1. The most widely used agent for the treatment of acute gouty arthritis is
2. The mechanism by which probenecid lowers plasma levels of uric acid is
(A) By inhibiting proximal tubular reabsorption of uric acid
(B) By inhibiting production of uric acid in the liver
(C) By promoting tubular secretion of uric acid
(D) By inhibiting breakdown of purines to uric acid
3. Allopurinol reduces serum urate levels by
(A) Promoting the active secretion of uric acid in kidneys
(B) Inhibiting uric acid synthesis
(C) Impairing renal urate reabsorption
(D) Decreasing metabolism of uric acid
4. The primary location in the kidney where both carrier-mediated reabsorption and secretion of urate occurs is the
(A) Ascending loop of Henle
(B) Distal tubules
(C) Collecting duct
(D) Proximal tubule
(E) Descending loop of Henle
5. Drug therapy is more effective in controlling uric acid production than is dietary restriction because
(A) Dietary restriction does not affect production of uric acid
(B) Drug therapy is more specific to the site of action
(C) Only a small portion of blood uric acid is derived from the diet
(D) The source of uric acid cannot be established ANSWERS
1. C. Colchicine is relatively selective for the treatment of acute gouty arthritis because it appears to prevent the release of inflammatory cytokines and chemotactic factors. Probenecid (A) blocks renal uric acid reabsorption but is generally not used alone during the acute phase of gout. Allopurinol (B) is the drug of choice in chronic tophaceous gout. Indomethacin (D) and phenylbutazone (E)
have antiinflammatory activity and are useful in treating acute gouty arthritis but are not used nearly as widely as colchicine for initial treatment.
2. A. Probenecid blocks active reabsorption of uric acid in the proximal tubules following glomerular filtration. It does not inhibit uric acid synthesis (B), stimulate tubular secretion (C), or inhibit the metabolism of purines (D).
3. B. Allopurinol inhibits xanthine oxidase, the enzyme involved in the conversion of hypoxanthine and xanthine to uric acid. It has no known ability to increase uric acid synthesis markedly (A), inhibit reabsorption (C), or impair uric acid breakdown (D).
4. D. While the other parts of the renal tubular system do contain active transport systems, these systems do not have an affinity of urate transport.
5. C. The dietary intake of purines is not a major contributing factor to uric acid blood levels. Therefore, pharmacological reduction of uric acid synthesis or increased excretion is required. Dietary restriction (A) can affect uric acid production if precursor molecules are lowered sufficiently, but this usually is not feasible. The question of drug specificity (B) is not germane to the question. Pathways of uric acid synthesis in the body (D) are well known.
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