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THE ANSWER IS D.

NSAIDs inhibit cyclooxygenase (COX) thereby inhibiting the synthesis of prostaglandin, a key mediator of inflammation. The analgesic effect of NSAIDs is peripherally mediated by decreasing prostaglandin and raising the threshold of activation of nocireceptors. There are two distinct COX isoenzymes: COX-1 and COX-2. Selective inhibition of COX-2 leads to greater inhibition of prostacyclin production than thromboxane which may lead to prothrombotic effects, increasing the risk of cardiovascular disease. These effects seem to be balanced out in non-selective COX inhibitors, resulting in few changes in cardiovascular risk.

Inhibition of COX-1, particularly in volume-depleted patients, can result in a decreased glomerular filtration rate and renal insufficiency (A). NSAIDs enhance lithium reabsorption (B) and may reduce lithium excretion leading to increased lithium levels and clinical effects. NSAIDs do displace protein-bound warfarin, but this may lead to an increase in prothrombin time (C), not decrease.

Reference

Miner JR, Paris PM, Yealy DM: Pain Management, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 186:p 2422-2424.

 

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