Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 971: A patient who is on treatment for hyperlipidemia develops gallstones. What is the mechanism of action of the causative drug that was given to this patient?

A. Binds to deoxycholic acid
B. Decreases VLDL
C. Activates PPAR alpha (Correct Answer)
D. Inhibits HMG CoA reductase

Explanation: ***Activates PPAR alpha*** * Activation of **PPAR alpha (Peroxisome Proliferator-Activated Receptor alpha)** by fibrates can lead to increased cholesterol secretion into bile [1]. * This increased biliary cholesterol saturation predisposes patients to **cholesterol gallstone** formation. *Decreases VLDL* * While fibrates do decrease **VLDL (Very Low-Density Lipoprotein)** production, this specific action is not the primary mechanism by which they cause gallstones [1]. * The reduction in VLDL is beneficial for triglyceride lowering, but the gallstone risk relates to cholesterol metabolism. *Binds to deoxycholic acid* * This mechanism is characteristic of **bile acid sequestrants** like cholestyramine, which bind to bile acids in the gut to prevent their reabsorption. * Bile acid sequestrants are not typically associated with an increased risk of gallstones; in fact, they can sometimes be used to reduce gallstones in specific contexts. *Inhibits HMG CoA reductase* * This is the mechanism of action for **statins**, which are highly effective in lowering LDL cholesterol by inhibiting the rate-limiting enzyme in cholesterol synthesis [2]. * Statins are not generally associated with an increased risk of gallstones; some studies even suggest a potential protective effect [3].

Question 972: Which among the following is the false statement regarding statins?

A. These drugs should not be stopped even in severe conditions like injury, surgery etc.
B. Although HMG-CoA reductase inhibitors substantially reduce the risk of cardiovascular events, there is mild increase in lipoprotein a (Lpa) levels.
C. With the long term use, there is slight increase in the incidence of type 2 diabetes mellitus.
D. They can be given with verapamil and other enzyme inhibitors (Correct Answer)

Explanation: ***They can be given with verapamil and other enzyme inhibitors*** - This statement is **FALSE** and is the correct answer because **verapamil** (a moderate CYP3A4 inhibitor) and other potent CYP3A4 inhibitors like **clarithromycin** or **azole antifungals** can significantly increase statin concentrations, raising the risk of adverse effects like **myopathy** and **rhabdomyolysis**. - **Co-administration** of statins with these inhibitors generally requires careful dose adjustments or avoidance, as they increase the systemic exposure to most statins (especially **simvastatin**, **atorvastatin**, and **lovastatin**). *These drugs should not be stopped even in severe conditions like injury, surgery etc.* - This statement could be considered false in certain contexts, as statins **can be temporarily held** in acute, severe conditions like sepsis, major trauma, or complex surgery, especially if there's a concern for **acute kidney injury** or **rhabdomyolysis** [1]. - However, in most routine surgical situations, statins are typically continued due to their cardiovascular protective effects. *Although HMG-CoA reductase inhibitors substantially reduce the risk of cardiovascular events, there is mild increase in lipoprotein a (Lpa) levels.* - This statement is **TRUE**. Statins are associated with a **modest increase in Lp(a) levels** (approximately 10-20%), which has been consistently demonstrated in clinical studies [2]. - While statins effectively lower **LDL cholesterol**, Lp(a) levels are largely **genetically determined** and may paradoxically increase with statin therapy, though this effect is generally considered clinically insignificant compared to the overall cardiovascular benefits [2]. *With the long term use, there is slight increase in the incidence of type 2 diabetes mellitus.* - This statement is **TRUE**. Long-term statin use is associated with a **small but statistically significant increase** in the risk of developing **type 2 diabetes mellitus** (approximately 9-12% increased risk), particularly in individuals with pre-existing risk factors like **metabolic syndrome**. - This risk, however, is generally **outweighed by the cardiovascular benefits** of statin therapy in at-risk patients, making it an acceptable trade-off.

Question 973: Preferred drug for the treatment of ventricular tachycardia is

A. Digoxin
B. Propranolol
C. Diltiazem
D. Lignocaine (Correct Answer)

Explanation: ***Lignocaine*** *(Historical Answer for FMGE-2019)* - **Lignocaine** (also known as **lidocaine**) is a **Class IB antiarrhythmic** drug that was historically the preferred treatment for **ventricular tachycardia (VT)**, especially in patients with **ischemic heart disease**. - It works by **blocking sodium channels** in the heart, specifically targeting depolarized or partially depolarized cells, which helps to stabilize the ventricular rhythm. - **⚠️ IMPORTANT UPDATE:** Current guidelines (AHA/ACC 2015 onwards) now recommend **amiodarone as the first-line antiarrhythmic** for hemodynamically stable VT, with lignocaine as a **second-line alternative**. This question reflects the teaching prevalent at the time of FMGE-2019. *Digoxin* - **Digoxin** is a **cardiac glycoside** primarily used for **atrial fibrillation** with rapid ventricular response and **heart failure**. - It is **not the preferred drug** for ventricular tachycardia and can even precipitate arrhythmias in some cases. *Propranolol* - **Propranolol** is a **beta-blocker** (Class II antiarrhythmic) typically used to treat **supraventricular tachycardias**, **hypertension**, and **angina**. - While beta-blockers can have some role in preventing recurrent VT, they are **not the first-line treatment** for acute VT. *Diltiazem* - **Diltiazem** is a **calcium channel blocker** (Class IV antiarrhythmic) primarily used for **supraventricular tachycardias** and to control ventricular rate in **atrial fibrillation**. - It is **not effective** for ventricular tachycardia and may worsen the condition in some cases.

Question 974: Which of the following drug causes postural hypotension commonly?

A. Alpha blocker (Correct Answer)
B. Angiotensin receptor blockers
C. Beta blocker
D. ACE inhibitor

Explanation: ***Alpha blocker*** - **Alpha-1 adrenergic blockers** cause common postural hypotension by blocking **alpha-1 receptors** on vascular smooth muscle, leading to vasodilation and reduced peripheral vascular resistance. - This vasodilation, especially in the upright position, can cause blood to pool in the lower extremities, decreasing venous return to the heart and thus lowering blood pressure. *Angiotensin receptor blockers* - These drugs block the effects of **angiotensin II**, leading to vasodilation and decreased aldosterone secretion, typically causing a more gradual and less pronounced drop in blood pressure. - While they can cause hypotension, **postural hypotension** is less common and usually less severe compared to alpha blockers due to their different mechanism of action and less abrupt vasodilation. *Beta blocker* - **Beta-blockers** primarily reduce heart rate and myocardial contractility, thereby decreasing cardiac output, which can contribute to generalized hypotension. - They do not directly cause significant **vasodilation** in the same manner as alpha-blockers, making postural hypotension less common unless there are other contributing factors. *ACE inhibitor* - **ACE inhibitors** prevent the conversion of angiotensin I to **angiotensin II**, leading to vasodilation and reduced aldosterone. - They can cause hypotension, especially with the first dose or in volume-depleted patients, but **postural hypotension** is typically less frequent and severe than with alpha-blockers.

Question 975: The drug that causes fall in elderly patients with postural hypotension is:-

A. Acarbose
B. Prazosin (Correct Answer)
C. Nor-adrenaline
D. Metformin

Explanation: ***Prazosin*** - **Alpha-1 adrenergic blocker** used to treat hypertension and benign prostatic hyperplasia (BPH) - Commonly causes **orthostatic hypotension (postural hypotension)** as a side effect by blocking alpha-1 receptors on vascular smooth muscle, preventing compensatory vasoconstriction upon standing - Leads to **dizziness, lightheadedness, and falls**, especially in elderly patients who have reduced baroreceptor sensitivity - **First-dose phenomenon** is particularly notable, with marked hypotension after the initial dose *Acarbose* - Alpha-glucosidase inhibitor used to treat type 2 diabetes by reducing carbohydrate absorption in the intestine - Primary side effects are **gastrointestinal** (flatulence, diarrhea, abdominal discomfort) - Does not affect blood pressure or cause postural hypotension *Nor-adrenaline (Norepinephrine)* - **Vasopressor** and sympathomimetic agent that causes vasoconstriction through alpha-adrenergic receptor stimulation - **Increases blood pressure** and is used to treat severe hypotension in critical care settings - Would not cause falls due to postural hypotension; rather, it counteracts hypotension *Metformin* - **Biguanide** oral hypoglycemic agent for type 2 diabetes that primarily decreases hepatic glucose production and increases insulin sensitivity - Main side effects include gastrointestinal disturbances and rare lactic acidosis - Not associated with postural hypotension or increased risk of falls

Question 976: Which of the following is a direct renin inhibitor?

A. Perindopril
B. Losartan
C. Vernakalant
D. Aliskiren (Correct Answer)

Explanation: ***Aliskiren*** - **Aliskiren** directly inhibits **renin**, the enzyme responsible for initiating the **renin-angiotensin-aldosterone system (RAAS)**, by preventing the conversion of **angiotensinogen to angiotensin I**. - This mechanism of action is distinct from other RAAS inhibitors that act further down the pathway. *Perindopril* - **Perindopril** is an **ACE inhibitor**, which works by blocking the enzyme that converts **angiotensin I to angiotensin II**. - It does not directly inhibit **renin** activity. *Losartan* - **Losartan** is an **angiotensin receptor blocker (ARB)**, which works by preventing **angiotensin II** from binding to its receptors. - It does not directly inhibit **renin** and primarily acts by blocking the effects of already formed **angiotensin II**. *Vernakalant* - **Vernakalant** is an antiarrhythmic drug primarily used for the acute conversion of **atrial fibrillation**. - It works by blocking specific **potassium and sodium channels** in the atria, and has no direct activity on the **renin-angiotensin-aldosterone system**.

Question 977: Coronary steal syndrome is associated with

A. Sevoflurane
B. Halothane
C. Isoflurane (Correct Answer)
D. Desflurane

Explanation: ***Isoflurane*** - **Isoflurane** is a potent coronary vasodilator which can cause coronary steal syndrome in patients with existing **coronary artery disease**. - It preferentially dilates normal coronary arteries, diverting blood flow away from stenotic areas, potentially worsening **myocardial ischemia**. *Sevoflurane* - **Sevoflurane** is also a vasodilator but is generally considered to have a lower risk of coronary steal compared to isoflurane. - Its vasodilatory effects are less pronounced in diseased arteries, making it a safer option for patients with **ischemic heart disease**. *Halothane* - **Halothane** is known for myocardial depression and arrhythmias, but its coronary dilating properties are less pronounced and it is infrequently associated with coronary steal. - It is an older inhalational anesthetic that has largely been replaced due to its side effect profile, including potential **hepatotoxicity**. *Desflurane* - **Desflurane** is a potent vasodilator, similar to isoflurane, but it typically causes peripheral vasodilation rather than significant coronary steal. - Its rapid onset and offset are beneficial, but it can cause **tachycardia** and **hypertension** with rapid increases in concentration.

Question 978: Drug of choice in cardiogenic shock is

A. Noradrenaline
B. Dopamine (Correct Answer)
C. Adrenaline
D. Phenylephrine

Explanation: ***Dopamine*** - **Dopamine** is often considered the **drug of choice** in cardiogenic shock because, at low to moderate doses, it increases myocardial contractility and heart rate (positive inotropic and chronotropic effects) while also improving renal perfusion. - Its ability to stimulate **alpha-1, beta-1, and dopaminergic receptors** makes it effective in improving cardiac output and maintaining organ perfusion in this critical condition. *Phenylephrine* - **Phenylephrine** is a selective **alpha-1 adrenergic agonist** that causes potent vasoconstriction and increases systemic vascular resistance. - While it effectively raises blood pressure, it **lacks inotropic effects** and can actually **reduce cardiac output** through reflex bradycardia and increased afterload. - Its strong vasoconstrictive effects without inotropic support make it **not suitable** as a primary agent in cardiogenic shock where cardiac contractility is already compromised. *Noradrenaline* - **Noradrenaline (norepinephrine)** is a potent vasoconstrictor primarily acting on alpha-1 receptors, leading to a significant increase in systemic vascular resistance and blood pressure. - While useful in some forms of shock, its strong vasoconstrictive effect can **increase afterload** and potentially worsen myocardial oxygen demand in cardiogenic shock with already compromised cardiac function. *Adrenaline* - **Adrenaline (epinephrine)** has strong **beta-1 and alpha-1 agonist effects**, leading to increased heart rate, contractility, and vasoconstriction. - While it can improve blood pressure and cardiac output, its significant **chronotropic and arrhythmogenic effects**, along with increased myocardial oxygen demand, make it less favorable than dopamine as a first-line agent in cardiogenic shock.

Question 979: Which of the following drugs decreases plasma renin activity

A. Nifedipine
B. Hydralazine
C. Enalapril
D. Clonidine (Correct Answer)

Explanation: ***Clonidine*** - **Clonidine** is a centrally acting alpha-2 adrenergic agonist that reduces **sympathetic outflow** from the brainstem. - This reduction in sympathetic activity leads to decreased release of **norepinephrine**, which in turn reduces renin secretion by the kidneys. *Nifedipine* - **Nifedipine** is a **dihydropyridine calcium channel blocker** that causes peripheral vasodilation. - The vasodilation often leads to a **reflex increase in sympathetic activity** and, consequently, an increase in plasma renin activity. *Hydralazine* - **Hydralazine** is a direct systemic **vasodilator** that decreases peripheral vascular resistance. - This vasodilation can cause a **reflex increase in sympathetic activity** and **renin release** as the body tries to compensate for the drop in blood pressure. *Enalapril* - **Enalapril** is an **ACE inhibitor** that blocks the conversion of angiotensin I to angiotensin II. - This action directly leads to **increased plasma renin activity** due to the disruption of the negative feedback loop on renin release.

Question 980: Intravenous furosemide is used for rapid control of symptoms in acute left ventricular failure. It provides quick relief of dyspnoea by :

A. Causing venodilation (Correct Answer)
B. Producing bronchodilation
C. Stimulating left ventricular contractility
D. Causing rapid diuresis and reducing circulating blood volume

Explanation: ***Causing venodilation*** - Furosemide, even before significant diuresis, causes rapid **venodilation**, leading to a decrease in **preload** and pulmonary congestion. This reduces the work of the heart and alleviates dyspnoea. - This effect is mediated by the release of **prostaglandins** and is observed within minutes of intravenous administration. *Producing bronchodilation* - Furosemide does not directly cause bronchodilation; it primarily acts on the kidneys and vasculature. - While improved pulmonary edema can secondarily ease breathing, its quick relief of dyspnoea is not due to direct airway relaxation. *Stimulating left ventricular contractility* - Furosemide is a loop diuretic and does not directly enhance **myocardial contractility**; it is not an inotropic agent. - In fact, by reducing preload and afterload, it can indirectly reduce the immediate demand on the failing ventricle. *Causing rapid diuresis and reducing circulating blood volume* - While furosemide does cause rapid diuresis and a reduction in circulating blood volume, these effects typically take longer to fully manifest (around 30 minutes to an hour) when compared to the immediate relief of dyspnoea seen after IV administration. - The initial rapid relief of dyspnoea is attributed more to its vasodilatory properties, reducing cardiac preload.

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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