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Gastritis
- 1. K O F I N T I B A F F O U R A B O A G Y E GASTRITIS
- 2. STOMACH • A glandular digestive and endocrine organ
- 3. STOMACH • Storage • Secretion – HCL, enzymes • Protein digestion • Protection – mucus, bicarbonate, tight intercellular junctions, HCL
- 4. GASTRITIS • Inflammation of the gastric mucosa Acute or chronic
- 5. ACUTE GASTRITIS • Acute gastritis: Acute mucosal inflammation, haemorrhage and sloughing of superficial mucosa • When inflammatory cells are rare or absent, the term gastropathy is applied • Acute gastritis often produces no symptoms but may cause dyspepsia, anorexia, nausea or vomiting, and hematemesis or melena.
- 6. CAUSES • Excessive use of NSAIDS • Excessive alcohol consumption • Cytotoxic drug therapy: radiation, chemotherapy • Uremia • H. pylori infection • Reduced mucin and bicarbonate secretion in the aged • Severe stress • Ischemia
- 8. PATHOPHYSIOLOGY • NSAIDS inhibit COX-1 and COX-2 dependent synthesis of prostaglandins E2 and I2 which stimulate mucus, bicarbonate, and phospholipid secretion, mucosal blood flow, and epithelial restitution while reducing acid secretion. • H. pylori infection and uraemia may cause inhibition of gastric bicarbonate transporters by ammonium ions. • Chemicals like alcohol, acids and bases, cytotoxic drugs and radiation therapy cause gastritis as a result of direct cellular damage
- 9. MORPHOLOGY
- 10. HISTOLOGY
- 11. CHRONIC GASTRITIS • H. pylori the most common cause. Mainly affects the antrum • Autoimmune gastritis mainly affects body • Persistent acute insults • Radiation injury, chronic bile reflux, mechanical injury (e.g. an indwelling nasogastric tube), and involvement by systemic diseases, such as Crohn disease, amyloidosis • Clinical symptoms are typically less severe but more persistent. • Nausea and upper abdominal pain are typical, sometimes with vomiting, but hematemesis is uncommon.
- 12. H. PYLORI
- 13. A, Spiral-shaped H. pylori are highlighted within surface mucus. B, Intraepithelial and lamina propria neutrophils are prominent. C, Lymphoid aggregates with germinal centers and abundant subepithelial plasma cells within the superficial lamina propria are characteristic of H. pylori gastritis.
- 14. AUTOIMMUNE GASTRITIS • Accounts for less than 10% of chronic gastritis • Mainly affects the body • Associated with hypergastrinemia • Antibodies to parietal cells and intrinsic factor • Reduced serum pepsinogen I concentration • Endocrine cell hyperplasia and glandular atrophy • Vitamin B12 deficiency • Defective gastric acid secretion (achlorhydria) • May be associated with autoimmune conditions like Hashimoto thyroiditis, Type 1 DM, Graves disease, Myasthenia Gravis
- 15. SEQUELAE AND COMPLICATIONS • Peptic ulcer • Adenocarcinoma • MALToma • Atrophy • Pernicious anaemia • Carcinoid tumor
- 16. LESS COMMON FORMS • Eosinophilic Gastritis: characterized by tissue damage associated with dense infiltrates of eosinophils in the mucosa and muscularis, usually in the antral or pyloric region • Granulomatous Gastritis: This descriptive term is applied to any gastritis that contains well-formed granulomas or aggregates of epithelioid macrophages.
- 17. DIFFERENTIAL DIAGNOSES Acute gastritis • Peptic ulcer disease • Cholecytitis • Chlolelithiasis • Gastric cancer • Viral gastroenteritis • B cell lymphoma • Complications of acute sarcoidosis • Crohn disease Chronic gastritis • Crohn disease • Gastroesophagial reflux disease • Atrophic gastritis • Chronic kidney disease
- 18. REFERENCES • Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease (Ninth edition.). Philadelphia, PA: Elsevier/Saunder • https://emedicine.medscape.com/article/175909
Editor's Notes
- Acute gastritis, and chronic gastritis can occur following disruption of any of these protective mechanisms.
- Hyperemia, multiple petechiae, edema, ulceration