Diuretics — MCQs
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Thiazide diuretics can be used for the treatment of all of these conditions EXCEPT :
Mechanism of action of thiazides is by -
Which of the following is NOT an effect of Mannitol?
All of the following diuretics increase K+ excretion EXCEPT:
All of the following are potassium sparing diuretic EXCEPT:
Which of the following thiazides can be used in severe renal failure?
Potassium-sparing diuretics act at the level of
Which of the following statements accurately compares the potency of amiloride and triamterene?
Which one of the following drugs causes increased concentration of Na+ & Cl- in urine with normal bicarbonate?
Which of the following diuretics can lead to erectile dysfunction?
Diuretics Indian Medical PG Practice Questions and MCQs
Question 171: Thiazide diuretics can be used for the treatment of all of these conditions EXCEPT :
- A. Hypertension
- B. Hyperlipidemia (Correct Answer)
- C. Congestive Heart Failure
- D. Idiopathic hypercalciuria with nephrocalcinosis
Explanation: ***Hyperlipidemia***- Thiazide diuretics are **not used to treat hyperlipidemia** and can sometimes have a mild **adverse effect of causing dyslipidemia** (increased LDL cholesterol and triglycerides).- Their mechanism of action primarily involves diuresis and vasodilation, not directly affecting lipid metabolism.*Hypertension*- Thiazide diuretics are **first-line agents** for the treatment of hypertension, especially for uncomplicated cases [3].- They reduce blood pressure by increasing sodium and water excretion, leading to a decrease in **extracellular fluid volume** and peripheral vascular resistance [2].*Congestive Heart Failure*- Thiazide diuretics are effective in managing **fluid overload** and **edema** associated with congestive heart failure [2].- While loop diuretics are often preferred for severe heart failure due to their greater diuretic potency, thiazides can be beneficial in milder cases or as adjuncts.*Idiopathic hypercalciuria with nephrocalcinosis*- Thiazide diuretics are used to treat **idiopathic hypercalciuria** because they promote **calcium reabsorption** in the renal tubules, thereby reducing urinary calcium excretion [1].- This property helps prevent the formation of calcium-containing kidney stones and can be beneficial in patients with **nephrocalcinosis**.
Question 172: Mechanism of action of thiazides is by -
- A. Inhibiting Na+K+2Cl- in ascending limb of loop of henle
- B. Inhibiting Na+/Cl- symporter in DCT (Correct Answer)
- C. Inhibiting Na+/Cl- symporter in PCT
- D. Inhibiting Na+K+2Cl- in descending limb of loop of henle
Explanation: **Inhibiting Na+/Cl- symporter in DCT** - Thiazide diuretics primarily act on the **distal convoluted tubule (DCT)** of the nephron [2]. - They inhibit the **Na+/Cl- symporter** (NCC channel) on the apical membrane, preventing reabsorption of sodium and chloride ions [1], [2]. *Inhibiting Na+K+2CI- in descending limb of loop of henle* - The descending limb of the loop of Henle is permeable to water but largely impermeable to solutes; there is no significant Na+K+2Cl- symporter activity here. - This mechanism describes the action of loop diuretics, but they act on the **ascending** limb, not the descending limb. *Inhibiting Na+K+2Cl- in ascending limb of loop of henle* - This mechanism describes the action of **loop diuretics** (e.g., furosemide, bumetanide) [3]. - Loop diuretics inhibit the **Na+K+2Cl- cotransporter (NKCC2)** in the thick ascending limb of the loop of Henle, leading to significant diuresis [3]. *Inhibiting Na+/Cl- symporter in PCT* - The **proximal convoluted tubule (PCT)** is primarily responsible for reabsorbing most of the filtered sodium, chloride, bicarbonate, and other solutes. - While sodium is reabsorbed in the PCT, it's mainly through Na+/H+ exchangers and other mechanisms, not a specific Na+/Cl- symporter that is targeted by thiazides [2].
Question 173: Which of the following is NOT an effect of Mannitol?
- A. Increases blood osmolality
- B. Increases GFR
- C. Decreases ICP
- D. Increases blood viscosity (Correct Answer)
Explanation: ***Increases blood viscosity*** - Mannitol is an **osmotic diuretic** that works by increasing the osmolality of the blood plasma, which draws water from the interstitial fluid and intracellular compartments into the intravascular space. - This process leads to **hemodilution**, which would decrease blood viscosity rather than increase it. *Increases blood osmolality* - Mannitol, as an **osmotic diuretic**, directly works by increasing the osmolality of the plasma. - This elevated plasma osmolality creates an osmotic gradient that pulls water from cells and interstitial spaces into the blood. *Increases GFR* - By increasing plasma volume through the movement of fluid from the interstitial space, mannitol can lead to **increased renal blood flow** and, consequently, an elevated GFR. - The increased fluid volume delivered to the kidneys also contributes to its diuretic effect. *Decreases ICP* - Mannitol is frequently used to reduce **intracranial pressure** (ICP) because it draws water out of the brain parenchyma into the blood vessels due to its osmotic effect. - This reduction in brain volume lessens the pressure within the skull.
Question 174: All of the following diuretics increase K+ excretion EXCEPT:
- A. Acetazolamide
- B. Triamterene (Correct Answer)
- C. Thiazide
- D. Furosemide
Explanation: ***Triamterene*** - **Triamterene** is a **potassium-sparing diuretic** that blocks epithelial sodium channels (ENaC) in the collecting duct, thereby reducing sodium reabsorption and potassium secretion. - Unlike most other diuretics, it causes **decreased K+ excretion** and can lead to hyperkalemia. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** that acts in the proximal tubule, inhibiting bicarbonate reabsorption. - This leads to increased delivery of sodium and bicarbonate to the collecting duct, which enhances **potassium secretion** and increases K+ excretion. *Thiazide* - **Thiazide diuretics** (e.g., hydrochlorothiazide) act by inhibiting the Na+/Cl- cotransporter in the **distal convoluted tubule**. - This increases the delivery of sodium to the collecting duct, which stimulates the exchange of sodium for **potassium**, leading to increased K+ excretion and hypokalemia. *Furosemide* - **Furosemide** is a **loop diuretic** that inhibits the Na+/K+/2Cl- cotransporter in the **thick ascending limb of the loop of Henle**. - This prevents the reabsorption of these ions, leading to increased delivery of sodium to the collecting duct, which promotes **potassium secretion** and increased K+ excretion.
Question 175: All of the following are potassium sparing diuretic EXCEPT:
- A. Indapamide (Correct Answer)
- B. Triamterene
- C. Amiloride
- D. Spironolactone
Explanation: ***Indapamide*** - **Indapamide** is a **thiazide-like diuretic**, acting primarily on the distal convoluted tubule to inhibit sodium and chloride reabsorption, thus promoting their excretion along with water. - Unlike potassium-sparing diuretics, it can cause **potassium wasting (hypokalemia)** due to increased delivery of sodium to the collecting duct, where it is exchanged for potassium. *Triamterene* - **Triamterene** is a **potassium-sparing diuretic** that directly inhibits epithelial sodium channels (ENaC) in the collecting tubule, reducing sodium reabsorption and potassium secretion. - This mechanism helps to conserve potassium, preventing hypokalemia often associated with other diuretic classes. *Amiloride* - **Amiloride** is another **potassium-sparing diuretic** that, like triamterene, blocks epithelial sodium channels (ENaC) in the late distal tubule and collecting duct. - By inhibiting sodium reabsorption in this segment, it reduces the electrochemical gradient for potassium secretion, leading to potassium retention. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist**, making it a potassium-sparing diuretic that competitively blocks aldosterone receptors in the collecting duct. - This blockage prevents aldosterone from promoting sodium reabsorption and potassium secretion, resulting in increased sodium excretion and **potassium retention**.
Question 176: Which of the following thiazides can be used in severe renal failure?
- A. Chlorthiazide
- B. Metolazone (Correct Answer)
- C. Bendroflumethiazide
- D. Trichloromethazide
Explanation: **Metolazone** - **Metolazone** is an exception among thiazides, as it retains its efficacy even in cases of **severe renal impairment** (creatinine clearance below 30 mL/min). - Its ability to act at more distal sites in the nephron and its different pharmacokinetic profile contribute to its effectiveness in reduced renal function. *Chlorthiazide* - This is a **thiazide diuretic** that loses significant efficacy when the **glomerular filtration rate (GFR)** falls below 30 mL/min. - It is generally not recommended for use in patients with **severe renal failure** due to diminished diuretic response. *Bendroflumethiazide* - Similar to most other **thiazide diuretics**, **bendroflumethiazide's** effectiveness is greatly reduced in **renal insufficiency**. - Its use is limited when the **creatinine clearance** drops below 30 mL/min, rendering it ineffective for diuresis in severe renal failure. *Trichloromethazide* - **Trichloromethazide** is another **thiazide diuretic** that shares the common characteristic of losing its diuretic effect in the presence of **significant renal impairment**. - It is not a suitable choice for managing fluid retention in patients with **severe renal failure**.
Question 177: Potassium-sparing diuretics act at the level of
- A. Carbonic anhydrase
- B. Aldosterone receptor (Correct Answer)
- C. NaCl symporter
- D. Na-K pump
Explanation: ***Aldosterone receptor*** - **Potassium-sparing diuretics** include two main classes: 1. **Aldosterone receptor antagonists** (e.g., **spironolactone**, **eplerenone**) that act on **aldosterone receptors** in the collecting tubules 2. **ENaC blockers** (e.g., **amiloride**, **triamterene**) that directly block **epithelial sodium channels (ENaC)** in the collecting duct - Both mechanisms reduce **sodium reabsorption** and **potassium secretion** in the **collecting tubule**, leading to retained potassium. - The aldosterone receptor is the most commonly tested site for this drug class. *Carbonic anhydrase* - **Carbonic anhydrase inhibitors** (e.g., **acetazolamide**) act primarily in the **proximal convoluted tubule**. - They inhibit **bicarbonate reabsorption**, leading to diuresis and metabolic acidosis, and are not considered potassium-sparing. *NaCl symporter* - **Thiazide diuretics** act on the **NaCl symporter (NCC)** in the **distal convoluted tubule**. - They inhibit sodium and chloride reabsorption but do not spare potassium; chronic use can lead to **hypokalemia**. *Na-K pump* - The **Na-K pump** (Na+/K+-ATPase) is found in many cells and maintains ion gradients, but it is not the primary target of potassium-sparing diuretics. - While involved in renal transport, diuretics targeting this pump have different primary mechanisms and therapeutic uses.
Question 178: Which of the following statements accurately compares the potency of amiloride and triamterene?
- A. Amiloride is more potent than triamterene
- B. Both drugs have equal potency
- C. Potency cannot be compared between these drugs
- D. Triamterene is more potent than amiloride (Correct Answer)
Explanation: ***Triamterene is more potent than amiloride*** - **Triamterene** is generally considered to be **more potent** than amiloride, with approximately **10-fold greater potency** on a weight basis. - This higher potency is reflected in the **lower effective dosing** of triamterene (50-100 mg/day) compared to amiloride (5-10 mg/day), though the starting doses appear different due to available formulations. - Both are **potassium-sparing diuretics** that block epithelial sodium channels (ENaC) in the collecting duct, but triamterene requires a smaller dose to achieve equivalent diuretic effects. *Amiloride is more potent than triamterene* - This statement is incorrect; **amiloride** is typically considered **less potent** than triamterene on a milligram-per-milligram basis. - The standard therapeutic doses reflect this difference in potency, with amiloride requiring relatively higher doses for comparable effects. *Both drugs have equal potency* - This statement is incorrect as there are well-documented differences in the **potency** of these two **potassium-sparing diuretics**. - While both work through the same mechanism (blocking ENaC channels in the collecting tubule), their individual pharmacological profiles result in different dose-response relationships. *Potency cannot be compared between these drugs* - This statement is incorrect; the **potency** of drugs within the same class and mechanism of action, such as these two potassium-sparing diuretics, **can and should be compared**. - Clinical and pharmacological studies routinely assess and compare the relative potencies of similar therapeutic agents to guide appropriate dosing.
Question 179: Which one of the following drugs causes increased concentration of Na+ & Cl- in urine with normal bicarbonate?
- A. Furosemide
- B. Ethacrynic acid (Correct Answer)
- C. Bumetanide
- D. Acetazolamide
Explanation: ***Ethacrynic acid*** - Ethacrynic acid is a **loop diuretic** that inhibits the Na+-K+-2Cl- cotransporter in the **thick ascending limb of the loop of Henle**. - It causes increased urinary excretion of **Na+ and Cl-** while maintaining **normal bicarbonate levels** (does not affect carbonic anhydrase). - **Key distinguishing feature**: Ethacrynic acid is a **phenoxyacetic acid derivative** (NOT a sulfonamide), making it useful in patients with **sulfonamide allergies**. - Note: All loop diuretics share the property of increasing Na+ and Cl- excretion with normal bicarbonate. *Furosemide* - Furosemide is a **sulfonamide-derived loop diuretic** with the same mechanism as ethacrynic acid (inhibits Na+-K+-2Cl- cotransporter). - It also increases Na+ and Cl- excretion with normal bicarbonate levels. - While pharmacologically equivalent to ethacrynic acid for this effect, it is structurally different (sulfonamide derivative). *Bumetanide* - Bumetanide is another **sulfonamide-derived loop diuretic** with identical mechanism to furosemide and ethacrynic acid. - It produces the same electrolyte effects: increased Na+ and Cl- excretion with normal bicarbonate. - Structurally, it is a sulfonamide derivative like furosemide. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** acting in the **proximal tubule**. - It increases excretion of **bicarbonate** (causing metabolic acidosis), along with Na+ and K+. - This would result in **elevated bicarbonate in urine**, NOT normal bicarbonate, making it incorrect.
Question 180: Which of the following diuretics can lead to erectile dysfunction?
- A. Thiazide diuretics (Correct Answer)
- B. Carbonic anhydrase inhibitor
- C. Loop diuretics
- D. Mannitol
Explanation: ***Thiazide diuretics*** - **Thiazide diuretics** can cause **erectile dysfunction**, possibly due to effects on vascular function and **reduced blood flow** to the penis. - This adverse effect is a known concern and can impact patient adherence to **antihypertensive therapy**. *Carbonic anhydrase inhibitor* - **Carbonic anhydrase inhibitors** like acetazolamide are primarily used for glaucoma, altitude sickness, and metabolic alkalosis, and do not typically cause **erectile dysfunction**. - Their primary side effects relate to **metabolic acidosis** and electrolyte imbalances, not sexual function. *Loop diuretics* - **Loop diuretics** like furosemide are potent diuretics used in conditions like heart failure and edema; **erectile dysfunction** is not a common or significant side effect. - Their main adverse effects include **hypokalemia**, ototoxicity, and hypovolemia. *Mannitol* - **Mannitol** is an osmotic diuretic used to reduce intracranial and intraocular pressure. - It is administered intravenously and its side effects primarily involve **fluid and electrolyte disturbances**, not **erectile dysfunction**.
Practice by Chapter
Carbonic Anhydrase Inhibitors
Practice Questions
Loop Diuretics
Practice Questions
Thiazide and Thiazide-Like Diuretics
Practice Questions
Potassium-Sparing Diuretics
Practice Questions
Carbonic Anhydrase Inhibitors
Practice Questions
Osmotic Diuretics
Practice Questions
Combination Diuretic Therapy
Practice Questions
Diuretics in Heart Failure
Practice Questions
Diuretics in Hypertension
Practice Questions
Diuretics in Renal Disorders
Practice Questions
Adverse Effects and Drug Interactions
Practice Questions
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