-threatening complication caused ous manifestation of the disorder. They usu-
by wearing soft contact lenses, particularly ally reabsorb without complications unless
when they are worn overnight beyond they penetrate into the vitreous. Intraretinal
doctor-recommended periods or when poor hemorrhages occur because of abnormalities
disinfection techniques are used. It also may of the retinal vessels, diseases of the blood, in-
occur in non–contact lens wearers after expo- creased pressure in the retinal vessels, or vitre-
sure to contaminated water or soil. It is char- ous traction on the vessels. Systemic causes
acterized by pain that is disproportionate to include diabetes mellitus, hypertension, and
the clinical manifestations, redness of the blood dyscrasias. Subretinal hemorrhages are
eye, and photophobia. those that develop between the choroid and
6. Changes in pupil size are controlled by con- pigment layer of the retina. A common cause
traction or relaxation of the sphincter and of subretinal hemorrhage is neovasculariza-
radial muscles of the iris. The pupillary reflex, tion. Photocoagulation may be used to treat
which controls the size of the pupillary open- microaneurysms and neovascularization.
ing, is controlled by the autonomic nervous 10. Proliferative diabetic retinopathy represents a
system, with the parasympathetic nervous more severe retinal change than background
system producing pupillary constriction or retinopathy. It is characterized by formation
miosis, and the sympathetic nervous system of new fragile blood vessels (i.e., neovascular-
producing pupillary dilation or mydriasis. ization) at the disk and elsewhere in the
The sphincter muscle that produces pupillary retina. These vessels grow in front of the
constriction is innervated by postganglionic retina, along the posterior surface of the vitre-
parasympathetic neurons of the ciliary gan- ous or into the vitreous. They threaten vision
glion and other scattered ganglion cells in two ways. First, because they are abnormal,
between the scleral and choroid layers. The they often bleed easily, leaking blood into
pupillary reflex is controlled by a region in the vitreous cavity and decreasing visual acu-
the midbrain called the pretectum. ity. Second, the blood vessels attach firmly to
7. Glaucoma usually results from congenital or the retinal surface and posterior surface of the
acquired lesions of the anterior segment of vitreous, such that normal movement of the
the eye that mechanically obstruct aqueous vitreous may exert a pull on the retina, causing

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500 ANSWERS

retinal detachment and progressive blind- are not present in great numbers; the cornea
ness. secretes immunosuppressive factors; and
11. Persistently elevated blood pressure results in corneal cells secrete substances (e.g., Fas lig-
the compensatory thickening of arteriolar and) that protect against apoptosis, thereby
walls, which effectively reduces capillary minimizing inflammation. The other answers
perfusion pressure. With severe uncontrolled are incorrect.
hypertension, there is disruption of the 6. d. Rationale: Miotic drugs (e.g., pilocarpine),
blood-retinal barrier, necrosis of smooth mus- which are used in the treatment of angle-
cle and endothelial cells, exudation of blood closure glaucoma (to be discussed), produce
and lipids, and retinal ischemia. These pupil constriction and, in that manner, facili-
changes are manifested in the retina by mi- tate aqueous humor circulation. The other
croaneurysms, intraretinal hemorrhages, answers are classes of drugs that do not affect
hard exudates, and cotton-wool spots. papillary constriction.
7. a. Rationale: Primary open-angle glaucoma
usually occurs because of an abnormality of
SECTION III: APPLYING YOUR
the trabecular meshwork that controls the
KNOWLEDGE
flow of aqueous humor into the canal of
Activity E Schlemm. The other answers are incorrect.
8. 1-d, 2-b, 3-a, 4-c, 5-e
1. The nurse would expect the doctor to order an
9. b. Rationale: Age-related cataracts, which are
ophthalmoscopic exam under anesthesia by
the most common type, are characterized by
an ophthalmologist. CT or MRI scans are used
increasingly blurred vision and visual distor-
to evaluate the extent of intraocular disease
tion. The other answers are incorrect.
and extraocular spread.
10. c. Rationale: With the loss of gel structure,
2. Treatment options for retinoblastoma are laser
fine fibers, membranes, and cellular debris
thermotherapy, cryotherapy, chemotherapy,
develop. When this occurs, floaters (images)
and nucleation.
can often be noticed because these substances
move within the vitreous cavity during head
SECTION IV: PRACTICING FOR NCLEX movement. Blind spots, meshlike structures,
Activity F and red spots are not seen during head move-
ment with a loss of the gel structure of the
1. a. Rationale: Neurologic causes of eyelid weak- vitreous humor.
ness include damage to the innervating cra- 11. d. Rationale: Neovascularization occurs in
nial nerves or to the nerve’s central nuclei in many conditions that impair retinal blood
the midbrain and the caudal pons. The other flow, including stasis because of hyperviscosity
answers have nothing to do with the central of blood or decreased flow, vascular occlu-
nuclei of the oculomotor and the facial nerve. sion, sickle cell disease, sarcoidosis, diabetes
2. b. Rationale: The symptoms include tearing mellitus, and retinopathy of prematurity. The
and discharge, pain, swelling, and tender- other answers are incorrect.
ness. The other answers are incorrect. 12. a. Rationale: Nonexudative age-related macu-
3. c. Rationale: Infection should be suspected lar degeneration is characterized by various
when conjunctivitis develops 48 hours after degrees of atrophy and degeneration of the
birth. The other answers are not correct. outer retina, Bruch membrane, and chorio-
4. c. Rationale: The treatment of herpes simplex capillary layer of the choroid. It does not in-
virus (HSV) keratitis focuses on eliminating volve leakage of blood or serum; hence, it is
viral replication within the cornea while min- called dry age-related macular degeneration.
imizing the damaging effects of the inflam- The other answers are characterizations of
matory process. The other answers are not the “wet” form of macular degeneration.
goals in the treatment of HSV keratitis. 13. b. Rationale: Crude analysis of visual stimula-
5. b, c, d. Rationale: The low rejection rate is tion at reflex levels, such as eye- and head-
due to several factors: the cornea is avascular, orienting responses to bright moving lights,
including lymphatics, thereby limiting perfu- pupillary reflexes, and blinking at sudden
sion by immune elements; major histocom- bright lights, may be retained even though
patibility complexes (class II) are virtually vision has been lost. The other answers are
absent in the cornea; antigen-presenting cells incorrect.

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ANSWERS 501

14. c. Rationale: Paralytic strabismus is uncom- 3. Otitis externa

mon in children, but accounts for nearly all 4. temporal
cases of adult strabismus. It can be caused by 5. eustachian
infiltrative processes, including Graves disease, 6. abnormally patent
myasthenia gravis, stroke, and direct optical 7. Otitis media
trauma. The other diseases have nothing to do 8. Acute otitis media
with adult strabismus. 9. Otosclerosis
15. b. Rationale: The reversibility of amblyopia 10. cochlea
depends on the maturity of the visual system 11. Wernicke area
at the time of onset and the duration of the 12. Sensorineural
abnormal experience. The other answers are 13. bacterial meningitis
incorrect. 14. cranial nerve VIII
15. cytomegalovirus
16. vestibular
CHAPTER 55 DISORDERS OF 17. vertigo
HEARING AND VESTIBULAR 18. Motion sickness
FUNCTION 19. paroxysmal positional
20. vestibular neuronitis
SECTION II: ASSESSING YOUR 21. Ménière
UNDERSTANDING 22. cerebellum

Activity A Activity B
1. ear
2. cerumen

Middle Inner
Cochlear
ear ear Cranial portion
nerve
Semicircular Vestibular
Tympanic VIII
canals portion
membrane

Incus

Cochlea

Eustachian
tube

Malleus
External Stapes
Auricle acoustic
meatus
Pharynx

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502 ANSWERS

Activity C jury, and cochlear or labyrinthine infection or

inflammation.
1. j 2. h 3. e 4. c 5. i 5. Conductive hearing loss occurs when auditory
6. a 7. g 8. d 9. b 10. f stimuli are not adequately transmitted
through the auditory canal, tympanic mem-
Activity D brane, middle ear, or ossicle chain to the inner
1. The eustachian tube serves three basic func- ear. Temporary hearing loss can occur as the
tions: (a) ventilation of the middle ear, along result of impacted cerumen in the outer ear or
with equalization of middle ear and ambient fluid in the middle ear. Foreign bodies, includ-
pressures; (b) protection of the middle ear ing pieces of cotton and insects, may impair
from unwanted nasopharyngeal sound waves hearing. More permanent causes of hearing
and secretions; and (c) drainage of middle ear loss are thickening or damage of the tympanic
secretions into the nasopharynx. membrane or involvement of the bony struc-
2. Hearing loss, which is a common complica- tures (ossicles and oval window) of the middle
tion of otitis media, is usually conductive and ear due to otosclerosis or Paget disease.
temporary based on the duration of the effu- 6. The hair cells in both utricular and saccular
sion. Hearing loss that is associated with fluid maculae are embedded in a flattened gelati-
collection usually resolves when the effusion nous mass, the otolithic membrane, which is
clears. Permanent hearing loss may occur as studded with tiny stones called otoliths. Al-
the result of damage to the tympanic mem- though they are small, the density of the
brane or other middle ear structures. Cases of otoliths increases the membrane’s weight
sensorineural hearing loss are rare. Persistent and its resistance to change in motion.
and episodic conductive hearing loss in chil- When the head is tilted, the gelatinous mass
dren may impair their cognitive, linguistic, shifts its position because of the pull of the
and emotional development. gravitational field, bending the stereocilia of
3. During active bone resorption, the bone struc- the macular hair cells. Although each hair
ture appears spongy and softer than normal. cell becomes more or less excitable depend-
The resorbed bone is replaced by an over- ing on the direction in which the cilia are
growth of new, hard, sclerotic bone. The bending, the hair cells are oriented in all di-
process is slowly progressive, involving more rections, making these sense organs sensitive
areas of the temporal bone, especially in front to static or changing head position in rela-
of and posterior to the stapes footplate. As it tion to the gravitational field. In a condition
invades the footplate, the pathologic bone in- called benign positional vertigo (to be dis-
creasingly immobilizes the stapes, reducing cussed), the otoliths become dislodged from
the transmission of sound. Pressure of otoscle- their gelatinous base, causing positional
rotic bone on middle ear structures or the vertigo.
vestibulocochlear nerve (cranial nerve VIII) 7. Caloric testing involves elevating the head
may contribute to the development of tinni- 30 degrees and irrigating each external audi-
tus, sensorineural hearing loss, and vertigo. tory canal separately with 30 to 50 mL of ice
4. A number of causes and conditions have been water. The resulting changes in temperature,
associated with subjective tinnitus. Intermit- which are conducted through the petrous
tent periods of mild, high-pitched tinnitus portion of the temporal bone, set up convec-
lasting for several minutes are common in tion currents in the endolymph that mimic
normal-hearing persons. Impacted cerumen is the effects of angular acceleration. In an un-
a benign cause of tinnitus, which resolves after conscious person with a functional brain
the earwax is removed. Medications such as as- stem and intact oculovestibular reflexes, the
pirin and stimulants such as nicotine and caf- eyes exhibit a jerk nystagmus lasting 2 to
feine can cause transient tinnitus. Conditions 3 minutes, with the slow component toward
associated with more persistent tinnitus in- the irrigated ear followed by rapid movement
clude noise-induced hearing loss, presbycusis away from the ear. With impairment of brain
(sensorineural hearing loss that occurs with stem function, the response becomes per-
aging), hypertension, atherosclerosis, head in- verted and eventually disappears.

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ANSWERS 503

panic membrane or involvement of the bony

SECTION III: APPLYING YOUR
structures (ossicles and oval window) of the
KNOWLEDGE
middle ear due to otosclerosis or Paget
Activity E disease. Huntington, Alzheimer, and Parkinson
diseases are not associated with conductive
1. When talking about ototoxicity, aminoglyco-
hearing loss.
sides, antimalarial drugs, chemotherapeutic
8. c. Rationale: Acoustic neuromas are benign
drugs, loop diuretics, and salicylates would be
Schwann cell tumors affecting cranial nerve
discussed.
VIII. The other answers are incorrect.
9. d. Rationale: Tuning forks are used to differen-
SECTION IV: PRACTICING FOR NCLEX tiate conductive and sensorineural hearing
Activity F loss. AudioScope, audiometer, and tone
analysis do not differentiate between conduc-
1. a. Rationale: The most common bacterial tive and sensorineural hearing loss.
pathogens are gram-negative rods 10. a. Rationale: Genetic causes are probably re-
(Pseudomonas aeruginosa, Proteus spp.) and sponsible for as much as 50% of sensori-
fungi (Aspergillus) that grow in the presence neural hearing loss in children. The other
of excess moisture. The other answers are not diseases are not the correct answer.
fungi. 11. b. Rationale: The disorder first reduces the
2. a. Rationale: The abnormally patent tube does ability to understand speech and, later, the
not close or does not close completely. In ability to detect, identify, and localize
infants and children with an abnormally sounds.
patent tube, air and secretions are often
pumped into the eustachian tube during cry-
ing and nose blowing. Cerumen and saliva CHAPTER 56 STRUCTURE
are not let into the eustachian tube. AND FUNCTION OF THE
3. a, b, d. Rationale: Risk factors include prema-
ture birth, male gender, ethnicity (Native MUSCULOSKELETAL SYSTEM
American, Inuit), family history of recurrent
otitis media, presence of siblings in the SECTION II: ASSESSING YOUR
household, genetic syndromes, and low so- UNDERSTANDING
cioeconomic status. Being an only child and Activity A
being a female are not risk factors for AOM.
4. c. Rationale: Because much of the conductive 1. muscles, tendons, ligaments
hearing loss associated with otosclerosis is 2. calcium, blood
caused by stapedial fixation, surgical treat- 3. axial, appendicular
ment involves stapedectomy with stapedial 4. Compact
reconstruction using the patient’s own stapes 5. Bones
or stapedial prosthesis. The other answers are 6. periosteum
incorrect. 7. marrow
5. d. Rationale: The scala vestibuli and scala 8. nutritional arteries
media are separated from each other by the 9. connective, calcium
vestibular membrane, also known as Reissner 10. osteoprogenitor
membrane. The other answers are incorrect. 11. Osteoclasts
6. a. Rationale: In some vascular disorders, 12. Elastic
sounds generated by turbulent blood flow 13. Fibrocartilage
(e.g., arterial bruits or venous hums) are con- 14. Hyaline
ducted to the auditory system. Vascular disor- 15. Calcitonin
ders typically produce a pulsatile form of 16. Tendons
tinnitus. The other answers are incorrect. 17. Ligaments
7. b. Rationale: More permanent causes of hear- 18. Synarthroses
ing loss are thickening or damage of the tym- 19. Synovial
20. bursae

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504 ANSWERS

Activity B Activity E
Compact bone Proximal epiphysis 1. A typical long bone has a shaft, or diaphysis,
Yellow and two ends, called epiphyses. Long bones
Epiphyseal
marrow
line are usually narrow in the midportion and
broad at the ends so that the weight they bear
Medullary
cavity can be distributed over a wider surface. The
shaft of a long bone is formed mainly of com-
pact bone roughly hollowed out to form a
Periosteum
marrow-filled medullary canal. The ends of
long bones are covered with articular cartilage.
2. Red bone marrow contains developing red
blood cells and is the site of blood cell forma-
A
tion. Yellow bone marrow is composed largely
Nutrient of adipose cells. At birth, nearly all marrow is
artery
Compact bone red and hematopoietically active. As the need
Spongy bone
for red blood cell production decreases during
postnatal growth, red marrow is gradually re-
placed with yellow bone marrow in most of
the bones. In the adult, red marrow persists in
the vertebrae, ribs, sternum, and ilia.
3. The intercellular matrix is composed of two
B C types of substances—organic matter and inor-
Epiphyseal
ganic salts. The organic matter, including
line bone cells, blood vessels, and nerves, consti-
Distal epiphysis tutes approximately one-third of the dry
weight of bone; the inorganic salts make up
Activity C the other two-thirds. The organic matter con-
sists primarily of collagen fibers embedded in
1. j 2. f 3. b 4. d 5. e
an amorphous ground substance. The inor-
6. i 7. a 8. c 9. g 10. h
ganic matter consists of hydroxyapatite, an in-
soluble macrocrystalline structure of calcium
Activity D
phosphate salts, and small amounts of calcium
Parathyroid
carbonate and calcium fluoride.
glands 4. Both connective tissue types consist of living
Kidney cells, nonliving intercellular fibers, and an
Reabsorption amorphous (shapeless) ground substance. The
of calcium tissue cells are responsible for secreting and
Bone maintaining the intercellular substances in
Release of
calcium and
which they are housed. However, cartilage
phosphate consists of more extracellular substance than
bone, and fibers are embedded in a firm gel
Calcium
concentration rather a calcified cement substance. Hence,
in extracellular cartilage has the flexibility of a firm plastic
fluid material rather than the rigid characteristics of
Urinary excretion
bone.
of phosphate 5. Parathyroid hormone (PTH) maintains serum
calcium levels by initiation of calcium release
from bone, by conservation of calcium by the
Activation of
vitamin D kidney, by enhanced intestinal absorption of
calcium through activation of vitamin D, and
Intestine by reduction of serum phosphate levels. PTH
Reabsorption of also increases the movement of calcium and
calcium via activated phosphate from bone into the extracellular
vitamin D
fluid.

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ANSWERS 505

6. The most potent of the vitamin D metabolites 6. a. Rationale: The most potent of the vitamin
is 1,25-(OH)2D3. This metabolite increases in- D metabolites is 1,25-(OH)2D3. This metabo-
testinal absorption of calcium and promotes lite increases intestinal absorption of calcium
the actions of parathyroid hormone on resorp- and promotes the actions of parathyroid hor-
tion of calcium and phosphate from bone. mone on resorption of calcium and phos-
Bone resorption by the osteoclasts is increased, phate from bone. None of the other answers
and bone formation by the osteoblasts is de- are correct.
creased; there is also an increase in acid phos- 7. b. Rationale: Synchondroses are joints in
phatase and a decrease in alkaline which bones are connected by hyaline carti-
phosphatase. Intestinal absorption and bone lage and have limited motion. The other an-
resorption increase the amount of calcium and swers are incorrect.
phosphorus available to the mineralizing sur- 8. c. Rationale: Diarthrodial joints are the joints
face of the bone. most frequently affected by rheumatic disor-
ders. The other types of joint are not the ones
SECTION III: APPLYING YOUR most frequently affected by rheumatic disor-
KNOWLEDGE ders.
9. d. Rationale: The tendons and ligaments of
Activity F the joint capsule are sensitive to position and
1. “Tendonitis occurs because of overuse of the movement, particularly stretching and twist-
tendon, which causes inflammation of the ing. The other answers are incorrect.
tendon.” 10. a. Rationale: These sacs, called bursae, contain
2. “Some tendons are enclosed in sheaths so that synovial fluid. Their purpose is to prevent fric-
they slide inside the sheath and are cushioned tion on a tendon. Bursae do not prevent injury
by synovial fluid. Other tendons are not en- to a joint, nor do they cushion joints. They
cased in a sheath. All tendons attach muscles also do not prevent friction on a ligament.
to bone and do not stretch very much.”
CHAPTER 57 DISORDERS OF
SECTION IV: PRACTICING FOR NCLEX MUSCULOSKELETAL FUNCTION:
Activity G TRAUMA, INFECTION, AND
1. a. Rationale: The metaphysis is composed of NEOPLASMS
bony trabeculae that have cores of cartilage.
The other answers are incorrect. SECTION II: ASSESSING YOUR
2. b. Rationale: Yellow bone marrow is com- UNDERSTANDING
posed largely of adipose cells. Hematopoietic
cells are in red bone marrow. Cancellous cells Activity A
are in spongy bone. Osteogenic cells line the 1. musculoskeletal
latticelike pattern that forms bone marrow. 2. falls
3. c. Rationale: Lamellar bone is composed 3. Soft tissue
largely of cylindrical units called osteons or 4. strain
haversian systems. Hematopoietic cells, 5. sprain
spicules, and macrocrystalline cells do not 6. dislocation
comprise lamellar bone. 7. Loose
4. d. Rationale: Fibrocartilage is found in the in- 8. Rotator cuff
tervertebral disks, in areas where tendons are 9. rotational
connected to bone, and in the symphysis 10. Dislocations
pubis. The other answers are incorrect. 11. sudden injury, pathologic
5. a, b, c. Rationale: Parathyroid hormone main- 12. pathologic
tains serum calcium levels by initiation of 13. fracture
calcium release from bone, conservation of 14. Traction
calcium by the kidney, enhanced intestinal 15. Fracture blisters
absorption of calcium through activation of 16. thromboemboli
vitamin D, and reduction of serum phos- 17. fat embolism
phate levels. 18. Tuberculosis

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506 ANSWERS

19. Osteonecrosis 2. If properly treated, injuries usually heal with

20. osteosarcoma the restoration of the original tensile strength.
21. Benign Repair is accomplished by fibroblasts from the
22. chondroma inner tendon sheath or, if the tendon has no
23. Chondrosarcoma sheath, from the loose connective tissue that
surrounds the tendon. Capillaries infiltrate the
Activity B injured area during the initial healing process
and supply the fibroblasts with the materials
they need to produce large amounts of colla-
Proximal gen. Formation of the long collagen bundles
occurs within the first 2 weeks and, although
Midshaft
tensile strength increases steadily thereafter, it
is not sufficient to permit strong tendon pulls
for 6 to 8 weeks. The danger is that muscle
contraction will pull the injured ends apart,
Distal causing the tendon to heal in the lengthened
position. Another danger is that adhesions will
Transverse Oblique Spiral develop in areas where tendons pass through
fibrous channels, such as in the distal palm of
the hands, rendering the tendon useless.
3. Motion of the arm involves the coordinated
movement of muscles of the rotator cuff
(supraspinous, teres minor, infraspinatus, and
subscapularis) and their musculotendinous at-
tachments. These muscles are separated from
the overlying coracoacromial arch by two bur-
sae, the subdeltoid and subcoracoid. These two
Impacted bursae, sometimes referred to as the subacro-
Comminuted Segmental Butterfly mial bursa, often communicate and are af-
fected by lesions of the rotator cuff. Rotator
Activity C cuff injuries and impingement disorders can
result from a number of causes, including ex-
1. a 2. e 3. i 4. c 5. j
cessive use, a direct blow, or stretch injury,
6. f 7. g 8. d 9. h 10. b
usually involving throwing or swinging, as
with baseball pitchers or tennis players.
Activity D
Overuse and degenerative disorders have a
1. slower onset and are seen in older persons
with minor or no trauma. The tendons of the
a c b d rotator cuff fuse together near their insertions
into the tuberosites of the humerus to form
Activity E the musculotendinous cuff.
4. A hip fracture is generally a fracture of the
1. Any joint can be sprained, but the ankle joint
proximal femur. Such fractures are commonly
is most commonly involved, especially in fast-
categorized according to the anatomic site in
moving injuries in which an ankle or knee can
which they occur. Femoral-neck fractures are
be suddenly twisted. Most ankle sprains occur
located in the area distal to the femoral head
in the lateral ankle when the foot is turned in-
but proximal to the greater and lesser
ward under a person, forcing the ankle into in-
trochanters and are considered intracapsular,
version beyond the structural limits. Other
because they are located within the capsule of
common sites of sprain are the knee (the col-
the hip joint. Intertrochanteric fractures occur
lateral ligament and anterior cruciate ligament)
in the metaphyseal region between the greater
and elbow (the ulnar side). As with a strain, the
and lesser trochanter. Subtrochanteric frac-
soft tissue injury that occurs with a sprain is not
tures are those that occur just below the
evident on the radiograph. Wrist sprains most
greater trochanter. Femoral-neck and in-
often occur with a fall on an outstretched hand.
tertrochanteric fractures account for more

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ANSWERS 507

than 90% of hip fractures, occurring in ap- mass depends on the location of the tumor; a
proximately equal proportions. small lump arising on the surface of the tibia is
5. The compartment syndrome has been de- easy to detect, whereas a tumor that is deep in
scribed as a condition of increased pressure the medial portion of the thigh may grow to a
within a limited space (e.g., abdominal and considerable size before it is noticed. Benign
limb compartments) that compromises the cir- and malignant tumors can cause the bone to
culation and function of the tissues within the erode to the point at which it cannot with-
space. The muscles and nerves of an extremity stand the strain of ordinary use. In such cases,
are enclosed in a tough, inelastic fascial enve- even a small amount of bone stress or trauma
lope called a muscle compartment. If the pres- precipitates a pathologic fracture. A tumor
sure in the compartment is sufficiently high, may produce pressure on a peripheral nerve,
tissue circulation is compromised, causing causing decreased sensation, numbness, a
death of nerve and muscle cells. Permanent limp, or limitation of movement.
loss of function may occur. The amount of 9. Metastatic lesions are seen most often in the
pressure required to produce a compartment spine, femur, pelvis, ribs, sternum, proximal
syndrome depends on many factors, including humerus, and skull, and are less common in
the duration of the pressure elevation, the anatomic sites that are further removed from
metabolic rate of the tissues, vascular tone, the trunk of the body that are secondary tu-
and local blood pressure. Compartment syn- mors. Tumors that frequently spread to the
drome can result from a decrease in compart- skeletal system are those of the breast, lung,
ment size, an increase in the volume of its prostate, kidney, and thyroid, although any
contents, or a combination of the two factors. cancer can ultimately involve the skeleton.
6. Osteomyelitis after trauma or bone surgery More than 85% of bone metastases result
usually is associated with persistent or recur- from primary lesions in the breast, lung, or
rent fevers, increased pain at the operative or prostate.
trauma site, and poor incisional healing,
which often is accompanied by continued SECTION III: APPLYING YOUR
wound drainage and wound separation. Pros-
KNOWLEDGE
thetic joint infections often present with joint
pain, fever, and cutaneous drainage. Activity F
7. The pathologic features of bone necrosis are 1. Magnetic resonance imaging (MRI) of the in-
the same, regardless of cause. The lesion site is jured knee
related to the vessels involved. There is necro- 2. Knee is place in removable knee immobilizer
sis of cancellous bone and marrow. The cortex and isometric quadriceps exercises
usually is not involved because of collateral 3. An arthroscopic meniscectomy may be per-
blood flow. In subchondral necrosis, a triangu- formed if there is recurrent or persistent lock-
lar or wedge-shaped segment of tissue that has ing, recurrent fluid build-up in the knee, or
the subchondral bone plate as its base and the disabling pain.
center of the epiphysis as its apex, undergoes
necrosis. When medullary infarcts occur in
fatty bone marrow, the death of bone cells SECTION IV: PRACTICING FOR NCLEX
causes calcium release and necrosis of fat cells, Activity G
with the formation of free fatty acids. Released
calcium forms an insoluble “soap” with free 1. a. Rationale: Overuse injuries have been de-
fatty acids. Because bone lacks mechanisms for scribed as chronic injuries, including stress
resolving the infarct, the lesions remain for life. fractures that result from constant high levels
8. The three major manifestations of bone tu- of physiologic stress without sufficient recov-
mors are pain, presence of a mass, and impair- ery time. They commonly occur in the elbow
ment of function. Pain is a feature common to (“Little League elbow” or “tennis elbow”) and
almost all malignant tumors, but may or may in tissue where tendons attach to the bone,
not occur with benign tumors. A mass or hard such as the heel, knee, and shoulder. The
lump may be the first sign of a bone tumor. A other answers are incorrect.
malignant tumor is suspected when a painful 2. 1-g, 2-d, 3-b, 4-f, 5-c, 6-a, 7-e
mass exists that is enlarging or eroding the 3. b, c, d. Rationale: Conservative treatment
cortex of the bone. The ease of discovery of a with anti-inflammatory agents, corticosteroid

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508 ANSWERS

injections, and physical therapy often is steroid therapy. Vessel injury, radiation ther-
undertaken. A period of rest is followed by a apy, and embolism can cause osteonecrosis,
customized exercise and rehabilitation pro- but prior steroid therapy is the most common
gram to improve strength, flexibility, and en- cause other than fracture.
durance. Pain medicine and anesthetic 12. c. Rationale: The primary clinical feature of
injections are not usually prescribed for con- osteosarcoma is deep localized pain with
servative treatment of a shoulder or rotator nighttime awakening and swelling in the af-
cuff injury. fected bone. In osteosarcoma the pain is
4. b. Rationale: Hip dislocation is an emergency. worse at night. There may be erythema in the
In the dislocated position, great tension is overlaying skin, but that is not the primary
placed on the blood supply to the femoral clinical feature of the disease. Osteosarcoma
head and avascular necrosis can result. Pain does not cause soreness in the nearest joint; it
caused by a dislocated knee is not considered may impede range of motion.
an emergency. The longer the hip is dislo- 13. a, c, e. Rationale: The primary goals in treat-
cated, the more time it takes to heal and re- ment of metastatic bone disease are to pre-
main in place, but this is not an emergency, vent pathologic fractures and promote
and dislocation of the hip does not interrupt survival with maximum functioning, allow-
the blood supply to the femoral head. ing the person to maintain as much mobility
5. b. Rationale: Various growth factors, such as and pain control as possible. Cure of the dis-
bone morphologic protein (BMP), are ease and preventing bone segment ischemia
thought to induce bone formation and repair are not primary goals of treatment in
bone defects. The other choices listed are not metastatic bone disease.
used to induce healing in fractures.
6. b, c, d. Rationale: A thorough history includes
the mechanism, time, and place of the injury;
CHAPTER 58 DISORDERS OF
first recognition of symptoms; and any treat- MUSCULOSKELETAL FUNCTION:
ment initiated. It is unimportant if anyone DEVELOPMENTAL AND METABOLIC
else in the family is susceptible to fractures.
It is also unimportant what the patient has DISORDERS
eaten. If surgery were indicated, then it
would be important to find out if the patient SECTION II: ASSESSING YOUR
had eaten. UNDERSTANDING
7. 1-a, 2-c, 3-b Activity A
8. c. Rationale: The main clinical features of fat
emboli syndrome (FES) are respiratory failure, 1. Skeletal
cerebral dysfunction, and skin and mucosal 2. epiphyseal growth plate
petechiae. Cerebral manifestations include 3. hypermobility, torsional
encephalopathy, seizures, and focal neuro- 4. Blount
logic deficits unrelated to head injury. The 5. polydactyly
other answers are incorrect. 6. type I collagen
9. d. Rationale: Intravenous therapy is usually 7. dysplasia
needed for up to 6 weeks. Initial antibiotic 8. clubfoot
therapy is followed by surgery to remove for- 9. avascular necrosis
eign bodies (e.g., metal plates, screws) or se- 10. Osgood-Schlatter
questra and by long-term antibiotic therapy. 11. osteoprogenitor
The other answers are incorrect. 12. Osteopenia
10. a. Rationale: Any bone, joint, or bursae can be 13. Osteoporosis
affected, but the spine is the most common 14. Postmenopausal
site, followed by the knees and hips. The an- 15. Secondary
kles and shoulders are not common sites for 16. Osteomalacia
tuberculosis to be found. 17. renal rickets
11. b. Rationale: Besides fracture, the most com- 18. calcification
mon causes of bone necrosis are idiopathic 19. turnover
(i.e., those of unknown cause) and prior 20. Paget

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ANSWERS 509

Activity B hypotonic muscles, loose-jointedness, scoliosis,

and a tendency toward hernia formation. Hear-
1. h 2. b 3. c 4. e 5. a ing loss owing to otosclerosis of the tiny bones
6. j 7. i 8. g 9. d 10. f in the middle ear is common in affected adults.
4. Congenital scoliosis can be divided into fail-
Activity C
ures of formation and failures of segmenta-
1. Epiphyseal separation can occur in children as tion. Failures of formation include the absence
the result of trauma. The separation usually oc- of a portion of the vertebra, such as hemiverte-
curs in the zone of the mature enlarged cartilage bra (absence of a whole side of the vertebra)
cells, which is the weakest part of the growth and wedge vertebra (missing only a portion of
plate. The blood vessels that nourish the epiph- the vertebra). Failure of segmentation is the
ysis pass through the growth plate. These vessels absence of the normal separations between the
are ruptured when the growth plate separates. vertebrae. The child may have other anomalies
This can cause cessation of growth and a short- and neurologic complications if the spine is
ened extremity. The growth plate also is sensi- involved. Neuromuscular scoliosis develops
tive to nutritional and metabolic changes. from neuropathic or myopathic diseases. It is
Scurvy (i.e., vitamin C deficiency) impairs the seen with cerebral palsy, myelodysplasia, and
formation of the organic matrix of bone, caus- poliomyelitis. There is often a long, “C”-
ing slowing of growth at the epiphyseal plate shaped curve from the cervical to the sacral re-
and cessation of diaphyseal growth. In rickets gion. In children with cerebral palsy, severe
(i.e., vitamin D deficiency), calcification of the deformity may make treatment difficult. Myo-
newly developed bone on the metaphyseal side pathic neuromuscular scoliosis develops with
of the growth plate is impaired. Thyroid and Duchenne muscular dystrophy and usually is
growth hormones are required for normal not severe. Idiopathic scoliosis is a structural
growth. Alterations in these and other hor- spinal curvature for which no cause has been
mones can also affect growth. established. It occurs in healthy, neurologi-
2. Toeing-in because of adduction of the forefoot cally normal children.
usually is the result of the fetal position main- 5. The sequence of bone resorption and bone
tained in utero. It can occur in one foot or both formation begins with osteoclastic resorption
feet. The forefoot commonly is adducted and of existing bone, during which the organic
gives the foot a kidney-shaped appearance, (protein matrix) and the inorganic (mineral)
whereas the hind foot is normal. It can be components are removed. The sequence
caused by torsion in the foot, lower leg, or en- proceeds to the formation of new bone by
tire leg. Toeing-out, a common problem in osteoblasts. In the adult, the length of one
children, is caused by external femoral torsion. sequence (i.e., bone resorption and forma-
This occurs when the femur can be externally tion) is approximately 4 months. Ideally, the
rotated to approximately 90 degrees but inter- replaced bone should equal the absorbed
nally rotated only to a neutral position or bone. If it does not, there is a net loss of bone.
slightly beyond. Because the femoral torsion In the elderly, for example, bone resorption
persists when a child habitually sleeps in the and formation no longer are perfectly coupled,
prone position, an external tibial torsion also and bone mass is lost.
may develop. If external tibial torsion is pres- 6. The pathogenesis of osteoporosis involves an
ent, the feet point lateral to the midline of imbalance between bone resorption and for-
the medial plane. External tibial torsion mation such that bone resorption exceeds
rarely causes toeing-out; it only intensifies bone formation. Exercise may prevent or delay
the condition. the onset of osteoporosis by increasing peak
3. The disorder, osteogenesis imperfecta, is char- bone mineral density during periods of
acterized by thin and poorly developed bones growth. Poor nutrition or an age-related de-
that are susceptible to multiple fractures. Chil- crease in intestinal absorption of calcium be-
dren with this disorder have short limbs and a cause of deficient activation of vitamin D may
soft, thin cranium with bifrontal prominences contribute to the development of osteoporo-
that give a triangular appearance to the face. sis, particularly in the elderly. Postmenopausal
Other problems associated with defective con- osteoporosis, which is caused by an estrogen
nective tissue synthesis include thin skin, blue deficiency, is manifested by a loss of cancel-
or gray sclera, abnormal tooth development, lous bone and a predisposition to fractures of

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510 ANSWERS

the vertebrae and distal radius. The loss of of disorders marked by extreme skeletal
bone mass is greatest during early menopause fragility. Four major subtypes of the disorder
when estrogen levels are withdrawing. have been identified. The disorder is charac-
7. Osteoporotic changes occur in the diaphysis terized by thin and poorly developed bones,
and metaphysis of bone. In severe osteoporo- which are susceptible to multiple fractures.
sis, the bones begin to resemble the fragile Children with osteogenesis imperfecta have
structure of a fine porcelain vase. There is loss short limbs and a soft, thin cranium with
of trabeculae from cancellous bone and thin- bifrontal prominences that give a triangular
ning of the cortex to such an extent that mini- appearance to the face. Other problems associ-
mal stress causes fractures. The changes that ated with defective connective tissue synthe-
occur with osteoporosis have been explained sis include thin skin, blue or gray sclera,
by two distinct disease processes: postmeno- abnormal tooth development, hypotonic
pausal and senile osteoporosis. In post- muscles, loose-jointedness, scoliosis, and a
menopausal women, the increase in tendency toward hernia formation. There are
osteoclastic activity affects mainly bones or neither thick bones in the lower extremities
portions of bone that have increased surface nor thick skin in osteogenesis imperfecta.
area, such as the cancellous compartment of 4. c. Rationale: The correction of clubfoot is
the vertebral bodies. The osteoporotic trabecu- maintained by full-time wear of a Denis
lae become thinned and lose their intercon- Browne splint for 3 months and part-time
nections, leading to microfractures and night and nap wear for approximately 2 to
eventual vertebral collapse. In senile osteo- 3 years. The other answers are incorrect.
porosis, the osteoporotic cortex is thinned by 5. a, b, c. Rationale: Treatment of Legg-Calvé-
subperiosteal and endosteal resorption and the Perthes disease involves periods of rest, use of
haversian systems are widened. Hip fractures, assistive devices for walking, non–weight-
which are seen later in life, are more com- bearing and abduction braces to keep the legs
monly associated with senile osteoporosis. separated in abduction with mild internal ro-
tation. The Atlanta Scottish Rite brace, which
SECTION III: APPLYING YOUR does not extend below the knee, is the most
KNOWLEDGE widely used orthosis because it provides con-
tainment while allowing free knee motion
Activity D
and ambulation without crutches or external
1. Drugs include nonsteroidal or other anti-in- support. Weight-bearing braces and adduc-
flammatory agents, and biphosphonates and tion braces are not used in the treatment of
calcitonin to manage pain and prevent further Legg-Calvé-Perthes disease.
spread of the disease and neurologic defects 6. d. Rationale: Osgood-Schlatter disease is char-
acterized by pain in the front of the knee that
SECTION IV: PRACTICING FOR NCLEX is associated with inflammation and thicken-
ing of the patellar tendon. The pain usually is
Activity E
associated with specific activities, such as
1. a. Rationale: Patellar subluxation can result in kneeling, running, bicycle riding, or stair
patellofemoral malalignment with patellar climbing. There are swelling, tenderness, and
subluxation or dislocation and pain. The increased prominence of the tibial tubercle.
other answers are incorrect. The symptoms usually are self-limiting. The
2. b. Rationale: Genu varum can cause gait awk- other answers are incorrect.
wardness and increased risk for sprains and 7. a. Rationale: Scoliosis usually is first noticed
fractures. Uncorrected genu valgum can because of the deformity it causes. A high
cause subluxation and recurrent dislocation shoulder, prominent hip, or projecting
of the patella, with a predisposition to chon- scapula may be noticed by a parent or seen in
dromalacia and joint pain and fatigue. The a school-based screening program A child
other answers are incorrect. with scoliosis can stand straight, does not feel
3. a, c, e. Rationale: The clinical manifestations pain, and can walk straight, so these answers
of osteogenesis imperfecta include a spectrum are incorrect.

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ANSWERS 511

8. b. Rationale: The clinical method of choice for Activity B

bone mineral density (BMD) studies is dual-
energy x-ray absorptiometry (DXA) of the Bone Osteophyte
spine and hip. The other answers will not di- cysts
agnose osteoporosis.
9. c. Rationale: The elderly with intestinal mal-
absorption also may benefit from vitamin D.
The least expensive and most effective long-
term treatment is a diet rich in vitamin D
(i.e., fish, dairy products, and margarine)
along with careful exposure to the midday
sun. The other answers are incorrect.
10. d. Rationale: As with osteomalacia in the
adult, rickets can result from kidney failure;
malabsorptive syndromes, such as celiac dis-
ease and cystic fibrosis; and medications, such
Erosion of
as anticonvulsants, which cause target organ Joint space cartilage and
resistance to vitamin D, and aluminum- narrows bone
containing antacids, which bind phospho-
rous and prevent its absorption. The other Activity C
drugs are not used to treat rickets.
1. c 2. e 3. f 4. j 5. a
6. b 7. d 8. g 9. h 10. i
CHAPTER 59 DISORDERS OF
MUSCULOSKELETAL FUNCTION: Activity D
RHEUMATIC DISORDERS 1.

SECTION II: ASSESSING YOUR e g d a

UNDERSTANDING
c f b
Activity A
1. rheumatoid arthritis Activity E
2. T cell-mediated
1. The pathogenesis of rheumatoid arthritis (RA)
3. chronic inflammatory
4. scleroderma can be viewed as an aberrant immune re-
5. Ankylosing spondylitis sponse that leads to synovial inflammation
6. arthropathies and destruction of the joint architecture. It
7. Reiter syndrome has been suggested that the disease is initiated
8. enteropathic by the activation of helper T cells, release of
9. Osteoarthritis cytokines, and antibody formation. Approxi-
10. wear and tear mately 70%–80% of those with the disease
11. Gout have a substance called the rheumatoid factor
12. Juvenile idiopathic arthritis (RF), which is an autologous (self-produced)
13. systemic lapis erythematosus antibody (Ig RF) that reacts with a fragment of
14. dermatomyositis immunoglobulin G (IgG) to form immune
15. Arthritis complexes. Immune complexes (IgG RF  IgG)
16. Osteoarthritis and complement components are found in
17. Polymyalgia rheumatica the synovium, synovial fluid, and extrarticular
lesions of persons with RA.

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512 ANSWERS

2. At the cellular level, neutrophils, macrophages, quence of enzyme defects that result in an
and lymphocytes are attracted to the area. The overproduction of UA; inadequate elimination
neutrophils and macrophages phagocytize the of UA by the kidney; or a combination of the
immune complexes and, in the process, re- two. In secondary gout, the hyperuricemia
lease lysosomal enzymes capable of causing may be caused by increased breakdown in the
destructive changes in the joint cartilage. The production of nucleic acids, as occurs with
inflammatory response that follows attracts rapid tumor cell lysis during treatment for
additional inflammatory cells, setting into mo- lymphoma or leukemia. Other cases of sec-
tion a chain of events that perpetuates the ondary gout result from chronic renal disease.
condition. As the inflammatory process pro-
gresses, the synovial cells and subsynovial tis- SECTION III: APPLYING YOUR
sues undergo reactive hyperplasia. KNOWLEDGE
Vasodilation and increased blood flow cause
warmth and redness. The joint swelling that Activity F
occurs is the result of the increased capillary 1. Juvenile idiopathic arthritis (JIA) can be re-
permeability that accompanies the inflamma- garded not as a single disease, but as a category
tory process. of diseases with three principal types of onset:
3. Arthralgias and arthritis are among the most (1) systemic onset disease, (2) pauciarticular
commonly occurring early symptoms of sys- arthritis, and (3) polyarticular disease.
temic lupus erythematosus (SLE). The pol- 2. You would expect blood work for rheumatoid
yarthritis of SLE initially can be confused with factor and a complete metabolic panel along
other forms of arthritis, especially rheumatoid with a complete blood count (CBC) to be or-
arthritis (RA), because of the symmetric dered.
arthropathy. Flexion contractures, hyperex-
tension of the interphalangeal joint, and sub-
luxation of the carpometacarpal joint SECTION IV: PRACTICING FOR NCLEX
contribute to the deformity and subsequent Activity G
loss of function in the hands. Other muscu-
loskeletal manifestations of SLE include 1. c, e, d, i, f, g, a, h, b. Rationale: The role of the
tenosynovitis, rupture of the intrapatellar and autoimmune process in the joint destruction
Achilles tendons, and avascular necrosis, fre- of rheumatoid arthritis (RA) remains obscure.
quently of the femoral head. At the cellular level, neutrophils, macro-
4. The joint changes associated with osteoarthri- phages, and lymphocytes are attracted to the
tis, which include a progressive loss of articu- area. The neutrophils and macrophages
lar cartilage and synovitis, result from the phagocytize the immune complexes and, in
inflammation caused when cartilage attempts the process, release lysosomal enzymes capa-
to repair itself, creating osteophytes or spurs. ble of causing destructive changes in the
These changes are accompanied by joint pain, joint cartilage. The inflammatory response
stiffness, limitation of motion, and, in some that follows attracts additional inflammatory
cases, by joint instability and deformity. cells, setting into motion a chain of events
5. The pathogenesis of gout resides in an eleva- that perpetuates the condition. As the inflam-
tion of the serum uric acid levels. Uric acid matory process continues, the synovial cells
(UA) is the end product of purine (adenine and subsynovial tissues undergo reactive hy-
and guanine from DNA and RNA) metabolism. perplasia. Vasodilation and increased blood
UA elevation and the subsequent development flow cause warmth and redness. The joint
of gout can result from overproduction of swelling that occurs is the result of the in-
purines, decreased salvage of free purine bases, creased capillary permeability that accompa-
augmented breakdown of nucleic acids be- nies the inflammatory process.
cause of increased cell turnover, or decreased 2. a. Rationale: Arthralgias and arthritis are
urinary excretion of UA. Primary gout, which among the most commonly occurring early
constitutes 90% of cases, may be a conse- symptoms of systemic lupus erythematosus

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ANSWERS 513

(SLE). The other answers are symptoms of SLE crystals are found in the synovial fluid or
in differing stages of the disease. in tissue sections of tophaceous deposits.
3. c, d. Rationale: Almost all persons with sclero- The other answers are not diagnostic of
derma develop polyarthritis and Raynaud gout.
phenomenon, a vascular disorder character- 10. c. Rationale: In terms of medications, the se-
ized by reversible vasospasm of the arteries lection of drugs used in the treatment of
supplying the fingers. Dumping syndrome, arthritic disorders and their dosages may
chronic diarrhea, and chronic vasoconstriction need to be considered when prescribing for
are not diseases developed by people with the elderly. For example, the nonsteroidal
scleroderma. anti-inflammatory drugs (NSAIDs) may be
4. b. Rationale: Corticosteroids are the mainstay less well tolerated by the elderly, and their
of treatment for polymyositis and dermato- side effects are more likely to be serious. In
myositis. The other drug types are not the addition to bleeding from the gastrointestinal
treatment of choice for polymyositis and der- tract and renal insufficiency, there may be
matomyositis. cognitive dysfunction, manifested by forget-
5. c. Rationale: The pain, which becomes worse fulness, inability to concentrate, sleepless-
when resting, particularly when lying in bed, ness, paranoid ideation, and depression.
initially may be blamed on muscle strain or Malaise, lethargy, and mania are not side
spasm from physical activity. The other an- effects of NSAIDs.
swers are incorrect.
6. d. Rationale: Reiter syndrome was the first
rheumatic disease to be recognized in associa-
CHAPTER 60 STRUCTURE
tion with human immunodeficiency virus AND FUNCTION OF THE SKIN
(HIV) infection. Symptoms of arthritis may
precede any overt signs of HIV disease. The SECTION II: ASSESSING YOUR
other sexually transmitted diseases (STDs) UNDERSTANDING
have not been associated with Reiter syn- Activity A
drome.
7. a. Rationale: The biologic response modifiers, 1. integumentum
specifically the tumor necrosis factor (TNF) 2. thickness
inhibitors (e.g., etanercept, infliximab, and 3. epidermis
adalimumab) have been found to be benefi- 4. stratum corneum
cial in controlling arthritis, as well as psoria- 5. Keratinocytes
sis in patients with psoriatic arthritis. The 6. Melanocytes
other drugs have not been found to be bene- 7. eumelanin
ficial in psoriatic arthritis. 8. Langerhans
8. a, c, e. Rationale: The joint changes associated 9. basal lamina
with osteoarthritis, which include a progres- 10. epidermis
sive loss of articular cartilage and synovitis, 11. dermis
result from the inflammation caused when 12. papillary
cartilage attempts to repair itself, creating os- 13. Eccrine
teophytes or spurs. These changes are accom- 14. Apocrine
panied by joint pain, stiffness, limitation of 15. keratinized
motion, and, in some cases, by joint instabil- 16. keratinized
ity and deformity. The other answers are in- 17. blister
correct. 18. callus
9. b. Rationale: A definitive diagnosis of gout 19. Corns
can be made only when monosodium urate 20. xerosis

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514 ANSWERS

Activity B
1.
Epidermis lifted to reveal
papillae of the dermis

Papillae

Dermis

Arrector pili muscle

Blood vessel

Sebaceous gland

Subcutaneous tissue

Nerve endings

Nerve to hair follicle

Sweat gland

2. Activity C

Hair shaft 1. d 2. j 3. i 4. c 5. a
6. h 7. f 8. g 9. b 10. e
Arrector pili muscle

Activity D
Epidermis
1. The skin serves several other vital functions,
Sebaceous including somatosensory function, tempera-
gland ture regulation, and vitamin D synthesis. The
Keratinized skin is richly innervated with pain, tempera-
cells ture, and touch receptors. Skin receptors relay
Dermis the numerous qualities of touch, such as pres-
Hair sure, sharpness, dullness, and pleasure to the
follicle central nervous system for localization and
Hair fine discrimination. The rate at which heat is
papilla
dissipated from the body is determined by con-
Dermal striction or dilation of the arterioles that sup-
blood ply blood to the skin and through evaporation
vessels of moisture and sweat from the skin surface.
Vitamin D3, the most important of these, is
formed in the skin as the result of irradiation

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ANSWERS 515

of 7-dehydrocholesterol, a substance normally

SECTION III: APPLYING YOUR
found in the skin, by ultraviolet rays from the
KNOWLEDGE
sun.
2. The epidermis is composed of stratified squa- Activity E
mous keratinized epithelium, which, when
1. Skin color is determined by the melanin pro-
viewed under the microscope, is seen to con-
duced by the melanocytes. Black skin produces
sist of five distinct layers, or strata, that repre-
more melanin and produces it faster than
sent a progressive differentiation or
white skin. Because of their skin color, dark-
maturation of the keratinocytes: the stratum
skinned persons are better protected against
germinativum, or basal layer; the stratum
skin cancer, premature wrinkling, and aging of
spinosum; the stratum granulosum; the stra-
the skin that occurs with sun exposure. Dry or
tum lucidum; and the stratum corneum.
“ashy” skin also can be a problem for people
3. The ability to synthesize melanin depends on
with dark skin. It often is uncomfortable, and
the ability of the melanocytes to produce an
it also is easily noticed because it gives the skin
enzyme called tyrosinase, which converts the
an ashen or grayish appearance. The darker
amino acid tyrosine to a precursor of melanin.
pigmentation can make skin pallor, cyanosis,
A genetic lack of this enzyme results in a clini-
and erythema more difficult to observe.
cal condition called albinism. Persons with this
Changes in skin color, in particular hypo- and
disorder lack pigmentation in the skin, hair,
hyperpigmentation, often accompany disor-
and iris of the eye.
ders of dark skin and are very important signs
4. Dark-skinned and light-skinned people have
to observe when diagnosing skin conditions.
approximately the same number of
melanocytes, but the production and packag-
ing of pigment differ. In dark-skinned people, SECTION IV: PRACTICING FOR NCLEX
larger melanin-containing melanosomes are Activity F
produced and transferred individually to the
keratinocyte; whereas, in light-skinned peo- 1. a. Rationale: The skin also serves as an im-
ple, smaller melanosomes are produced and munologic barrier. The Langerhans cells de-
then packaged together in a membrane be- tect foreign antigens, playing an important
fore being transferred to the keratinocyte. Al- part in allergic skin conditions and skin graft
though the number of melanosomes in dark rejections. The other cell types are not part of
and white skin is the same, black skin pro- the immunologic barrier.
duces more melanin and produces it faster 2. 1-c, 2-b, 3-a, 4-d
than white skin. 3. b. Rationale: The basement membrane is also
5. The sebaceous glands are located over the en- a major site of immunoglobulin and comple-
tire skin surface except for the palms, soles, ment deposition in skin disease. The other
and sides of the feet. They are part of the answers are incorrect.
pilosebaceous unit. They secrete a mixture of 4. c. Rationale: The reticular dermis (pars reticu-
lipids, including triglycerides, cholesterol, and laris) is the thicker area of the dermis and
wax. This mixture is called sebum; it lubricates forms the bulk of the dermal layer. The other
hair and skin. Sebum is not the same as the three answers are part of the reticular dermis
surface lipid film. Sebum prevents undue but it is not characterized by them.
evaporation of moisture from the stratum 5. a, c, e. Rational: Because the eccrine glands
corneum during cold weather and helps to and deep hair follicles extend to this layer
conserve body heat. Sebum production is and several skin diseases involve the subcuta-
under the control of genetic and hormonal neous tissue, the subcutaneous tissue may be
influences. considered part of the skin. The keratinocytes
6. It is generally agreed that itch is a sensation and the Merkel cells are not part of the sub-
that originates in free nerve endings in the cutaneous tissue.
skin, is carried by small myelinated type C 6. d. Rationale: This mixture is called sebum; it
nerve fibers to the dorsal horn of the spinal lubricates hair and skin. Sweat comes from
cord, and is then transmitted to the somato- sweat glands. Chalasia is an abnormal relax-
sensory cortex via the spinothalamic tract, dif- ation or the cardiac sphincter of the stomach.
fering from the pain pathways. Cerumen is found in the ear.

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516 ANSWERS

7. a. Rationale: The nearly transparent nail plate 20. Papulosquamous

provides a useful window for viewing the 21. Lichen planus
amount of oxygen in the blood, providing a 22. repeated
view of the color of the blood in the dermal 23. scabies
vessels. The other answers are incorrect. 24. UVB rays
8. b. Rationale: When a blister occurs, histologi- 25. photosensitive
cally, there is degeneration of the epidermal 26. Sunburn
cells and a disruption of the intercellular 27. Burns
junctions that causes the layers of the skin to 28. Burn
separate. Lichenifications are thickened areas 29. ischemic
of the skin. Petechiae are pinpoint rashes on 30. dysplastic nevus
the skin. A pressure ulcer is sometimes re- 31. melanocytes
ferred to as a “bed sore” and is caused by con- 32. melanoma
tinuous pressure on a bony prominence. 33. Basal cell carcinoma
9. c. Rationale: Given these new findings, it has 34. Squamous cell carcinomas
been postulated that itch exists both locally 35. birthmarks
and centrally, that, in addition to localized 36. Hemangiomas
itch, an “itch center” exists in the somatosen- 37. Port-wine stains
sory cortex. The other answers are incorrect. 38. Irritant diaper dermatitis
10. d. Rationale: Moisturizing agents are the cor- 39. Prickly heat
nerstone of treatment for dry skin. These 40. Cradle cap
agents exert their effects by repairing the skin
barrier, increasing the water content of the Activity B
skin, reducing transepidermal water loss, and
1.
restoring the lipid barrier’s ability to attract,
1. b 2. e 3. a 4. g 5. f
hold, and redistribute water. The other an-
6. h 7. d 8. c 9. j 10. i
swers are incorrect.
2.
1. h 2. a 3. j 4. e 5. d
CHAPTER 61 DISORDERS OF SKIN 6. g 7. b 8. f 9. c 10. i
INTEGRITY AND FUNCTION Activity C
SECTION II: ASSESSING YOUR 1. The most common type of albinism is reces-
UNDERSTANDING sively inherited oculocutaneous albinism,
Activity A
in which there are a normal number of
melanocytes, but they lack tyrosinase, the
1. Primary enzyme needed for synthesis of melanin. In-
2. melanin dividuals have pale or pink skin, white or yel-
3. Albinism low hair, and light-colored or sometimes pink
4. Fungi eyes. Persons with albinism have ocular prob-
5. Candidiasis lems, such as extreme sensitivity to light, re-
6. bacterial fractive errors, lack of stereopsis, and
7. Impetigo nystagmus.
8. Cellulitis 2. The fungi that cause superficial mycoses live
9. Verrucae plantaris, verrucae palmaris on the dead keratinized cells of the epider-
10. zoster mis. They emit an enzyme that enables them
11. Acne to digest keratin, which results in superficial
12. Sebum skin scaling, nail disintegration, or hair
13. comedones, blackheads, whiteheads breakage, depending on the location of the
14. Inflammatory infection. Deeper reactions involving vesi-
15. dermatoses cles, erythema, and infiltration are caused by
16. Allergic contact the inflammation that results from exotoxins
17. nummular liberated by the fungus. Fungi also are capa-
18. urticaria ble of producing an allergic or immune re-
19. Topical, systemic sponse.

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ANSWERS 517

3. The two common types of tinea capitis are onization and proliferation of Propionibac-
primary (noninflammatory) and secondary terium acnes, and (4) inflammation
(inflammatory). The infection is spread most 7. Atopic dermatitis (atopic eczema) is an itchy,
often among household members who share inflammatory skin disorder that is character-
combs and brushes on which the spores are ized by poorly defined erythema with edema,
shed and remain viable for long periods. De- vesicles, and weeping at the acute stage and
pending on the invading fungus, the lesions skin thickening (lichenification) in the
of the noninflammatory type can vary from chronic stage. The infantile form of atopic
grayish, round, hairless patches to balding dermatitis is characterized by vesicle forma-
spots, with or without black dots on the tion, oozing, and crusting with excoriations.
head. The individual usually is asympto- The skin of the cheeks may be paler, with
matic, although pruritus may exist. The in- extra creases under the eyes. Adolescents and
flammatory type of tinea capitis is caused by adults usually have dry, red patches affecting
virulent strains. The onset is rapid, and in- the face, neck, and upper trunk, but without
flamed lesions usually are localized to one the thickening and discrete demarcation as-
area of the head. The inflammation is be- sociated with psoriasis. The bends of the el-
lieved to be a delayed hypersensitivity reac- bows and knees are usually involved. In
tion to the invading fungus. The initial lesion chronic cases, the skin is dry, leathery, and
consists of a pustular, scaly, round patch with lichenified.
broken hairs. A secondary bacterial infection 8. It is thought that activated T lymphocytes
is common and it may lead to a painful, cir- (mainly CD4 helper cells) produce chemical
cumscribed, boggy, and indurated lesion messengers that stimulate abnormal growth
called a kerion. of keratinocytes and dermal blood vessels.
4. Preexisting wounds (e.g., ulcers, erosions) Accompanying inflammatory changes are
and tinea pedis are often portals of entry. caused by infiltration of neutrophils and
Legs are the most common sites, followed by monocytes. Skin trauma (i.e., prepsoriasis) is
the hands and pinnas of the ears, but celluli- a common precipitating factor in people pre-
tis may be seen on many body parts. The le- disposed to psoriasis. The reaction of the skin
sion consists of an expanding red, swollen, to an original trauma of any type is called the
tender plaque with an indefinite border, cov- Köebner reaction. Stress, infections, trauma,
ering a small to wide area. Cellulitis is fre- xerosis, and use of medications, such as an-
quently accompanied by fever, erythema, giotensin-converting enzyme inhibitors,
heat, edema, and pain. Cellulitis often in- -adrenergic blocking drugs, lithium, and the
volves the lymph system and, once compro- antimalarial agent, hydroxychloroquine
mised, repeat infections may impair (Plaquenil), may precipitate or exacerbate the
lymphatic drainage, leading to chronically condition.
swollen legs, and eventually dermal fibrosis 9. A mite, Sarcoptes scabiei, which burrows into
and lymphedema. the epidermis, causes scabies. After a female
5. The recurrent lesions of HSV-1 usually begin mite is impregnated, she burrows into the
with a burning or tingling sensation. Umbili- skin and lays two to three eggs each day for 4
cated vesicles and erythema follow and or 5 weeks. The eggs hatch after 3–4 days,
progress to pustules, ulcers, and crusts before and the larvae migrate to the skin surface. At
healing. Lesions are most common on the this point, they burrow into the skin only for
lips, face, mouth, nasal septum, and nose. food or protection. The larvae molt and be-
When a lesion is active, HSV-1 is shed and come nymphs; they molt once more to be-
there is risk of transmitting the virus to oth- come adults. After the new adult females are
ers. Pain is common, and healing takes place impregnated, the cycle is repeated. Small
within 10–14 days. Precipitating factors may vesicles may cover the burrows. Pruritus is
be stress, menses, or injury. In particular, common and may result from the burrows,
UVB exposure seems to be a frequent trigger the fecal material of the mite, or both. Excori-
for recurrence. Individuals who are immuno- ations may develop from scratching, leaving
compromised may have severe attacks. the host vulnerable to secondary bacterial in-
6. (1) Increased sebum production, (2) increased fections and severe skin lesions if left un-
proliferation of the keratinizing epidermal treated.
cells that form the sebaceous cells, (3) the col-

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518 ANSWERS

10. Skin damage induced by UVB is believed to with temperature regulation; imposes exces-
be caused by the generation of reactive oxy- sive demands on the metabolic system; and
gen species and by damage to melanin. Cellu- challenges the immune system
lar proteins and DNA are primarily damaged 2. Hemodynamic instability owing to fluid loss;
because of their abundance and ability to ab- smoke inhalation and postburn lung injury;
sorb UV radiation. Both UVA and UVB also hypermetabolism, characterized by increased
deplete Langerhans cells and immune cells. It oxygen consumption, increased glucose use,
is believed that these effects prevent immune and protein and fat wasting; impaired func-
cells from detecting and removing sun-dam- tion of the kidneys; hypovolemic shock and
aged cells with malignant potential. impaired organ perfusion; and sepsis
11. A patient should (a) wear a wide-brimmed
hat, (b) cover up in the sun, (c) seek shade, SECTION IV: PRACTICING FOR NCLEX
(d) wear wrap-around sunglasses, and (e)
Activity E
avoid the sun during the hours of 10 AM to
4 PM, while using a broad spectrum sunscreen 1. 1-a, 2-c, 3-b
with an SPF of 15 or higher. It is also important 2. a. Rationale: Treatment of fungal infections
to avoid sun tanning booths, perform a self- usually follows diagnosis confirmed by KOH
assessment of the skin every month, and obtain preparation or culture. The other answers are
a professional skin examination every year. incorrect.
12. The massive loss of skin tissue not only predis- 3. 1-b, 2-a, 3-f, 4-g, 5-e, 6-d, 7-c
poses to attack by microorganisms that are 4. b. Rationale: Benzoyl peroxide is a topical
present in the environment but it allows for agent that has both antibacterial and
the massive loss of body fluids and their con- comedolytic properties. It is the topical agent
tents, it interferes with temperature regulation, most effective in reducing P. acnes. The other
it challenges the immune system, and it im- topical agents do not act both as comedolytic
poses excessive demands on the metabolic and and antibacterial agents.
reparative processes that are needed to restore 5. a, c, e. Rationale: Prominent symptoms in-
the body’s interface with the environment. clude eyes that are itchy, burning, or dry; a
13. Basal cell carcinoma usually is a nonmetasta- gritty or foreign sensation; and erythema and
sizing tumor that extends wide and deep if swelling of the eyelid. Heat sensitivity and
left untreated. Nodular ulcerative basal cell telangiectasia occur later in the disease and
carcinoma is the most common, accounting are not considered prominent symptoms.
for 60% of all basal cell carcinoma. It has a 6. c. Rationale: The lesions of allergic contact
nodulocystic structure that begins as a small, dermatitis range from a mild erythema with
flesh-colored or pink, smooth, translucent edema to vesicles or large bullae. The other
nodule that enlarges over time. Telangiectatic answers are incorrect.
vessels frequently are seen beneath the sur- 7. d. Rationale: In persons with black skin, pig-
face. Over the years, a central depression mentation may be lost from lichenified skin.
forms that progress to an ulcer surrounded by The other answers do not occur in people
the original shiny, waxy border. The second with black skins who have eczema.
most common form is superficial basal cell 8. a. Rationale: Intravenous immunoglobulin
carcinoma, which is seen most often on the may hasten the healing response of the skin.
chest or back. It begins as a flat, nonpalpable, Broad-spectrum antibiotics and cortico-
erythematous plaque. The red, scaly areas steroids may be given but they do not hasten
slowly enlarge, with nodular borders and the healing response of the skin. Diflucan is
telangiectatic bases. This type of skin cancer given for vaginal candidiasis.
is difficult to diagnose because it mimics 9. b. Rationale: In psoriasis vulgaris, the primary
other dermatologic problems. lesions are sharply demarcated thick red
plaques with a silvery scale that vary in size
SECTION III: APPLYING YOUR and shape. The other answers are incorrect.
KNOWLEDGE 10. c. Rationale: Most persons with lichen planus
who have skin lesions also have oral lesions,
Activity D
appearing as milky white lacework on the
1. Attack by microorganisms in the environ- buccal mucosa or tongue. The other answers
ment; massive loss of body fluids; interferes are incorrect.

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ANSWERS 519

11. d. Rationale: Oral ivermectin, a broad-spec- cryosurgery and chemosurgery are effective
trum antiparasitic agent, has been used for in removing all cancerous cells. The other an-
treatment-resistant scabies. The other drugs swers are incorrect.
are not used for treatment-resistant scabies. 16. b. Rationale: In black-skinned persons, the le-
12. b. Rationale: Methods for preventing pressure sions may appear as hyperpigmented nodules
ulcers include frequent position change, and occur more frequently on non–sun-
meticulous skin care, and frequent and care- exposed areas. The other answers do not
ful observation to detect early signs of skin describe squamous cell carcinoma in black-
breakdown. The other answers are incorrect. skinned people.
13. c. Rationale: Another form of nevi, the dys- 17. c. Rationale: Hemangiomas of infancy typi-
plastic nevus, is important because of its ca- cally undergo an early period of proliferation
pacity to transform to malignant melanoma. during which they enlarge, followed by a pe-
The other answers are incorrect. riod of slow involution where the growth is
14. d. Rationale: Other risk factors include a reversed until complete resolution. Surgical
family history of malignant melanoma, excision, laser surgery, and chemotherapy are
presence of marked freckling on the upper not used for hemagiomas of infancy.
back, history of three or more blistering 18. d. Rationale: Immunization is accomplished
sunburns before 20 years of age, and pres- by live-virus injection. Rubella vaccination
ence of actinic keratoses. The other answers has close to 100% immunity response in im-
are incorrect. munized children. The other answers are in-
15. a. Rationale: The most important treatment correct.
goal for basal cell carcinoma is complete 19. a. Rationale: Lentigines can be removed surgi-
elimination of the lesion. Also important is cally (cryotherapy, laser therapy, liquid nitro-
the maintenance of function and optimal gen). Topical creams and lotions containing
cosmetic effect. Curettage with electrodesic- adapalene, tertinoin, have been used. The
cation, surgical excision, irradiation, laser, other answers are incorrect.

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