Diuretics — MCQs
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Acetazolamide is administered to a glaucoma patient. Given that this drug inhibits carbonic anhydrase in the renal proximal tubule, which of the following substances will be excreted at a lower rate?
A 68-year-old woman presents for a routine check-up with occasional ankle swelling. Her serum potassium is 3.5 mEq/L. Which of the following diuretics would be most appropriate for this patient, considering the need to avoid unnecessary potassium losses?
Which of the following is an adverse effect of thiazide diuretics?
Which of the following inhibits the Na+-K+-2Cl- cotransporter?
Acetazolamide acts at which part of the nephron?
What is the mechanism of action of furosemide as a diuretic?
Acetazolamide side effects include all except:
Which of the following potassium-sparing diuretics alters cardiac mortality?
What is the diuretic of choice for rapid relief of congestive symptoms in a patient with congestive heart failure?
What is the drug of choice in lithium-induced diabetes insipidus?
Diuretics Indian Medical PG Practice Questions and MCQs
Question 71: Acetazolamide is administered to a glaucoma patient. Given that this drug inhibits carbonic anhydrase in the renal proximal tubule, which of the following substances will be excreted at a lower rate?
- A. Na+
- B. H2O
- C. HCO3-
- D. NH4+ (Correct Answer)
Explanation: **Explanation:** **Mechanism of Action & The Correct Answer (NH4+):** Acetazolamide is a Carbonic Anhydrase (CA) inhibitor. In the proximal convoluted tubule (PCT), CA is essential for the reabsorption of bicarbonate ($HCO_3^-$) and the secretion of Hydrogen ions ($H^+$). By inhibiting CA, the drug reduces the availability of $H^+$ ions in the tubular lumen. Ammonia ($NH_3$) is produced by tubular cells and diffuses into the lumen, where it normally combines with secreted $H^+$ to form Ammonium ($NH_4^+$). This process, known as **"Ammonia Trapping,"** renders the molecule non-diffusible, ensuring its excretion. Since Acetazolamide decreases $H^+$ secretion, $NH_3$ cannot be converted to $NH_4^+$. Consequently, $NH_4^+$ formation decreases, and $NH_3$ diffuses back into the systemic circulation. Therefore, the **excretion rate of $NH_4^+$ decreases.** **Why Other Options are Incorrect:** * **A & B (Na+ and H2O):** Inhibition of CA prevents $NaHCO_3$ reabsorption. This leads to increased luminal osmolarity, causing **Natriuresis** (increased $Na^+$ excretion) and **Diuresis** (increased $H_2O$ excretion). * **C (HCO3-):** The primary effect of Acetazolamide is the inhibition of $HCO_3^-$ reabsorption, leading to significant **Bicarbonaturia** (increased $HCO_3^-$ excretion) and subsequent hyperchloremic metabolic acidosis. **High-Yield NEET-PG Pearls:** * **Clinical Uses:** Glaucoma (decreases aqueous humor), Mountain Sickness (induces metabolic acidosis to stimulate respiration), and Urinary Alkalinization (to excrete acidic drugs like uric acid). * **Side Effects:** Hypokalemia, Metabolic Acidosis, and **Hyperammonemia** (contraindicated in Liver Cirrhosis as it can precipitate hepatic encephalopathy due to decreased $NH_4^+$ excretion). * **Site of Action:** Proximal Convoluted Tubule (PCT).
Question 72: A 68-year-old woman presents for a routine check-up with occasional ankle swelling. Her serum potassium is 3.5 mEq/L. Which of the following diuretics would be most appropriate for this patient, considering the need to avoid unnecessary potassium losses?
- A. Furosemide
- B. Hydrochlorothiazide
- C. Spironolactone
- D. Amiloride (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Amiloride** **1. Why Amiloride is the Correct Choice:** The patient has a serum potassium level of 3.5 mEq/L, which is at the lower limit of normal (3.5–5.0 mEq/L). To manage her edema without causing further hypokalemia, a **Potassium-Sparing Diuretic** is indicated. Amiloride works by directly blocking the **Epithelial Sodium Channels (ENaC)** in the late distal tubule and collecting duct. By preventing sodium reabsorption at this site, it reduces the negative luminal potential, thereby inhibiting the secretion of potassium into the urine. Unlike other diuretics, it preserves serum potassium levels. **2. Why the Other Options are Incorrect:** * **A. Furosemide:** A loop diuretic that inhibits the Na⁺-K⁺-2Cl⁻ symporter in the thick ascending limb. It causes significant potassium loss (hypokalemia) due to increased sodium delivery to the distal tubule and activation of the RAAS. * **B. Hydrochlorothiazide:** A thiazide diuretic that inhibits the Na⁺-Cl⁻ symporter in the distal convoluted tubule. Like loop diuretics, it is "potassium-wasting" and would likely push this patient into clinical hypokalemia. * **C. Spironolactone:** While also potassium-sparing, it is an **Aldosterone Antagonist**. It has a slow onset of action (taking days to work) and carries side effects like gynecomastia due to its non-specific binding to androgen receptors. Amiloride is often preferred when a direct ENaC blockade is sufficient. **3. NEET-PG High-Yield Pearls:** * **Liddle’s Syndrome:** Amiloride is the drug of choice for this rare genetic condition (overactive ENaC channels). * **Lithium-Induced Diabetes Insipidus:** Amiloride is the treatment of choice as it blocks lithium entry through ENaC in the collecting ducts. * **Site of Action:** Remember that potassium-sparing diuretics are the only class that acts on the **Collecting Duct**. * **Side Effect:** The most serious complication of this class is **hyperkalemia**, especially if used with ACE inhibitors or in patients with renal impairment.
Question 73: Which of the following is an adverse effect of thiazide diuretics?
- A. Hyperkalemic metabolic acidosis
- B. Hypolipidemia
- C. Hypouricemia
- D. Erectile dysfunction (Correct Answer)
Explanation: **Explanation:** Thiazide diuretics (e.g., Hydrochlorothiazide, Chlorthalidone) are a cornerstone of hypertension management, but they are associated with several metabolic and systemic side effects. **Why Erectile Dysfunction is Correct:** Erectile dysfunction (ED) is a well-documented, though often under-reported, adverse effect of thiazide diuretics. The exact mechanism is multifactorial; it is thought to be caused by a decrease in total peripheral resistance and a reduction in zinc levels (which are necessary for testosterone production), as well as direct effects on vascular smooth muscle. In clinical trials, thiazides are more frequently associated with ED compared to ACE inhibitors or Calcium Channel Blockers. **Analysis of Incorrect Options:** * **A. Hyperkalemic metabolic acidosis:** Thiazides cause **Hypokalemic metabolic alkalosis**. They increase sodium delivery to the distal tubule, promoting K+ and H+ secretion into the urine. * **B. Hypolipidemia:** Thiazides actually cause **Hyperlipidemia**. They can lead to a transient increase in total cholesterol, LDL, and triglycerides. * **C. Hypouricemia:** Thiazides cause **Hyperuricemia**. They compete with uric acid for the organic acid secretory secretory pump in the proximal tubule, leading to uric acid retention, which can precipitate gout. **NEET-PG High-Yield Pearls:** * **The "Hyper" Rule:** Thiazides cause **Hyper**glycemia, **Hyper**lipidemia, **Hyper**uricemia, and **Hyper**calcemia (useful in preventing calcium stones). * **The "Hypo" Rule:** They cause **Hypo**kalemia, **Hypo**natremia, and **Hypo**magnesemia. * **Chlorthalidone** is currently preferred over Hydrochlorothiazide due to its longer half-life and better evidence in reducing cardiovascular events.
Question 74: Which of the following inhibits the Na+-K+-2Cl- cotransporter?
- A. Mannitol
- B. Carbonic anhydrase inhibitor
- C. Thiazide
- D. Loop diuretic (Correct Answer)
Explanation: **Explanation:** **Correct Option: D (Loop Diuretics)** Loop diuretics (e.g., Furosemide, Torsemide, Bumetanide) exert their primary effect on the **Thick Ascending Limb (TAL)** of the Loop of Henle [4]. They act by inhibiting the **Na+-K+-2Cl- symporter (NKCC2)** on the apical membrane [1]. By blocking this transporter, they prevent the reabsorption of sodium, potassium, and chloride, leading to potent natriuresis [5]. Because the TAL is responsible for reabsorbing ~25% of filtered sodium, these are the most efficacious diuretics ("High-ceiling diuretics"). **Incorrect Options:** * **A. Mannitol:** This is an **Osmotic Diuretic**. It works primarily in the Proximal Convoluted Tubule (PCT) and the Descending Limb of the Loop of Henle by increasing the osmolarity of the tubular fluid, thereby retaining water in the lumen [3]. * **B. Carbonic Anhydrase Inhibitors (e.g., Acetazolamide):** These act in the **PCT** by inhibiting the enzyme carbonic anhydrase, which prevents the reabsorption of sodium bicarbonate ($NaHCO_3$) [2]. * **C. Thiazides:** These act on the **Distal Convoluted Tubule (DCT)** by inhibiting the **Na+-Cl- symporter**. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Action:** Loop diuretics act on the TAL; Thiazides act on the DCT. * **Calcium Dynamics:** Loop diuretics **increase** urinary calcium excretion ("Loops Lose Calcium"), making them useful in treating hypercalcemia [5]. Conversely, Thiazides **decrease** urinary calcium (useful in idiopathic hypercalciuria/stones). * **Ototoxicity:** This is a unique side effect of loop diuretics (especially Ethacrynic acid) due to the presence of NKCC transporters in the inner ear. * **Drug of Choice:** Loop diuretics are the preferred agents for acute pulmonary edema and congestive heart failure.
Question 75: Acetazolamide acts at which part of the nephron?
- A. Proximal Convoluted Tubule (PCT) (Correct Answer)
- B. Distal Convoluted Tubule (DCT)
- C. Ascending loop of Henle
- D. Descending loop of Henle
Explanation: **Explanation:** **Acetazolamide** is a potent **Carbonic Anhydrase (CA) inhibitor** [2]. Its primary site of action is the **Proximal Convoluted Tubule (PCT)** [4]. In the PCT, carbonic anhydrase (specifically the CA-IV isoenzyme on the brush border and CA-II in the cytoplasm) is responsible for the reabsorption of sodium bicarbonate ($NaHCO_3$) [3]. By inhibiting this enzyme, acetazolamide prevents the dehydration of carbonic acid and the subsequent reabsorption of bicarbonate, leading to alkaline diuresis and a mild diuretic effect [2]. **Analysis of Incorrect Options:** * **Distal Convoluted Tubule (DCT):** This is the site of action for **Thiazide diuretics**, which inhibit the $Na^+/Cl^-$ symporter. * **Ascending loop of Henle:** Specifically the Thick Ascending Limb (TAL), this is the site of action for **Loop diuretics** (e.g., Furosemide), which inhibit the $Na^+/K^+/2Cl^-$ cotransporter. * **Descending loop of Henle:** This segment is highly permeable to water but impermeable to solutes; it is primarily influenced by **Osmotic diuretics** like Mannitol [1]. **Clinical Pearls for NEET-PG:** * **Therapeutic Uses:** Glaucoma (decreases aqueous humor production), Acute Mountain Sickness (counteracts respiratory alkalosis), and Urinary Alkalinization (to excrete acidic drugs like uric acid or cystine). * **Adverse Effects:** Hyperchloremic metabolic acidosis, hypokalemia, and paresthesia. * **Contraindications:** Avoid in patients with hepatic cirrhosis, as it can decrease ammonia excretion, potentially precipitating hepatic encephalopathy.
Question 76: What is the mechanism of action of furosemide as a diuretic?
- A. Inhibition of Na-K-Cl ion symporter (Correct Answer)
- B. Aldosterone antagonism
- C. Inhibition of Na-Cl symporter in distal tubules
- D. Carbonic anhydrase inhibition
Explanation: **Explanation:** **1. Why Option A is Correct:** Furosemide is a potent **Loop Diuretic**. Its primary mechanism of action is the reversible inhibition of the **Naⁱ-Kⁱ-2Cl⁻ symporter (NKCC2)** [2] located in the luminal membrane of the **Thick Ascending Limb (TAL)** of the Loop of Henle [4]. By blocking this transporter, it prevents the reabsorption of these electrolytes, leading to a significant increase in the excretion of sodium, chloride, and water [2]. Because the TAL is responsible for reabsorbing ~25% of filtered sodium, loop diuretics are the most efficacious diuretics ("High-ceiling diuretics") [3]. **2. Why Other Options are Incorrect:** * **Option B (Aldosterone antagonism):** This describes **Spironolactone** and Eplerenone. These are potassium-sparing diuretics that act on the mineralocorticoid receptors in the collecting ducts. * **Option C (Inhibition of Na-Cl symporter):** This is the mechanism of **Thiazide diuretics** (e.g., Hydrochlorothiazide), which act specifically on the **Distal Convoluted Tubule (DCT)** [3]. * **Option D (Carbonic anhydrase inhibition):** This describes **Acetazolamide**, which acts primarily in the **Proximal Convoluted Tubule (PCT)** [5]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Electrolyte Changes:** Furosemide causes **Hypokalemia**, **Hypomagnesemia**, and notably **Hypocalcemia** (unlike Thiazides, which cause hypercalcemia) [4]. "Loop loses calcium." * **Drug of Choice:** It is the treatment of choice for **Acute Pulmonary Edema** due to its rapid onset and additional vasodilator effect. * **Adverse Effects:** Watch for **Ototoxicity** (especially when combined with aminoglycosides), Hyperuricemia (can precipitate Gout), and Sulfa-allergy cross-reactivity [1]. * **Site of Action:** Always remember—Loop diuretics act on the **Thick Ascending Limb** [2].
Question 77: Acetazolamide side effects include all except:
- A. Hypokalemia
- B. Drowsiness
- C. Diarrhea (Correct Answer)
- D. Paresthesia
Explanation: **Explanation:** Acetazolamide is a **Carbonic Anhydrase Inhibitor** that acts primarily at the proximal convoluted tubule (PCT). It inhibits the enzyme carbonic anhydrase, leading to the excretion of sodium, potassium, and bicarbonate. **Why "Diarrhea" is the correct answer:** Diarrhea is not a recognized side effect of Acetazolamide. In fact, the most common gastrointestinal side effect associated with its use is **nausea or anorexia**, but it does not typically cause increased bowel motility or diarrhea. **Analysis of Incorrect Options:** * **Hypokalemia (Option A):** By increasing the delivery of sodium and water to the distal tubule, Acetazolamide promotes potassium secretion into the urine. This is a classic side effect of most diuretics (except potassium-sparing ones). * **Drowsiness (Option B):** Acetazolamide can cause Central Nervous System (CNS) depression, leading to sedation, fatigue, and drowsiness, especially in patients with hepatic impairment. * **Paresthesia (Option C):** This is a very common and high-yield side effect. Patients often report "pins and needles" sensations in the extremities and face due to the metabolic acidosis and electrolyte shifts induced by the drug. **High-Yield Clinical Pearls for NEET-PG:** * **Metabolic Acidosis:** Acetazolamide causes **Hyperchloremic Metabolic Acidosis** (due to bicarbonate loss). * **Therapeutic Uses:** Glaucoma (decreases aqueous humor), Altitude Sickness (prophylaxis), and Urinary Alkalization (to excrete acidic drugs like aspirin). * **Contraindication:** Avoid in patients with **Liver Cirrhosis**, as it decreases ammonia excretion, potentially precipitating hepatic coma. * **Renal Stones:** It can cause calcium phosphate stones because calcium is less soluble in alkaline urine.
Question 78: Which of the following potassium-sparing diuretics alters cardiac mortality?
- A. Spironolactone (Correct Answer)
- B. Amiloride
- C. Triamterene
- D. Eplerenone
Explanation: **Explanation:** **1. Why Spironolactone is Correct:** Spironolactone is a competitive **Aldosterone Receptor Antagonist (MRA)**. In chronic heart failure, aldosterone levels are chronically elevated, leading to pathological cardiac remodeling and myocardial fibrosis. Spironolactone inhibits these effects, thereby reducing cardiac stiffness and arrhythmias. The landmark **RALES trial** demonstrated that adding spironolactone to standard therapy significantly reduces morbidity and mortality in patients with severe Heart Failure with Reduced Ejection Fraction (HFrEF). **2. Why the Other Options are Incorrect:** * **Amiloride & Triamterene (Options B & C):** These are **epithelial sodium channel (ENaC) blockers** acting directly on the late distal tubule and collecting duct. Unlike MRAs, they do not antagonize the systemic effects of aldosterone on the heart. They are primarily used to prevent hypokalemia induced by other diuretics and have no proven mortality benefit in heart failure. * **Eplerenone (Option D):** While Eplerenone is also an MRA and *does* reduce mortality (proven in the **EMPHASIS-HF** trial), it is a more selective antagonist with fewer side effects (like gynecomastia). However, in the context of standard NEET-PG questions, **Spironolactone** is the classic, first-line answer as it was the first to demonstrate this benefit and remains the prototype drug for this category. **3. High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** Spironolactone causes **gynecomastia** and impotence due to its non-selective binding to androgen and progesterone receptors. Eplerenone is the preferred alternative if these occur. * **Contraindication:** Both are contraindicated in patients with **hyperkalemia** or significant renal impairment (Serum Creatinine >2.5 mg/dL). * **Site of Action:** They act on the **Collecting Duct** (the "late" part of the nephron). * **Other Mortality-Reducing Drugs in HF:** ACE inhibitors, ARBs, Beta-blockers, and SGLT2 inhibitors.
Question 79: What is the diuretic of choice for rapid relief of congestive symptoms in a patient with congestive heart failure?
- A. Hydrochlorothiazide
- B. Furosemide (Correct Answer)
- C. Metolazone
- D. Amiloride
Explanation: **Furosemide** is the diuretic of choice for the rapid relief of congestive symptoms (such as pulmonary edema or peripheral edema) in patients with Congestive Heart Failure (CHF) [1]. **Why Furosemide is the Correct Answer:**Furosemide is a **Loop Diuretic** that acts by inhibiting the $Na^+-K^+-2Cl^-$ symporter in the Thick Ascending Limb (TAL) of the Loop of Henle [2]. It is preferred in acute CHF for two primary reasons:1. **High Efficacy:** Known as "high-ceiling" diuretics, loop diuretics have the highest natriuretic capacity, capable of excreting up to 25% of filtered sodium [2].2. **Rapid Action:** When given intravenously, it produces rapid venodilation (via prostaglandin release) even before the diuretic effect begins, which immediately reduces cardiac preload and relieves pulmonary congestion.**Why Other Options are Incorrect:** * **A. Hydrochlorothiazide:** Thiazides are "low-ceiling" diuretics. They are less potent than loop diuretics and are generally used for long-term management of hypertension rather than acute relief of CHF symptoms [1, 2].* **C. Metolazone:** While a potent thiazide-like diuretic, it is typically used as an "add-on" to loop diuretics in cases of diuretic resistance rather than as a first-line monotherapy for rapid relief.* **D. Amiloride:** This is a potassium-sparing diuretic with very weak natriuretic activity. It is used primarily to counteract hypokalemia caused by other diuretics [1].**High-Yield Clinical Pearls for NEET-PG:** * **DOC for Acute Pulmonary Edema:** IV Furosemide.* **Ototoxicity:** A key side effect of loop diuretics, especially when used with aminoglycosides.* **Metabolic Profile:** Loop diuretics cause **Hypokalemic Metabolic Alkalosis**, Hypomagnesemia, and Hyperuricemia (can precipitate Gout) [2].* **Calcium Handling:** Loop diuretics "Lose" calcium (used in hypercalcemia), whereas Thiazides "Thrive" on calcium (cause hypercalcemia; used in idiopathic hypercalciuria).
Question 80: What is the drug of choice in lithium-induced diabetes insipidus?
- A. Amiloride (Correct Answer)
- B. Vasopressin
- C. Thiazide diuretics
- D. Diclofenac
Explanation: ### Explanation **Correct Option: A. Amiloride** Lithium-induced Nephrogenic Diabetes Insipidus (NDI) occurs because lithium enters the principal cells of the collecting duct through **ENaC (Epithelial Sodium Channels)**. Once inside, lithium inhibits glycogen synthase kinase-3β, interfering with the action of ADH (Vasopressin) and reducing aquaporin-2 expression. **Amiloride** is the drug of choice because it blocks these ENaC channels, preventing lithium from entering the cells and thereby restoring the kidney's concentrating ability. **Why other options are incorrect:** * **B. Vasopressin:** In NDI, the kidneys are resistant to ADH. Therefore, administering exogenous vasopressin will not improve urine concentration. * **C. Thiazide diuretics:** While thiazides are used to treat other forms of NDI (by causing mild volume depletion and increasing proximal water reabsorption), they are not the specific treatment for lithium-induced cases and can actually increase lithium toxicity by decreasing its clearance. * **D. Diclofenac:** NSAIDs can be used in NDI to decrease GFR and inhibit prostaglandins (which antagonize ADH), but they are secondary treatments and carry risks of renal impairment. **High-Yield Clinical Pearls for NEET-PG:** * **Lithium Toxicity:** Thiazides, ACE inhibitors, and NSAIDs (except Aspirin) increase lithium levels and can lead to toxicity. * **Amiloride vs. Triamterene:** Both are K+-sparing diuretics (ENaC blockers), but Amiloride is specifically preferred for lithium-induced NDI. * **DOC for Central DI:** Desmopressin (dDAVP). * **DOC for General NDI:** Thiazides (e.g., Hydrochlorothiazide).
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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