Diuretics Practice Questions

Q: Furosemide -induced hearing loss occurs primarily by damaging which structure?

Na⁺-K⁺-2Cl⁻cotransporter in stria vascularis. ### ***Na⁺-K⁺-2Cl⁻ cotransporter in stria vascularis*** - Furosemide is a **loop diuretic** that inhibits the **Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2)** in the thick ascending limb of the loop of Henle, but it also inhibits the **NKCC1** isoform found in the **stria vascularis** of the inner ear. - This inhibition disrupts the **endocochlear potential** by reducing potassium secretion into the endolymph, leading to temporary or permanent **sensorineural hearing loss**. *Outer hair cells in Organ of Corti* - While aminoglycosides are known to be directly **ototoxic** to the **outer hair cells** of the Organ of Corti, this is not the primary site of damage for loop diuretics. - Loop diuretics specifically alter the ionic gradient between the **endolymph** and the **perilymph** rather than causing direct cellular toxicity to hair cells. *Vestibulocochlear nerve* - The **vestibulocochlear nerve (CN VIII)** is typically damaged by acoustic neuromas or toxins like heavy metals, but it is not the target of furosemide-induced injury. - Symptoms of loop diuretic toxicity involve hearing loss rather than the primary neuropathic deficits associated with direct nerve toxicity. *Cochlear duct basement membrane* - Damage to the **basilar membrane** (often via noise-induced trauma or mechanical injury) results in hearing loss, but this is a structural failure unrelated to furosemide. - Furosemide mechanism is **biochemical/metabolic** regarding electrolyte transport, not an injury to the physical architecture of the membrane.

Q: Which drug commonly causes gynecomastia?

Spironolactone. **Explanation:** **Spironolactone** is a potassium-sparing diuretic and a competitive aldosterone antagonist. It is the most common pharmacological cause of gynecomastia. The underlying mechanism is twofold: 1. **Anti-androgenic effect:** It binds to and blocks androgen receptors. 2. **Hormonal imbalance:** It inhibits testosterone synthesis and increases the peripheral conversion of testosterone to estradiol. This shift in the estrogen-to-androgen ratio leads to the development of glandular breast tissue in males. **Analysis of Incorrect Options:** * **B. Rifampicin:** This is an enzyme inducer (CYP450). While it can alter the metabolism of various hormones, it is not classically associated with gynecomastia. * **C. Penicillin:** This is a beta-lactam antibiotic with no hormonal activity; it does not cause gynecomastia. * **D. Bumetanide:** This is a potent loop diuretic. Unlike spironolactone, loop diuretics do not interfere with steroid hormone receptors. **High-Yield Clinical Pearls for NEET-PG:** * **Eplerenone:** A selective aldosterone antagonist that does **not** cause gynecomastia because it has low affinity for androgen and progesterone receptors. It is the preferred alternative if a patient develops breast tenderness on spironolactone. * **Mnemonic for drugs causing Gynecomastia (DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone, **C**imetidine, **O**estrogens/Ketoconazole. * **Cimetidine:** Another high-yield cause; it acts as a H2 blocker and also has significant anti-androgenic properties.

Q: Which diuretic can be used in renal failure?

Furosemide. **Explanation:** **Furosemide** is the correct answer because it is a high-ceiling loop diuretic that remains effective even when the Glomerular Filtration Rate (GFR) falls below 30 mL/min. In renal failure, the delivery of solutes to the distal nephron is reduced; loop diuretics are potent enough to inhibit the $Na^+-K^+-2Cl^-$ symporter in the thick ascending limb, maintaining diuresis and managing fluid overload in patients with chronic kidney disease (CKD). **Why the other options are incorrect:** * **Chlorothiazide & Chlorthalidone:** These are Thiazide/Thiazide-like diuretics. They generally lose their efficacy when GFR is less than 30 mL/min (except for Metolazone and Indapamide). Using them in advanced renal failure is ineffective for fluid management. * **Mannitol:** This is an osmotic diuretic. In renal failure, Mannitol is not excreted efficiently, leading to its accumulation in the extracellular fluid. This causes "osmotic shift," drawing water out of cells and potentially leading to acute pulmonary edema or congestive heart failure. It is contraindicated in established anuria. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Furosemide is the drug of choice for acute pulmonary edema and edema associated with CKD. * **Metolazone Exception:** While most thiazides fail in renal failure, Metolazone can be combined with Loop diuretics (Sequential Nephron Blockade) to treat refractory edema in CKD patients. * **Ototoxicity:** Furosemide can cause dose-dependent ototoxicity, especially when administered rapidly IV or combined with aminoglycosides. * **Electrolyte Profile:** Loop diuretics cause "Hypo-everything" (Hypokalemia, Hypomagnesemia, Hypocalcemia), except for Hyperuricemia and Hyperglycemia.

Q: Which of the following side effects is associated with Spironolactone?

Hyperkalemia. **Explanation:** **Spironolactone** is a potassium-sparing diuretic that acts as a competitive antagonist of the **Mineralocorticoid Receptor (Aldosterone receptor)** in the late distal tubule and collecting duct. **Why Hyperkalemia is Correct:** Aldosterone normally promotes the reabsorption of sodium ($Na^+$) and the excretion of potassium ($K^+$) and hydrogen ions ($H^+$). By blocking this receptor, Spironolactone prevents $K^+$ secretion into the tubular lumen. This leads to the retention of potassium in the blood, resulting in **Hyperkalemia**, its most significant and potentially life-threatening side effect. **Analysis of Incorrect Options:** * **A. Alkalosis:** Spironolactone causes **Metabolic Acidosis** (not alkalosis) because it inhibits the excretion of $H^+$ ions. * **B. Hirsutism:** Spironolactone actually has **anti-androgenic** properties (it blocks androgen receptors and inhibits steroidogenesis). Therefore, it is used to *treat* hirsutism in conditions like PCOS. A common side effect in males, however, is **gynecomastia**. * **D. Hyperglycemia:** This is a classic side effect of **Thiazides and Loop diuretics**, which can impair insulin release. Spironolactone does not typically affect blood glucose levels. **High-Yield Clinical Pearls for NEET-PG:** * **Eplerenone** is a more selective aldosterone antagonist with fewer endocrine side effects (less risk of gynecomastia) compared to Spironolactone. * **Drug Interaction:** Avoid combining Spironolactone with ACE inhibitors or ARBs, as this significantly increases the risk of severe hyperkalemia. * **Indication of Choice:** It is the diuretic of choice for patients with **Cirrhosis with Ascites** and is proven to reduce mortality in **Chronic Heart Failure (NYHA Class II-IV)**.

Q: A 64-year-old man with heart failure is recently started on 80 mg/day of furosemide. He now feels weak and tired, but notes that his heart failure symptoms have improved. There is no change in his urine output and he gets a good diuretic response every time he takes his furosemide. Which are the characteristic ECG findings?

lengthened QU interval. ### Explanation **Correct Answer: C. Lengthened QU interval** **1. Underlying Medical Concept:** Furosemide is a potent loop diuretic that inhibits the Na⁺/K⁺/2Cl⁻ symporter in the thick ascending limb of the Loop of Henle. A common and significant side effect of loop diuretics is **hypokalemia** (low serum potassium). In hypokalemia, the ECG undergoes characteristic changes due to delayed ventricular repolarization. The most classic finding is the appearance of **prominent U waves**. As the U wave becomes more pronounced and the T wave flattens, the T and U waves often merge. This creates the appearance of a **"lengthened QU interval"** (or a pseudo-prolonged QT interval), which is a hallmark of potassium depletion. The patient’s symptoms of weakness and fatigue are clinical indicators of this electrolyte imbalance. **2. Why the other options are incorrect:** * **A & B (PR Interval):** Changes in the PR interval are typically associated with calcium abnormalities or AV nodal blocks (e.g., Digoxin toxicity), not primarily with the hypokalemia caused by diuretics. * **D (Shortened QT interval):** A shortened QT interval is characteristic of **hypercalcemia**. In contrast, hypokalemia (and hypocalcemia) typically leads to a prolonged appearance of the repolarization phase (prolonged QU/QT). **3. NEET-PG High-Yield Pearls:** * **ECG findings in Hypokalemia:** Flattening/inversion of T waves, ST-segment depression, prominent U waves, and QU prolongation. * **Loop Diuretics Side Effects (Mnemonic: OH DANG!):** **O**totoxicity, **H**ypokalemia, **D**ehydration, **A**llergy (sulfa), **N**ephritis (interstitial), **G**out (hyperuricemia). * **Metabolic state:** Loop diuretics cause **Hypokalemic Metabolic Alkalosis**. * **U wave:** A positive deflection after the T wave, representing slow repolarization of Purkinje fibers. It is most visible in precordial leads V2–V4.

Q: What is the mechanism of action of furosemide in left ventricular failure (LVF)?

Inhibitor of Na-K-Cl ion symporter. **Mechanism of Action:** Furosemide is a potent **Loop Diuretic**. Its primary mechanism involves the inhibition of the **Naⁱ-Kⁱ-2Clⁱ symporter (NKCC2)** [1] located in the luminal membrane of the **Thick Ascending Limb (TAL)** of the Henle’s loop [2]. By blocking this transporter, it prevents the reabsorption of these electrolytes, leading to profound diuresis and natriuresis [3]. **Role in Left Ventricular Failure (LVF):** In acute LVF (Pulmonary Edema), furosemide acts via two distinct phases [4]: 1. **Immediate Effect (Vascular):** It causes rapid **venodilation** (mediated by prostaglandins), which increases venous capacitance and decreases preload. This provides symptomatic relief even before the onset of diuresis. 2. **Delayed Effect (Renal):** It reduces fluid overload through diuresis, further decreasing the workload on the failing heart. **Analysis of Incorrect Options:** * **B. Aldosterone antagonist:** This describes **Spironolactone** or Eplerenone, which act on the distal tubule and collecting ducts. * **C. Mercurial derivative:** These are obsolete diuretics (e.g., Mersalyl) rarely used today due to toxicity. * **D. Carbonic anhydrase inhibitor:** This describes **Acetazolamide**, which acts on the proximal convoluted tubule and is primarily used for glaucoma or altitude sickness, not LVF [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Action:** Thick Ascending Limb (TAL) – the "diluting segment." * **Side Effects (The "Hypo"s):** Hypokalemia, Hypomagnesemia, Hypocalcemia (Loop loses Calcium), and Hyperuricemia. * **Ototoxicity:** Furosemide can cause dose-dependent hearing loss, especially when combined with aminoglycosides [2]. * **Drug of Choice:** Furosemide is the DOC for **Acute Pulmonary Edema** and edema associated with CHF, Cirrhosis, and Renal failure [4].

Q: Which of the following thiazide diuretics remains active when the Glomerular Filtration Rate (GFR) is 30-40 mL/min?

Metolazone. ### Explanation\n\n**1. Why Metolazone is Correct:**\nMost thiazide diuretics lose their efficacy when the Glomerular Filtration Rate (GFR) falls below **30–40 mL/min** [1], [2]. This is because they must be secreted into the tubular lumen to act on the Na⁺-Cl⁻ symporter in the distal convoluted tubule; in renal failure, their delivery to the site of action is significantly impaired. **Metolazone** (and to some extent Indapamide) is a "thiazide-like" diuretic that is uniquely potent. It maintains its diuretic efficacy even in advanced renal insufficiency (GFR as low as 10–20 mL/min) [1].\n\n**2. Why the Other Options are Incorrect:**\n* **Benzthiazide & Chlorothiazide:** These are classical thiazides. They are ineffective in patients with significant renal impairment (GFR < 30 mL/min) because they cannot reach therapeutic concentrations in the tubular fluid [1].\n* **Chlorthalidone:** While it is highly potent and has a long half-life (making it a preferred agent for hypertension), it generally loses its effectiveness as a diuretic when renal function is significantly compromised, unlike Metolazone [1].\n\n**3. High-Yield Clinical Pearls for NEET-PG:**\n* **Synergistic Effect:** Metolazone is frequently added to Loop diuretics (e.g., Furosemide) to overcome **"diuretic resistance"** in patients with refractory edema or congestive heart failure. This is known as **Sequential Nephron Blockade**.\n* **Metabolic Side Effects:** Remember the mnemonic **"Hyper GLUC"** for thiazides: Hyper**G**lycemia, Hyper**L**ipidemia, Hyper**U**ricemia, and Hyper**C**alcemia.\n* **Hypokalemia:** Like loop diuretics, thiazides cause potassium wasting [1].\n* **Indapamide:** Another thiazide-like diuretic often preferred in diabetics as it is considered "metabolically neutral."

Question 1

Furosemide -induced hearing loss occurs primarily by damaging which structure?

Accepted Answer

Na⁺-K⁺-2Cl⁻cotransporter in stria vascularis

Answer

Outer hair cells in Organ of Corti

Answer

Vestibulocochlear nerve

Answer

Cochlear duct basement membrane

Question 2

A 26-year-old man diagnosed with diabetes insipidus was started on hydrochlorothiazide. The beneficial effect of hydrochlorothiazide in this patient is due to which of the following mechanisms?

Accepted Answer

Inhibition of Na+ reabsorption in DCT, leading to mild volume depletion and increased proximal water reabsorption

Answer

Direct stimulation of V2 receptors in the collecting duct

Answer

Blocking aquaporin -2 channels in the collecting duct

Answer

Increasing medullary interstitial osmolarity

Question 3

Which drug commonly causes gynecomastia?

Accepted Answer

Spironolactone

Answer

Rifampicin

Answer

Penicillin

Answer

Bumetanide

Question 4

Which diuretic can be used in renal failure?

Accepted Answer

Furosemide

Answer

Chlorothiazide

Answer

Mannitol

Answer

Chlorthalidone

Question 5

Which of the following side effects is associated with Spironolactone?

Accepted Answer

Hyperkalemia

Answer

Alkalosis

Answer

Hirsutism

Answer

Hyperglycemia

Question 6

A 64-year-old man with heart failure is recently started on 80 mg/day of furosemide. He now feels weak and tired, but notes that his heart failure symptoms have improved. There is no change in his urine output and he gets a good diuretic response every time he takes his furosemide. Which are the characteristic ECG findings?

Accepted Answer

lengthened QU interval

Answer

shortened PR interval

Answer

lengthened PR interval

Answer

shortening of the QT interval

Question 7

What is the drug of choice for hypertension in a patient with osteoporosis?

Accepted Answer

Thiazide diuretics

Answer

ACE inhibitors

Answer

Beta-blockers

Answer

Loop diuretics

Question 8

What is the mechanism of action of furosemide in left ventricular failure (LVF)?

Accepted Answer

Inhibitor of Na-K-Cl ion symporter

Answer

Aldosterone antagonist

Answer

Mercurial derivative

Answer

Carbonic anhydrase inhibitor

Question 9

A patient arrives in the emergency room in a coma and has a serum Ca 2+ of 4.5 mM. You start a saline infusion of which of the following drugs?

Accepted Answer

Ethacrynic acid

Answer

Calcitonin

Answer

Hydrochlorothiazide

Answer

Spironolactone

Question 10

Which of the following thiazide diuretics remains active when the Glomerular Filtration Rate (GFR) is 30-40 mL/min?

Accepted Answer

Metolazone

Answer

Benzthiazide

Answer

Chlorothiazide

Answer

Chlorthalidone

Diuretics — MCQs

Diuretics — MCQs

On this page

Practice by Chapter

Want unlimited practice?