Pathology of stomach

3,915 views

Published on

0 Comments
10 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
3,915
On SlideShare
0
From Embeds
0
Number of Embeds
3
Actions
Shares
0
Downloads
235
Comments
0
Likes
10
Embeds 0
No embeds

No notes for slide

Pathology of stomach

  1. 1. Pathology of Stomach Dr. Saifeldenn Hussein Pathologist IMS-MSU PATHOLOGY DEPARTMENT
  2. 2. TOPICS1) CONGENITAL ABNORMALITIES2) ACUTE GASTRITIS3) CHRONIC GASTRITIS4) PEPTIC ULCER DISEASE5) BENIGN TUMORS6) GASTRIC CARCINOMA
  3. 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. 4. Diaphragmatic Hernia:• Congenital opening defect on the diaphragm keep the stomach and intestines move up into the chest cavity.
  5. 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. 6. CLINICAL FEATURES:a) Asymptomaticb) Nausea, vomitingc) Epigastric paind) In severe cases: hemorrhage = severe hematemesis - melena
  7. 7. Pathology :• Erosion of the superficial epithelial with petechial hemorrahge any where in the stomach• Patchy mucosal necrosis
  8. 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. 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. 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. 11. Investigation:i) Serologic test for Abii) Fecal bacteria detectioniii) Urea breath testiv) Gastric biopsy- histology visualization
  12. 12. PATHOLOGY :• lymphocytes and plasma cells seen in the lamina propria• Lymphoid hyperplasia• H. pylori seen on the surface mucus of epith cells
  13. 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. 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. 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. 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. 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. 18. Microscopically:• 4 zones identifiable:• Superficial necrotic layer• Zone of inflammation• Layer of granulation tissue• Underlying fibrous scar
  19. 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. 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. 21. TREATMENT:• Antibiotics to eliminate H. pylori• Blocking gastric acid secretion with histamine-receptor blockers and proton pump inhibitors.
  22. 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. 23. THANK YOU

×