Level of

competent : 4

GASTROPATHY/ GASTRITIS

Definition : any disease or inflammation of the

stomach
Increased frequency with age

Gastric carcinoma
Surgery/chemothera
py

Gastric lymphoma
Chemo/debulking
agent

Specific gastritis
Eosinophilic gastritis :
corticosteroid
Granulomatous gastritis
Portalhypertensive
gastropathy : BB, nitrate,

Hypertropic folds
Zollinger-Ellison Syd

Nonspesific gastritis
Nonerosive gastritis :
Type A & B
Erosive gastritis : H.pylori

GASTRITIS

Acute gastritis is a term

covering a broad spectrum of
entities that induce
inflammatory changes in the
gastric mucosa
Chronic gastritis is a
histopathological entity
characterized by chronic
inflammation of the stomach The inflammation may involve the
mucosa.
entire stomach (eg, pangastritis) or
a region of the stomach (eg, antral
gastritis).

Causes
CHRONIC GASTRITIS :

ACUTE GASTRITIS : certain

drugs; alcohol; bacterial,
viral, and fungal
infections; acute stress
(shock); radiation; allergy
and food poisoning; bile;
ischemia; and direct
trauma.

Infectious gastritis (bacterial,

viral, and fungal infections)

Noninfectious gastritis

Chronic gastritis of
undetermined etiology or
gastritis of undetermined type

H pylori infection - is the most common cause of

chronic gastritis.

Pathophysiology
Acute/stress gastropathy
NSAID, alcohol, corticosteroids
Stress gastritis : any critical illness under perfusion, within 24 hours,
GI bleeding 30% (respiratory failure, liver/renal disease with
coagulopathy, sepsis, surgery/trauma(Cushings ulcer), burns
(Curlings ulcer), CNS insult)

Chronic gastritis

Chronic Antral gastritis (Type B): H.pylori

Chronic Fundal gastritis (Type A) : autoantibody against intrinsic factor
& parietal cell loss intrinsic factor & achlorhydria

Congestive gastropathy
Cirrhosis & portal hypertension

Clinical manifestation

Many asymptomatic
Dyspepsia (epigastric
discomfort), N/V,
postprandial fullness,
bloating, occasionally
GI bleeding

Diagnostic study

EGD : scattered
mucosal erosion
or foci of
intramucosal
hemorrage

Treatment

Increased stomach
pH>4 (pepsin is
inactivated & blood
coagulation is
enhanced) : Proton
pump inhibitor
drugs & supportive
measures

Helicobacter pylori (Hp)

Flagellated gram negative bacilli

with urease activity :
hydrolyzes urea >> ammonia
(NH3) & CO2 (help resist
stomatch acid)
Transmission : fecal-oral, oral-oral
and most infection acquired in
childhood
Natural habit :
gastric mucosa of the antrum,
if found in duodenum,
associated with metaplastic
gastric epithelium

90% duodenal ulcer and

70% gastric ulcer

Pathophysiology

Inflammation
Toxin : vacuolating
cytotoxin (VacA),
cytotoxin-associated
gene A (CagA)
Acid

Moayyedi P. In Clinical Gastroenterology and Hepatology. 2005; p.2

Clinical
presentation

Majority individuals
(app. 80%) remain
asymptomatic
Small subset patients
: dyspeptic
symptoms (epigastric
pain, fullness, early
satiety & nausea)

Diagnostic
methods
Performed only if treatment
intended
INVASIVE TEST
Endoscopic
Rapid urease/CLO (>95%)
Biopsy/histology using HE
(>95%)
Biopsy/culture ( highly
spesific only)

NON-INVASIVE TEST

UBT = urea breath test

(> 90%)
Serology IgG Anti-Hp
serum (85-90%), urine
(85%), saliva +IgA (7085%)
Stool test Ag Hp= HpSA
(>95%)

Treatment

Complication

In 1994, WHO classified

H.pylori as group I
carcinogen3-6 fold higher
incidence of gastric ca.
Strong association with
mucosal associated
Lymphoid tumors (MALT) :
treatment Hp
regression/cure 90%
patient

With acid hyposecretion (left),

the main effect of H pylori
gastritis affecting the gastric
body is to suppress parietal cells,
leading to low acid secretion,
which is associated with gastric
cancer. With acid hypersecretion
(right), antral H pylori gastritis
increases acid secretion by
suppressing somatostatin and
elevating gastrin release,
increasing the risk of duodenal
ulceration. Orange areas indicate
extent and location of gastritis

Autoregulation of acid
secretion. Food stimulates
release of gastrin from antral
G cells (G). Gastrin stimulates
enterochromaffin-like cells
(ECL) to release histamine,
which stimulates parietal cells
(P) in the gastric corpus to
secrete acid. Acid stimulates
release of somatostatin from
somatostatin cells (S) in the
antrum, inhibiting further
gastrin release