Acute gastritis: acute haemorrhagic/erosive gastritis is usually antral and drug related (aspirin, NSAIDs, alcohol), or, less commonly in the body secondary to shock and hypoperfusion, e.g., post trauma, sepsis or burns, and therefore not biopsied. Acute neutrophilic gastritis is seen in food poisoning, sepsis and Helicobacter pylorii (HP) infection.
Chronic gastritis: with poor correlation between symptoms, endoscopic appearances and histology it is very common in biopsy material and is autoimmune, bacterial or chemical in nature (types A, B and C). The latter is usually antral, related to drug ingestion or bile reflux and comprises a reactive mucosa with a lack of inflammatory cells. Autoimmune gastritis affects the corpus resulting in a spectrum of atrophic gastritis and gastric atrophy with hypochlorhydria, pernicious anaemia and a predisposition to gastric cancer. It is associated with other autoimmune diseases, e.g., diabetes and mucosal damage is mediated by circulating antibodies to gastrin receptors on the parietal cells. The anaemia is due to lack of gastric intrinsic factor with decreased vitamin B12 absorption in the terminal ileum. HP infection is the commonest form of chronic gastritis and increases in incidence with age. The Gram negative, curved bacillus is readily identified (H and E, Cresyl Violet, Giemsa) lying under the surface mucous layer damaging the epithelium and producing a chronic inflammatory reaction in the lamina propria with focal neutrophil polymorph cryptitis. Treatment is by antibiotic eradication.
The Sydney System classifies and grades chronic gastritis based on an assessment of histological (neutrophils, chronic inflammation, atrophy, intestinal metaplasia), topographical (antral/ corpus predominant or pangastritis) and aetiological (HP, drugs) factors.
Chronic gastritis predisposes to peptic ulceration, gastric carcinoma and malignant lymphoma. Unusual variants such as lymphocytic, granulomatous or eosinophilic gastritis are occasionally seen - infective gastritis occurs in immunosuppressed patients (e.g., CMV) or opportunistically overlying ulceration (e.g., candida fungus). Peptic ulceration: there are two patient groups:
1. HP antral gastritis ^ loss of acid regulatory feedback ^ hyperchlorhydria ^ duodenitis ^ duodenal gastric metaplasia with HP colonisation ^ further duodenitis and duodenal ulcer (DU), or
2. HP pangastritis ^ hypoacidity ^ weakening of the mucosal mucous barrier ^ further gastritis ^ erosion and gastric ulceration (GU).
Further risk factors include smoking, alcohol and drugs (NSAIDs, aspirin, steroids). DU outnumbers GU (4:1). Benign gastric ulcers are usually on the lesser curve in the vicinity of the incisura.
Complications include acute or chronic bleeding from the ulcer base, perforation with peritonitis, penetration and fistula to an adjacent organ (e.g., colon or pancreas), fibrotic repair resulting in mechanical obstruction such as pyloric stenosis, and rarely, cancer. Surgery for peptic ulceration has decreased dramatically in the last two decades with the evolution of effective anti-ulcer treatments based largely on antibiotic eradication of HP infection and acid suppression (H2 receptor antagonists, proton pump inhibitors (PPIs)). It is now reserved for those peptic ulcers refractory to medical treatment, in which complications have arisen or there is a suspicion of malignancy. Acute haemorrhage is managed conservatively by laser, electrocoagulation or injection of sclerosant.
Hyperplastic polyps: commonest in the antrum and up to 1.5 cm in size, they form 60% of gastric mucosal polyps and are characterised by dilated, hyperplastic glands in oedematous, inflamed lamina propria. Single or multiple, they probably represent healing of the mucosa after erosion - malignant change is extremely rare although there can be cancer elsewhere in the stomach.
Other non-neoplastic polyps: rare, e.g., hamartomatous polyps (Peutz Jegher's/Cronkhite -Canada syndromes), inflammatory fibroid polyp, or common, such as fundic gland cyst polyps - small, multiple, gastric body, cystic dilatation of specialised glands, incidental or associated with PPI therapy/familial adenomatous polyposis coli (FAPC).
Note that various diseases can present as polypoidal gastric folds or hypertrophic gastropathy, e.g., Menetrier's disease (hypochlordydria, protein loss from elongated gastric pits), ZollingerEllison syndrome (pancreatic/duodenal gastrinomas, hyperchlorhydria, multiple peptic ulcers), Crohn's disease, carcinoma or malignant lymphoma.
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