Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 291: Antihypertensives act by all of the following mechanisms except?

A. Na+-ATPase inhibition (Correct Answer)
B. Alpha adrenergic blockade
C. Beta adrenergic blockade
D. Potassium channel opener

Explanation: **Explanation:** The goal of antihypertensive therapy is to reduce peripheral vascular resistance or cardiac output. **Why Option A is the Correct Answer:** **Na⁺/K⁺-ATPase inhibition** is the mechanism of action for **Cardiac Glycosides (e.g., Digoxin)**, not antihypertensives. Inhibiting this pump increases intracellular sodium, which subsequently leads to increased intracellular calcium via the Na⁺/Ca²⁺ exchanger. This results in **positive inotropy** (increased contractility), which is used in heart failure and supraventricular arrhythmias. It does not lower blood pressure; in fact, acute toxicity can sometimes cause vasoconstriction. **Analysis of Other Options:** * **Alpha-adrenergic blockade (Option B):** Drugs like Prazosin and Doxazosin block $\alpha_1$ receptors on vascular smooth muscle, leading to vasodilation and decreased peripheral resistance. * **Beta-adrenergic blockade (Option C):** Drugs like Propranolol and Atenolol reduce blood pressure by decreasing cardiac output, inhibiting renin release from the juxtaglomerular apparatus, and reducing central sympathetic outflow. * **Potassium channel openers (Option D):** Drugs like Minoxidil and Nicorandil open $K_{ATP}$ channels, causing hyperpolarization of smooth muscle cells. This leads to potent relaxation of arterioles and a drop in blood pressure. **High-Yield Clinical Pearls for NEET-PG:** * **First-line antihypertensives (A-B-C-D):** **A**CE inhibitors/ARBs, **B**eta-blockers (no longer first-line for uncomplicated HTN), **C**alcium channel blockers, and **D**iuretics. * **Minoxidil** is a potent vasodilator but can cause hypertrichosis (used topically for baldness). * **Sodium Nitroprusside** acts via NO release and is used in hypertensive emergencies; watch for cyanide toxicity. * **Digoxin** (Na⁺/K⁺-ATPase inhibitor) is contraindicated in WPW syndrome and hypertrophic cardiomyopathy (HOCM).

Question 292: Which antihypertensive medication is not contraindicated in pregnancy?

A. Spironolactone
B. Labetalol (Correct Answer)
C. Sodium Nitroprusside
D. ACE inhibitor

Explanation: **Explanation:** Management of hypertension in pregnancy requires drugs that are effective without being teratogenic or compromising uteroplacental blood flow. **1. Why Labetalol is Correct:** Labetalol is a combined **alpha and beta-adrenergic blocker**. It is considered a first-line agent for pregnancy-induced hypertension (PIH) and pre-eclampsia. It works by reducing peripheral vascular resistance while maintaining cardiac output and placental perfusion. It has a proven safety profile with minimal risk of fetal bradycardia compared to pure beta-blockers. **2. Why the Other Options are Incorrect:** * **Spironolactone (Option A):** This is an aldosterone antagonist with **anti-androgenic effects**. It can interfere with the sexual differentiation of a male fetus (feminization), making it contraindicated. * **Sodium Nitroprusside (Option C):** It is generally avoided because its metabolism releases **cyanide**, which can lead to fetal cyanide toxicity and death. It is only used as a last resort in life-threatening hypertensive emergencies. * **ACE Inhibitors (Option D):** These are strictly contraindicated (Category X/D). They cause **fetal dysgenesis**, specifically renal tubular dysgenesis, oligohydramnios, skull hypoplasia, and fetal anuria. **High-Yield Clinical Pearls for NEET-PG:** * **First-line drugs in pregnancy:** Labetalol (most common), Oral Methyldopa (safest long-term), and Nifedipine (long-acting). * **Drug of choice for Hypertensive Emergency in pregnancy:** IV Labetalol or IV Hydralazine. * **Drug of choice for Eclampsia (Seizures):** Magnesium Sulfate ($MgSO_4$). * **Avoid:** ACEIs, ARBs, Direct Renin Inhibitors, and Diuretics (unless there is pre-existing heart failure).

Question 293: Which drug is used for Buerger's disease?

A. Xanthinol nicotinate (Correct Answer)
B. Propranolol
C. Glyceryl trinitrate
D. All the above

Explanation: **Explanation:** **Buerger’s Disease (Thromboangiitis Obliterans)** is a non-atherosclerotic, inflammatory occlusive disease of small and medium-sized arteries and veins, strongly associated with tobacco use. The primary goal of pharmacological therapy (when smoking cessation is insufficient) is to improve peripheral blood flow through vasodilation. **Why Xanthinol Nicotinate is correct:** Xanthinol nicotinate is a peripheral vasodilator. It is a combination of theophylline and niacin (nicotinic acid). It works by causing direct relaxation of the vascular smooth muscles and improving microcirculation. In Buerger’s disease, it helps alleviate symptoms of intermittent claudication and rest pain by increasing blood flow to the ischemic distal extremities. **Analysis of Incorrect Options:** * **Propranolol:** This is a non-selective beta-blocker. It is actually **contraindicated** in peripheral vascular diseases like Buerger’s or Raynaud’s because blocking $\beta_2$ receptors leads to unopposed $\alpha$-adrenergic vasoconstriction, which can worsen ischemia. * **Glyceryl Trinitrate (GTN):** While GTN is a potent vasodilator, it acts primarily on the venous system and large coronary arteries. It is the drug of choice for Angina Pectoris but is not a standard or effective long-term treatment for the structural peripheral occlusions seen in Buerger’s disease. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Treatment:** The only definitive treatment to prevent progression and amputation in Buerger’s disease is **absolute smoking cessation**. * **Iloprost:** A synthetic analogue of Prostacyclin ($PGI_2$) is often considered the most effective pharmacological agent for limb salvage in severe cases. * **Cilostazol:** A PDE-3 inhibitor used for intermittent claudication; it provides both vasodilation and inhibition of platelet aggregation. * **Diagnosis:** Look for the "corkscrew collaterals" sign on angiography.

Question 294: Hyperkalemia is associated with which of the following drug classes?

A. ACE inhibitors (Correct Answer)
B. Chlorthalidone
C. Amphotericin-B
D. Amiodarone

Explanation: **Explanation:** **1. Why ACE Inhibitors (ACEIs) cause Hyperkalemia:** ACE inhibitors (e.g., Enalapril, Lisinopril) inhibit the Angiotensin-Converting Enzyme, preventing the conversion of Angiotensin I to Angiotensin II. Since Angiotensin II is the primary stimulus for **Aldosterone** secretion from the adrenal cortex, its deficiency leads to reduced aldosterone levels. Aldosterone normally promotes sodium reabsorption and potassium excretion in the distal tubules; thus, its inhibition results in **potassium retention**, leading to hyperkalemia. **2. Analysis of Incorrect Options:** * **Chlorthalidone:** This is a thiazide-like diuretic. Like loop diuretics, it increases sodium delivery to the distal tubule, promoting potassium excretion, which leads to **hypokalemia**. * **Amphotericin-B:** This antifungal is notorious for nephrotoxicity. It increases the permeability of the distal tubular membrane, causing significant wasting of potassium and magnesium, resulting in **hypokalemia**. * **Amiodarone:** While it has many side effects (thyroid dysfunction, pulmonary fibrosis), it does not typically affect serum potassium levels directly. However, hypokalemia can increase the risk of Torsades de Pointes in patients taking Amiodarone. **3. Clinical Pearls for NEET-PG:** * **K-Sparing Synergism:** The risk of hyperkalemia is significantly increased when ACEIs are combined with Potassium-sparing diuretics (e.g., Spironolactone) or NSAIDs. * **Other Hyperkalemic Drugs:** Remember the mnemonic **"K-BANK"**: **K**-sparing diuretics, **B**eta-blockers, **A**CEIs/ARBs, **N**SAIDs, and **K**-supplementation/Digitalis toxicity. * **Management:** If a patient on ACEIs develops serum $K^+ > 5.5$ mEq/L, the drug should be discontinued.

Question 295: All of the following decrease AV conduction EXCEPT:

A. Esmolol
B. Digitalis
C. Lignocaine (Correct Answer)
D. Verapamil

Explanation: **Explanation:** The conduction of impulses through the Atrioventricular (AV) node is primarily mediated by calcium channels and regulated by the autonomic nervous system. Drugs that block calcium channels, inhibit sympathetic activity, or increase vagal tone will decrease AV conduction (prolonging the PR interval). **Why Lignocaine is the correct answer:** Lignocaine is a **Class IB antiarrhythmic**. It acts specifically on sodium channels in the ventricular myocardium and Purkinje fibers, particularly in ischemic tissues. Crucially, Class IB agents have **no significant effect on the SA node or AV node conduction**. Therefore, it does not decrease AV conduction, making it the correct "except" choice. **Why the other options are incorrect:** * **Esmolol (Option A):** A cardioselective Beta-1 blocker (Class II). It decreases AV conduction by inhibiting sympathetic stimulation, making it useful for rate control in atrial fibrillation. * **Digitalis (Option B):** It increases vagal (parasympathetic) tone to the heart, which slows conduction through the AV node. This is its primary mechanism for controlling ventricular rate in supraventricular tachycardias. * **Verapamil (Option D):** A non-dihydropyridine Calcium Channel Blocker (Class IV). It directly blocks L-type calcium channels in the AV node, significantly slowing conduction and increasing the refractory period. **High-Yield Clinical Pearls for NEET-PG:** * **AV Node Blockers (Mnemonic: ABCD):** **A**denosine, **B**eta-blockers, **C**alcium channel blockers (Verapamil/Diltiazem), and **D**igoxin. * **Lignocaine** is the drug of choice for **ventricular arrhythmias** associated with acute myocardial infarction but is ineffective for supraventricular arrhythmias because it does not affect the AV node. * **Esmolol** is the shortest-acting beta-blocker (half-life ~9 minutes) due to metabolism by RBC esterases.

Question 296: Which drug inhibits the absorption of cholesterol from the intestine?

A. Resins
B. Ezetimibe (Correct Answer)
C. Niacin
D. Orlistat

Explanation: **Explanation:** **Ezetimibe** is the correct answer because it specifically inhibits the intestinal absorption of dietary and biliary cholesterol. It acts by binding to and blocking the **Niemann-Pick C1-Like 1 (NPC1L1) protein**, a key cholesterol transporter located on the brush border of enterocytes in the small intestine. This reduction in cholesterol delivery to the liver leads to an up-regulation of LDL receptors, subsequently lowering plasma LDL levels. **Analysis of Incorrect Options:** * **Resins (Bile Acid Sequestrants):** Drugs like Cholestyramine bind to bile acids in the gut, preventing their enterohepatic circulation. While they indirectly affect cholesterol levels, they do not block the direct absorption of cholesterol itself. * **Niacin (Vitamin B3):** This drug primarily acts on the liver and adipose tissue. It inhibits the enzyme **DGAT-2**, reducing VLDL synthesis, and inhibits lipolysis in adipose tissue by acting on G-protein coupled receptors. * **Orlistat:** Although it acts in the intestine, it is a **gastric and pancreatic lipase inhibitor**. It prevents the breakdown and absorption of dietary **triglycerides (fats)**, not cholesterol, and is primarily used for weight loss. **High-Yield Clinical Pearls for NEET-PG:** * **Synergistic Effect:** Ezetimibe is frequently combined with Statins (e.g., Vytorin) because it counteracts the compensatory increase in cholesterol absorption often seen with statin therapy. * **Side Effects:** Unlike resins, Ezetimibe does not cause significant malabsorption of fat-soluble vitamins. * **Key Marker:** It reduces LDL-C by approximately 15-20% when used as monotherapy.

Question 297: A pregnant patient is admitted for workup of hemolytic anemia. She reports taking an antihypertensive drug after the beginning of her pregnancy. What is the most likely cause?

A. Minoxidil
B. Clonidine
C. Methyldopa (Correct Answer)
D. Labetalol

Explanation: **Explanation:** **1. Why Methyldopa is correct:** Methyldopa is a centrally acting alpha-2 agonist and remains a first-line antihypertensive in pregnancy (alongside Labetalol and Nifedipine). However, a classic and high-yield side effect of Methyldopa is **Autoimmune Hemolytic Anemia (AIHA)**. * **Mechanism:** It induces the formation of autoantibodies against Rh antigens on the red blood cell (RBC) surface. * **Diagnosis:** This is characterized by a **Positive Direct Coombs Test**. While 10-20% of patients on long-term therapy develop a positive Coombs test, only about 1% develop clinically significant hemolysis. **2. Why the other options are incorrect:** * **Minoxidil:** A potent vasodilator used in resistant hypertension. Its primary side effects are hypertrichosis (excessive hair growth) and fluid retention/tachycardia. It is not associated with hemolysis. * **Clonidine:** Like methyldopa, it is a central alpha-2 agonist. While it can cause sedation and dry mouth, it does not cause autoimmune hemolysis. * **Labetalol:** A combined alpha and beta-blocker, it is the preferred drug for hypertensive emergencies in pregnancy. Its side effects include bradycardia and bronchospasm, but not hemolytic anemia. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Methyldopa is the DOC for chronic hypertension in pregnancy, whereas Labetalol is often preferred for acute management of pregnancy-induced hypertension (PIH). * **Coombs Test:** If a patient on Methyldopa develops anemia, the first step is to perform a Direct Coombs Test. If positive, the drug must be discontinued. * **Contraindicated in Pregnancy:** ACE inhibitors and ARBs (due to teratogenicity/renal dysgenesis) and Nitroprusside (due to cyanide toxicity).

Question 298: Which of the following fibrinolytic agents can be given as a single weight-based intravenous bolus over 10 seconds?

A. Tissue plasminogen activator (tPA)
B. Tenecteplase (TNK) (Correct Answer)
C. Reteplase (rPA)
D. Any of the above

Explanation: **Explanation:** The correct answer is **Tenecteplase (TNK)**. The primary pharmacological goal in thrombolysis is to achieve rapid reperfusion with minimal bleeding complications. Tenecteplase is a genetically engineered mutant of Alteplase (tPA) designed to optimize these goals. **Why Tenecteplase is correct:** Tenecteplase has three key modifications that make it superior for bolus administration: 1. **Longer Half-life:** It has a significantly longer half-life (~20–24 minutes) compared to Alteplase, allowing it to be administered as a **single weight-based IV bolus over 5–10 seconds**. 2. **Higher Fibrin Specificity:** It is more specific to fibrin-bound plasminogen, reducing the risk of systemic fibrinogen depletion. 3. **PAI-1 Resistance:** It is highly resistant to inhibition by Plasminogen Activator Inhibitor-1 (PAI-1). **Why other options are incorrect:** * **Tissue plasminogen activator (Alteplase):** It has a very short half-life (4–6 minutes) and requires a complex administration protocol involving an initial bolus followed by a 90-minute continuous infusion. * **Reteplase:** While it has a longer half-life than Alteplase, it is administered as **two fixed-dose IV boluses** (10 units each) given 30 minutes apart, not as a single bolus. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Tenecteplase is currently the preferred fibrinolytic for ST-Elevation Myocardial Infarction (STEMI) in the pre-hospital setting due to its ease of administration. * **Mechanism:** All these agents act by converting plasminogen to plasmin, which then degrades fibrin clots. * **Antidote:** In cases of life-threatening bleeding due to fibrinolytics, **Epsilon-aminocaproic acid** or **Tranexamic acid** can be used as inhibitors.

Question 299: In which of the following patients would enalapril be the best first-line agent for high blood pressure control?

A. A 62-year-old man with renal artery stenosis
B. A 32-year-old pregnant female
C. A 41-year-old woman with hyperkalemia
D. A 56-year-old diabetic woman (Correct Answer)

Explanation: **Explanation:** **Why Option D is Correct:** Enalapril is an ACE inhibitor (ACEi). In patients with **Diabetes Mellitus**, ACE inhibitors are the first-line antihypertensive agents because they provide significant **nephroprotection**. They dilate the efferent arteriole more than the afferent arteriole, thereby reducing intraglomerular pressure. This mechanism slows the progression of diabetic nephropathy and reduces albuminuria, making it the drug of choice for this patient. **Why Other Options are Incorrect:** * **Option A (Renal Artery Stenosis):** ACE inhibitors are **contraindicated** in bilateral renal artery stenosis (or stenosis in a solitary kidney). These patients depend on Angiotensin II-mediated vasoconstriction of the efferent arteriole to maintain Glomerular Filtration Rate (GFR). Blocking this can precipitate acute renal failure. * **Option B (Pregnancy):** ACE inhibitors are **teratogenic** (Category D). They can cause fetal renal dysgenesis, oligohydramnios, and skull hypoplasia. Preferred agents in pregnancy include Labetalol, Methyldopa, or Hydralazine. * **Option C (Hyperkalemia):** ACE inhibitors reduce Aldosterone secretion, which leads to potassium retention. Administering enalapril to a patient with existing hyperkalemia can lead to life-threatening arrhythmias. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** ACE inhibitors are DOC for HTN in patients with Diabetes, Chronic Kidney Disease (proteinuric), and Heart Failure (reduced ejection fraction). * **Side Effects:** Remember the mnemonic **CAPTOPRIL** (Cough, Angioedema, Proteinuria, Taste changes, Orthostatic hypotension, Pregnancy contraindication, Renal artery stenosis contraindication, Increased potassium, Leukopenia). * **Dry Cough:** Caused by the accumulation of **Bradykinin** and Substance P in the lungs. If a patient develops a cough, switch them to an ARB (e.g., Losartan).

Question 300: A drug is a classical example of pharmacological success but therapeutic failure due to the coronary steal phenomenon. Which drug is it?

A. Glyceryl trinitrate
B. Dipyridamole (Correct Answer)
C. Propranolol
D. Diltiazem

Explanation: ### Explanation **Correct Option: B. Dipyridamole** **The Concept: Coronary Steal Phenomenon** Dipyridamole is a potent coronary vasodilator that acts by inhibiting adenosine deaminase and phosphodiesterase, leading to increased adenosine levels. While it is a "pharmacological success" because it effectively dilates coronary arteries, it is a "therapeutic failure" in treating angina due to the **Coronary Steal Phenomenon**. In a patient with coronary artery disease, vessels supplying ischemic areas are already maximally dilated by local metabolites. When dipyridamole is administered, it dilates the healthy, non-ischemic vessels. This reduces resistance in the healthy zones, "stealing" blood flow away from the stenosed, ischemic areas and diverting it to well-perfused areas, potentially worsening the ischemia. **Why other options are incorrect:** * **A. Glyceryl trinitrate (GTN):** GTN primarily causes venodilation (reducing preload) and dilates large epicardial coronary arteries without causing steal. It is the drug of choice for acute angina. * **C. Propranolol:** A beta-blocker that reduces myocardial oxygen demand by decreasing heart rate and contractility. It does not cause vasodilation or coronary steal. * **D. Diltiazem:** A calcium channel blocker that reduces heart rate and causes coronary vasodilation, but it does not typically induce the steal phenomenon to a clinically significant degree compared to dipyridamole. **High-Yield NEET-PG Pearls:** * **Clinical Use:** Because of its ability to induce "steal," Dipyridamole is used in **Thallium/Persantine Stress Testing** to identify ischemic areas in patients unable to exercise. * **Antiplatelet Action:** Dipyridamole is also used in combination with Aspirin for secondary stroke prevention. * **Other "Steal" drugs:** Hydralazine and Isoflurane are also associated with coronary steal.

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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