Cardiovascular Drugs Practice Questions

Q: Which of the following graphs of cardiac action potential represents mechanism of action of lignocaine?

Second graph from the left. ***Correct: Second graph from the left*** - Lignocaine is a **Class IB antiarrhythmic drug** that works by *selectively blocking activated and inactivated sodium channels*. This action **reduces the slope of phase 0 depolarization** (upstroke velocity) and **shortens the action potential duration** (phase 3 repolarization). - The graph shows a decreased steepness of phase 0 and a **shorter overall action potential duration** compared to the baseline (solid line), which is characteristic of Class IB antiarrhythmics like lignocaine. *Incorrect: First graph from the left* - This graph represents a drug that **significantly decreases the slope of phase 0** and **markedly prolongs the action potential duration** and **effective refractory period**. This is typical of **Class IA antiarrhythmics** (e.g., quinidine, procainamide, disopyramide). - Lignocaine shortens, not prolongs, the action potential duration. *Incorrect: Third graph from the left* - This graph primarily illustrates a **prolongation of the repolarization phase (phase 3)**, leading to an increased action potential duration, but with little to no change in the phase 0 upstroke. This effect is characteristic of **Class III antiarrhythmics** (e.g., amiodarone, sotalol, dronedarone, dofetilide, ibutilide), which primarily block potassium channels. - Lignocaine's primary effect is on sodium channels with a resultant shortening of the action potential. *Incorrect: Fourth graph from the left* - This graph likely represents **Class II antiarrhythmics (beta-blockers)** or shows minimal effect on action potential morphology, possibly representing a different mechanism that doesn't significantly alter the ventricular action potential configuration. - Lignocaine has a distinctive effect of shortening action potential duration with reduced phase 0 slope, which is not shown in this graph.

Q: A 30-year-old male chronic smoker presents with this condition. Which of the following drugs is the preferred drug for improving circulation?

Cilostazol. ***Cilostazol*** - The image shows **gangrenous toes** in a **chronic smoker**, suggesting peripheral arterial disease (PAD) or Buerger's disease (thromboangiitis obliterans), which is typically seen in young to middle-aged males who are heavy smokers and presents with limb ischemia. - **Cilostazol** is a phosphodiesterase-3 inhibitor that inhibits platelet aggregation and is a direct arterial vasodilator, making it the preferred drug for improving **claudication** and circulation in PAD. *Prasugrel* - **Prasugrel** is an antiplatelet drug used primarily in acute coronary syndromes undergoing percutaneous coronary intervention (PCI) to reduce thrombotic events. - While it reduces platelet aggregation, it does not directly improve peripheral circulation or symptoms of claudication as effectively as cilostazol in PAD. *Naftidrofuryl* - **Naftidrofuryl** is a peripheral vasodilator and serotonin 5-HT2 receptor antagonist used primarily for treating intermittent claudication and has some evidence for improving pain-free walking distance. - However, it is generally considered a second-line agent, and its efficacy is often less pronounced than cilostazol, particularly in severe cases of peripheral ischemia. *Xanthine nicotinate* - **Xanthine nicotinate** is a derivative of nicotinic acid with vasodilator properties, sometimes used to improve circulation in peripheral vascular disease. - Its efficacy in severe peripheral ischemia or symptomatic claudication is generally considered limited compared to other agents like cilostazol, and it is not typically a preferred first-line treatment.

Q: A patient with rheumatic heart disease is in atrial fibrillation. The ECG shows irregularly irregular heart rhythm with absent P waves and down-sloping ST segment depression pronounced in V2-V3 and in the rhythm strip. The patient is experiencing general unwell being. Given the ECG findings and history, which medication is most likely causing the patient's symptoms?

Digoxin. ***Digoxin*** - The ECG findings of **irregularly irregular rhythm with absent P waves** (atrial fibrillation), combined with **down-sloping ST segment depression** (often described as "digoxin effect" or "digitalis effect"), are classic signs of **digoxin toxicity**. - **General unwell being** is a common non-specific symptom of digoxin toxicity, which can manifest as fatigue, malaise, or gastrointestinal upset. *Flecainide* - Flecainide is a Class Ic antiarrhythmic and can cause various ECG changes, including **PR interval prolongation** and **QRS widening**, but not typically the characteristic down-sloping ST segment changes associated with digoxin. - While it can be proarrhythmic, leading to symptoms of general unwell being, the specific ECG pattern described points away from flecainide and more towards digoxin. *Amiodarone* - Amiodarone is a Class III antiarrhythmic that primarily **prolongs the QT interval** on an ECG. - It does not typically cause the down-sloping ST segment depression seen in this patient, although it can cause bradyarrhythmias or other proarrhythmic effects. *Quinidine* - Quinidine is a Class Ia antiarrhythmic that typically causes **QRS widening** and **QT prolongation**, and can also lead to U waves. - While it can be associated with "quinidine syncope" due to arrhythmias like Torsades de pointes, it does not produce the specific down-sloping ST segment changes seen here that are characteristic of digoxin.

Q: Which of the following anti-hypertensive drugs is/are best avoided during pregnancy ?

Angiotensin converting enzyme inhibitors. ***Angiotensin converting enzyme inhibitors*** - **ACE inhibitors** are contraindicated in pregnancy due to their association with **fetal renal abnormalities**, **oligohydramnios**, and **fetal death**. - They can cause severe **birth defects** and are categorized as pregnancy category D drugs, meaning there is positive evidence of human fetal risk. *Nifedipine* - **Nifedipine**, a dihydropyridine calcium channel blocker, is considered a **safe** and effective antihypertensive in pregnancy. - It is frequently used for managing **hypertension** and **preterm labor** in pregnant women. *Methyldopa* - **Methyldopa** is often considered the **first-line drug** for chronic hypertension in pregnancy due to its established safety profile for both mother and fetus. - It has a long history of use and is one of the most studied antihypertensives in pregnancy. *Labetalol* - **Labetalol**, a combined alpha and beta-blocker, is also considered a **safe** and effective option for managing hypertension in pregnancy. - It is often used for **gestational hypertension** and **preeclampsia** and has a good fetal safety record.

Q: Match the following antiarrhythmic drugs with their mechanism of action: | Mechanism of action | Drug | | :-- | :-- | | 1. Na+ channel blocker | A. Quinidine | | 2. K+ channel blocker | B. Digoxin | | 3. Na+K+ ATPase inhibitor | C. Esmolol | | 4. Beta-blocker | D. Ibutilide |

1-A, 2-D, 3-B, 4-C. ***1-A, 2-D, 3-B, 4-C*** - **Quinidine** is a Class IA antiarrhythmic drug that primarily blocks **sodium channels**, prolonging the action potential duration and refractoriness. - **Ibutilide** is a Class III antiarrhythmic drug that blocks **potassium channels**, leading to delayed repolarization and increased effective refractory period. - **Digoxin** inhibits the **Na+/K+ ATPase pump**, increasing intracellular calcium and affecting AV nodal conduction. - **Esmolol** is a **beta-blocker** (Class II antiarrhythmic) that reduces heart rate and contractility by blocking β1-adrenergic receptors. *1-A, 2-C, 3-D, 4-B* - This option incorrectly matches **Esmolol** (a beta-blocker) with **K+ channel blocker** and **Ibutilide** (K+ channel blocker) with **Na+K+ ATPase inhibitor**. - It also incorrectly matches **Digoxin** (Na+K+ ATPase inhibitor) with **beta-blocker**. *1-D, 2-C, 3-A, 4-B* - This option incorrectly matches **Ibutilide** (K+ channel blocker) with **Na+ channel blocker** and incorrectly matches **Quinidine** (Na+ channel blocker) with **Na+K+ ATPase inhibitor**. - It also incorrectly matches **Digoxin** (Na+K+ ATPase inhibitor) with **beta-blocker**. *1-D, 2-B, 3-A, 4-C* - This option incorrectly matches **Ibutilide** (K+ channel blocker) with **Na+ channel blocker** and **Digoxin** (Na+K+ ATPase inhibitor) with **K+ channel blocker**. - It also incorrectly matches **Quinidine** (Na+ channel blocker) with **Na+K+ ATPase inhibitor**.

Q: Identify the correct match, regarding the drug and its adverse effect.

Verapamil - constipation. ***Verapamil - Constipation*** - **Verapamil**, a **non-dihydropyridine calcium channel blocker**, frequently causes constipation due to its effect on smooth muscle in the gastrointestinal tract, leading to **decreased intestinal motility**. - This adverse effect is common and often dose-dependent, making it a significant consideration in patient management. *Aliskiren - hypokalemia* - **Aliskiren**, a **direct renin inhibitor**, can cause **hyperkalemia** by reducing angiotensin II levels, which normally stimulate aldosterone secretion. - It does not typically cause hypokalemia; rather, potassium-sparing effects are often observed. *Hydralazine - heart failure* - **Hydralazine** is a **vasodilator** used to treat hypertension and **heart failure** with reduced ejection fraction by reducing afterload. - It does not cause heart failure; instead, it is often prescribed to improve cardiac function in patients with heart failure. *Atenolol - hemolytic anemia* - **Atenolol** is a **beta-blocker** primarily used for hypertension, angina, and arrhythmias. - **Hemolytic anemia** is a rare adverse effect associated with certain drugs, but it is not a known or common side effect of atenolol.

Q: A patient who is on treatment for hyperlipidemia develops gallstones. What is the mechanism of action of the causative drug that was given to this patient?

Activates PPAR alpha. ***Activates PPAR alpha*** * Activation of **PPAR alpha (Peroxisome Proliferator-Activated Receptor alpha)** by fibrates can lead to increased cholesterol secretion into bile [1]. * This increased biliary cholesterol saturation predisposes patients to **cholesterol gallstone** formation. *Decreases VLDL* * While fibrates do decrease **VLDL (Very Low-Density Lipoprotein)** production, this specific action is not the primary mechanism by which they cause gallstones [1]. * The reduction in VLDL is beneficial for triglyceride lowering, but the gallstone risk relates to cholesterol metabolism. *Binds to deoxycholic acid* * This mechanism is characteristic of **bile acid sequestrants** like cholestyramine, which bind to bile acids in the gut to prevent their reabsorption. * Bile acid sequestrants are not typically associated with an increased risk of gallstones; in fact, they can sometimes be used to reduce gallstones in specific contexts. *Inhibits HMG CoA reductase* * This is the mechanism of action for **statins**, which are highly effective in lowering LDL cholesterol by inhibiting the rate-limiting enzyme in cholesterol synthesis [2]. * Statins are not generally associated with an increased risk of gallstones; some studies even suggest a potential protective effect [3].

Q: Preferred drug for the treatment of ventricular tachycardia is

Lignocaine. ***Lignocaine*** *(Historical Answer for FMGE-2019)* - **Lignocaine** (also known as **lidocaine**) is a **Class IB antiarrhythmic** drug that was historically the preferred treatment for **ventricular tachycardia (VT)**, especially in patients with **ischemic heart disease**. - It works by **blocking sodium channels** in the heart, specifically targeting depolarized or partially depolarized cells, which helps to stabilize the ventricular rhythm. - **⚠️ IMPORTANT UPDATE:** Current guidelines (AHA/ACC 2015 onwards) now recommend **amiodarone as the first-line antiarrhythmic** for hemodynamically stable VT, with lignocaine as a **second-line alternative**. This question reflects the teaching prevalent at the time of FMGE-2019. *Digoxin* - **Digoxin** is a **cardiac glycoside** primarily used for **atrial fibrillation** with rapid ventricular response and **heart failure**. - It is **not the preferred drug** for ventricular tachycardia and can even precipitate arrhythmias in some cases. *Propranolol* - **Propranolol** is a **beta-blocker** (Class II antiarrhythmic) typically used to treat **supraventricular tachycardias**, **hypertension**, and **angina**. - While beta-blockers can have some role in preventing recurrent VT, they are **not the first-line treatment** for acute VT. *Diltiazem* - **Diltiazem** is a **calcium channel blocker** (Class IV antiarrhythmic) primarily used for **supraventricular tachycardias** and to control ventricular rate in **atrial fibrillation**. - It is **not effective** for ventricular tachycardia and may worsen the condition in some cases.

Question 1

Which of the following graphs of cardiac action potential represents mechanism of action of lignocaine?

Accepted Answer

Second graph from the left

Answer

First graph from the left

Answer

Third graph from the left

Answer

Fourth graph from the left

Question 2

A 30-year-old male chronic smoker presents with this condition. Which of the following drugs is the preferred drug for improving circulation?

Accepted Answer

Cilostazol

Answer

Prasugrel

Answer

Naftidrofuryl

Answer

Xanthine nicotinate

Question 3

A patient with rheumatic heart disease is in atrial fibrillation. The ECG shows irregularly irregular heart rhythm with absent P waves and down-sloping ST segment depression pronounced in V2-V3 and in the rhythm strip. The patient is experiencing general unwell being. Given the ECG findings and history, which medication is most likely causing the patient's symptoms?

Accepted Answer

Digoxin

Answer

Flecainide

Answer

Amiodarone

Answer

Quinidine

Question 4

Which one of the following responses to intravenous adenosine is correctly matched?

Accepted Answer

Atrio-ventricular nodal reentrant tachycardia - Termination and complete recovery

Answer

Atrial flutter - Termination and complete recovery

Answer

Ventricular tachycardia - Termination and complete recovery

Answer

Atrial fibrillation - Termination

Question 5

Which of the following anti-hypertensive drugs is/are best avoided during pregnancy ?

Accepted Answer

Angiotensin converting enzyme inhibitors

Answer

Nifedipine

Answer

Methyldopa

Answer

Labetalol

Question 6

Match the following antiarrhythmic drugs with their mechanism of action:

Accepted Answer

1-A, 2-D, 3-B, 4-C

Answer

1-D, 2-B, 3-A, 4-C

Answer

1-A, 2-C, 3-D, 4-B

Answer

1-D, 2-C, 3-A, 4-B

Question 7

Identify the correct match, regarding the drug and its adverse effect.

Accepted Answer

Verapamil - constipation

Answer

Aliskiren - hypokalemia

Answer

Hydralazine - heart failure

Answer

Atenolol - hemolytic anemia

Question 8

A patient who is on treatment for hyperlipidemia develops gallstones. What is the mechanism of action of the causative drug that was given to this patient?

Accepted Answer

Activates PPAR alpha

Answer

Binds to deoxycholic acid

Answer

Decreases VLDL

Answer

Inhibits HMG CoA reductase

Question 9

Which among the following is the false statement regarding statins?

Accepted Answer

They can be given with verapamil and other enzyme inhibitors

Answer

These drugs should not be stopped even in severe conditions like injury, surgery etc.

Answer

Although HMG-CoA reductase inhibitors substantially reduce the risk of cardiovascular events, there is mild increase in lipoprotein a (Lpa) levels.

Answer

With the long term use, there is slight increase in the incidence of type 2 diabetes mellitus.

Question 10

Preferred drug for the treatment of ventricular tachycardia is

Accepted Answer

Lignocaine

Answer

Digoxin

Answer

Propranolol

Answer

Diltiazem

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

On this page

Practice by Chapter

Want unlimited practice?