Diuretics — MCQs
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Gout can be precipitated by -
Which of the following is not caused by furosemide?
All of the following drugs are known to worsen hyperkalemia except
In the presence of renal failure, which of the following should not be given?
All of the following adverse effects can be caused by loop diuretics except :
Thiazide diuretics cause all except:
Which potassium-sparing diuretic alters cardiac morphology and is associated with anti-androgenic side effects?
Chronic thiazide therapy causes persistent hypercalcemia which is due to:
Amiloride can cause hyperkalemia due to its action on:
Thiazides and loop diuretics both have opposite action on which of the following ions ?
Diuretics Indian Medical PG Practice Questions and MCQs
Question 151: Gout can be precipitated by -
- A. Digitalis
- B. Calcium channel blockers
- C. Thiazide diuretics (Correct Answer)
- D. Omeprazole
Explanation: ***Thiazide diuretics*** - **Thiazide diuretics** reduce the renal excretion of **uric acid**, leading to increased serum uric acid levels (hyperuricemia). - This elevation in uric acid can lead to the formation of **uric acid crystals** in joints, precipitating a gout attack. *Digitalis* - **Digitalis** (digoxin) is a cardiac glycoside used for heart failure and arrhythmias; it does not directly affect uric acid metabolism. - Its primary mechanism involves inhibiting the **Na+/K+-ATPase pump**, increasing intracellular calcium, and enhancing myocardial contractility. *Calcium channel blockers* - **Calcium channel blockers** primarily act by blocking calcium influx into vascular smooth muscle and cardiac cells. - They are generally considered **neutral** or even slightly beneficial for uric acid levels; some, like amlodipine, have shown potential to lower uric acid slightly. *Omeprazole* - **Omeprazole** is a proton pump inhibitor (PPI) that reduces stomach acid production. - It does not have a direct mechanism that would significantly impact **uric acid metabolism** or precipitate gout.
Question 152: Which of the following is not caused by furosemide?
- A. Hyponatremia
- B. Hyperuricemia
- C. Hypokalemia
- D. Hypercalcemia (Correct Answer)
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**. - Its mechanism of action directly contrasts with conditions that cause elevated calcium levels. *Hyponatremia* - Furosemide inhibits the reabsorption of sodium and chloride in the loop of Henle, leading to increased excretion of these electrolytes and **free water**. - This can result in a state of **sodium depletion** and dilutional hyponatremia. *Hyperuricemia* - Furosemide competes with uric acid for secretion into the renal tubule. - This competition leads to **decreased renal excretion of uric acid**, which can result in elevated blood uric acid levels. *Hypokalemia* - Furosemide increases the delivery of sodium to the collecting ducts, which enhances the activity of the sodium-potassium ATPase pump and potassium secretion. - This leads to increased excretion of potassium in the urine and can cause **low serum potassium levels**.
Question 153: All of the following drugs are known to worsen hyperkalemia except
- A. Furosemide (Correct Answer)
- B. ACE inhibitors
- C. Amiloride
- D. Spironolactone
Explanation: ***Furosemide*** - **Furosemide** is a loop diuretic that acts on the **thick ascending limb of the loop of Henle**, inhibiting the reabsorption of sodium, chloride, and potassium. - This action leads to increased excretion of potassium in the urine, thus **preventing hyperkalemia** and often causing hypokalemia. *ACE inhibitors* - **ACE inhibitors** block the production of angiotensin II, leading to decreased aldosterone secretion. - Reduced aldosterone levels decrease potassium excretion in the renal tubules, which can **worsen hyperkalemia**. *Amiloride* - **Amiloride** is a potassium-sparing diuretic that blocks sodium channels in the collecting duct. - This action reduces potassium secretion, making it a drug that can **worsen hyperkalemia**. *Spironolactone* - **Spironolactone** is an aldosterone antagonist that also acts as a potassium-sparing diuretic. - By blocking aldosterone's effects, it **decreases potassium excretion** in the renal tubules and can therefore worsen hyperkalemia.
Question 154: In the presence of renal failure, which of the following should not be given?
- A. Bumetanide
- B. Furosemide
- C. Spironolactone (Correct Answer)
- D. None of the options
Explanation: ***Spironolactone*** - **Spironolactone** is an **aldosterone antagonist**, a **potassium-sparing diuretic**, which can cause **hyperkalemia**, especially in patients with **renal impairment** where potassium excretion is already compromised - Due to the risk of severe **hyperkalemia**, which can lead to life-threatening **cardiac arrhythmias**, spironolactone is **contraindicated** or used with extreme caution in **renal failure** - In renal failure, the kidneys cannot adequately excrete potassium, and adding a potassium-sparing diuretic significantly increases the risk of dangerous hyperkalemia *Bumetanide* - **Bumetanide** is a **loop diuretic** that primarily acts on the **ascending limb of the loop of Henle** to inhibit sodium and chloride reabsorption - While its efficacy may be reduced in severe renal failure, it is still commonly used at higher doses and can be effective in managing fluid overload in these patients - Loop diuretics remain the mainstay of diuretic therapy in renal failure, unlike potassium-sparing diuretics *Furosemide* - **Furosemide** is another **loop diuretic** that is often used in patients with **renal failure** to promote diuresis and manage fluid overload - Even with impaired kidney function, it can still exert its diuretic effect, although higher doses may be required - It does not cause significant potassium retention and is safe to use in renal failure *None of the options* - This option is incorrect because **spironolactone** is specifically contraindicated in patients with **renal failure** due to the high risk of **hyperkalemia**
Question 155: All of the following adverse effects can be caused by loop diuretics except :
- A. Hypomagnesemia
- B. Hyperglycemia
- C. Hypercalcemia (Correct Answer)
- D. Hyperuricemia
Explanation: ***Hypercalcemia*** - Loop diuretics inhibit the reabsorption of calcium in the thick ascending limb of the loop of Henle, leading to **increased calcium excretion** and thus **hypocalcemia**, not hypercalcemia [2]. - This property makes them useful in treating conditions like hypercalcemia, but it means they do not cause hypercalcemia themselves. *Hypomagnesemia* - Loop diuretics inhibit magnesium reabsorption in the thick ascending limb, leading to **increased urinary magnesium excretion** and potential **hypomagnesemia** [1], [2]. - This electrolyte imbalance can contribute to cardiac arrhythmias and muscle weakness [2]. *Hyperglycemia* - Loop diuretics, particularly in high doses, can decrease **insulin secretion** and increase **insulin resistance**, leading to **hyperglycemia**. - This effect is generally mild but can be significant in patients with **diabetes mellitus**. *Hyperuricemia* - Loop diuretics compete with uric acid for secretion into the renal tubules, leading to **reduced uric acid excretion** and elevated serum uric acid levels, also known as **hyperuricemia** [1]. - This can precipitate or exacerbate **gout attacks** in susceptible individuals [1].
Question 156: Thiazide diuretics cause all except:
- A. Decreased uric acid excretion
- B. Hyperkalemia
- C. Hyperglycemia
- D. Increased calcium excretion (Correct Answer)
Explanation: ***Increased calcium excretion*** - Thiazide diuretics are known to **decrease urinary calcium excretion**, leading to an increase in serum calcium levels. - This property makes them useful in the treatment of **calcium nephrolithiasis** and **osteoporosis**. *Decreased uric acid excretion* - Thiazide diuretics compete with uric acid for secretion in the **proximal tubule**, leading to decreased uric acid excretion and potential **hyperuricemia**. - This can precipitate or exacerbate **gout**. *Hyperkalemia* - Thiazide diuretics cause **hypokalemia**, NOT hyperkalemia, by increasing potassium excretion in the **distal convoluted tubule**. - Thiazides block Na-Cl cotransporter, leading to increased sodium delivery to collecting duct where **sodium-potassium exchange** occurs, causing potassium loss. *Hyperglycemia* - Thiazide diuretics can cause **hyperglycemia** by impairing insulin secretion from the pancreas and increasing insulin resistance in peripheral tissues. - This effect is more prominent in patients with **pre-existing diabetes** or impaired glucose tolerance.
Question 157: Which potassium-sparing diuretic alters cardiac morphology and is associated with anti-androgenic side effects?
- A. Amiloride
- B. Triamterene
- C. Spironolactone (Correct Answer)
- D. Eplerenone
Explanation: ***Spironolactone*** - **Spironolactone** is a **non-selective aldosterone antagonist** that blocks mineralocorticoid receptors - It has significant **anti-androgenic effects** due to binding to androgen receptors, causing gynecomastia, decreased libido, and menstrual irregularities - Aldosterone promotes **cardiac remodeling** (hypertrophy and fibrosis) in heart failure; spironolactone's antagonistic action **reverses or prevents** these detrimental changes, thus altering cardiac morphology favorably - Used in **heart failure with reduced ejection fraction** (HFrEF) to improve outcomes and reduce mortality *Amiloride* - **Amiloride** is a direct epithelial sodium channel (ENaC) blocker - Its primary action is to inhibit sodium reabsorption in the collecting tubule - While it helps in treating hypertension and heart failure through its diuretic effect, it does **not directly alter cardiac morphology** like aldosterone antagonists - No anti-androgenic effects *Triamterene* - **Triamterene** is another direct ENaC blocker, similar in mechanism to amiloride - Promotes sodium excretion and potassium retention, often combined with loop or thiazide diuretics - Does **not have direct effects on aldosterone-mediated cardiac remodeling** - No anti-androgenic effects *Eplerenone* - **Eplerenone** is a **selective aldosterone receptor antagonist**, similar to spironolactone in altering cardiac morphology - However, it is **more selective** for mineralocorticoid receptors and has **minimal anti-androgenic effects** - This selectivity reduces hormonal side effects like gynecomastia - Also used in heart failure and post-MI, but the question specifically asks about the drug associated with anti-androgenic effects
Question 158: Chronic thiazide therapy causes persistent hypercalcemia which is due to:
- A. Fanconi's syndrome
- B. Hypervitaminosis D
- C. Renal tubular acidosis
- D. Increased distal tubular calcium reabsorption (Correct Answer)
Explanation: ***Increased distal tubular calcium reabsorption*** - Thiazide diuretics work by inhibiting the **sodium-chloride cotransporter** in the **distal convoluted tubule**, leading to increased sodium and water excretion. - This inhibition also leads to enhanced **calcium reabsorption** in the distal tubule by increasing the electrochemical gradient and affecting transmembrane calcium channels, resulting in **hypercalcemia**. *Fanconi's syndrome* - This is a generalized dysfunction of the **proximal renal tubules**, leading to the excretion of amino acids, glucose, phosphate, and bicarbonate in the urine. - It typically causes **hypophosphatemia** and **renal osteodystrophy**, not primary hypercalcemia. *Hypervitaminosis D* - This condition results from excessive intake of **vitamin D**, leading to increased intestinal calcium absorption and bone resorption, causing hypercalcemia. - It is not directly caused by chronic thiazide therapy. *Renal tubular acidosis* - This is a group of disorders characterized by a defect in renal acid excretion or bicarbonate reabsorption, leading to **metabolic acidosis**. - While it can be associated with various electrolyte disturbances, it does not directly cause persistent hypercalcemia.
Question 159: Amiloride can cause hyperkalemia due to its action on:
- A. Electrogenic K+ channels
- B. Electrogenic Na+ channels (Correct Answer)
- C. Non-electrogenic Na+-Cl- symporter
- D. H+-K+ ATPase
Explanation: ***Correct: Electrogenic Na+ channels*** - Amiloride is a **potassium-sparing diuretic** that blocks the **epithelial sodium channels (ENaC)** in the apical membrane of the collecting duct cells. - By blocking **ENaC**, amiloride reduces the reabsorption of sodium, which in turn diminishes the negative potential in the tubular lumen, thereby reducing the driving force for **potassium secretion** and leading to hyperkalemia. *Incorrect: Electrogenic K+ channels* - While potassium channels are involved in potassium balance, amiloride's primary action is not directly on these channels. - Its effects on potassium are secondary to its impact on sodium reabsorption and the resulting electrochemical gradient. *Incorrect: Non-electrogenic Na+-Cl- symporter* - The **Na+-Cl- symporter (NCC)** is located in the distal convoluted tubule and is the target of **thiazide diuretics**, not amiloride. - Blocking NCC leads to increased delivery of sodium and water to the collecting duct, but does not directly cause hyperkalemia. *Incorrect: H+-K+ ATPase* - The **H+-K+ ATPase** in the collecting duct is involved in potassium reabsorption and hydrogen ion secretion. - Amiloride does not directly inhibit this pump; instead, it affects potassium handling by altering the electrical gradient associated with sodium reabsorption.
Question 160: Thiazides and loop diuretics both have opposite action on which of the following ions ?
- A. Potassium
- B. Sodium
- C. Chloride
- D. Calcium (Correct Answer)
Explanation: ***Calcium*** - Thiazide diuretics **increase calcium reabsorption** in the distal convoluted tubule, leading to decreased urinary calcium excretion. - Loop diuretics **decrease calcium reabsorption** in the thick ascending limb of the loop of Henle, resulting in increased urinary calcium excretion. *Potassium* - Both thiazide and loop diuretics can cause **hypokalemia** by increasing potassium excretion in the urine. - This is due to increased sodium delivery to the collecting duct, which stimulates potassium secretion. *Sodium* - Both thiazide and loop diuretics inhibit sodium reabsorption at different sites in the nephron, leading to **increased urinary sodium excretion** (natriuresis). - This is their primary mechanism of action for diuresis. *Chloride* - Both thiazide and loop diuretics inhibit **chloride reabsorption** as they block specific sodium-chloride cotransporters. - Thiazides inhibit the Na-Cl cotransporter in the DCT, while loop diuretics inhibit the Na-K-2Cl cotransporter in the thick ascending limb.
Practice by Chapter
Carbonic Anhydrase Inhibitors
Practice Questions
Loop Diuretics
Practice Questions
Thiazide and Thiazide-Like Diuretics
Practice Questions
Potassium-Sparing Diuretics
Practice Questions
Carbonic Anhydrase Inhibitors
Practice Questions
Osmotic Diuretics
Practice Questions
Combination Diuretic Therapy
Practice Questions
Diuretics in Heart Failure
Practice Questions
Diuretics in Hypertension
Practice Questions
Diuretics in Renal Disorders
Practice Questions
Adverse Effects and Drug Interactions
Practice Questions
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