Drugs Used in Gout and Hyperuricemia — MCQs
A drug used in acute gout -
A 55-year-old patient with gout has high uric acid levels; which drug should be avoided?
What is the mechanism of action of colchicine in acute gout?
What is the drug of choice for the treatment of acute gout in patients in whom NSAIDs are contraindicated?
A patient with recurrent gout attacks was started on a drug that inhibits uric acid synthesis. His symptoms were reduced after therapy. Which drug was he started on?
Gout is NOT caused by which of the following?
Furosemide causes all except -
Pegloticase is used in:
Which of the following drugs is useful in acute attack of gout ?
Which of the following is not used in acute attack of severe pain due to gout ?
Drugs Used in Gout and Hyperuricemia Indian Medical PG Practice Questions and MCQs
Question 1: A drug used in acute gout -
- A. Colchicine (Correct Answer)
- B. Sulfinpyrazone
- C. Allopurinol
- D. Probenecid
Explanation: ***Colchicine*** - **Colchicine** is an anti-inflammatory drug that is effective in treating acute gout flares by inhibiting neutrophil migration and activation. - It is often used as a first-line treatment for acute gout, particularly in its early stages. *Sulfinpyrazone* - **Sulfinpyrazone** is a uricosuric agent, meaning it increases the excretion of uric acid via the kidneys. - It is used for **long-term management** of chronic gout, not for acute attacks. *Probenecid* - **Probenecid** is also a uricosuric drug that works by inhibiting the reabsorption of uric acid in the renal tubules. - Like sulfinpyrazone, it is used for **prophylaxis** in chronic gout to lower serum uric acid levels, not for an acute flare. *Allopurinol* - **Allopurinol** is a xanthine oxidase inhibitor, which reduces the production of uric acid in the body. - It is a cornerstone of **chronic gout management** to prevent future attacks but is not indicated for the immediate treatment of an acute flare as it can sometimes worsen the acute attack initially.
Question 2: A 55-year-old patient with gout has high uric acid levels; which drug should be avoided?
- A. Probenecid
- B. Allopurinol
- C. Febuxostat
- D. Aspirin (Correct Answer)
Explanation: ***Aspirin*** - High doses of **aspirin** can increase serum uric acid levels, which is detrimental for a patient with gout desiring to lower uric acid. - While low-dose aspirin (<300 mg/day) might have a minor uricosuric effect, higher doses are **anti-uricosuric** and should generally be avoided in gout. *Probenecid* - **Probenecid** is a **uricosuric agent** that helps excrete uric acid via the kidneys, making it beneficial for patients who underexcrete uric acid. - It works by inhibiting the reabsorption of uric acid in the renal tubules, thereby lowering serum uric acid levels. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** that reduces the production of uric acid by blocking the enzyme responsible for its synthesis. - It is a cornerstone treatment for chronic gout to lower uric acid levels and prevent recurrent attacks. *Febuxostat* - **Febuxostat** is also a **xanthine oxidase inhibitor**, similar to allopurinol, used to reduce uric acid production. - It is often considered an alternative for patients who cannot tolerate allopurinol or who do not achieve target uric acid levels with allopurinol.
Question 3: What is the mechanism of action of colchicine in acute gout?
- A. Renal disease involving interstitial tissues
- B. Uric acid nephrolithiasis
- C. Deficiency of enzyme Xanthine oxidase
- D. Inhibition of leukocyte migration and phagocytosis (Correct Answer)
Explanation: ***Inhibition of leukocyte migration and phagocytosis*** - Colchicine primarily exerts its anti-inflammatory effect in acute gout by **binding to tubulin**, which inhibits microtubule polymerization. - This action disrupts essential cellular functions in inflammatory cells, particularly **neutrophils**, thereby reducing their migration to inflamed sites and their ability to phagocytose uric acid crystals. *Renal disease involving interstitial tissues* - This option describes a potential complication or manifestation of gout, such as **urate nephropathy**, rather than the mechanism of action of colchicine. - Colchicine does not directly target or treat pre-existing renal interstitial tissue disease as its primary mechanism for acute gout relief. *Uric acid nephrolithiasis* - This condition involves the formation of **kidney stones from uric acid** and is a consequence of chronic hyperuricemia. - Colchicine is not used to acutely treat or prevent the formation of uric acid kidney stones; its role is in managing the inflammatory arthritis of gout. *Deficiency of enzyme Xanthine oxidase* - **Xanthine oxidase** is an enzyme involved in the production of uric acid, and its inhibition (e.g., by allopurinol or febuxostat) is a strategy to lower uric acid levels in the blood. - Colchicine does not affect xanthine oxidase activity; it works downstream by modulating the inflammatory response to uric acid crystals.
Question 4: What is the drug of choice for the treatment of acute gout in patients in whom NSAIDs are contraindicated?
- A. Colchicine (Correct Answer)
- B. Allopurinol
- C. Paracetamol
- D. Febuxostat
Explanation: ***Colchicine*** * **Colchicine** is a highly effective anti-inflammatory agent for acute gout flares, particularly when initiated early in the attack. * It is often the drug of choice when **NSAIDs are contraindicated** due to renal, gastrointestinal, or cardiovascular issues. *Allopurinol* * **Allopurinol** is a **xanthine oxidase inhibitor** used for long-term **gout prophylaxis** by reducing uric acid levels, not for acute attacks. * Initiating allopurinol during an acute flare can sometimes *exacerbate* the attack by transiently shifting uric acid levels. *Febuxostat* * **Febuxostat** is another **xanthine oxidase inhibitor** used for **chronic management of hyperuricemia** in gout patients, similar to allopurinol. * It is not indicated for the **acute treatment of gout** due to its mechanism of action, which focuses on reducing uric acid production over time. *Paracetamol* * **Paracetamol (acetaminophen)** is an **analgesic** and **antipyretic** but possesses very limited anti-inflammatory properties. * It is generally **ineffective** for the intense inflammatory pain and swelling characteristic of an acute gout attack.
Question 5: A patient with recurrent gout attacks was started on a drug that inhibits uric acid synthesis. His symptoms were reduced after therapy. Which drug was he started on?
- A. Probenecid
- B. Colchicine
- C. Diclofenac
- D. Allopurinol (Correct Answer)
Explanation: ***Allopurinol*** - **Allopurinol** is a **xanthine oxidase inhibitor** that effectively reduces uric acid synthesis by blocking the enzyme responsible for converting hypoxanthine and xanthine to uric acid. - It is a cornerstone therapy for preventing recurrent gout attacks in patients with **hyperuricemia**. *Probenecid* - **Probenecid** is a **uricosuric agent** that increases the excretion of uric acid in the urine, rather than inhibiting its synthesis. - It works by inhibiting the reabsorption of uric acid in the renal tubules. *Colchicine* - **Colchicine** is an **anti-inflammatory agent** primarily used to treat acute gout flares and prevent future attacks by disrupting microtubule function and inhibiting neutrophil migration. - It does not affect uric acid synthesis or excretion. *Diclofenac* - **Diclofenac** is a **non-steroidal anti-inflammatory drug (NSAID)** used to manage the pain and inflammation associated with acute gout attacks. - It works by inhibiting prostaglandin synthesis and has no effect on uric acid levels.
Question 6: Gout is NOT caused by which of the following?
- A. Sulfinpyrazone (Correct Answer)
- B. Aspirin
- C. Chlorthalidone
- D. Pyrazinamide
Explanation: ***Sulfinpyrazone*** - **Sulfinpyrazone** is a **uricosuric agent** [1] that *increases* the excretion of uric acid, thereby *reducing* serum uric acid levels. - This medication is used to *treat* gout by preventing attacks, rather than causing them [3]. *Aspirin* - **Low-dose aspirin** can *inhibit* the renal tubular secretion of uric acid, which can lead to an *increase* in serum uric acid levels and potentially precipitate a gout attack [4]. - High doses of aspirin are uricosuric, meaning they increase uric acid excretion, but the more commonly used low doses tend to cause hyperuricemia. *Chlorthalidone* - **Chlorthalidone** is a **thiazide-like diuretic** that *reduces* uric acid excretion by the kidneys, thus *elevating* serum uric acid levels [2]. - Increased serum uric acid levels can lead to the formation of uric acid crystals and trigger acute gout attacks [5]. *Pyrazinamide* - **Pyrazinamide**, an anti-tuberculosis drug, is well-known to *inhibit* the renal tubular excretion of uric acid. - This inhibition leads to **hyperuricemia** and can consequently cause or exacerbate gout.
Question 7: Furosemide causes all except -
- A. Hypokalemia
- B. Ototoxicity
- C. Hypercalcemia (Correct Answer)
- D. Hyperuricemia
Explanation: ***Hypercalcemia*** - Furosemide, a **loop diuretic**, inhibits the reabsorption of calcium in the thick ascending limb of the loop of Henle, leading to increased urinary calcium excretion and thus **hypocalcemia**, not hypercalcemia. - This effect makes loop diuretics useful in managing **hypercalcemia** by promoting calcium excretion. *Hypokalemia* - Furosemide inhibits the Na-K-2Cl cotransporter, leading to increased delivery of sodium to the collecting duct, which enhances potassium secretion and can cause **hypokalemia**. - Monitoring serum potassium levels and potassium supplementation are often necessary during furosemide therapy. *Ototoxicity* - Furosemide can cause **ototoxicity**, particularly with rapid intravenous administration or in patients with renal impairment. - This adverse effect typically manifests as **tinnitus** or **hearing loss**, which can be transient or permanent. *Hyperuricemia* - Furosemide competes with uric acid for secretion in the proximal tubule, leading to decreased uric acid excretion and subsequently **hyperuricemia**. - This can precipitate or exacerbate **gout attacks** in susceptible individuals.
Question 8: Pegloticase is used in:
- A. Rheumatoid arthritis
- B. Paralytic ileus
- C. Chronic gout (Correct Answer)
- D. Psoriatic arthritis
Explanation: ***Chronic gout*** - Pegloticase is an enzyme that converts **uric acid to allantoin**, a more water-soluble compound readily excreted by the kidneys. - It is specifically approved for the treatment of **chronic, refractory gout** in patients who have failed to achieve target serum uric acid levels with conventional therapies. *Rheumatoid arthritis* - This condition is an **autoimmune inflammatory disease** primarily affecting the joints. - Treatment typically involves **DMARDs** (disease-modifying antirheumatic drugs) such as methotrexate, biologics, and corticosteroids, not pegloticase. *Paralytic ileus* - This is a condition characterized by the **absence of bowel motility**, often due to surgery, medications, or electrolyte imbalances. - Management focuses on supportive care, addressing the underlying cause, and sometimes prokinetic agents, but not pegloticase. *Psoriatic arthritis* - This is a specific type of **inflammatory arthritis** associated with psoriasis. - Treatment regimens for psoriatic arthritis usually involve DMARDs, biologics (like TNF inhibitors), and NSAIDs, rather than pegloticase.
Question 9: Which of the following drugs is useful in acute attack of gout ?
- A. Furosemide
- B. Sulfinpyrazone
- C. Allopurinol
- D. Piroxicam (Correct Answer)
Explanation: ***Piroxicam*** - **Piroxicam** is a **non-steroidal anti-inflammatory drug (NSAID)**, which are the first-line treatment for acute gout attacks. - NSAIDs work by inhibiting **prostaglandin synthesis**, thereby reducing inflammation and pain associated with the acute crystal-induced arthritis. *Furosemide* - **Furosemide** is a loop diuretic that can **raise uric acid levels** by increasing reabsorption in the renal tubules. - Therefore, it would exacerbate **gout** and is contraindicated during an acute attack. *Sulfinpyrazone* - **Sulfinpyrazone** is a **uricosuric agent** used for chronic gout management to increase uric acid excretion. - It is **not used for acute attacks** as it can precipitate or worsen an attack by mobilizing uric acid crystals. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** used for long-term management of hyperuricemia and chronic gout. - Starting allopurinol during an **acute attack** can worsen or prolong the attack by causing rapid changes in serum uric acid levels.
Question 10: Which of the following is not used in acute attack of severe pain due to gout ?
- A. Colchicine
- B. Febuxostat (Correct Answer)
- C. Corticosteroids
- D. Indomethacin
Explanation: ***Febuxostat*** - **Febuxostat** is a xanthine oxidase inhibitor used for **long-term prevention** of gout attacks by lowering uric acid levels. - It is **not indicated for acute attacks** of gout because it does not have immediate anti-inflammatory or analgesic effects. *Colchicine* - **Colchicine** is an **anti-inflammatory agent** commonly used for the **acute treatment** of gout, particularly if started within 24-36 hours of symptom onset. - It works by inhibiting neutrophil migration and activation, reducing the inflammatory response to uric acid crystals. *Indomethacin* - **Indomethacin** is a powerful **non-steroidal anti-inflammatory drug (NSAID)** frequently used for the **acute management** of gout. - It rapidly reduces pain and inflammation by inhibiting prostaglandin synthesis. *Corticosteroids* - **Corticosteroids** (e.g., prednisone) are effective **anti-inflammatory agents** that can be used for **acute gout attacks**, especially when NSAIDs or colchicine are contraindicated or ineffective. - They can be administered orally, intravenously, or via intra-articular injection to quickly alleviate symptoms.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free