Diseases of the stomach:-

Objectives
1. Normal gastric physiology.
2. Why a normal person does n't autolyze his stomach?
3. Types of gastritis
4. A medical student had a history of epigastric pain one day before the
exam, what are the causes?
Gastric emptying:-
a. When food enters the proximal stomach, a vagally mediated
inhibition of fundic tone (receptive relaxation) permits storage
of food with out arises in intra gastric pressure.
b. Liquid dispersed through out the stomach in rapid fashion and
then emptied primarily by low level tonic contraction.
c. Solids:-after an initial period in the proximal stomach (30
min), solid are re distributed to the antrum, where they are
mixed by segmental contraction. These contractions occur up
to three times per min. and originate in a pacemaker situated in
the mid body along the great curvature.
d. The pyloric valve allows particles less than one mm to pass
through by wave contraction, while non digestive particles
pass by inter digestive migrating motor complex. This
contraction occur every 90-120 min in fasting.
Gastric secretion:-
From body and fundus of the stomach: -
1. Parietal cells --- HCL
2. Chief cells -pepsinogen.

From antrum of the stomach ---chief cells –gastrin.

Gastric wall mast cell in close proximity of chief cells—histamine.
Acid secretion in resting unfed stomach does not correlate with serum
gastrin concentration and is primarily related to vagal tone and presence of
H.Pylori infection.
Basal secretion of acid average is one to two meq \hour.
Maximal acid secretion. Is 50 meq\hour.

Normal mucosal defense:-

To protect the mucus from acid gastric juice.
a. a thin coat of mucus is formed continuously
b. Sodium bicarbonate is secreted from surface epith. Cells to
neutralize HCL. Secretion occurs in response to Ph less than 3.
c. Epithelial cell are continuously shed and rebleed.
d. Prostaglandins stimulate mucus and bicarbonate. Secretion is
protected and maintains blood flow during period of protection.
Prostaglandin is decreasing with ageing with ingestion of NSAID.

Erosive and hemorrhagic gastritis:-

Essentials of diagnosis:-
1. Most commonly seen in alcoholic in west and in NSAIDS in
east.
2. Often asymptomatic, may cause epigastric pain, nausea and
vomiting.
3. May cause hematemesis, usually not significant.

Clinical considerations:-
The most common cause is NSAIDS ingestion and alcohol intake; stress
due to medical and serious surgical causes is another cause (stress gastritis).
Uncommon causes as radiation and caustic ingestion.
Endoscopic finding:-
Including sub epithelial hemorrhage, petechae, erosion, they very in
size and number may be focal or diffuse.
Symptoms and signs:-
Usually asymptomatic, may present with anorexia epigastric pain, nausea
and vomiting, there is a poor correlation between severity of endoscopic
findings .it may present commonly with upper GIT bleeding rarely give
hemodynamic instability.

Pathology:
 Differential diagnosis:-

Epigastric pain may be due to:-

- peptic ulcer - food poisoning
- GERD - viral GE
- CA stomach - functional dyspepsia
- Biliary tract disease
In severe pain:-
- Perforated peptic ulcer or penetrating peptic ulcer.
- Pancreatic disease.
- Oesophageal rupture.
- Rupture aortic aneurysm
- Gastric valvulus
- Myocardial infarction.

In upper GIT bleeding:-

- Oesophageal varices.
- Mallory- Weiss tear.
- Arteriovenous malformation.
Specific causes and treatment:-

1. stress gastritis:-
Developed with in 18 hours in the majority of critically ill pt.
clinically important bleeding occurs in 2-3% rarely associated with
high mortality. Major risk factors including: - trauma, burn,
hypotension, sepsis, CNS injury, coagulopathy mechanical
respiration, hepatic and renal failure and multi organ failure.
Pharmacological prophylactic:-
Sucralfate or H2 receptor antagonist sucralfate suspension one gram
orally 4-6 hours
Cimetidine 900-1200, ranitidine 150mg by continuous iv infusion
over 24 hours.
Ph must be more than 4 that checked after four hours in critically ill pt
from N|G.
Treatment:-
- Continuous infusions of sucralfate +cimetidine.
- Endoscoptic therapy may be of benefit.
NSAIDS gastritis:-

Half of the pt. receiving NSAIDS have endoscopic finding, one

fourth has dyspepsia on chronic use to these drugs. the effect varies from
mild to severe ,it may occur immediately or little bite late ,it may be
associated with enteritis and colicky abdominal pain to severe dull epigastric
pain or upper GIT bleeding. NSAIDs varies in their effect some have a mild
effect others severe one and some of them are non selective in their work
that work on Cox 1 and Cox 2 receptors while others work on selective Cox
2 receptors.

Treatment:-
Symptoms may improve with discontinuation of the agent, reduction of the
dose to the lowest effective dose or administration with meals.
Endoscope indicated in persistent symptoms despite conservative measures
or pt at high risk for NSAID induced ulcer. The pt may need:-
Sucralfate one gram four times daily.
Cimetidine 400 mg twice daily
Ranitidine 150 mg twice daily.
Famotidine 20 mg twice daily
Proton pump inhibitor (PPI).

ALCOHOLIC GASTRITIS:
The pt may need therapy, with sucralfate or H2receptor antagonist for 4-6
weeks

Portal hypertensive gastropathy:-

Occurs usually with liver cirrhosis or portal hypertension, pt may present
with acute haematemesis,or chronic iron deficiency anemia.
Treatment with propranolol to decrease portal pressure, surgery if B-blocker
fails

Non erosive gastritis

This form of gastritis involves diffuse inflammation changes in the
mucosa. They are classified into:
1. fundal type (type A)
2. antral type (type B)
Fundal type (type A):-
The maximum inflammatory changes occur at the greater curvature in the
fundus and body with minimal or no inflammation in the antrum. Parietal
cells antibodies and intrinsic factor antibodies appear in most pt and
pernicious anemia may develop suggesting an immunological mechanism.
Hypo secretion of acid result from fundic gland atrophy(atrophic gastritis )
,with sparing of the antral secretion ,this will leads to hypergastrinemia as
the feedback inhibition of acid on gastrin release is lost .this may be a
normal process in few aged pt .it carries a risk for
1. Pernicious anemia
2. Gastric carcinoids
3. Adenocarcinoma

Endoscope of atrophic gastritis

Histopathology in patient with atrophic gastritis

Treatment;-
No specific therapy exists.

Antral gastritis:-
It is usually caused by H.pylori infection and leads to chronic infection.
The effect of H.pylori in the antrum may leads to:

1. peptic ulcer
2. H .pylori infection.

Specific type gastritis:-

1. Infection: - acute bacterial infection of gastric submucosa and
muscularis with variety of aerobic and anaerobic organism produces
a rare , rapidly progressive , life threatening condition known as
phlegmonous or necrotizing gastritis which requires emergency
gastric resection and antibiotic therapy.
 Viral infection with CMV in AIDS or fungal infection in
immunocopromised pt ,pt may has abdominal pain which may persist for
several days.
2. granulomatous gastritis :-
Chronic granulomatous dis as syphilis, TB, fugal infection, Crohn’s dis, it
may produce variety of symptoms
3. eosinophilic gastritis
Eosinophilic infiltration of the antrum and proximal intestine may involve
the mucosa; peripheral eosinophilia is predominant symptoms as anemia,
abd pain, early satiety &post prandial vomiting, treatment with steroid.
4. Lymphomatous gastritis diagnosed by biopsy, no treatment is
effective.
5. mentrier’s dis:- (hypertrophy gastropathy )
replacement of parietal cells and chief cell by mucus secreting cells with
excessive secretion of protein through the stomach (mucus).this will lead to
protein losing enteropathy ,it occur in middle age and elderly.
Diagnosis by barium meal and endoscope .shows enlarged folds and nodular
appearance.
Treatment: - antisecritary drugs or parietal gastrectomy.