Hyperuricemia MCQs With Answer

Hyperuricemia MCQs With Answer provide B. Pharm students a focused, practical way to master hyperuricemia’s pharmacology, pathophysiology, diagnosis, and drug therapy. This concise introduction and question set emphasize serum uric acid regulation, xanthine oxidase inhibitors, uricosurics, biologics, adverse effects, drug interactions, genetic risk factors (e.g., HLA-B*5801), and special populations such as renal impairment and tumour lysis syndrome. Questions also cover monitoring parameters, mechanisms of urate transporters (URAT1, GLUT9, ABCG2), and evidence-based prevention strategies. These targeted MCQs help strengthen clinical reasoning and dispensing decisions relevant to B. Pharm training. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. Which enzyme catalyzes the final steps in uric acid production?

  • Xanthine oxidase
  • Uricase
  • Hypoxanthine phosphoribosyltransferase (HPRT)
  • Adenine deaminase

Correct Answer: Xanthine oxidase

Q2. Hyperuricemia is defined as fasting serum uric acid concentration typically above which value in adult males?

  • 4 mg/dL
  • 6 mg/dL
  • 7 mg/dL
  • 9 mg/dL

Correct Answer: 7 mg/dL

Q3. The primary mechanism of action of allopurinol is:

  • Inhibition of URAT1 transporter
  • Competitive inhibition of xanthine oxidase via alloxanthine (oxypurinol)
  • Enhancing renal uric acid excretion by alkalinizing urine
  • Neutralizing urate crystals in synovial fluid

Correct Answer: Competitive inhibition of xanthine oxidase via alloxanthine (oxypurinol)

Q4. Which uricosuric drug works primarily by inhibiting URAT1 to increase renal uric acid excretion?

  • Allopurinol
  • Febuxostat
  • Probenecid
  • Colchicine

Correct Answer: Probenecid

Q5. Febuxostat differs from allopurinol because it:

  • Is a purine analogue metabolized to oxypurinol
  • Non-competitively inhibits xanthine oxidase and is non-purine based
  • Directly degrades uric acid to allantoin
  • Acts as a uricosuric agent at high doses

Correct Answer: Non-competitively inhibits xanthine oxidase and is non-purine based

Q6. A major severe adverse reaction associated with allopurinol, especially in HLA-B*5801 carriers, is:

  • Hepatic failure
  • Stevens-Johnson syndrome/TEN
  • Peripheral neuropathy
  • Ototoxicity

Correct Answer: Stevens-Johnson syndrome/TEN

Q7. Pegloticase treats refractory gout by:

  • Inhibiting xanthine oxidase
  • Enhancing renal urate secretion
  • Converting uric acid to allantoin via recombinant uricase
  • Blocking IL-1 mediated inflammation

Correct Answer: Converting uric acid to allantoin via recombinant uricase

Q8. Which of the following increases serum uric acid by reducing renal uric acid excretion?

  • Thiazide diuretics
  • ACE inhibitors
  • Beta blockers
  • Calcium channel blockers

Correct Answer: Thiazide diuretics

Q9. In tumour lysis syndrome, hyperuricemia occurs primarily due to:

  • Decreased uric acid production
  • Massive nucleic acid breakdown releasing purines
  • Excess dietary purine intake
  • Increased uricase activity

Correct Answer: Massive nucleic acid breakdown releasing purines

Q10. Which laboratory parameter is most directly used to diagnose hyperuricemia?

  • Serum creatinine
  • Serum uric acid concentration
  • Urine protein
  • Serum urea

Correct Answer: Serum uric acid concentration

Q11. Monitoring of patients on allopurinol should include which test due to potential toxicity?

  • Complete blood count and liver function tests
  • Serum magnesium
  • Serum troponin
  • Pulmonary function tests

Correct Answer: Complete blood count and liver function tests

Q12. Colchicine’s mechanism in gout prophylaxis is mainly:

  • Inhibition of xanthine oxidase
  • Depolymerization of microtubules reducing neutrophil chemotaxis
  • Activation of uricase
  • Inducing diuresis to increase uric acid excretion

Correct Answer: Depolymerization of microtubules reducing neutrophil chemotaxis

Q13. Which transporter mutation is associated with increased intestinal urate excretion and protection against hyperuricemia?

  • URAT1 gain-of-function
  • ABCG2 loss-of-function
  • GLUT9 loss-of-function
  • HPRT deficiency

Correct Answer: ABCG2 loss-of-function

Q14. Which drug requires HLA-B*5801 screening in certain populations due to high risk of severe cutaneous adverse reactions?

  • Febuxostat
  • Allopurinol
  • Probenecid
  • Colchicine

Correct Answer: Allopurinol

Q15. Which of the following is a uricase enzyme not naturally present in humans but used therapeutically?

  • Rasburicase
  • Allopurinol
  • Febuxostat
  • Probenecid

Correct Answer: Rasburicase

Q16. Which dietary change most effectively reduces risk of hyperuricemia?

  • Increased intake of red meat and seafood
  • Increased consumption of fructose-sweetened beverages
  • Reduced intake of high-purine foods and alcohol
  • Increased dairy fat intake

Correct Answer: Reduced intake of high-purine foods and alcohol

Q17. The first-line chronic urate-lowering therapy for most gout patients is:

  • Probenecid
  • Colchicine
  • Allopurinol
  • Rasburicase

Correct Answer: Allopurinol

Q18. Which adverse effect is a dose-limiting toxicity of colchicine?

  • Nephrotoxicity
  • Gastrointestinal upset and diarrhea
  • Hypoglycemia
  • Cardiotoxicity

Correct Answer: Gastrointestinal upset and diarrhea

Q19. Febuxostat is preferable over allopurinol in patients with:

  • Severe hepatic impairment only
  • Severe allergy or intolerance to allopurinol
  • Pregnancy
  • Children under 12 years

Correct Answer: Severe allergy or intolerance to allopurinol

Q20. Urate nephropathy is primarily caused by:

  • Deposition of urate crystals in renal tubules leading to obstruction and inflammation
  • Excessive uricase activity in kidneys
  • Autoimmune glomerulonephritis
  • Liver failure

Correct Answer: Deposition of urate crystals in renal tubules leading to obstruction and inflammation

Q21. Which of the following is TRUE regarding urinary alkalinization for uric acid stones?

  • It decreases uric acid solubility and promotes stone formation
  • It increases uric acid solubility and helps dissolve uric acid stones
  • It is contraindicated when using allopurinol
  • It increases serum uric acid concentration

Correct Answer: It increases uric acid solubility and helps dissolve uric acid stones

Q22. Secondary hyperuricemia causes include all EXCEPT:

  • Chronic kidney disease
  • Leukemia undergoing chemotherapy
  • High-purine diet
  • Congenital HPRT overactivity

Correct Answer: Congenital HPRT overactivity

Q23. Which drug interaction increases risk of allopurinol toxicity by inhibiting its renal excretion or enhancing oxypurinol levels?

  • Probenecid coadministration
  • ACE inhibitors coadministration
  • Rifampicin coadministration
  • Warfarin coadministration

Correct Answer: Probenecid coadministration

Q24. HPRT deficiency (Lesch-Nyhan syndrome) leads to severe hyperuricemia due to:

  • Increased salvage of purines leading to low uric acid
  • Overproduction of uric acid from impaired purine salvage
  • Excess uricase activity
  • Increased renal excretion of uric acid

Correct Answer: Overproduction of uric acid from impaired purine salvage

Q25. Which monitoring parameter is most important when using rasburicase for tumour lysis syndrome?

  • Blood glucose
  • Methemoglobin level and hemolysis risk in G6PD deficiency
  • Thyroid function tests
  • Serum potassium only

Correct Answer: Methemoglobin level and hemolysis risk in G6PD deficiency

Q26. Which statement about uric acid physiology is correct?

  • Humans express uricase and convert uric acid to allantoin
  • Uric acid is the end product of purine metabolism in humans
  • Uric acid is highly soluble at acidic pH
  • All purines are exclusively excreted via bile

Correct Answer: Uric acid is the end product of purine metabolism in humans

Q27. Which transporter is primarily responsible for renal reabsorption of uric acid in the proximal tubule?

  • NKCC2
  • URAT1
  • ENaC
  • Na+/K+ ATPase

Correct Answer: URAT1

Q28. An acute gout attack should generally NOT be initiated with which approach?

  • Immediate initiation of urate-lowering therapy with allopurinol at full dose
  • NSAIDs for acute pain control
  • Colchicine started early for anti-inflammatory effect
  • Short course corticosteroids if NSAIDs contraindicated

Correct Answer: Immediate initiation of urate-lowering therapy with allopurinol at full dose

Q29. Which lab finding is typical during an acute gout flare?

  • Synovial fluid with negatively birefringent, needle-shaped crystals
  • Synovial fluid high in cholesterol crystals
  • Positively birefringent, rhomboid crystals
  • Synovial fluid sterile with no crystals

Correct Answer: Synovial fluid with negatively birefringent, needle-shaped crystals

Q30. Long-term urate-lowering therapy target for serum uric acid in gout patients is typically:

  • Above 8 mg/dL
  • Less than 6 mg/dL
  • Exactly 7.5 mg/dL
  • Greater than 10 mg/dL

Correct Answer: Less than 6 mg/dL

Q31. Which adverse effect is specifically associated with febuxostat in some studies prompting caution?

  • Increased cardiovascular mortality risk in certain populations
  • Severe ototoxicity
  • Renal tubular necrosis
  • Hyperthyroidism

Correct Answer: Increased cardiovascular mortality risk in certain populations

Q32. For patients with frequent uric acid kidney stones, which pharmacologic strategy is commonly recommended?

  • Urine acidification with ammonium chloride
  • Urine alkalinization with potassium citrate
  • High-purine diet to increase urine flow
  • Allopurinol discontinuation

Correct Answer: Urine alkalinization with potassium citrate

Q33. Which of the following increases uric acid production leading to hyperuricemia?

  • Rapid cell turnover such as in leukemia
  • Use of xanthine oxidase inhibitors
  • Low purine diet
  • Activation of uricase

Correct Answer: Rapid cell turnover such as in leukemia

Q34. Which statement about probenecid is TRUE?

  • It is effective in patients with severe renal impairment (CrCl <30 mL/min)
  • It blocks URAT1 increasing renal uric acid excretion
  • It directly degrades uric acid to allantoin
  • It is a xanthine oxidase inhibitor

Correct Answer: It blocks URAT1 increasing renal uric acid excretion

Q35. Which condition is a contraindication to rasburicase administration?

  • Pregnancy
  • G6PD deficiency due to hemolysis risk
  • Hypertension
  • Hyperlipidemia

Correct Answer: G6PD deficiency due to hemolysis risk

Q36. Which of the following best describes the role of ABCG2 transporter in urate homeostasis?

  • Renal reabsorption of urate in the late distal tubule
  • Facilitates extra-renal (intestinal) urate excretion
  • Direct enzymatic degradation of uric acid
  • Activation of xanthine oxidase

Correct Answer: Facilitates extra-renal (intestinal) urate excretion

Q37. During initiation of urate-lowering therapy, prophylaxis to prevent gout flares is commonly given. Which is used?

  • Low-dose colchicine or low-dose NSAID for several months
  • High-dose corticosteroids indefinitely
  • Immediate high-dose allopurinol without prophylaxis
  • Rasburicase monthly

Correct Answer: Low-dose colchicine or low-dose NSAID for several months

Q38. Which medication decreases uric acid production but is contraindicated or used with caution in severe hepatic impairment?

  • Probenecid
  • Febuxostat
  • Colchicine
  • Rasburicase

Correct Answer: Febuxostat

Q39. A patient with gout on allopurinol develops a maculopapular rash. The correct immediate step is:

  • Ignore rash and continue allopurinol
  • Stop allopurinol and evaluate for severe hypersensitivity
  • Increase the allopurinol dose
  • Switch to probenecid immediately without assessment

Correct Answer: Stop allopurinol and evaluate for severe hypersensitivity

Q40. Which laboratory ratio or calculation can help distinguish overproduction from underexcretion of uric acid?

  • Fractional excretion of uric acid (FEUA) or 24‑hour urinary uric acid excretion
  • Serum potassium to sodium ratio
  • Serum phosphate level
  • Urine osmolality alone

Correct Answer: Fractional excretion of uric acid (FEUA) or 24‑hour urinary uric acid excretion

Q41. Which of the following is the MAIN reason to avoid initiating urate-lowering therapy during an acute gout flare?

  • It will always worsen renal function
  • It can exacerbate or prolong the flare if started at full dose
  • It is ineffective unless given intravenously
  • Urate-lowering drugs are contraindicated with NSAIDs

Correct Answer: It can exacerbate or prolong the flare if started at full dose

Q42. Prolonged use of which medication class commonly used for hypertension is associated with increased serum urate?

  • Thiazide diuretics
  • ACE inhibitors
  • Calcium channel blockers
  • Angiotensin receptor blockers (all except losartan)

Correct Answer: Thiazide diuretics

Q43. Which statement about allopurinol dose adjustment is correct for renal impairment?

  • Allopurinol dose should always be increased in renal impairment
  • Dose of allopurinol or oxypurinol accumulation must be considered and adjusted in renal impairment
  • Renal function has no impact on allopurinol dosing
  • Allopurinol is contraindicated in any renal impairment

Correct Answer: Dose of allopurinol or oxypurinol accumulation must be considered and adjusted in renal impairment

Q44. Which metabolic condition is commonly associated with hyperuricemia and gout?

  • Hypothyroidism
  • Metabolic syndrome and insulin resistance
  • Type 1 hypersensitivity
  • Iron deficiency anemia

Correct Answer: Metabolic syndrome and insulin resistance

Q45. Which of the following is TRUE about uric acid solubility?

  • Uric acid is more soluble at acidic pH
  • Uric acid solubility decreases at lower pH and increases with alkalinization
  • Solubility is independent of urine pH
  • Alkalinization always causes uric acid stones

Correct Answer: Uric acid solubility decreases at lower pH and increases with alkalinization

Q46. Drug-induced hyperuricemia can occur with which anticancer agent due to tumour lysis risk?

  • All chemotherapy agents uniformly
  • Agents causing rapid tumour cell lysis such as certain cytotoxic regimens—e.g., high‑burden lymphoma therapy
  • Only hormonal therapies
  • Only targeted small molecules with no cell kill

Correct Answer: Agents causing rapid tumour cell lysis such as certain cytotoxic regimens—e.g., high‑burden lymphoma therapy

Q47. Which of the following is indicated for rapid reduction of extremely high serum uric acid in tumour lysis syndrome?

  • Oral allopurinol only
  • Rasburicase (IV recombinant urate oxidase)
  • Probenecid orally
  • Low-dose aspirin

Correct Answer: Rasburicase (IV recombinant urate oxidase)

Q48. In a patient with gout and chronic kidney disease (CKD), which urate-lowering agent might require cautious use or dose adjustment?

  • Febuxostat without caution
  • Probenecid, which is less effective and may be contraindicated in advanced CKD
  • Pegloticase as first-line in CKD stage 4
  • High-dose potassium citrate as sole therapy

Correct Answer: Probenecid, which is less effective and may be contraindicated in advanced CKD

Q49. Which genetic test may be considered before starting allopurinol in high-risk ethnic groups?

  • HLA-B*5801 screening
  • BRCA1 testing
  • CYP2D6 genotyping
  • HLA-A*0201 screening

Correct Answer: HLA-B*5801 screening

Q50. Which patient counselling point is important when dispensing urate-lowering therapy?

  • Stop urate-lowering therapy as soon as the first gout flare resolves
  • Adherence is important; therapy is usually long-term and serum uric acid target should be maintained
  • There is no need for monitoring serum uric acid once therapy starts
  • Increase intake of alcoholic beverages to improve efficacy

Correct Answer: Adherence is important; therapy is usually long-term and serum uric acid target should be maintained

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