Diuretics Practice Questions

Q: Furosemide causes all except -

Hypercalcemia. ***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.

Q: A drug that can be used for producing alkalinization of urine is?

Acetazolamide. ***Acetazolamide*** - This drug is a **carbonic anhydrase inhibitor** that works in the **proximal tubule** of the kidney to decrease bicarbonate reabsorption. - By inhibiting **carbonic anhydrase**, it increases the excretion of **bicarbonate**, leading to an **alkaline urine** and mild systemic acidosis. *Spironolactone* - This is a **potassium-sparing diuretic** that acts as an **aldosterone antagonist** in the collecting duct. - It increases sodium excretion and potassium retention, but does not primarily cause **urine alkalinization**. *Furosemide* - This is a **loop diuretic** that acts on the **thick ascending limb of the loop of Henle** to inhibit the Na-K-2Cl cotransporter. - While it can increase urine output, it primarily increases the excretion of sodium, potassium, and chloride, and typically causes a **mild metabolic alkalosis** in the blood, but does not directly alkalinize the urine. *Hydrochlorothiazide* - This is a **thiazide diuretic** that acts in the **distal convoluted tubule** to inhibit the Na-Cl cotransporter. - It promotes the excretion of sodium and chloride, and can cause **hypokalemia** and metabolic alkalosis, but does not primarily induce **urine alkalinization**.

Q: Free water clearance is decreased by?

Chlorpropamide. ***Chlorpropamide*** - **Chlorpropamide** is a sulfonylurea oral hypoglycemic agent that is a **classic and well-documented cause of SIADH (Syndrome of Inappropriate Antidiuretic Hormone)**. - **SIADH** leads to increased ADH secretion, causing increased water reabsorption in the collecting ducts and thus **decreased free water clearance**. - Among the options listed, chlorpropamide is the **prototypical drug** associated with drug-induced SIADH in pharmacology teaching. *Furosemide* - **Furosemide** is a loop diuretic that inhibits the reabsorption of sodium and chloride in the **loop of Henle**. - This disrupts the medullary concentration gradient and leads to increased excretion of water and electrolytes, thereby **increasing free water clearance**. *Vinblastine* - **Vinblastine** is a vinca alkaloid chemotherapeutic agent primarily used in cancer treatment. - It does not significantly affect renal water handling or ADH secretion and does **not typically cause SIADH**. *Vincristine* - **Vincristine** is another vinca alkaloid chemotherapy drug that **can also cause SIADH** and decrease free water clearance. - However, in the context of standard pharmacology teaching and board examinations, **chlorpropamide** is the more classical example emphasized for drug-induced SIADH and decreased free water clearance. - Vincristine is primarily known for its **neurotoxicity** as a major side effect.

Q: Which of the following is NOT known as adverse drug reaction of furosemide?

Hyperkalemia. ***Hyperkalemia*** - Furosemide is a **loop diuretic** that primarily acts on the **thick ascending limb of the loop of Henle**, inhibiting the Na-K-2Cl cotransporter. - This action leads to increased excretion of potassium in the distal tubule, therefore, **hypokalemia** is a common adverse effect, not hyperkalemia. - **Hyperkalemia is NOT an adverse effect of furosemide** - it causes the opposite effect (hypokalemia). *Hypomagnesemia* - Furosemide inhibits magnesium reabsorption in the **loop of Henle**, leading to increased urinary excretion of magnesium. - This can result in clinically significant **hypomagnesemia**, especially with long-term use. - This IS a well-recognized adverse effect. *Hyperuricemia* - Furosemide competes with uric acid for secretion into the renal tubule at the **proximal tubule**. - This competition reduces uric acid excretion, causing an increase in serum **uric acid levels** and potentially precipitating **gout attacks**. - This IS a well-recognized adverse effect. *Acidosis* - Furosemide characteristically causes **metabolic alkalosis** (not acidosis) due to: - Contraction alkalosis from volume depletion - Enhanced H+ secretion in the distal tubule - Loss of Cl- in urine - **Metabolic acidosis is NOT a typical adverse effect** of furosemide. - While severe volume depletion theoretically could contribute to lactic acidosis, this is not a recognized or standard adverse drug reaction of furosemide.

Q: One of the following diuretics does not require its presence in the tubular lumen for its pharmacological effects

Aldosterone antagonists. ***Aldosterone antagonists*** - These diuretics act from the **basolateral side** of the renal tubular cells, binding to **cytoplasmic mineralocorticoid receptors**. - Their action is independent of their concentration within the **tubular lumen**, as they modulate gene transcription rather than directly blocking ion channels from the luminal side. *Loop diuretics* - These agents, such as **furosemide**, must reach the **tubular lumen** via **active secretion** in the proximal tubule to exert their effect. - They inhibit the **Na+-K+-2Cl− cotransporter (NKCC2)** on the luminal membrane in the thick ascending limb of the loop of Henle. *Carbonic anhydrase inhibitors* - Drugs like **acetazolamide** primarily act within the **tubular lumen** and in the cytoplasm of proximal tubule cells. - They inhibit **carbonic anhydrase**, reducing bicarbonate reabsorption and thus requiring luminal presence for part of their effect. *Thiazide diuretics* - Similar to loop diuretics, thiazides must be **secreted into the tubular lumen** by the organic acid transporter in the proximal tubule. - They then inhibit the **Na+-Cl− cotransporter (NCC)** on the luminal membrane of the distal convoluted tubule.

Q: What is the mechanism of action of thiazides?

Na+Cl- co-transporter inhibitor. **Na+Cl- co-transporter inhibitor** - Thiazide diuretics primarily act by inhibiting the **Na+Cl- cotransporter** (also known as the **NCC cotransporter**) in the **distal convoluted tubule** of the nephron. - This inhibition reduces the reabsorption of **sodium chloride**, leading to increased excretion of sodium, chloride, and water. *Carbonic anhydrase inhibitor* - **Carbonic anhydrase inhibitors** like acetazolamide primarily act in the **proximal convoluted tubule**. - They inhibit carbonic anhydrase, reducing bicarbonate reabsorption and leading to increased excretion of bicarbonate, sodium, and potassium, as well as a subsequent diuresis. *Osmotic diuresis* - **Osmotic diuretics** (e.g., mannitol) are filtered by the glomeruli but poorly reabsorbed, creating an **osmotic gradient** in the renal tubule. - This osmotic effect prevents water reabsorption, leading to increased urinary flow and excretion of solutes. *Na+K+ co-transporter inhibitor* - This refers to the **Na+K+2Cl- cotransporter** (NKCC2) which is inhibited by **loop diuretics** in the **thick ascending limb of the loop of Henle**. - Inhibition of this cotransporter leads to significant diuresis due to the large amount of sodium reabsorbed in this segment.

Q: Which diuretic causes impaired glucose tolerance?

Thiazide. ***Thiazide*** - **Thiazide diuretics** can cause **impaired glucose tolerance** or even exacerbate existing diabetes due to several mechanisms, including **hypokalemia**, which impairs insulin secretion. - They may also reduce **peripheral glucose utilization** and increase hepatic glucose production. - This is a well-known adverse effect that requires monitoring in diabetic patients. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** primarily used for glaucoma, altitude sickness, and metabolic alkalosis. - It does not typically cause **impaired glucose tolerance** as a significant side effect. *Triamterene* - **Triamterene** is a **potassium-sparing diuretic** that acts by blocking sodium channels in the collecting duct. - It is not commonly associated with **impaired glucose tolerance**. *Amiloride* - **Amiloride** is another **potassium-sparing diuretic** with a mechanism similar to triamterene. - It is not known to cause **impaired glucose tolerance** as a side effect.

Q: Thiazide diuretics act on:

DCT mainly. ***DCT mainly*** - Thiazide diuretics primarily act on the **distal convoluted tubule (DCT)** [2, 3]. - They inhibit the **sodium-chloride cotransporter (NCC)** in the luminal membrane of the DCT cells, blocking the reabsorption of Na+ and Cl- [1, 2, 3].*Loop of henle* - The loop of Henle is the site of action for **loop diuretics**, which inhibit the Na-K-2Cl cotransporter. - While it's an important part of the nephron for fluid balance, it's not the primary target for thiazide diuretics.*PCT mainly* - The **proximal convoluted tubule (PCT)** is where the majority of solute and water reabsorption occurs. - **Carbonic anhydrase inhibitors** (e.g., acetazolamide) primarily act in the PCT, not thiazides.*All part of tubule* - No single class of diuretic acts on **all parts of the renal tubule**. - Each class has a specific site of action to allow for selective modulation of electrolyte and water balance.

Q: The site of action of the loop diuretic furosemide is:

Thick ascending limb of loop of Henle. ***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.

Q: Thiazides cause -

Metabolic alkalosis. ***Metabolic alkalosis*** - Thiazide diuretics cause increased excretion of **potassium** and **hydrogen ions** in the urine, leading to **hypokalemia** and an increase in serum bicarbonate [1]. - This increased bicarbonate reabsorption by the kidneys, coupled with an increase in extracellular fluid volume contraction, results in **metabolic alkalosis** [1]. *Respiratory alkalosis* - This condition is characterized by a decrease in **arterial carbon dioxide (PaCO2)** due to **hyperventilation**, which is not directly caused by thiazide diuretics. - While electrolyte imbalances can indirectly affect respiration, thiazides primarily influence metabolic acid-base balance. *Metabolic acidosis* - This occurs due to a decrease in **serum bicarbonate** or an increase in acid, which is the opposite effect of thiazide diuretics. - Thiazides, by promoting hydrogen ion excretion, would tend to prevent rather than cause metabolic acidosis. *Respiratory acidosis* - Characterized by an increase in **arterial carbon dioxide (PaCO2)** due to **hypoventilation**, which is not a direct effect of thiazide diuretics. - Thiazide use does not typically lead to impaired ventilation.

Question 1

Furosemide causes all except -

Accepted Answer

Hypercalcemia

Answer

Hypokalemia

Answer

Ototoxicity

Answer

Hyperuricemia

Question 2

A drug that can be used for producing alkalinization of urine is?

Accepted Answer

Acetazolamide

Answer

Spironolactone

Answer

Furosemide

Answer

Hydrochlorothiazide

Question 3

Free water clearance is decreased by?

Accepted Answer

Chlorpropamide

Answer

Furosemide

Answer

Vinblastine

Answer

Vincristine

Question 4

Which of the following is NOT known as adverse drug reaction of furosemide?

Accepted Answer

Hyperkalemia

Answer

Hypomagnesemia

Answer

Hyperuricemia

Answer

Acidosis

Question 5

One of the following diuretics does not require its presence in the tubular lumen for its pharmacological effects

Accepted Answer

Aldosterone antagonists

Answer

Loop diuretics

Answer

Carbonic anhydrase inhibitors

Answer

Thiazide diuretics

Question 6

What is the mechanism of action of thiazides?

Accepted Answer

Na+Cl- co-transporter inhibitor

Answer

Carbonic anhydrase inhibitor

Answer

Osmotic diuresis

Answer

Na+K+ co-transporter inhibitor

Question 7

Which diuretic causes impaired glucose tolerance?

Accepted Answer

Thiazide

Answer

Acetazolamide

Answer

Triamterene

Answer

Amiloride

Question 8

Thiazide diuretics act on:

Accepted Answer

DCT mainly

Answer

Loop of Henle

Answer

PCT mainly

Answer

All parts of tubule

Question 9

The site of action of the loop diuretic furosemide is:

Accepted Answer

Thick ascending limb of loop of Henle

Answer

Distal convoluted tubule

Answer

Descending limb of loop of Henle

Answer

Proximal convoluted tubule

Question 10

Thiazides cause -

Accepted Answer

Metabolic alkalosis

Answer

Respiratory alkalosis

Answer

Metabolic acidosis

Answer

Respiratory acidosis

Diuretics — MCQs

Diuretics — MCQs

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