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home - Stomach - Gastritis and Gastropathy - Gastritis Overview Written by Dr Sebastian Zeki

Gastritis Overview

Surveillance endoscopy IM alone doesnt need surveillanceFamily history or background High grade dysplasia needs resection (local or gastrectomy)Pernicious anaemia may need a single OGD to identify specific lesions but not routine Metaplastic (chronic) atrophic gastritis Autoimmune Environmental Types Both have metaplasia as defining feature: TypesPseudopyloric metaplasia-Replacement of parietal and chief cells in oxyntic glands by mucus-secreting cells of the type found in antral (ie, pyloric) mucosa Type I- Complete intestinali-sation Types II and III incomplete intestinalisation (ie goblet cells but no Paneth cells) Autoimmune metaplasticAtrophic gastritis Immune response in the oxyntic mucosa directed against parietal cells and intrinsic factor. Associations:HLA B-8 and DR-3Pernicious anaemia and hypochlo-rhydria.Autoimmune thyroid diseaseClinical features — Autosomal dominant disorder that commonly affects people of northern Europe or northern European extractionM:F is 1:3 Pathology — The proportion of pseudopyloric and intestinal metaplasia within the body and fundus vary widely among patients, and either form can predominate. Gastric adenocarcinoma In 1-3% AMAGHighest risk 1 year after diagnosis of pernicious anemia. Get focal lymphocytic infiltration including epithelial lymphocyto-sis with destruction of oxyntic glands. Pseudohypertro-phy of parietal cells resembling that seen during treatment with omeprazole may be present in the islands of surviving mucosa Early stages(active autoimmune gastritis): The metaplasia, glandular atrophy, and inflammation are confined to the gastric body and fundusThe gastric body and fundus may appear to contain multiple polyps (=islands of normal tissue) End-stage AMAG:Lack of rugal foldsVisible blood vessels Oxyntic glands replaced by metaplastic glands Carcinoid tumors Macroscopi-cally: Mucosal nodules/polyps ECL cell hyperplasia is also observed in PPI induced hypergastrinae-mia but not associated with carcinoid G-cellshyperplasia Gastrin Trophic effect on enterochromaffin-like cells (ECL cells- usually produce histamine), within the metaplastic and atrophic body mucosa. Gastrin normalDecreased gastric acid production Inflammation Metaplasia Atrophy Inflammation Metaplasia Atrophy Proximal migration of transitional zone (between body and antrum) with intestinalisationOxyntic mucosa (normal mucosa in body and fundus) may become atrophied and thin Progression from IM to Gastric Cancer Risk Factors:-Family history of gastric cancer. -Residence in or migration from a high risk location. -Member of a high risk ethnic population. -Dysplasia on biopsy. -Extensive IM on biopsies (more important then metaplastic subtype) Intestinal metaplasia Gastric Cancer Hypochlorhydria Trophic Effect Complications of AMAG AMAG EMAG Metaplasia Metaplastic Gastritis Gastric CancerGastric ulceration Focally distributed areas in antrum Risk factors —Nitroso compounds ( by bacterial metabolism of nitrates).Helicobacter pylori — Written by Dr Sebastian Zeki

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