Diuretics Practice Questions

Q: Vasopressin antagonists act on which part of the nephron?

Medullary collecting duct. **Explanation:** Vasopressin (Antidiuretic Hormone/ADH) antagonists, also known as **Vaptans** (e.g., Tolvaptan, Conivaptan), exert their primary diuretic effect by blocking **V2 receptors**. These receptors are located on the basolateral membrane of the principal cells in the **medullary collecting duct**. **Mechanism of Action:** Under normal physiological conditions, ADH binds to V2 receptors, triggering the insertion of **Aquaporin-2 (AQP2)** water channels into the apical membrane. This allows for free water reabsorption. By antagonizing these receptors, Vaptans prevent water reabsorption, leading to **aquaresis** (excretion of solute-free water) without significant loss of electrolytes like sodium or potassium. **Analysis of Options:** * **A. Proximal Convoluted Tubule:** This is the site of action for Carbonic Anhydrase inhibitors (Acetazolamide) and SGLT2 inhibitors. * **B. Distal Convoluted Tubule:** This is the site of action for Thiazide diuretics, which inhibit the Na+-Cl- symporter. * **C. Cortical Collecting Tubule:** While some V2 receptors exist here, the **medullary** portion of the collecting duct has the highest density of these receptors and is the critical site for establishing the final urine concentration. Potassium-sparing diuretics (Amiloride, Spironolactone) act primarily in the cortical segment. **NEET-PG High-Yield Pearls:** * **Indications:** Vaptans are the treatment of choice for **SIADH** and are used in hypervolemic hyponatremia (e.g., CHF, Cirrhosis). * **Tolvaptan:** Oral, selective V2 antagonist. * **Conivaptan:** IV, non-selective (blocks both V1a and V2 receptors). * **Side Effect:** Rapid correction of hyponatremia with Vaptans carries a risk of **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis).**

Q: Which of the following can lead to Megaloblastic anemia?

Triamterene. **Explanation:** **Triamterene** is the correct answer because it is a potassium-sparing diuretic that acts as a **weak folic acid antagonist**. It structurally resembles pyrimethamine and methotrexate, inhibiting the enzyme **dihydrofolate reductase (DHFR)**. This inhibition prevents the conversion of dihydrofolate to tetrahydrofolate, which is essential for DNA synthesis. In patients with low folate stores (e.g., those with liver cirrhosis or pregnancy), triamterene can precipitate **megaloblastic anemia**. **Analysis of Incorrect Options:** * **Dorzolamide (Option A):** A topical carbonic anhydrase inhibitor used primarily in the treatment of glaucoma to reduce intraocular pressure. It does not interfere with folate metabolism. * **Chlorthiazide (Option B):** A thiazide diuretic that acts on the distal convoluted tubule. Its primary side effects include hypokalemia, hyperuricemia, and hyperglycemia, but not megaloblastic anemia. * **Canrenone (Option C):** An active metabolite of Spironolactone. While it is also a potassium-sparing diuretic, it acts as a competitive **aldosterone receptor antagonist** and does not inhibit dihydrofolate reductase. **High-Yield Clinical Pearls for NEET-PG:** 1. **Other drugs causing Megaloblastic Anemia (DHFR Inhibitors):** Methotrexate, Trimethoprim, Pyrimethamine, and Phenytoin (interferes with absorption). 2. **Triamterene Specifics:** It can cause **nephrolithiasis** (kidney stones) as the drug is poorly soluble and can crystallize in the urine. 3. **Potassium-Sparing Diuretics Classification:** * *Aldosterone Antagonists:* Spironolactone, Eplerenone. * *Renal Epithelial Na+ Channel Inhibitors:* Triamterene, Amiloride.

Q: Which diuretic agent is most useful in the treatment of recurrent calcium stones?

Hydrochlorothiazide. ### Explanation **Correct Answer: D. Hydrochlorothiazide** **Mechanism and Rationale:** Thiazide diuretics (like Hydrochlorothiazide) are the drugs of choice for preventing recurrent calcium oxalate stones. Their effectiveness lies in their ability to **decrease urinary calcium excretion (hypocalciuria)**. Thiazides inhibit the $Na^+/Cl^-$ symporter in the Distal Convoluted Tubule (DCT). This reduction in intracellular sodium enhances the activity of the $Na^+/Ca^{2+}$ exchanger on the basolateral membrane, which in turn creates a gradient that promotes **increased reabsorption of calcium** from the tubular lumen into the blood. By lowering the concentration of calcium in the urine, the likelihood of stone precipitation is significantly reduced. **Why the other options are incorrect:** * **A. Mannitol:** An osmotic diuretic used primarily to reduce intracranial or intraocular pressure. It does not specifically target calcium handling and can cause electrolyte imbalances. * **B. Furosemide:** A loop diuretic that **increases** urinary calcium excretion ("Loops Lose Calcium"). It is used to treat hypercalcemia but would worsen the risk of calcium stone formation. * **C. Spironolactone:** A potassium-sparing diuretic (aldosterone antagonist). While it prevents potassium loss, it has no significant effect on renal calcium reabsorption. **NEET-PG High-Yield Pearls:** * **Mnemonic:** **L**oops **L**ose calcium; **T**hiazides **T**ake it up (reabsorb). * **Paradoxical Use:** Thiazides are also used in **Nephrogenic Diabetes Insipidus** to reduce polyuria by inducing mild volume depletion and increasing proximal water reabsorption. * **Metabolic Side Effects of Thiazides:** Hyper**G**lycemia, Hyper**L**ipidemia, Hyper**U**ricemia, and Hyper**C**alcemia (Mnemonic: **GLUC**).

Q: All of the following about loop diuretics are true EXCEPT:

Furosemide is the most potent loop diuretic.. **Explanation:** **1. Why Option D is the correct (False) statement:** While Furosemide is the most commonly used loop diuretic, it is **not** the most potent. In the context of loop diuretics, potency refers to the dose required to achieve a specific effect. **Bumetanide** is the most potent loop diuretic (approximately 40 times more potent than Furosemide), followed by Torsemide. Furosemide actually has the lowest potency among the commonly used sulfonamide loop diuretics. **2. Analysis of other options:** * **Option A:** **Ethacrynic acid** is a non-sulfonamide loop diuretic. It is associated with the highest incidence of **ototoxicity** (tinnitus and deafness) compared to others and is generally reserved for patients with sulfonamide allergies. * **Option B:** Loop diuretics stimulate the intrarenal synthesis of **prostaglandins (PGE2)**. This leads to renal and systemic vasodilation, which is why IV Furosemide provides rapid symptomatic relief in acute pulmonary edema even before the diuresis begins. * **Option C:** By inhibiting the Na⁺-K⁺-2Cl⁻ symporter in the Thick Ascending Limb (TAL), more Na⁺ reaches the distal tubule. This promotes K⁺ and H⁺ secretion, leading to **hypokalemia** and **metabolic alkalosis** (contraction alkalosis). **NEET-PG High-Yield Pearls:** * **Mechanism:** Inhibits Na⁺-K⁺-2Cl⁻ cotransporter in the TAL of the Loop of Henle. * **Electrolyte Profile:** Causes "Hypo-everything" (Hypokalemia, Hypomagnesemia, Hypocalcemia, Hyponatremia) **EXCEPT** Hyperuricemia and Hyperglycemia. * **Drug of Choice:** Furosemide is the DOC for acute pulmonary edema and edema associated with CHF, cirrhosis, and renal failure. * **Torsemide:** Has a longer half-life and better oral bioavailability than Furosemide.

Q: An adolescent developed metabolic acidosis after taking a certain medication. What is the causative drug?

Acetazolamide. ### Explanation **Correct Option: A. Acetazolamide** Acetazolamide is a **Carbonic Anhydrase (CA) inhibitor** that acts primarily on the proximal convoluted tubule (PCT) of the kidney. It inhibits the enzyme carbonic anhydrase, preventing the reabsorption of sodium bicarbonate ($NaHCO_3$). This leads to increased urinary excretion of bicarbonate (alkaline urine), resulting in a depletion of the body's alkali reserve. The clinical consequence is a **Hyperchloremic Normal Anion Gap Metabolic Acidosis**. **Analysis of Incorrect Options:** * **B. Phenformin:** While Biguanides (like Phenformin and Metformin) are notorious for causing **Lactic Acidosis**, Phenformin has been largely withdrawn globally due to this high risk. However, in the context of standard pharmacological mechanisms involving bicarbonate loss, Acetazolamide is the classic textbook cause of metabolic acidosis. * **C. Verapamil:** This is a Calcium Channel Blocker (CCB) used for hypertension and arrhythmias. Its primary side effects include constipation, peripheral edema, and bradycardia, but it does not typically cause metabolic acidosis. * **D. Triamterene:** This is a potassium-sparing diuretic. While it can cause hyperkalemia and a mild metabolic acidosis (similar to Spironolactone), it is less commonly associated with significant systemic acidosis compared to the direct bicarbonate-wasting effect of Acetazolamide. **High-Yield Clinical Pearls for NEET-PG:** * **Acetazolamide Uses:** Glaucoma (decreases aqueous humor), Mountain Sickness (induces mild acidosis to stimulate respiration), and Urinary Alkalization. * **Side Effects:** Metabolic acidosis, hypokalemia, paresthesia, and sulfonamide-like hypersensitivity reactions. * **Acid-Base Tip:** Remember that "Proximal Renal Tubular Acidosis (Type 2 RTA)" is the physiological equivalent of Acetazolamide's mechanism of action.

Q: Glycerol is classified as which of the following?

Osmotic diuretic. **Explanation:** **Glycerol** is a low-molecular-weight, pharmacologically inert substance that acts as an **Osmotic Diuretic**. When administered (usually orally), it increases the osmolality of the plasma and tubular fluid. This creates an osmotic gradient that draws water out of the intracellular and interstitial compartments into the vascular space and prevents water reabsorption in the proximal convoluted tubule and descending limb of Henle's loop. **Why the other options are incorrect:** * **Purgative:** While some osmotic agents like Lactulose or Magnesium salts are used as purgatives, Glycerol's primary systemic classification in pharmacology is an osmotic agent. (Note: Glycerin suppositories can be used for constipation, but it is not its primary systemic classification). * **Antidiabetic:** Glycerol is actually a precursor for gluconeogenesis; it does not lower blood glucose. * **Antiemetic:** Glycerol has no action on the chemoreceptor trigger zone (CTZ) or the vomiting center. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Use:** Glycerol is most commonly used to rapidly reduce **intraocular pressure (IOP)** in acute glaucoma and **intracranial pressure (ICP)** in cerebral edema. * **Route:** Unlike Mannitol (which must be given IV), Glycerol is **effective orally**. * **Metabolism:** Unlike Mannitol, Glycerol is metabolized in the body and provides approximately **4.3 kcal/g**, which can lead to hyperglycemia. * **Caution:** Use with extreme caution in **Diabetic patients** (due to hyperglycemia) and **Congestive Heart Failure (CHF)** patients (due to rapid expansion of extracellular fluid volume).

Q: In the proximal convoluted tubule (PCT), sodium reabsorption is prevented by which class of drugs?

Osmotic diuretics. ### Explanation **Correct Answer: C. Osmotic diuretics** **Mechanism of Action:** Osmotic diuretics (e.g., **Mannitol**) are pharmacologically inert substances that are freely filtered at the glomerulus but undergo minimal reabsorption. Their primary site of action is the **Proximal Convoluted Tubule (PCT)** and the descending limb of the Loop of Henle. By increasing the osmotic pressure of the tubular fluid, they counteract the osmotic force of sodium, thereby **preventing the passive reabsorption of water and sodium**. This leads to an increase in urine volume (diuresis) and sodium excretion (natriuresis). **Analysis of Incorrect Options:** * **A. Ethacrynic acid:** This is a **Loop diuretic**. It acts on the **Thick Ascending Limb (TAL)** of the Loop of Henle by inhibiting the $Na^+-K^+-2Cl^-$ symporter. * **B. Acetazolamide:** While it acts on the PCT, its primary mechanism is the inhibition of **Carbonic Anhydrase**. This prevents the reabsorption of **Bicarbonate ($HCO_3^-$)** rather than primarily targeting sodium reabsorption directly. * **D. Triamterene:** This is a **Potassium-sparing diuretic**. It acts on the **Late Distal Tubule and Collecting Duct** by blocking the Epithelial Sodium Channels (ENaC). **High-Yield Clinical Pearls for NEET-PG:** * **Mannitol** must be administered **intravenously**; it is not absorbed orally. * **Therapeutic Uses:** Reduction of intracranial pressure (cerebral edema) and intraocular pressure (acute glaucoma). * **Contraindications:** It is strictly contraindicated in **Acute Pulmonary Edema** and **Congestive Heart Failure** because it initially expands the extracellular fluid volume before diuresis occurs. * **Side Effect:** Can cause "Dialysis Disequilibrium Syndrome" if cleared too rapidly.

Q: Which of the following adverse effects is NOT caused by thiazide diuretics?

Hypernatremia. Thiazide diuretics (e.g., Hydrochlorothiazide, Chlorthalidone) act on the **Distal Convoluted Tubule (DCT)** by inhibiting the **Na⁺-Cl⁻ symporter**. ### Why Hypernatremia is the Correct Answer Thiazides inhibit the reabsorption of Sodium (Na⁺) and Chloride (Cl⁻) in the DCT, leading to increased excretion of these ions in the urine. This loss of sodium typically results in **Hyponatremia**, not hypernatremia. In fact, thiazides are one of the most common drug-related causes of hyponatremia in clinical practice. ### Explanation of Incorrect Options (Adverse Effects of Thiazides) * **Hypercalcemia (A):** Thiazides increase Ca²⁺ reabsorption in the DCT (via the Na⁺/Ca²⁺ exchanger on the basolateral membrane). This makes them useful in treating idiopathic hypercalciuria and calcium stones. * **Hypomagnesemia (B):** Long-term use of thiazides leads to increased renal excretion of Magnesium, though the exact mechanism is less defined than that of loop diuretics. * **Hyperuricemia (D):** Thiazides compete with uric acid for the organic acid secretory secretory system in the proximal tubule, leading to decreased uric acid excretion. This can precipitate acute gouty arthritis. ### NEET-PG High-Yield Pearls: "The Hypo-Hyper Rule" To remember Thiazide side effects, think of **4 Hypos** and **4 Hypers**: * **HYPO:** Hyponatremia, Hypokalemia, Hypomagnesemia, Hypochloremic alkalosis. * **HYPER:** Hypercalcemia, Hyperuricemia, Hyperglycemia (due to decreased insulin release), Hyperlipidemia (increased LDL/Cholesterol). **Key Distinction:** Loop diuretics cause **Hypocalcemia** ("Loops lose calcium"), whereas Thiazides cause **Hypercalcemia**.

Q: Which diuretic can be considered appropriate for combining with ACE inhibitors?

Hydrochlorothiazide. **Explanation:** The combination of **Hydrochlorothiazide (HCTZ)** and ACE inhibitors (ACEIs) is a standard, synergistic therapeutic strategy in managing hypertension and heart failure. **Why Hydrochlorothiazide is correct:** 1. **Synergistic BP Lowering:** Thiazides cause sodium depletion, which activates the Renin-Angiotensin-Aldosterone System (RAAS). ACE inhibitors block this compensatory RAAS activation, leading to a more profound drop in blood pressure. 2. **Potassium Homeostasis:** This is the most critical clinical reason. ACE inhibitors cause **potassium retention** (hyperkalemia) by inhibiting aldosterone. Thiazides are **potassium-wasting** diuretics. When used together, they counteract each other's effects on serum potassium, maintaining electrolyte balance. **Why the other options are incorrect:** * **Spironolactone & Eplerenone (Options A & B):** These are Potassium-Sparing Diuretics (Mineralocorticoid Receptor Antagonists). Combining them with ACEIs significantly increases the risk of **severe, life-threatening hyperkalemia**, as both drug classes promote potassium retention. * **Amiloride (Option D):** This is an epithelial sodium channel (ENaC) blocker, also classified as a potassium-sparing diuretic. Like Spironolactone, it carries a high risk of hyperkalemia when combined with ACEIs. **High-Yield Clinical Pearls for NEET-PG:** * **First-Dose Hypotension:** ACEIs can cause a sharp drop in BP if the patient is already volume-depleted by diuretics. It is often advised to stop the diuretic for 24–48 hours before starting an ACEI. * **Metabolic Neutrality:** ACEIs can mitigate the hyperglycemia and hyperuricemia sometimes induced by high-dose Thiazides. * **Preferred Combination:** Fixed-dose combinations of ACEIs/ARBs with HCTZ are among the most commonly prescribed antihypertensives worldwide.

Question 1

Hypokalemia is seen with which of the following?

Accepted Answer

Addison's disease

Answer

Frusemide

Answer

Cortisol

Answer

Amiloride

Question 2

Vasopressin antagonists act on which part of the nephron?

Accepted Answer

Medullary collecting duct

Answer

Proximal convoluted tubule

Answer

Distal convoluted tubule

Answer

Cortical collecting tubule

Question 3

Which of the following can lead to Megaloblastic anemia?

Accepted Answer

Triamterene

Answer

Dorzolamide

Answer

Chlorthiazide

Answer

Canrenone

Question 4

Which diuretic agent is most useful in the treatment of recurrent calcium stones?

Accepted Answer

Hydrochlorothiazide

Answer

Mannitol

Answer

Furosemide

Answer

Spironolactone

Question 5

All of the following about loop diuretics are true EXCEPT:

Accepted Answer

Furosemide is the most potent loop diuretic.

Answer

Ethacrynic acid is the most ototoxic loop diuretic.

Answer

They release prostaglandins and lead to vasodilation.

Answer

Loop diuretics lead to hypokalemia and metabolic alkalosis.

Question 6

An adolescent developed metabolic acidosis after taking a certain medication. What is the causative drug?

Accepted Answer

Acetazolamide

Answer

Phenformin

Answer

Verapamil

Answer

Triamterene

Question 7

Glycerol is classified as which of the following?

Accepted Answer

Osmotic diuretic

Answer

Purgative

Answer

Antidiabetic

Answer

Antiemetic

Question 8

In the proximal convoluted tubule (PCT), sodium reabsorption is prevented by which class of drugs?

Accepted Answer

Osmotic diuretics

Answer

Ethacrynic acid

Answer

Acetazolamide

Answer

Triamterene

Question 9

Which of the following adverse effects is NOT caused by thiazide diuretics?

Accepted Answer

Hypernatremia

Answer

Hypercalcemia

Answer

Hypomagnesemia

Answer

Hyperuricemia

Question 10

Which diuretic can be considered appropriate for combining with ACE inhibitors?

Accepted Answer

Hydrochlorothiazide

Answer

Spironolactone

Answer

Eplerenone

Answer

Amiloride

Diuretics — MCQs

Diuretics — MCQs

On this page

Practice by Chapter

Want unlimited practice?