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GASTRITIS & PEPTIC ULCER DISEASE

GASTRITIS & PEPTIC ULCER DISEASE. EKATA ANTHONIA ABHULIMEN 617. GASTRITIS. DEFINITION. Gastritis is an inflammation, irritation, or erosion of the lining of the stomach. It can occur suddenly (acute) or gradually (chronic). CLASSIFICATION. ACUTE GASTRITIS.

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GASTRITIS & PEPTIC ULCER DISEASE

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  1. GASTRITIS &PEPTIC ULCER DISEASE EKATA ANTHONIA ABHULIMEN 617

  2. GASTRITIS

  3. DEFINITION Gastritis is an inflammation, irritation, or erosion of the lining of the stomach. It can occur suddenly (acute) or gradually (chronic).

  4. CLASSIFICATION

  5. ACUTE GASTRITIS Acute gastritis is sudden inflammation of the stomach lining resulting in abdominal pain, bleeding, or other gastrointestinal symptoms.

  6. Pathogenesis The common mechanism of injury is an imbalance between the aggressive (acidic) and the defensive(protective) factors that maintain the integrity of the gastric mucosa. Factors involved in the pathogenesis include: • increased H⁺ • decreased HCO3⁻ • decreased blood flow • epithelial damage • Decreased mucus production

  7. Consequences of Acidic damage

  8. RISK FACTORS INCLUDE: • NSAIDS – aspirin • Smoking and alcohol consumption • Chemotherapy • Severe burn (curling ulcer) • Increased intracranial pressure (Cushing ulcer) • Shock • H. Pylori infection

  9. PRESENTATION: • epigastric pain • nausea and vomiting • melena • Hematemesis • appetite loss • indigestion

  10. INVESTIGATION • Presentation and history • endoscopy Normal Diffuse mild erythema of the corpus

  11. TREATMENT • Non Pharmacologic • Avoid mucosal irritants (NSAIDs , alcohol) • Cessation of smoking • Pharmacologic • Misoprostol • Proton pump inhibitors • Rx h. pylori infection

  12. CHRONIC GASTRITIS It is the chronic inflammation of the gastric mucosa and is divided into two based on etiology: • Type A chronic atrophic gastritis : Autoimmune gastritis • Type B chronic atrophic gastritis Helicobacter pylori gastritis

  13. Symptoms • Mainly assymptomatic • Upper abdominal pain , possibly made worse by eating • Dark stools • Loss of appetite • Nausea • hematemesis

  14. Autoimmune gastritis • Accounts for 10% of chronic gastritis • Involves the fundus and body of the stomach • It is associated with serum antiparietal and anti-intrinsic factor (IF) antibodies. • There may also be achloridia • There may also be g-cell hyperplasia and increased gastrin levels • Lack of intrinsic factor leads to pernicious anemia(due to vitamin B12 malabsorption)

  15. Gross appearance on endoscopy • There is loss of rugal folds in the body and fundus • Atrophic changes • Visible blood vessels (late stage)

  16. The degree of atrophic changes on endoscopic findings. • (A) No atrophy (grade 0). There is no atrophic change on the endoscopic finding. • (B) Mild atrophy (grade 1). Patchy atrophic changes are noticed without transparent vessels. • (C) Moderate atrophy (grade 2). Transparent vessels are noticed on the antrum. • (D) Severe atrophy (grade 3). Transparent vessels are noticed throughout the antrum and corpus.

  17. Histologic appearance • Loss of glands and parietal cells • Chronic lymphoplasmacytic inflammation • Intestinal metaplasia (increased risk for gastric carcinoma)

  18. Normal histology

  19. Intestinal metaplasia

  20. Treatment • No treatment is needed other than parenteral replacement of vitamin B12.

  21. Helicobacter pylori gastritis • The corkscrew-shaped bacterium H pylori is the most common cause of gastritis • These are urease producing gram-negative rods that have the ability to colonize and infect the stomach. • There is no association with pernicious anemia, antibodies to parietal cells, or reduced gastric acid secretion.

  22. Diagnosis: • urea breath test • serology (Ag or Ab detection) • endoscopic biopsy + tissue sampling

  23. an antral gland of the stomach with a large Giemsa-stained colony of Helicobacter pylori in the lumen (arrow) at 250X power. Helicobacter pylori bacteria can be identified by immunohistochemistry Original magnification (400X).

  24. PEPTIC ULCER DISEASE

  25. Definition Mucosal defects penetrating through the muscularis mucosa of the upper gastrointestinal tract that occur as a result of an imbalance between aggressive factors (gastric acid, pepsin) and gastroduodenaldefense mechanisms.

  26. ETIOLOGY -infection w/ gram-negative Helicobacter pylori (MCC)-use of NSAIDs (2nd MMC)-increased hydrochloric acid secretion-inadequate mucosal defense against gastric acid • Less common causes of peptic ulcers are: • Burns • Head trauma • Gastrinoma(Zollinger-Ellison syndrome)

  27. CLASSIFICATION

  28. Comparison Table of Gastric vs. Duodenal Ulcers

  29. Pathogenesis: H. pylori is the most important causative agent in causing PUD - H pylori induces an inflammatory response production of pro-inflammatory cytokines ( i.e IL-1, IL-6, TNF, IL-8) IL-8 recruits neutrophils further damage

  30. NSAIDs inhibit the production of prostaglandins in the gastric mucosa. These prostaglandins normally function to protect the gastric mucosa by increasing mucus and bicarbonate secretion and by stimulating local vasodilation, which maintains mucosal perfusion and prevents ischemic injury.

  31. Diagnosis • The gold standard is endoscopy (most sensitive test), but an upper gastrointestinal (GI) barium study is cheaper and less invasive. • If endoscopy is done, a biopsy of any gastric ulcer is mandatory to exclude malignancy. • Use urea breath test (more accurate) and IgM serum antibody test to diagnose current H. pylori infection

  32. This is a typical punched out and circular lesion in the stomach, with clean base and normal margins.

  33. Treatment approachesfor PUD 1) Eradicating H. pylori infection2) Reducing secretion of gastric acid3) Providing agents that protect the gastric mucosa from damage

  34. Drugs • Current tx H. pylori: administered for a 2-week course (90% OR > ERADICATION) 1) Triple therapy: 2) Quadruple therapy PPI ALWAYS Retest with stool antigen or breath test to confirm cure of Helicobacter.

  35. Treatment to reduce secretion of gastric acid • H2 receptor antagonist: • Cimetidine • Ranitidine • Famotidine • Nizatidine • H+/k+ atpase proton pump inhibitors • Omeprazole • Lansoprazole • Pantoprazole • Esomeprazole • Rabeprazole • Anticholinergics: • Dicyclomine

  36. Treatment to increase protection of lining: • Prostaglanding analogue • Misoprostol • Mucosal protective agents • Sucralfate • Bismuth subsalicylate

  37. Complications of peptic ulcer disease • Hemorrhage: Potential sources of hemorrhage include a posterior penetrating duodenal ulcer (gastroduodenal artery) or penetrating gastric ulcer on the lesser curvature (gastric artery). • Perforation • Chronic gastritis and H. pylori predispose to development of gastric carcinoma.

  38. References http://umm.edu/health/medical/altmed/condition/gastritis#ixzz34p63N7yn http://www.webmd.com/digestive-disorders/digestive-diseases-gastritis http://umm.edu/health/medical/altmed/condition/gastritis http://www.gastrosource2.com/stomach/menu/Stomach_MAIN.htm

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