Cardiovascular Drugs — MCQs

A 60-year-old male with angina presents with severe chest pain unresponsive to sublingual nitroglycerin. An ECG shows ST segment elevation in the anterolateral leads, and thrombolytic therapy is initiated. If streptokinase is given to this patient, it may produce thrombolysis after binding to which of the following proteins?

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 321: A 42-year-old woman with a 20-year history of Type II diabetes has hypertension with a BP in the 150/94 mmHg range and mild proteinuria on urinalysis. Which drug would be the best to treat the hypertension in this individual?

A. Enalapril (Correct Answer)
B. Hydrochlorothiazide
C. Propranolol
D. Nifedipine

Explanation: ### Explanation **Correct Answer: A. Enalapril** The clinical scenario describes a patient with **Type II Diabetes Mellitus, Hypertension, and Proteinuria**. In such patients, **ACE inhibitors (like Enalapril)** or Angiotensin Receptor Blockers (ARBs) are the first-line antihypertensive agents. The underlying medical concept is **Renoprotection**. ACE inhibitors dilate the **efferent arteriole** of the glomerulus more than the afferent arteriole. This reduces intraglomerular capillary pressure, thereby decreasing albuminuria and slowing the progression of diabetic nephropathy. Regardless of the blood pressure-lowering effect, these drugs are preferred for their specific ability to preserve renal function in diabetics. **Why other options are incorrect:** * **B. Hydrochlorothiazide:** While effective for hypertension, thiazides can cause metabolic side effects like hyperglycemia and hyperlipidemia, which may worsen glycemic control in diabetic patients. * **C. Propranolol:** Non-selective beta-blockers are generally avoided in diabetics because they can mask the autonomic symptoms of hypoglycemia (like tachycardia and tremors) and may delay recovery from hypoglycemic episodes. * **D. Nifedipine:** While Calcium Channel Blockers (CCBs) are metabolically neutral and effective for BP control, they do not offer the same level of superior renoprotection as ACE inhibitors in the presence of proteinuria. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** ACE inhibitors/ARBs are the DOC for hypertension in patients with Diabetes, Chronic Kidney Disease (CKD), and Heart Failure. * **Contraindications:** ACE inhibitors are strictly contraindicated in **pregnancy** (teratogenic), **bilateral renal artery stenosis**, and patients with **hyperkalemia**. * **Side Effect:** The most common side effect of ACE inhibitors is a **dry cough**, mediated by increased levels of Bradykinin and Substance P. If a cough develops, the patient should be switched to an ARB (e.g., Losartan).

Question 322: What is the most common side effect of dihydropyridine calcium channel blockers?

A. Headache (Correct Answer)
B. Constipation
C. Diarrhoea
D. Muscle cramps

Explanation: **Explanation:** Dihydropyridine (DHP) Calcium Channel Blockers (CCBs), such as **Amlodipine** and **Nifedipine**, act primarily by inhibiting L-type calcium channels in the vascular smooth muscle. This leads to potent **peripheral vasodilation**. **1. Why Headache is the correct answer:** The primary mechanism of DHP-CCBs is the relaxation of arterial smooth muscle. This causes significant vasodilation of the meningeal and cerebral vessels. The resulting increase in intracranial blood flow and stretching of vessel walls triggers sensory nerves, leading to **vasodilatory headaches**. This is the most frequently reported side effect, especially during the initiation of therapy. Other common side effects due to this same mechanism include **peripheral edema** (due to precapillary dilation) and **flushing**. **2. Why the other options are incorrect:** * **B. Constipation:** This is a classic side effect of **Verapamil** (a non-dihydropyridine CCB). Verapamil inhibits calcium channels in the gastrointestinal smooth muscle, leading to decreased motility. It is rarely seen with DHPs. * **C. Diarrhoea:** This is not a characteristic side effect of CCBs. In fact, CCBs are more likely to cause decreased bowel motility. * **D. Muscle cramps:** While occasionally reported, these are not a "most common" or "classic" side effect compared to the vascular symptoms of DHPs. **High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Edema:** A highly characteristic side effect of Amlodipine; it is **not** due to fluid overload but due to increased capillary hydrostatic pressure (pre-capillary dilation). * **Reflex Tachycardia:** Common with short-acting DHPs (like Nifedipine) due to rapid vasodilation triggering the baroreceptor reflex. * **Gingival Hyperplasia:** A shared side effect of CCBs (especially Nifedipine), Phenytoin, and Cyclosporine.

Question 323: Which of the following drugs can cause coronary steal phenomenon?

A. Hydralazine (Correct Answer)
B. Glyceryl trinitrate
C. Disopyramide
D. Diltiazem

Explanation: ### Explanation **Coronary Steal Phenomenon** occurs when a drug causes potent vasodilation of healthy coronary arterioles, leading to a diversion of blood flow away from ischemic (stenosed) areas toward well-perfused areas. In ischemic regions, arterioles are already maximally dilated due to local metabolites; therefore, they cannot dilate further. When a vasodilator acts on healthy vessels, it reduces resistance there, "stealing" the blood from the high-resistance ischemic zones, potentially worsening angina or myocardial infarction. **Why Hydralazine is Correct:** **Hydralazine** is a potent direct-acting arteriolar vasodilator. It primarily affects the resistance vessels (arterioles). By dilating non-ischemic coronary arterioles, it triggers the coronary steal phenomenon. Other classic examples of drugs causing this effect include **Dipyridamole** and **Adenosine** (often used in pharmacological stress testing for this very reason). **Why the Other Options are Incorrect:** * **B. Glyceryl trinitrate (GTN):** Unlike hydralazine, nitrates primarily cause **venodilation** (reducing preload) and dilate large epicardial coronary arteries rather than peripheral arterioles. They improve subendocardial perfusion and do not typically cause coronary steal. * **C. Disopyramide:** This is a Class IA antiarrhythmic drug. Its primary side effects are anticholinergic (dry mouth, urinary retention) and negative inotropy; it does not have significant vasodilatory properties. * **D. Diltiazem:** This is a non-dihydropyridine Calcium Channel Blocker (CCB). While it causes some vasodilation, it also decreases heart rate and myocardial oxygen demand, making it protective in stable angina rather than causative of steal. **High-Yield Clinical Pearls for NEET-PG:** * **Dipyridamole** is the most frequently cited drug in exams for causing coronary steal. * **Isoflurane** (inhalational anesthetic) is also known to potentially cause coronary steal. * **Nitroprusside** can cause coronary steal because it dilates both arterioles and venules. * **Clinical Sign:** If a patient’s chest pain worsens after administering a potent arteriolar vasodilator, suspect coronary steal.

Question 324: Aspirin is used for secondary prevention of ischemic heart disease because it:

A. Inhibits TXA2 synthesis by platelets (Correct Answer)
B. Inhibits prostacyclin synthesis
C. Inhibits the release of EDRF
D. Inhibits the synthesis of endothelins

Explanation: **Explanation:** Aspirin (Acetylsalicylic acid) is a mainstay in the secondary prevention of ischemic heart disease due to its role as an antiplatelet agent. **1. Why Option A is Correct:** Aspirin works by **irreversibly inhibiting the enzyme Cyclooxygenase-1 (COX-1)** via acetylation. In platelets, COX-1 is responsible for the synthesis of **Thromboxane A2 (TXA2)**, a potent vasoconstrictor and mediator of platelet aggregation. Since platelets are anuclear and cannot synthesize new enzymes, the inhibition lasts for the entire lifespan of the platelet (approx. 7–10 days). Reducing TXA2 levels prevents thrombus formation over atherosclerotic plaques, thereby reducing the risk of myocardial infarction. **2. Why Other Options are Incorrect:** * **Option B:** While aspirin can inhibit **Prostacyclin (PGI2)** synthesis in vascular endothelial cells, PGI2 is a vasodilator and anti-aggregatory agent. At low doses (75–150 mg), aspirin is "platelet-selective" because endothelial cells can regenerate COX enzymes, whereas platelets cannot. Inhibiting PGI2 is actually an unwanted effect. * **Option C & D:** Aspirin does not have a direct inhibitory effect on **Endothelium-Derived Relaxing Factor (EDRF/Nitric Oxide)** or **Endothelins**. These are regulated by different pathways (e.g., NO synthase and Endothelin-converting enzyme). **High-Yield Clinical Pearls for NEET-PG:** * **Low-dose Aspirin (75–150 mg/day):** Preferred for cardioprotection to achieve selective TXA2 inhibition while sparing PGI2. * **Irreversible Action:** Aspirin is the only NSAID that binds irreversibly to COX. * **Primary vs. Secondary Prevention:** Aspirin is strongly indicated for *secondary* prevention (post-MI/Stroke). Its use in *primary* prevention is now limited due to the increased risk of major GI bleeding. * **Aspirin Resistance:** Can be seen in patients with high platelet turnover or genetic polymorphisms.

Question 325: ACE inhibitors are contraindicated in:

A. Hypertension
B. Myocardial infarction
C. Renal artery stenosis (Correct Answer)
D. Left ventricular dysfunction

Explanation: **Explanation:** **Why Renal Artery Stenosis (RAS) is the Correct Answer:** In patients with bilateral renal artery stenosis (or stenosis in a solitary kidney), renal perfusion pressure is significantly reduced. To maintain the **Glomerular Filtration Rate (GFR)**, the body relies on Angiotensin II to cause **vasoconstriction of the efferent arteriole**. ACE inhibitors block the production of Angiotensin II, leading to efferent arteriolar vasodilation. This causes a sharp drop in intraglomerular pressure, resulting in acute renal failure. Therefore, ACE inhibitors are strictly contraindicated in these patients. **Why Other Options are Incorrect:** * **A. Hypertension:** ACE inhibitors are first-line agents for hypertension, especially in patients with diabetes or proteinuric kidney disease. * **B. Myocardial Infarction (MI):** They are standard of care post-MI to prevent "ventricular remodeling" and reduce mortality. * **D. Left Ventricular Dysfunction:** ACE inhibitors are the cornerstone of treatment for Heart Failure with Reduced Ejection Fraction (HFrEF) as they reduce both preload and afterload. **High-Yield NEET-PG Pearls:** * **Teratogenicity:** ACE inhibitors are contraindicated in **pregnancy** (cause fetal renal dysgenesis and skull hypoplasia). * **Side Effects:** The most common side effect is a **dry cough** (due to increased Bradykinin); the most serious is **angioedema**. * **Monitoring:** Always monitor serum creatinine and potassium levels. A minor rise in creatinine (up to 30%) is acceptable, but **hyperkalemia** is a known contraindication. * **Drug of Choice:** ACE inhibitors are the DOC for **Diabetic Nephropathy** because they are renoprotective (reduce proteinuria).

Question 326: Which of the following is a beta-blocker with a beta-2 receptor agonist action?

A. Labetalol
B. Carvedilol
C. Celiprolol (Correct Answer)
D. Tilisolol

Explanation: **Explanation:** The correct answer is **Celiprolol**. **1. Why Celiprolol is correct:** Celiprolol is a unique, third-generation beta-blocker. Its pharmacological profile is characterized by **selective $\beta_1$ antagonism** (cardioselective) combined with **partial $\beta_2$ receptor agonism** (Intrinsic Sympathomimetic Activity - ISA) [1]. This $\beta_2$ agonist action leads to peripheral vasodilation and bronchodilation, which helps counteract the typical side effects of beta-blockers, such as cold extremities or bronchospasm. It also possesses weak $\alpha_2$ blocking and nitric oxide-modulating properties. **2. Analysis of Incorrect Options:** * **A. Labetalol:** This is a non-selective $\beta$ blocker with additional **$\alpha_1$ blocking** activity. It does not have $\beta_2$ agonist action. It is a drug of choice in pregnancy-induced hypertension. * **B. Carvedilol:** This is a non-selective $\beta$ blocker with **$\alpha_1$ blocking** and potent antioxidant properties. It is widely used in chronic heart failure but lacks $\beta_2$ agonism. * **C. Tilisolol:** This is a non-selective beta-blocker used primarily in Japan. It is unique because it has **potassium channel opening** properties (vasodilation), but it does not act as a $\beta_2$ agonist [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Vasodilatory Beta-blockers:** Remember them by the mechanism [1]: * **$\alpha_1$ blockade:** Labetalol, Carvedilol. * **$\beta_2$ agonism:** Celiprolol, Carteolol. * **NO (Nitric Oxide) release:** Nebivolol (most cardioselective), Nipradilol. * **$K^+$ channel opening:** Tilisolol. * **Celiprolol** is particularly useful in hypertensive patients with asthma or peripheral vascular disease due to its $\beta_2$ agonist-mediated bronchodilation and vasodilation.

Question 327: What is the most suitable antiarrhythmic drug for counteracting ventricular extrasystoles due to digoxin toxicity?

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

Explanation: ### Explanation **Correct Option: C. Lignocaine** Lignocaine (Lidocaine) is the drug of choice for ventricular arrhythmias (like ventricular extrasystoles or tachycardia) caused by digoxin toxicity. * **Mechanism:** Digoxin toxicity causes increased automaticity and delayed after-depolarizations (DADs) due to intracellular calcium overload. Lignocaine, a Class IB antiarrhythmic, selectively blocks activated and inactivated sodium channels with rapid dissociation [1]. * **Key Advantage:** Unlike other antiarrhythmics, Lignocaine does not significantly depress myocardial contractility or slow AV conduction, making it safe in the context of digitalis-induced conduction blocks [2]. **Why Other Options are Incorrect:** * **A. Verapamil:** This Calcium Channel Blocker can worsen AV block and may increase digoxin levels by competing for renal/biliary excretion (P-glycoprotein inhibition). Verapamil's cardiotoxic effects include inducing AV block and negative inotropic effects, limiting its use in diseased hearts [3]. * **B. Quinidine:** It is strictly contraindicated. Quinidine reduces the renal and tissue clearance of digoxin, potentially doubling its plasma concentration and worsening toxicity. * **D. Amiodarone:** While an effective antiarrhythmic, it can increase digoxin levels [4] and further depress the SA and AV nodes, increasing the risk of high-grade heart block. Amiodarone potently inhibits the hepatic metabolism or renal elimination of many compounds, including digoxin, often requiring a reduction in digoxin dosage during co-administration [4]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Management Priority:** The first step in digoxin toxicity is to stop the drug and correct hypokalemia (if present). 2. **Specific Antidote:** **Digibind** (Digoxin-specific Fab fragments) is the definitive treatment for life-threatening toxicity. 3. **Electrolyte Interaction:** Hypokalemia, hypomagnesemia, and hypercalcemia predispose a patient to digoxin toxicity. 4. **Phenytoin:** Also used for digitalis-induced arrhythmias, especially if there is associated AV block, as it can improve AV conduction.

Question 328: Lipid-lowering agents, statins, act in all the following ways except:

A. Decreased hepatic cholesterol synthesis
B. Decreased LDL receptors (Correct Answer)
C. Inhibiting HMG CoA reductase
D. Decreasing VLDL

Explanation: ### Explanation Statins (HMG-CoA reductase inhibitors) are the first-line agents for hypercholesterolemia. The core mechanism involves the competitive inhibition of the rate-limiting enzyme in cholesterol biosynthesis. **Why "Decreased LDL receptors" is the correct answer (the exception):** Statins actually **increase** the expression of LDL receptors. When statins inhibit hepatic cholesterol synthesis, the intracellular pool of cholesterol drops. To compensate, the liver upregulates the synthesis of LDL receptors on the hepatocyte surface. These receptors then clear more LDL and VLDL remnants from the circulation, leading to a significant drop in plasma LDL levels. Therefore, saying statins *decrease* these receptors is physiologically incorrect. **Analysis of Incorrect Options:** * **A & C (Inhibiting HMG CoA reductase / Decreased hepatic synthesis):** These are the primary actions of statins. By mimicking the substrate HMG-CoA, they block the conversion of HMG-CoA to mevalonate, directly halting endogenous cholesterol production. * **D (Decreasing VLDL):** Since VLDL is a precursor to LDL and requires cholesterol for its assembly, the reduction in hepatic cholesterol availability leads to a secondary decrease in VLDL secretion. **High-Yield Clinical Pearls for NEET-PG:** * **Pleiotropic Effects:** Statins have "extra" benefits beyond lipid lowering, including plaque stabilization, anti-inflammatory properties, and improved endothelial function. * **Timing:** Most statins (except Atorvastatin and Rosuvastatin) should be taken at **bedtime** because peak cholesterol synthesis occurs during the night. * **Side Effects:** Monitor for **myopathy** (elevated CPK) and hepatotoxicity. Risk increases when combined with Fibrates or Cytochrome P450 inhibitors. * **Contraindication:** Statins are strictly **Teratogenic** (Category X).

Question 329: What is the drug of choice in digitalis-induced ventricular arrhythmia?

A. IV Lignocaine (Correct Answer)
B. Phenytoin
C. Quinidine
D. Procainamide

Explanation: **Explanation:** **1. Why IV Lignocaine is the Correct Answer:** Lignocaine (Lidocaine) is a Class IB anti-arrhythmic that is the **drug of choice (DOC)** for digitalis-induced ventricular arrhythmias. Digitalis toxicity causes increased automaticity and delayed after-depolarizations (DADs). Lignocaine works by blocking activated and inactivated sodium channels, specifically shortening the action potential duration and decreasing automaticity in the ventricular myocardium without significantly affecting AV conduction. Crucially, it does not worsen the AV block often associated with digitalis toxicity. **2. Why Other Options are Incorrect:** * **Phenytoin:** Historically, Phenytoin was the DOC for digitalis-induced arrhythmias (especially those with AV block). While still effective, **Lignocaine is now preferred** due to its superior safety profile and ease of administration. * **Quinidine (Class IA):** This is strictly **contraindicated** in digitalis toxicity. Quinidine reduces the renal clearance of Digoxin and displaces it from tissue binding sites, effectively doubling plasma Digoxin levels and worsening toxicity. * **Procainamide (Class IA):** Like Quinidine, it can worsen AV conduction disturbances and is generally avoided in the setting of digitalis-induced arrhythmias. **3. High-Yield Clinical Pearls for NEET-PG:** * **Antidote of Choice:** For life-threatening digitalis toxicity (hemodynamic instability or hyperkalemia), the definitive treatment is **Digoxin-specific antibody fragments (DigiFab/Digibind).** * **Electrolyte Management:** Hypokalemia predisposes to toxicity. However, if toxicity causes **hyperkalemia**, it is a sign of severe poisoning (inhibition of Na+/K+ ATPase) and indicates the need for DigiFab. * **Atropine:** Used for digitalis-induced bradycardia or high-grade AV block. * **Avoid DC Cardioversion:** It can precipitate ventricular fibrillation in a digitalis-toxic heart unless absolutely necessary (use low energy).

Question 330: A 60-year-old male with angina presents with severe chest pain unresponsive to sublingual nitroglycerin. An ECG shows ST segment elevation in the anterolateral leads, and thrombolytic therapy is initiated. If streptokinase is given to this patient, it may produce thrombolysis after binding to which of the following proteins?

A. Antithrombin III
B. Fibrin
C. Plasminogen (Correct Answer)
D. Protein C

Explanation: ### Explanation **Mechanism of Action (Why Option C is Correct):** Streptokinase is a first-generation thrombolytic agent derived from *beta-hemolytic streptococci*. Unlike tissue plasminogen activator (tPA), streptokinase is **not fibrin-specific**. It works by forming a stable **1:1 stoichiometric complex with plasminogen**. This streptokinase-plasminogen complex undergoes a conformational change that exposes an active site, which then enzymatically converts free circulating plasminogen into **plasmin**. Plasmin subsequently degrades fibrin clots, as well as fibrinogen and other clotting factors (factors V and VII). **Analysis of Incorrect Options:** * **A. Antithrombin III:** This is a natural anticoagulant that inhibits thrombin and Factor Xa. It is the site of action for **Heparin**, not thrombolytics. * **B. Fibrin:** While newer agents like Alteplase, Reteplase, and Tenecteplase are "fibrin-selective" (binding preferentially to plasminogen already bound to fibrin), **Streptokinase does not bind directly to fibrin**. It acts systemically on all circulating plasminogen. * **D. Protein C:** This is a vitamin K-dependent natural anticoagulant that inactivates Factors Va and VIIIa. It is not involved in the mechanism of streptokinase. **High-Yield NEET-PG Pearls:** * **Antigenicity:** Because it is a bacterial protein, streptokinase is antigenic. It can cause **hypersensitivity reactions** (anaphylaxis) and should not be repeated in the same patient within 6–12 months due to neutralizing antibodies. * **Side Effects:** The most common side effect is bleeding. Unlike tPA, streptokinase can also cause significant **hypotension**. * **Comparison:** Tenecteplase is currently the preferred thrombolytic in STEMI due to its high fibrin specificity, long half-life (bolus dose), and lower bleeding risk compared to streptokinase.

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