Cardiovascular Drugs — MCQs

Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs

Question 681: What is the drug of choice for persistent unstable ventricular arrhythmia?

A. Procainamide
B. Calcium gluconate
C. Amiodarone (Correct Answer)
D. Digoxin

Explanation: **Explanation:** **Amiodarone** is the drug of choice for persistent unstable ventricular arrhythmias (such as Ventricular Tachycardia or Ventricular Fibrillation) that are refractory to electrical cardioversion or defibrillation. As a Class III antiarrhythmic, its primary mechanism is blocking potassium channels, which prolongs the action potential duration and effective refractory period. However, it also possesses Class I (sodium channel), Class II (beta-blocking), and Class IV (calcium channel) properties, making it highly effective across various myocardial tissues. **Why other options are incorrect:** * **Procainamide (Option A):** While a Class IA antiarrhythmic used for stable VT (especially in Wolff-Parkinson-White syndrome), it is not the first-line choice for persistent unstable arrhythmias due to its slower onset and risk of hypotension. * **Calcium Gluconate (Option B):** This is used for cardioprotection in hyperkalemia or for calcium channel blocker toxicity; it has no direct antiarrhythmic effect on ventricular tachycardia. * **Digoxin (Option C):** Used primarily for rate control in atrial fibrillation or in heart failure. It can actually *induce* ventricular arrhythmias in toxic doses. **NEET-PG High-Yield Pearls:** * **ACLS Protocol:** In pulseless VT/VF, Amiodarone is administered after the third shock. Lidocaine is the alternative if Amiodarone is unavailable. * **Side Effects:** Long-term use is associated with "6 Ps": **P**ulmonary fibrosis, **P**hotodermatitis (Blue-grey skin), **P**rolonged QT, **P**eripheral neuropathy, and **P**eripapillary (corneal) deposits, and Thyroid **P**athology (Hypo/Hyperthyroidism due to high iodine content). * **Drug of Choice:** Amiodarone is also the drug of choice for arrhythmias in patients with structural heart disease or decreased ejection fraction.

Question 682: Important adverse effect of nesiritide is

A. Dysgeusia
B. Hypotension (Correct Answer)
C. Cough
D. Angioedema

Explanation: **Explanation:** **Nesiritide** is a recombinant form of human **B-type Natriuretic Peptide (BNP)**. It is primarily used in the management of acutely decompensated heart failure with dyspnea at rest. **1. Why Hypotension is the Correct Answer:** Nesiritide works by binding to particulate guanylyl cyclase receptors, leading to increased intracellular **cGMP**. This results in potent **vasodilation** of both arteries and veins (reducing both preload and afterload) and promotes natriuresis. Because of its potent vasodilatory properties, **dose-dependent hypotension** is its most common and significant adverse effect. It can sometimes be prolonged and require careful blood pressure monitoring during infusion. **2. Analysis of Incorrect Options:** * **A. Dysgeusia (Taste perversion):** This is a classic side effect associated with **Captopril** (an ACE inhibitor), often due to its sulfhydryl group. * **C. Cough:** This is a hallmark side effect of **ACE Inhibitors** (like Enalapril or Lisinopril) caused by the accumulation of bradykinin and substance P in the lungs. * **D. Angioedema:** This is a rare but life-threatening adverse effect primarily linked to **ACE Inhibitors** and, to a lesser extent, ARBs and Neprilysin inhibitors (Sacubitril). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Increases cGMP $\rightarrow$ Vasodilation + Natriuresis. * **Indication:** Acutely decompensated heart failure (ADHF). * **Key Side Effects:** Hypotension (most common) and potential renal impairment (azotemia). * **Half-life:** Short (approx. 18 minutes), administered via IV bolus followed by continuous infusion.

Question 683: Which drug is used for the management of atrial fibrillation and atrial flutter?

A. Verapamil
B. Digitalis (Correct Answer)
C. Quinidine
D. Diphenylhydantoin

Explanation: **Explanation:** The primary goal in managing atrial fibrillation (AF) and atrial flutter is **ventricular rate control**. **Digitalis (Digoxin)** is the correct answer because of its unique electrophysiological properties. It increases vagal tone (parasympathomimetic effect), which **decreases conduction velocity and increases the refractory period of the Atrioventricular (AV) node**. By slowing AV conduction, it prevents the rapid atrial impulses from reaching the ventricles, thereby controlling the ventricular rate. It is particularly preferred in patients with co-existing heart failure due to its positive inotropic effect. **Analysis of Incorrect Options:** * **Verapamil (Option A):** While Verapamil (a Calcium Channel Blocker) is also used for rate control in AF, in the context of classic pharmacology questions, Digitalis is often highlighted for its specific vagal mechanism. However, Verapamil is contraindicated in patients with heart failure. * **Quinidine (Option C):** This is a Class IA antiarrhythmic used for **rhythm control** (converting AF to sinus rhythm). It is rarely used now due to its potential to cause "Quinidine syncope" (Torsades de Pointes) and its vagolytic effect, which can paradoxically increase ventricular rate if used without a prior AV nodal blocker. * **Diphenylhydantoin (Option D):** Also known as Phenytoin, this is a Class IB antiarrhythmic. It is specifically the drug of choice for **Digitalis-induced atrial tachycardia** with AV block, but not for routine AF/flutter. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Digoxin inhibits Na+/K+ ATPase, leading to increased intracellular Ca²⁺ (inotropy) and increased vagal tone (negative dromotropy). * **ECG Changes:** Digoxin can cause "sagging" ST-segment depression (Hockey-stick appearance). * **Toxicity:** Hypokalemia predisposes to Digoxin toxicity. The most common arrhythmia in toxicity is Ventricular Bigeminy; the most characteristic is Atrial Tachycardia with AV block.

Question 684: What is the mechanism of action of Telmisartan?

A. Blocks alpha adrenergic receptors
B. AT-2 receptor antagonist
C. Blocks AT-1 receptors (Correct Answer)
D. Mast cell stabilizer

Explanation: **Explanation:** **Mechanism of Action:** Telmisartan belongs to the class of **Angiotensin II Receptor Blockers (ARBs)**. It acts by selectively and competitively antagonizing the **AT-1 receptors**. Under normal physiological conditions, Angiotensin II binds to AT-1 receptors to cause potent vasoconstriction, aldosterone release, and sympathetic activation. By blocking these receptors, Telmisartan promotes vasodilation and reduces peripheral resistance, thereby lowering blood pressure. **Analysis of Options:** * **Option A (Alpha blockers):** Drugs like Prazosin or Terazosin block alpha-1 receptors. Telmisartan does not interact with the adrenergic system. * **Option B (AT-2 antagonist):** While there are two main types of Angiotensin receptors (AT-1 and AT-2), the beneficial cardiovascular effects of ARBs come from blocking **AT-1**. AT-2 receptors are generally associated with vasodilation and anti-proliferation; blocking them would be counterproductive. * **Option D (Mast cell stabilizer):** This describes drugs like Sodium Cromoglycate, used in asthma and allergic rhinitis, which have no relation to the renin-angiotensin system. **High-Yield Clinical Pearls for NEET-PG:** * **Unique Property:** Telmisartan has a dual mechanism; it also acts as a partial agonist of **PPAR-gamma** (Peroxisome Proliferator-Activated Receptor gamma), which may provide additional metabolic benefits like improved insulin sensitivity. * **Pharmacokinetics:** It has the **longest half-life** (~24 hours) among all ARBs, allowing for once-daily dosing. * **Advantage over ACE Inhibitors:** ARBs do not inhibit the breakdown of bradykinin; therefore, they **do not cause the dry cough** or angioedema typically seen with Enalapril or Lisinopril. * **Contraindication:** Like all drugs acting on the RAAS, Telmisartan is strictly **teratogenic** and contraindicated in pregnancy.

Question 685: Aliskiren is a:

A. Endothelin receptor antagonist
B. Antiplatelet
C. Renin inhibitor (Correct Answer)
D. Diuretic

Explanation: **Explanation:** **Aliskiren** is the first and only clinically approved **Direct Renin Inhibitor (DRI)**. It acts at the rate-limiting step of the Renin-Angiotensin-Aldosterone System (RAAS) by directly binding to the catalytic site of renin [2]. This prevents the conversion of Angiotensinogen to Angiotensin I, leading to a decrease in levels of Angiotensin II and Aldosterone, which results in vasodilation and reduced blood pressure [2]. **Analysis of Incorrect Options:** * **Option A (Endothelin receptor antagonist):** These drugs (e.g., **Bosentan, Ambrisentan**) block endothelin receptors and are primarily used in the management of Pulmonary Arterial Hypertension (PAH). * **Option B (Antiplatelet):** These agents (e.g., **Aspirin, Clopidogrel**) inhibit platelet aggregation to prevent thromboembolic events. * **Option D (Diuretic):** These drugs (e.g., **Furosemide, Hydrochlorothiazide**) increase urine output by inhibiting sodium reabsorption in the nephron. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Unlike ACE inhibitors or ARBs, Aliskiren does not increase bradykinin levels; therefore, the incidence of **dry cough** is significantly lower [1]. * **Pharmacokinetics:** It has very low oral bioavailability (~2.5%) and its absorption is significantly decreased by high-fat meals [1]. * **Contraindications:** It is strictly **contraindicated in pregnancy** (teratogenic) and should not be combined with ACE inhibitors or ARBs in patients with diabetes due to the risk of hyperkalemia and renal impairment (ALTITUDE trial) [1]. * **Side Effects:** Hyperkalemia, diarrhea (at high doses), and angioedema (rare) [1].

Question 686: Daltroban is an antagonist of which of the following?

A. Angiotensin
B. Nitric oxide
C. Thromboxane A2 (Correct Answer)
D. Oxytocin

Explanation: **Explanation:** **Daltroban** is a selective and potent **Thromboxane A2 (TXA2) receptor antagonist**. Thromboxane A2 is a powerful mediator released by platelets that causes potent vasoconstriction and promotes platelet aggregation [1]. By blocking the TXA2 (TP) receptors, Daltroban inhibits these effects, making it useful in research and clinical studies for conditions involving pathological platelet activation and vasospasm, such as myocardial ischemia and renal disorders. **Analysis of Options:** * **Option A (Angiotensin):** Antagonists of Angiotensin II are known as ARBs (e.g., Losartan, Valsartan). They act on AT1 receptors to lower blood pressure. * **Option B (Nitric Oxide):** Nitric oxide is a vasodilator. Antagonists are rarely used clinically, though NOS inhibitors (like L-NAME) are used in research. * **Option D (Oxytocin):** Antagonists of oxytocin (e.g., Atosiban) are used as tocolytics to inhibit premature labor. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism Distinction:** While **Aspirin** inhibits TXA2 *synthesis* (by inhibiting COX-1), **Daltroban** and **Ifetroban** act by *blocking the receptor* itself. * **Dual Action:** Some newer agents like **Ridogrel** act as both TXA2 synthase inhibitors and TXA2 receptor antagonists. * **Clinical Utility:** TXA2 antagonists are primarily studied for their potential to prevent thrombosis without significantly increasing bleeding time compared to traditional antiplatelet agents.

Question 687: Food reduces the oral bioavailability of the following angiotensin converting enzyme inhibitors EXCEPT?

A. Enalapril (Correct Answer)
B. Captopril
C. Ramipril
D. Fosinopril

Explanation: **Explanation:** The oral bioavailability of most ACE inhibitors is affected by the presence of food in the gastrointestinal tract, which typically delays or reduces absorption. However, **Enalapril** is a notable exception. **1. Why Enalapril is Correct:** Enalapril is a prodrug that is converted into its active metabolite, enalaprilat, in the liver. Its gastrointestinal absorption is **not significantly affected by food**. This clinical advantage allows for flexible dosing (with or without meals), ensuring consistent therapeutic levels regardless of dietary timing. **2. Analysis of Incorrect Options:** * **Captopril:** This is the classic example of an ACE inhibitor whose bioavailability is significantly **reduced (by 30–40%)** when taken with food. It should ideally be taken one hour before meals. * **Ramipril:** Similar to many other ACE inhibitors, food can delay the rate of absorption of Ramipril, although the extent of reduction is less severe than Captopril. * **Fosinopril:** The absorption of Fosinopril is also slightly reduced or delayed by the presence of food. **3. High-Yield Clinical Pearls for NEET-PG:** * **Prodrug Status:** All ACE inhibitors are prodrugs **EXCEPT Captopril and Lisinopril**. * **Elimination:** All ACE inhibitors are primarily excreted renally **EXCEPT Fosinopril and Spirapril**, which have balanced hepatobiliary and renal excretion (making them safer in renal failure). * **Duration of Action:** Captopril has the shortest half-life and requires multiple daily dosing, whereas most others (like Enalapril and Ramipril) are suitable for once or twice-daily dosing. * **Key Side Effects:** Remember the mnemonic **CAPTOPRIL** (Cough, Angioedema, Proteinuria, Taste changes, Orthostatic hypotension, Pregnancy contraindication, Renal artery stenosis contraindication, Increased Potassium, Leukopenia).

Question 688: The dose of digoxin is NOT altered in which of the following conditions?

A. Old age
B. Hepatic disease (Correct Answer)
C. Renal disease
D. Hypercalcemia

Explanation: **Explanation:** The correct answer is **Hepatic disease** because of the pharmacokinetic profile of Digoxin. **1. Why Hepatic Disease is the correct answer:** Digoxin is a polar glycoside that is primarily excreted **unchanged by the kidneys** (approx. 60-80%) via glomerular filtration and tubular secretion (P-glycoprotein mediated) [2], [3]. It undergoes minimal hepatic metabolism [2]. Therefore, its clearance is not significantly affected by liver dysfunction, and dose adjustment is generally not required in patients with hepatic disease [1]. **2. Why the other options are incorrect:** * **Old Age:** Renal function naturally declines with age (reduced GFR). Additionally, elderly patients have lower skeletal muscle mass (the primary tissue reservoir for digoxin), leading to higher serum levels. Dose reduction is mandatory to avoid toxicity. * **Renal Disease:** Since the kidneys are the primary route of elimination, any degree of renal impairment increases the half-life of digoxin significantly (from 36 hours up to 5 days), necessitating strict dose reduction based on creatinine clearance [2], [3]. * **Hypercalcemia:** Digoxin works by inhibiting the Na+/K+ ATPase pump, which indirectly increases intracellular calcium. Hypercalcemia synergizes with digoxin, increasing the risk of cardiac arrhythmias. In this state, the heart is "sensitized" to digoxin, requiring a lower dose or cautious monitoring [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Digitoxin vs. Digoxin:** Unlike Digoxin, **Digitoxin** is primarily metabolized by the liver and is the drug of choice in patients with renal failure (though rarely used now) [2]. * **Electrolyte Triad:** Digoxin toxicity is precipitated by **Hypokalemia, Hypomagnesemia, and Hypercalcemia.** * **Monitoring:** The therapeutic range for digoxin is narrow (**0.5–2 ng/mL**) [2]. * **Antidote:** Digibind (Digoxin-specific Fab fragments) is used for life-threatening toxicity.

Question 689: Which of the following anti-arrhythmic drugs decreases the action potential duration in Purkinje fibers?

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

Explanation: **Explanation:** The question tests the understanding of the **Vaughan-Williams classification** of anti-arrhythmic drugs, specifically their effects on the cardiac action potential. **1. Why Lignocaine is Correct:** Lignocaine (Lidocaine) is a **Class IB sodium channel blocker**. Unlike Class IA drugs, Class IB agents preferentially bind to sodium channels in the inactivated state and dissociate rapidly. Crucially, they **shorten the Action Potential Duration (APD)** and the Effective Refractory Period (ERP) in Purkinje fibers and ventricular myocytes. They achieve this by blocking the small "late" inward sodium current that normally persists during the plateau phase (Phase 2), leading to earlier repolarization. **2. Why the Other Options are Incorrect:** * **A. Quinidine (Class IA):** These drugs block sodium channels and potassium channels. By blocking K+ channels, they **prolong** the APD and the QT interval. * **B. Flecainide (Class IC):** These are the most potent sodium channel blockers but have a **neutral effect** (no significant change) on the APD. * **C. Amiodarone (Class III):** The primary mechanism of Class III drugs is potassium channel blockade, which significantly **prolongs** the APD and ERP. **3. High-Yield Clinical Pearls for NEET-PG:** * **Class IB Selectivity:** Lignocaine is selective for **ischemic tissues** and depolarized cells, making it the drug of choice for post-myocardial infarction ventricular arrhythmias. * **ERP/APD Ratio:** Although Lignocaine decreases APD, it decreases it less than the ERP, effectively **increasing the ERP/APD ratio**, which underlies its anti-arrhythmic efficacy. * **Route of Administration:** Lignocaine undergoes extensive first-pass metabolism; therefore, it is given only **intravenously**. * **Toxicity:** Neurological side effects (seizures, tremors, "Lidocaine crazies") are common signs of toxicity.

Question 690: Which antihypertensive causes decreased libido and impotence?

A. Atenolol (Correct Answer)
B. Enalapril
C. Prazosin
D. Diltiazem

Explanation: **Explanation:** **Atenolol (Correct Answer):** Atenolol is a cardioselective **$\beta_1$-blocker**. Beta-blockers are the most common class of antihypertensives associated with sexual dysfunction, specifically decreased libido and erectile dysfunction (impotence). The mechanism is multifactorial: they cause a decrease in central sympathetic outflow, lower systemic blood pressure (reducing penile perfusion), and may interfere with the relaxation of corpus cavernosum smooth muscle. Additionally, non-selective beta-blockers can lead to peripheral vasoconstriction, further exacerbating the issue. **Why the other options are incorrect:** * **Enalapril (ACE Inhibitor):** ACE inhibitors and ARBs are generally considered "sexually neutral" or may even improve sexual function by increasing nitric oxide availability and improving endothelial health. * **Prazosin ($\alpha_1$-blocker):** These drugs are rarely associated with impotence. In fact, $\alpha$-blockers are sometimes used to treat BPH and can improve sexual function by causing vasodilation. However, they are notorious for causing **first-dose hypotension** and **retrograde ejaculation**. * **Diltiazem (Calcium Channel Blocker):** CCBs are typically neutral regarding sexual desire and performance. **NEET-PG High-Yield Pearls:** * **Diuretics (especially Thiazides)** and **Beta-blockers** are the two primary antihypertensive classes linked to impotence. * **Spironolactone** (K+-sparing diuretic) causes decreased libido and gynecomastia due to its anti-androgenic effects. * **Nebivolol** is a unique $\beta$-blocker that increases Nitric Oxide (NO) release, making it the $\beta$-blocker least likely to cause erectile dysfunction. * **Drug of choice** for hypertension in a patient concerned about sexual dysfunction: **ACE inhibitors or ARBs.**

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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