Gout: acute and chronic pharmacotherapy MCQs With Answer

Introduction: This quiz collection focuses on acute and chronic pharmacotherapy of gout tailored for M.Pharm students preparing for Pharmacotherapeutics I (MPP 102T). It summarizes core concepts — mechanisms of action, drug selection for flares and long-term urate-lowering therapy, dosing considerations in renal impairment, major adverse effects, important drug interactions, and monitoring strategies. Questions emphasize clinical pharmacology and rational drug use: when to use NSAIDs, colchicine, corticosteroids, xanthine oxidase inhibitors, uricosurics and recombinant uricases; genetic and comorbidity-related precautions; and prophylaxis during initiation of urate-lowering therapy. Use these MCQs to test knowledge depth and readiness for practical therapeutics decisions in managing gout.

Q1. What is the primary molecular mechanism of action of colchicine in acute gout?

• Inhibits cyclooxygenase-2 (COX-2) selectively
• Inhibits xanthine oxidase, lowering uric acid formation
• Inhibits microtubule polymerization by binding tubulin
• Blocks interleukin-1β receptor signaling directly

Correct Answer: Inhibits microtubule polymerization by binding tubulin

Q2. In an otherwise healthy patient presenting with an acute gout flare, which is the preferred first-line pharmacologic option?

• Initiate long-term allopurinol immediately
• High-dose NSAIDs (e.g., indomethacin or naproxen)
• Daily low-dose colchicine for chronic prophylaxis
• Oral pegloticase

Correct Answer: High-dose NSAIDs (e.g., indomethacin or naproxen)

Q3. How does allopurinol lower serum uric acid concentration?

• Inhibits renal URAT1 transporter to increase uric acid excretion
• Catalyzes conversion of uric acid to allantoin
• Inhibits xanthine oxidase, reducing formation of uric acid
• Enhances hepatic metabolism of purines via CYP3A4 induction

Correct Answer: Inhibits xanthine oxidase, reducing formation of uric acid

Q4. What is the generally recommended timing to initiate urate-lowering therapy (ULT) in patients with a first acute gout flare?

• Start ULT immediately during the acute flare without anti-inflammatory cover
• Begin ULT only after the acute flare has resolved
• Never start ULT; treat only symptomatically
• Initiate ULT and stop anti-inflammatory therapy

Correct Answer: Begin ULT only after the acute flare has resolved

Q5. What is the appropriate initial dosing approach for allopurinol in patients with significant renal impairment?

• Start at full dose (300 mg daily) regardless of renal function
• Start low (e.g., 50–100 mg daily) and titrate cautiously
• Avoid allopurinol entirely and use febuxostat exclusively
• Double the usual starting dose to overcome decreased clearance

Correct Answer: Start low (e.g., 50–100 mg daily) and titrate cautiously

Q6. Which best describes febuxostat’s pharmacologic profile and an important safety consideration?

• Non-purine xanthine oxidase inhibitor with hepatic metabolism and a cardiovascular safety signal
• Uricosuric that blocks URAT1 and causes frequent nephrolithiasis
• Recombinant uricase given orally to convert uric acid to allantoin
• Pyrimidine analog that directly inhibits purine salvage pathway enzymes

Correct Answer: Non-purine xanthine oxidase inhibitor with hepatic metabolism and a cardiovascular safety signal

Q7. Why must azathioprine dosing be adjusted when given concomitantly with allopurinol?

• Allopurinol induces azathioprine metabolism, reducing efficacy
• Allopurinol inhibits xanthine oxidase, increasing azathioprine/6-MP toxicity
• Allopurinol blocks azathioprine absorption in the gut
• There is no significant interaction between allopurinol and azathioprine

Correct Answer: Allopurinol inhibits xanthine oxidase, increasing azathioprine/6-MP toxicity

Q8. What is the principal mechanism of action of probenecid in managing hyperuricemia?

• Enhances hepatic xanthine oxidase activity
• Inhibits renal URAT1-mediated tubular reabsorption of uric acid (uricosuric)
• Acts as a synthetic uricase to degrade uric acid to allantoin
• Blocks prostaglandin synthesis in synovial tissue

Correct Answer: Inhibits renal URAT1-mediated tubular reabsorption of uric acid (uricosuric)

Q9. Which clinical condition is a contraindication to using probenecid for gout management?

• History of recurrent calcium oxalate kidney stones
• History of uric acid nephrolithiasis (kidney stones)
• Mild hyperuricemia without past gout flares
• Concurrent use of xanthine oxidase inhibitors

Correct Answer: History of uric acid nephrolithiasis (kidney stones)

Q10. Pegloticase is indicated for which of the following scenarios and what is a major safety concern?

• First-line for new gout; major concern is hypertension
• Refractory chronic gout with tophi; major concern is infusion reactions and anaphylaxis
• Mild gout with preserved renal function; major concern is nephrolithiasis
• As prophylaxis during ULT initiation; major concern is bone marrow suppression

Correct Answer: Refractory chronic gout with tophi; major concern is infusion reactions and anaphylaxis

Q11. What is the generally accepted serum urate treatment target for most patients on long-term urate-lowering therapy?

• Maintain serum urate >8 mg/dL
• Less than 6 mg/dL (less than 5 mg/dL if tophi present)
• Exactly 7 mg/dL for all patients
• Serum urate is not a useful treatment target

Correct Answer: Less than 6 mg/dL (less than 5 mg/dL if tophi present)

Q12. If NSAIDs are contraindicated (e.g., active peptic ulcer) for an acute gout patient, which alternative is commonly recommended?

• Immediate initiation of allopurinol
• Systemic or intra-articular corticosteroids
• Start long-term probenecid therapy
• Daily pegloticase infusions

Correct Answer: Systemic or intra-articular corticosteroids

Q13. What are the notable toxicities of colchicine, especially when combined with CYP3A4 or P-gp inhibitors?

• Hypertension and hyperglycemia
• Severe diarrhea, gastrointestinal intolerance and neuromyopathy
• Renal failure due to direct nephrotoxicity in all patients
• Thrombocytosis and polycythemia

Correct Answer: Severe diarrhea, gastrointestinal intolerance and neuromyopathy

Q14. What prophylactic strategy is recommended when initiating urate-lowering therapy to reduce the risk of precipitating gout flares?

• No prophylaxis is needed; stop all anti-inflammatory drugs
• Low-dose colchicine or a low-dose NSAID for 3–6 months during ULT initiation
• High-dose corticosteroids indefinitely
• Immediate pegloticase infusion before ULT

Correct Answer: Low-dose colchicine or a low-dose NSAID for 3–6 months during ULT initiation

Q15. Which commonly used antihypertensive class is associated with increasing serum uric acid and precipitating gout?

• ACE inhibitors (e.g., lisinopril)
• Thiazide diuretics (e.g., hydrochlorothiazide) and loop diuretics
• Angiotensin receptor blockers (e.g., losartan)
• Calcium channel blockers (e.g., amlodipine)

Correct Answer: Thiazide diuretics (e.g., hydrochlorothiazide) and loop diuretics

Q16. After effective xanthine oxidase inhibition, which pattern of purine metabolites is expected?

• Increased uric acid and decreased xanthine/hypoxanthine
• Decreased uric acid with increased xanthine and hypoxanthine
• Increased purine nucleotide synthesis causing hyperuricemia
• No change in purine metabolites

Correct Answer: Decreased uric acid with increased xanthine and hypoxanthine

Q17. Which genetic allele is strongly associated with severe allopurinol hypersensitivity (SJS/TEN) and is screened in high‑risk populations?

• HLA-B*1502
• HLA-B*5801
• HLA-DR4
• CYP2C9*3

Correct Answer: HLA-B*5801

Q18. Which agent is preferred for treatment of tumor lysis–related hyperuricemia and which for refractory chronic gout?

• Allopurinol for tumor lysis; probenecid for refractory gout
• Rasburicase for tumor lysis syndrome; pegloticase for refractory chronic gout
• Pegloticase for tumor lysis; febuxostat for refractory gout
• Colchicine for tumor lysis; allopurinol for refractory gout

Correct Answer: Rasburicase for tumor lysis syndrome; pegloticase for refractory chronic gout

Q19. How does urinary alkalinization affect uric acid and stone risk?

• It decreases uric acid solubility and increases stone formation
• It increases uric acid solubility, reducing the risk of uric acid stones
• It converts uric acid to calcium oxalate, increasing stone risk
• It has no effect on uric acid solubility

Correct Answer: It increases uric acid solubility, reducing the risk of uric acid stones

Q20. Before initiating allopurinol therapy, which monitoring or screening step is important in patients from high-risk ethnic groups or with CKD?

• No baseline testing is needed prior to allopurinol
• Screen for HLA-B*5801 allele and assess renal function
• Only measure fasting blood glucose
• Obtain a baseline ECG to rule out QT prolongation

Correct Answer: Screen for HLA-B*5801 allele and assess renal function

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