1. A. By blocking renal prostaglandin synthesis, COX-2 inhibitors, such as rofecoxib, decrease the blood flow to the juxtaglomerular apparatus, thus stimulating the release of renin and subsequent Na+ retention and blood pressure elevation. Rofecoxib is neither metabolized nor induced by CYP2C9. It decreases rather than increases renal blood flow and does not increase the excretion of hy-drochlorothiazide. Item D is incorrect because rofe-coxib has very little effect on COX-1 and prostaglandins are not a major controlling factor of peripheral vascular tone. Rofecoxib does not decrease basal metabolic rate.
2. E. Treatment guidelines suggest the use of DMARDs early in the course of rheumatoid arthritis to slow the joint deterioration associated with the disease. Methotrexate is the DMARD of choice for people with moderate to severe forms of rheumatoid arthritis. Although NSAIDs can decrease methotrexate clearance, NSAIDs can be safely used with the low doses of methotrexate used in the therapy of rheumatoid arthritis. Methotrexate is highly teratogenic and should not be used by women who are or may become pregnant.
3. C. The likelihood of gastric ulceration and GI bleeding is increased by heavy alcohol use, poor health, advanced age, long-term NSAID use, and use of drugs such as corticosteroids and anticoagulants. Ibuprofen is not converted to a cardiotoxic metabolite. Dermal toxicities, such as epidermal necrolysis, are rare complications of ibuprofen therapy, but necrotizing fasciitis is not one of them. Confusion and ataxia are not side effects associated with ibuprofen, nor is eosinophilia.
4. D. Etanercept is a recombinant fusion protein consisting of two TNF receptor domains linked to one IgG Fc molecule. It binds to soluble TNF-a and TNF-p and forms inactive complexes. It does not directly affect cAMP phosphodiesterase, leukotriene synthesis, or autoantibody production.
5. A. Celecoxib selectively inhibits COX-2, so it does not inhibit the constitutive activity of COX-1 in the regulation of gastric acid secretion. When prostaglandin synthesis by COX-1 or COX-2 is blocked, eicosanoids are shifted into the leukotriene pathway, so bronchospasm and hypersensitivity reactions are favored. The shorter half-life of cele-coxib does not allow once-daily dosing. This drug is no less able than other NSAIDs to close the ductus arteriosus during the third trimester. None of the NSAIDs is empirically more efficacious than the others; a patient's own response and side effects determine the best drug for him or her.
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