Gastritis

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GASTRITIS

• Gastritis is an inflammation, irritation, or


erosion of the lining of the stomach /
gastric mucosa. It can occur suddenly
(acute) or gradually (chronic).

RISK FACTOR OF GASTRITIS


 H. pylori infection
 Regular use of aspirin or other NSAIDs
 Older age
ETIOLOGY OF GASTRITIS
• Bacterial infection
• Regular use of pain relievers
• Excessive alcohol use
• Stress
• Bile reflux disease
• Your own body attacking cells in your stomach
(autoimmune gastritis)
• Other diseases and conditions
CLASSIFICATION OF GASTRITIS
• Acute gastritis
– Acute H. pylori infection
– Other acute infectious gastritis
• Chronic atrophic gastritis
– Type A
– Type B
– Indeterminant
• Uncommon forms of gastritis
– Lymphocytic
– Eosinophilic
– Crohn’s disease
– Sarcoidosis
– Isolated granulomatous gastritis
SYMPTOMS OF GASTRITIS
• Nausea or recurrent upset stomach
• Abdominal bloating
• Abdominal pain
• Vomiting
• Indigestion
• Burning or gnawing feeling in the stomach
between meals or at night
• Vomiting blood or coffee ground-like material
• Black, tarry stools
Infection of H. PILORY

gastritis TH 1 motility
H.Pylory
infects gaster
urease
protective TH2
Vac A Urea
ammonia
+CO2
Provides a survival needs for bacteria
Causes epithelial injury
Pathogenesis of Helicobacter pylori infection

• An ability to colonize and adhere to gastric


epithelial cells.
• The possesion of flagella that allows movement
through the luminal mucous layer to site of higher
Ph.
• An ability of adherent strains to supress acid
secretion to improve their survival.
• Secretion of urease that produces ammonia
results in a more alkaline environment.
• Release of vacuolating cytotoxin (VacA) that
promotes bacterial survival and causes epithelial
injury.
• The presence of cytotoxin-assosiated gene (CagA) strains that can escape
normal immune responses and cause inflammation with release of
inflammatory cytokines and reactive oxygen metabolites that damages
mucosal epitelial cells and loss of the protective mucosal barrier.
• Recruitment and activation of neutrophils,macrophages,and mast cells
with release of inflammatory cytokines that promote celllar injury.
• Down-regulation of antral somatostatin leading to increased
gastrin,acid,impaired mucosal bicarbonat production and increased
mucosal exposure to acid and pepsin.
• Activation/inhibition of T-and B- cell immune
responses that may contribute to mucosal
injury.
• Release of cytokines and chemokines that
promote gastric epithelial cell death and cell
proliferation that can result in
atrophy,ulcers,or malignant growth.
Examination
• Urea breath test
• Serologi
• Biopsy urea test
• Manifestacion:
– Burn feeling (in epigastrium)
– Nausea
– Bitter in the tounge
– Disfagia

Complication:
Esophagitis is classified into the following 4
gradesI,II,III,IV.

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