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Lec.4 Dr. Basim

Lec.4 Dr. Basim. Note: Other etiological factors for D.U: Positive family history present in 20 – 40% of D.U. Blood group O in 30% of patients with D.U. Alcoholic liver cirrhosis. Obstructive lung diseases. hyperparathyroidism Chronic renal failure. Hyperacidity (high HCL LEVEL).

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Lec.4 Dr. Basim

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  1. Lec.4 Dr. Basim

  2. Note: Other etiological factors for D.U: • Positive family history present in 20 – 40% of D.U. • Blood group O in 30% of patients with D.U. • Alcoholic liver cirrhosis. • Obstructive lung diseases. • hyperparathyroidism • Chronic renal failure. • Hyperacidity (high HCL LEVEL). • Zollinger Ellison syndrome (Gastrinoma……. High level of gastrin…… multiple ulcers in stomach, duodenum & even jejunum).

  3. Morphology of Peptic ulcer: 1.Site:G.U. usually at the lesser curvature at the antral area (antral gastritis). D.U. at anterior or posterior wall of first part of duodenum. 2. Size:2 – 4cm. 3. Number: Usually solitary (sometime two). 4. Shape: round – oval , punched out appearance. 5. Depth:defect in mucosa, submucosa, & muscularis layer. 6. Margins: margins of benign peptic ulcer are not elevated, not beaded, & margins of crater are perpendicular to the base with edema of immediate surrounding mucosa.

  4. 7. Mic:four zones are identified. a. base & margins have thin superficial layer of necrotic fibrinoid debris. b. beneath, is a layer of active non specific inflammatory infiltration with neutrophils predominance. c. deeper granulation layer. d. fibrous scar tissue that is radiate from margins of ulcer, with vessels trapped within scarred tissue. Note: Chronic gastritis is extremely common in patient with chronic peptic ulcer (H.pylori); unlike acute ulcer usually not associated with gastritis. Clinical features: Epigastric pain: (hunger pain, worse at night, relieved by meal for ….. for D.U).

  5. COMPLICATIONS: 1. Healing & Scarring: Scarring mainly at pyloric area ……… pyloric outlet obstruction; usually with ulcer at prepyloric area………….. Vomiting & dehydration & hyperkalemic acidosis. (Hour glass deformity ………. If ulcer more higher in the stomach) This complication is characteristic complication of D.U. 2. Bleeding: Either hematemesis &/ or melena. Is more with D.U than G.U. In chronic condition can result in Iron deficiency anemia. 3. Perforation: escaping of gastric contents into peritoneal cavity…….. Chemical peritonitis… then bacterial peritonitis. Early cause severe generalized abdominal pain with board like rigidity……. In chemical peritonitis. Less pain in bacterial peritonitis (just distension with less rigidity). This complication more in D.U than G.U.

  6. 4. Penetration: Ulcer penetrates into adjacent structure like small intestine. (more with D.U). 5. Malignant transformation: D.U NEVER SHOWS MALIGNANT TRANSFORMATION. G.U in less than 1% of cases shows malignant transformation. 6. Abscess formation.

  7. Tumors of stomach: Divided into polyps & carcinomas Polyps: Any nodule or mass that project above the mucosal surface, (including leiomyoma, lipoma). Gastric polyps are less common than those of colon (0.4% of general population). Types : Hyperplastic polyps (80 -85% of cases, benign). Fundic gland polyp (10% 0f cases, benign). Adenomatous polyps (5%, predisposing to adenocarcinoma). Gastric carcinoma: Is one of important cause of death from malignancy (3%). Types: Adenocarcinoma (90%- 95%). Lymphoma (4%). Carcinoid tumor (3%). Mesenchymal tumors (2%).

  8. Adenocarcinoma: • Sex: M/F = 2/1 • Age: 5th – 6th decades. • Geograghic differences: high incidence in japan, costarica, hungary. Morphological types: 1.Intestinal type. 2. Diffuse type. Etiological factors: I. Those of intestinal type: 1. Dietary factors: • Nitrites derived from nitrate (preservatives of diet)……. Undergo nitrosation by the action of intragastric bacteria to the nitrosamines & nitrosamides (carcinogenics). • Smoked & salted food. • Decreased intake of fresh fruits & vegetables (contain antioxidants that inhibit nitrosation). 2. Chronic gastritis & intestinal metaplasia. • Infection with H.pylori • Pernicious anemia.

  9. 4. Host factors: • Gastric adenoma • Partial gastrectomy. • Barrett esophagus. 5. Genetic factors: • Blood group A II. Etiological factors of diffuse type: mostly unknown except for inheritant type (mutation in E- cadherin).

  10. Morphology of gastric carcinoma: 1.Site: • pyloric & antrum (at lesser curvature)(50% -60%). • Cardia 40% Note (large ulcer at greater curvature is more likely to be malignant). 2. Gross: • Exophytic mass (protruded mass). • Flat (depressed) type ……no obvious mass. • Ulcerative type (excavated)….. show ulcer with headed-up margins, surrounding mucosal folds appear to be arise from the margins of ulcer. • Diffuse type…. Entire stomach is extensively infiltrated by malignancy…… rigid & thickened stomach….. look like leather bottle ( linitisplastica).

  11. 3.Microscopic : i. Intestinal type: • Composed of well differentiated malignant intestinal type glands (look like colon). • Good prognosis. ii. Diffuse type: • Composed of gastric type mucous cells; that do not form glands but rather invade the mucosa & submucosa in scattered individual cell pattern. • These cells accumulate mucin …… signet ring cells. • Poor prognosis.

  12. 4. Spread: • Local spread……. To adjacent organs like esophagus, duodenum. • Lymphatic spread……. To regional lymph nodes, sometime earliest lymph node involve by metastases is supraclavicular lymph node (Virchow's node). • Transcoelomic spread (along body cavities): Invade peritoneal cavity ……. Implanted on ovaries….. (Krukenberg tumor). • Hematogenous spread ……. Liver, lung. Clinical features: usually delay…….. presented with 3As (Anemia, Anorexia, & Asthenia). Note: gastric carcinoma can be classified according to depth of invasion into: • Early gastric carcinoma (limited to the mucosa & submucosa) regardless lymph node & distant metastases & this type derived from dysplastic lesion. • Advanced carcinoma (involve mucosa, submucosa & muscularis layer).

  13. Pathology of intestine: Histology of intestine: • Small intestinal mucosa usually have mucosal villi & crypts lined by columnar epithelium. • Large intestine have a flat mucosa with numerous vertical oriented crypts. Congenital anomalies of intestine: • Atresia & stenosis of intestine……. Intestinal obstruction. • Duplication of intestine. • Malrotation of whole intestine.

  14. 4. Meckeldiverticulum: • Is the most common anomalies. • Result from failure of involution of the omphalomesentric duct….. leaving blind present tubular structure of about 2 inches. • It is true diverticulum (contain three layers of intestine in its wall). • It is a lesion of (2s). • in 2% of population. • Lies about 2 feet from ileocecal valve. • It is length is about 2 inches. • 20% of cases contain heterotopic tissue (gastric mucosa…… gastric ulcer, bleeding & perforation) or sometimes contain pancreatic tissue. Complications: • Diverticulitis. • Intestinal obstruction. • Peptic ulcer, bleeding & perforation. • B12 deficiency (bacteria growth)……. Pernicious anemia.

  15. 5.Hirschsprung disease: (congenital aganglionic megacolon). This is a disorder result from arrest of migration of neural crest cells at any level of GIT before reaching the anal area……….leading to functional obstruction & dilatation of colonic segment proximal to the affected segment (due to lack of both meissner & auerbach plexuses in this area). • 50% of cases are associated with mutation in RET GENE (responsible for synthesis of these plexus). • More in male with other congenital anomalies (like Meckel diverticulum, hydrocephalus). Clinical features: • Failure to pass meconium. • Constipation. • Abdominal distension Complications: • Enterocolitis with electrolyte & water imbalance. • Perforation of colon with peritonitis.

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