Diuretics and Fluid Balance Drugs MCQs

Pharmacology · 77 free questions with answers & explanations.

1. A patient on furosemide for heart failure has been given regular NSAIDs post-surgery for pain. His urine output drops markedly. The mechanism of NSAID-furosemide interaction reducing diuretic efficacy is:
2. A patient with hypertension on hydrochlorothiazide develops hypokalemia and metabolic alkalosis. The mechanism of thiazide-induced hypokalemia is:
3. Mannitol is an osmotic diuretic used in cerebral edema. Which property makes mannitol effective for lowering intracranial pressure?
4. A patient on loop diuretics develops severe hypokalemia. The mechanism by which furosemide causes hypokalemia involves which tubular segment and which electrophysiological consequence in the heart?
5. Tolvaptan (vasopressin V2 receptor antagonist) is used in polycystic kidney disease (ADPKD) and hyponatremia. Which specific cellular mechanism in the renal collecting duct does it block?
6. Acetazolamide, a carbonic anhydrase inhibitor, is used for altitude sickness prophylaxis. The mechanism by which it prevents acute mountain sickness (AMS) is:
7. Tolvaptan is a vasopressin V2 receptor antagonist used for hyponatraemia in SIADH. Unlike conventional diuretics, tolvaptan produces 'aquaresis' (electrolyte-free water excretion). The mechanism is:
8. A patient with nephrotic syndrome and severe edema is on furosemide 80 mg twice daily without adequate diuretic response ('diuretic resistance'). The nephrologist adds metolazone. What is the pharmacological rationale for this combination specifically in nephrotic syndrome?
9. Tolvaptan is used in autosomal dominant polycystic kidney disease (ADPKD). Its mechanism to slow cyst growth involves:
10. Acetazolamide is used in the prevention of high-altitude cerebral oedema (HACE). The pharmacological rationale is:
11. Tolvaptan, a selective V2 receptor antagonist (aquaporin), is used in SIADH and autosomal dominant polycystic kidney disease (ADPKD). In ADPKD, tolvaptan slows cyst growth by which mechanism beyond simple aquaresis?
12. Acetazolamide is used acutely in metabolic alkalosis. It corrects alkalosis by which mechanism?
13. Acetazolamide (carbonic anhydrase inhibitor) is used to prevent high-altitude sickness. The mechanism by which it prevents acute mountain sickness is:
14. A patient with cirrhosis and refractory ascites is started on tolvaptan. The mechanism of action of tolvaptan and the specific contraindication in liver disease relates to:
15. Tolvaptan is used in autosomal dominant polycystic kidney disease (ADPKD) to slow cyst growth. Its mechanism of action in ADPKD beyond simple aquaresis is:
16. Tolvaptan (a vasopressin V2 receptor antagonist) is used in hyponatremia. In which specific type of hyponatremia is tolvaptan most efficacious, and why is it contraindicated in hypovolemic hyponatremia?
17. A patient on a high-ceiling loop diuretic develops metabolic alkalosis. Which mechanism specifically accounts for furosemide-induced metabolic alkalosis?
18. Tolvaptan is a vasopressin V2-receptor antagonist (aquaretic) used in hyponatraemia due to SIADH. The risk of osmotic demyelination syndrome (ODS) with tolvaptan is most pronounced when:
19. Acetazolamide, a carbonic anhydrase inhibitor, is used in altitude sickness prophylaxis. The mechanism by which it prevents acute mountain sickness relates to:
20. Acetazolamide is used in altitude sickness prophylaxis. Beyond its inhibition of carbonic anhydrase in the kidney producing metabolic acidosis, what is the mechanism by which the induced metabolic acidosis helps acclimatization?
21. Tolvaptan is a vasopressin V2 receptor antagonist (vaptans) used in hyponatremia and ADPKD. In SIADH, why can tolvaptan cause rapid correction of sodium that risks osmotic demyelination syndrome (ODS)?
22. Tolvaptan is used in autosomal dominant polycystic kidney disease (ADPKD) to slow cyst growth. Its mechanism in ADPKD is:
23. Acetazolamide prevents acute mountain sickness (AMS) by a mechanism that involves:
24. A patient with heart failure on furosemide develops diuretic resistance. Metolazone is added. The synergistic mechanism of metolazone with loop diuretics is:
25. Tolvaptan is a selective V2 receptor antagonist approved for autosomal dominant polycystic kidney disease (ADPKD). The mechanism by which V2 blockade slows renal cyst growth is:
26. Tolvaptan is a vaptane class diuretic. Its mechanism and the clinical scenario where it is specifically superior to furosemide involve which of the following?
27. Tolvaptan, a vasopressin V2 receptor antagonist (vaptans), is specifically used in hyponatremia. Which type of hyponatremia does it NOT effectively treat?
28. Acetazolamide, a carbonic anhydrase inhibitor, causes metabolic acidosis as an adverse effect. Which biochemical mechanism explains this?
29. Furosemide causes hypomagnesaemia in addition to hypokalaemia. The mechanism is:
30. Acetazolamide is used as prophylaxis for high-altitude cerebral/pulmonary oedema. The mechanism enabling altitude acclimatisation is:
31. A patient with cirrhosis and resistant ascites is started on tolvaptan. Its mechanism of action and the specific FDA black box warning are:
32. Spironolactone in heart failure reduces mortality primarily by blocking:
33. A patient with syndrome of inappropriate antidiuretic hormone secretion (SIADH) is treated with tolvaptan. Tolvaptan corrects hyponatraemia by:
34. Acetazolamide causes metabolic acidosis as a side effect of its primary mechanism. This occurs because:
35. Acetazolamide is a carbonic anhydrase inhibitor used as a diuretic and for altitude sickness. Which acid-base disturbance does chronic acetazolamide use predictably cause?
36. A patient is taking spironolactone for heart failure. Its mechanism of action is best described as:
37. Furosemide is given IV to a patient in acute pulmonary edema. Before significant diuresis occurs, the patient feels relief of dyspnea. This early benefit is due to:
38. Tolvaptan is a selective vasopressin V2 receptor antagonist (vaptан) used for hyponatraemia in SIADH. Why is it CONTRAINDICATED in hypovolaemic hyponatraemia?
39. Loop diuretics (furosemide) cause hypokalaemic metabolic alkalosis. Which mechanism BEST explains the metabolic alkalosis?
40. Acetazolamide, a carbonic anhydrase inhibitor, is used for altitude sickness. Its prophylactic benefit comes from:
41. A patient with chronic heart failure is on furosemide. Over time, she develops 'diuretic resistance.' Thiazide addition (e.g., metolazone) is recommended. Which pharmacological principle underlies this combination?
42. Acetazolamide (carbonic anhydrase inhibitor) used as a diuretic causes metabolic acidosis rather than alkalosis. Why?
43. Tolvaptan is a vasopressin V2 receptor antagonist (vaptans) used in hyponatraemia and autosomal dominant polycystic kidney disease (ADPKD). Its mechanism produces:
44. Acetazolamide is a carbonic anhydrase inhibitor used in altitude sickness prophylaxis. Its benefit in acute mountain sickness is primarily through:
45. Loop diuretics like furosemide can cause metabolic alkalosis. The mechanism is best explained by:
46. Tolvaptan is a vaptane used for hyponatraemia in SIADH. Its mechanism of action is:
47. Acetazolamide is used to prevent acute mountain sickness (AMS). The mechanism by which it accelerates acclimatization involves:
48. A patient with heart failure and moderate hyponatremia (Na+ = 128 mEq/L) related to inappropriate ADH secretion is started on tolvaptan. Unlike loop diuretics, tolvaptan corrects hyponatremia without worsening hypokalemia because it:
49. Amiloride is used as potassium-sparing diuretic and also in Liddle syndrome. In Liddle syndrome, its mechanism differs from the primary action in normal physiology because:
50. A 75-year-old woman on furosemide for heart failure develops severe hyponatraemia (Na+ 118 mEq/L). Her urine osmolality is 450 mOsm/kg. The physician suspects SIADH triggered by the loop diuretic. Furosemide treatment of SIADH paradoxically can help correct it. The mechanism is:
51. A 55-year-old man with resistant hypertension is found to have hypokalaemia (K+ 2.9 mEq/L) and metabolic alkalosis while on high-dose chlorthalidone. The physician adds a potassium-sparing diuretic. Which drug among the following blocks the mineralocorticoid receptor AND is additionally a diuretic, rather than acting on the epithelial sodium channel?
52. Acetazolamide inhibits carbonic anhydrase in the proximal convoluted tubule. The metabolic consequence of prolonged acetazolamide use is:
53. Tolvaptan, a vasopressin V2 receptor antagonist (vaptans), is used in hyponatraemia due to SIADH and in autosomal dominant polycystic kidney disease (ADPKD). In SIADH, its mechanism of correcting hyponatraemia is:
54. Spironolactone reduces mortality in severe (NYHA III-IV) heart failure with reduced ejection fraction (HFrEF). Its benefit in HFrEF extends beyond diuresis through which additional mechanism?
55. Furosemide causes hypokalemia and metabolic alkalosis. The mechanism by which furosemide produces metabolic alkalosis is:
56. Spironolactone is used in heart failure with reduced ejection fraction (HFrEF) beyond its diuretic effect. The key additional pharmacological benefit in heart failure is:
57. Acetazolamide is a carbonic anhydrase inhibitor used in altitude sickness. The mechanism by which it reduces altitude sickness is:
58. Tolvaptan is used in hyponatremia associated with SIADH and in ADPKD. Its mechanism of action is best described as:
59. Carbonic anhydrase inhibitors (acetazolamide) cause metabolic acidosis and are used in glaucoma and altitude sickness. In altitude sickness, the pharmacological rationale is:
60. Furosemide inhibits the Na-K-2Cl cotransporter (NKCC2) in the thick ascending limb of Henle. The secondary effect of loop diuretics that makes them life-saving in acute pulmonary edema even before diuresis begins is:
61. A patient with nephrotic syndrome is on furosemide but shows poor diuretic response. The mechanism of this 'loop diuretic resistance' unique to the nephrotic state is:
62. A patient with SIADH (syndrome of inappropriate ADH secretion) secondary to lung cancer has plasma Na+ of 118 mEq/L with neurological symptoms. Which drug selectively antagonizes the V2 vasopressin receptor in the collecting duct?
63. Acetazolamide inhibits carbonic anhydrase. In acute mountain sickness (AMS), acetazolamide is given prophylactically. The mechanism by which it facilitates acclimatization is:
64. Furosemide acts by inhibiting the Na-K-2Cl cotransporter (NKCC2) in the thick ascending limb of the loop of Henle. Which electrolyte abnormality is a direct consequence of this inhibition that is not seen with thiazide diuretics?
65. Spironolactone is a potassium-sparing diuretic used in primary hyperaldosteronism and heart failure. Its mechanism of action is:
66. Acetazolamide acts by inhibiting carbonic anhydrase in the proximal tubule. Which acid-base disturbance is a predictable consequence of prolonged acetazolamide use?
67. Eplerenone is preferred over spironolactone in male patients with heart failure with reduced ejection fraction (HFrEF) because:
68. Tolvaptan is used in autosomal dominant polycystic kidney disease (ADPKD) to slow cyst growth. Its mechanism is:
69. Furosemide's diuretic effect is diminished in nephrotic syndrome despite normal renal function. The primary reason is:
70. Acetazolamide causes a self-limiting diuresis because:
71. A patient with cirrhosis and refractory ascites is given tolvaptan. Its mechanism differs from all other diuretics because:
72. Acetazolamide is used for prophylaxis of high-altitude sickness. Its beneficial mechanism at altitude is:
73. Spironolactone is used in heart failure with reduced ejection fraction (HFrEF). Its benefit beyond diuresis involves:
74. Furosemide is a loop diuretic. The electrolyte abnormality most likely with chronic high-dose furosemide therapy, and its mechanism, is:
75. Acetazolamide is used in high-altitude sickness. The mechanism by which it reduces symptoms of altitude illness is:
76. Loop diuretics cause hypokalaemia and metabolic alkalosis. Which mechanism best explains the alkalosis?
77. Tolvaptan is used in hyponatraemia associated with SIADH and in autosomal dominant polycystic kidney disease (ADPKD). Its mechanism is: