Potassium-Sparing Diuretics — MCQs
Severe hyperkalemia is seen in combination with:
Potassium-sparing diuretics act at the level of
Which medication is commonly used in heart failure that also has aldosterone antagonistic properties?
Which one of the following is not a clinical use of spironolactone?
Which diuretic is known to cause the maximum potassium loss?
All of the following diuretics increase K+ excretion EXCEPT:
The site of action of the loop diuretic furosemide is:
All of the following drugs are known to worsen hyperkalemia except
Which of the following potassium-sparing diuretics was the first to be shown to reduce cardiac mortality in chronic heart failure patients?
Which electrolyte shows the most significant increase in urinary excretion within 24 hours of initiating thiazide diuretic therapy for hypertension?
Potassium-Sparing Diuretics Indian Medical PG Practice Questions and MCQs
Question 1: Severe hyperkalemia is seen in combination with:
- A. Amiloride and Furosemide
- B. Lisinopril and Furosemide
- C. Losartan and amiloride (Correct Answer)
- D. Propranolol and verapamil
Explanation: ***Losartan and amiloride*** - **Losartan** is an **angiotensin receptor blocker (ARB)**, often leading to **hyperkalemia** by inhibiting aldosterone secretion. - **Amiloride** is a **potassium-sparing diuretic**, directly interfering with sodium reabsorption and potassium excretion in the **collecting duct**. The combination of Na⁺-channel inhibitors like amiloride with angiotensin-converting enzyme inhibitors (or ARBs) carries a risk of life-threatening hyperkalemia [1].*Amiloride and Furosemide* - **Furosemide** is a **loop diuretic** that causes **potassium wasting**, thus counteracting the potassium-sparing effect of amiloride [2]. - Combining these two drugs typically results in a **neutral or mildly hypokalemic effect**, not severe hyperkalemia.*Lisinopril and furosemide* - **Lisinopril** is an **ACE inhibitor** that causes **hyperkalemia** by reducing aldosterone levels. - However, **furosemide** induces **hypokalemia**, significantly mitigating the hyperkalemic potential of lisinopril [2].*Propranolol and verapamil* - **Propranolol** (a beta-blocker) and **verapamil** (a calcium channel blocker) primarily affect heart rate and contractility, and blood pressure. - Neither of these drugs is directly associated with significant alterations in **potassium levels** to cause severe hyperkalemia.
Question 2: Potassium-sparing diuretics act at the level of
- A. Carbonic anhydrase
- B. Aldosterone receptor (Correct Answer)
- C. NaCl symporter
- D. Na-K pump
Explanation: ***Aldosterone receptor*** - **Potassium-sparing diuretics** include two main classes: 1. **Aldosterone receptor antagonists** (e.g., **spironolactone**, **eplerenone**) that act on **aldosterone receptors** in the collecting tubules 2. **ENaC blockers** (e.g., **amiloride**, **triamterene**) that directly block **epithelial sodium channels (ENaC)** in the collecting duct - Both mechanisms reduce **sodium reabsorption** and **potassium secretion** in the **collecting tubule**, leading to retained potassium. - The aldosterone receptor is the most commonly tested site for this drug class. *Carbonic anhydrase* - **Carbonic anhydrase inhibitors** (e.g., **acetazolamide**) act primarily in the **proximal convoluted tubule**. - They inhibit **bicarbonate reabsorption**, leading to diuresis and metabolic acidosis, and are not considered potassium-sparing. *NaCl symporter* - **Thiazide diuretics** act on the **NaCl symporter (NCC)** in the **distal convoluted tubule**. - They inhibit sodium and chloride reabsorption but do not spare potassium; chronic use can lead to **hypokalemia**. *Na-K pump* - The **Na-K pump** (Na+/K+-ATPase) is found in many cells and maintains ion gradients, but it is not the primary target of potassium-sparing diuretics. - While involved in renal transport, diuretics targeting this pump have different primary mechanisms and therapeutic uses.
Question 3: Which medication is commonly used in heart failure that also has aldosterone antagonistic properties?
- A. Carvedilol
- B. Spironolactone (Correct Answer)
- C. Abiraterone
- D. Sacubitril/Valsartan
Explanation: ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that acts as a **competitive antagonist of aldosterone** receptors, primarily in the collecting ducts of the kidneys. - This action leads to increased excretion of sodium and water, and retention of potassium, which is beneficial in **heart failure** by reducing fluid overload and mitigating the detrimental effects of aldosterone on cardiac remodeling. *Carvedilol* - **Carvedilol** is a **beta-blocker** with additional **alpha-1 blocking** properties, commonly used in heart failure to reduce heart rate, blood pressure, and myocardial oxygen demand. - It does not possess significant aldosterone antagonistic properties. *Sacubitril/Valsartan* - **Sacubitril/Valsartan** is an **angiotensin receptor-neprilysin inhibitor (ARNI)**. Valsartan is an **angiotensin receptor blocker (ARB)**, and sacubitril inhibits neprilysin, an enzyme that degrades natriuretic peptides. - While it modulates the **renin-angiotensin-aldosterone system (RAAS)** and is highly effective in heart failure, it does not directly antagonize aldosterone receptors. *Abiraterone* - **Abiraterone** is an **androgen-biosynthesis inhibitor** used in the treatment of **prostate cancer**. - Its primary mechanism involves inhibiting **CYP17**, an enzyme critical for androgen production, and it has no role in the management of heart failure or aldosterone antagonism.
Question 4: Which one of the following is not a clinical use of spironolactone?
- A. Pulmonary edema (Correct Answer)
- B. Congestive heart failure
- C. Hypertension
- D. To counteract hypokalemia due to thiazide diuretics
Explanation: ***Pulmonary edema*** - While spironolactone is a **diuretic**, its onset of action is relatively slow (days to weeks), making it unsuitable for the acute management of **pulmonary edema**, which requires rapid fluid removal. - For acute pulmonary edema, fast-acting loop diuretics like **furosemide** are preferred due to their potent and rapid diuresis. *Congestive heart failure* - Spironolactone is a **potassium-sparing diuretic** and an **aldosterone antagonist**, which improves outcomes in **congestive heart failure** by reducing fluid retention, myocardial fibrosis, and sympathetic activation. - It specifically helps in preventing **cardiac remodeling** and has been shown to reduce mortality in patients with heart failure. *Hypertension* - Spironolactone is used as an **adjunctive treatment for hypertension**, particularly in cases of **resistant hypertension** or when there is evidence of primary hyperaldosteronism. - It helps lower **blood pressure** by blocking aldosterone's effects, leading to increased sodium and water excretion. *To counteract hypokalemia due to thiazide diuretics* - As a **potassium-sparing diuretic**, spironolactone directly counteracts the **hypokalemia** (low potassium) that can be induced by other diuretics, such as **thiazide diuretics** and **loop diuretics**. - Its mechanism involves blocking **aldosterone receptors** in the collecting duct, reducing potassium secretion and sodium reabsorption.
Question 5: Which diuretic is known to cause the maximum potassium loss?
- A. Spironolactone
- B. Furosemide (Correct Answer)
- C. Thiazide diuretics
- D. Acetazolamide
Explanation: ***Furosemide*** - Furosemide is a **loop diuretic** that inhibits the Na-K-2Cl cotransporter in the **thick ascending limb of the loop of Henle**, leading to significant excretion of sodium, chloride, potassium, and water. - Its potent diuresis and impact on potassium reabsorption result in a **high risk of hypokalemia**. *Thiazide* - Thiazide diuretics inhibit the **Na-Cl cotransporter** in the **distal convoluted tubule**, causing moderate sodium and water excretion, and some potassium loss. - While they can cause hypokalemia, their effect on potassium excretion is generally **less pronounced than loop diuretics**. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that acts primarily in the **proximal tubule**, inhibiting bicarbonate reabsorption and leading to increased excretion of bicarbonate, sodium, potassium, and water. - The potassium loss is due to increased delivery of sodium to the collecting duct, leading to enhanced potassium secretion, but it is typically **less severe than with loop diuretics**. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that acts as an **aldosterone antagonist** in the collecting duct, inhibiting sodium reabsorption and potassium secretion. - Instead of causing potassium loss, spironolactone actually **conserves potassium** and can lead to hyperkalemia.
Question 6: All of the following diuretics increase K+ excretion EXCEPT:
- A. Acetazolamide
- B. Triamterene (Correct Answer)
- C. Thiazide
- D. Furosemide
Explanation: ***Triamterene*** - **Triamterene** is a **potassium-sparing diuretic** that blocks epithelial sodium channels (ENaC) in the collecting duct, thereby reducing sodium reabsorption and potassium secretion. - Unlike most other diuretics, it causes **decreased K+ excretion** and can lead to hyperkalemia. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** that acts in the proximal tubule, inhibiting bicarbonate reabsorption. - This leads to increased delivery of sodium and bicarbonate to the collecting duct, which enhances **potassium secretion** and increases K+ excretion. *Thiazide* - **Thiazide diuretics** (e.g., hydrochlorothiazide) act by inhibiting the Na+/Cl- cotransporter in the **distal convoluted tubule**. - This increases the delivery of sodium to the collecting duct, which stimulates the exchange of sodium for **potassium**, leading to increased K+ excretion and hypokalemia. *Furosemide* - **Furosemide** is a **loop diuretic** that inhibits the Na+/K+/2Cl- cotransporter in the **thick ascending limb of the loop of Henle**. - This prevents the reabsorption of these ions, leading to increased delivery of sodium to the collecting duct, which promotes **potassium secretion** and increased K+ excretion.
Question 7: The site of action of the loop diuretic furosemide is:
- A. Distal convoluted tubule
- B. Descending limb of loop of Henle
- C. Proximal convoluted tubule
- D. Thick ascending limb of loop of Henle (Correct Answer)
Explanation: ***Thick ascending limb of loop of Henle*** - Furosemide, a **loop diuretic**, acts by inhibiting the **Na+-K+-2Cl- cotransporter (NKCC2)** in the luminal membrane of the epithelial cells in the thick ascending limb. - This inhibition prevents the reabsorption of these ions, leading to increased excretion of **sodium**, **potassium**, **chloride**, and water. *Distal convoluted tubule* - This is the primary site of action for **thiazide diuretics**, which inhibit the **Na+-Cl- cotransporter**. - While some water reabsorption occurs here, it is not the main target for loop diuretics like furosemide. *Descending limb of loop of Henle* - This segment is primarily permeable to **water** due to aquaporins but impermeable to solutes, allowing for passive water reabsorption. - No significant transport mechanisms are directly targeted by furosemide here. *Proximal convoluted tubule* - The proximal tubule is where the majority of filtered **sodium**, **water**, and other solutes are reabsorbed. - **Carbonic anhydrase inhibitors** (e.g., acetazolamide) primarily act here.
Question 8: 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 9: Which of the following potassium-sparing diuretics was the first to be shown to reduce cardiac mortality in chronic heart failure patients?
- A. Spironolactone (Correct Answer)
- B. Amiloride
- C. Triamterene
- D. Eplerenone
Explanation: ***Spironolactone*** - **Spironolactone** was the first potassium-sparing diuretic shown to reduce **cardiac mortality** in patients with **chronic heart failure** in the **RALES trial** (Randomized Aldactone Evaluation Study). - Its beneficial effects in heart failure are primarily attributed to its **aldosterone receptor antagonist** properties, which counteract the harmful effects of aldosterone on the myocardium and vasculature, rather than just its diuretic effect. *Amiloride* - **Amiloride** is a potassium-sparing diuretic that works by directly inhibiting **epithelial sodium channels (ENaC)** in the collecting duct. - While it helps in potassium conservation, it has not been shown to significantly reduce cardiac mortality in chronic heart failure patients in clinical trials. *Triamterene* - **Triamterene** is another potassium-sparing diuretic that also directly inhibits **ENaC** in the collecting duct, similar to amiloride. - Like amiloride, it is used to prevent hypokalemia but lacks evidence for significant **cardiac mortality reduction** in chronic heart failure. *Eplerenone* - **Eplerenone** is a selective **aldosterone receptor antagonist**, similar to spironolactone, with fewer hormonal side effects. - While it has been shown to reduce **cardiac mortality** in chronic heart failure (e.g., in the EMPHASIS-HF trial), it was introduced later than spironolactone and was not the *first* to demonstrate this benefit.
Question 10: Which electrolyte shows the most significant increase in urinary excretion within 24 hours of initiating thiazide diuretic therapy for hypertension?
- A. Sodium (Correct Answer)
- B. Potassium
- C. Magnesium
- D. Calcium
Explanation: ***Sodium*** - Thiazide diuretics primarily act on the **distal convoluted tubule** by inhibiting the **Na+/Cl- cotransporter**, leading to increased excretion of **sodium** and water [1]. - The initial and most significant pharmacological effect of thiazides is to promote **natriuresis**, removing excess sodium from the body [2]. - Within **24 hours**, sodium excretion shows the most pronounced increase, which is the primary mechanism for blood pressure reduction [2]. *Potassium* - While thiazides do cause **potassium excretion**, this effect is less significant than sodium excretion initially and is partly due to increased flow to the collecting duct and elevated aldosterone levels [2]. - Hypokalemia is a known side effect of long-term thiazide use, but the **immediate increase in urinary sodium** is more pronounced. *Magnesium* - Thiazide diuretics are known to cause **increased urinary excretion of magnesium**, which can lead to hypomagnesemia with chronic use [3]. - However, the initial increase in magnesium excretion is generally **less pronounced** compared to sodium excretion within the first 24 hours of therapy. *Calcium* - Uniquely among diuretics, thiazides **decrease** urinary calcium excretion, promoting calcium retention and reabsorption in the distal tubule [1], [3]. - This is why thiazides are sometimes used therapeutically in **hypercalciuric nephrolithiasis** and can cause hypercalcemia as a side effect. - Calcium excretion is **reduced**, not increased, making this the opposite of the correct answer.
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