Acute gastric mucosal injury: pathogenesis and therapy.
Our knowledge concerning the pathogenesis and treatment of acute gastric mucosal injury is rapidly expanding. The gastric mucosa maintains its integrity despite exposure to hydrochloric acid, pepsin, bile, and potentially damaging ingested substances. The balance between gastric mucosal injury and repair is a dynamic process involving multiple complex mechanisms. Clinically, when this process breaks down, acute gastric musocal injury results. Therapy of this disorder has included the use of antisecretory drugs and antacids, while more recent research efforts are exploring the use of cytoprotective agents.
D000208:Acute Disease; D000535:Aluminum / Q000008:administration & dosage / Q000627:therapeutic use; D000818:Animals; D000863:Antacids / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D001639:Bicarbonates / Q000378:metabolism; D002986:Clinical Trials as Topic; D004285:Dogs; D004847:Epithelial Cells; D005753:Gastric Mucosa / Q000166:cytology / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D006801:Humans; D009093:Mucus / Q000378:metabolism; D011453:Prostaglandins / Q000096:biosynthesis / Q000627:therapeutic use; D051381:Rats; D013276:Stomach Ulcer / Q000139:chemically induced / Q000188:drug therapy* / Q000209:etiology*; D013312:Stress, Physiological; D013392:Sucralfate
D000863:Antacids; D000897:Anti-Ulcer Agents; D001639:Bicarbonates; D011453:Prostaglandins; D013392:Sucralfate; D000535:Aluminum