Diuretics — MCQs

Diuretics Indian Medical PG Practice Questions and MCQs

Question 61: At equally natriuretic doses, which of the following drugs causes maximum potassium excretion?

A. Spironolactone
B. Furosemide
C. Acetazolamide (Correct Answer)
D. Aldosterone

Explanation: **Explanation:** The correct answer is **Acetazolamide**. **1. Why Acetazolamide is correct:** Acetazolamide is a Carbonic Anhydrase Inhibitor (CAI) that acts on the proximal convoluted tubule (PCT). It inhibits the reabsorption of sodium bicarbonate ($NaHCO_3$). This results in a large delivery of sodium and non-reabsorbable bicarbonate ions to the distal segments of the nephron. To compensate for the high sodium load, the distal tubule and collecting ducts exchange sodium for potassium. Furthermore, the presence of bicarbonate (a negative anion) in the distal tubule creates a negative luminal potential that further "pulls" $K^+$ out of the cells. Consequently, at doses that produce the same level of natriuresis as other diuretics, CAIs cause the **highest magnitude of potassium loss.** **2. Why the other options are incorrect:** * **Spironolactone:** This is a potassium-sparing diuretic. It antagonizes aldosterone receptors, leading to potassium retention rather than excretion. * **Furosemide:** While loop diuretics cause significant hypokalemia, their primary site of action is the Thick Ascending Limb. At *equally natriuretic doses*, the distal delivery of bicarbonate seen with CAIs makes Acetazolamide more potent at inducing kaliuresis. * **Aldosterone:** This is a mineralocorticoid, not a diuretic. While it increases $K^+$ excretion, it causes sodium *retention* (edema), making it the opposite of a natriuretic agent. **3. NEET-PG High-Yield Pearls:** * **Site of Action:** Acetazolamide (PCT), Furosemide (TAL of Loop of Henle), Thiazides (DCT). * **Metabolic Effect:** Acetazolamide causes **Hyperchloremic Metabolic Acidosis** (due to $HCO_3$ loss), whereas Loop and Thiazide diuretics cause **Metabolic Alkalosis**. * **Clinical Use:** Acetazolamide is the drug of choice for Glaucoma and Mountain Sickness, but it is a weak diuretic due to compensatory reabsorption in distal segments.

Question 62: Side effects of thiazides may include:

A. Hypokalemia
B. Hyperuricemia
C. Hyperglycemia
D. All of the above (Correct Answer)

Explanation: Thiazide diuretics (e.g., Hydrochlorothiazide, Chlorthalidone) act on the **Distal Convoluted Tubule (DCT)** by inhibiting the $Na^+/Cl^-$ symporter [1]. Their side effect profile is a high-yield topic for NEET-PG, often remembered by the mnemonic **"Hyper-GLUC"** (Hyper-Glycemia, Lipidemia, Uricemia, Calcemia). ### **Explanation of Options:** * **Hypokalemia (Option A):** By inhibiting sodium reabsorption in the DCT, more sodium is delivered to the collecting ducts. This triggers the aldosterone-sensitive $Na^+/K^+$ exchange, leading to increased potassium excretion in the urine. * **Hyperuricemia (Option B):** Thiazides compete with uric acid for the organic acid secretory secretory transport system in the proximal tubule [1]. This decreases uric acid excretion, potentially precipitating **Gout** [1]. * **Hyperglycemia (Option C):** Thiazides cause hypokalemia, which inhibits the release of insulin from pancreatic beta cells (as insulin release is K-dependent). They also decrease peripheral glucose utilization, worsening glycemic control in diabetics. ### **Why "All of the Above" is Correct:** Since thiazides concurrently cause potassium loss, elevate serum uric acid levels, and impair glucose tolerance, all three listed side effects are characteristic of this drug class. ### **High-Yield Clinical Pearls for NEET-PG:** 1. **Hypercalcemia:** Unlike Loop diuretics (which cause hypocalcemia), Thiazides **increase** calcium reabsorption [1][2]. This makes them useful in treating **Idiopathic Hypercalciuria** (kidney stones). 2. **Hyponatremia:** Thiazides are a common cause of drug-induced hyponatremia, especially in elderly patients. 3. **Lipid Profile:** They can cause a transient increase in LDL cholesterol and triglycerides (**Hyperlipidemia**). 4. **Erectile Dysfunction:** A frequently overlooked but common clinical side effect of thiazides.

Question 63: Spironolactone is least commonly used in which of the following conditions?

A. Congestive heart failure
B. Cirrhotic edema
C. Hypertension (Correct Answer)
D. Primary hyperaldosteronism

Explanation: The correct answer is **Hypertension**. While Spironolactone is a diuretic, it is considered a **weak diuretic** when used alone because it acts on the late distal tubule and collecting duct, where only about 2–3% of sodium reabsorption occurs [1]. In the management of essential hypertension, Thiazides or Calcium Channel Blockers are preferred as first-line agents. Spironolactone is typically reserved for resistant hypertension or specific cases where hyperaldosteronism is a contributing factor. **Why other options are incorrect:** * **Congestive Heart Failure (CHF):** Spironolactone is a cornerstone therapy (RALES trial). It prevents myocardial remodeling and fibrosis caused by aldosterone, significantly reducing mortality in patients with NYHA Class II-IV heart failure. * **Cirrhotic Edema:** It is the **drug of choice** for edema and ascites in liver cirrhosis. In cirrhosis, there is secondary hyperaldosteronism due to decreased hepatic clearance of aldosterone; Spironolactone directly antagonizes this effect [2]. * **Primary Hyperaldosteronism (Conn’s Syndrome):** It is used as the primary medical treatment to block the effects of excessive aldosterone secretion [1, 3], especially in patients who are not candidates for surgery. **NEET-PG High-Yield Pearls:** * **Mechanism:** Competitive antagonist at the Mineralocorticoid Receptor (MR) in the cortical collecting duct [1, 2, 3]. * **Side Effects:** Hyperkalemia (most common) [1, 3] and **Gynecomastia** (due to non-specific binding to androgen and progesterone receptors) [2]. * **Eplerenone:** A more selective mineralocorticoid antagonist with fewer endocrine side effects (no gynecomastia) [2]. * **Contraindication:** Should not be used if serum potassium is >5.0 mEq/L or in severe renal impairment (CrCl <30 mL/min) [1, 3].

Question 64: High ceiling diuretics are useful in the treatment of all of the following conditions except?

A. Generalized edema
B. Cerebral edema
C. Acute pulmonary edema
D. Pulmonary hypertension (Correct Answer)

Explanation: **Explanation:** High-ceiling diuretics (Loop diuretics like Furosemide) act on the thick ascending limb of the Henle’s loop by inhibiting the **Na⁺-K⁺-2Cl⁻ symporter**. They are the most potent diuretics, capable of excreting up to 25% of filtered sodium. **Why Pulmonary Hypertension is the Correct Answer:** Pulmonary hypertension is primarily a vascular remodeling and vasoconstrictive disease. While diuretics may be used cautiously in associated right-sided heart failure to reduce congestion, they are **not** a primary treatment for pulmonary hypertension itself. The mainstay of treatment involves vasodilators (e.g., Sildenafil, Bosentan, Epoprostenol). In fact, aggressive diuresis can decrease preload too much, leading to a drop in cardiac output in these patients. **Analysis of Other Options:** * **Generalized Edema:** Loop diuretics are the first-line treatment for edema associated with Congestive Heart Failure (CHF), Nephrotic syndrome, and Liver cirrhosis due to their high efficacy. * **Cerebral Edema:** While Mannitol (Osmotic diuretic) is the drug of choice, high-dose loop diuretics are used as adjuncts to reduce intracranial pressure by decreasing CSF formation and inducing systemic dehydration. * **Acute Pulmonary Edema:** Furosemide is the **drug of choice**. It works via two mechanisms: a rapid **venodilatory effect** (mediated by prostaglandins) that reduces preload within minutes, followed by the slower diuretic effect. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Furosemide is the DOC for Acute Pulmonary Edema and Hypercalcemia (with saline). * **Ototoxicity:** Ethacrynic acid is the most ototoxic; Furosemide is the most common cause of drug-induced deafness among diuretics. * **Metabolic Profile:** They cause "Hypo-everything" (Hypokalemia, Hyponatremia, Hypomagnesemia, Hypocalcemia) **except** Hyperuricemia and Hyperglycemia.

Question 65: Which of the following is the drug of choice for the treatment of inappropriate anti-diuretic hormone secretion?

A. Furosemide
B. Hydrochlorothiazide
C. Spironolactone
D. Demeclocycline (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Demeclocycline** **Mechanism and Rationale:** Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by excessive ADH release, leading to water retention and dilutional hyponatremia. **Demeclocycline**, a tetracycline derivative, is the drug of choice for chronic SIADH because it acts as an **ADH antagonist** at the level of the collecting duct. It induces a state of "nephrogenic diabetes insipidus" by interfering with the intracellular signaling (cAMP) triggered by ADH, thereby promoting the excretion of free water. **Analysis of Incorrect Options:** * **A. Furosemide:** While loop diuretics can be used in acute, symptomatic SIADH to increase free water clearance (usually alongside hypertonic saline), they are not the primary long-term treatment of choice. * **B. Hydrochlorothiazide:** Thiazides are contraindicated in SIADH. They inhibit sodium reabsorption in the distal tubule and can actually **worsen hyponatremia** by increasing ADH sensitivity and causing volume depletion-induced ADH release. * **C. Spironolactone:** This is a potassium-sparing diuretic (aldosterone antagonist) used primarily in hyperaldosteronism or heart failure; it has no role in antagonizing ADH. **High-Yield Clinical Pearls for NEET-PG:** * **Vaptans:** Tolvaptan (oral) and Conivaptan (IV) are "selective V2 receptor antagonists" and are now frequently preferred over demeclocycline for SIADH due to a better side-effect profile. * **Side Effect:** A major side effect of Demeclocycline is **nephrotoxicity** and photosensitivity. * **Correction Rate:** In SIADH, avoid rapid correction of hyponatremia to prevent **Osmotic Demyelination Syndrome** (Central Pontine Myelinolysis). Rule of thumb: <10–12 mEq/L in 24 hours. * **First-line treatment:** For mild/asymptomatic SIADH, the initial step is always **fluid restriction**.

Question 66: Hypercalcemia is seen in all of the following conditions except:

A. Lithium
B. Multiple myeloma
C. Loop diuretics (Correct Answer)
D. Hypervitaminosis D

Explanation: **Explanation:** The correct answer is **Loop diuretics** because they are the only option listed that causes **hypocalcemia** (decreased calcium levels) rather than hypercalcemia. **1. Why Loop Diuretics (Option C) is correct:** Loop diuretics (e.g., Furosemide) inhibit the **Na+/K+/2Cl- symporter** in the Thick Ascending Limb (TAL) of the Loop of Henle. This inhibition abolishes the positive transepithelial potential (lumen-positive voltage) that normally drives the paracellular reabsorption of divalent cations like **Calcium (Ca2+)** and **Magnesium (Mg2+)**. Consequently, calcium is excreted in the urine (hypercalciuria), leading to a decrease in serum calcium levels. **2. Why the other options are incorrect:** * **Lithium (Option A):** Lithium can cause hypercalcemia by increasing the set-point of the Calcium-Sensing Receptor (CaSR) in the parathyroid gland, leading to inappropriately high PTH secretion (Lithium-induced hyperparathyroidism). * **Multiple Myeloma (Option B):** This malignancy causes extensive bone resorption through the activation of osteoclasts by cytokines (RANKL, IL-6), leading to significant hypercalcemia. * **Hypervitaminosis D (Option D):** Vitamin D increases intestinal absorption of calcium and phosphate, as well as bone resorption, directly leading to elevated serum calcium levels. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** "Loop diuretics **Lose** calcium; Thiazides **Throw** it back into the blood." * **Thiazide Diuretics:** These cause **hypercalcemia** and are used in the management of idiopathic hypercalciuria to prevent calcium stones. * **Loop Diuretics:** These are used in the emergency management of **acute hypercalcemia** (along with aggressive saline hydration). * **Other causes of hypercalcemia:** Hyperparathyroidism (most common cause), Sarcoidosis (due to extra-renal 1-alpha hydroxylase activity), and Milk-Alkali Syndrome.

Question 67: Loop diuretics act by which of the following mechanisms?

A. Inhibition of Na+-Cl- Symport
B. Inhibition of Na+-K+-2 Cl- cotransport (Correct Answer)
C. Inhibition of Na+-K+ ATPase
D. Inhibition of H+-K+ ATPase

Explanation: **Explanation:** **Correct Option: B. Inhibition of Na+-K+-2 Cl- cotransport** Loop diuretics (e.g., Furosemide, Torsemide, Bumetanide) exert their primary effect by inhibiting the **Na+-K+-2Cl- (NKCC2) symporter** located in the luminal membrane of the **Thick Ascending Limb (TAL)** of the Loop of Henle. By blocking this transporter, these drugs prevent the reabsorption of sodium, potassium, and chloride. This leads to a significant increase in the excretion of these ions and water, making them the most potent diuretics ("High-ceiling" diuretics). **Analysis of Incorrect Options:** * **Option A (Na+-Cl- Symport):** This is the mechanism of action for **Thiazide diuretics**, which act on the Distal Convoluted Tubule (DCT). * **Option C (Na+-K+ ATPase):** This enzyme is located on the basolateral membrane of most renal cells. While it provides the energy gradient for transport, it is the primary target of **Cardiac Glycosides (Digoxin)**, not diuretics. * **Option D (H+-K+ ATPase):** This is the "proton pump" found in the gastric parietal cells. It is inhibited by **Proton Pump Inhibitors (PPIs)** like Omeprazole. **High-Yield Clinical Pearls for NEET-PG:** 1. **Site of Action:** Thick Ascending Limb (TAL) of the Loop of Henle. 2. **Electrolyte Changes:** Loop diuretics cause **Hypokalemia, Hypomagnesemia, and Hypocalcemia** (unlike Thiazides, which cause Hypercalcemia). 3. **Ototoxicity:** Ethacrynic acid is the most ototoxic, while Bumetanide is the least. 4. **Drug of Choice:** Furosemide is the drug of choice for **Acute Pulmonary Edema** due to its rapid action and additional venodilatory effect. 5. **Metabolic Effect:** They can cause **Hypokalemic Metabolic Alkalosis** and Hyperuricemia (precipitating Gout).

Question 68: A new diuretic is being studied in human volunteers. Compared with placebo, the new drug increases urine volume, decreases urinary Ca2+, increases body pH, and decreases serum K+. If this new drug has a similar mechanism of action to an established diuretic, it probably what?

A. Blocks the NaCl cotransporter in the distal convoluted tubule. (Correct Answer)
B. Blocks aldosterone receptors in the collecting tubule.
C. Inhibits carbonic anhydrase in the proximal convoluted tubule.
D. Inhibits the Na/K/2Cl cotransporter in the thick ascending limb.

Explanation: ### Explanation The drug described exhibits the classic profile of a **Thiazide diuretic**. **1. Why Option A is Correct:** Thiazides block the **Na+/Cl- cotransporter** in the **distal convoluted tubule (DCT)**. * **Urine Volume:** Increased due to inhibition of Na+ reabsorption. * **Urinary Ca2+:** Decreased (Hypocalciuria). Thiazides enhance Ca2+ reabsorption in the DCT, making them useful in preventing calcium oxalate stones. * **Body pH:** Increases (Metabolic Alkalosis). Increased Na+ delivery to the collecting duct promotes H+ and K+ secretion. * **Serum K+:** Decreased (Hypokalemia). Increased flow and Na+ delivery to the late distal tubule/collecting duct stimulate K+ excretion. **2. Why the Other Options are Incorrect:** * **Option B (Aldosterone Antagonists):** These are "potassium-sparing." They would **increase** serum K+ and **decrease** body pH (causing metabolic acidosis), which contradicts the question. * **Option C (Carbonic Anhydrase Inhibitors):** These cause **metabolic acidosis** (decreased pH) due to bicarbonate loss in the urine, whereas the drug in the question increases pH. * **Option D (Loop Diuretics):** While they cause hypokalemia and alkalosis, they **increase** urinary Ca2+ ("Loops lose calcium"). The drug in the question decreases urinary Ca2+. **3. NEET-PG High-Yield Pearls:** * **Thiazide Mnemonic:** "Thiazides treat Stones (hypercalciuria) but cause Bones (hypercalcemia)." * **Metabolic Profile:** Thiazides cause **"Hyper-GLUC"** (Hyperglycemia, Hyperlipidemia, Hyperuricemia, and Hypercalcemia). * **Drug of Choice:** Thiazides are often preferred for hypertension in patients with concomitant osteoporosis due to their calcium-sparing effect.

Question 69: On which part of the nephron do loop diuretics act?

A. Descending limb
B. Thick ascending limb (Correct Answer)
C. Cortical segment
D. Collecting duct

Explanation: **Explanation:** **Mechanism of Action (The Correct Answer):** Loop diuretics (e.g., Furosemide, Torsemide, Bumetanide) primarily act on the **Thick Ascending Limb (TAL)** of the Loop of Henle [1, 2]. They work by inhibiting the **Na⁺-K⁺-2Cl⁻ symporter (NKCC2)** on the luminal membrane [1, 2]. By blocking this transporter, they prevent the reabsorption of sodium, potassium, and chloride, leading to potent natriuresis and diuresis [1]. Because the TAL is responsible for reabsorbing approximately 25% of filtered sodium, these are the most efficacious diuretics ("High-ceiling diuretics") [2]. **Analysis of Incorrect Options:** * **A. Descending limb:** This segment is highly permeable to water but impermeable to solutes. No major diuretics act here. * **C. Cortical segment:** This usually refers to the Distal Convoluted Tubule (DCT), which is the site of action for **Thiazide diuretics** (inhibiting the Na⁺-Cl⁻ symporter). * **D. Collecting duct:** This is the site of action for **Potassium-sparing diuretics** (e.g., Spironolactone, Amiloride) and ADH antagonists (Vaptans). **High-Yield Clinical Pearls for NEET-PG:** * **Abolition of Corticomedullary Gradient:** By inhibiting solute reabsorption in the TAL, loop diuretics interfere with the kidney's ability to concentrate urine. * **Calcium Excretion:** Unlike Thiazides (which cause hypercalcemia), loop diuretics cause **hypocalcemia** ("Loops lose Calcium"). They are used in the emergency management of hypercalcemia. * **Ototoxicity:** This is a unique side effect of loop diuretics (especially Ethacrynic acid) due to the presence of the NKCC transporter in the stria vascularis of the inner ear. * **Drug of Choice:** Furosemide is the drug of choice for acute pulmonary edema due to its rapid action and additional venodilatory effect.

Question 70: Mannitol when given intravenously causes which of the following changes?

A. Decrease in blood viscosity (Correct Answer)
B. Increase in blood viscosity
C. Increase in GFR
D. Increase in ICT

Explanation: **Explanation:** Mannitol is an osmotic diuretic that remains confined to the extracellular compartment. When administered intravenously, it creates an osmotic gradient that draws water from the intracellular space into the vascular compartment. **1. Why Option A is Correct:** The rapid shift of water from cells into the bloodstream leads to **hemodilution**. This expansion of plasma volume decreases the hematocrit and reduces the overall **blood viscosity**. This reduction in viscosity is clinically significant as it improves microcirculatory blood flow, particularly in the brain, which is one of the mechanisms by which mannitol reduces intracranial pressure (ICP). **2. Why the other options are incorrect:** * **Option B:** Mannitol decreases viscosity via hemodilution; it does not increase it. * **Option C:** While mannitol can increase renal blood flow, it does not consistently increase the **Glomerular Filtration Rate (GFR)**. In fact, its primary site of action is the Loop of Henle and the proximal tubule, where it limits water reabsorption. * **Option D:** Mannitol is used to **decrease** Intracranial Tension (ICT) and Intraocular Pressure (IOP) by drawing fluid out of the brain parenchyma and vitreous humor into the blood. It does not increase ICT. **High-Yield NEET-PG Pearls:** * **Mechanism:** Osmotic effect in the proximal tubule and descending limb of the Loop of Henle. * **Contraindications:** Acute Pulmonary Edema and Congestive Heart Failure (due to the initial rapid expansion of extracellular fluid volume) and Anuria. * **Clinical Uses:** Cerebral edema (to lower ICT), acute congestive glaucoma (to lower IOP), and prevention of cisplatin-induced nephrotoxicity. * **Side Effect:** Acute expansion of ECF can lead to "dialysis disequilibrium" or pulmonary congestion.

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Carbonic Anhydrase Inhibitors

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Loop Diuretics

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Thiazide and Thiazide-Like Diuretics

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Potassium-Sparing Diuretics

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Carbonic Anhydrase Inhibitors

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Osmotic Diuretics

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Combination Diuretic Therapy

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Diuretics in Heart Failure

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Diuretics in Hypertension

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Diuretics in Renal Disorders

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Adverse Effects and Drug Interactions

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Diuretics — MCQs

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