Diuretics Practice Questions

Q: Acetazolamide decreases intraocular pressure by what mechanism?

Decreases aqueous humor production. **Explanation:** **Mechanism of Action (Why A is correct):** Acetazolamide is a potent **Carbonic Anhydrase Inhibitor (CAI)**. In the eye, the enzyme carbonic anhydrase is present in the non-pigmented ciliary epithelium. It facilitates the reaction: $CO_2 + H_2O \rightleftharpoons H_2CO_3 \rightleftharpoons H^+ + HCO_3^-$. The secretion of aqueous humor is an active process dependent on the transport of sodium and bicarbonate ions. By inhibiting carbonic anhydrase, acetazolamide reduces the availability of bicarbonate ions, which in turn decreases the active transport of sodium into the posterior chamber. This osmotic shift leads to a **reduction in aqueous humor production by approximately 50-60%**, thereby lowering intraocular pressure (IOP). **Analysis of Incorrect Options:** * **B. Decreases vitreous volume:** This is the mechanism of **Hyperosmotic agents** (e.g., Mannitol, Glycerol). They create an osmotic gradient that draws water out of the vitreous into the bloodstream. * **C. Increased drainage of aqueous:** This is the mechanism of **Miotics** (pilocarpine - increases trabecular outflow) or **Prostaglandin analogues** (latanoprost - increases uveoscleral outflow). Acetazolamide has no effect on the outflow pathways. **High-Yield Clinical Pearls for NEET-PG:** * **Route:** Systemic (Oral/IV). Topical CAIs include Dorzolamide and Brinzolamide. * **Indications:** Acute Angle Closure Glaucoma (emergency management) and prophylaxis before intraocular surgery. * **Side Effects:** Paresthesia (most common), metabolic acidosis, hypokalemia, and renal calculi. * **Contraindication:** It is a sulfonamide derivative; avoid in patients with **sulfa allergy** and those with severe hepatic or renal impairment.

Q: Which of the following is a non-competitive inhibitor of carbonic anhydrase?

Acetazolamide. ### Explanation **Correct Option: B. Acetazolamide** Acetazolamide is a sulfonamide derivative that acts as a potent, **non-competitive inhibitor** of the enzyme **carbonic anhydrase (CA)**, primarily the Type II isoenzyme found in the proximal convoluted tubule (PCT) and the ciliary body of the eye. By inhibiting CA, it prevents the dehydration of $H_2CO_3$ and the rehydration of $CO_2$, leading to a decrease in $H^+$ secretion and a subsequent increase in the excretion of sodium, potassium, and bicarbonate. This results in alkaline urine and a mild metabolic acidosis. **Analysis of Incorrect Options:** * **A. Allopurinol:** This is a hypuricemic agent that acts as a competitive inhibitor of **Xanthine Oxidase**. It is used in the chronic management of Gout. * **C. Bimatoprost:** This is a **Prostaglandin $F_{2\alpha}$ analogue**. It reduces intraocular pressure by increasing the uveoscleral outflow of aqueous humor, rather than inhibiting CA. * **D. Dipivefrine:** This is a prodrug of **Epinephrine**. It acts as a sympathomimetic to reduce intraocular pressure by increasing aqueous outflow; it does not inhibit enzymes. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Acetazolamide is the DOC for **Acute Mountain Sickness** (prevents cerebral/pulmonary edema and counteracts respiratory alkalosis). * **Glaucoma:** Used to rapidly decrease intraocular pressure in acute angle-closure glaucoma by reducing aqueous humor formation. * **Side Effects:** Drowsiness, paresthesia, and the formation of **calcium phosphate renal stones** (due to alkaline urine). * **Contraindication:** Avoid in patients with hepatic cirrhosis, as it can precipitate **hepatic encephalopathy** by decreasing ammonia excretion.

Q: Aldosterone antagonists are not useful in the treatment of which of the following conditions?

Gynaecomastia. **Explanation:** Aldosterone antagonists (Spironolactone and Eplerenone) are potassium-sparing diuretics that act by inhibiting the mineralocorticoid receptor [1]. **Why Gynaecomastia is the correct answer:** Aldosterone antagonists, specifically **Spironolactone**, are a **cause** of gynaecomastia, not a treatment for it [2]. Spironolactone is structurally similar to steroids and acts as a non-specific antagonist at androgen receptors while also increasing the peripheral conversion of testosterone to estradiol [4]. This hormonal imbalance leads to breast tissue enlargement in males (gynaecomastia) and erectile dysfunction as common side effects [2]. **Analysis of Incorrect Options:** * **Hypertension:** Aldosterone antagonists are used as add-on therapy in resistant hypertension to counteract the effects of sodium and water retention. * **Congestive Heart Failure (CHF):** They are "life-saving" drugs in CHF (NYHA Class II-IV). They prevent aldosterone-mediated cardiac remodeling and fibrosis, significantly reducing mortality. * **Hirsutism:** Due to its anti-androgenic properties (blocking androgen receptors and inhibiting steroidogenesis), Spironolactone is clinically used to treat hirsutism and acne in females [4]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Eplerenone** is a more selective mineralocorticoid antagonist; it has a lower affinity for androgen receptors and is therefore **less likely** to cause gynaecomastia compared to Spironolactone [2]. 2. **Hyperkalemia** is the most significant and life-threatening metabolic side effect of these drugs [3]. 3. **Drug of Choice:** Spironolactone is the drug of choice for **Primary Hyperaldosteronism (Conn’s Syndrome)** and edema associated with **Liver Cirrhosis** (where secondary hyperaldosteronism is present) [3].

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

Acidosis. Furosemide is a high-ceiling loop diuretic that acts by inhibiting the **Na⁺-K⁺-2Cl⁻ symporter** in the Thick Ascending Limb (TAL) of the Loop of Henle [1]. **Why Acidosis is the Correct Answer:** Furosemide does **not** cause acidosis; instead, it causes **Metabolic Alkalosis** [1, 3]. This occurs via two mechanisms: 1. **Contraction Alkalosis:** Loss of isotonic fluid (NaCl and water) leads to a decrease in extracellular fluid volume, concentrating the remaining bicarbonate [3]. 2. **Increased H⁺ secretion:** Increased delivery of Na⁺ to the distal tubule stimulates Na⁺ reabsorption in exchange for H⁺ and K⁺ (via aldosterone), leading to net acid loss in the urine [1, 3]. **Analysis of Incorrect Options:** * **Hyperglycemia:** Loop diuretics can impair insulin release from the pancreas and decrease peripheral glucose utilization, often secondary to hypokalemia. * **Hypomagnesemia:** By abolishing the positive transepithelial potential in the TAL, loop diuretics inhibit the paracellular reabsorption of divalent cations (Mg²⁺ and Ca²⁺) [1, 2]. * **Hypokalemia:** Increased Na⁺ delivery to the distal nephron promotes K⁺ excretion via the Na⁺/K⁺ exchange pump, a classic side effect of all diuretics acting proximal to the collecting duct [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Loop Diuretic Side Effects (OH DANG!):** **O**totoxicity, **H**ypokalemia, **D**ehydration, **A**llergy (Sulfa), **N**ephritis (Interstitial), **G**out (Hyperuricemia) [2]. * **Calcium Handling:** Loop diuretics cause **Hypocalcemia** ("Loops Lose Calcium") [1], whereas Thiazides cause **Hypercalcemia**. * **Drug of Choice:** Furosemide is the drug of choice for acute pulmonary edema and symptomatic hypercalcemia.

Q: Hyperuricemia is seen with which of the following drugs?

Chlorthiazide. **Explanation:** **Chlorthiazide** (a Thiazide diuretic) causes hyperuricemia primarily through two mechanisms: 1. **Competition for Secretion:** Thiazides are organic acids that compete with uric acid for the Organic Anion Transporter (OAT) in the proximal convoluted tubule, reducing uric acid secretion into the tubular lumen. 2. **Enhanced Reabsorption:** Diuretic-induced hypovolemia triggers the proximal tubule to increase the reabsorption of sodium and water, which leads to a compensatory increase in the reabsorption of uric acid. **Analysis of Incorrect Options:** * **Acetazolamide (Carbonic Anhydrase Inhibitor):** While it acts on the proximal tubule, it actually increases the excretion of uric acid (uricosuric effect) by inhibiting its reabsorption. * **Mannitol (Osmotic Diuretic):** It acts by increasing the osmolarity of the tubular fluid. It does not significantly interfere with the organic acid transport system and does not typically cause hyperuricemia. * **Triamterene (K+-Sparing Diuretic):** It acts on the late distal tubule and collecting duct by blocking ENaC channels. It does not affect the proximal tubule’s uric acid transport mechanisms. **NEET-PG High-Yield Pearls:** * **The "Hyper" Rule for Thiazides:** Thiazides cause **Hyper**uricemia, **Hyper**glycemia, **Hyper**lipidemia, and **Hyper**calcemia (unlike Loop diuretics, which cause *hypo*calcemia). * **Loop Diuretics (e.g., Furosemide):** These also cause hyperuricemia via similar mechanisms (competition at OAT and volume depletion). * **Clinical Contraindication:** Thiazides and Loop diuretics should be used with caution in patients with a history of **Gout**, as they can precipitate an acute attack.

Q: Which drug abolishes the corticomedullary osmotic gradient?

Furosemide. ### Explanation **Correct Option: A. Furosemide** The **corticomedullary osmotic gradient** is the increasing osmolality of the renal interstitium from the cortex (300 mOsm/L) to the deep medulla (1200 mOsm/L). This gradient is primarily established and maintained by the **Countercurrent Multiplier system** in the Thick Ascending Limb (TAL) of the Loop of Henle. Furosemide (a loop diuretic) inhibits the **Na⁺-K⁺-2Cl⁻ (NKCC2) symporter** in the TAL. By blocking the reabsorption of these electrolytes into the medullary interstitium, it prevents the buildup of high osmotic pressure in the medulla. Consequently, the gradient is "abolished" or washed out. Without this gradient, the collecting duct cannot reabsorb water even in the presence of ADH, leading to the excretion of large volumes of dilute urine. **Why Incorrect Options are Wrong:** * **B. Thiazides:** These act on the **Distal Convoluted Tubule (DCT)**. Since the DCT is located entirely within the renal cortex and does not participate in the countercurrent multiplier system, thiazides do not affect the medullary osmotic gradient. * **C & D. Spironolactone and Triamterene:** These are **Potassium-sparing diuretics** acting on the late distal tubule and collecting ducts. Their site of action is beyond the segment responsible for generating the medullary gradient. **High-Yield NEET-PG Pearls:** * **Loop Diuretics** are the most potent diuretics ("High-ceiling") because the TAL reabsorbs ~25% of filtered sodium. * Because they abolish the gradient, loop diuretics impair the kidney's ability to both **concentrate** urine (during dehydration) and **dilute** urine. * **Clinical Correlation:** Loop diuretics are the drugs of choice for acute pulmonary edema and generalized edema (CHF, Nephrotic syndrome). * **Side Effects:** Hypokalemia, Hyperuricemia, Ototoxicity, and Hypocalcemia ("Loops Lose Calcium").

Q: Which of the following diuretics acts on the nephron through the interstitium?

Spironolactone. ### Explanation **Correct Option: D (Spironolactone)** The fundamental concept here is the **site of action** and the **route of access** to the receptor. Most diuretics (Thiazides, Loop diuretics, Carbonic anhydrase inhibitors) act from the **luminal side** of the nephron. They must be filtered at the glomerulus or secreted into the tubular fluid to reach their target transporters. **Spironolactone**, however, is a competitive **Aldosterone Antagonist**. Aldosterone receptors (Mineralocorticoid Receptors) are located in the **cytoplasm** of the principal cells in the late distal tubule and collecting duct. Spironolactone reaches these receptors by diffusing from the **peritubular capillaries through the interstitium** into the basolateral side of the cell. It does not need to be present in the tubular lumen to exert its effect. **Analysis of Incorrect Options:** * **A. Thiazides:** Act on the $Na^+/Cl^-$ symporter in the Distal Convoluted Tubule (DCT) from the **luminal side**. * **B. Furosemide:** A loop diuretic that inhibits the $Na^+/K^+/2Cl^-$ cotransporter in the Thick Ascending Limb (TAL). It is highly protein-bound and reaches the **lumen** via organic acid secretory pumps in the proximal tubule. * **C. Acetazolamide:** Inhibits Carbonic Anhydrase primarily at the **luminal brush border** of the Proximal Convoluted Tubule (PCT). **High-Yield NEET-PG Pearls:** * **Potassium Sparing:** Spironolactone is the drug of choice for **Primary Hyperaldosteronism (Conn’s Syndrome)** and edema associated with **Liver Cirrhosis**. * **Side Effects:** Due to its steroid structure, it can cause **Gynecomastia** and impotence in males (anti-androgenic effect). **Eplerenone** is a more selective alternative with fewer endocrine side effects. * **Clinical Marker:** It is proven to reduce mortality in patients with **Chronic Heart Failure** (NYHA Class II-IV).

Question 1

Acetazolamide decreases intraocular pressure by what mechanism?

Accepted Answer

Decreases aqueous humor production

Answer

Decreases vitreous volume

Answer

Increased drainage of aqueous

Answer

None of the above

Question 2

Which of the following is a non-competitive inhibitor of carbonic anhydrase?

Accepted Answer

Acetazolamide

Answer

Allopurinol

Answer

Bimatoprost

Answer

Dipivefrine

Question 3

Aldosterone antagonists are not useful in the treatment of which of the following conditions?

Accepted Answer

Gynaecomastia

Answer

Hypertension

Answer

Congestive heart failure

Answer

Hirsutism

Question 4

Which of the following adverse effects is NOT caused by furosemide?

Accepted Answer

Acidosis

Answer

Hyperglycemia

Answer

Hypomagnesemia

Answer

Hypokalemia

Question 5

Hyperuricemia is seen with which of the following drugs?

Accepted Answer

Chlorthiazide

Answer

Acetazolamide

Answer

Mannitol

Answer

Triamterene

Question 6

Which drug abolishes the corticomedullary osmotic gradient?

Accepted Answer

Furosemide

Answer

Thiazide

Answer

Spironolactone

Answer

Triamterene

Question 7

All of the following are true about osmotic diuretics except:

Accepted Answer

Osmotic diuretics are used in active cerebral bleeding.

Answer

They expand the extracellular fluid compartment and increase renal blood flow.

Answer

Osmotic diuretics are used in cerebral edema.

Answer

Mannitol is used in acute congestive glaucoma.

Question 8

In patients with decompensated cirrhosis on diuretic therapy presenting with tender gynecomastia, which diuretic is the best substitution?

Accepted Answer

Amiloride to substitute spironolactone

Answer

Furosemide to substitute spironolactone

Answer

Spironolactone to substitute amiloride

Answer

Torsemide to substitute spironolactone

Question 9

Which of the following diuretics acts on the nephron through the interstitium?

Accepted Answer

Spironolactone

Answer

Thiazide

Answer

Furosemide

Answer

Acetazolamide

Question 10

What is true about triamterene?

Accepted Answer

Its saluretic effect is greater than that of thiazides.

Answer

It is often combined with thiazide diuretics.

Answer

Its action is similar to that of amiloride.

Answer

It is a potassium-sparing diuretic.

Diuretics — MCQs

Diuretics — MCQs

On this page

Practice by Chapter

Want unlimited practice?