Diuretics — MCQs
On this page
Which of the following is a potassium-sparing diuretic?
Which is the most potent loop diuretic?
Which drug causes hypercalcemia?
Canrenone is a metabolite of which drug?
All of the following statements about amiloride are true EXCEPT:
What is the mechanism of action of acetazolamide?
Which group of diuretics does not require access to the tubular lumen to induce diuresis?
Potassium supplementation is often necessary for patients taking which of the following drugs?
Which of the following diuretics can lead to hyperglycemia and hyperlipidemia?
What is true about Acetazolamide?
Diuretics Indian Medical PG Practice Questions and MCQs
Question 91: Which of the following is a potassium-sparing diuretic?
- A. Furosemide
- B. Spironolactone (Correct Answer)
- C. Thiazide
- D. None of the above
Explanation: **Explanation:** **Correct Answer: B. Spironolactone** **Mechanism of Action:** Spironolactone is a competitive antagonist of the **Mineralocorticoid Receptor (Aldosterone receptor)** located in the late distal tubule and collecting duct. Normally, aldosterone promotes the reabsorption of Na⁺ and the secretion of K⁺ and H⁺. By blocking this receptor, spironolactone inhibits Na⁺-K⁺ exchange, leading to sodium excretion (natriuresis) while retaining potassium in the blood. Hence, it is classified as a **Potassium-Sparing Diuretic**. **Why other options are incorrect:** * **A. Furosemide:** This is a **Loop Diuretic** that inhibits the Na⁺-K⁺-2Cl⁻ symporter in the Thick Ascending Limb of Henle. It causes significant potassium loss (hypokalemia) because the increased sodium delivery to the distal tubule stimulates K⁺ secretion. * **C. Thiazide:** These act on the Distal Convoluted Tubule (DCT) by inhibiting the Na⁺-Cl⁻ symporter. Like loop diuretics, they increase sodium delivery to the late distal segments, leading to compensatory K⁺ excretion and **hypokalemia**. **High-Yield NEET-PG Pearls:** 1. **Classification:** Potassium-sparing diuretics are divided into **Aldosterone Antagonists** (Spironolactone, Eplerenone) and **Direct ENaC Blockers** (Amiloride, Triamterene). 2. **Clinical Use:** Spironolactone is the drug of choice for **Primary Hyperaldosteronism (Conn’s Syndrome)** and edema associated with **Liver Cirrhosis**. 3. **Side Effects:** A classic side effect of Spironolactone is **Gynecomastia** (due to its non-specific anti-androgenic activity). Eplerenone is a more selective alternative with fewer endocrine side effects. 4. **Contraindication:** These drugs should be avoided in patients with **Hyperkalemia** or chronic kidney disease (CKD) to prevent life-threatening arrhythmias.
Question 92: Which is the most potent loop diuretic?
- A. Furosemide
- B. Bumetanide (Correct Answer)
- C. Torsemide
- D. Ethacrynic acid
Explanation: **Explanation:** **Bumetanide** is the correct answer because it is the most potent loop diuretic currently available in clinical practice. Potency in pharmacology refers to the amount of drug (dose) required to produce a specific effect. Bumetanide is approximately **40 times more potent** than Furosemide; typically, 1 mg of Bumetanide achieves the same diuresis as 40 mg of Furosemide. It also possesses superior and more predictable oral bioavailability (80-100%). **Analysis of Incorrect Options:** * **Furosemide (A):** While it is the most commonly used loop diuretic, it is significantly less potent than Bumetanide. Its oral absorption is erratic (10-90%), making it less predictable in patients with gut edema (e.g., CHF). * **Torsemide (C):** It is more potent than Furosemide (ratio 1:2) and has a longer half-life, but it remains less potent than Bumetanide. It is often preferred for chronic heart failure due to its anti-aldosterone properties. * **Ethacrynic Acid (D):** This is the least potent loop diuretic listed. It is a non-sulfonamide derivative, making it the drug of choice only for patients with a true sulfonamide allergy. It carries the highest risk of **ototoxicity**. **High-Yield NEET-PG Pearls:** 1. **Mechanism of Action:** Loop diuretics inhibit the **Na+-K+-2Cl- symporter** in the Thick Ascending Limb (TAL) of the Loop of Henle. 2. **Site of Action:** They are also called "High-ceiling diuretics" because they act on the segment with the highest reabsorptive capacity. 3. **Metabolic Side Effects:** Remember the mnemonic **"Hypo-everything"** (Hypokalemia, Hyponatremia, Hypomagnesemia, Hypocalcemia) EXCEPT for **Hyperuricemia** and **Hyperglycemia**. 4. **Drug of Choice:** Loop diuretics are the first-line treatment for **Acute Pulmonary Edema**.
Question 93: Which drug causes hypercalcemia?
- A. Bumetanide
- B. Spironolactone
- C. Thiazide (Correct Answer)
- D. Furosemide
Explanation: **Explanation:** **Thiazide diuretics** (e.g., Hydrochlorothiazide, Chlorthalidone) are the correct answer because they promote the renal reabsorption of calcium [1]. They act on the **Distal Convoluted Tubule (DCT)** by inhibiting the $Na^+/Cl^-$ symporter [2]. This decrease in intracellular sodium enhances the activity of the $Na^+/Ca^{2+}$ exchanger on the basolateral membrane, which in turn drives more calcium reabsorption from the tubular lumen into the blood. Consequently, Thiazides cause **hypercalcemia** and **hypocalciuria** [1], [2]. **Analysis of Incorrect Options:** * **Bumetanide & Furosemide (Options A & D):** These are **Loop diuretics** that inhibit the $Na^+/K^+/2Cl^-$ cotransporter in the Thick Ascending Limb of Henle. This action abolishes the lumen-positive potential required for the paracellular reabsorption of divalent cations. Therefore, Loop diuretics cause **hypocalcemia** (calcium excretion). *Mnemonic: "Loops Lose Calcium." * **Spironolactone (Option B):** This is a **Potassium-sparing diuretic** (Aldosterone antagonist). While it significantly affects potassium and hydrogen ion excretion, it has no clinically significant effect on serum calcium levels. **NEET-PG High-Yield Pearls:** * **Clinical Utility:** Because Thiazides decrease urinary calcium, they are the drug of choice for patients with **idiopathic hypercalciuria** and recurrent **calcium oxalate stones**. * **Bone Health:** Thiazides are preferred for hypertensive patients with **osteoporosis** as they help preserve bone mineral density. * **Metabolic Side Effects:** Thiazides are associated with the "4 Hypers and 2 Hypos": **Hyper**uricemia, **Hyper**glycemia, **Hyper**lipidemia, **Hyper**calcemia; **Hypo**kalemia, and **Hypo**natremia [1].
Question 94: Canrenone is a metabolite of which drug?
- A. Ampicillin
- B. Spironolactone (Correct Answer)
- C. Furosemide
- D. Acetazolamide
Explanation: **Explanation:** **Correct Answer: B. Spironolactone** Spironolactone is a synthetic steroid that acts as a competitive antagonist of the mineralocorticoid receptor (Aldosterone antagonist) [1]. It is a **prodrug** that undergoes extensive first-pass metabolism in the liver. Its primary active metabolite is **Canrenone**, which accounts for a significant portion of its long-lasting antimalarials activity [2]. Canrenone has a much longer half-life (approx. 16.5 hours) compared to parent spironolactone (approx. 1.5 hours), contributing to the drug's prolonged clinical effect [2]. **Why other options are incorrect:** * **A. Ampicillin:** An aminopenicillin antibiotic. It is excreted mostly unchanged in the urine; it does not produce canrenone. * **C. Furosemide:** A loop diuretic acting on the Na⁺-K⁺-2Cl⁻ symporter in the thick ascending limb. It is primarily excreted unchanged and does not have steroid-based metabolites. * **D. Acetazolamide:** A carbonic anhydrase inhibitor acting on the proximal convoluted tubule. It is excreted unchanged by the kidneys. **High-Yield Clinical Pearls for NEET-PG:** * **Potassium-Sparing:** Spironolactone and Eplerenone are the only diuretics that can cause **hyperkalemia** [1]. * **Side Effects:** Due to its non-specific binding to androgen and progesterone receptors, spironolactone can cause **gynecomastia**, impotence, and menstrual irregularities [1]. **Eplerenone** is a more selective alternative with fewer endocrine side effects [1]. * **Clinical Use:** It is the drug of choice for **primary hyperaldosteronism (Conn’s Syndrome)** and is used to improve survival in **Congestive Heart Failure (NYHA Class II-IV)** and to manage ascites in **liver cirrhosis**.
Question 95: All of the following statements about amiloride are true EXCEPT:
- A. It antagonizes the action of aldosterone. (Correct Answer)
- B. It is the drug of choice for the treatment of lithium-induced diabetes insipidus.
- C. It decreases calcium loss in the urine.
- D. It is more potent than triamterene.
Explanation: **Explanation:** Amiloride is a **Potassium-Sparing Diuretic** that belongs to the class of **Renal Epithelial Sodium Channel (ENaC) blockers**. **1. Why Option A is the correct answer (The False Statement):** Amiloride does **not** antagonize the action of aldosterone. Instead, it acts independently of aldosterone by directly blocking the ENaC channels in the late distal tubule and collecting duct. In contrast, drugs like Spironolactone and Eplerenone are the ones that competitively antagonize the Mineralocorticoid (Aldosterone) Receptor. **2. Analysis of Incorrect Options (True Statements):** * **Option B:** Amiloride is the **drug of choice for Lithium-induced Nephrogenic Diabetes Insipidus**. Lithium enters the collecting duct cells through ENaC channels; amiloride blocks these channels, preventing lithium from accumulating and interfering with ADH action. * **Option C:** Like thiazides, amiloride **decreases urinary calcium excretion** (hypocalciuric effect), which can be beneficial in patients with calcium-containing kidney stones. * **Option D:** Amiloride is significantly **more potent** than Triamterene (the other ENaC blocker), requiring a much lower dose (5 mg vs. 50-100 mg) to achieve the same effect. **NEET-PG High-Yield Pearls:** * **Mechanism:** Direct ENaC blockade $\rightarrow$ decreased Na+ reabsorption $\rightarrow$ decreased K+ and H+ secretion (hence "potassium-sparing"). * **Liddle’s Syndrome:** Amiloride is the treatment of choice for this rare genetic condition characterized by overactive ENaC channels. * **Side Effect:** The most serious adverse effect is **Hyperkalemia**, especially when used with ACE inhibitors or in patients with renal impairment.
Question 96: What is the mechanism of action of acetazolamide?
- A. Inhibition of aldosterone
- B. Stimulation of aldosterone
- C. Inhibition of carbonic anhydrase (Correct Answer)
- D. Stimulation of carbonic anhydrase
Explanation: **Explanation:** **Mechanism of Action:** Acetazolamide is a potent inhibitor of the enzyme **carbonic anhydrase (CA)**, primarily located in the **proximal convoluted tubule (PCT)** of the nephron. Under normal conditions, CA facilitates the conversion of $H_2CO_3$ into $H_2O$ and $CO_2$ in the lumen, and the reverse reaction inside the cell. By inhibiting this enzyme, acetazolamide prevents the reabsorption of sodium bicarbonate ($NaHCO_3$). This leads to increased urinary excretion of bicarbonate, sodium, and water, resulting in alkaline urine and a mild diuretic effect. **Analysis of Options:** * **Option A & B (Aldosterone):** Aldosterone acts on the distal tubule and collecting ducts to increase sodium reabsorption and potassium excretion. Drugs that inhibit aldosterone are known as Potassium-Sparing Diuretics (e.g., Spironolactone). Acetazolamide has no direct effect on aldosterone receptors. * **Option D (Stimulation of CA):** Stimulating carbonic anhydrase would theoretically increase bicarbonate reabsorption, which is the opposite of the desired diuretic effect. **High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Uses:** Glaucoma (decreases aqueous humor production), Acute Mountain Sickness (induces metabolic acidosis to stimulate respiration), and Urinary Alkalinization (to excrete acidic drugs like aspirin). * **Side Effects:** Hyperchloremic metabolic acidosis, hypokalemia, and sulfonamide-like hypersensitivity reactions. * **Contraindication:** It should be avoided in patients with hepatic cirrhosis as it decreases ammonia excretion, potentially precipitating hepatic encephalopathy.
Question 97: Which group of diuretics does not require access to the tubular lumen to induce diuresis?
- A. Carbonic anhydrase inhibitor
- B. Na-Cl symporter inhibitor
- C. Mineralocorticoid antagonist (Correct Answer)
- D. Na-K-2Cl symporter inhibitor
Explanation: ### Explanation **Correct Option: C. Mineralocorticoid antagonist** **Mechanism of Action:** Most diuretics act from the **luminal side** of the nephron. However, Mineralocorticoid Antagonists (e.g., Spironolactone, Eplerenone) are unique because they are **lipid-soluble steroids**. They do not need to be secreted into the tubular lumen; instead, they cross the basolateral membrane from the bloodstream to reach the cytoplasm of the principal cells in the late distal tubule and collecting duct. Once inside, they bind to and inhibit the **intracellular Mineralocorticoid Receptor (MR)**, preventing the expression of ENaC (epithelial sodium channels) and Na+/K+ ATPase. **Why Incorrect Options are Wrong:** * **A. Carbonic anhydrase inhibitors (Acetazolamide):** These must be filtered or secreted into the proximal convoluted tubule to inhibit the membrane-bound carbonic anhydrase enzyme on the luminal brush border. * **B. Na-Cl symporter inhibitors (Thiazides):** These act on the Distal Convoluted Tubule (DCT). They are organic acids that are secreted into the lumen via the organic acid transport system to inhibit the NCC transporter from the luminal side. * **D. Na-K-2Cl symporter inhibitors (Loop diuretics):** Drugs like Furosemide are highly protein-bound and are not filtered at the glomerulus. They must be actively secreted into the tubular lumen by the proximal tubule to reach the Thick Ascending Limb (TAL) and inhibit the NKCC2 transporter. **NEET-PG High-Yield Pearls:** 1. **Site of Action:** Spironolactone is the only diuretic that acts on the **cytosolic receptor** rather than a membrane protein. 2. **Pharmacokinetics:** Because they act via gene transcription and protein synthesis, mineralocorticoid antagonists have a **slow onset of action** (several days). 3. **Clinical Use:** Spironolactone is the drug of choice for edema in **liver cirrhosis** (due to secondary hyperaldosteronism) and is proven to reduce mortality in **Congestive Heart Failure (CHF)**.
Question 98: Potassium supplementation is often necessary for patients taking which of the following drugs?
- A. Spironolactone
- B. Triamterene
- C. Furosemide (Correct Answer)
- D. Amiloride
Explanation: **Explanation:** **Correct Option: C. Furosemide** Furosemide is a potent **Loop Diuretic** that acts by inhibiting the **Na⁺-K⁺-2Cl⁻ cotransporter** in the Thick Ascending Limb (TAL) of the Loop of Henle. By preventing sodium reabsorption, it increases the delivery of Na⁺ to the distal nephron. This triggers the renin-angiotensin-aldosterone system (RAAS), leading to increased Na⁺-K⁺ exchange in the collecting ducts. Consequently, there is significant urinary excretion of potassium (**Hypokalemia**). To prevent cardiac arrhythmias and muscle weakness, patients on long-term loop diuretics often require exogenous potassium supplementation. **Why other options are incorrect:** * **A, B, and D (Spironolactone, Triamterene, Amiloride):** These are all **Potassium-Sparing Diuretics**. Spironolactone is an aldosterone antagonist, while Triamterene and Amiloride block the Epithelial Sodium Channels (ENaC). These drugs prevent K⁺ secretion into the urine. Therefore, they carry a risk of **Hyperkalemia**, and potassium supplementation is strictly contraindicated as it could lead to fatal potassium levels. **High-Yield Clinical Pearls for NEET-PG:** * **Loop Diuretics (Furosemide):** Cause "Hypo-everything" (Hypokalemia, Hypomagnesemia, Hypocalcemia) except for Hyperuricemia and Hyperglycemia. * **Thiazides:** Also cause hypokalemia but, unlike loop diuretics, they cause **Hypercalcemia** (useful in patients with osteoporosis or calcium stones). * **Drug of Choice:** Furosemide is the DOC for acute pulmonary edema; Spironolactone is the DOC for edema in hepatic cirrhosis and Conn’s syndrome.
Question 99: Which of the following diuretics can lead to hyperglycemia and hyperlipidemia?
- A. Carbonic anhydrase inhibitors
- B. Loop diuretics
- C. Thiazide diuretics (Correct Answer)
- D. Vasopressin antagonists
Explanation: **Explanation:** **Thiazide diuretics** (e.g., Hydrochlorothiazide, Chlorthalidone) are well-known for causing metabolic side effects, specifically **hyperglycemia** and **hyperlipidemia**. 1. **Hyperglycemia:** Thiazides inhibit insulin release from the pancreas (due to hypokalemia-induced closure of ATP-sensitive K+ channels) and decrease peripheral glucose utilization, leading to impaired glucose tolerance. 2. **Hyperlipidemia:** They cause a transient increase in serum total cholesterol, LDL, and triglycerides, likely due to altered lipid metabolism and insulin resistance. **Analysis of Incorrect Options:** * **Carbonic Anhydrase Inhibitors (e.g., Acetazolamide):** These primarily cause metabolic acidosis and hypokalemia. They are not typically associated with significant glucose or lipid elevations. * **Loop Diuretics (e.g., Furosemide):** While they can cause mild hyperglycemia (also via hypokalemia), the effect is significantly less pronounced than with Thiazides. Their hallmark side effects are ototoxicity and profound hypocalcemia. * **Vasopressin Antagonists (e.g., Tolvaptan):** These are "aquaretics" used in SIADH. Their main side effect is thirst, dry mouth, and potential hepatotoxicity (with Tolvaptan). **High-Yield Clinical Pearls for NEET-PG:** * **The "Hyper" Rule for Thiazides:** They cause **Hyper**glycemia, **Hyper**lipidemia, **Hyper**uricemia (can precipitate Gout), and **Hyper**calcemia (useful in nephrolithiasis). * **The "Hypo" Rule for Thiazides:** They cause **Hypo**kalemia, **Hypo**natremia, and **Hypo**magnesemia. * **Drug of Choice:** Thiazides are the preferred diuretics for hypertension in patients with osteoporosis because they decrease urinary calcium excretion.
Question 100: What is true about Acetazolamide?
- A. Decreased GFR (Correct Answer)
- B. Action similar to sulphonamide
- C. It decreases Na, K, and Glucose excretion
- D. It causes metabolic alkalosis
Explanation: **Explanation:** **Acetazolamide** is a potent Carbonic Anhydrase (CA) inhibitor that acts primarily at the Proximal Convoluted Tubule (PCT). **Why Option A is Correct:** Acetazolamide causes a **decrease in Glomerular Filtration Rate (GFR)** through a mechanism known as **Tubuloglomerular Feedback (TGF)**. By inhibiting CA, it prevents the reabsorption of NaHCO₃, leading to an increased delivery of solutes (sodium and chloride) to the Macula Densa in the distal tubule. The Macula Densa senses this high solute load and triggers afferent arteriolar vasoconstriction, thereby reducing the GFR. **Analysis of Incorrect Options:** * **Option B:** While Acetazolamide is chemically a **sulfonamide derivative**, its *action* is not similar to sulfonamide antibiotics (which inhibit dihydropteroate synthase). It is used for its enzyme-inhibiting properties, not antimicrobial ones. * **Option C:** It **increases** the excretion of Sodium (Na⁺), Potassium (K⁺), and Bicarbonate (HCO₃⁻). It does not significantly affect glucose excretion. * **Option D:** By causing significant loss of bicarbonate in the urine (bicarbonaturia), it leads to **Hyperchloremic Metabolic Acidosis**, not alkalosis. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Indications:** Glaucoma (decreases aqueous humor production), Acute Mountain Sickness (counteracts respiratory alkalosis), and Urinary Alkalinization (to excrete acidic drugs like uric acid or aspirin). * **Side Effects:** Hypokalemia, Paresthesia, Renal stones (due to calcium phosphate precipitation in alkaline urine), and Sulfonamide hypersensitivity. * **Contraindication:** Hepatic Cirrhosis (it decreases ammonia excretion, potentially precipitating hepatic encephalopathy).
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
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free