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- W25114501 abstract "This chapter discusses the pathophysiology and pathology of gastritis and gastricmucosal hypertrophy. It also discusses the symptoms, diagnosis, and treatment of gastritis and gastricmucosal hypertrophy. The mucosa of the stomach may be injured by a variety of agents, ethyl alcohol, aspirin, other inhibitors of prostaglandin (PG) synthesis, bile salts, and certain bacterial toxins being prominent offenders. Where the exposure to noxious agents is protracted, chronic persistent inflammatory changes may occur, particularly in the antrum or at the antral-oxyntic junction. On the other hand, chronic gastritis of the fundus and body appears to be predominantly the result of autoimmune phenomena. Superficial gastritis may be diffusely distributed throughout the stomach, and consists of hyperemia and edema, especially of the lamina propria with some extension into the submucosa. There is moderate infiltration of segmented granulocytes and a slight focal degranulation but not disruption of the surface epithelium. Erosive gastritis is similar to superficial gastritis except that the delicate neck region of the gastric gland tends to undergo necrosis so that in addition to the changes described above, there is also focal sloughing of the mucosa. Management of acute gastritis consists of controlling blood loss, identifying and discontinuing any noxious agents, and providing a milieu for the gastritis or lacerations to heal. This latter aspect of treatment is usually managed adequately by reducing the secretion of acid with cimetidine or by raising intragastric pH with doses of oral antacids capable of neutralizing HCl every two to four hours. While they are potentially attractive therapeutic agents, methylated prostaglandins are not yet available for clinical use." @default.
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- W25114501 date "1982-01-01" @default.
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- W25114501 title "Gastritis and Gastric Mucosal Hypertrophy" @default.
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- W25114501 doi "https://doi.org/10.1016/b978-0-409-95021-2.50010-8" @default.
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