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1. Pathology of the Stomach. Ileus. Vascular Diseases of the Bowels and the Peritoneum

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1. Pathology of the Stomach. Ileus. Vascular Diseases of the Bowels and the Peritoneum 1. Pathology of the stomach. Ileus. Vascular diseases of the bowels and the peritoneum. PATHOLOGY OF THE STOMACH Stomach mucosa • Gastric mucosa is covered by a layer of mucus. The mucosal glands comprise the cardiac glands, the fundic glands in the fundus and body of the stomach, and the pyloric glands in the antrum. • The surface mucous cells and the cardiac and pyloric glands secrete mucus which protects the stomach from self- digestion. • In fundic glands, the chief cells secrete pepsinogen; the parietal cells secrete HCl, bicarbonate, and intrinsic factor, and the endocrine cells release histamine. • Pyloric endocrine cells secrete gastrin, somatostatine, etc. Glossary • Gastritis - inflammation of the gastric mucosa associated with gastric mucosal injury • Gastropathy - epithelial cell damage and regeneration without associated inflammation • Erosion - circumscribed necrosis-induced defect of mucosa that does not cross the muscularis mucosae • Ulcer - the defect extends beyond the mucosa ACUTE GASTRITIS Pathogenesis Common condition, induced by acute damage to the gastric mucosa due to • alcohol, NSAIDs (nonsteroidal anti-inflammatory drugs, e.g., aspirin) or steroids • stress situations, e.g., severe burns, hypothermia, shock, CNS trauma, etc. • Helicobacter pylori infection Pathological features • Hemorrhagic-erosive inflammation of gastric mucosa affecting the entire stomach (pangastritis) or the antrum of stomach (antral gastritis) • Mucosal hyperemia, punctate hemorrhages, multiple erosions • + Acute ulcers: anywhere in the stomach (rarely in the proximal duodenum); multiple, <1 cm; usually do not penetrate through the muscularis propria layer • Healing is complete Clinical features • Epigastric pain, nausea, vomiting • On occasion, massive bleeding with hematemesis and melena ± hemorrhagic shock • Dg.: via endoscopy of stomach CHRONIC GASTRITIS • Common features: atrophy of the gastric mucosa and metaplastic transformation of the gastric glands Helicobacter pylori-induced gastritis (also termed as environmental metaplastic atrophic gastritis; EMAG) • Very common; in the absence of antibiotic therapy, it persists for life • Diagnosed histologically in biopsy samples obtained endoscopically • Associated with increased risk of peptic ulcer, gastric adenocarcinoma, and gastric MALT-lymphoma • HP eradication therapies reduce the risk of these pathologies Pathogenesis • HP microbes colonize on and injure the mucous cells • HP is protected from the acidic gastric juice because the microbes produce urease; the ammonia and bicarbonate produced neutralize the acid Morphology • Chronic active gastritis, most marked in the antrum • Gram-negative, spiral-shaped bacilli are attached to the mucous cells; infiltration of the lamina propria by lymphocytes and plasma cells + lymphoid follicles; neutrophilic infiltration of the mucous neck region • Longstanding inflammation: multifocal mucosal atrophy, characterized by loss of specialized cells in gastric glands, and their metaplastic replacement by columnar absorptive cells and goblet cells (intestinal metaplasia); fibrosis of the lamina propria; + dysplasia (intraepithelial neoplasia) in the glands Clinical features • No symptoms or epigastric discomfort • Patients with antral predominant gastritis have increased gastrin release and reduced somatostatin release → high HCl production → frequent development of duodenal peptic ulcer • Patients with multifocal atrophic gastritis have decreased acid production, may develop gastric peptic ulcers and have an increased risk for gastric adenocarcinoma Autoimmune metaplastic atrophic gastritis (AMAG) Pathogenesis • Rare • Autoantibodies to the gastric parietal cells. Can be isolated or associated with other autoimmune disorders Morphology Chronic atrophic corpus gastritis: lymphoplasmocytic infiltration of the lamina propria, extensive loss of the parietal cells, and intestinal metaplasia in the glands; + dysplasia (intraepithelial neoplasia) in the glands • Antrum: G-cell hyperplasia Clinical features • Reduced acid secretion: hypochlorhydria • Hypergastrinemia: response to hypochlorhydria to stimulate HCl production in the vanishing parietal cells • Intrinsic factor is not produced → disturbed vitamin B12 absorption → pernicious anemia • High risk for the development of gastric adenocarcinoma 1 1. Pathology of the stomach. Ileus. Vascular diseases of the bowels and the peritoneum. Reactive gastropathy • Frequent condition Pathogenesis • Reflux of bilious duodenal secretions or long-term usage of NSAIDs Morphology • The chemicals cause foveolar hyperplasia, mucosal edema, congestion of capillaries, and smooth muscle proliferation in the lamina propria • No significant increase in chronic inflammatory cells Clinical features • Mild dyspepsia + epigastric pain CHRONIC PEPTIC ULCER DISEASE Pathogenesis • Most ulcers are caused by HP infection or drugs (NSAID, steroids), both factors disrupt normal mucosal defense and repair, making the mucosa more susceptible to acid and pepsin • Other ulcerogenic effects: smoking, hypergastrinemia, emotional stress • Duodenal ulcer: increased production of gastric acid and HP-gastritis. The mechanism by which HP promotes duodenal ulcerogenesis is not known. Location • Stomach, usually the antrum and the lesser curvature • Postpyloric duodenum: in the first 2 cm-s distal to the pylorus on the anterior or posterior wall. • Within Barrett’s mucosa in esophagus Gross • Single, sharply demarcated round ulcer 1 to 2.5 cm in diameter • Healing: epithelium covers the defect, the smooth muscle cells do NOT regenerate, fibrosis takes place at the site of the injury Clinical features • Epigastrial pain releaved by food or antacids Complications Gastric ulcer • Mild to severe hemorrhage from eroded vessels • Perforation peritonitis • Pyloric stenosis due to the progressive shrinkage of fibrotic tissue proximal stomach becomes greatly dilated; persistent vomiting • Malignant change Duodenal ulcer • Penetration into the pancreas • Profuse bleeding from erosion of branches of the superior pancreatico-duodenal artery hemorrhagic shock • Perforation peritonitis • No risk of malignant transformation Good news: complex therapy has decreased advanced peptic ulcer disease (eradication of H. pylori infection, proton pump inhibitor treatment of hyperacidity, and modification of lifestyle) Acute upper gastrointestinal bleeding - summary Symptoms • Hematemesis - vomiting of blood • Melena – passage of black tarry stools • On occasion: hemorrhagic shock - life-threatening condition: pallor, cold nose, systolic BP below 100 mmHg, pulse above 100 b.p.m Common causes • Esophageal varices • Mallory-Weiss sy • Chronic peptic ulcer of duodenum or stomach • Acute erosive/hemorrhagic gastritis GASTRIC EPITHELIAL TUMORS Benign Hyperplastic (regenerative) polyps • Non-neoplastic small, often multiple polyps; mostly in the antrum • Seen in the setting of chronic gastritis Intestinal-type adenoma • Strong potential for malignant change • Gross: solitary polyp, greater than 1 cm; mainly in the antrum • LM: proliferation of dysplastic tubules that form polyp Clinical features • Extensive metaplastic atrophic gastritis mostly coexists • Mainly asymptomatic; recurrent bleeding of large adenomas may result in anemia Malignant Adenocarcinoma • High incidence in central and eastern Asia, eastern Europe, South America 2 1. Pathology of the stomach. Ileus. Vascular diseases of the bowels and the peritoneum. • Peak: between 50-60 ys Etiology • Multifactorial • 90% of cases - sporadic, 10% - familial/hereditary • Environmental factors: H. pylori infection, EBV infection, tobacco smoking, and diet high in smoked and/or salt- preserved foods and low in fruits and vegetables Anatomical location • Usually along the lesser curvature of the antropyloric region • Less common: cardia Gross Early carcinomas • Polypoid (>3 mm) or flat lesions in the form of mucosal patches or a loss of rugae • May not be recognized on endoscopy Advanced carcinomas • Localized growth with a fungating or ulcerated appearance • Infiltrative growth with or without ulceration • Linitis plastica (tube-like alteration of the stomach): no obvious tumour mass is visible on the mucosal surface; however, the gastric wall becomes thickened by the tumorous infiltration Histological and molecular features, and prognosis 1) Intestinal adenocarcinomas • Well or moderately differentiated; form tubular structures reminiscent of adenocarcinomas of colon • Chromosomally instable tumors; display DNA aneuploidy, translocations, and mutations in proto-oncogens (receptor tyrosine kinase-RAS activation) and tumor suppressor genes (TP53) • Better prognosis than the diffuse type 2) Diffuse carcinomas • Poorly differentiated; composed of poorly cohesive tumor cells or signet-ring cells; desmoplastic reaction leads to linitis plastica • Genomically stable tumors; display epithelial-cadherin gene (CDH1) mutations or RHOA mutations • Highly malignant; poor prognosis 3) Other histological subtypes • Microsatellite instabile tumors, or positive for Epstein-Barr virus Patterns of spread • Directly to the serosa; local invasion of the duodenum, pancreas, and retroperitoneum • Peritoneal dissemination: carcinosis of peritoneum • Lymphatic metastases: local lymph nodes; Virchow node: supraclavicular lymph node • Retrograde lymphatic spread: signet-ring carcinoma metastasis to both ovaries (Krukenberg tumor) • Hematogeneous metastases: liver Stage Early carcinoma • Invades no more deeply than the submucosa,
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