By Robert Logan, Adam Harris, J. J. Misiewicz, J. H. Baron
(BMJ Books) Univ. sanatorium, Nottingham, united kingdom. presents a concise consultant to issues of the higher gastrointestinal tract. hugely illustrated with charts, diagrams, and colour photos. displays newest advances in knowing the pathophysiology and pathogenesis of this sickness. For scientific scholars, nurses, and clinicians. Softcover.
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Additional info for ABC of the Upper Gastrointestinal
After exclusion of surreptitious use of ulcerogenic drugs and the rarer causes of duodenal ulcer, such patients need long term maintenance treatment with antisecretory drugs. 1 Causes of duodenal ulcer Common causes x H pylori infection x Non-steroidal anti-inflammatory drugs Rare causes x Zollinger-Ellison syndrome x Hypercalcaemia x Granulomatous diseases (Crohn’s disease, sarcoidosis) x Neoplasia (carcinoma, lymphoma, leiomyoma, leiomyosarcoma) x Infections (tuberculosis, syphilis, herpes simplex, cytomegalovirus) x Ectopic pancreatic tissue Management of Helicobacter pylori infection Gastric ulcer Gastric ulcer found after barium meal Diagnosis The main difference in the management of gastric ulcers from that of duodenal ulcers is the need to exclude malignancy in an apparently benign gastric ulcer.
4 In these studies omeprazole protected against ulcers, both gastric and particularly duodenal, and erosions. Misoprostol was associated with the same rate of duodenal ulcer formation as placebo but was particularly effective in preventing multiple erosions. In these studies the site of the initial lesion was a strong predictor of the site of subsequent relapse. NSAID users without ulcers Many studies have shown that misoprostol can inhibit ulcer development in such patients, as can famotidine 40 mg twice daily and omeprazole.
The unreliability of dyspepsia as a pointer to ulceration underlies many of the problems of managing patients taking NSAIDs. Within 90 minutes of taking 300 mg or 600 mg of aspirin, nearly everyone develops acute injury consisting of intramucosal petechiae and erosions. Non-aspirin NSAIDs cause less florid acute injury, but endoscopic studies show that about 20% of those taking non-aspirin NSAIDs or aspirin at anti-inflammatory doses chronically have a gastric or duodenal ulcer. Many patients who start NSAIDs will not be able to continue because of drug associated dyspepsia.