Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 981: Plasma Renin activity is lowered by which of the following group of drugs?

A. Arteriolar dilators
B. Alpha 2 agonists (Correct Answer)
C. Calcium channel blockers
D. ACE inhibitors

Explanation: ***Alpha 2 agonists*** - **Alpha-2 agonists** (e.g., clonidine) work by stimulating central alpha-2 adrenergic receptors, which reduces **sympathetic outflow** from the CNS. - This reduction in sympathetic tone decreases **renin release** from the juxtaglomerular cells in the kidney, thereby lowering plasma renin activity. *Arteriolar dilators* - **Arteriolar dilators** (e.g., hydralazine, minoxidil) decrease peripheral vascular resistance and lower blood pressure. - This reduction in blood pressure and renal perfusion can activate the **renin-angiotensin-aldosterone system (RAAS)**, leading to an **increase** in plasma renin activity as a compensatory mechanism. *Calcium channel blockers* - **Calcium channel blockers** (e.g., nifedipine, amlodipine) directly relax vascular smooth muscle and reduce peripheral resistance. - Some calcium channel blockers, particularly **dihydropyridines**, can cause reflex sympathetic activation due to vasodilation, potentially **increasing** renin release. *ACE inhibitors* - **ACE inhibitors** (e.g., enalapril, lisinopril) block the conversion of angiotensin I to angiotensin II. - By inhibiting the negative feedback that angiotensin II typically exerts on renin release, ACE inhibitors actually lead to an **increase** in plasma renin activity.

Question 982: Drug used for euvolemic hyponatremia in patient with advanced congestive heart failure is?

A. Nesiritide
B. Tolvaptan (Correct Answer)
C. Metoprolol
D. Hydrocortisone

Explanation: ***Tolvaptan*** - **Tolvaptan** is a selective **vasopressin V2-receptor antagonist** that promotes free water excretion (aquaresis) without significantly altering electrolyte balance, making it suitable for euvolemic hyponatremia [1]. - It works by blocking the action of **antidiuretic hormone (ADH)**, which is often elevated in patients with **congestive heart failure (CHF)** leading to water retention and hyponatremia [2]. *Nesiritide* - **Nesiritide** is a **recombinant human B-type natriuretic peptide (BNP)** that causes vasodilation and diuresis, but it is primarily used for acutely decompensated heart failure with signs of congestion, not specifically for euvolemic hyponatremia [1]. - While it can induce diuresis, its main role is to reduce **preload** and **afterload**, and it does not directly target the mechanism of euvolemic hyponatremia as effectively as an aquaretic agent [1]. *Metoprolol* - **Metoprolol** is a **beta-blocker** used to reduce heart rate and blood pressure, improving cardiac function in CHF patients. - It does not directly address **hyponatremia** and its mechanism of action is unrelated to water balance or sodium concentration. *Hydrocortisone* - **Hydrocortisone** is a **corticosteroid** used for conditions like adrenal insufficiency, inflammation, or allergic reactions. - It has no direct role in the management of **hyponatremia** or **congestive heart failure**.

Question 983: The cardiovascular side effects of Dexmedetomidine are as follows:

A. Hypertension and Tachycardia
B. Hypertension and Bradycardia
C. Hypotension and Bradycardia (Correct Answer)
D. Hypotension and Tachycardia

Explanation: ***Hypotension and Bradycardia*** - **Dexmedetomidine** is an **alpha-2 adrenergic agonist** that causes a dose-dependent decrease in heart rate (bradycardia) and blood pressure (hypotension) due to reduced sympathetic outflow. - The initial hypertensive effect seen with rapid IV administration is usually transient and followed by sustained hypotension. *Hypertension and Tachycardia* - This combination is not typical for **dexmedetomidine**, which primarily exerts its effects by centrally reducing sympathetic tone, leading to lowered heart rate and blood pressure. - **Tachycardia** is a rare and usually reflex-mediated response if severe hypotension occurs, but it's not a primary effect. *Hypertension and Bradycardia* - While an initial, transient **hypertension** can occur with rapid **dexmedetomidine** infusion due to peripheral alpha-2 stimulation, this is not its predominant long-term cardiovascular effect. - The sustained effect is usually **hypotension**, not hypertension, making this option incorrect as a primary side effect. *Hypotension and Tachycardia* - Although **hypotension** is a common side effect of **dexmedetomidine**, **tachycardia** is generally not. - The drug mainly causes a reduction in heart rate (**bradycardia**) as part of its central sympatholytic action.

Question 984: Hypokalemia is seen in therapy with

A. Diazepam
B. Corticosteroids (Correct Answer)
C. Ibuprofen
D. Digitalis

Explanation: ***Corticosteroids*** - **Corticosteroids** can cause **hypokalemia** due to their mineralocorticoid activity, which promotes renal potassium excretion. - This effect is often dose-dependent and more pronounced with certain corticosteroids like **fludrocortisone** or high doses of prednisolone. *Diazepam* - **Diazepam** is a **benzodiazepine** that acts on GABA receptors in the brain. - It primarily causes central nervous system effects like sedation and anxiolysis, without directly affecting **potassium levels**. *Ibuprofen* - **Ibuprofen** is a **non-steroidal anti-inflammatory drug (NSAID)**. - It can lead to **renal dysfunction** and **fluid retention**, but it does not directly cause **hypokalemia**. *Digitalis* - **Digitalis** (digoxin) is a cardiac glycoside used to treat **heart failure** and **arrhythmias**. - While **hypokalemia** can exacerbate **digitalis toxicity**, digitalis therapy itself does not significantly cause **hypokalemia**; rather, it's a critical electrolyte to monitor.

Question 985: Ductus arteriosus closes in response to ?

A. Decrease in peripheral oxygen saturation
B. Indomethacin therapy (Correct Answer)
C. Increase in pulmonary vascular resistance
D. Prostaglandin E1

Explanation: ***Indomethacin therapy*** - **Indomethacin** is a **prostaglandin synthesis inhibitor**, which reduces the levels of prostaglandins (specifically **PGE2**) that keep the ductus arteriosus open. - Its use, particularly in premature infants, promotes the **constriction and functional closure** of the ductus arteriosus. *Decrease in peripheral oxygen saturation* - **Low oxygen saturation** during fetal life actually helps to **keep the ductus arteriosus open** by maintaining vasodilation. - An **increase in oxygen saturation** after birth is a key trigger for ductal closure. *Increase in pulmonary vascular resistance* - An **increase in pulmonary vascular resistance** is a characteristic of pulmonary hypertension and would **impede pulmonary blood flow**, potentially causing blood to shunt through a patent ductus arteriosus (PDA) from the aorta to the pulmonary artery, or even worsen right-to-left shunting. - Normal physiological changes after birth involve a **decrease in pulmonary vascular resistance**, which contributes to the closure of the ductus arteriosus. *Prostaglandin E1* - **Prostaglandin E1 (PGE1)** is a potent **vasodilator** that is used therapeutically to **maintain the patency of the ductus arteriosus** in infants with certain congenital heart defects. - Its presence **prevents closure**, rather than promoting it.

Question 986: Effect of dopamine on renal vessels?

A. Increased permeability
B. No effect
C. Vasodilatation (Correct Answer)
D. Vasoconstriction

Explanation: ***Vasodilatation*** - Dopamine, at **low doses**, acts on D1 receptors in the renal vasculature, leading to **renal vasodilation**. - This effect increases **renal blood flow** and **glomerular filtration rate**, improving kidney perfusion. *Increased permeability* - **Increased permeability** of renal vessels is not a primary direct effect of dopamine but rather a feature of inflammatory processes or damage. - This typically leads to protein leakage, which is distinct from dopamine's hemodynamic actions. *No effect* - This option is incorrect because dopamine has distinct and well-documented effects on renal vessels. - Dopamine is commonly used in clinical practice for its **pharmacological effects** on the kidneys, such as increasing urine output and renal blood flow. *Vasoconstriction* - While dopamine can cause vasoconstriction at **high doses** by activating alpha-1 adrenergic receptors, its primary and most significant effect on renal vessels at **lower, therapeutic doses** is vasodilation. - **Vasoconstriction** would decrease renal blood flow, which is contrary to the desired effect of dopamine in renal support.

Question 987: All are vasodilators except –

A. Lidocaine
B. Procaine
C. Bupivacaine
D. Cocaine (Correct Answer)

Explanation: ***Cocaine*** - Cocaine is unique among local anesthetics because it causes **vasoconstriction** rather than vasodilation. - This vasoconstrictive effect is due to its blocking of **norepinephrine reuptake** at adrenergic nerve terminals, leading to an accumulation of norepinephrine and subsequent adrenergic stimulation. *Lidocaine* - Lidocaine is a common **amide-type local anesthetic** known for its vasodilatory properties that contribute to its systemic absorption. - Its vasodilatory effect can lead to a **flushing** sensation and increased blood flow in the area of injection. *Procaine* - Procaine is an **ester-type local anesthetic** that causes vasodilation, which results in a relatively short duration of action. - This vasodilation increases **local blood flow**, speeding up the systemic absorption and metabolism of the drug. *Bupivacaine* - Bupivacaine is an **amide-type local anesthetic** with longer duration of action compared to lidocaine, and like most local anesthetics, it causes vasodilation. - The vasodilatory effect of bupivacaine can lead to increased **systemic absorption** and potential for systemic toxicity if not managed carefully.

Question 988: All of the following may precipitate digitalis toxicity except :

A. Hypocalcemia (Correct Answer)
B. Hypomagnesemia
C. Hypokalemia
D. Hypothyroidism

Explanation: ***Hypocalcemia*** - **Hypocalcemia** actually **antagonizes** the effects of digitalis, thereby *reducing* the risk of toxicity. - Digitalis primarily acts by inhibiting the **Na+/K+-ATPase pump**, leading to increased intracellular calcium, while hypocalcemia would counteract this increase. *Hypomagnesemia* - **Hypomagnesemia** can precipitate digitalis toxicity because magnesium normally **competes with calcium** for binding sites and also helps regulate the **Na+/K+-ATPase pump**. - A deficiency in magnesium can enhance the overall proarrhythmic effects of digitalis. *Hypokalemia* - **Hypokalemia** significantly increases the risk of digitalis toxicity as digitalis normally binds to the **K+ binding site** on the Na+/K+-ATPase pump. - Lower extracellular potassium levels allow more **digitalis to bind** to the pump, increasing its inhibitory effects and intracellular calcium. *Hypothyroidism* - Patients with **hypothyroidism** have a **reduced metabolism** of digitalis, leading to higher serum drug levels at standard doses. - This slower clearance necessitates a **lower maintenance dose** of digitalis in hypothyroid patients to avoid toxicity.

Question 989: A patient with pulmonary fibrosis comes to the emergency with arrhythmia. Which anti-arrhythmic drug should be avoided?

A. Lignocaine
B. Procainamide
C. Verapamil
D. Amiodarone (Correct Answer)

Explanation: ***Amiodarone*** - **Amiodarone** is known to cause **pulmonary toxicity** as a significant adverse effect, which can exacerbate pre-existing **pulmonary fibrosis**. - Its long half-life and **iodine content** contribute to its potential for delayed and severe pulmonary side effects, making it contraindicated in patients with existing lung disease. *Lignocaine* - **Lignocaine** (lidocaine) is a **Class IB antiarrhythmic** primarily used for **ventricular arrhythmias** and is generally safe in patients with pulmonary disease as it does not have significant pulmonary side effects. - Its main toxicities involve the **central nervous system** and cardiovascular system (at high doses). *Procainamide* - **Procainamide** is a **Class IA antiarrhythmic** that can be used for both **atrial and ventricular arrhythmias**, and it does not typically cause pulmonary toxicity. - Potential side effects include a **lupus-like syndrome**, agranulocytosis, and cardiotoxicity, none of which are exacerbated by pulmonary fibrosis. *Verapamil* - **Verapamil** is a **non-dihydropyridine calcium channel blocker** used for **supraventricular tachycardias** and rate control in atrial fibrillation, which does not have significant pulmonary side effects. - Its main concerns relate to **cardiac depression** and **hypotension**, but it is not contraindicated in the context of pulmonary fibrosis.

Question 990: Hypertension and pulmonary edema associated with scorpion sting is managed by :-

A. Prazosin (Correct Answer)
B. Phentolamine
C. Spironolactone
D. Carvedilol

Explanation: ***Prazosin*** - **Prazosin** is an **alpha-1 adrenergic receptor blocker** that causes vasodilation, reducing both preload and afterload, which is crucial in managing scorpion sting-induced **hypertension** and **pulmonary edema** [1]. - It effectively counteracts the massive catecholamine release triggered by scorpion venom, which leads to widespread vasoconstriction and increased cardiac workload [1]. *Phentolamine* - **Phentolamine** is a non-selective alpha-adrenergic blocker, but it has a shorter duration of action and is typically used for managing **hypertensive crises** during pheochromocytoma surgery. - While it can lower blood pressure, its rapid onset and short half-life make it less suitable for sustained management of scorpion sting complications compared to prazosin. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist** and a potassium-sparing diuretic, primarily used in conditions like heart failure, cirrhosis, and primary hyperaldosteronism. - It is not an acute treatment for hypertension or pulmonary edema caused by scorpion venom, as its mechanism of action is too slow and indirect to counteract the immediate effects of catecholamine surge. *Carvedilol* - **Carvedilol** is a non-selective beta-blocker with alpha-1 blocking activity, commonly used in chronic heart failure and hypertension [2]. - While it has some alpha-blocking properties, its dominant **beta-blocking effects** can exacerbate pulmonary edema in an acute setting and may worsen cardiac output if bradycardia or myocardial depression occurs [2].

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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free