Other causes of GI mucosal injury: upper intestinal content.
Factors in upper intestinal content that can produce acute injury to the gastric mucosa include lysolecithin and the bile acids. Both damage the gastric mucosal barrier by increasing mucosal permeability. The secondary and deconjugated bile acids are more toxic in this regard than are the primary or conjugated ones. The extent of injury is highly pH-dependent. Although the bile acids do not affect the gel properties of gastric mucus, they do produce significant inhibition of carbonic anhydrase activity and gastric bicarbonate secretion. In concert with other topical damaging agents, bile acids increase mucosal blood flow. However, gross mucosal lesions are rarely observed under these circumstances. Chronic exposure of acid-peptic-secreting mucosa to upper intestinal content results in the development of a severe atrophic gastritis within 6 months. The ability of atrophic mucosa to maintain an intraluminal pH gradient is impaired, and it ulcerates with great regularity when exposed to a highly acid environment. Clinically, excessive enterogastric reflux has been implicated in the pathogenesis of both benign gastric ulcer and the post-gastrectomy syndrome of alkaline reflux gastritis. The evidence to support this view for both disease entities is reviewed.
D001647:Bile Acids and Salts / Q000502:physiology*; D005743:Gastrectomy / Q000009:adverse effects; D005753:Gastric Mucosa / Q000098:blood supply / Q000473:pathology*; D005756:Gastritis / Q000209:etiology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007421:Intestine, Small / Q000502:physiology*; D008244:Lysophosphatidylcholines / Q000502:physiology; D010179:Pancreas / Q000201:enzymology; D010434:Pepsin A / Q000378:metabolism; D013276:Stomach Ulcer / Q000209:etiology*
D001647:Bile Acids and Salts; D008244:Lysophosphatidylcholines; D010434:Pepsin A