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Pathology Lecture 42 Gastritis, Peptic Ulcer Disease & Gastric Neoplasms 1) To be familiar with the etiology, pathogenesis, and morphologic features of chronic gastritis and peptic ulcer disease. Disease Etiology Pathogenesis Morphology Chronic gastritis Infectious: Helicobacter pylori Immunologic: autoimmune gastritis Toxic: alcohol and cigarettes Chemical: reflux of bilious and what most secretions after antrectomy and gastroenterostomy Motor and mechanical: obstruction, bezoars and gastric atony Other: radiation, granulomatous conditions, amyloidosis, GVHD Helicobacter pylori, motile gram-negative rods, colonize the surface of gastric-type epithelium producing cytotoxin, endotoxin, and other protein products that stimulate inflammation. Autoimmune gastritis is the development of antibodies to parietal cells, intrinsic factor, and acid producing enzyme H+/K+ATPase. Leads to achlorhydria & pernicious anemia Gross: normal to slight erythema (redness) Micro: neutrophilic infiltrate within the glandular and surface epithelium, regenerative epithelial changes, and ultimate mucosal atrophy. Peptic ulcer disease US: incidence 10% men, 4% women Duodenal ulcers: 99% have H. pylori gastritis, ulcers are more common with alcoholic liver cirrhosis, COPD, CRF, and hyperparathyroidism. Gastric ulcers: NSAIDs are ulcerogenic. 70% of those not a tribute to NSAIDs have H. pylori. Produced by an imbalance between the gastroduodenal mucosal defense mechanisms in the damaging forces. Mucosal exposure to gastric acid and pepsin is essential for the development of peptic ulcers. H. pylori: directly damages mucosa and attract inflammatory cells, more damage. NSAIDs suppressed mucosal prostaglandin synthesis. Gross: located primarily in duodenum (other locations possible), 10-20% have multiple ulcers. Ulcers are small (<2 cm), round to oval, smooth and clean, penetrating muscularis mucosae into muscularis propria (may perforate wall) Micro: ulcer base has amorphous, fibrinoid eosinophilic debris. Inflammatory infiltrate with neutrophils, granulation tissue, and collagenous scarring. 2) To know the main types of stomach polyps and their significance with respect to cancer. In the alimentary, tract term polyp is applied to any nodule or mass the projects above the level of the surrounding mucosa. Mucosal polyps are classified as non-neoplastic or neoplastic (gastric polyps are uncommon). Most (up to 90%) are non-neoplastic and appear to be of a hyperplastic nature, and regarded as having no malignant potential (although they are found in 20% of carcinomas). Adenoma of the stomach constitutes 5-10% of stomach polyps and the associated risk of cancer can be as high as 30%. Other types are uncommon including fundic gland polyps, hamartomatous Peutz-Jeghers polyps, and juvenile polyps. The inflammatory fibroid polyp (eosinophilic granuloma) is a striking lesion that is a bulky submucosal growth composed of inflamed desk terrorized fibromuscular tissue with a prominent use in the select infiltrate and a tenuous mucosa stretched over the surface 3) To be familiar with epidemiology, pathogenesis, morphologic alterations and clinical implications of stomach cancer. Cancer Epidemiology Pathogenesis Morphologic alterations Clinical implications Gastric adenocarcinoma Geographic: Japan, Finland, Columbia >US and Canada Intestinal type: ~55 years, male 2x >female Diffuse type: ~48 years, male ≈ female Environmental: diet, low socioeconomic status, smoking Host factors: H. pylori infection leading to chronic gastritis & intestinal metaplasia (may become dysplastic) Genetic: family history, blood group A Intestinal type: an exophitic, flat or excavated lesion, on the antro-pyloric region (mostly), gland formation Diffuse type: "leather bottle" shape and consistency, Micro: poorly differentiated "signet ring" cell. Gastric lymphoma 5% of all gastric malignancies, nearly all RP cell lymphomas of MALT >80% are associated with chronic gastritis and H. pylori infection. Mucosal lymphocytic infiltrate in the lamina propria surrounding gastric glands infiltrated with atypical lymphocytes and undergoing destruction. Initially asymptomatic. Later, weight loss, abdominal pain, anorexia, and chronic blood loss. Gastric outlet obstruction possible. Metastasize via lymph nodes. 4) To be familiar with the information contained in this handout. Review handout.