Diuretics — MCQs
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What is a known adverse effect of Triamterene?
A group of people are travelling to the mountains, and a girl starts complaining of mountain sickness. What is the drug of choice?
A patient having hypertension is on thiazides and is complaining of fatigue and hypokalemia. Which of the following drugs can prevent potassium loss?
A 35-year-old male experiences headache, nausea, and shortness of breath while trekking. The physician prescribes a drug to alleviate his symptoms. The drug administered primarily acts on which part of the nephron?
Which of the following diuretics primarily acts on the part labeled 'D' in the given diagram of a nephron?
A 50-year-old woman was prescribed a diuretic by a doctor to manage hypertension. Which of the following diuretics acts on site 'A' as marked in the given image?
A patient on hydrochlorothiazide develops renal stones. What explains this adverse effect?
By what primary mechanism does hydrochlorothiazide help prevent the formation of calcium stones?
A patient is started on hydrochlorothiazide for hypertension and later develops renal stones. Which metabolic effect of hydrochlorothiazide is most likely responsible?
The image shows drug 'X' blocking a channel in the renal tubule. Which of the following drugs is 'X'?
Diuretics Indian Medical PG Practice Questions and MCQs
Question 131: What is a known adverse effect of Triamterene?
- A. Improved glucose tolerance
- B. Muscle cramps (Correct Answer)
- C. Decrease in urea level
- D. Hypokalemia
Explanation: **Explanation:** **Triamterene** is a potassium-sparing diuretic that acts by directly blocking the epithelial sodium channels (ENaC) in the late distal tubule and collecting duct [1], [2]. Unlike spironolactone, its action is independent of aldosterone. **Why Muscle Cramps?** Muscle cramps are a frequently reported side effect of Triamterene. This occurs due to the rapid alteration in electrolyte balance and the contraction of extracellular fluid volume. While it spares potassium, the net loss of sodium and water can lead to localized electrolyte imbalances in muscle tissue, triggering involuntary contractions. **Analysis of Incorrect Options:** * **A. Improved glucose tolerance:** Diuretics, particularly thiazides, are known to *worsen* glucose tolerance (hyperglycemia). Triamterene does not improve it; in some cases, it may impair it. * **C. Decrease in urea level:** Diuretics can cause a decrease in effective circulating volume, leading to pre-renal azotemia, which actually **increases** blood urea nitrogen (BUN) levels. * **D. Hypokalemia:** As a potassium-sparing diuretic, Triamterene causes **hyperkalemia**, not hypokalemia [1]. This is its most dangerous potential side effect, especially when used with ACE inhibitors [1]. **High-Yield Facts for NEET-PG:** 1. **Triamterene & Kidney Stones:** A unique side effect of Triamterene is that it is poorly soluble and can precipitate in the urine, leading to **crystalluria and kidney stones** (triamterene casts). 2. **Mechanism:** It is a "renal epithelial sodium channel blocker," similar to Amiloride [2]. 3. **Liddle’s Syndrome:** While Amiloride is the drug of choice, this class is used to treat Liddle’s syndrome (pseudo-hyperaldosteronism).
Question 132: A group of people are travelling to the mountains, and a girl starts complaining of mountain sickness. What is the drug of choice?
- A. Thiazide
- B. Acetazolamide (Correct Answer)
- C. Promethazine
- D. Dimenhydrinate
Explanation: ***Acetazolamide*** - This drug is the agent of choice for prophylaxis and treatment of **Acute Mountain Sickness (AMS)** due to its ability to accelerate **acclimatization**. - It functions as a **carbonic anhydrase inhibitor**, inducing a mild metabolic acidosis that stimulates the respiratory center, thereby increasing ventilation and improving blood oxygen saturation. *Promethazine* - This is an **antihistamine** (H1 blocker) often used for its potent **antiemetic** (nausea) and sedative effects. - While it may relieve nausea symptoms associated with AMS, it does not address the underlying physiological disturbances or enhance **acclimatization**. *Dimenhydrinate* - This medication is also an **antihistamine** typically employed to treat and prevent **motion sickness** and vertigo. - It lacks the crucial physiological mechanism (carbonic anhydrase inhibition) required to improve breathing efficiency and accelerate the body's response to **hypoxia**. *Thiazide* - This category of drugs, such as hydrochlorothiazide, are **diuretics** primarily used for hypertension and edema. - They do not possess the necessary respiratory stimulation properties of **Acetazolamide** and are therefore ineffective in treating or preventing mountain sickness.
Question 133: A patient having hypertension is on thiazides and is complaining of fatigue and hypokalemia. Which of the following drugs can prevent potassium loss?
- A. Acetazolamide
- B. Indapamide
- C. Furosemide
- D. Amiloride (Correct Answer)
Explanation: ***Amiloride***- Amiloride is a **potassium-sparing diuretic** that acts by blocking the **Epithelial Sodium Channel (ENaC)** in the collecting duct. [5]- By inhibiting Na+ reabsorption here, it decreases the electrical gradient that drives **potassium secretion**, effectively counteracting the hypokalemic effect of thiazides. [2]*Furosemide*- Furosemide is a **loop diuretic** that inhibits the Na-K-2Cl cotransporter in the thick ascending limb.- It is notorious for causing significant urinary **potassium loss** and would worsen the patient's **hypokalemia** and fatigue. [5]*Acetazolamide*- Acetazolamide is a **carbonic anhydrase inhibitor** that increases the delivery of Na+ and bicarbonate (HCO3-) to the collecting duct. [4]- The increased delivery of these ions promotes the secretion and loss of **potassium** in the urine, thus failing to prevent hypokalemia. [4]*Indapamide*- Indapamide is a **thiazide-like diuretic** that, similar to thiazides, inhibits the NaCl cotransporter in the distal convoluted tubule. [1]- Like other thiazides, Indapamide is a **potassium-wasting diuretic** and would exacerbate the existing **hypokalemia**. [3]
Question 134: A 35-year-old male experiences headache, nausea, and shortness of breath while trekking. The physician prescribes a drug to alleviate his symptoms. The drug administered primarily acts on which part of the nephron?
- A. Loop of Henle
- B. Collecting duct (CD)
- C. Proximal convoluted tubule (PCT) (Correct Answer)
- D. Distal convoluted tubule (DCT)
Explanation: ***Proximal convoluted tubule (PCT)***- The clinical presentation (headache, nausea, shortness of breath while trekking) is consistent with **Acute Mountain Sickness (AMS)**, which is typically prevented or treated with **Acetazolamide**.- **Acetazolamide** is a **carbonic anhydrase inhibitor** that acts primarily in the PCT, reducing bicarbonate reabsorption and inducing metabolic acidosis, which stimulates ventilation to counteract altitude-induced respiratory alkalosis.*Loop of Henle*- This segment is the primary site for **Loop Diuretics** (e.g., **Furosemide**), which inhibit the **Na+-K+-2Cl- cotransporter** in the thick ascending limb.- Loop diuretics promote powerful diuresis but are not the standard pharmacological choice for treating or preventing the symptoms of AMS.*Distal convoluted tubule (DCT)*- The DCT is the target site for **Thiazide Diuretics** (e.g., **Hydrochlorothiazide**), which block the **Na+-Cl- cotransporter**.- Thiazides primarily manage hypertension and edema and lack the necessary mechanism (carbonic anhydrase inhibition) to directly increase ventilation required for AMS treatment.*Collecting duct (CD)*- The collecting duct is where **Potassium-sparing diuretics** and **Aldosterone antagonists** (e.g., **Spironolactone**) exert their effects by controlling final sodium and potassium balance.- While these drugs can influence fluid balance, their primary actions are far removed from the need to induce metabolic acidosis to stimulate central respiratory drives in high-altitude illness.
Question 135: Which of the following diuretics primarily acts on the part labeled 'D' in the given diagram of a nephron?
- A. Acetazolamide
- B. Mannitol
- C. Hydrochlorothiazide (Correct Answer)
- D. Furosemide
Explanation: ***Hydrochlorothiazide*** - The part labeled 'D' in the diagram is the **Distal Convoluted Tubule (DCT)**. **Thiazide diuretics**, such as hydrochlorothiazide, primarily act on this segment of the nephron. - They work by inhibiting the **Na+/Cl- cotransporter** in the DCT, which reduces the reabsorption of sodium and chloride from the tubular fluid, leading to increased water excretion. *Furosemide* - Furosemide is a **loop diuretic** that acts on the **thick ascending limb of the Loop of Henle** (part of B), not the DCT. - It is a more potent diuretic than thiazides because it inhibits the **Na+-K+-2Cl- cotransporter**, which is responsible for reabsorbing a significant portion of filtered sodium. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that primarily acts on the **Proximal Convoluted Tubule (PCT)** (labeled 'A'). - Its mechanism involves reducing the reabsorption of **bicarbonate (HCO3-)**, which leads to a mild diuretic effect and can cause metabolic acidosis. *Mannitol* - Mannitol is an **osmotic diuretic** that acts mainly in the **Proximal Convoluted Tubule (PCT)** and the **descending limb of the Loop of Henle**. - It is a pharmacologically inert substance that increases the **osmolarity** of the tubular fluid, thereby preventing water reabsorption.
Question 136: A 50-year-old woman was prescribed a diuretic by a doctor to manage hypertension. Which of the following diuretics acts on site 'A' as marked in the given image?
- A. Acetazolamide
- B. Mannitol
- C. Hydrochlorothiazide (Correct Answer)
- D. Furosemide
Explanation: ***Hydrochlorothiazide*** - Hydrochlorothiazide is a **thiazide diuretic** that acts on the **Distal Convoluted Tubule (DCT)**, which is indicated by the letter 'A' in the provided diagram. - It works by inhibiting the **Na+/Cl- cotransporter** in the early DCT, leading to increased excretion of sodium and water, which helps lower blood pressure. *Furosemide* - Furosemide is a potent **loop diuretic** that acts on the **thick ascending limb of the loop of Henle** (labeled as 'G'). - It inhibits the **Na+/K+/2Cl- cotransporter**, causing a significant increase in sodium and water excretion, making it more powerful than thiazides. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor**, and its primary site of action is the **Proximal Convoluted Tubule (PCT)** (labeled as 'D'). - It is a weak diuretic and is more commonly used for glaucoma, metabolic alkalosis, or altitude sickness rather than as a primary agent for hypertension. *Mannitol* - Mannitol is an **osmotic diuretic** that exerts its effect primarily in the **Proximal Convoluted Tubule (PCT)** and the **descending limb of the loop of Henle**. - It is administered intravenously and is used to reduce intracranial or intraocular pressure, not for the chronic management of hypertension.
Question 137: A patient on hydrochlorothiazide develops renal stones. What explains this adverse effect?
- A. Decreased urinary citrate (Correct Answer)
- B. Increased urinary citrate
- C. Decrease urinary calcium
- D. Increase urinary calcium
Explanation: ***Decreased urinary citrate*** - **Hydrochlorothiazide** (HCTZ) can cause hypokalemia associated with **metabolic alkalosis** - Metabolic alkalosis leads to **decreased urinary citrate** excretion (hypocitraturia) - **Citrate is a key inhibitor** of calcium oxalate and calcium phosphate stone formation by complexing with urinary calcium - Hypocitraturia theoretically increases stone formation risk by reducing this protective effect - **Clinical Note:** Despite this mechanism, thiazides are actually used to **prevent** recurrent calcium stones due to their dominant effect of reducing urinary calcium excretion *Increased urinary calcium* - This would promote stone formation, but thiazides actually **decrease** urinary calcium excretion (hypocalciuria) - The calcium-lowering effect is why thiazides are used therapeutically for **preventing** calcium nephrolithiasis - In this question, the mechanism relates to altered citrate, not calcium excretion *Decreased urinary calcium* - Thiazides do decrease urinary calcium, which is **protective** against stones, not causative - This is the primary beneficial effect that makes thiazides useful in preventing recurrent calcium nephrolithiasis - The stone formation in the question stem relates to the **citrate** mechanism, not calcium *Increased urinary citrate* - Increased citrate would be **protective** against stone formation by binding urinary calcium - Thiazides cause the opposite effect: **hypocitraturia** (decreased citrate) due to associated metabolic alkalosis - Higher urinary citrate is actually a therapeutic goal in stone prevention
Question 138: By what primary mechanism does hydrochlorothiazide help prevent the formation of calcium stones?
- A. It directly dissolves existing calcium stones by altering urinary pH and increasing their solubility.
- B. It increases the urinary excretion of citrate, which acts as a chelating agent.
- C. It increases calcium reabsorption in the distal convoluted tubule, leading to a decrease in urinary calcium excretion. (Correct Answer)
- D. It increases the filtration of calcium at the glomerulus, thereby reducing serum calcium levels.
Explanation: ***It increases calcium reabsorption in the distal convoluted tubule, leading to a decrease in urinary calcium excretion.*** - By inhibiting the **sodium-chloride cotransporter (NCC)** in the **distal convoluted tubule (DCT)**, thiazides indirectly enhance calcium reabsorption via the basolateral Na+/Ca2+ exchanger. - This pharmacological effect causes **hypocalciuria**, which reduces the supersaturation of calcium oxalate/phosphate in the urine, thereby preventing stone formation. *It increases the urinary excretion of citrate, which acts as a chelating agent.* - While citrate is a powerful inhibitor of stones, thiazides are **not** primarily known to substantially increase urinary citrate excretion. - Other measures, such as oral **potassium citrate**, are used specifically to increase urinary citrate levels in stone formers. *It increases the filtration of calcium at the glomerulus, thereby reducing serum calcium levels.* - Thiazides actually tend to cause a slight **increase** in serum calcium (due to enhanced reabsorption in the DCT and bone effects), a condition known as thiazide-induced hypercalcemia. - Their mechanism of stone prevention is focused on reducing **urinary** calcium, not primarily filtering more calcium. *It directly dissolves existing calcium stones by altering urinary pH and increasing their solubility.* - Thiazides are primarily **preventative** medications for stone formation; they do not have a role in directly dissolving existing calcium stones. - The dissolution of some stones (like uric acid stones) is usually achieved by urinary alkalinization (e.g., using **potassium citrate**), which is not the main action of HCTZ.
Question 139: A patient is started on hydrochlorothiazide for hypertension and later develops renal stones. Which metabolic effect of hydrochlorothiazide is most likely responsible?
- A. Hypocitraturia
- B. Hypocalciuria
- C. Hypomagnesemia
- D. Hyperuricemia (Correct Answer)
Explanation: ***Hyperuricemia*** * Hydrochlorothiazide causes **hyperuricemia** by competing with uric acid for secretion in the proximal tubule, leading to decreased uric acid excretion. * Elevated serum uric acid levels increase the risk of **uric acid stone formation**, which is a well-recognized adverse effect of thiazide diuretics. * This is why thiazides can precipitate gout attacks and increase uric acid stone risk. *Hypocalciuria* * HCTZ causes **decreased urinary calcium excretion** (hypocalciuria) by enhancing calcium reabsorption in the DCT. * This effect is **stone-PROTECTIVE**, not causative - thiazides are actually used therapeutically to prevent recurrent calcium stones. * This would NOT explain stone formation in this patient. *Hypomagnesemia* * While HCTZ can cause magnesium loss, hypomagnesemia is not a primary mechanism for stone formation with thiazide use. * Magnesium is actually a stone inhibitor, so low levels could theoretically contribute, but this is not the main mechanism. *Hypocitraturia* * HCTZ does not typically cause significant citrate wasting or hypocitraturia. * Hypocitraturia is more characteristic of **carbonic anhydrase inhibitors** and chronic metabolic acidosis, not thiazide diuretics.
Question 140: The image shows drug 'X' blocking a channel in the renal tubule. Which of the following drugs is 'X'?
- A. Eplerenone
- B. Canrenone
- C. Indapamide
- D. Amiloride (Correct Answer)
Explanation: ***Amiloride*** - The image shows drug 'X' inhibiting the **epithelial sodium channel (ENaC)** in the kidney tubule. **Amiloride** is a potassium-sparing diuretic that directly blocks ENaC. - By blocking ENaC, amiloride reduces sodium reabsorption and thereby reduces potassium excretion, making it a **potassium-sparing diuretic**. *Eplerenone* - **Eplerenone** is a selective aldosterone receptor antagonist. It blocks the action of aldosterone, not directly the ENaC. - While it has a similar overall effect of potassium-sparing, its mechanism is upstream of the ENaC receptor itself, by preventing aldosterone from increasing ENaC expression. *Canrenone* - **Canrenone** is an active metabolite of spironolactone, which is also an aldosterone receptor antagonist. - Like eplerenone, it works by blocking aldosterone receptors, preventing aldosterone from increasing ENaC activity, rather than directly blocking the channel itself. *Indapamide* - **Indapamide** is a thiazide-like diuretic that acts on the distal convoluted tubule. - It inhibits the **Na+/Cl- symporter**, which is different from the ENaC shown in the image, affecting a different part of the nephron and mechanism of action.
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
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Diuretics in Renal Disorders
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Adverse Effects and Drug Interactions
Practice Questions
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