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Pathology of stomach

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  • 1. Pathology of Stomach Dr. Saifeldenn Hussein Pathologist IMS-MSU PATHOLOGY DEPARTMENT
  • 2. TOPICS1) CONGENITAL ABNORMALITIES2) ACUTE GASTRITIS3) CHRONIC GASTRITIS4) PEPTIC ULCER DISEASE5) BENIGN TUMORS6) GASTRIC CARCINOMA
  • 3. CONGENITAL ABNORMALITIESPyloric stenosis:Males 3:1 vs. femalesMay occur with Turner syndrome, trisomy 18, esophageal atresiaClinical features: i) Narrowing of pyloris - hypertrophy and possibly hyperplasia (muscularis) ii) Projectile vomiting within first 3 week after birth- dehydration iii) Palpable mass iv) Surgical splitting is curative
  • 4. Diaphragmatic Hernia:• Congenital opening defect on the diaphragm keep the stomach and intestines move up into the chest cavity.
  • 5. ACUTE GASTRITIS• Gastritis (inflammation of gastric mucosa) usually transient inflammation lead to bleeding and erosion of mucosaPathogenesis: associated factors: a) NSAID (e.g., aspirin) b) Alcohol c) Heavy smoking d) Stress (trauma, burns, surgery) e) Trauma to CNS Acid secretion damage to epithelium active inflammation HCO3
  • 6. CLINICAL FEATURES:a) Asymptomaticb) Nausea, vomitingc) Epigastric paind) In severe cases: hemorrhage = severe hematemesis - melena
  • 7. Pathology :• Erosion of the superficial epithelial with petechial hemorrahge any where in the stomach• Patchy mucosal necrosis
  • 8. CHRONIC GASTRITISPresence of chronic mucosal inflammation leading to:a) mucosal atrophyb) intestinal metaplasiac) usually no erosionEtiology: a) Chronic infection (Helicobacter pylori) b) Autoimmune (Pernicious anemia) c) Alcohol, smoking d) Post surgery (i.e., gastric) e) Radiation
  • 9. • Helicobacter pylori most important etiologic association with chronic gastritis( Gram –ve rods with polar flagella) found only on the epithelial surface and dose not invade.• Urease +ve (produces NH 3 and CO2 from urea)• Plays role in other diseases: a) Peptic ulcer b) Gastric carcinoma c) Gastric MALT
  • 10. • H. pylori-induced gastritis: i) Pangastritis – (multifocal gastric atrophy) high level of IL-B (potent pro-inflammatory cytokines) inhibit gastric acid- lower H + production - risk of adenocarcinoma ii) Antral-type – low level of IL-B - high H + production - risk of peptic ulcer
  • 11. Investigation:i) Serologic test for Abii) Fecal bacteria detectioniii) Urea breath testiv) Gastric biopsy- histology visualization
  • 12. PATHOLOGY :• lymphocytes and plasma cells seen in the lamina propria• Lymphoid hyperplasia• H. pylori seen on the surface mucus of epith cells
  • 13. Autoimmune gastritis: Chronic diffuse inflammatory disease of the body and fundus of the stomach High risk of gastric CA.• < 10% of gastritis cases due to Ab against parietal cell and IF lead to: a) mucosal atrophy loss of acid production ( achlorhydria) b) increased serum gastrin (G- cell hyperplasia) c) Pernicious anemia seen with other autoimmune diseases i) Type 1 diabetes ii) Addison disease iii) Hashimoto thyroiditis
  • 14. PEPTIC ULCER DISEASE• PU is chronic lesions, solitary occur any part of the alimentary tract due to exposed to the aggressive acid-peptic juicesSites : Duodenum = 1st part Stomach usually = antrum Gastroesophageal junction = reflux Duodenum, stomach in Zollinger-Ellison syndromeEtiology:1) H.pylori infection: 100% in duodenal ulcers and 75% in gastric ulcers
  • 15. Other factors promoting peptic ulceration:• Zollinger-Ellison syndrome – multiple ulcers in stomach, duodenum due to excess gastrin• Chronic NSAID use – suppress prostaglandin syn• Cigarette smoking – impair mucosal blood flow• Corticosteroids• Alcoholic cirrhosis, COAD – duodenal ulcer• Chronic renal failure and hyperparathyroidism = hypercalcemia – stimulate gastrin – acid prod.
  • 16. Pathogenesis :• Imbalance between defense and damaging forces• Severe inflammation - IL-1, IL-6, IL-8,TNF - IL-8 recruits neutrophils• H. pylori produces proteases and phospholipases enzymes i) break down protective actions of mucus vi) HCO 3 - in duodenum v) H + secretion in stomach vi) damage to mucosa and epithelial cells leakage of nutrients (sustain H. pylori)
  • 17. Pathology: grossGastric ulcer:Site: Lesser gastric curvature in the antral and prepyloric region= a/e chronic gastritis Great curvature = NSAIDSize: Single, round, less than 4 cmEdges: Sharp, not heaped-upBase of ulcer: Smooth and clean due to peptic digestionDuodenal ulcer:Site : anterior or posterior wall of the first part of the duodenumSize : solitary some time paired ulcer on both wall (kissing ulcer)Edges: sharply demarcated
  • 18. Microscopically:• 4 zones identifiable:• Superficial necrotic layer• Zone of inflammation• Layer of granulation tissue• Underlying fibrous scar
  • 19. Clinical features:Epigastric pain is main presentation.• The classic duodenal ulcer is characterized by epigastric pain 1 to 3 hours after a meal.• Gastric ulcer pain relieved by food
  • 20. Complications:1) Hemorrhage2) Perforation3) Pyloric obstruction (gastric outlet obstruction) :caused by muscular spasm, edema, muscular hypertrophy or contraction of scar tissue, 4) Development of combined ulcers 5) Malignant transformation of benign gastric ulcer and dose not occur in DU.
  • 21. TREATMENT:• Antibiotics to eliminate H. pylori• Blocking gastric acid secretion with histamine-receptor blockers and proton pump inhibitors.
  • 22. Acute gastric ulceration:• Focal acutely development of gastric mucosal defect due to:1) NSAID2) Physiological Stress (stress ulcer)3) Severe burn or trauma (Curling ulcer)4) Intracranial injury (Cushing ulcer)• Gross: Small and multiple ulcer found any where in stomach and duodenum .
  • 23. THANK YOU

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