1. NSAID Gastropathy Group B Lim, Imee – Lim, Mary

2. NSAIDS Weak organic acids that inhibit biosynthesis of prostaglandins Anti-inflammatory, analgesic, antipyretic, antiplatelet effects Ex: Aspirin, Ibuprofen

4. Prostaglandin Regulate the release of mucosal bicarbonate and mucus Inhibit parietal cell secretion Important in maintaining mucosal blood flow Epithelial cell restitution

6. 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

7. 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

8. – 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

9. Risk Factors Advanced age History of ulcer Concomitant use of glucocorticoids High dose or multiple NSAIDS Concomitant of use anticoagulants Serious or multisystem disease

10. Diagnosis - Screening for Aspirin or NSAIDs in Blood and urine

11. Treatment Goals of therapy -Treatment of active ulcer -Prevention of future injury

12. 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

13. 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

14. Prevention of NSAID induced Ulceration H2 receptor antagonist Misoprostol PPI

15. 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