Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 1051: What type of drug is Sacubitril?

A. ACE inhibitor
B. Neutral endopeptidase inhibitor (Correct Answer)
C. Calcium channel inhibitor
D. Beta adrenergic blocker

Explanation: ***Neutral endopeptidase inhibitor*** - **Sacubitril** is specifically a **neprilysin inhibitor**, which is a type of neutral endopeptidase. - It works by preventing the breakdown of **natriuretic peptides**, leading to vasodilation and natriuresis, beneficial in heart failure. *ACE inhibitor* - **ACE inhibitors** block the conversion of angiotensin I to angiotensin II, leading to vasodilation and reduced aldosterone. - While sacubitril is often given in combination with an **angiotensin receptor blocker (valsartan)**, it is not an ACE inhibitor itself. *Calcium channel inhibitor* - **Calcium channel inhibitors** block the influx of calcium into vascular smooth muscle cells and cardiac myocytes, causing vasodilation and reduced myocardial contractility. - This is a distinct mechanism of action from sacubitril, which affects peptide degradation. *Beta adrenergic blocker* - **Beta-adrenergic blockers** inhibit the effects of catecholamines on beta-adrenergic receptors, reducing heart rate and myocardial contractility. - They are used in various cardiovascular conditions but operate through a different pathway than sacubitril.

Question 1052: What is the drug of choice for treating tachycardia induced by digitalis?

A. Phenytoin (Correct Answer)
B. Lidocaine
C. Reducing the dosage of digoxin
D. Verapamil

Explanation: ***Phenytoin*** - Phenytoin is the traditional drug of choice for **digitalis-induced tachyarrhythmias** as it blocks **sodium channels**, suppresses **automaticity**, and uniquely improves **AV conduction**. - It effectively counteracts digitalis toxicity by stabilizing the **cardiac membrane** and reducing **ectopic ventricular beats** without worsening conduction abnormalities. *Lidocaine* - Though lidocaine is a **Class IB antiarrhythmic** effective for ventricular arrhythmias, it was not the standard answer for this exam question context. - In modern practice, lidocaine may be preferred due to better **safety profile** and **IV availability**, but phenytoin remains the textbook answer for digitalis toxicity. *Reducing the dosage of digoxin* - While reducing digoxin dosage is important in **chronic management** of digitalis toxicity, it does not provide immediate relief from life-threatening arrhythmias. - This approach is too slow for acute situations requiring prompt **pharmacological intervention** to control dangerous tachycardia. *Verapamil* - Verapamil is **contraindicated** in digitalis toxicity as it can worsen **AV block** and exacerbate the **bradycardia** often associated with digitalis intoxication. - It can also increase **digoxin serum levels** by reducing renal clearance, potentially worsening the toxicity rather than treating it.

Question 1053: Which of the following medications is primarily used to decrease serum triglycerides?

A. Fibrates (Correct Answer)
B. Ezetimibe
C. Niacin
D. Statin

Explanation: ***Fibrates*** - Fibrates, such as **gemfibrozil** and **fenofibrate**, are primarily used to activate **PPAR-alpha**, leading to increased lipoprotein lipase activity and reduced hepatic triglyceride synthesis. - This effectively lowers **serum triglyceride levels** by 20-50% and can also increase HDL cholesterol. *Statin* - Statins primarily inhibit **HMG-CoA reductase**, the rate-limiting enzyme in cholesterol synthesis, which makes them highly effective at lowering **LDL cholesterol**. - While they can cause a modest reduction in triglycerides (10-30%), this is not their primary mechanism or indication. *Ezetimibe* - Ezetimibe works by inhibiting the absorption of **cholesterol** at the brush border of the small intestine, thereby lowering **LDL cholesterol**. - It has minimal effect on **triglyceride levels** and is not indicated for primary triglyceride reduction. *Niacin* - Niacin, or **nicotinic acid**, reduces the liver's production of VLDL (which contains triglycerides) and LDL, and also increases HDL cholesterol. - While it can significantly lower triglycerides, its use is often limited by bothersome side effects such as **flushing** and itchiness, making fibrates generally preferred for primary triglyceride lowering due to better tolerability.

Question 1054: Digitalis is used in mitral stenosis to control the ventricular rate when the patient develops which condition?

A. Atrial fibrillation (Correct Answer)
B. Right ventricular failure
C. Acute pulmonary edema
D. Myocarditis

Explanation: ***Atrial fibrillation*** - **Digitalis** (digoxin) is effective in **slowing the ventricular rate** in atrial fibrillation by increasing vagal tone and prolonging the refractory period of the AV node. - In **mitral stenosis**, an uncontrolled rapid ventricular rate due to atrial fibrillation can significantly reduce cardiac output and worsen symptoms. *Right ventricular failure* - While digitalis can improve contractility, its primary role in **RV failure** is not rate control; diuretics and afterload reduction are more commonly used. - A patient with isolated right ventricular failure due to mitral stenosis would not directly benefit from digitalis for rate control. *Acute pulmonary edema* - **Acute pulmonary edema** requires rapid diuresis, oxygen, and vasodilators to reduce preload and afterload. - Digitalis has a slower onset of action and is not the first-line treatment for acute pulmonary edema, especially if the cause is not related to a rapid ventricular rate. *Myocarditis* - **Myocarditis** is an inflammation of the heart muscle, and digitalis is generally avoided due to concerns about potentially worsening arrhythmias and myocardial damage in an inflamed heart. - Treatment for myocarditis focuses on supportive care and addressing the underlying cause, not rate control with digitalis unless specific arrhythmias develop.

Question 1055: Beta-blockers should be used with caution in patients with?

A. Hypertension
B. CHF
C. Conduction defect (Correct Answer)
D. Glaucoma

Explanation: ***Conduction defect*** - Beta-blockers **slow heart rate** and **decrease AV nodal conduction**, which can worsen pre-existing conduction defects like **AV block** or **sick sinus syndrome**. - Their use can lead to **symptomatic bradycardia** or complete heart block in susceptible individuals. - This represents a **strong relative contraindication** requiring significant caution. *Hypertension* - Beta-blockers are a **first-line treatment for hypertension**, effectively lowering blood pressure by reducing cardiac output and renin release. - They are generally **well-tolerated** and beneficial in most hypertensive patients. *Glaucoma* - Topical beta-blockers, such as **timolol**, are a common treatment for open-angle glaucoma as they **reduce aqueous humor production**, thereby lowering intraocular pressure. - Systemic use of beta-blockers does not typically worsen glaucoma and may even offer some benefit. *CHF* - While certain beta-blockers (**carvedilol, metoprolol succinate, bisoprolol**) are now proven beneficial in **chronic heart failure with reduced ejection fraction (HFrEF)**, they do require careful use. - They must be **initiated at low doses and carefully titrated** to avoid acute decompensation, and are **contraindicated in acute decompensated heart failure**. - However, **conduction defects** represent a **stronger contraindication** where beta-blockers can cause life-threatening bradycardia or complete heart block, making it the best answer for conditions requiring the most caution.

Question 1056: Fenoldopam is used in the management of?

A. Hypertensive emergencies (Correct Answer)
B. Congestive heart failure
C. Migraine prophylaxis
D. Tachyarrhythmias

Explanation: ***Hypertensive emergencies*** - **Fenoldopam** is a **dopamine D1 receptor agonist** that causes rapid, dose-dependent peripheral vasodilation and increased renal blood flow, making it suitable for acute blood pressure reduction during hypertensive emergencies. - Its **rapid onset** and short half-life allow for precise control of blood pressure, and its **benefit** in preserving or improving renal function is particularly beneficial in patients with renal impairment. *Congestive heart failure* - While fenoldopam can increase renal blood flow, it is not a primary treatment for **congestive heart failure (CHF)** and is not typically used for its management. - Other drug classes, such as **diuretics**, **ACE inhibitors**, and **beta-blockers**, are the mainstays of CHF treatment. *Migraine prophylaxis* - Fenoldopam has **no role** in the prevention or acute treatment of migraines. - **Beta-blockers**, **calcium channel blockers**, and certain **antidepressants** are commonly used for migraine prophylaxis. *Tachyarrhythmias* - Fenoldopam **does not have antiarrhythmic properties** and is not indicated for the treatment of tachyarrhythmias. - **Beta-blockers**, **calcium channel blockers**, and specific **antiarrhythmic drugs** are used to manage tachyarrhythmias.

Question 1057: Which of the following is a lipid insoluble beta-blocker?

A. Timolol
B. Carvedilol
C. Pindolol
D. Celiprolol (Correct Answer)

Explanation: ***Celiprolol*** - **Celiprolol** is a **hydrophilic** (lipid-insoluble) beta-blocker, meaning it has low lipid solubility and does not readily cross the blood-brain barrier. - This property reduces the likelihood of **CNS side effects** such as nightmares and insomnia. *Timolol* - **Timolol** is a **lipophilic** (lipid-soluble) beta-blocker, allowing it to penetrate the central nervous system. - Its high lipid solubility contributes to a higher incidence of **CNS side effects**. *Carvedilol* - **Carvedilol** is a **lipophilic** mixed alpha and beta-blocker, which means it can cross the blood-brain barrier. - This can lead to central nervous system effects, although its primary clinical use is in heart failure and hypertension. *Pindolol* - **Pindolol** is a **lipophilic** beta-blocker with intrinsic sympathomimetic activity (ISA). - Its lipid solubility allows it to enter the brain, potentially causing **CNS-related side effects**.

Question 1058: Which of the following adverse effects of ACE inhibitors is primarily due to the inhibition of aldosterone secretion?

A. Hyperkalemia (Correct Answer)
B. Respiratory tract irritation
C. Facial swelling
D. Hypotension

Explanation: ***Hyperkalemia*** - **Angiotensin II** stimulates aldosterone secretion, and **ACE inhibitors** block angiotensin II formation, leading to reduced aldosterone. - **Aldosterone** promotes sodium reabsorption and potassium excretion in the renal tubules, so its reduction causes **potassium retention** and **hyperkalemia**. - This is the primary adverse effect mediated through the **aldosterone pathway**. *Respiratory tract irritation* - This is primarily due to the accumulation of **bradykinin** and **substance P** in the airways, not due to the inhibition of aldosterone. - ACE is responsible for bradykinin breakdown, so its inhibition leads to **bradykinin accumulation** causing cough. *Facial swelling* - This is a symptom of **angioedema**, which is related to the accumulation of **bradykinin** due to ACE inhibition, not due to aldosterone inhibition. - Bradykinin causes **vasodilation** and increased vascular permeability. *Hypotension* - While hypotension can occur with ACE inhibitors, it is primarily due to reduced formation of the potent vasoconstrictor **angiotensin II**, causing **decreased systemic vascular resistance**. - This is NOT primarily mediated through the aldosterone pathway, but through direct vascular effects.

Question 1059: What is the mechanism of action of ticagrelor?

A. Reversible inhibition of ADP action (Correct Answer)
B. Irreversible inhibition of ADP action
C. Reversible inhibition of GPIIb/IIIa
D. Irreversible inhibition of GPIIb/IIIa

Explanation: ***Reversible inhibition of ADP action*** - **Ticagrelor** is a **P2Y12 receptor antagonist** that works by preventing ADP from binding to its receptor on platelets [2]. - This binding is **reversible**, meaning ticagrelor can dissociate from the receptor, allowing for some recovery of platelet function over time [2]. *Irreversible inhibition of ADP action* - **Clopidogrel** and **prasugrel** are examples of **irreversible P2Y12 inhibitors**, forming a permanent bond with the receptor [2]. - Irreversible inhibition leads to a longer duration of platelet inhibition, as new platelets must be generated for function to return [2]. *Reversible inhibition of GPIIb/IIIa* - **GPIIb/IIIa inhibitors** like **eptifibatide** and **tirofiban** block the final common pathway of platelet aggregation by preventing fibrinogen binding [1]. - While their action is reversible, they target a *different* mechanism than ticagrelor. *Irreversible inhibition of GPIIb/IIIa* - **Abciximab** is a GPIIb/IIIa inhibitor that binds **irreversibly** (or with very slow dissociation) to the receptor [1]. - Unlike reversible GPIIb/IIIa inhibitors, abciximab is a monoclonal antibody with a prolonged antiplatelet effect [1]. - This is still an incorrect answer as ticagrelor targets the P2Y12 receptor, not GPIIb/IIIa.

Question 1060: Which class of antihypertensive drugs is known to cause erectile dysfunction?

A. Calcium channel blocker
B. ACE inhibitors
C. AT1 receptor antagonists
D. Beta-blockers (Correct Answer)

Explanation: ***Beta-blockers*** - **Beta-blockers** are the antihypertensive class most commonly associated with **erectile dysfunction** - Mechanism: Reduced cardiac output, decreased peripheral blood flow, central nervous system effects reducing libido, and blockade of β2-mediated vasodilation - **Non-selective beta-blockers** (propranolol, nadolol) have higher incidence of ED compared to selective β1-blockers (metoprolol, atenolol) - Newer vasodilating beta-blockers (nebivolol, carvedilol) have lower risk of sexual dysfunction *Calcium channel blockers* - Generally have **neutral or minimal effect** on erectile function - May even improve ED in some patients due to **vasodilatory properties** - Side effects include peripheral edema and headache, but not sexual dysfunction *ACE inhibitors* - Associated with **lower risk of erectile dysfunction** compared to other antihypertensives - May have neutral or even protective effects on sexual function - Preferred choice for hypertensive patients with existing sexual dysfunction concerns - Common side effects: dry cough and angioedema (not related to sexual function) *AT1 receptor antagonists* - **ARBs have neutral to potentially beneficial effects** on sexual function - Considered an excellent alternative for patients experiencing sexual side effects with other antihypertensive medications - Some studies suggest they may improve erectile function in hypertensive patients

Practice by Chapter

Antihypertensive Agents

Practice Questions

Drugs for Heart Failure

Practice Questions

Antiarrhythmic Drugs

Practice Questions

Antianginal Agents

Practice Questions

Lipid-Lowering Drugs

Practice Questions

Anticoagulants and Antiplatelet Drugs

Practice Questions

Thrombolytic Agents

Practice Questions

Drugs Used in Pulmonary Hypertension

Practice Questions

Drugs Used in Shock

Practice Questions

Cardiovascular Effects of Non-Cardiovascular Drugs

Practice Questions

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