Bumetanide MCQs With Answer

Bumetanide MCQs With Answer: A focused review for B. Pharm students covering the pharmacology and clinical use of bumetanide. Key topics include mechanism of action (NKCC2 inhibition in the thick ascending limb), pharmacokinetics (high oral bioavailability, short half‑life), therapeutic indications (edema in heart failure, hepatic and renal disease), and adverse effects (hypokalemia, metabolic alkalosis, ototoxicity). Emphasis is placed on dosing, monitoring (electrolytes, renal function, hearing), drug interactions (NSAIDs, aminoglycosides, digoxin), contraindications, and clinical problem‑solving to build exam readiness and safe prescribing knowledge. These Bumetanide MCQs With Answer will reinforce concepts in mechanism, pharmacokinetics, adverse effects, interactions, and clinical applications. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. What is the primary mechanism of action of bumetanide?

  • Inhibition of Na+/K+/2Cl− cotransporter (NKCC2) in the thick ascending limb
  • Inhibition of Na+/Cl− cotransporter (NCC) in the distal tubule
  • Activation of epithelial sodium channels (ENaC) in the collecting duct
  • Inhibition of carbonic anhydrase in the proximal tubule

Correct Answer: Inhibition of Na+/K+/2Cl− cotransporter (NKCC2) in the thick ascending limb

Q2. Which of the following is the most common clinical indication for bumetanide?

  • Treatment of bacterial infections
  • Management of edema associated with heart failure
  • Long‑term control of asthma
  • Primary prevention of myocardial infarction

Correct Answer: Management of edema associated with heart failure

Q3. Compared to furosemide, bumetanide is:

  • Less potent than furosemide
  • Approximately equally potent
  • Approximately 40 times more potent than furosemide
  • Approximately 100 times more potent than furosemide

Correct Answer: Approximately 40 times more potent than furosemide

Q4. Which electrolyte disturbance is most characteristically caused by bumetanide therapy?

  • Hyperkalemia
  • Hypokalemia
  • Hypermagnesemia
  • Hypercalcemia

Correct Answer: Hypokalemia

Q5. The primary route of elimination for bumetanide is:

  • Hepatic metabolism with biliary excretion
  • Fecal excretion unchanged
  • Primarily renal excretion
  • Pulmonary exhalation

Correct Answer: Primarily renal excretion

Q6. Which statement best describes the oral bioavailability of bumetanide?

  • Very low (<10%)
  • Moderate (30–50%)
  • High (~80–100%)
  • Completely inactivated by first‑pass metabolism

Correct Answer: High (~80–100%)

Q7. What is the approximate elimination half‑life of bumetanide in adults?

  • 30 minutes
  • 1–1.5 hours
  • 8–12 hours
  • 24–48 hours

Correct Answer: 1–1.5 hours

Q8. Bumetanide’s effect on urinary calcium is to:

  • Decrease calcium excretion and cause hypercalcemia
  • Increase calcium excretion, potentially leading to hypocalcemia
  • No significant effect on calcium handling
  • Increase calcium reabsorption in the proximal tubule

Correct Answer: Increase calcium excretion, potentially leading to hypocalcemia

Q9. Which drug class increases the risk of bumetanide‑induced ototoxicity when coadministered?

  • Beta‑blockers
  • Aminoglycoside antibiotics
  • ACE inhibitors
  • Statins

Correct Answer: Aminoglycoside antibiotics

Q10. How do NSAIDs typically affect the diuretic effect of bumetanide?

  • They potentiate the diuretic effect by increasing renal blood flow
  • They have no interaction
  • They reduce the diuretic effect by inhibiting renal prostaglandin synthesis
  • They cause additive hyperkalemia with bumetanide

Correct Answer: They reduce the diuretic effect by inhibiting renal prostaglandin synthesis

Q11. The primary anatomical site of action for bumetanide is the:

  • Proximal convoluted tubule
  • Thick ascending limb of the loop of Henle
  • Distal convoluted tubule
  • Collecting duct

Correct Answer: Thick ascending limb of the loop of Henle

Q12. Bumetanide belongs to which chemical/class group?

  • Thiazide diuretic
  • Loop diuretic; sulfonamide derivative
  • Potassium‑sparing diuretic
  • Carbonic anhydrase inhibitor

Correct Answer: Loop diuretic; sulfonamide derivative

Q13. In patients with low glomerular filtration rate (GFR), bumetanide is:

  • Less effective than thiazides and should be avoided
  • Generally effective even with reduced GFR
  • Contraindicated if GFR <60 mL/min
  • Only effective when combined with ACE inhibitors

Correct Answer: Generally effective even with reduced GFR

Q14. Which laboratory parameter requires frequent monitoring during bumetanide therapy?

  • Fasting blood glucose only
  • Liver function tests only
  • Serum electrolytes, especially potassium
  • Thyroid function tests

Correct Answer: Serum electrolytes, especially potassium

Q15. Bumetanide is contraindicated in which clinical condition?

  • Controlled hypertension
  • Anuria (absence of urine production)
  • Osteoarthritis
  • Mild seasonal allergies

Correct Answer: Anuria (absence of urine production)

Q16. What is the usual pregnancy classification advice for bumetanide?

  • Category A — safe in pregnancy
  • Category B — no risk shown in humans
  • Category C — use only if potential benefit justifies risk
  • Category X — contraindicated in pregnancy

Correct Answer: Category C — use only if potential benefit justifies risk

Q17. Why does bumetanide increase the risk of digoxin toxicity?

  • It directly inhibits digoxin metabolism
  • It increases digoxin renal clearance
  • Hypokalemia caused by bumetanide sensitizes the myocardium to digoxin
  • It competes with digoxin for plasma protein binding sites

Correct Answer: Hypokalemia caused by bumetanide sensitizes the myocardium to digoxin

Q18. The typical onset of action after oral administration of bumetanide is:

  • 5–10 minutes
  • 30–60 minutes
  • 4–6 hours
  • 24 hours

Correct Answer: 30–60 minutes

Q19. The onset of diuretic action after intravenous bumetanide is approximately:

  • Less than 1 minute
  • About 5 minutes
  • 1–2 hours
  • 6–8 hours

Correct Answer: About 5 minutes

Q20. A common oral dosing range for bumetanide in adults is:

  • 0.5–2 mg daily
  • 20–40 mg daily
  • 50–200 mg daily
  • 500–1000 mg daily

Correct Answer: 0.5–2 mg daily

Q21. Bumetanide can cause which acid–base disturbance?

  • Metabolic acidosis
  • Respiratory acidosis
  • Metabolic alkalosis
  • Respiratory alkalosis

Correct Answer: Metabolic alkalosis

Q22. The natriuretic effect of bumetanide is due to:

  • Increased aldosterone secretion
  • Enhanced sodium reabsorption in proximal tubule
  • Blockade of sodium reabsorption in the thick ascending limb
  • Inhibition of water channels in the collecting duct

Correct Answer: Blockade of sodium reabsorption in the thick ascending limb

Q23. For hypertension management, bumetanide is:

  • First‑line agent for uncomplicated hypertension
  • Rarely used and has no role in hypertension
  • Not first‑line; used in resistant hypertension or volume overload
  • Preferred in pregnancy for blood pressure control

Correct Answer: Not first‑line; used in resistant hypertension or volume overload

Q24. In patients with a documented sulfonamide allergy, bumetanide should be:

  • Administered routinely without concern
  • Avoided entirely in all cases
  • Used with caution due to possible cross‑reactivity
  • Preferred over thiazides

Correct Answer: Used with caution due to possible cross‑reactivity

Q25. Bumetanide typically affects magnesium balance by:

  • Decreasing urinary magnesium excretion
  • Increasing urinary magnesium excretion, risking hypomagnesemia
  • Causing hypermagnesemia through renal retention
  • No significant effect on magnesium

Correct Answer: Increasing urinary magnesium excretion, risking hypomagnesemia

Q26. Which laboratory trend suggests overdiuresis or intravascular volume depletion with bumetanide?

  • Decreasing blood urea nitrogen (BUN) with stable creatinine
  • Rising BUN and creatinine indicating prerenal azotemia
  • Markedly reduced serum uric acid
  • Improved potassium and sodium levels

Correct Answer: Rising BUN and creatinine indicating prerenal azotemia

Q27. Which statement correctly contrasts loop diuretics (like bumetanide) with thiazide diuretics?

  • Loop diuretics inhibit NCC in the distal tubule; thiazides inhibit NKCC2
  • Both act primarily at the collecting duct
  • Loop diuretics inhibit NKCC2 in TAL; thiazides inhibit NCC in distal tubule
  • Thiazides are more effective than loops at very low GFR

Correct Answer: Loop diuretics inhibit NKCC2 in TAL; thiazides inhibit NCC in distal tubule

Q28. In acute hypercalcemia, bumetanide can be useful when combined with saline because it:

  • Increases renal calcium excretion
  • Enhances intestinal calcium absorption
  • Directly binds circulating calcium
  • Suppresses parathyroid hormone immediately

Correct Answer: Increases renal calcium excretion

Q29. Bumetanide is characterized by which of the following protein binding properties?

  • Not protein bound (<10%)
  • Moderately protein bound (30–50%)
  • Highly protein bound (~95%)
  • Irreversibly bound to plasma proteins

Correct Answer: Highly protein bound (~95%)

Q30. When high doses of bumetanide or combination therapy with ototoxic drugs is required, what monitoring is recommended?

  • Serial audiometry and hearing assessment
  • Daily chest X‑ray
  • Weekly liver biopsy
  • No special monitoring is necessary

Correct Answer: Serial audiometry and hearing assessment

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