Diuretics in Hypertension — MCQs

10 questions

All of the following adverse effects can be caused by loop diuretics except :

A patient with hypertension, peripheral edema, and chronic kidney disease (CKD) presents for management. Which of the following medications would be the best choice?

Thiazide diuretics can be used for the treatment of all of these conditions EXCEPT :

Side effects of thiazide diuretics include all of the following except?

What is the mechanism of action of thiazides?

Which of the following potassium-sparing diuretics was the first to be shown to reduce cardiac mortality in chronic heart failure patients?

Furosemide causes all except -

Drug of choice for Liddle syndrome

Which electrolyte shows the most significant increase in urinary excretion within 24 hours of initiating thiazide diuretic therapy for hypertension?

Q10

Drugs acting on K+ channels include which of the following?

Diuretics in Hypertension Indian Medical PG Practice Questions and MCQs

Question 1: All of the following adverse effects can be caused by loop diuretics except :

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

Explanation: ***Hypercalcemia*** - Loop diuretics inhibit the reabsorption of calcium in the thick ascending limb of the loop of Henle, leading to **increased calcium excretion** and thus **hypocalcemia**, not hypercalcemia [2]. - This property makes them useful in treating conditions like hypercalcemia, but it means they do not cause hypercalcemia themselves. *Hypomagnesemia* - Loop diuretics inhibit magnesium reabsorption in the thick ascending limb, leading to **increased urinary magnesium excretion** and potential **hypomagnesemia** [1], [2]. - This electrolyte imbalance can contribute to cardiac arrhythmias and muscle weakness [2]. *Hyperglycemia* - Loop diuretics, particularly in high doses, can decrease **insulin secretion** and increase **insulin resistance**, leading to **hyperglycemia**. - This effect is generally mild but can be significant in patients with **diabetes mellitus**. *Hyperuricemia* - Loop diuretics compete with uric acid for secretion into the renal tubules, leading to **reduced uric acid excretion** and elevated serum uric acid levels, also known as **hyperuricemia** [1]. - This can precipitate or exacerbate **gout attacks** in susceptible individuals [1].

Question 2: A patient with hypertension, peripheral edema, and chronic kidney disease (CKD) presents for management. Which of the following medications would be the best choice?

A. Aliskiren
B. Beta blocker
C. Prazosin
D. Chlorthalidone (Correct Answer)
E. Furosemide

Explanation: ***Chlorthalidone*** - **Chlorthalidone** is a **thiazide-type diuretic** that is effective in managing hypertension and associated edema, even in patients with moderate CKD (eGFR >30 mL/min/1.73m²). - Its long duration of action and proven cardiovascular benefits make it a good choice for hypertension control in this clinical context. - **Superior to loop diuretics for blood pressure control** and has better evidence for reducing cardiovascular events. *Aliskiren* - **Aliskiren** is a **direct renin inhibitor** that blocks the renin-angiotensin-aldosterone system (RAAS). - However, in patients with CKD, particularly those with existing hypertension and peripheral edema, it is generally **not preferred due to potential risks** of hyperkalemia, renal impairment, and hypotension, especially when combined with ACE inhibitors or ARBs. *Beta blocker* - While **beta-blockers** can treat hypertension, they are **not the first-line choice** for patients with both hypertension and significant peripheral edema. - They also have potential side effects like bradycardia, fatigue, and bronchospasm, and may mask symptoms of hypoglycemia in diabetic patients. *Prazosin* - **Prazosin** is an **alpha-1 adrenergic blocker** that can reduce blood pressure but is primarily used for **hypertension with benign prostatic hyperplasia (BPH)** due to its dilating effect on the bladder neck. - It's **not typically a first-line agent** for essential hypertension with peripheral edema and carries a risk of **first-dose syncope**. *Furosemide* - **Furosemide** is a **loop diuretic** that is more effective than thiazides for managing edema, especially in severe CKD (eGFR <30). - However, for **blood pressure control** in patients with moderate CKD and edema, **thiazide-type diuretics like chlorthalidone are preferred** due to their superior antihypertensive efficacy and cardiovascular benefits. - Loop diuretics have a shorter duration of action and are less effective for chronic hypertension management.

Question 3: 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 4: Side effects of thiazide diuretics include all of the following except?

A. Hypokalemia
B. Erectile dysfunction
C. Hyponatremia
D. Hypocalcemia (Correct Answer)

Explanation: ***Hypocalcemia*** - Thiazide diuretics are known to cause **hypercalcemia** (increased calcium reabsorption), NOT hypocalcemia, due to their action on the distal convoluted tubule. - This property makes them useful in treating conditions like **idiopathic hypercalciuria** and **calcium-containing kidney stones**. - The mechanism involves enhanced passive calcium reabsorption in the proximal tubule and active reabsorption in the distal tubule. *Hyponatremia* - Thiazide diuretics impair the kidney's ability to dilute urine and reabsorb sodium in the distal tubule, leading to **increased sodium excretion** and potential hyponatremia. - This effect is more pronounced in **elderly patients** and those with increased free water intake. - Hyponatremia is one of the most common electrolyte disturbances with thiazides. *Hypokalemia* - Thiazides increase the delivery of sodium and water to the collecting duct, leading to increased activity of the **renin-angiotensin-aldosterone system** and enhanced potassium secretion. - This results in **potassium wasting** and hypokalemia, which may require potassium supplementation or combination with potassium-sparing diuretics. *Erectile dysfunction* - Thiazide diuretics can cause **erectile dysfunction** through mechanisms including effects on vascular smooth muscle, reduced blood flow, and possible hormonal effects. - This is a common side effect reported in male patients using these medications for hypertension and may affect compliance.

Question 5: What is the mechanism of action of thiazides?

A. Carbonic anhydrase inhibitor
B. Na+Cl- co-transporter inhibitor (Correct Answer)
C. Osmotic diuresis
D. Na+K+ co-transporter inhibitor

Explanation: **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.

Question 6: Which of the following potassium-sparing diuretics was the first to be shown to reduce cardiac mortality in chronic heart failure patients?

A. Spironolactone (Correct Answer)
B. Amiloride
C. Triamterene
D. Eplerenone

Explanation: ***Spironolactone*** - **Spironolactone** was the first potassium-sparing diuretic shown to reduce **cardiac mortality** in patients with **chronic heart failure** in the **RALES trial** (Randomized Aldactone Evaluation Study). - Its beneficial effects in heart failure are primarily attributed to its **aldosterone receptor antagonist** properties, which counteract the harmful effects of aldosterone on the myocardium and vasculature, rather than just its diuretic effect. *Amiloride* - **Amiloride** is a potassium-sparing diuretic that works by directly inhibiting **epithelial sodium channels (ENaC)** in the collecting duct. - While it helps in potassium conservation, it has not been shown to significantly reduce cardiac mortality in chronic heart failure patients in clinical trials. *Triamterene* - **Triamterene** is another potassium-sparing diuretic that also directly inhibits **ENaC** in the collecting duct, similar to amiloride. - Like amiloride, it is used to prevent hypokalemia but lacks evidence for significant **cardiac mortality reduction** in chronic heart failure. *Eplerenone* - **Eplerenone** is a selective **aldosterone receptor antagonist**, similar to spironolactone, with fewer hormonal side effects. - While it has been shown to reduce **cardiac mortality** in chronic heart failure (e.g., in the EMPHASIS-HF trial), it was introduced later than spironolactone and was not the *first* to demonstrate this benefit.

Question 7: 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 8: Drug of choice for Liddle syndrome

A. Furosemide
B. Amiloride (Correct Answer)
C. Spironolactone
D. Acetazolamide

Explanation: ***Amiloride*** - **Amiloride** is a potassium-sparing diuretic that directly blocks the **epithelial sodium channel (ENaC)** in the collecting duct. - Liddle syndrome is caused by a gain-of-function mutation in ENaC, leading to excessive sodium reabsorption and potassium excretion, which **amiloride directly counters**. - This makes it the **specific and most effective treatment** for this genetic condition. *Furosemide* - **Furosemide** is a loop diuretic that blocks the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle. - While it can induce diuresis, it does not specifically target the **ENaC overactivity** seen in Liddle syndrome, making it less effective. *Spironolactone* - **Spironolactone** is an aldosterone antagonist that blocks the mineralocorticoid receptor. - Liddle syndrome involves a **defect in ENaC function directly**, not excess aldosterone, so spironolactone is generally ineffective. *Acetazolamide* - **Acetazolamide** is a carbonic anhydrase inhibitor that acts primarily in the proximal tubule to reduce bicarbonate reabsorption. - Its mechanism of action is unrelated to the **excessive ENaC activity** characteristic of Liddle syndrome.

Question 9: Which electrolyte shows the most significant increase in urinary excretion within 24 hours of initiating thiazide diuretic therapy for hypertension?

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

Explanation: ***Sodium*** - Thiazide diuretics primarily act on the **distal convoluted tubule** by inhibiting the **Na+/Cl- cotransporter**, leading to increased excretion of **sodium** and water [1]. - The initial and most significant pharmacological effect of thiazides is to promote **natriuresis**, removing excess sodium from the body [2]. - Within **24 hours**, sodium excretion shows the most pronounced increase, which is the primary mechanism for blood pressure reduction [2]. *Potassium* - While thiazides do cause **potassium excretion**, this effect is less significant than sodium excretion initially and is partly due to increased flow to the collecting duct and elevated aldosterone levels [2]. - Hypokalemia is a known side effect of long-term thiazide use, but the **immediate increase in urinary sodium** is more pronounced. *Magnesium* - Thiazide diuretics are known to cause **increased urinary excretion of magnesium**, which can lead to hypomagnesemia with chronic use [3]. - However, the initial increase in magnesium excretion is generally **less pronounced** compared to sodium excretion within the first 24 hours of therapy. *Calcium* - Uniquely among diuretics, thiazides **decrease** urinary calcium excretion, promoting calcium retention and reabsorption in the distal tubule [1], [3]. - This is why thiazides are sometimes used therapeutically in **hypercalciuric nephrolithiasis** and can cause hypercalcemia as a side effect. - Calcium excretion is **reduced**, not increased, making this the opposite of the correct answer.

Question 10: Drugs acting on K+ channels include which of the following?

A. Nicorandil (Correct Answer)
B. Methyldopa
C. Amiloride
D. Spironolactone

Explanation: ***Nicorandil*** - **Nicorandil** is a **potassium channel activator** that causes vasodilation by opening ATP-sensitive potassium channels in vascular smooth muscle cells. - This action leads to hyperpolarization of the cell membrane, making it more difficult for calcium influx and thus promoting relaxation and **vasodilation**. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist** that works by blocking aldosterone receptors in the renal collecting tubules. - Its main effect is to increase sodium and water excretion while **conserving potassium**, making it a potassium-sparing diuretic, but it does not directly act on potassium channels for its primary mechanism. *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that directly inhibits **epithelial sodium channels (ENaC)** in the collecting duct. - By blocking sodium reabsorption, it indirectly reduces potassium secretion, thus conserving potassium, but it does not directly affect potassium channels. *Methyldopa* - **Methyldopa** is a **centrally acting alpha-2 adrenergic agonist** that reduces sympathetic outflow from the central nervous system. - It decreases peripheral vascular resistance and heart rate, leading to a reduction in blood pressure, and does not directly interact with potassium channels.

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