Cardiovascular Drugs Practice Questions

Q: Which of the following is a direct renin inhibitor?

Aliskiren. ***Aliskiren*** - **Aliskiren** directly inhibits **renin**, the enzyme responsible for initiating the **renin-angiotensin-aldosterone system (RAAS)**, by preventing the conversion of **angiotensinogen to angiotensin I**. - This mechanism of action is distinct from other RAAS inhibitors that act further down the pathway. *Perindopril* - **Perindopril** is an **ACE inhibitor**, which works by blocking the enzyme that converts **angiotensin I to angiotensin II**. - It does not directly inhibit **renin** activity. *Losartan* - **Losartan** is an **angiotensin receptor blocker (ARB)**, which works by preventing **angiotensin II** from binding to its receptors. - It does not directly inhibit **renin** and primarily acts by blocking the effects of already formed **angiotensin II**. *Vernakalant* - **Vernakalant** is an antiarrhythmic drug primarily used for the acute conversion of **atrial fibrillation**. - It works by blocking specific **potassium and sodium channels** in the atria, and has no direct activity on the **renin-angiotensin-aldosterone system**.

Q: Drug of choice in cardiogenic shock is

Dopamine. ***Dopamine*** - **Dopamine** is often considered the **drug of choice** in cardiogenic shock because, at low to moderate doses, it increases myocardial contractility and heart rate (positive inotropic and chronotropic effects) while also improving renal perfusion. - Its ability to stimulate **alpha-1, beta-1, and dopaminergic receptors** makes it effective in improving cardiac output and maintaining organ perfusion in this critical condition. *Phenylephrine* - **Phenylephrine** is a selective **alpha-1 adrenergic agonist** that causes potent vasoconstriction and increases systemic vascular resistance. - While it effectively raises blood pressure, it **lacks inotropic effects** and can actually **reduce cardiac output** through reflex bradycardia and increased afterload. - Its strong vasoconstrictive effects without inotropic support make it **not suitable** as a primary agent in cardiogenic shock where cardiac contractility is already compromised. *Noradrenaline* - **Noradrenaline (norepinephrine)** is a potent vasoconstrictor primarily acting on alpha-1 receptors, leading to a significant increase in systemic vascular resistance and blood pressure. - While useful in some forms of shock, its strong vasoconstrictive effect can **increase afterload** and potentially worsen myocardial oxygen demand in cardiogenic shock with already compromised cardiac function. *Adrenaline* - **Adrenaline (epinephrine)** has strong **beta-1 and alpha-1 agonist effects**, leading to increased heart rate, contractility, and vasoconstriction. - While it can improve blood pressure and cardiac output, its significant **chronotropic and arrhythmogenic effects**, along with increased myocardial oxygen demand, make it less favorable than dopamine as a first-line agent in cardiogenic shock.

Q: Which of the following drugs decreases plasma renin activity

Clonidine. ***Clonidine*** - **Clonidine** is a centrally acting alpha-2 adrenergic agonist that reduces **sympathetic outflow** from the brainstem. - This reduction in sympathetic activity leads to decreased release of **norepinephrine**, which in turn reduces renin secretion by the kidneys. *Nifedipine* - **Nifedipine** is a **dihydropyridine calcium channel blocker** that causes peripheral vasodilation. - The vasodilation often leads to a **reflex increase in sympathetic activity** and, consequently, an increase in plasma renin activity. *Hydralazine* - **Hydralazine** is a direct systemic **vasodilator** that decreases peripheral vascular resistance. - This vasodilation can cause a **reflex increase in sympathetic activity** and **renin release** as the body tries to compensate for the drop in blood pressure. *Enalapril* - **Enalapril** is an **ACE inhibitor** that blocks the conversion of angiotensin I to angiotensin II. - This action directly leads to **increased plasma renin activity** due to the disruption of the negative feedback loop on renin release.

Q: Plasma Renin activity is lowered by which of the following group of drugs?

Alpha 2 agonists. ***Alpha 2 agonists*** - **Alpha-2 agonists** (e.g., clonidine) work by stimulating central alpha-2 adrenergic receptors, which reduces **sympathetic outflow** from the CNS. - This reduction in sympathetic tone decreases **renin release** from the juxtaglomerular cells in the kidney, thereby lowering plasma renin activity. *Arteriolar dilators* - **Arteriolar dilators** (e.g., hydralazine, minoxidil) decrease peripheral vascular resistance and lower blood pressure. - This reduction in blood pressure and renal perfusion can activate the **renin-angiotensin-aldosterone system (RAAS)**, leading to an **increase** in plasma renin activity as a compensatory mechanism. *Calcium channel blockers* - **Calcium channel blockers** (e.g., nifedipine, amlodipine) directly relax vascular smooth muscle and reduce peripheral resistance. - Some calcium channel blockers, particularly **dihydropyridines**, can cause reflex sympathetic activation due to vasodilation, potentially **increasing** renin release. *ACE inhibitors* - **ACE inhibitors** (e.g., enalapril, lisinopril) block the conversion of angiotensin I to angiotensin II. - By inhibiting the negative feedback that angiotensin II typically exerts on renin release, ACE inhibitors actually lead to an **increase** in plasma renin activity.

Q: Drug used for euvolemic hyponatremia in patient with advanced congestive heart failure is?

Tolvaptan. ***Tolvaptan*** - **Tolvaptan** is a selective **vasopressin V2-receptor antagonist** that promotes free water excretion (aquaresis) without significantly altering electrolyte balance, making it suitable for euvolemic hyponatremia [1]. - It works by blocking the action of **antidiuretic hormone (ADH)**, which is often elevated in patients with **congestive heart failure (CHF)** leading to water retention and hyponatremia [2]. *Nesiritide* - **Nesiritide** is a **recombinant human B-type natriuretic peptide (BNP)** that causes vasodilation and diuresis, but it is primarily used for acutely decompensated heart failure with signs of congestion, not specifically for euvolemic hyponatremia [1]. - While it can induce diuresis, its main role is to reduce **preload** and **afterload**, and it does not directly target the mechanism of euvolemic hyponatremia as effectively as an aquaretic agent [1]. *Metoprolol* - **Metoprolol** is a **beta-blocker** used to reduce heart rate and blood pressure, improving cardiac function in CHF patients. - It does not directly address **hyponatremia** and its mechanism of action is unrelated to water balance or sodium concentration. *Hydrocortisone* - **Hydrocortisone** is a **corticosteroid** used for conditions like adrenal insufficiency, inflammation, or allergic reactions. - It has no direct role in the management of **hyponatremia** or **congestive heart failure**.

Q: The drug that can cause hirsutism is

Minoxidil. ***Minoxidil*** - **Minoxidil** is a potent **vasodilator** that can cause **hirsutism** as a common side effect, especially when used orally. - Due to its hair growth stimulating effect, it is also topically used to treat **androgenetic alopecia** [1]. *Dactinomycin* - **Dactinomycin** is an **antineoplastic antibiotic** primarily used in cancer chemotherapy. - Its main side effects include **myelosuppression**, nausea, vomiting, and mucositis, not hirsutism. *Cycloserine* - **Cycloserine** is an antibiotic mainly used to treat **tuberculosis** [2]. - Its adverse effects are predominantly **neurological** and psychiatric, such as seizures and psychosis, not affecting hair growth [2]. *Valsartan* - **Valsartan** is an **angiotensin receptor blocker (ARB)** used to treat hypertension and heart failure. - Common side effects include dizziness and hyperkalemia; it does not cause hirsutism.

Q: A drug used to prevent niacin-induced flushing is

Aspirin. ***Aspirin*** - Niacin-induced flushing is mediated by **prostaglandins**, primarily prostaglandin D2 (PGD2), which cause vasodilation. - **Aspirin**, being a non-steroidal anti-inflammatory drug (NSAID) and a cyclooxygenase (COX) inhibitor, blocks the synthesis of prostaglandins, thereby reducing flushing. *Cetirizine* - Cetirizine is a **second-generation H1 antihistamine** primarily used to treat allergic symptoms like rhinitis or urticaria. - It does not significantly affect prostaglandin pathways implicated in niacin-induced flushing. *Dexamethasone* - Dexamethasone is a **corticosteroid** with potent anti-inflammatory and immunosuppressive effects. - While it can broadly reduce inflammation, it is not the primary or most appropriate treatment for niacin-induced flushing, which is better managed with prostaglandin inhibitors. *Paracetamol* - Paracetamol (acetaminophen) is an **analgesic and antipyretic** that works primarily by inhibiting prostaglandin synthesis in the central nervous system. - It has minimal anti-inflammatory effects and does not effectively reduce peripheral prostaglandin production responsible for niacin flush.

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.

Question 1

Which of the following is a direct renin inhibitor?

Accepted Answer

Aliskiren

Answer

Perindopril

Answer

Losartan

Answer

Vernakalant

Question 2

Drug of choice in cardiogenic shock is

Accepted Answer

Dopamine

Answer

Noradrenaline

Answer

Adrenaline

Answer

Phenylephrine

Question 3

Which of the following drugs decreases plasma renin activity

Accepted Answer

Clonidine

Answer

Nifedipine

Answer

Hydralazine

Answer

Enalapril

Question 4

Plasma Renin activity is lowered by which of the following group of drugs?

Accepted Answer

Alpha 2 agonists

Answer

Arteriolar dilators

Answer

Calcium channel blockers

Answer

ACE inhibitors

Question 5

Drug used for euvolemic hyponatremia in patient with advanced congestive heart failure is?

Accepted Answer

Tolvaptan

Answer

Nesiritide

Answer

Metoprolol

Answer

Hydrocortisone

Question 6

The drug that can cause hirsutism is

Accepted Answer

Minoxidil

Answer

Dactinomycin

Answer

Cycloserine

Answer

Valsartan

Question 7

A drug used to prevent niacin-induced flushing is

Accepted Answer

Aspirin

Answer

Dexamethasone

Answer

Paracetamol

Answer

Cetirizine

Question 8

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 9

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 10

All of the following may precipitate digitalis toxicity except :

Accepted Answer

Hypocalcemia

Answer

Hypomagnesemia

Answer

Hypokalemia

Answer

Hypothyroidism

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

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