This document summarizes acute and chronic gastritis. Acute gastritis is caused by factors like NSAID use, alcohol, smoking, infections, and stress. It involves neutrophil infiltration and can cause erosions and ulceration. Chronic gastritis is defined by long-term inflammation leading to atrophy and intestinal metaplasia. Helicobacter pylori infection is a major cause and results in urease production and cytotoxins that drive chronic inflammation. Autoimmune mechanisms can also lead to chronic gastritis, seen as lymphocytes and plasma cells in the lamina propria and intestinal metaplasia.

1. Acute & chronic
gastritis
Etiology, pathogenesis & morphology

2. Acute Gastritis:
• Gastritis: inflammation of the gastric mucosa.
• Diagnosis mostly histological.
• Acute Gastritis:acute mucosal inflammatory
process usually of a transient nature.
• neutrophilic infiltration
• Etiology:
Heavy use of NSAID’s, particularly aspirin
Excessive alcohol consumption&Heavy smoking

3. Treatment with cancer chemotherapeutic drugs Gastric
irradiation or freezing
 Systemic bacterial or viral infections
 Severe stress& Mechanical trauma
 Ischemia, shock & uremia
 Distal gastrectomy.
• Pathogenesis:
increased acid secretion with back-diffusion,
 decreased production of bicarbonate buffer,
reduced blood flow,
disruption of the adherent mucus layer,
 direct damage to the epithelium.

4. • Morphology:
the gastric mucosa demonstrates
edema, neutrophilic infiltrates, mucosal
erosions, and, if severe, ulceration &
hemorrhage.
 FIGURE 17–13 B.Low-power microscopic view of focal mucosal disruption with hemorrhage;
the adjacent mucosa is normal.

5. Chronic Gastritis:
• Chronic gastritis is defined as the presence of
chronic mucosal inflammatory changes leading
eventually to mucosal atrophy and intestinal
metaplasia, usually in the absence of erosions
• Etiology:
Chronic infection by H. pylori
 Immunologic,(in association with pernicious
anemia)

6. Toxic,(alcohol &cigarette smoking)
 Postsurgical,(esp following antrectomy with
gastroenterostomy)
 Motor and mechanical,(obstruction, bezoars&
gastric atony)
Radiation
 Granulomatous conditions (e.g., Crohn disease)
 Misc.—amyloidosis, graft-versus-host disease
,uremia.
• Pathogenesis:

7. oChronic atrophic gastritis caused by H.pylori:
• (1) Gram-negative, curved rod
• (2) Produces urease, proteases, cytotoxins
(a) Urease converts amino groups in proteins to
ammonia
(b) Secretion products produce chronic gastritis
and PUD,
• (3) Colonizes mucus layer lining
oAutoimmune atrophic gastritis:
• Autoantibodies to parietal cells (H/K ATPase
proton pump) and intrinsic factor

8. • Morphology:
• Chronic inflammatory infiltrate(lymphocytes
&/or plasma cells) in the lamina propria
• Intestinal metaplasia(Precursor lesion for
adenocarcinoma)
• Intestinal atrophy
• Epithelial dysplasia
• FIGURE 17–14 Chronic gastritis, showing partial replacement of the gastric mucosal epithelium by
intestinal metaplasia (upper left) and inflammation of the lamina propria (right) containing
lymphocytes and plasma cells.

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