Diuretics Practice Questions

Q: Which drug causes hypercalcemia?

Thiazide. **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].

Q: All of the following statements about amiloride are true EXCEPT:

It antagonizes the action of aldosterone.. **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.

Q: Canrenone is a metabolite of which drug?

Spironolactone. **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**.

Q: Potassium supplementation is often necessary for patients taking which of the following drugs?

Furosemide. **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.

Q: Which of the following diuretics can lead to hyperglycemia and hyperlipidemia?

Thiazide diuretics. **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.

Q: What is true about Acetazolamide?

Decreased GFR. **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).

Q: Thiazide diuretics do not produce which of the following adverse effects?

Hypoglycemia. **Explanation:** Thiazide diuretics are known for causing a variety of metabolic disturbances, but **Hypoglycemia** is not one of them. In fact, Thiazides are notorious for causing **Hyperglycemia**. **1. Why Hypoglycemia is the correct answer:** Thiazides impair glucose tolerance by inhibiting insulin release from the pancreas (partially due to hypokalemia, which hyperpolarizes beta cells) and decreasing peripheral glucose utilization. Therefore, they cause an *increase* in blood sugar levels, making "hypoglycemia" the incorrect clinical effect. **2. Analysis of Incorrect Options:** * **Hyponatremia (B):** Thiazides inhibit the $Na^+/Cl^-$ symporter in the distal convoluted tubule. They increase sodium excretion while the body’s ability to dilute urine is impaired, frequently leading to low serum sodium. * **Hypokalemia (C):** Increased sodium delivery to the collecting ducts stimulates the exchange of $Na^+$ for $K^+$, leading to significant potassium loss in the urine. * **Hyperuricemia (D):** Thiazides compete with uric acid for the organic acid secretory secretory pathway in the proximal tubule. This leads to uric acid retention, which can precipitate acute gouty arthritis. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Thiazide side effects:** **"Hyper GLUC"** – **G**lycemia, **L**ipidemia (Hyperlipidemia), **U**ricemia, and **C**alcemia (Hypercalcemia). * **Calcium Sparing:** Unlike Loop diuretics ("Loops Lose Calcium"), Thiazides *increase* calcium reabsorption and are used clinically to prevent calcium-containing renal stones. * **Drug of Choice:** Thiazides are often the first-line treatment for essential hypertension in patients without co-morbidities.

Question 1

Which of the following medications can be used to treat hypercalciuria?

Accepted Answer

Indapamide

Answer

Torsemide

Answer

Acetazolamide

Answer

Frusemide

Question 2

Which drug causes hypercalcemia?

Accepted Answer

Thiazide

Answer

Bumetanide

Answer

Spironolactone

Answer

Furosemide

Question 3

All of the following statements about amiloride are true EXCEPT:

Accepted Answer

It antagonizes the action of aldosterone.

Answer

It is the drug of choice for the treatment of lithium-induced diabetes insipidus.

Answer

It decreases calcium loss in the urine.

Answer

It is more potent than triamterene.

Question 4

Canrenone is a metabolite of which drug?

Accepted Answer

Spironolactone

Answer

Ampicillin

Answer

Furosemide

Answer

Acetazolamide

Question 5

Which group of diuretics does not require access to the tubular lumen to induce diuresis?

Accepted Answer

Mineralocorticoid antagonist

Answer

Carbonic anhydrase inhibitor

Answer

Na-Cl symporter inhibitor

Answer

Na-K-2Cl symporter inhibitor

Question 6

Potassium supplementation is often necessary for patients taking which of the following drugs?

Accepted Answer

Furosemide

Answer

Spironolactone

Answer

Triamterene

Answer

Amiloride

Question 7

Which of the following diuretics can lead to hyperglycemia and hyperlipidemia?

Accepted Answer

Thiazide diuretics

Answer

Carbonic anhydrase inhibitors

Answer

Loop diuretics

Answer

Vasopressin antagonists

Question 8

What is true about Acetazolamide?

Accepted Answer

Decreased GFR

Answer

Action similar to sulphonamide

Answer

It decreases Na, K, and Glucose excretion

Answer

It causes metabolic alkalosis

Question 9

Thiazide diuretics do not produce which of the following adverse effects?

Accepted Answer

Hypoglycemia

Answer

Hyponatremia

Answer

Hypokalemia

Answer

Hyperuricemia

Question 10

A 68-year-old woman presents with symptoms and signs of congestive heart failure. Which of the following is a contraindication to the use of furosemide?

Accepted Answer

A history of rash with trimethoprim-sulfamethoxazole

Answer

Hypoalbuminemia

Answer

Oliguria

Answer

Acidosis

Diuretics — MCQs

Diuretics — MCQs

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