Cardiovascular Drugs Practice Questions

Q: Ductus arteriosus closes in response to ?

Indomethacin therapy. ***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.

Q: A patient given one of the following drug develops low grade fever, muscle and joint ache, chest pain and skin rashes. Lab investigations showed presence of antihistone antibodies. Symptoms however subsided after discontinuation of the drug. Which is the drug that caused the reaction?

Hydralazine. ***Hydralazine*** - This drug is a well-known cause of **drug-induced lupus erythematosus (DILE)**, which presents with symptoms like fever, myalgia, arthralgia, pleuritic chest pain, and skin rashes. - The presence of **antihistone antibodies** is a hallmark laboratory finding in DILE, and symptoms typically resolve upon discontinuation of the causative drug. *Paracetamol* - Paracetamol (acetaminophen) is an **analgesic** and **antipyretic** and is generally well-tolerated. - It does not typically cause a lupus-like syndrome or induce the formation of antihistone antibodies. *Furosemide* - Furosemide is a **loop diuretic** primarily used for treating edema and hypertension. - While it can cause side effects like electrolyte imbalances, it is not associated with drug-induced lupus or antihistone antibodies. *Rifampicin* - Rifampicin is an **antibiotic** used to treat tuberculosis and other bacterial infections. - Its side effects can include hepatotoxicity, gastrointestinal disturbances, and reddish discoloration of body fluids, but not typically a lupus-like syndrome with antihistone antibodies.

Q: All of the following may precipitate digitalis toxicity except :

Hypocalcemia. ***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.

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

Amiodarone. ***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.

Q: Drug of choice for Digoxin induced Ventricular Tachycardia:

Lignocaine. ***Lignocaine*** - **Lignocaine** (also known as lidocaine) is the drug of choice for digoxin-induced ventricular tachycardia due to its ability to suppress ventricular arrhythmias without further compromising cardiac contractility [1]. - It works by blocking **sodium channels** in the myocardium, reducing automaticity and stabilizing the cardiac membrane [1]. *Diltiazem* - **Diltiazem** is a calcium channel blocker primarily used for supraventricular tachycardias and angina [1]. - It is contraindicated in digoxin toxicity as it can worsen myocardial depression and AV nodal blockade [1]. *Propranolol* - **Propranolol** is a beta-blocker that can suppress some arrhythmias but is generally not the first-line treatment for digoxin-induced ventricular tachycardia [1]. - Beta-blockers can worsen **bradycardia** and **AV block** often seen in digoxin toxicity [1]. *Verapamil* - **Verapamil** is a calcium channel blocker similar to diltiazem and can exacerbate digoxin toxicity [1]. - It is known to increase serum **digoxin levels** and can worsen the underlying cardiotoxic effects.

Q: Which of the following causes vasodilation?

Histamine. ***Histamine*** - Histamine is a **potent vasodilator**, primarily through its effects on H1 receptors, leading to the relaxation of **vascular smooth muscle**. - This vasodilation contributes to the increased blood flow and **erythema** observed during inflammatory and allergic responses. - Acts via H1 receptors on endothelial cells to release **nitric oxide** and **prostacyclin**. *Thromboxane A2* - **Thromboxane A2** is a potent **vasoconstrictor** and platelet aggregator, playing a key role in hemostasis and thrombosis. - It is synthesized from **arachidonic acid** via COX-1 and is predominantly found in platelets. *Angiotensin II* - **Angiotensin II** is a powerful **vasoconstrictor** that increases blood pressure through direct arterial smooth muscle contraction. - Part of the **renin-angiotensin-aldosterone system (RAAS)**, it also promotes sodium retention and aldosterone release. - Targeted by ACE inhibitors and ARBs for hypertension management. *Serotonin* - Serotonin (5-hydroxytryptamine, 5-HT) has **complex effects on vascular tone**, causing both vasodilation and vasoconstriction depending on the receptor subtype and vascular bed. - In many contexts, particularly in damaged vessels, it acts as a **vasoconstrictor** and promotes platelet aggregation.

Q: Major mechanism of action of nitrates in acute attack of angina is:

Decreases in preload. ***Decreases in preload*** - Nitrates primarily cause systemic **venodilation**, leading to pooling of blood in the peripheral veins and reducing venous return to the heart. - This reduction in venous return directly decreases the **left ventricular end-diastolic volume** and pressure, thereby lowering myocardial oxygen demand. *Coronary vasodilation* - While nitrates can cause some **coronary vasodilation**, especially in epicardial arteries, this effect is less significant in relieving acute angina compared to their systemic venodilating effects, particularly in areas of fixed stenosis. - In atherosclerotic vessels, the ability to dilate is impaired, making the **reduction in demand** more critical than increased supply. *Decreases in afterload* - Nitrates can cause some **arterial vasodilation** leading to a modest decrease in afterload, but this is a secondary effect. - The primary and most profound action, especially at therapeutic doses for angina, is on the **venous system**. *Decreases in heart rate* - Nitrates generally do not directly decrease heart rate; in fact, a reflex **tachycardia** can sometimes occur due to the drop in blood pressure. - A decrease in heart rate would reduce myocardial oxygen demand, but this is not the **major mechanism of nitrates**.

Q: Which of the following is not used in heart failure?

Trimetazidine. ***Trimetazidine*** - While it has an anti-ischemic effect and can be used in **stable angina**, trimetazidine is *not* a primary or established drug for **heart failure** treatment. - Its mechanism involves metabolic modulation rather than direct hemodynamic or neurohormonal benefits critical for heart failure. *Sacubitril* - Sacubitril is a **neprilysin inhibitor**, often combined with valsartan (an ARB) as **sacubitril/valsartan**, and is a cornerstone in managing **heart failure with reduced ejection fraction (HFrEF)**. - It enhances beneficial natriuretic peptides, leading to vasodilation, natriuresis, and reduced cardiac remodeling. *Metoprolol* - **Beta-blockers** like metoprolol are essential in heart failure management, particularly in **HFrEF**, to reduce mortality and morbidity. - They work by blocking the effects of norepinephrine and epinephrine, thereby reducing heart rate, myocardial contractility, and preventing adverse cardiac remodeling. *Nesiritide* - Nesiritide is a **recombinant human B-type natriuretic peptide (BNP)** that is used intravenously in the acute setting for **decompensated heart failure**. - It promotes vasodilation, diuresis, and natriuresis, helping to reduce preload and afterload.

Q: Assertion: ACE inhibitors are contraindicated in bilateral renal artery stenosis. Reason: They cause acute kidney injury by reducing efferent arteriolar tone.

Both A & R true, R explains A. ***Correct: Both A & R true, R explains A*** - **Assertion is TRUE**: ACE inhibitors are absolutely contraindicated in bilateral renal artery stenosis due to risk of acute kidney injury - **Reason is TRUE**: In bilateral renal artery stenosis, the kidneys depend on **angiotensin II** to maintain GFR by constricting the efferent arteriole - **R explains A**: ACE inhibitors block angiotensin II production → **efferent arteriolar dilation** → drastically reduced GFR → **acute kidney injury (AKI)** - This direct mechanistic link makes the reason a complete explanation of the assertion *Incorrect: A true R false* - While the assertion is true, the reason is also **true** (not false) - ACE inhibitors do reduce efferent arteriolar tone by blocking angiotensin II - This is the precise mechanism causing AKI in these patients *Incorrect: Both A & R true, R doesn't explain A* - Both statements are indeed true, but this option is incorrect because the reason **does explain** the assertion - The mechanism (reduced efferent arteriolar tone → decreased GFR) directly explains why ACE inhibitors are contraindicated - The causal relationship is clear and direct *Incorrect: A false R true* - The assertion is **true**, not false - ACE inhibitors are definitively contraindicated in bilateral renal artery stenosis - This is a well-established clinical contraindication to prevent renal failure

Q: A 70-year-old patient with heart failure and low potassium is on digoxin and furosemide. Which medication addition could safely counteract hypokalemia without risking digoxin toxicity?

Spironolactone. ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that helps counteract potassium loss caused by furosemide, thereby reducing the risk of **hypokalemia** - By preventing hypokalemia, spironolactone indirectly reduces the risk of **digoxin toxicity**, as hypokalemia potentiates the cardiac effects of digoxin and increases myocardial sensitivity to digoxin - This is the **standard of care** in heart failure patients on loop diuretics and digoxin *Amlodipine* - **Amlodipine** is a **calcium channel blocker** primarily used for **hypertension** and **angina** - It does not directly affect **potassium levels** and would not address the patient's hypokalemia - While safe with digoxin, it doesn't solve the underlying electrolyte problem *Calcium gluconate* - **Calcium gluconate** is primarily used to treat **hyperkalemia** or **hypocalcemia** - While it can be used to treat digoxin toxicity in emergency settings by stabilizing cardiac membranes, it does not prevent **hypokalemia** - It does not replenish potassium stores and is not appropriate for chronic management *Hydrochlorothiazide* - **Hydrochlorothiazide** is a **thiazide diuretic** that, like furosemide, causes **potassium wasting** through increased renal excretion - Adding it would **exacerbate** the patient's existing **hypokalemia**, significantly increasing the risk of **digoxin toxicity** - This combination would be potentially dangerous in this clinical scenario

Question 1

Ductus arteriosus closes in response to ?

Accepted Answer

Indomethacin therapy

Answer

Decrease in peripheral oxygen saturation

Answer

Increase in pulmonary vascular resistance

Answer

Prostaglandin E1

Question 2

A patient given one of the following drug develops low grade fever, muscle and joint ache, chest pain and skin rashes. Lab investigations showed presence of antihistone antibodies. Symptoms however subsided after discontinuation of the drug. Which is the drug that caused the reaction?

Accepted Answer

Hydralazine

Answer

Paracetamol

Answer

Furosemide

Answer

Rifampicin

Question 3

All of the following may precipitate digitalis toxicity except :

Accepted Answer

Hypocalcemia

Answer

Hypomagnesemia

Answer

Hypokalemia

Answer

Hypothyroidism

Question 4

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

Accepted Answer

Amiodarone

Answer

Lignocaine

Answer

Procainamide

Answer

Verapamil

Question 5

Drug of choice for Digoxin induced Ventricular Tachycardia:

Accepted Answer

Lignocaine

Answer

Diltiazem

Answer

Propranolol

Answer

Verapamil

Question 6

Which of the following causes vasodilation?

Accepted Answer

Histamine

Answer

Thromboxane A2

Answer

Angiotensin II

Answer

Serotonin

Question 7

Major mechanism of action of nitrates in acute attack of angina is:

Accepted Answer

Decreases in preload

Answer

Coronary vasodilation

Answer

Decreases in afterload

Answer

Decreases in heart rate

Question 8

Which of the following is not used in heart failure?

Accepted Answer

Trimetazidine

Answer

Sacubitril

Answer

Metoprolol

Answer

Nesiritide

Question 9

Assertion: ACE inhibitors are contraindicated in bilateral renal artery stenosis. Reason: They cause acute kidney injury by reducing efferent arteriolar tone.

Accepted Answer

Both A & R true, R explains A

Answer

A true R false

Answer

Both A & R true, R doesn't explain A

Answer

A false R true

Question 10

A 70-year-old patient with heart failure and low potassium is on digoxin and furosemide. Which medication addition could safely counteract hypokalemia without risking digoxin toxicity?

Accepted Answer

Spironolactone

Answer

Amlodipine

Answer

Calcium gluconate

Answer

Hydrochlorothiazide

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

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