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NSAID Gastropathy Group B Lim, Imee – Lim, Mary
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NSAIDS Weak organic acids that inhibit biosynthesis of prostaglandins Anti-inflammatory, analgesic, antipyretic, antiplatelet effects Ex: Aspirin, Ibuprofen
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Prostaglandin Regulate the release of mucosal bicarbonate and mucus Inhibit parietal cell secretion Important in maintaining mucosal blood flow Epithelial cell restitution
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Symptoms: Epigastric pain (burning or gnawing) – Ill-defined, aching sensation, hunger pain – DU: 90min-3hrs after meals Relieved by antacids or food Pain that awakes the patient from sleep – GU: pain precipitated by food acid-induced activation of chemical receptors in the duodenum enhanced duodenal sensitivity to bile acids and pepsin or altered gastroduodenal motility
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Complications – Variation in intensity or distribution of pain as well as onset of associated symptoms – Penetrating Ulcer: Dyspepsia that is no longer relieved by food or antacids and radiates to the back – Bleeding: Tarry stool, coffee ground emesis
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– Perforation: Severely tender, board-like abdomen Sudden onset of severe generalized abdominal pain – Gastric outlet obstruction Pain worsening with meals, nausea and vomiting Presence of succussion splash
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Risk Factors Advanced age History of ulcer Concomitant use of glucocorticoids High dose or multiple NSAIDS Concomitant of use anticoagulants Serious or multisystem disease
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Diagnosis - Screening for Aspirin or NSAIDs in Blood and urine
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Treatment Goals of therapy -Treatment of active ulcer -Prevention of future injury
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Harrison's Principles of Internal Medicine 17th Ed Recommendation for Treatment of NSAID related mucosal injury Clinical SettingRecommendation Active ulcer NSAID discontinued NSAID continued H 2 receptor antagonist or PPI PPI Prophylactic therapyMisoprostol PPI Selective COX-2 inhibitor H. Pylori infectionEradication if active ulcer is present or there is a past history of peptic ulcer disease
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Harrison's Principles of Internal Medicine 17th Ed Guide to NSAID Therapy No/ Low NSAID GI RiskNSAID GI Risk No CV risk (no Aspirin) Traditional NSAIDCoxib or Traditional NSAID + PPI Consider non-NSAID therapy CV risk (consider Aspirin) Traditional NSAID + PPI if GI risk warrants gastroprotection Consider non-NSAID therapy A gastroprotective agent must be added if a traditional NSAID is prescribed Consider non-NSAID therapy
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Prevention of NSAID induced Ulceration H2 receptor antagonist Misoprostol PPI
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NSAID gastropathy Patient’s history of taking diclofenac Na with concomitant use of clopidogrel Patient’s advanced age (65 years old) Bleeding as complication of NSAID-induced disease
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