Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 661: What is the primary reason for using aspirin in the prophylaxis of myocardial infarction (MI)?

A. It possesses analgesic properties.
B. It exhibits antiplatelet action. (Correct Answer)
C. It has a sedative effect.
D. It inhibits prostaglandin synthesis.

Explanation: ### Explanation **1. Why Option B is Correct:** The primary mechanism for myocardial infarction (MI) is the rupture of an atherosclerotic plaque, which triggers platelet aggregation and subsequent thrombus formation in the coronary arteries. Aspirin (Acetylsalicylic acid) acts as an **irreversible inhibitor of the enzyme Cyclooxygenase-1 (COX-1)**. This inhibition prevents the synthesis of **Thromboxane A2 (TXA2)**, a potent platelet aggregator and vasoconstrictor. By inhibiting TXA2, aspirin reduces platelet "stickiness," preventing the formation of an occlusive clot. This antiplatelet effect is achieved at low doses (75–150 mg/day). **2. Why Other Options are Incorrect:** * **Option A:** While aspirin is an analgesic, pain relief is not the goal of *prophylaxis*. In an acute MI, stronger analgesics like Morphine are preferred. * **Option C:** Aspirin has no sedative properties; it does not act on the CNS to induce sleep or calmness. * **Option D:** While aspirin *does* inhibit prostaglandin synthesis, this is a broad pharmacological mechanism. The **specific** reason for its use in MI prophylaxis is the downstream effect on platelets (antiplatelet action), not general anti-inflammatory or prostaglandin inhibition. **3. NEET-PG High-Yield Pearls:** * **Irreversibility:** Aspirin is the only NSAID that binds irreversibly to COX; the effect lasts for the life of the platelet (7–10 days). * **Dose-Dependent Effect:** Low doses (75–150 mg) selectively inhibit TXA2, whereas high doses inhibit Prostacyclin (PGI2), which is a vasodilator and anti-aggregator. * **Primary vs. Secondary Prophylaxis:** Aspirin is a cornerstone for secondary prophylaxis (preventing a second MI) and is used selectively in primary prophylaxis for high-risk patients. * **Side Effect:** Watch for **Reye’s Syndrome** in children and **Aspirin-induced Asthma** (due to leukotriene shift).

Question 662: Cardiac glycosides are obtained from which plant source?

A. Rauwolfia serpentina.
B. Strophanthus gratus. (Correct Answer)
C. Ricinus communis.
D. Atropa belladonna.

Explanation: **Explanation:** **Cardiac glycosides** (like Digoxin and Ouabain) are naturally occurring compounds used to increase myocardial contractility. They are primarily derived from two plant genera: **Digitalis** (Foxglove) and **Strophanthus** [1], [2]. * **Why Option B is correct:** **Strophanthus gratus** is the primary source of **G-strophanthin**, also known as **Ouabain** [4]. Another species, *Strophanthus kombe*, provides K-strophanthin. These glycosides inhibit the Na+/K+-ATPase pump, leading to an increase in intracellular calcium and improved cardiac output in heart failure [2], [3]. **Analysis of Incorrect Options:** * **A. Rauwolfia serpentina:** Known as Indian Snakeroot, it is the source of **Reserpine**. It was historically used as an antihypertensive and antipsychotic by depleting catecholamines, not as a cardiac glycoside. * **C. Ricinus communis:** This is the source of **Castor oil** (a stimulant laxative) and the potent toxin **Ricin**. It has no therapeutic role in cardiac contractility. * **D. Atropa belladonna:** Known as Deadly Nightshade, it is a source of **Atropine**. While it affects the heart (increasing heart rate by blocking M2 receptors), it is an anticholinergic, not a cardiac glycoside. **High-Yield Clinical Pearls for NEET-PG:** * **Digoxin** is derived from *Digitalis lanata* (Grecian foxglove). * **Digitoxin** is derived from *Digitalis purpurea* (Purple foxglove) [2]. * **Mechanism:** Inhibition of Na+/K+-ATPase → Increased intracellular Na+ → Decreased Na+/Ca2+ exchange → Increased intracellular Ca2+ (**Positive Inotropy**) [3]. * **ECG Changes:** Characterized by the "reverse tick" or "sagging" ST-segment depression (Salvador Dali sign).

Question 663: Which of the following possesses the highest efficacy to increase HDL cholesterol?

A. Gemfibrosil
B. Enoic acid
C. Atorvastatin
D. Nicotinic acid (Correct Answer)

Explanation: **Explanation:** **Nicotinic Acid (Niacin)** is the correct answer because it is the most potent agent currently available for increasing HDL cholesterol levels. It typically raises HDL by **15% to 35%**. It achieves this by inhibiting the hepatic breakdown of Apolipoprotein A-I (the primary protein component of HDL), thereby increasing its half-life and circulating levels. Additionally, Niacin inhibits the peripheral mobilization of free fatty acids, reducing VLDL and LDL synthesis. **Analysis of Incorrect Options:** * **Gemfibrozil (Fibrates):** While Fibrates are the drugs of choice for reducing **Triglycerides**, their effect on HDL is modest (usually a 10–15% increase), making them less efficacious than Niacin for this specific purpose. * **Atorvastatin (Statins):** Statins are the gold standard for lowering **LDL cholesterol**. Although they do increase HDL, the effect is minimal (5–10%). * **Enoic acid:** This is likely a distractor referring to fatty acids (like Eicosapentaenoic acid/Omega-3). These are primarily used to lower triglycerides and have negligible effects on raising HDL. **NEET-PG High-Yield Pearls:** * **Side Effects of Niacin:** The most common side effect is **cutaneous flushing** (mediated by Prostaglandin D2/E2), which can be minimized by taking **Aspirin** 30 minutes prior. It can also cause hyperuricemia (precipitating gout) and hyperglycemia. * **Mechanism of Fibrates:** They act as **PPAR-α agonists**, increasing the activity of Lipoprotein Lipase (LPL). * **Drug of Choice Summary:** * To lower LDL: Statins. * To lower Triglycerides: Fibrates. * To raise HDL: Niacin.

Question 664: Nitroglycerine can be administered by all of the following routes except?

A. Oral
B. Sublingual
C. Intramuscular (Correct Answer)
D. Intravenous

Explanation: **Explanation:** Nitroglycerine (Glyceryl Trinitrate - GTN) is a potent vasodilator used primarily for angina pectoris. The correct answer is **Intramuscular (C)** because this route is not used clinically for GTN. Intramuscular injections are avoided due to unpredictable absorption rates and the risk of local tissue irritation, especially when more efficient and titratable routes are available. **Analysis of Options:** * **Oral (A):** GTN can be given orally (sustained-release tablets), but it undergoes **extensive first-pass metabolism** in the liver (bioavailability <1%). Therefore, oral doses must be significantly higher than sublingual doses to be effective. * **Sublingual (B):** This is the **route of choice for acute anginal attacks**. It bypasses the liver (avoiding first-pass metabolism), ensuring rapid onset of action (1–3 minutes). * **Intravenous (D):** Used in **emergency settings** such as unstable angina, acute heart failure, or hypertensive emergencies. It allows for precise titration and immediate effect. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** GTN is a prodrug that releases **Nitric Oxide (NO)**, increasing cGMP and causing smooth muscle relaxation (primarily venodilation, reducing preload). * **Storage:** GTN is volatile and light-sensitive; it must be stored in **dark glass containers** with tight metal caps. * **Tolerance:** Continuous use leads to "Nitrate Tolerance" (depletion of free sulfhydryl groups). A **nitrate-free interval** of 8–12 hours (usually at night) is required to restore sensitivity. * **Contraindication:** Never co-administer with **Sildenafil** (PDE-5 inhibitors) as it can cause life-threatening hypotension.

Question 665: A 60-year-old man with unstable angina is treated with an intravenously administered glycoprotein IIb-IIIa inhibitor. What is the mechanism of action of this agent?

A. Dilate coronary arteries.
B. Inhibit atherogenesis.
C. Inhibit platelet adhesion.
D. Inhibit platelet aggregation. (Correct Answer)

Explanation: ### Explanation **Mechanism of Action: Inhibition of Platelet Aggregation** Glycoprotein (GP) IIb/IIIa inhibitors (e.g., **Abciximab, Eptifibatide, and Tirofiban**) act on the "final common pathway" of platelet activation. The GP IIb/IIIa receptor is a surface integrin that, when activated, binds to **fibrinogen** and von Willebrand factor. Fibrinogen acts as a bridge, linking multiple platelets together to form a stable plug. By blocking this receptor, these drugs prevent fibrinogen binding, thereby directly inhibiting **platelet aggregation**. **Analysis of Incorrect Options:** * **A. Dilate coronary arteries:** This is the mechanism of Nitrates or Calcium Channel Blockers, not antiplatelets. * **B. Inhibit atherogenesis:** Atherogenesis is a chronic inflammatory process involving LDL oxidation and foam cell formation. While Statins may slow this, GP IIb/IIIa inhibitors are acute-phase antithrombotics. * **C. Inhibit platelet adhesion:** Adhesion is the initial step where platelets bind to the subendothelial matrix (via GP Ib-IX-V and vWF). GP IIb/IIIa inhibitors act later in the process during the aggregation phase. **High-Yield Clinical Pearls for NEET-PG:** * **The "Final Common Pathway":** GP IIb/IIIa inhibitors are more potent than Aspirin or Clopidogrel because they block the final step of aggregation regardless of the initial stimulus (ADP, Thrombin, or TXA2). * **Abciximab:** A monoclonal antibody; it is non-competitive and has the longest biological half-life (irreversible binding). * **Eptifibatide & Tirofiban:** Small molecules; they are competitive, reversible inhibitors with shorter durations of action. * **Major Side Effect:** Bleeding and **thrombocytopenia** (especially with Abciximab). * **Clinical Use:** Primarily used in Acute Coronary Syndrome (ACS) undergoing Percutaneous Coronary Intervention (PCI).

Question 666: Which drug is typically administered in cardiogenic shock?

A. Dopamine (Correct Answer)
B. Phenylephrine
C. Atropine
D. Digoxin

Explanation: **Explanation:** **Cardiogenic shock** is characterized by a primary failure of the heart to pump blood effectively, leading to low cardiac output and hypotension. The goal of treatment is to increase cardiac contractility (inotropy) and maintain blood pressure without excessively increasing the workload of the heart. **Why Dopamine is correct:** Dopamine is a dose-dependent catecholamine. At **medium doses (5–10 µg/kg/min)**, it primarily stimulates **$\beta_1$ receptors**, increasing myocardial contractility and heart rate. At **higher doses (>10 µg/kg/min)**, it stimulates **$\alpha_1$ receptors**, causing vasoconstriction to raise systemic blood pressure. This dual action makes it a classic choice for stabilizing patients in cardiogenic shock. (Note: While Dobutamine is often preferred if blood pressure is stable, Dopamine is the preferred choice among these options, especially when hypotension is prominent). **Why other options are incorrect:** * **B. Phenylephrine:** A pure $\alpha_1$ agonist. It causes intense vasoconstriction which increases afterload. In cardiogenic shock, increasing afterload makes it harder for the failing heart to pump, potentially worsening the condition. * **C. Atropine:** An anticholinergic used primarily for symptomatic bradycardia. It does not provide the necessary inotropic support required for shock. * **D. Digoxin:** While it is a positive inotrope, its onset of action is too slow for acute shock management, and it carries a high risk of arrhythmias in the setting of acute myocardial ischemia. **High-Yield NEET-PG Pearls:** * **Dobutamine** is often considered the "Inotrope of Choice" for cardiogenic shock if the systolic BP is >90 mmHg, as it reduces afterload (via $\beta_2$). * **Dopamine** is preferred if the patient is severely hypotensive (SBP <70-80 mmHg). * **Low-dose Dopamine (0.5–2 µg/kg/min)** acts on $D_1$ receptors (renal vasodilation), but clinical studies have shown it does not prevent acute renal failure (the "renal dose" myth).

Question 667: Which nitrate does not undergo first-pass metabolism?

A. Isosorbide mononitrate (Correct Answer)
B. Nitroglycerine
C. Pentaerythritol tetranitrate
D. Isosorbide dinitrate

Explanation: ### Explanation **Correct Answer: A. Isosorbide mononitrate** **1. Why Isosorbide mononitrate is correct:** Isosorbide mononitrate (ISMN) is the active metabolite of Isosorbide dinitrate. Unlike most other nitrates, it possesses **100% oral bioavailability** because it does not undergo hepatic first-pass metabolism. This characteristic makes its pharmacokinetics highly predictable, allowing for consistent plasma levels when administered orally. **2. Why the other options are incorrect:** * **Nitroglycerine (Glyceryl Trinitrate):** It undergoes extensive (nearly 90-95%) first-pass metabolism in the liver. This is why it is primarily administered via sublingual, transdermal, or intravenous routes to bypass the liver and achieve rapid action. * **Isosorbide dinitrate (ISDN):** It undergoes significant first-pass metabolism (oral bioavailability is only ~20-25%). It is metabolized in the liver into two active metabolites: Isosorbide-2-mononitrate and Isosorbide-5-mononitrate. * **Pentaerythritol tetranitrate:** This is a long-acting nitrate that also undergoes significant hepatic metabolism, resulting in lower systemic bioavailability compared to ISMN. **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for Acute Angina:** Sublingual Nitroglycerine (due to rapid onset). * **Longest Acting Nitrate:** Pentaerythritol tetranitrate. * **Nitrate Tolerance:** Continuous exposure leads to reduced efficacy (depletion of free sulfhydryl groups). To prevent this, a **"Nitrate-free interval"** of 8–12 hours (usually at night) is recommended. * **Monday Disease:** Workers in explosive factories exposed to nitrates develop tolerance during the week but lose it over the weekend, leading to headaches and tachycardia upon returning to work on Monday. * **Contraindication:** Never co-administer nitrates with **Sildenafil** (PDE-5 inhibitors) as it can cause life-threatening hypotension.

Question 668: Beta-blockers are used in which of the following conditions?

A. Postural hypotension
B. Alcohol withdrawal
C. Anxiety
D. All of the above (Correct Answer)

Explanation: **Explanation:** Beta-blockers (β-adrenoceptor antagonists) are versatile drugs used across multiple specialties due to their ability to antagonize the effects of catecholamines. 1. **Alcohol Withdrawal:** During withdrawal, there is massive sympathetic overactivity. Beta-blockers (like Propranolol) are used to control the **autonomic symptoms** such as tachycardia, palpitations, and tremors. They are often used as adjuncts to benzodiazepines. 2. **Anxiety:** They are highly effective for **"Performance Anxiety"** (stage fright). They do not treat the psychological fear but suppress the peripheral physical manifestations (tremors, sweating, and palpitations), helping the patient remain calm. 3. **Postural Hypotension:** While it seems counterintuitive (as beta-blockers usually lower BP), they are used in specific types of **orthostatic intolerance**, such as **Postural Orthostatic Tachycardia Syndrome (POTS)**. By blocking the compensatory tachycardia and improving stroke volume, they help stabilize the hemodynamic response in these patients. **Clinical Pearls for NEET-PG:** * **Propranolol** is the most lipid-soluble beta-blocker, allowing it to cross the blood-brain barrier, making it the drug of choice for tremors and prophylaxis of migraine. * **Esmolol** is the shortest-acting beta-blocker (T½ ≈ 9 mins), administered IV for intraoperative arrhythmias. * **Contraindications:** Always remember the "ABCDE" contraindications: **A**sthma/COPD, **B**lock (Heart block), **C**onstrictive vascular disease (Raynaud's), **D**iabetes (masks hypoglycemia), and **E**lectrolyte imbalance (Hyperkalemia). * **Specific Indication:** Beta-blockers are the first-line treatment for **Hypertrophic Obstructive Cardiomyopathy (HOCM)** and **Thyrotoxicosis** (to control symptoms and inhibit peripheral conversion of T4 to T3).

Question 669: Which of the following drugs causes an increase in the effective refractory period of the atrioventricular (AV) node?

A. bretylium
B. amiodarone (Correct Answer)
C. procainamide
D. quinidine

Explanation: **Explanation:** **Amiodarone** is a Class III antiarrhythmic drug with a complex mechanism of action. While its primary role is blocking potassium channels (prolonging the action potential duration), it also possesses significant Class I (sodium channel), Class II (beta-blocking), and Class IV (calcium channel) properties. The **Class II and IV effects** specifically target the AV node, leading to a decrease in conduction velocity and an **increase in the effective refractory period (ERP)**. This makes it highly effective in controlling the ventricular rate in supraventricular tachycardias like atrial fibrillation. **Analysis of Incorrect Options:** * **Bretylium (Option A):** A pure Class III agent that primarily affects the ventricular myocardium. It does not have significant effects on the AV node's refractory period. * **Procainamide (Option C):** A Class IA agent that mainly blocks sodium channels. While it increases the ERP of the atrium and ventricle, its effect on the AV node is minimal and can sometimes be offset by its weak anticholinergic properties. * **Quinidine (Option D):** A Class IA agent that has significant **anticholinergic (vagolytic) properties**. This actually *decreases* the refractory period of the AV node and increases AV conduction, which is why it must be preceded by an AV nodal blocking agent (like a beta-blocker) when treating atrial flutter/fibrillation. **High-Yield NEET-PG Pearls:** * **Amiodarone** is the drug of choice for both ventricular and supraventricular arrhythmias in patients with structural heart disease or heart failure. * **Side Effects:** Remember the "6 Ps": **P**ulmonary fibrosis, **P**hotodermatitis (Blue-grey skin), **P**eripheral neuropathy, **P**rolonged QT, **P**apillary/corneal microdeposits, and **P**roblems with thyroid (Hypo/Hyperthyroidism due to high iodine content). * **Vagolytic effect:** Quinidine and Disopyramide are the Class IA drugs with the strongest vagolytic effects on the AV node.

Question 670: Which endogenous peptide causes vasodilation and is inactivated by angiotensin-converting enzyme?

A. Angiotensinogen
B. Angiotensin–I
C. Angiotensin–II
D. Bradykinin (Correct Answer)

Explanation: **Explanation:** The correct answer is **Bradykinin**. **1. Why Bradykinin is correct:** Bradykinin is a potent endogenous vasodilator peptide belonging to the kinin system. It acts on $B_2$ receptors to release nitric oxide and prostacyclin. Crucially, **Angiotensin-Converting Enzyme (ACE)**, also known as **Kininase II**, is the primary enzyme responsible for the degradation (inactivation) of bradykinin. When ACE is inhibited (e.g., by Enalapril), bradykinin levels rise, leading to vasodilation but also common side effects like dry cough and angioedema. **2. Why the other options are incorrect:** * **Angiotensinogen:** This is an α-2-globulin produced by the liver. It is the precursor protein acted upon by *renin* to form Angiotensin-I, not a vasodilator. * **Angiotensin-I:** This is a decapeptide formed from angiotensinogen. It is biologically inactive and is **converted** (not inactivated) by ACE into the potent vasoconstrictor Angiotensin-II. * **Angiotensin-II:** This is the primary effector molecule of the RAAS system. It is a potent **vasoconstrictor** (not a vasodilator) and is produced by the action of ACE, not inactivated by it. **3. NEET-PG Clinical Pearls:** * **ACE Inhibitor-induced Cough:** The accumulation of bradykinin in the lungs is the classic cause of the dry, irritating cough seen in patients on ACE inhibitors. * **Dual Role of ACE:** Remember that ACE has two primary functions: converting Angiotensin-I to Angiotensin-II (vasoconstriction) and inactivating Bradykinin (preventing vasodilation). * **Icatibant:** A selective $B_2$ receptor antagonist used in the treatment of Hereditary Angioedema (where bradykinin levels are excessively high).

Practice by Chapter

Antihypertensive Agents

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Drugs for Heart Failure

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Antiarrhythmic Drugs

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Antianginal Agents

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Lipid-Lowering Drugs

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Anticoagulants and Antiplatelet Drugs

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Thrombolytic Agents

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Drugs Used in Pulmonary Hypertension

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Drugs Used in Shock

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Cardiovascular Effects of Non-Cardiovascular Drugs

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