Current views on pathogenesis of peptic ulcer.
In duodenal ulcer disease, peptic digestion and ulceration of the duodenal mucosa can be related to increased duodenal acidity, which in about half the patients is due to inherited gastric hypersecretion, with too many parietal and chief cells. The others, normosecretors, may have parietal and chief cells excessively stimulated by, and/or specially sensitive to, gastrins and the vagus, together with inadequate suppression of the release of antral gastrin and the secretion of gastric acid. The abnormality is gastric hypersecretion with inappropriate hypergastrinaemia. The reserve capacities of the duodenal defence mechanisms are probably normal, but there seems to be a functional impairment with inadequate defence by decreased bicarbonate secretion into the duodenum, but as yet no clear impairment of the release of mucosal hormones. There are marked hereditary factors in gastric ulcer too. Some ulcers are related to gastric irritants (salicylates, tobacco). Oi's anatomical dual-control mechanism explains why gastric ulcers are usually solitary and at one site. Gastritis and duodenal reflux are probably the most important factors in type 1, body ulcers. Gastric stasis may be a factor in type 2, combined ulcers. Type 3 prepyloric ulcers resemble duodenal ulcers, both in blood group and hypersecretion.
D004386:Duodenum / Q000503:physiopathology; D004777:Environment; D005744:Gastric Acid / Q000502:physiology; D005753:Gastric Mucosa / Q000503:physiopathology; D005768:Gastrointestinal Hormones / Q000502:physiology; D006632:Histamine / Q000502:physiology; D006801:Humans; D007413:Intestinal Mucosa / Q000503:physiopathology; D010434:Pepsin A / Q000502:physiology; D010437:Peptic Ulcer / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D013276:Stomach Ulcer / Q000503:physiopathology
D005768:Gastrointestinal Hormones; D006632:Histamine; D010434:Pepsin A