Diuretics Practice Questions

Q: Mannitol is most commonly used for which of the following conditions?

Raised intracranial tension (ICT). ***Raised intracranial tension (ICT)*** - **Mannitol** is an osmotic diuretic that creates an osmotic gradient, drawing water from the **brain parenchyma** into the vascular space, thereby reducing brain volume and **intracranial pressure**. - It is particularly effective in acute settings for managing **cerebral edema** associated with trauma, stroke, or tumors. *Glaucoma* - While mannitol can reduce **intraocular pressure** in acute glaucoma, it is not the most common or first-line treatment. - Other medications like topical beta-blockers, alpha-agonists, and prostaglandin analogs are typically preferred for long-term management and acute relief. *Impending renal failure* - **Mannitol** can induce osmosis of fluid, which could increase urine output. However, it is **contraindicated** in established **renal failure** due to the risk of exacerbating fluid overload and electrolyte imbalances. - Its use in impending renal failure is limited and typically reserved for specific situations like preventing acute kidney injury during cardiac surgery, and it is not a primary treatment. *Pulmonary edema* - **Mannitol** can increase **intravascular volume** as it draws fluid from interstitial spaces, which can worsen **pulmonary edema**, especially in patients with heart failure. - Diuretics like furosemide (loop diuretics) are the preferred treatment for pulmonary edema.

Q: A patient who is a known case of hypertension on multiple anti-hypertensive medications came to OPD. His ECG finding is given below. Which of the following drugs is responsible for the ECG finding? (Image of ECG finding)

Spironolactone. ***Spironolactone*** - The ECG shows a **tall, peaked T wave**, which is characteristic of **hyperkalemia**. - **Spironolactone** is a **potassium-sparing diuretic**, and its use, especially in combination with other medications or in patients with **renal impairment**, can lead to **hyperkalemia**. *Prazosin* - Prazosin is an **alpha-1 adrenergic blocker** used for **hypertension**. - It does **not directly affect potassium levels** and is not associated with the ECG changes seen in hyperkalemia. *Metoprolol* - Metoprolol is a **beta-blocker** primarily used for **hypertension**, **angina**, and **arrhythmias**. - It does **not significantly cause hyperkalemia** or the characteristic ECG changes shown. *Hydrochlorothiazide* - Hydrochlorothiazide is a **thiazide diuretic** that typically causes **hypokalemia**, not hyperkalemia, by **increasing potassium excretion**. - The ECG findings associated with hypokalemia would include **flattened T waves** or **prominent U waves**.

Q: Theophylline by what mechanism causes diuresis?

Adenosine A1 receptor antagonism. ***Adenosine A1 receptor antagonism*** - Theophylline is an **adenosine receptor antagonist**, primarily blocking A1 and A2A receptors at therapeutic concentrations. - **Adenosine A1 receptor antagonism** in the kidney leads to increased renal blood flow and glomerular filtration rate, resulting in a diuretic effect. *Phosphodiesterase 3 inhibition* - While theophylline is a **non-specific phosphodiesterase inhibitor**, its diuretic effect is not primarily mediated by PDE3 inhibition at clinical concentrations. - PDE3 inhibition is more commonly associated with **cardiac contractility** and **vasodilation**, but not direct diuresis. *Phosphodiesterase 4 inhibition* - **PDE4 inhibition** is a mechanism shared by some other bronchodilators (e.g., roflumilast) but is not the primary mechanism by which theophylline exerts its diuretic action. - PDE4 inhibition mainly affects **inflammatory cells** and smooth muscle, contributing to bronchodilation and anti-inflammatory effects. *Beta-2 adrenergic agonist action* - Theophylline has **no significant direct beta-2 adrenergic agonist action**; it primarily works through adenosine receptor antagonism and phosphodiesterase inhibition. - Beta-2 agonists (e.g., albuterol) act by stimulating beta-2 receptors, leading to **bronchodilation**, not diuresis.

Q: How do thiazides cause hypercalcemia?

Decreased calcium excretion. ***Decreased calcium excretion*** - Thiazides inhibit the **Na-Cl co-transporter** in the **distal convoluted tubule**, leading to increased reabsorption of calcium [1], [2]. - This increased reabsorption of calcium is mediated by a low intracellular sodium concentration, which enhances the activity of the **Na+/Ca2+ exchanger** on the basolateral membrane [1]. *Increased parathyroid hormone secretion* - Thiazides **do not directly stimulate** parathyroid hormone (PTH) secretion; instead, they *decrease* calcium excretion, which would typically *lower* PTH levels through negative feedback. - Elevated PTH would lead to increased bone resorption and kidney calcium reabsorption, but this is not the **primary mechanism** for thiazide-induced hypercalcemia [2]. *Decreased calcitonin secretion* - **Calcitonin** is a hormone that *lowers* blood calcium levels, and its decrease would theoretically contribute to hypercalcemia. - However, thiazides have **no direct effect** on calcitonin secretion, making this an unlikely primary mechanism. *Increased calcium absorption* - While increased calcium absorption from the gut can contribute to hypercalcemia, thiazides do **not directly increase intestinal calcium absorption**. - Their primary action for influencing calcium levels is within the **kidney**, specifically on reabsorption, not absorption from the GI tract [1], [2].

Q: Which of the following is not a side effect of thiazide diuretics?

Hypocalcemia. ***Hypocalcemia*** - Thiazide diuretics are known to cause **hypercalcemia** (increased calcium levels) by enhancing calcium reabsorption in the distal convoluted tubule. - Therefore, hypocalcemia is not a direct side effect of thiazide diuretics. *Hypokalemia* - Thiazide diuretics inhibit the Na+/Cl- cotransporter in the **distal convoluted tubule**, leading to increased sodium delivery to the collecting duct. - This increased sodium delivery promotes potassium secretion and can result in **hypokalemia**. *Hepatic coma* - Thiazide diuretics can exacerbate or precipitate **hepatic encephalopathy** and coma in patients with pre-existing liver disease. - This is primarily due to diuretic-induced **hypokalemia** and metabolic alkalosis, which increase renal ammonia production. *Impotence* - Thiazide diuretics, particularly at higher doses, have been associated with various sexual side effects, including **erectile dysfunction (impotence)** in men. - While the exact mechanism is not fully understood, it is a recognized adverse effect.

Q: Which diuretic is most likely to cause hyponatremia by impairing free water excretion?

Thiazide diuretics. ***Thiazide diuretics*** - **Thiazide diuretics** inhibit the **Na-Cl cotransporter in the distal convoluted tubule (DCT)**, impairing the kidney's ability to dilute urine and excrete free water - This impaired urinary dilution leads to **water retention relative to sodium**, resulting in **dilutional hyponatremia** - **Most common in elderly patients**, those on low-salt diets, or with pre-existing volume depletion - **Mechanism**: By blocking sodium reabsorption in the DCT (a key site for urinary dilution), thiazides prevent the generation of free water, leading to hyponatremia when water intake continues *Loop diuretics* - **Loop diuretics** inhibit the **Na-K-2Cl cotransporter in the thick ascending limb of Henle**, causing significant diuresis - They impair the medullary concentration gradient, **enhancing free water excretion** - **Less likely to cause hyponatremia** compared to thiazides because they promote rather than impair free water clearance - When hyponatremia occurs with loop diuretics, it's usually due to concurrent SIADH or excessive free water intake *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** acting primarily on the **proximal tubule** - Causes **bicarbonate and sodium excretion**, leading to mild diuresis - Main side effect is **metabolic acidosis** (type 2 RTA) - **Does not significantly impair free water excretion**, making hyponatremia uncommon *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that blocks **epithelial sodium channels (ENaC) in the collecting duct** - Weak diuretic effect, primarily used to prevent potassium loss - **Does not impair urinary dilution mechanisms**, so hyponatremia is rare - Main concern is **hyperkalemia**, especially with ACE inhibitors or in renal insufficiency

Q: Which diuretic is known to cause the maximum potassium loss?

Furosemide. ***Furosemide*** - Furosemide is a **loop diuretic** that inhibits the Na-K-2Cl cotransporter in the **thick ascending limb of the loop of Henle**, leading to significant excretion of sodium, chloride, potassium, and water. - Its potent diuresis and impact on potassium reabsorption result in a **high risk of hypokalemia**. *Thiazide* - Thiazide diuretics inhibit the **Na-Cl cotransporter** in the **distal convoluted tubule**, causing moderate sodium and water excretion, and some potassium loss. - While they can cause hypokalemia, their effect on potassium excretion is generally **less pronounced than loop diuretics**. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that acts primarily in the **proximal tubule**, inhibiting bicarbonate reabsorption and leading to increased excretion of bicarbonate, sodium, potassium, and water. - The potassium loss is due to increased delivery of sodium to the collecting duct, leading to enhanced potassium secretion, but it is typically **less severe than with loop diuretics**. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that acts as an **aldosterone antagonist** in the collecting duct, inhibiting sodium reabsorption and potassium secretion. - Instead of causing potassium loss, spironolactone actually **conserves potassium** and can lead to hyperkalemia.

Q: Which diuretic inhibits the Na+-K+-2Cl- symporter in the thick ascending limb of the loop of Henle?

Furosemide. ***Furosemide*** - Furosemide is a **loop diuretic** that acts by inhibiting the **Na+-K+-2Cl- symporter** (NKCC2) in the luminal membrane of the epithelial cells in the thick ascending limb of the **loop of Henle** [1], [2]. - This inhibition prevents the reabsorption of sodium, potassium, and chloride ions, leading to increased excretion of these ions and water [1]. *Thiazides* - Thiazide diuretics, such as **hydrochlorothiazide**, primarily act on the **distal convoluted tubule** [4]. - They inhibit the **Na+-Cl- cotransporter**, not the Na+-K+-2Cl- symporter [4]. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that primarily acts in the **proximal convoluted tubule** [3]. - It inhibits the reabsorption of bicarbonate, leading to increased excretion of bicarbonate, sodium, and water [3]. *Amiloride* - Amiloride is a **potassium-sparing diuretic** that acts on the **collecting duct**. - It inhibits the **epithelial sodium channel (ENaC)**, leading to reduced sodium reabsorption and potassium secretion.

Q: Gynaecomastia is caused by which drug?

Spironolactone. ***Spironolactone*** - Spironolactone is a **well-established cause of gynaecomastia**, occurring in 5-10% of patients in a dose-dependent manner. - It acts as an **anti-androgen** by blocking androgen receptors and inhibiting testosterone synthesis, thereby increasing the estrogen to androgen ratio. - It is a **potassium-sparing diuretic** and aldosterone antagonist, commonly used in heart failure, hypertension, and conditions requiring androgen blockade. *Rifampicin* - Rifampicin is an **antibiotic** primarily used to treat tuberculosis and acts as a **strong inducer of cytochrome P450 enzymes**. - While rare hormonal effects have been reported, it is **not a recognized common cause** of gynaecomastia. - Main side effects include hepatotoxicity, orange discoloration of bodily fluids, and drug interactions. *Thiazide* - Thiazide diuretics work by inhibiting the **sodium-chloride cotransporter** in the distal convoluted tubule. - They are **not commonly associated** with gynaecomastia; typical side effects include hypokalemia, hyponatremia, and hyperglycemia. *Propranolol* - Propranolol is a **non-selective beta-blocker** used for hypertension, angina, arrhythmias, and anxiety. - While beta-blockers have rarely been implicated, propranolol is **not a well-established cause** of gynaecomastia compared to spironolactone. - Common side effects include bradycardia, fatigue, and bronchospasm.

Q: Thiazides act on which part of the nephron?

Distal Convoluted Tubule. ***Distal Convoluted Tubule*** - **Thiazide diuretics** specifically inhibit the **sodium-chloride cotransporter (NCC)** in the apical membrane of cells in the distal convoluted tubule. - This inhibition leads to decreased reabsorption of sodium and chloride, resulting in increased excretion of water, sodium, and chloride. *Proximal Convoluted Tubule* - The proximal convoluted tubule is the primary site for reabsorption of the majority of filtered substances, including sodium, bicarbonate, glucose, and amino acids. - While some diuretics like **acetazolamide** (a carbonic anhydrase inhibitor) act here, thiazides do not. *Glomerulus* - The **glomerulus** is primarily responsible for the **filtration** of blood, forming the initial filtrate. - It is not a site for diuretic action as it does not participate in active reabsorption or secretion of electrolytes. *Descending limb of loop of Henle* - The descending limb is highly permeable to **water** but impermeable to solutes, leading to water reabsorption due to the hyperosmotic medulla. - Diuretics typically do not act on this segment to inhibit solute transport, though osmotic diuretics can affect water movement here.

Question 1

Mannitol is most commonly used for which of the following conditions?

Accepted Answer

Raised intracranial tension (ICT)

Answer

Impending renal failure

Answer

Glaucoma

Answer

Pulmonary edema

Question 2

A patient who is a known case of hypertension on multiple anti-hypertensive medications came to OPD. His ECG finding is given below. Which of the following drugs is responsible for the ECG finding? (Image of ECG finding)

Accepted Answer

Spironolactone

Answer

Prazosin

Answer

Metoprolol

Answer

Hydrochlorothiazide

Question 3

Theophylline by what mechanism causes diuresis?

Accepted Answer

Adenosine A1 receptor antagonism

Answer

Phosphodiesterase 3 inhibition

Answer

Phosphodiesterase 4 inhibition

Answer

Beta-2 adrenergic agonist action

Question 4

How do thiazides cause hypercalcemia?

Accepted Answer

Decreased calcium excretion

Answer

Increased parathyroid hormone secretion

Answer

Decreased calcitonin secretion

Answer

Increased calcium absorption

Question 5

Which of the following is not a side effect of thiazide diuretics?

Accepted Answer

Hypocalcemia

Answer

Hypokalemia

Answer

Impotence

Answer

Hepatic coma

Question 6

Which diuretic is most likely to cause hyponatremia by impairing free water excretion?

Accepted Answer

Thiazide diuretics

Answer

Loop diuretics

Answer

Acetazolamide

Answer

Amiloride

Question 7

Which diuretic is known to cause the maximum potassium loss?

Accepted Answer

Furosemide

Answer

Spironolactone

Answer

Thiazide diuretics

Answer

Acetazolamide

Question 8

Which diuretic inhibits the Na+-K+-2Cl- symporter in the thick ascending limb of the loop of Henle?

Accepted Answer

Furosemide

Answer

Thiazides

Answer

Amiloride

Answer

Acetazolamide

Question 9

Gynaecomastia is caused by which drug?

Accepted Answer

Spironolactone

Answer

Rifampicin

Answer

Thiazide

Answer

Propranolol

Question 10

Thiazides act on which part of the nephron?

Accepted Answer

Distal Convoluted Tubule

Answer

Proximal Convoluted Tubule

Answer

Descending limb of loop of Henle

Answer

Glomerulus

Diuretics — MCQs

Diuretics — MCQs

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