Cardiovascular Drugs Practice Questions

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

Q: A patient on atorvastatin presents with myalgia; which test is recommended?

Creatine kinase. ***Creatine kinase*** - **Myalgia** in a patient on **atorvastatin** raises concern for **statin-induced myopathy**, which can range from mild muscle aches to severe **rhabdomyolysis** [1]. - **Creatine kinase (CK)** levels are commonly used to assess muscle damage, with significantly elevated levels (e.g., >10 times normal) indicating rhabdomyolysis [1]. *Liver function test* - While atorvastatin can cause **hepatic dysfunction**, **myalgia** is not a primary symptom of liver injury [1]. - **Liver function tests (LFTs)** would be more relevant if the patient presented with jaundice, dark urine, or other signs of liver damage [1]. *Blood urea nitrogen* - **Blood urea nitrogen (BUN)** is a marker of **kidney function**, not directly related to muscle pain or statin-induced myopathy. - While severe **rhabdomyolysis** can lead to **acute kidney injury (AKI)**, BUN would be checked *after* CK levels indicate significant muscle breakdown. *Serum potassium* - **Serum potassium** levels are important for **cardiac and muscle function**, but myalgia itself does not directly indicate a potassium imbalance. - **Hyperkalemia** can occur secondary to severe **rhabdomyolysis** due to the release of intracellular potassium from damaged muscle cells, but CK is the initial diagnostic test for muscle injury.

Q: What is the usual daily dose of fenofibrate for managing hyperlipidemia in adults?

200 mg. ***200 mg*** - The usual daily dose of **fenofibrate (non-micronized formulation)** for managing hyperlipidemia in adults is **200 mg once daily**. - This dose effectively reduces **triglycerides** and increases **HDL cholesterol** in patients with dyslipidemia. - **Micronized formulations** may use 160 mg or 145 mg daily due to better bioavailability. - Dose adjustment is required in **renal impairment** to reduce the risk of myopathy. *300 mg* - A 300 mg dose **exceeds the standard recommended daily dose** for fenofibrate and increases the risk of adverse effects including myopathy, hepatotoxicity, and gastrointestinal disturbances. - Higher doses do not provide additional lipid-lowering benefit and are not recommended. *150 mg* - While 150 mg is close to the therapeutic range, it represents a **submaximal dose** for standard non-micronized fenofibrate formulations. - Some micronized formulations use 145-160 mg, but **200 mg is the standard dose for conventional fenofibrate**. *250 mg* - A 250 mg dose is **not a standard therapeutic dose** for fenofibrate in managing hyperlipidemia. - This dose would increase adverse effects without additional clinical benefit and is not supported by clinical guidelines.

Q: What is the primary mechanism by which digoxin improves symptoms in heart failure?

Inhibits Na+/K+ ATPase. Inhibits Na+/K+ ATPase - Digoxin's primary mechanism involves inhibiting the Na+/K+ ATPase pump in cardiac myocytes [1]. - This inhibition leads to an increase in intracellular sodium, which in turn reduces the efficiency of the Na+/Ca2+ exchanger, ultimately increasing intracellular calcium [1]. Increases intracellular calcium levels - While digoxin does increase intracellular calcium, this is a downstream effect of its initial action on the Na+/K+ ATPase pump, not its primary mechanism of action [2]. - The elevated calcium then leads to increased contractility of the cardiac muscle [2]. Increases heart rate - Digoxin actually tends to decrease heart rate by increasing vagal tone, which is beneficial in heart failure, especially in patients with atrial fibrillation [1], [3]. - An increased heart rate would worsen cardiac output in a failing heart. Decreases heart rate - While digoxin does decrease heart rate, this is an indirect effect through vagal stimulation, and not its primary cellular mechanism of action for improving contractility in heart failure [3]. - The direct and primary mechanism is the inhibition of the Na+/K+ ATPase [1].

Question 1

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 2

Drug of choice for Digoxin induced Ventricular Tachycardia:

Accepted Answer

Lignocaine

Answer

Diltiazem

Answer

Propranolol

Answer

Verapamil

Question 3

Which of the following causes vasodilation?

Accepted Answer

Histamine

Answer

Thromboxane A2

Answer

Angiotensin II

Answer

Serotonin

Question 4

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 5

Which of the following is not used in heart failure?

Accepted Answer

Trimetazidine

Answer

Sacubitril

Answer

Metoprolol

Answer

Nesiritide

Question 6

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 7

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

Question 8

A patient on atorvastatin presents with myalgia; which test is recommended?

Accepted Answer

Creatine kinase

Answer

Liver function test

Answer

Blood urea nitrogen

Answer

Serum potassium

Question 9

What is the usual daily dose of fenofibrate for managing hyperlipidemia in adults?

Accepted Answer

200 mg

Answer

300 mg

Answer

150 mg

Answer

250 mg

Question 10

What is the primary mechanism by which digoxin improves symptoms in heart failure?

Accepted Answer

Inhibits Na+/K+ ATPase

Answer

Increases intracellular calcium levels

Answer

Increases heart rate

Answer

Decreases heart rate

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

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