Gastrointestinal system

Gastrointestinal system
disorders
disorders
by:-Muhumed Hashi Aden.

1
Introduction: Gastrointestinal system (GIS), Structure

2
I. Functional structures, Different Organs & Accessories of the GI-
System

GI-Organs Accessories
1. Mouth
2. Pharynx 1. Salivary
3. Esophagus glands
4. Stomach 2. Pancreas
5. Small 3. Liver
intestine 4. Gallbladder
6. Large
intestine
7. Rectum
(Anus)
3
4
Parts of GIT

5
Brief Review of Anatomy & physiology of Gastro-intestinal Tract
Gastrointestinal Tract, the stomach and
intestines as they function to digest food and
provide its nutrients to the body
The gastrointestinal tract is subject to a
variety of disorders and diseases.
The stomach, located in the upper abdomen
just below the diaphragm, is a saclike
structure with strong, muscular walls

6
The stomach can expand significantly to store
all the food from a meal for both mechanical
and chemical processing.
The stomach contracts about three times per
minute, churning the food and mixing it with
gastric juice. This fluid, secreted by
thousands of gastric glands in the lining of
the stomach, consists of water, hydrochloric
acid, an enzyme called pepsin, and mucin (the
main component of mucus).

7
Hydrochloric acid creates the acidic
environment that pepsin needs to begin
breaking down proteins.
It also kills microorganisms that may have
been ingested in the food.
Mucin coats the stomach, protecting it
from the effects of the acid and pepsin.
About four hours or less after a meal, food
processed by the stomach, called chyme,
begins passing a little at a time through
the pyloric sphincter into the duodenum,
the first portion of the small intestine.
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During this time, the liver secretes bile into
the small intestine through the bile duct. Bile
breaks large fat globules into small droplets,
which enzymes in the small intestine can act
up on. Pancreatic juice, secreted by the
pancreas, enters the small intestine through
the pancreatic duct.
Pancreatic juice contains enzymes that break
down sugars and starches into simple sugars,
fats into fatty acids and glycerol, and proteins
into amino acids

9
 Small intestine

Most digestion, as well as absorption of

digested food, occurs in the small intestine.
This narrow, twisting tube, about 2.5 cm in
diameter, fills most of the lower abdomen,
extending about 6 m in length.

Over a period of three to six hours, peristalsis
moves chyme through the duodenum into the
next portion of the small intestine, the
jejunum, and finally into the ileum, the last
section of the small intestine
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Large intestine
Functions. It absorbs water—about 6 liters
daily
 as well as dissolved salts from the residue
passed on by the small intestine.
 In addition, bacteria in the large intestine
promote the breakdown of undigested
materials and make several vitamins, notably
vitamin K, which the body needs for blood
clotting.
 The large intestine moves its remaining
contents toward the rectum, which makes up
11
A watery residue of indigestible food and
digestive juices remains unabsorbed.
This residue leaves the ileum of the small
intestine and moves by peristalsis into the
large intestine, where it spends 12 to 24
hours.
The large intestine forms an inverted U
over the coils of the small intestine. It
starts on the lower right-hand side of the
body and ends on the lower left-hand side.
The large intestine is 1.5 to 1.8 m (5 to 6
ft) long and about 6 cm (2.5 in) in
diameter 12
The rectum :-
stores the feces—waste material that
consists largely of undigested food,
digestive juices, bacteria, and mucus—
until elimination.
Then, muscle contractions in the walls of
the rectum push the feces toward the
anus.
When sphincters between the rectum and
anus relax, the feces pass out of the body.

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 Dyspepsia: indigestion; upper abdominal
discomfort associated with eating
Definition of key terms

Elimination: phase of digestive process that

occurs after digestion and absorption, when
waste products are evacuated from the body
Esophagus: collapsible tube connecting the
mouth to the stomach, through which food
passes as it is ingested
Fibroscopy (gastrointestinal): intubation
of a part of the GI system with a flexible,
lighted tube to assist in diagnosis and
treatment of diseases of that area
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Hydrochloric acid: acid secreted by the glands
in the stomach; mixes with chyme to break it
down into absorbable molecules and to aid in the
destruction of bacteria
Ingestion: phase of the digestive process that
occurs when food is taken into the GI tract via the
mouth and esophagus
Intrinsic factor: a gastric secretion that
combines with vitamin B12 so that the vitamin
can be absorbed
Large intestine: the portion of the GI tract into
which waste material from the small intestine
passes as absorption continues and elimination
begins; consists of several parts—ascending
segment, transverse segment, descending
segment, sigmoid colon, and rectum 15
Lipase: an enzyme that aids in the digestion of fats
Pepsin: a gastric enzyme that is important in protein
digestion
Small intestine: longest portion of the GI tract,
consisting of three parts—duodenum, jejunum, and
ileum—through which food mixed with all secretions
and enzymes passes as it continues to be digested
and begins to be absorbed into the bloodstream
Stomach: distensible pouch into which the food
bolus passes to be digested by gastric enzymes
Trypsin: enzyme that aids in the digestion of protein
Absorption: phase of the digestive process that
occurs when small molecules, vitamins, and minerals
pass through the walls of the small and large
intestine and into the bloodstream

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Achalasia: absence of peristalsis of the lower
esophagus resulting in difficulty swallowing,
regurgitation, and sometimes pain
Amylase: an enzyme that aids in the digestion of
starch
Anus: last section of the GI tract; outlet for waste
products from the system
Chyme: mixture of food with saliva, salivary enzymes,
and gastric secretions that is produced as the food
passes through the mouth, esophagus, and stomach
Digestion: phase of the digestive process that occurs
when digestive enzymes and secretions mix with
ingested food and when proteins, fats, and sugars are
broken down into their component smaller molecules

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Patients with gastrointestinal disorders may
present with a variety of symptoms that are
specific to the gastrointestinal tract and/or
general systemic symptoms. Disorders of the
gastrointestinal tract also give a variety of
signs

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Common symptoms include:
Abdominal pain, abdominal distension
Dyspepsia
Diarrhea or constipation
Gastrointestinal bleeding
Jaundice
Change in weight and change in appetite
Nausea and vomiting
Change in stool color
During history taking, detailed analysis of the
above symptoms should be done

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 Assessment
History and Physical examination
begins by taking a complete history, focusing on
symptoms common to GI dysfunction. These
symptoms include :
Pain
Indigestion
 Intestinal gas
 Nausea and vomiting
Hematemesis
 Changes in bowel habits and stool
characteristics

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Cont…

Information about any previous GI disease is

important
 Notes past and current medication use and any
previous treatment or surgery
Information pertaining to medications is of
particular interest because medications are a
frequent cause of GI symptoms
A dietary history to assess nutritional status
Questioning about the use of tobacco and alcohol
includes details about type and amount
Changes in appetite or eating patterns and any
examples of unexplained weight gain or loss over
the past year
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Cont…
Pain: Pain can be a major symptom of GI disease

The character,
 duration,
 pattern,
 frequency,
location,
 distribution of referred pain,
time of the pain vary greatly depending on the
underlying cause

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Cont’d

Indigestion/ Dyspepsia Upper abdominal discomfort

or distress associated with eating (commonly called
indigestion) is the most common symptom of
patients with GI dysfunction
The basis for this abdominal distress may be the
patient’s own gastric peristaltic movements
 Bowel movements may or may not relieve the pain
Indigestion can result from disturbed nervous
system control of the stomach or from a disorder in
the GI tract or else where in the body
Fatty foods tend to cause the most discomfort,
because they remain in the stomach longer than
proteins or carbohydrates do

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Cont…

Intestinal Gas: The accumulation of gas in the

GI tract may result in belching (the expulsion of
gas from the stomach through the mouth) or
flatulence (the expulsion of gas from the rectum)

 Usually, gases in the small intestine pass into the

colon and are released as flatus

 Patients often complain of bloating, distention,

or being “full of gas.”

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Cont…
Nausea and Vomiting: Vomiting is another major
symptom of GI disease
 Vomiting is usually preceded by nausea, which
can be triggered by odors, activity, or food intake
 The emesis, or vomit us, may vary in color and
content
 It may contain undigested food particles or blood
(hematemesis)
 When vomiting occurs soon after hemorrhage,
the emesis is bright red
 If blood has been retained in the stomach, it
takes on a coffee-ground appearance because of
the action of the digestive enzymes

25
The causes of nausea and vomiting are
many:-
Dys-motility
peritoneal irritation
infections
hepatobiliary or pancreatic disorders
mechanical obstruction);
increased intracranial pressure
systemic disorders, and
antitumor chemotherapy medications.

26
.Change in bowel habits and stool
characteristics: Changes in bowel habits may
signal colon disease
 Diarrhea (an abnormal increase in the frequency
and liquidity of the stool or in daily stool weight
or volume) commonly occurs when the contents
move so rapidly through the intestine and colon
that there is inadequate time for the GI
secretions to be absorbed
 Diarrhea is sometimes associated with
abdominal pain or cramping and nausea or
vomiting
 Constipation (a decrease in the frequency of
stool, or stools that are hard, dry, and of smaller
volume than normal) may be associated with anal
discomfort and rectal bleeding 27
 Physical examination
The physical examination includes
assessment of the mouth, abdomen, and
rectum
The mouth, tongue, buccal mucosa, teeth,
and gums are inspected, and ulcers,
nodules, swelling, discoloration, and
inflammation are noted
The patient lies supine with knees flexed
slightly for inspection, auscultation,
palpation, and percussion of the abdomen
 The nurse performs inspection first,
noting skin changes and scars from
previous surgery 28
Cont…
It also is important to note the contour and
symmetry of the abdomen, to identify any
localized bulging, distention, or peristaltic waves

The nurse performs auscultation before

percussion and palpation (which can increase
intestinal motility and thereby change bowel
sounds) and notes the character, location, and
frequency of bowel sounds

The nurse assesses bowel sounds in all four

quadrants using the stethoscope

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Cont…
Document the frequency of the sounds, using the terms:
 normal (sounds heard about every 5 to 20 seconds),
hypoactive (one or two sounds in 2 minutes),
 hyperactive (5 to 6 sounds heard in less than 30
seconds),
absent (no sounds in 3 to 5 minutes)
Notes tympany or dullness during percussion
Use of light palpation is appropriate for identifying
areas of tenderness or swelling;
Deep palpation to identify masses in any of the four
quadrant
If the patient identifies any area of discomfort, the
nurse can assess for rebound tenderness

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 STOOL TESTS
.

Basic examination of the stool includes inspecting

the specimen for consistency and color and
testing for occult (not visible) blood.
Special tests, including tests for fecal
urobilinogen, fat
Parasite
Virus
Bacteria
Poor absorption

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32
 Gastro-esophageal Reflux Disease

Some degree of gastro esophageal reflux (back-

flow of gastric or duodenal contents into the
esophagus) is normal in both adults and children

 Excessive reflux may occur because of an

incompetent lower esophageal sphincter, pyloric
stenosis, or a motility disorder.

The incidence of reflux seems to increase with

aging

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Cont’d
Clinical Manifestations
 Pyrosis (burning sensation in the esophagus),
 dyspepsia (indigestion),
 regurgitation,
 dysphagia or odynophagia (pain on swallowing),
hypersalivation, and esophagitis
 The symptoms may mimic those of a heart attack.
The patient's history aids in obtaining an accurate
diagnosis.
Assessment and Diagnostic Findings
Endoscopy
Ambulatory 12- to 36-hour esophageal pH
monitoring is used to evaluate the degree of acid
reflux
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 Management
Teach the patient to avoid situations that
decrease lower esophageal sphincter
pressure or cause esophageal irritation.
The patient is instructed to eat a low-fat
diet; to avoid caffeine, tobacco, beer, milk,
foods containing peppermint or spearmint,
and carbonated beverages;
To maintain normal body weight;
To elevate the head of the bed on 6- to 8-
inch (15- to 20-cm) blocks; and to elevate
the upper body on pillows.
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Antacids- 1 to 2 hrs after meals and at bed time
Metoclopramide
If reflux persists, the patient may be given
antacids or H2 receptor antagonists, such as
famotidine, nizatidine, or ranitidine.
 Proton pump inhibitors (medications that
decrease the release of gastric acid, such as
lansoprazole, rabeprazole , omeprazole
If medical management is unsuccessful, surgical
intervention may be necessary.

36
 Candida species are normal commensals in the
CANDIDA ESOPHAGITIS

throat but become pathogenic and produce

esophagitis in immunodeficiency states
 Candida esophagitis can occur without any
predisposing factors
Patients may be asymptomatic or complain of
odynophagia and dysphagia
 Oral thrush or other evidence of mucocutaneous
candidiasis may be absent
 Rarely, Candida esophagitis is complicated by
esophageal bleeding, perforation, and stricture or
by systemic invasion

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Cont.
Cause
Candida albicans
Diagnosis
Diagnosis is made by demonstration of yeast or
hyphal forms in plaque smears and exudate stained
with periodic acid–Schiff or Gomori silver stains
Histologic examination is often negative
Culture is not useful in diagnosis
Treatment
Empirical therapy with fluconazole for 7 days is
appropriate for suspected cases. Oral fluconazole
(200 mg on the first day, followed by 100 mg daily)
is the preferred treatment

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Gastriti
s
39
Gastritis

Gastritis (inflammation of the gastric or stomach

mucosa) is a common GI problem
 Is an inflammation of the gastric or stomach
mucosa
 Is the result of a breakdown in the normal gastric
barrier (mucosa), which normally protects the
stomach tissue from auto-digestion by acid

40
Types / Gastritis may be:
1.Acute Gastritis
2.Chronic Gastritis
Acute, lasting several hours to a few days,
Chronic, resulting from repeated exposure
to irritating agents or recurring episodes of
acute gastritis

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 Etiology --Acute Gastritis
o Drugs: • Physiologic stress:
shock, sepsis, burns
o Overuse of
NSAIDs • Psychologic stress

o Alcohol • irritating foods

o Radiation • Ingestion of strong

acid or alkali
o Helicobacter pylori
• Trauma: naso-gastric
o Staphylococcus suction, large hiatal
organisms hernia, endoscopic
o Bile and pancreatic techniques
secretions
42
Acute gastritis ……..
Dietary indiscretion—the person eats food that is
contaminated with disease-causing
microorganisms or that is irritating or too highly
seasoned
Other causes of acute gastritis include
Bile reflux, and radiation therapy
 A more severe form of acute gastritis is caused
by the ingestion of strong acid or alkali, which
may cause the mucosa to become gangrenous or
to perforate ,Scarring can occur, resulting in
pyloric obstruction

43
 Chronic gastritis
: prolonged inflammation of the stomach
 May result from repeated episodes of acute gastritis
 Benign or malignant ulcers of the stomach
Bacteria Helicobacter pylori
 Chronic gastritis is sometimes associated with
autoimmune diseases such as pernicious
anemia
Dietary factors such as caffeine
The use of medications, especially NSAIDs
Alcohol; smoking
 Reflux of intestinal contents into the stomach

44
Pathophysiology
Gastritis the result of a breakdown in the normal
mucosal barrier
A mucousal barrier normally protects the
stomach tissue from auto digestion by acid
When the barrier broken, acid can dissfuse back
in to the mucosa
This allows hydrochloric acid (HCI) to enter and
there by increase the secretion of pepisinogen
and the release of histamine from mast cells
The combined result of these occurrence is tissue
edema, loss of plasma in to gastric lumen with
disruption of capillary walls, and possible
hemorrhage

45
Cont…

In gastritis, the gastric mucous membrane

becomes edematous and hyperemic (congested
with fluid and blood) and undergoes superficial
erosion

It secretes a scanty amount of gastric juice,

containing very little acid but much mucus.

Superficial ulceration may occur and can lead to

hemorrhage

46
47
 Clinical Manifestation
Acute gastritis
 Anorexia, nausea and vomiting, hiccupping,
 Epigastric tenderness
 Feeling of fullness and abdominal
discomfort
 Hemorrhage associated with alcohol abuse
 Headache,
 fatigue
 Usually self-limited lasting from a few
hours to a few days
48
Chronic gastritis
anorexia, heartburn after eating
belching, a sour taste in the mouth, or
nausea and vomiting
 S/S are similar to that of acute gastritis

 Anemia because of atrophy of cells

producing intrinsic factor

49
Assessment and Diagnostic Findings
Diagnosis can be determined
Endoscopy,
 Upper GI radiographic studies
Histologic examination of a tissue
specimen obtained by biopsy
Complete blood count (CBC)
Stool exam for occult blood
For detecting H. pylori:
serologic testing for antibodies against
the H. pylori antigen

50
Medical Management
Acute gastritis

Instructing the patient to refrain from alcohol

and food until symptoms subside

After the patient can take nourishment by mouth,

a non-irritating diet is recommended

If the symptoms persist, fluids may need to be

administered parenterally

If bleeding is present, blood transfusion and fluid

replacement
51
 Management of Acute Gastritis
Antiemetis for nausea and vomiting
Antiacids
H2 antagonists
Blood transfusion and fluid replacement
if gastritis is hemorrhage
Emergency surgery:
 Partial Gastrectomy
 Vagotomy

52
Cont…

 If corrosion is extensive or severe, emetics and

lavage are avoided because of the danger of
perforation and damage to the esophagus

53
Cont.

Chronic gastritis
Focuses on evaluating and eliminating the
specific causes
Chronic gastritis is managed by modifying the
patient’s diet,
Promoting rest
Reducing stress
Initiating pharmacotherapy
Regular injection of vitamine B 12 are needed for
patients with pernicious anemia

54
Triple Rx for H. Pylori

Amoxicillin + PPI + Clarithromycin

TTC + PPI + Clarithromycin
Metronidazole + PPI + Clarithromycin

55
Peptic Ulcer Disease(PUD)
Gastric and Duodenal
Ulcers

56
Gastric and Duodenal Ulcers / PUD
A peptic ulcer is an excavation (hollowed-
out area) that forms in
1. the mucosal wall of the stomach
2. the pylorus (opening between stomach
and duodenum)
3. the duodenum (first part of small
intestine)
4. the esophagus

57
Ulcers are defined as breaks in the mucosal
surface >5 mm in size, with depth to the
submucosa
 A peptic ulcer is frequently referred to as a
gastric, duodenal, or esophageal ulcer,
depending on its location, or as peptic ulcer
disease
 Erosion of a circumscribed area of mucous
membrane is the cause
 This erosion may extend as deeply as the muscle
layers or through the muscle to the peritoneum

58
Cont’d

Peptic ulcers are more likely to be in the

duodenum than in the stomach

Peptic ulcer disease (PUD) causes inflammatory

injuries in either the gastric or duodenal mucosa,
with extension beyond the submucosa into the
muscularis mucosa

59
Damage of gastric mucosa from irritants

60
Causes
Infection with the gram-negative bacteria H. pylori
excessive secretion of HCl in the stomach may
contribute to the formation of gastric ulcers
stress may be associated with its increased secretion
The ingestion of caffeinated beverages, smoking,
and alcohol also may increase HCl secretion
Familial tendency may be a significant predisposing
factor
 A further genetic link is noted in the finding that
people with blood type O are more susceptible to
peptic ulcers than are those with blood type A, B, or
AB
Other predisposing factors associated with peptic
ulcer include chronic use of NSAIDs,

61
Cont.
Three major causes of peptic ulcer disease are now
recognized:

1. NSAIDs
2. Chronic H pylori infection
3. Acid hypersecretory states

62
63
The end results of H. pylori infection are:-

ο Gastritis
ο peptic ulcer diseases
ο Gastric cancer

64
Pathophysiology
The main cause of peptic ulcer is an imbalance
between gastric acidity and the strength of mucosal
barrier against auto digestion
This imbalance result from;
1. Exposure of the mucosal lining to excessive gastric
secretion
 Gastroesophgeal reflux: this expose the lowest part
of the esophagus to relatively high acidity of the
stomach
 Gastric hypersecretion: excessive HCL secretion and
pepsin overcomes the barrier against auto digestion
 Rapid emptying of gastric contents in to duodenum:
this occurs due to failure of enerogastric control
mechanisms to limit the rate of gastric emptying.
The duodenum mucosa will be exposed to big shots
of gastric HCI- duodenal ulceration
65
Cont.
2. Disruption of mucosal barrier against auto
digestion
 Diminished secretion of mucous as in anxiety and
nervous tension

 Failure of secretin hormone to stimulate enough

alkaline pancreatic or bile secretion to neutralize
gastric juice as it enters the duodenum
3. The role of NSAIDS:
 Inhibition of gastric mucosal prostaglandin synthesis
 These drugs inhibit prostaglandin synthesis, which
maintains gastro- duodenal mucosal integrity and
repair
 Gastric prostaglandin production appears to sustain
mucus production

66
Peptic ulcers occur mainly in the gastroduodenal
mucosa because this tissue cannot withstand the
digestive action of gastric acid (HCl) and pepsin

The erosion is caused by the increased

concentration or activity of acid-pepsin, or by
decreased resistance of the mucosa

 A damaged mucosa cannot secrete enough

mucus to act as a barrier against HCl

67
Pathophysiology
Acids, bile salts, aspirin, ischemia, H. pylori

Breakdown of gastric mucosal barrier

Acid back-diffusion into mucosa

Histamine release
Destruction of mucosal cells from damaged
mucosa

 Acid & Pepsin release

 Vasodilation
 Capillary
Further mucosal erosion permeability
Destruction of B/Vs
Bleeding
 Loss of plasma
proteins into gastric
ULCERATIO lumen
 Mucosal edema
N 68
Cont.

Mucosa defense
 Mucus
 Blood flow
 Bicarbonate secreted by gastric neutralize the acid
 Cellular tight junction

Aggressors
 Increased vagal nerve stimulation from variety
causes(emotion) hyper secretion of HCI and pepsin
 Bile salts

N.B. If imbalance occur between mucosal defense

and aggressors, there will be disruption of
mucosal layer

69
 Duodenal vs Gastric Ulcers

Duodenal Ulcer Gastric Ulcer

•Lesion
• Superficial; smooth margins; • Penetrating
round, oval, or cone shaped
•Incidence
• Age 30–60 • Usually 50 and over
• Male: female 2–3:1 • Male: female 1:1
• 80% of peptic ulcers • 15% of peptic ulcers
•Risk Factors
• H. pylori, alcohol, smoking, • H. pylori, gastritis, alcohol,
stress smoking, use of NSAIDs, stress 70
 GUs Vs DUs Cont’d…
Duodenal Ulcer Gastric Ulcer
•Signs, Symptoms, and Clinical Findings
• Hypersecretion of HCl • Normal—hyposecretion of HCl
• May have weight gain • Weight loss may occur
• Pain occurs 2-3 hrs after a meal • Pain 1⁄2 -1 hr after a meal
• Often awakened b/n 1-2 AM • Rarely occurs at night
• Ingestion of food relieves pain • May be relieved by vomiting
• Ingestion of food does not help
• Vomiting is uncommon • Vomiting common
• Hemorrhage less likely • Hemorrhage more likely
• Melena more common than • Hematemesis more common
hematemesis than melena
• More likely to perforate

•Malignancy Possibility
• Rare • Occasionally 71
Assessment and Diagnostic Findings
A physical examination may reveal pain, epigastric
tenderness, or abdominal distention
 A barium study of the upper GI tract may show an
ulcer; however, endoscopy is the preferred
diagnostic procedure because it allows direct
visualization of inflammatory changes, ulcers, and
lesions
Through endoscopy, a biopsy of the gastric mucosa
and of any suspicious lesions can be obtained
 Endoscopy may reveal lesions that are not evident
on x-ray studies because of their size or location
H. pylori infection may be determined by biopsy
and histology with culture

72
Medical Management
The goals are to eradicate H. pylori and to
manage gastric acidity

Methods used include:

 Medications
 lifestyle changes
Surgical intervention

73
1. PHARMACOLOGIC THERAPY
 Currently, the most commonly used therapy in the
treatment of ulcers is a combination of antibiotics, proton
pump inhibitors, and bismuth salts that suppresses or
eradicates H. pylori

 Recommended therapy for 10 to 14 days includes triple

therapy with two antibiotics (eg, metronidazole or
amoxicillin and clarithromycin ]) plus a proton pump
inhibitor (eg, lansoprazole or omeprazole ), or

 Quadruple therapy with two antibiotics (metronidazole

and tetracycline) plus a proton pump inhibitor and
bismuth salts

 Histamine 2 (H2) receptor antagonists and proton pump

inhibitors are used to treat NSAID-induced and other
ulcers not associated with H. pylori ulcers. 74
 Pharmacologic Mgt Cont’d…
Antibiotics for H. pylori
Amoxicillin + clarithromycin + proton
pump inhibitor
Tetracycline + proton pump inhibitor +
bismuth salts
Metronidazole + clarithromycin + proton
pump inhibitor

75
PUD Rx-- DACA-Ethiopia
I. PUD only
• First Line
• Ranitidine
• 150 mg P.O. BID OR 300 mg at bedtime for 4-6 weeks
• Maintenance therapy: 150 mg at bedtime.
• Alternatives
• Cimetidine
• 400 mg P.O. BID, with breakfast and at night, OR
• 800 mg at night for 4 - 6 weeks

OR
• Famotidine, 40 mg, P.O. at night for 4-6 weeks
OR
• Omeprazole
• 20 mg P.O. QD for 4 weeks (DU) or 8 weeks (GU)
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 Pharmacologic Mgt Cont’d…
II. PUD associated with H. pylori
First Line
Amoxicillin, 1g, P.O. BID
PLUS
Clarithromycin, 500mg P.O. BID
PLUS
Omeprazole, 20mg P.O. BID (OR 40mg QD)
 All for 7 - 14 days
Alternative
Amoxicillin, 1g, P.O. BID
PLUS
Metronidazole, 500mg, P.O. BID
PLUS
Omeprazole, 20mg P.O. BID OR 40mg QD for
7-14 days
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Cont’d
Initial Helicobacter pylori therapy
First-line therapy:
PPI twice a day plus clarithromycin 500 mg twice a
day plus amoxicillin 1000 mg twice a day or
metronidazole 500 mg twice a day for 10-14 days
Second-line therapy:
Pepto-Bismol 2 tabs four times a day plus tetra cycline
250 mg four times a day plus metron idazole 250 mg
four times a day (optional: add PPI daily) for 14 days
Therapy for retreatment of H. pylori therapy
failure
Repeat first-line therapy, substitute metronidazole for
amoxicillin (or vice versa) for 14 days; may add Pepto-
Bismol.
Add second-line H. pylori therapy.
78
Cont.

The patient is advised to adhere to the

medication regimen to ensure complete healing
of the ulcer
 Because most patients become symptom-free
within a week, it becomes a nursing responsibility
to stress the importance of following the
prescribed regimen so that the healing process
can continue uninterrupted and the return of
chronic ulcer symptoms can be prevented
Maintenance dosages of H2 receptor antagonists
are usually recommended for 1 year

79
Cont.
1. Drugs which neutralize the excess released
gastric acid (antacid)

2. Drugs which can inhabit gastric acid secretion

(H2 blocker, anticholnergic, proton pump
inhibitors, prostaglandins, sedatives and dietary
fats)

3. Cytoprotective agents which can enhance

secretion of the protective mucin

4. Antibiotics to destroy the causative organism

80
 2. Lifestyle modification
Stress Reduction and Rest
Reducing environmental stress requires physical
and psychological modifications on the patient's
part as well as the aid and cooperation of family
members and significant others
Smoking Cessation
Studies have shown that smoking decreases the
secretion of bicarbonate from the pancreas into
the duodenum, resulting in increased acidity of
the duodenum.
Research indicates that continued smoking may
significantly inhibit ulcer repair . Therefore, the
patient is strongly encouraged to stop smoking.
81
Cont’d

Dietary Modification
The intent of dietary modification for patients
with peptic ulcers is to avoid over secretion of
acid and hyper motility in the GI tract.
These can be minimized by
 avoiding extremes of temperature of food and
beverage and overstimulation from consumption
of meat extracts,
alcohol, coffee (including decaffeinated coffee,
which also stimulates acid secretion)
other caffeinated beverages (which stimulate acid
secretion)

82
 3. Surgery
Surgery is usually recommended:
for patients with intractable ulcers (those that
fail to heal after 12 to 16 weeks of medical
treatment)
Life-threatening hemorrhage
Perforation
Obstruction
Surgical procedures include :
Vagotomy, with or without pyloroplasty
 Billroth I
 Billroth II procedures

83
84
Vagotomy: Severing of the vagus nerve
 Decreases gastric acid by diminishing cholinergic
stimulation to the parietal cells, making them less
responsive to gastrin
May be done via open surgical
approach,laparoscopy
Billroth I (Gastroduodenostomy)
Removal of the lower portion of the antrum of the
stomach (which contains the cells that secrete
gastrin) as well as a small portion of the duodenum
and pylorus

The remaining segment is anastomosed to the

duodenum (Billroth I) or to the jejunum (Billroth II)

85
86
87
Potential complications

 Hemorrhage

 Perforation

 Penetration

 Pyloric obstruction (gastric outlet obstruction)

88