Gastric Disorders (Dyspeptic Diseases)

Anatomy of the Stomach

J-shaped enlargement of the GI tract

Has four regions: cardia, fundus, body, and pyloric
part.
The gastric glands contain three types of exocrine
gland cells that secrete their products into the
stomach lumen.
1. Mucous neck
2. Chief cells
3. Parietal cells
 Their secretions form gastric juice, which totals
2000–3000 mL day
2
3
How parietal cell produce the acid?

4
Cont…d

5
6
 Gastritis

 Inflammation of the gastric or stomach mucosa is one

of the most common GI problems affecting the
stomach.
 Is the result of a breakdown in the normal gastric
barrier (mucosa), which normally protects the
stomach tissue from auto-digestion by acid.

7
 Types of Gastritis

A. Acute gastritis
B. Chronic gastritis
C. Type A (fundal)
D. Type B (antral)

8
9
 Etiology
Acute Chronic

Drugs: NSAIDs- inhibit Repeated episodes of acute

the synthesis of gastritis
prostaglandins, which Benign or malignant ulcers
results in increased acid of the stomach
secretion and can Bacteria H. pylori
directly irritate the
Dietary factors such as
gastric mucosa
caffeine
Alcohol
Radiation
Helicobacter pylori
10
 Etiology …
Staphylococcus organisms
Salmonella
Bile and pancreatic secretions
Physiology stress: shock,
sepsis, burns
Psychologic stress
Renal failure (uremia)
Spicy, irritating foods
Ingestion of strong acid or
alkali
Trauma: nasogastric suction,
large hiatal hernia, endoscopic
techniques
Use of medications,
especially excess
ingestion of NSAIDs
Chronic alcohol abuse
Smoking
Reflux of intestinal
contents into the
stomach
11
 Clinical Manifestation

Acute gastritis
Anorexia, nausea and vomiting, hiccupping,
epigastric tenderness, feeling of fullness, and
abdominal discomfort
Hemorrhage associated with alcohol abuse
Headache, lassitude
Usually self-limited lasting from a few hours to a few
days

12
 Clinical Manifestation
Chronic gastritis
 S/S are similar to that of acute gastritis including anorexia,
heartburn after eating, belching, a sour taste in the mouth, or
nausea and vomiting
 Anemia
Because of gastric lesions, the acid-secreting cells are lost or
do not function as a result of atrophy, the source of intrinsic
factor is also lost.
Intrinsic factor, which normally combines with VitB12, is
unavailable, and thus VitB12 can’t be reabsorbed in the ileum.
Intrinsic factor protects VitB12 from digestion by the GI
enzymes.
Depilation of VitB12, which is essential for the growth and
maturation of RBCs results in development of pernicious
anemia. 13
 Diagnosis

Endoscopic examination with biopsy

Complete blood count (CBC)
Stool exam for occult blood
Serologic testing for antibodies against the H. pylori
antigen

14
 Management
• The gastric mucosa is capable of repairing itself after a
bout of gastritis, in about 1 day, although the appetite may
be diminished for an additional 2 or 3 days.
Acute Gastritis
♠ Bed rest
♠ Instructing the patient to refrain from alcohol and food
until symptoms subside
♠ Parentral fluid—if symptoms persist
♠ If gastritis is caused by ingestion of strong acids
neutralizing with anti-acids like aluminum hydroxide and
if caused by strong alkalis neutralizing with diluted lemon
juice or diluted vinegar
15
 Management …

♠ Antiemetis for nausea and vomiting

♠ Antiacids or H2 antagonists
♠ Blood transfusion and fluid replacement if gastritis is
hemorrhage
♠ In extreme cases, emergency surgery may be required
to remove gangrenous or perforated tissue.
Partial gastrectomy,
Vagotomy, or
Pyloroplasty
16
 Management …
Chronic Gastritis
Modifying the patient’s diet and lifestyles like
reducing stress
Promoting rest
Initiating pharmacotherapy
Antibiotics (e.g., tetracycline or amoxicillin,
combined with clarithromycin) to treat H. pylori
Proton pump inhibitor (e.g., omeprazole), and
possibly bismuth salts
Regular injections of VitB12—for patients with
pernicious anemia
17
 Nursing Management

Major Nursing Diagnoses

a. Imbalanced nutrition, less than body requirements,
related to inadequate intake of nutrients
b. Risk for imbalanced fluid volume related to
insufficient fluid intake and excessive fluid loss
subsequent to vomiting
c. Deficient knowledge about dietary management and
disease process
d. Acute pain related to irritated stomach mucosa

18
 Nursing Management …
Promoting optimal nutrition
Providing physical and emotional support to manage
the symptoms, including nausea, vomiting, heartburn,
and fatigue.
The patient should be NPO—possibly for days—
until the acute symptoms subside, thus allowing the
gastric mucosa to heal.
Discourages the intake of caffeinated beverages,
cigarette smoking and alcohol

19
 Nursing Management …
Promoting fluid balance
Daily fluid intake and output monitoring
If food and fluids are withheld, IV fluids (3 L/day)
usually are prescribed
Electrolyte monitoring
Be alert for any indicators of hemorrhagic gastritis,
which include hematemesis (vomiting of blood),
tachycardia, and hypotension

20
 Nursing Management …
Relieving pain
Instruct pt:
To avoid foods and beverages that may be
irritating to the gastric mucosa (described earlier)
About using medications to relieve chronic
gastritis
Patient education about dietary management and
disease process

21
Peptic Ulcer Disease (PUD)
Gastric and Duodenal Ulcers
 PUD
• A peptic ulcer is an excavation (hollowed-out area) that
forms in the mucosal wall of the stomach, in the pylorus
(opening between stomach and duodenum), in the
duodenum, or in the esophagus resulting from the
digestive action of HCl acid and pepsin.
• Occurs with the greatest frequency in people between the
ages of 40 and 60 years
• In the body of the stomach it can occur without excessive
acid secretion
• Ulcers are defined as breaks in the mucosal surface >5
mm in size, with depth to the sub-mucosa.

23
 Types of PUD …

Depending on the location of erosion

I. Gastric ulcer
II. Duodenal ulcer

24
25
 Cont…d

Path physiology of PUD

• GI mucosal ulceration occurs when there is
imbalance on the following two mechanisms
A. Increased level of mucosal aggressive factors
(Increased acid and pepsin production) OR
B. Inability of the mucosal barrier to resist the
destructive action of the gastric secretions
(enzymes & acids).

26
 Physiology of Gastric Secretion
HCl and pepsinogen are the two principal gastric
secretory products capable of inducing mucosal
injury.
Basal acid production occurs in a circadian pattern,
with highest levels occurring during the night and
lowest levels during the morning hours
The enzyme H+, K+-ATPase is responsible for
generating the large concentration of H+.
The chief cell, found primarily in the gastric fundus,
synthesizes and secretes pepsinogen, which will be
activated to pepsin within the acidic environment of
stomach (2 to 3 pH).
27
 Gastro-duodenal Mucosal Defense

• The gastric epithelium is under constant assault by a

series of endogenous noxious factors (like HCl,
pepsinogen/pepsin, and bile salts) exogenous
substances (like medications, alcohol, and bacteria
encounter the gastric mucosa).

28
 Mucosal Defense System

1. Pre-epithelial
• Mucus-bicarbonate layer, which serves as a
physicochemical barrier to multiple molecules,
including hydrogen ions
• Mucus primarily consists of water (95%) and a
mixture of lipids and glycoprotein (mucin),
which used to impede the diffusion of ions and
molecules such as pepsin.

29
 Mucosal Defense System …
2. Epithelial
• Prostaglandin- regulates the release of mucosal
bicarbonate and mucus, inhibits parietal cell
secretion, and is important in maintaining mucosal
blood flow and epithelial cell restitution
• Restitution- a process gastric epithelial cells
bordering a site of injury can migrate to restore a
damaged region as the pre-epithelial barrier were
breached
• Cell proliferation- GI tract has a very high cell
turnover rate, and the surface mucosa of the stomach
is renewed about every 3 days
30
 Mucosal Defense System …

3. Sub-epithelial Elements
• Elaborate micro-vascular system providing
• HCO3–neutralizes the acid generated by parietal cells
• An adequate supply of micronutrients and oxygen
while removing toxic metabolic by-products.

31
 Cont…d

Path physiology of PUD

• GI mucosal ulceration occurs when there is
imbalance on the following two mechanisms
A. Increased level of mucosal aggressive factors
(Increased acid and pepsin production) OR
B. Inability of the mucosal barrier to resist the
destructive action of the gastric secretions
(enzymes & acids).

32
 Cont…d
• Damaging/aggressive factors include Acid, pepsin,
duodenal reflux of bile, smoking, ethanol,NSAIDs,
steroids, ischemia, hypoxia, stress and most notably
H.pylori
• Protective/defensive factors are mucus, bicarbonate,
mucosal blood flow, prostaglandins, epithelial cell
renewal and growth factors
• When ever there is an imbalance occurs,
PUD will develops!!!

33
Balance of Aggressive and Defensive factors

34
 Cont…d

• Although the stomach contains acidic secretions

that can digest substances, intrinsic defenses
protect the gastricmucosal membrane from injury.
• A thick, tenacious layer of gastric mucus protects
the stomach from autodigestion, mechanical
trauma, and chemical trauma.
• Prostaglandins provide another line of defense.
• Gastric ulcers may be a result of destruction of
the mucosal barrier.
35
 Cont…d
• The duodenum is protected from ulceration by
the function of Brunner's glands.
• These glands produce a viscid, mucoid,
alkaline secretion that neutralizes the acid
chyme.
• Duodenal ulcers appear to result from
excessive acid production.

36
 Pathophysiology and Etiology cont…d
 Stress and anxiety
 H. pylori: Generate ammonia in the mucous layer, creating a
condition of chronic inflammation, which renders the mucosa
especially vulnerable to other noxious substances.

 Ulcerogenic drugs
– Aspirin and NSAID- inhibit the synthesis of mucus and
prostaglandins and cause abnormal permeability
– Corticosteroids- decrease the rate of mucous cell renewal
and thereby decrease its protective effects

37
 Pathophysiology and Etiology…

Excessive secretion of HCl in the stomach because of

the following conditions
Psychological stress and physiological stress (like in
case of burn, shock, surgery)
Ingestion of milk and caffeinated beverages
Smoking (also decreases pancreatic bicarbonate
secretion) and Alcohol
NB: The critical pathologic process in gastric ulcer
formation may not be the amount of acid that is
secreted but the amount that is able to penetrate the
mucosal barrier
38
 Pathophysiology and Etiology…

 Familial tendency-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
 Excessive amounts of the hormone gastrin, produced by
tumors, like in case of Zollinger-Ellison syndrome (ZES),
resulting in severe peptic ulcers, extreme gastric hyperacidity,
and excess gastrin secretion
 Gastroesophageal reflux disease [GERD]- resulting
esophageal ulcer
 Stress ulcer is the acute mucosal ulceration of the duodenal or
gastric area that occurs after physiologically stressful events,
such as burns, shock, severe sepsis, and multiple organ
traumas which may result in decreased gastric mucosal blood
flow and to reflux of duodenal contents into the stomach.
39
 Pathophysiology and Etiology…

Ingestion of hot, rough, or spicy foods

Acids, bile salts, aspirin, ischemia, H. pylori
Pregnancy appears to protect women from
developing ulcers.
– Estrogen and progesterone have a positive effect
on ulcer healing.
– Progesterone has also the effect of decreasing acid
secretion.

40
Disruption of gastric mucosa and pathophysiologic
consequences of back-flow of acids
 Acids, bile salts, aspirin, ischemia, H. pylori

Breakdown of gastric mucosal barrier

Acid back-diffusion into mucosa

Destruction of mucosal cells

Histamine release from
damaged mucosa
↑ Acid & Pepsin release

↑ Vasodilation
•Further mucosal erosion ↑Capillary permeability
•Destruction of blood vessels
•Bleeding •Loss of plasma proteins
into gastric lumen
•Mucosal edema
Ulceration 42
 Clinical Manifestations
Because gastric and duodenal mucosa do not have pain
sensory fibers, no pain or other symptoms.
However, as symptoms develop they may last for a few
days, weeks, or months and may disappear only to
reappear, often without an identifiable cause
Dull, gnawing pain or a burning sensation in the mid-
epigastrum or in the back
Pain of gastric ulcer origin:
Pain located high in the epigastrium
Occurs spontaneously about 1 to 2 hours after meals
Can be described as “burning” or “gaseous”

43
 Clinical Manifestations …
• Pain of duodenal ulcer origin
Pain described as “burning” or “cramping”
Most often located in the mid-epigastrum region
beneath the xyphoid process
Back pain—if ulcer is located on the posterior
aspect of the duodenum
Usually relieved by eating, because food
neutralizes the acid, or by taking alkali; however,
once the stomach has emptied or the alkali’s effect
has decreased, the pain returns

44
 Clinical Manifestations …

Sharply localized tenderness around the epigastrium

at or slightly to the right of the midline
Pyrosis (heartburn)
Vomiting (emesis often contains undigested food
eaten many hours earlier)
Constipation or diarrhea
Bleeding (evidenced by the passage of tarry stools)
Epigastric tenderness, or abdominal distention

45
 Complications
• The three major complications which are considered
as emergency are:
1. Hemorrhage
– Is the most common complication observed in
PUD
– Develops from erosion of the granulation tissue
found at the base of the ulcer during healing or
from erosion of the ulcer through a major blood
vessels

46
 Complications…
2. Perforation
The second most common ulcer-related complication
Commonly seen in large penetrating DUs that have not
healed
Occurs when the ulcer penetrates the serosal surface, with
spillage of either gastric or duodenal contents in to the
peritoneal cavity
S/S
Sudden, severe upper abdominal pain that quickly
spread throughout the abdomen
Shallow and rapid respiration
Bowel sounds are usually absent
Nausea and vomiting 47
 Complications…
3. Gastric outlet obstruction
Is the least common ulcer-related complication
A patient may have relative obstruction secondary to
ulcer-related inflammation and edema in the peripyloric
region. This process often resolves with ulcer healing.
S/S
Long history of ulcer pain
Pain
Short duration or complete absence of pain
Progresses to a more generalized upper abdominal
discomfort that becomes worse towards the end of
the day as the area filled and dilated
Relieved by belching or by self-induced vomiting 48
 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
Signs, Symptoms, and Clinical Findings
 Hypersecretion HCl  Normal—hyposecretion of HCl
 May have weight gain  Weight loss may occur
 Pain occurs 2–3 hours after a  Pain occurs 1⁄2 to 1 hour after a
meal meal
 Often awakened between 1–2  Rarely occurs at night
AM 49
Signs, Symptoms, and Clinical Findings … (Cont’d)
 Ingestion of food relieves pain  May be relieved by vomiting
 Vomiting uncommon  Ingestion of food does not help,
 Hemorrhage less likely than with sometimes increases pain
gastric ulcer  Vomiting common
 If present melena more common  Hemorrhage more likely to occur
than hematemesis than with duodena ulcer
 More likely to perforate than  Hematemesis more common than
gastric ulcers melena

Malignancy Possibility
 Rare  Occasionally
Risk Factors
 H. pylori, alcohol, smoking,  H. pylori, gastritis, alcohol,
cirrhosis, stress smoking, use of NSAIDs, stress
50
 Diagnosis
Fiberoptic endoscopy
Allows direct visualization of inflammatory changes,
ulcers, and lesions
Helps also to obtain a biopsy of the gastric mucosa
Upper GI barium-contrast study
Gastric secretory studies to:
Identify a possible gastrinoma (Zollinger-Ellison
Syndrome)
Determine the degree of gastric hyperacidity
Evaluate the results of therapy such as vagotomy and
H2-antagonist therapy

51
 Diagnosis …
CBC: determine anemia secondary to bleeding
Liver enzyme studies: to determine liver diseases
like cirrhosis that may complicate the treatment of the
ulcer
Urine and stool tests: for the presence of blood
Serologic test for antibodies to the H. pylori antigen

52
 Management
Aim of the treatment
i. To decrease the amount of gastric acidity
ii. To enhance mucosal defense mechanisms
iii. To minimize the harmful effects on the mucosa
Conservative mgt/minimum medical treatments
Adequate rest
Dietary interventions
Medications
Elimination of smoking
Long-term follow-up care

53
 Management …
Lifestyle Modifications
Adequate rest, both physical and emotional
A quite, calm environment at home or on the job
Elimination of stress helps to decrease the stimulus
for overproduction of gastric secretion
Moderate in daily activity –because excessive
physical activity can result in increased gastric
secretions through increased motor activity

54
 Nutritional Management
Avoiding foods and beverages irritating to the patient
Food known to irritate gastric mucosa include hot,
spicy foods and pepper; alcohol; carbonated
beverages; tea; and coffee
Foods high in roughage, such as raw fruits, salads,
and vegetables may irritate an inflamed mucosa
Proteins – is best neutralizing food, but also
stimulates HCl secretion
Carbohydrates and fats – the least to stimulate HCl
secretion, but they don’t neutralize well

55
 Nutritional Management …
Milk: milk proteins and calcium are stimulant to
gastric acid production, however, milk can neutralize
gastric acidity and contains prostaglandins and
growth factors, both of which known to protect the GI
mucosa from injury.
Generally:
No specific diet seems totally appropriate in the
treatment of ulcer disease
Each patient should be instructed to eat and drink
foods and fluids that do not cause and distressing
or harmful side effects

56
 Pharmacologic Therapy
1. Neutralizing agents – Antiacids
☺Initial drugs of choice in the treatment of PUD
☺Decrease gastric acidity and the acid content of
chyme reaching the duodenum
☺Block the conversion of pepesinogen to pepsin by
raising the pH to above 3.5
☺Some (like aluminum hydroxide) can bind to bile
salts and decreasing their effects on the gastric
mucosa
E.g. Aluminum hydroxide & magnesium trisilcates

57
 Pharmacologic Therapy …
2. Antisecretory
a. Histamine H2-receptor antagonists
• Inhibit the action of histamine at histamine H2 receptor
cells of the stomach, which then reduces the secretion of
gastric acid and reduces total pepsin output. The decrease
in acid allows the ulcerated areas to heal.
E.g. cimetidine, famotidine, nizatidine, ranitidine
b. Proton pump inhibitors (H+, K+, ATPase inhibitors)
• Suppress gastric acid secretion by inhibition of the
hydrogen-potassium adenosine triphosphatase (ATPase)
enzyme system at the secretory surface of the gastric
parietal cells.
• Block the last step of acid production
E.g. Omeprazole, Lansoprazole, Rabeprazole 58
 Pharmacologic Therapy …
3. Cytoprotective
A. Sucralfate
♠ Accelerate healing through covering the ulcer and
thereby protecting it from erosion caused by pepsin,
acid and bile salts
♠ Doesn’t have acid neutralizing effect
♠ Should be given at least 30 minutes before or after an
antiacid
B. Misoprostol
Is a synthetic prostaglandin; protects the gastric
mucosa from ulcerogenic agents; also increases
mucus production and bicarbonate levels

59
 Pharmacologic Therapy …
C. Bismuth subsalicylate
• Suppresses H. pylori bacteria in the gastric mucosa
and assists with healing of mucosal lesions
4. Antibiotics for H. Pylori
Tetracycline + proton pump inhibitor + bismuth salts
Amoxicillin + clarithromycin + proton pump
inhibitor
Metronidazole + clarithromycin + proton pump
inhibitor
Clarithromycin + proton pump inhibitor +
amoxicillin
60
 Surgical Management
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, or
obstruction, and
Those with ZES not responding to medications
Surgical interventions include:
A. Vagotomy: severing of the vagus nerve to decrease
gastric acid by diminishing cholinergic stimulation
to the parietal cells, and making them less
responsive to gastrin. It can be done with or without
pyloroplasty
61
 Surgical Management …
B. Pyloroplasty:
• Is a surgical procedure in which a longitudinal
incision is made into the pylorus and transversely
sutured closed to enlarge the outlet and relax the
muscle.
• Is an elective surgical procedure in which the lower
portion of the stomach, the pylorus, is cut and
resutured, to relax the muscle and widen the opening
into the intestine.

62
 Surgical Management …
C. Antrectomy
 Resection or surgical removal of antrum which is the
lower third of the stomach that lies between the
body of the stomach and the pyloric canal, which
empties into the first part of the small intestine.
 Antrum produces gastrin, which is a hormone that
stimulates the production of stomach acid
 Types:
Billroth I
Billroth II procedures

63
 Surgical Management …

C. Antrectomy …
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).

64
65
 Nursing Management
Based on assessment, the patients’ nursing diagnoses
may include:
Acute pain related to the effect of gastric acid
secretion on damaged tissue
Imbalanced nutrition, less than body requirement
related to changes in diet
Deficient knowledge about prevention of symptoms
and management of the condition

66
 Nursing Interventions
1. Relieving Pain
Patient education:
To take the prescribed drugs
To avoid aspirin, foods and beverages that contain
caffeine, and decaffeinated coffee,
To eat meals at regularly paced intervals in a relaxed
setting
Teaching relaxation techniques to help manage stress
and pain
Enhance smoking cessation efforts

67
 Nursing Interventions …
2. Maintaining Optimal Nutritional Status
Assesses the patient for malnutrition and weight loss
Advise the patient about the importance of complying
with the medication regimen and dietary restrictions
3. Teaching Patients Self-Care
Instruct the patient the factors that will help or
aggravate the condition
Give drug information
Avoiding foods that exacerbate symptoms as well as
substances that have acid-producing potential (e.g.,
alcohol; caffeinated beverages such as coffee, tea, and
colas) 68
 Nursing Interventions …
3. Teaching Patients Self-Care (Cont’d)….
Counsel the patient to eat meals at regular times and in a
relaxed setting, and to avoid Overeating
Inform the patient about the irritant effects of smoking on
the ulcer and cessation of smoking
Teach about the signs and symptoms of complications:
– Hemorrhage—cool skin, confusion, increased heart
rate, labored breathing, blood in stool
– Penetration and perforation—severe abdominal pain,
rigid and tender abdomen, vomiting, elevated
temperature, increased heart rate
– Pyloric obstruction—nausea and vomiting, distended
abdomen, abdominal pain 69
Thank You!!!

70