Loop Diuretics — MCQs

10 questions

Mechanism of action of thiazides is by -

A patient presents with hypertension and has a history of renal stones, along with several episodes of renal colic. Which diuretic is the most appropriate to use?

Which one of the following drugs causes increased concentration of Na+ & Cl- in urine with normal bicarbonate?

Furosemide causes all except -

All the following adverse effects can be caused by Loop Diuretics EXCEPT -

Thiazides and loop diuretics both have opposite action on which of the following ions ?

All of the following diuretics increase K+ excretion EXCEPT:

The site of action of the loop diuretic furosemide is:

In which segment of the nephron does ethacrynic acid exert its diuretic action?

Q10

Which of the following drugs decreases free water clearance?

Loop Diuretics Indian Medical PG Practice Questions and MCQs

Question 1: 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 2: A patient presents with hypertension and has a history of renal stones, along with several episodes of renal colic. Which diuretic is the most appropriate to use?

A. Furosemide
B. Hydrochlorothiazide (Correct Answer)
C. Ethacrynic acid
D. Spironolactone
E. Indapamide

Explanation: **Hydrochlorothiazide** - **Thiazide diuretics** like hydrochlorothiazide reduce urinary calcium excretion, which is beneficial in patients with a history of **calcium renal stones**. - This effect helps prevent the recurrence of renal stones while also treating hypertension. - Among thiazide and thiazide-like diuretics, hydrochlorothiazide has the **most established evidence** for preventing calcium stone recurrence. *Furosemide* - Furosemide is a **loop diuretic** that increases urinary calcium excretion, which would exacerbate the risk of renal stone formation. - While effective for hypertension, its effect on calcium makes it unsuitable for this patient. *Ethacrynic acid* - Ethacrynic acid is also a **loop diuretic** with similar effects to furosemide, including increasing urinary calcium excretion. - This makes it an inappropriate choice for a patient with a history of renal stones. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that works by antagonizing aldosterone, primarily affecting sodium and potassium excretion. - It does not significantly impact urinary calcium excretion in a way that would prevent calcium renal stones, nor is it a first-line agent for hypertension with co-existing renal stones. *Indapamide* - Indapamide is a **thiazide-like diuretic** with some calcium-retaining properties, but it is less effective than hydrochlorothiazide in reducing calcium excretion. - While it can be used for hypertension, **hydrochlorothiazide is preferred** specifically for preventing calcium stone recurrence due to stronger evidence and greater effect on reducing urinary calcium.

Question 3: 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 4: Furosemide causes all except -

A. Hypokalemia
B. Ototoxicity
C. Hypercalcemia (Correct Answer)
D. Hyperuricemia

Explanation: ***Hypercalcemia*** - Furosemide, a **loop diuretic**, inhibits the reabsorption of calcium in the thick ascending limb of the loop of Henle, leading to increased urinary calcium excretion and thus **hypocalcemia**, not hypercalcemia. - This effect makes loop diuretics useful in managing **hypercalcemia** by promoting calcium excretion. *Hypokalemia* - Furosemide inhibits the Na-K-2Cl cotransporter, leading to increased delivery of sodium to the collecting duct, which enhances potassium secretion and can cause **hypokalemia**. - Monitoring serum potassium levels and potassium supplementation are often necessary during furosemide therapy. *Ototoxicity* - Furosemide can cause **ototoxicity**, particularly with rapid intravenous administration or in patients with renal impairment. - This adverse effect typically manifests as **tinnitus** or **hearing loss**, which can be transient or permanent. *Hyperuricemia* - Furosemide competes with uric acid for secretion in the proximal tubule, leading to decreased uric acid excretion and subsequently **hyperuricemia**. - This can precipitate or exacerbate **gout attacks** in susceptible individuals.

Question 5: All the following adverse effects can be caused by Loop Diuretics EXCEPT -

A. Hypomagnesemia
B. Hypercalcemia (Correct Answer)
C. Hyperuricemia
D. Hyperglycemia

Explanation: ***Hypercalcemia*** - Loop diuretics inhibit the reabsorption of calcium in the thick ascending limb of the loop of Henle, leading to **increased urinary calcium excretion** and, consequently, **hypocalcemia** [2], [3]. - Therefore, loop diuretics actively decrease calcium levels, so hypercalcemia is not an adverse effect. *Hypomagnesemia* - Loop diuretics interfere with magnesium reabsorption in the thick ascending limb, which can lead to **increased urinary excretion of magnesium** and subsequently cause **hypomagnesemia** [1], [2]. - This effect is clinically significant as it can exacerbate other electrolyte imbalances or cause symptoms like muscle weakness or arrhythmias. *Hyperuricemia* - Loop diuretics can lead to **hyperuricemia** by competing with uric acid for secretion into the renal tubule and by increasing its reabsorption, thereby decreasing its excretion [1]. - This can precipitate or worsen gout, especially in susceptible individuals [1]. *Hyperglycemia* - Loop diuretics, like thiazide diuretics, can cause **hyperglycemia** by impairing insulin secretion and increasing peripheral insulin resistance. - This effect is more pronounced with higher doses and prolonged use, potentially worsening glycemic control in diabetic patients or unmasking latent diabetes.

Question 6: Thiazides and loop diuretics both have opposite action on which of the following ions ?

A. Potassium
B. Sodium
C. Chloride
D. Calcium (Correct Answer)

Explanation: ***Calcium*** - Thiazide diuretics **increase calcium reabsorption** in the distal convoluted tubule, leading to decreased urinary calcium excretion. - Loop diuretics **decrease calcium reabsorption** in the thick ascending limb of the loop of Henle, resulting in increased urinary calcium excretion. *Potassium* - Both thiazide and loop diuretics can cause **hypokalemia** by increasing potassium excretion in the urine. - This is due to increased sodium delivery to the collecting duct, which stimulates potassium secretion. *Sodium* - Both thiazide and loop diuretics inhibit sodium reabsorption at different sites in the nephron, leading to **increased urinary sodium excretion** (natriuresis). - This is their primary mechanism of action for diuresis. *Chloride* - Both thiazide and loop diuretics inhibit **chloride reabsorption** as they block specific sodium-chloride cotransporters. - Thiazides inhibit the Na-Cl cotransporter in the DCT, while loop diuretics inhibit the Na-K-2Cl cotransporter in the thick ascending limb.

Question 7: 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 8: The site of action of the loop diuretic furosemide is:

A. Distal convoluted tubule
B. Descending limb of loop of Henle
C. Proximal convoluted tubule
D. Thick ascending limb of loop of Henle (Correct Answer)

Explanation: ***Thick ascending limb of loop of Henle*** - Furosemide, a **loop diuretic**, acts by inhibiting the **Na+-K+-2Cl- cotransporter (NKCC2)** in the luminal membrane of the epithelial cells in the thick ascending limb. - This inhibition prevents the reabsorption of these ions, leading to increased excretion of **sodium**, **potassium**, **chloride**, and water. *Distal convoluted tubule* - This is the primary site of action for **thiazide diuretics**, which inhibit the **Na+-Cl- cotransporter**. - While some water reabsorption occurs here, it is not the main target for loop diuretics like furosemide. *Descending limb of loop of Henle* - This segment is primarily permeable to **water** due to aquaporins but impermeable to solutes, allowing for passive water reabsorption. - No significant transport mechanisms are directly targeted by furosemide here. *Proximal convoluted tubule* - The proximal tubule is where the majority of filtered **sodium**, **water**, and other solutes are reabsorbed. - **Carbonic anhydrase inhibitors** (e.g., acetazolamide) primarily act here.

Question 9: In which segment of the nephron does ethacrynic acid exert its diuretic action?

A. Proximal convoluted tubule
B. Collecting duct
C. Distal convoluted tubule
D. Thick ascending limb of loop of Henle (Correct Answer)

Explanation: ***Thick ascending limb of loop of Henle*** - Ethacrynic acid is a **loop diuretic** that acts by inhibiting the **Na+-K+-2Cl- cotransporter** (NKCC2) in the luminal membrane of the thick ascending limb. - This inhibition prevents the reabsorption of ions, leading to increased excretion of water, sodium, chloride, and potassium. *Proximal convoluted tubule* - The proximal convoluted tubule is the primary site of reabsorption of most filtered substances, but loop diuretics like ethacrynic acid do not primarily act here. - Carbonic anhydrase inhibitors and SGLT2 inhibitors are examples of diuretics that exert their effects in this segment. *Collecting duct* - The collecting duct is the site where aldosterone antagonists (e.g., spironolactone) and epithelial sodium channel (ENaC) inhibitors (e.g., amiloride, triamterene) exert their diuretic effects. - Its primary role involves fine-tuning water reabsorption under the influence of ADH and regulating potassium excretion. *Distal convoluted tubule* - Thiazide diuretics primarily act in the distal convoluted tubule by inhibiting the **Na+-Cl- cotransporter** (NCC). - This segment is responsible for further diluting the urine and reabsorbing a small percentage of filtered sodium and chloride.

Question 10: Which of the following drugs decreases free water clearance?

A. Vincristine (Correct Answer)
B. Vinblastine
C. Chlorpropamide
D. Furosemide

Explanation: ***Vincristine*** - **Vincristine** is a chemotherapeutic agent (vinca alkaloid) that commonly causes **syndrome of inappropriate antidiuretic hormone secretion (SIADH)**. - SIADH leads to **excessive ADH secretion**, causing increased water reabsorption in the collecting ducts. - This results in **decreased free water clearance**, hyponatremia, and concentrated urine with low serum osmolality [2]. *Furosemide* - **Furosemide** is a loop diuretic that inhibits the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle. - By reducing solute reabsorption, it impairs the medullary concentration gradient [2]. - This leads to impaired urinary concentration and **increased free water clearance** (dilute urine) [2]. *Vinblastine* - **Vinblastine** is another vinca alkaloid that can also cause SIADH, similar to vincristine. - However, vincristine is more commonly associated with SIADH than vinblastine. *Chlorpropamide* - **Chlorpropamide** is a first-generation sulfonylurea that can potentiate ADH action at the collecting duct [1]. - This leads to increased water reabsorption and decreased free water clearance [1]. - However, this effect is less clinically significant compared to SIADH-inducing drugs.

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