Chapter 22: Prostaglandins, NSAIDs, and Pharmacotherapy of Gout
Which NSAID has the least anti-inflammatory efficacy?
Answer is b. Acetaminophen, is antipyretic and analgesic, but is largely devoid of anti-inflammatory activity.
Which NSAID permanently inactivates TxA2 synthesis by platelets?
Answer is a. Aspirin is an irreversible inhibitor of COX-1. Because platelets are anucleate and have minimal capacity for synthesis of new protein, inhibition of platelet COX-1 lasts for the lifetime of the platelet (8-12 days).
What is the primary mechanism of action of allopurinol in treating gout?
a. It is an analgesic agent.
b. It is an anti-inflammatory agent.
c. It blocks inflammatory responses to urate crystals.
d. It inhibits urate formation.
e. It augments urate excretion.
Answer is d. Allopurinol inhibits xanthine oxidase and prevents the synthesis of urate from hypoxanthine and xanthine.
The cardiovascular risk associated with celecoxib results from
a. inhibition of prostaglandin production in the gastric epithelium.
b. inhibition of platelet thromboxane production.
c. effects on myocardial ion channels.
d. inhibition of prostaglandin in the kidney.
e. enhanced prostacyclin production by vascular endothelium.
Answer is d. Inhibition of PG production in the kidney, which increases the likelihood of hypertension and edema, occurs with celecoxib, as well as nonselective COX inhibitors. The lack of an effect on COX-1 production in platelets and the inhibition of prostacyclin synthesis by COX-2 in vascular endothelium increase the risk of thrombosis resulting in myocardial infarction and ischemic stroke.
Diclofenac has a t1/2 in plasma of 1 to 2 hours, yet its therapeutic effects in treating rheumatoid arthritis last for much longer. This prolongation of therapeutic effect is due to