Gastrointestinal System

1. Oral structures: lips, teeth,

gingivae, oral mucosa, tongue,
hard and soft palate, pharynx,
and salivary glands
2. Esophagus
a. Upper esophageal
sphincter
b. Lowe Esophageal
Sphincter (normally
remains closed, and opens
only to pass food into the
stomach
3. Stomach (Fundus, Body, Antrum)
4. Sphincters
a. LES- allows food to enter
the stomach and prevents
reflux into the esophagus
b. Pyloric sphincter-
regulates flow of stomach
contents (chime) into the
duodenum Functions of Gastrointestinal System:
5. Small intestine (Duodenum,
jejunum, ileum)  Digestion
6. Large intestine (Cecum, colon, o Ptyalin- enzyme contained
rectum) in the saliva that breaks
7. Ileocecal valve- prevents the down starch
return of feces from the cecum o Gastric juices containing
into the small intestine hydrochloric acid and
8. Appendix- collects lymphoid enzymes (pepsin and
tissues lipase) in the stomach
o Peristaltic action
o Most nutrient absorption
and food digestion is
completed in the small
intestine
 Elimination
o Occurs in the large
intestine and rectum
o Cecum and ascending
colon- absorb water and
electrolytes
 o Rectum- stores feces for o Barium swallow (Upper
elimination GI)- visualization by
fluoroscopy of the
Symptoms of altered GI function:
esophagus and stomach
 Food intolerance/ Lack of after the client swallows
appetite barium; shows outline of
 Pain structures
 Altered bowel elimination o Barium Enema (Lower GI)-
patterns instillation of barium into
 Presence of dark urine, jaundice, the large intestine, with
weight loss, N and V fluoroscopy and filming
 Previous GI tract surgery used to visualize
structures and determine
Physical Examination: Inspection, efficiency of emptying
Auscultation, Percussion, Palpation  Motility studies- use manometric
(always palpate the abdomen last so catheters to measure intraluminal
that sounds from palpation are not pressure in GI structures
auscultated)  Endoscopic studies- provide
Lab tests: direct visualization of internal GI
structures (e.g. esophagoscopy,
 Blood and serum studies gastroscopy, colonoscopy,
o Albumin- globulin ratio and sigmoidoscopy, and
total protein, alkaline esophagogastroduodenoscopy)
phosphatase levels  Ultrasonography, CT, MRI
(measures enzyme activity
in bone, intestine, liver,
and biliary systems) Gastroesophageal Reflux Disease
o Miscellaneous (iron, (GERD)
calcium, cholesterol,
prothrombin time, - Excessive reflux of hydrochloric
carotenes, and vitamin A) acid into the esophagus
 Fecal fat studies - Usually results from an
o Qualitative evaluation incompetent LES, pyloric
stenosis, or a motility disorder
(neutral (ingested mineral
oil) or fatty acid (lipids)) Clinical Manifestations:
o Quantitative evaluation (fat
 Pyrosis (burning sensation in
content)
the esophagus)
o Stool guaiac (detects
 Regurgitation of sour- tasting
occult blood in stool-
secretions
indicating GI bleed)
 Dysphagia (difficulty
 Radiographic studies
swallowing) and odynophagia
(pain on swallowing)
  Symptoms mimicking those of  Burning, aching, or
a heart attack gnawing pain in the right
epigastrium
Nursing Management:
 Administer medications
(antacids, histamine- receptor
antagonists, and PPIs)
 Low fat, high- fiber diet
 Avoid irritants (spicy, acidic
foods, alcohol, caffeine,
tobacco)
 Avoid food or drinks 2 hours
before bedtime or lying down
after eating
 Elevate head of the bed
 Lose weight, if necessary
 Pyrosis (heartburn),
nausea and vomiting
Peptic Ulcer Disease  Epigastric tenderness
- Thought to result from  Barium swallow shows an
helicobacter pylori infection ulcerated area
- Contributing factors:  Endoscopy identifies
o Altered gastric acid levels inflammation of gastric
o Tobacco and alcohol use mucosa, ulcers, and
lesions
o Use of NSAIDS and
 Biopsy can determine the
steroids
presence of H. pylori
o Genetic predisposition
o Psychosomatic factors Nursing Management:
- Involves ulcers (breaks in the
 Antacids, anticholinergics,
mucosa) occurring in the:
histamine- receptor
o Duodenum (duodenal
antagonist, PPIs, and
ulcer)—related to
mucosal protective agents
hypersecretion of acid,
 Medications for ulcers
possibly caused by
caused by H. pylori
overactive vagal
(metronidazole and
stimulation
tetracycline)
o Stomach (gastric ulcer)-
 Avoid foods that previously
may be related to back-
have caused pain
diffusion of acid through
damaged mucosa  Smoking cessation
 Prepare the client for
Clinical Manifestations: diagnostic procedures
 o Barium swallow (no irritating substances affect the
oral intake after GI tract)
midnight and  Diarrhea (produced by toxins
possible laxatives to that stimulate secretion of
clean the GI tract. water and electrolytes)
Stools are  Fever and malaise
monitored until all  Borborygmi (rumbling,
barium has been gurgling sound) heard on
eliminated) auscultation
o Gastroscopy
Lab tests:
(informed consent,
NPO for 8 hours  Stool specimen (shows
before the leukocytes, blood, mucus,
procedure. Assess parasite ova)
for gag reflex after,  Hemoglobin and
before the client hematocrit levels are
consumes food) elevated because of
o Prepare the client dehydration from vomiting
for surgery and diarrhea
 Creatinine and blood urea
nitrogen levels are
Gastroenteritis elevated with acute
- Inflammation of stomach (gastric diarrhea
mucosa) and small intestine, Nursing management:
resulting in vomiting
- Possible causes: bacterial  Medications (antidiarrheal,
(staphylococcus aureus, antiemetics)
salmonella, shigella) food  NPO and bed rest (allow
poisoning, amoeba, adenovirus, GI to rest)
enterovirus, and coxsackievirus,  Clear liquid diet to bland
parasites, non- bacterial food diet to regular diet
poisoning from toxins in plants,  Monitor I and O and fluid/
seafood, contaminated food, electrolyte status; monitor
certain drugs (antibiotics) for dehydration; increase
fluid intake, if necessary
Clinical manifestations:
 Abdominal cramping
 Nausea and vomiting
(protective mechanism that
empties the contents of the
stomach when noxious or
Peritonitis  Radiograph (may reveal location
of perforation)
- Acute or chronic inflammation of
the peritoneum Nursing Management:
 Medications (antibiotics,
antiemetics, opioid analgesic)
 Monitor respiratory status
 Minimize pain
 Reduce/ prevent the spread of
infection

Appendicitis
- Usually results from E. coli or - Inflammation of the vermiform
Streptococcus faecalis invasion appendix
of the peritoneum, chemical
irritation (due to ruptured bladder,
ovary, or fallopian tube), bile
spillage into the peritoneal cavity,
contamination from surgical glove
talc, particles of suture materials
or lint from surgical drapes,
penetrating abdominal wound or
bowel strangulation’
Clinical Manifestations:
 Severe localized abdominal - Caused by obstruction of the
pain with or without guarding appendix lumen, which can result
and rebound tenderness from a fecalith, kinking of the
 Abdomen is rigid and board- appendix, inflammation, or a
like neoplasm
 Fever, tachycardia, and chills - Obstruction of the appendix
 Shallow, guarded respirations lumen causes increased
 Signs of dehydration and intraluminal pressure and trigger
acidosis---late manifestations an inflammatory process that can
lead to infection, necrosis, and
Lab tests: perforation
 WBC count (may reveal Clinical manifestations:
leukocytosis or leukopenia)
 Paracentesis (identifies the  McBurney’s point (right lower
causative agent) quadrant) pain, rebound
tenderness
  Nausea and vomiting Nursing Management:
 Low- grade fever
 Prompt surgery; provide general
preop and postop care
 Provide discharge teaching

Dunphy’s sign- increased pain with

coughing
Psoas sign- pain on passive extension
of the right thigh
Obturator sign- pain on passive internal
rotation of the hip when the right knee is
flexed
Respiratory System Pulmonary Ventilation
Upper Respiratory Tract: nose, nasal - Breathing
cavity, sinuses, pharynx, larynx - Movement of gases through a
pressure gradient (high to low)
- Inspiration- when atmospheric
pressure is greater than lung
pressure
- Expiration- when lung pressure is
greater than atmospheric
pressure
Volumes of air exchange:
Tidal volume- amount of air exhaled
normally after a typical inspiration (normal:
500 ml)
Expiratory reserve volume- additional
amount of air forcibly expired after tidal
Lower Respiratory Tract: trachea, expiration (normal: 1000-1200 ml)
bronchial tree, and lungs
Inspiratory reserve volume- amount of air
that can be forcibly inhaled over and above
normal
Residual volume- amount of air that stays
trapped in the alveoli (normal 1.2 L)

Functions:
 Air distributor
 Gas exchanger
 Filters, warms, and humidifies air
 Influences speech
 Allows for sense of smell
Acute Respiratory Failure during exercise but not at
rest
- When the exchange of oxygen for
carbon dioxide in the normal 4. Alveolar Hypoventilation
lungs cannot match the rate of Hypercapnic (high levels
oxygen consumption and carbon of carbon dioxide)
dioxide production in the body respiratory failure
cells
1. Airway obstruction
2. Restrictive lung disease Clinical Manifestations:
3. Central nervous system disorder
(head trauma, stroke) a. Dyspnea
4. Drug overdose b. Tachypnea
5. Anesthesia and surgical c. Tachycardia
procedures d. Headache
e. Cyanosis
Hypoxemia- low blood oxygen; f. Anxiety, confusion, restlessness
indicates oxygenation failure g. Decreases, absent breath sounds
h. Adventitious breath sounds
4 major physiologic events:
Hypoxemia
1. V/Q mismatch
a. Paradoxical breathing- chest and
Ventilation (amount of gas
abdomen expands during
that reaches the alveoli)
exhalation
and Perfusion (amount of
b. Retractions
blood perfusing the lungs)
c. Cyanosis (late)
Ventilation problems: d. Prolonged expiration (trying to
Pneumonia, asthma, excrete excess carbon dioxide)
COPD, pain e. Nasal flaring
f. Tachypnea
Perfusion problems:
pulmonary embolism, Hypercapnia
decreased cardiac output
a. Pursed lip breathing
2. Shunting b. Rapid, shallow breathing
V/Q mismatch!!! c. Tripod positioning
Acute Respiratory Distress
Syndrome, septal defects
of the heart Acute Respiratory Distress
Syndrome (ARDS)
3. Diffusion Limitation
- Clinical syndrome characterized
Alveolar membranes by pulmonary edema and
thickened, hypoxemia progressive decrease in arterial
oxygen
 - Occurs after a serious illness or Pulmonary Embolism
injury and accumulation of lung
- Obstruction of one or more
fluids (noncardiogenic pulmonary
pulmonary arteries by a thrombus
edema)
or thrombi
Causes:
Causes:
 Aspiration
 Prolonged immobility
 Drug overdose
 Heart failure
 Prolonged inhalation of high
 Thrombophlebitis
concentrations of oxygen, smoke,
 Hematologic disorders
or corrosive substances
 Shock  Lower extremity fractures or
surgery
 Trauma
 Pregnancy or hormonal
 Systemic infection
contraceptive use
Manifestations (usually occur 12- 48 
hours after injury or illness)
 Decreased LOC
 Dyspnea
 Tachypnea
 Auscultated crackles
 Severe hypoxia
 Marked buccal peripheral
cyanosis
 Hypocapnia
Lab:
 Chest radiograph
 ABG studies
Nursing management:
 Medications (corticosteroids)
 Maintain adequate airway
 Monitor for signs and symptoms
of fluid volume overload
(peripheral edema and jugular
vein distention)
 Decrease carbohydrate intake
(which metabolize to form excess
CO2)