Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 1071: Which of the following is NOT a side effect of digitalis?

A. Nausea and vomiting
B. Ventricular Bigeminy
C. Vasodilatation (Correct Answer)
D. Ventricular tachycardia

Explanation: **Vasodilatation** - **Digitalis**, primarily digoxin, is known for its **positive inotropic effect**, increasing myocardial contractility, and for its **vasoconstrictive properties** at higher doses due to sympathetic activation and direct smooth muscle effects, not vasodilatation. - While it can indirectly improve cardiac output and thus tissue perfusion, its direct vascular effects do not typically include widespread vasodilatation. *Ventricular tachycardia* - **Digitalis toxicity** can lead to various arrhythmias, including **ventricular tachycardia**, which is a potentially life-threatening side effect. - This occurs due to increased automaticity and delayed afterdepolarizations in ventricular myocytes. *Nausea and vomiting* - **Gastrointestinal symptoms** such as **nausea and vomiting** are common early signs of digitalis toxicity. - These effects are thought to be mediated by the drug's action on the chemoreceptor trigger zone in the brainstem. *Ventricular Bigeminy* - **Ventricular bigeminy**, characterized by alternating normal and premature ventricular beats, is another classic manifestation of **digitalis toxicity**. - This arrhythmia results from enhanced automaticity and altered conduction properties in the ventricles.

Question 1072: Which of the following statements about hypolipidemic drugs is false?

A. Gemfibrozil causes myopathy
B. Gemfibrozil can increase myopathy caused by statins
C. Lovastatin can cause hepatic dysfunction
D. Cholesterol reducing drugs are contraindicated in child less than 8 years (Correct Answer)

Explanation: ***Cholesterol reducing drugs are contraindicated in child less than 8 years*** - While cholesterol-lowering drugs are generally avoided in young children, there are specific **genetic dyslipidemias** where treatment may be initiated earlier under specialist supervision [1]. - The statement is **false** because some genetic conditions may necessitate earlier treatment, making a blanket contraindication for all children under 8 inaccurate [1]. *Gemfibrozil causes myopathy* - **Gemfibrozil** (a fibric acid derivative) can indeed cause **myopathy**, especially when used alone or in combination with other lipid-lowering agents [2]. - This adverse effect is thought to be due to its mechanism of action affecting fatty acid metabolism and muscle integrity. *Gemfibrozil can increase myopathy caused by statins* - The co-administration of **gemfibrozil** with **statins** significantly increases the risk of **myopathy** and **rhabdomyolysis** [2]. - This is primarily due to gemfibrozil inhibiting the **glucuronidation** of statins, which increases statin plasma concentrations [2]. *Lovastatin can cause hepatic dysfunction* - **Statins**, including **lovastatin**, can cause **elevations in liver transaminases** and, in rare cases, lead to **drug-induced liver injury** [1]. - Regular monitoring of liver function tests is recommended when initiating statin therapy and during follow-up [2].

Question 1073: What is the drug of choice for a classical angina attack?

A. CCBs
B. β-blocker
C. GTN (Correct Answer)
D. Prazosin

Explanation: ***GTN*** - **Glyceryl trinitrate (GTN)** is the drug of choice for immediate relief of a classical angina attack because it rapidly dilates coronary arteries and peripheral blood vessels, reducing **myocardial oxygen demand** and improving blood flow [2]. - Its **nitric oxide** mediated vasodilatory effects quickly alleviate chest pain by decreasing **preload** and afterload [2], [3]. *CCBs* - **Calcium channel blockers (CCBs)** are used for long-term prevention of angina by reducing myocardial oxygen demand, but they are not the first-line treatment for acute relief due to their slower onset of action [1]. - While they can dilate coronary arteries and reduce heart rate/contractility, their role is more in **prophylaxis** rather than acute symptom management [1]. *β-blocker* - **Beta-blockers** are primarily used for chronic management and prevention of angina by reducing heart rate, contractility, and blood pressure, thereby decreasing myocardial oxygen demand. - They are generally avoided for acute angina attacks as they do not provide rapid symptomatic relief and can potentially worsen symptoms in some acute ischemic conditions. *Prazocin* - **Prazosin** is an **alpha-1 adrenergic blocker** primarily used to treat hypertension and benign prostatic hyperplasia. - It causes vasodilation but is not indicated for the treatment of acute angina, as its mechanism of action and onset of effect are not suitable for rapid relief of myocardial ischemia.

Question 1074: Which of the following is a renin inhibitor?

A. Losartan
B. Benazepril
C. Remikiren (Correct Answer)
D. Imidapril

Explanation: **Remikiren** - **Remikiren** is a direct **renin inhibitor** that acts by binding to the active site of renin, preventing its interaction with angiotensinogen. - This inhibition reduces the formation of **angiotensin I** and subsequently **angiotensin II**, leading to decreased blood pressure. *Losartan* - **Losartan** is an **Angiotensin II Receptor Blocker (ARB)**, meaning it blocks AT1 receptors, preventing angiotensin II from binding. - It does not inhibit renin activity directly but rather acts downstream in the **renin-angiotensin-aldosterone system (RAAS)**. *Benazepril* - **Benazepril** is an **Angiotensin-Converting Enzyme (ACE) inhibitor**, which blocks the enzyme responsible for converting **angiotensin I** to **angiotensin II**. - It does not directly inhibit renin production or activity. *Imidapril* - **Imidapril** is also an **Angiotensin-Converting Enzyme (ACE) inhibitor**, similar to benazepril. - Its mechanism of action involves inhibiting ACE, thereby reducing **angiotensin II** levels, rather than directly inhibiting renin.

Question 1075: Drug of choice for familial hypercholesterolemia?

A. Nicotinic acid
B. Lovastatin (Correct Answer)
C. Cholestyramine
D. Gemfibrozil

Explanation: ***Lovastatin*** - **Statins** (HMG-CoA reductase inhibitors) are the **first-line therapy** for familial hypercholesterolemia as they effectively lower **LDL cholesterol** levels by inhibiting cholesterol synthesis [1]. - While other agents can be used adjunctively, statins like lovastatin are the cornerstone for managing this genetic condition [2]. *Nicotinic acid* - **Nicotinic acid** (niacin) primarily lowers **triglycerides** and increases **HDL cholesterol**, but it is less potent than statins for reducing LDL-C, especially in familial hypercholesterolemia [1]. - Its use is often limited by significant **side effects** like flushing. *Cholestyramine* - **Cholestyramine** is a **bile acid sequestrant** that binds to bile acids in the intestine, preventing their reabsorption and mildly lowering LDL cholesterol. - It is less effective than statins and often causes **gastrointestinal side effects** such as constipation and bloating. *Gemfibrozil* - **Gemfibrozil** is a **fibrate**, primarily used to lower **triglyceride levels** and increase HDL cholesterol. - It has minimal impact on LDL cholesterol compared to statins and is not the primary treatment for familial hypercholesterolemia [2].

Question 1076: Which of the following medications is most likely to cause reflex tachycardia?

A. Nifedipine (Correct Answer)
B. Verapamil
C. Propranolol
D. Amlodipine

Explanation: ***Nifedipine*** - Nifedipine is a **dihydropyridine calcium channel blocker** that causes significant peripheral vasodilation, leading to a rapid drop in blood pressure. - This sudden drop in blood pressure triggers a **baroreflex response**, compensatory increase in heart rate. *Verapamil* - Verapamil is a **non-dihydropyridine calcium channel blocker** that primarily acts on the cardiac pacemaker cells and slows AV nodal conduction. - While it can cause vasodilation, its direct negative chronotropic effect on the heart often **blunts or prevents reflex tachycardia**. *Propranolol* - Propranolol is a **non-selective beta-blocker** that blocks beta-1 and beta-2 adrenergic receptors. - It directly **decreases heart rate and myocardial contractility**, thereby preventing reflex tachycardia. *Amlodipine* - Amlodipine is a **dihydropyridine calcium channel blocker**, similar to nifedipine, but it has a **slower onset of action and a longer half-life**. - Its more gradual onset of vasodilation often results in a significantly **less pronounced or absent reflex tachycardia** compared to nifedipine.

Question 1077: Which of the following is not a cardioselective beta blocker?

A. Nebivolol
B. Atenolol
C. Betaxolol
D. Oxprenolol (Correct Answer)

Explanation: ***Oxprenolol*** - **Oxprenolol** is a non-selective beta-blocker with **intrinsic sympathomimetic activity (ISA)**, meaning it blocks both β1 and β2 receptors and partially stimulates them. - Its non-selective action means it affects both the heart (β1) and other organs like the lungs (β2), making it less suitable for patients with respiratory conditions. *Nebivolol* - **Nebivolol** is a highly cardioselective beta-blocker that primarily blocks **β1 receptors** and also has **vasodilatory properties** due to nitric oxide release. - Its high selectivity translates to fewer β2-mediated side effects, such as bronchoconstriction. *Atenolol* - **Atenolol** is a **cardioselective beta-blocker** that predominantly blocks **β1 receptors** at therapeutic doses. - This selectivity makes it a common choice for cardiovascular conditions, reducing the risk of bronchospasm compared to non-selective agents. *Betaxolol* - **Betaxolol** is a **cardioselective beta-blocker** primarily used for the treatment of hypertension and glaucoma. - It selectively blocks **β1 adrenergic receptors**, minimizing effects on the lungs compared to non-selective beta-blockers.

Question 1078: Which of the following is a second-generation beta blocker?

A. Timolol
B. Atenolol (Correct Answer)
C. Nadolol
D. Propranolol

Explanation: ***Atenolol*** - **Atenolol** is a **second-generation beta blocker** characterized by its **cardioselectivity**, meaning it primarily blocks beta-1 receptors in the heart. - This selectively reduces heart rate and contractility with fewer respiratory side effects compared to non-selective agents. *Propranolol* - **Propranolol** is a **first-generation non-selective beta blocker**, meaning it blocks both beta-1 and beta-2 adrenergic receptors. - Its non-selective action can cause significant bronchoconstriction, making it less suitable for patients with respiratory conditions. *Timolol* - **Timolol** is also a **first-generation non-selective beta blocker** commonly used in ophthalmic preparations for glaucoma. - It blocks both beta-1 and beta-2 receptors and does not possess the cardioselectivity of second-generation agents. *Nadolol* - **Nadolol** is another **first-generation non-selective beta blocker** with a long duration of action due to its extensive plasma half-life. - Like other first-generation agents, it lacks cardioselectivity and blocks both beta-1 and beta-2 receptors.

Question 1079: Which beta-1 antagonist is used in congestive cardiac failure?

A. Atenolol
B. Metoprolol (Correct Answer)
C. Esmolol
D. Bisoprolol

Explanation: ***Metoprolol*** - **Metoprolol succinate** (extended-release formulation) is a selective **beta-1 antagonist** proven to reduce mortality and hospitalizations in **chronic heart failure with reduced ejection fraction (HFrEF)**. - It works by **reducing heart rate, myocardial oxygen demand**, and preventing adverse cardiac remodeling through inhibition of chronic sympathetic activation. - Along with **bisoprolol and carvedilol**, it is one of the **three beta-blockers with proven mortality benefit** in heart failure trials. *Atenolol* - While atenolol is a selective beta-1 antagonist, it **lacks evidence for mortality benefit** in heart failure. - It has **high hydrophilicity** and renal elimination, leading to less favorable pharmacokinetics compared to metoprolol. - More commonly used for **hypertension and angina** rather than heart failure management. *Esmolol* - **Esmolol** is an ultra-short-acting selective beta-1 antagonist used for **acute control of heart rate** in perioperative and critical care settings. - Its **very short half-life (9 minutes)** makes it unsuitable for chronic management of heart failure. - Administered only **intravenously** and requires continuous infusion. *Bisoprolol* - While **bisoprolol is also approved** for heart failure and has proven mortality benefit (CIBIS-II trial), this question likely expects **metoprolol** as the answer given the historical context. - Both bisoprolol and metoprolol are acceptable answers, but **metoprolol** has been more widely studied and is more commonly cited in Indian medical exams. - Bisoprolol has **greater beta-1 selectivity** than metoprolol but similar clinical outcomes in heart failure.

Question 1080: What is the correct sequence of medication administration for pre-operative prophylaxis in pheochromocytoma?

A. Beta blockade followed by alpha blockade
B. Simultaneous alpha and beta blockade
C. Alpha blockade followed by beta blockade (Correct Answer)
D. Alpha blockade only

Explanation: ***Alpha blockade followed by beta blockade*** - **Alpha blockade** should always be initiated first to control **hypertension** and prevent a **hypertensive crisis** during surgery. This is critical because pheochromocytoma causes excessive catecholamine release, leading to profound vasoconstriction. - **Beta blockade** is then added only after adequate alpha blockade has been achieved to control **tachycardia** and arrhythmias, preventing **unopposed alpha-adrenergic stimulation** which could paradoxically worsen hypertension. *Simultaneous alpha and beta blockade* - Administering both simultaneously is dangerous because **beta blockade** can mask the effects of inadequate alpha blockade. - This can lead to **unopposed alpha-adrenergic stimulation** after beta blockade, causing severe **vasoconstriction** and hypertensive crisis. *Beta blockade followed by alpha blockade* - Initiating with **beta blockade** without prior **alpha blockade** is absolutely contraindicated in pheochromocytoma. - This can lead to severe and potentially fatal **hypertension** due to **unopposed alpha-adrenergic stimulation** as beta blockade prevents vasodilation. *Alpha blockade only* - While essential for initial management, **alpha blockade alone** might not fully control all symptoms, especially **tachycardia** and **arrhythmias** caused by high circulating catecholamine levels. - Adding a **beta blocker** after achieving adequate alpha blockade helps in controlling these cardiac effects, optimizing patient preparation for surgery.

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

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Cardiovascular Effects of Non-Cardiovascular Drugs

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