Cardiovascular Drugs Practice Questions

Q: A 50-year-old patient with type IIA hyperlipoproteinemia is started on intestinal cholesterol absorption inhibitor. Which drug and its receptor combination is correct?

X = Ezetimibe, Y = NPC1L1 receptor. ***$X=$ Ezetimibe, $Y=$ NPC1L1 receptor*** - The image depicts the mechanism of **cholesterol absorption in the enterocyte**, where dietary cholesterol enters the cell. The arrow labeled 'X' points to an inhibitor of this absorption, and 'Y' points to the receptor involved. - **Ezetimibe** (X) is a specific inhibitor of intestinal cholesterol absorption, acting by binding to the **Niemann-Pick C1-like 1 (NPC1L1)** protein (Y) on the brush border of enterocytes. *X = Ezetimibe, Y = PPAR $\alpha$ receptor* - While Ezetimibe (X) correctly identifies the drug, **PPAR $\alpha$ receptors** (Y) are nuclear receptors primarily involved in lipid and lipoprotein metabolism, and they are the target of fibrates, not ezetimibe. - **PPAR $\alpha$ receptors** regulate the expression of genes involved in fatty acid oxidation and triglyceride metabolism, distinct from direct cholesterol absorption inhibition. *X = Mipomersen, Y = ABCD1 receptor* - **Mipomersen** (X) is an oligonucleotide inhibitor of apolipoprotein B-100 synthesis, used to treat homozygous familial hypercholesterolemia. It is not an intestinal cholesterol absorption inhibitor. - The **ABCD1 receptor** (ATP-binding cassette transporter D1) is involved in peroxisomal transport of very long-chain fatty acids, not directly related to intestinal cholesterol absorption or Mipomersen's mechanism. *X = Mipomersen, Y = LDL receptor* - As mentioned, **Mipomersen** (X) inhibits apoB-100 synthesis and does not directly act on intestinal cholesterol absorption. - The **LDL receptor** (Y) is primarily responsible for clearing LDL particles from circulation but is not the target of Mipomersen, nor is it the intestinal cholesterol absorption receptor.

Q: A 1-year-old child with moderate VSD is scheduled for surgery next month. For control of symptoms of CHF, a drug $X$ was given. The uneducated parents gave double the dose of drug resulting in the child developing listlessness and poor feeding. Based on the ECG shown, what is the drug prescribed and its side effect?

Digoxin toxicity, ventricular bigeminy. ***Digoxin toxicity, ventricular bigeminy*** - The ECG shows a regular rhythm with alternating normal sinus beats and **premature ventricular contractions (PVCs)**, indicating **ventricular bigeminy**. This is a classic arrhythmia associated with **digoxin toxicity**, especially in a child being treated for CHF. - **Digoxin** is commonly used in pediatric CHF to improve myocardial contractility, and overdose (as suggested by double dosing) can lead to symptoms like **listlessness and poor feeding** due to its narrow therapeutic window and central nervous system effects. *Spironolactone, hypokalemia* - **Spironolactone** is a potassium-sparing diuretic and would primarily cause **hyperkalemia**, not hypokalemia. - While used in CHF, it primarily acts on renal electrolyte balance and would not directly cause ventricular arrhythmias like bigeminy. *Furosemide, hypokalemia* - **Furosemide** is a loop diuretic that can cause **hypokalemia**, which is indeed a risk factor for arrhythmias, but the ECG pattern of **bigeminy** is more specific to **digoxin toxicity**. - While hypokalemia *can* predispose to arrhythmias, furosemide itself is not directly indicated by the bigeminy pattern; the symptoms of toxicity (listlessness, poor feeding) for furosemide overdose would primarily involve dehydration and electrolyte imbalances, not specifically cardiac rhythm disturbances like bigeminy. *Beta blocker, third-degree heart block* - **Beta-blockers** are used in some forms of CHF but an overdose typically causes **bradycardia** and **varying degrees of AV block**, potentially a third-degree heart block, but not **ventricular bigeminy**. - The ECG does not show dissociated P waves and QRS complexes characteristic of third-degree heart block; instead, it shows a patterned alternation of normal and ectopic beats.

Q: A young air force pilot complains of palpitations and recurrent pre-syncope like condition during training exercises. He passed out in the cockpit in last training exercise after which he is grounded and sent for medical examination. ECG was done. Which of the following drugs is absolutely contraindicated in this condition?

Adenosine. ***Adenosine*** - The ECG shows a **delta wave** characteristic of **Wolff-Parkinson-White (WPW) syndrome**, indicating ventricular pre-excitation via an accessory pathway (Bundle of Kent). - **Adenosine is absolutely contraindicated** in WPW syndrome when there is risk of **atrial fibrillation or atrial flutter**, as it blocks the **AV node** preferentially while having minimal effect on the accessory pathway. - This causes all atrial impulses to be conducted exclusively through the **accessory pathway**, which can lead to extremely **rapid ventricular rates** and potentially **ventricular fibrillation**. - Given the patient's symptoms of syncope and palpitations during stress (which can trigger AF), adenosine poses significant risk. *Flecainide* - **Class IC antiarrhythmic** that blocks fast sodium channels in both the **AV node AND the accessory pathway**. - Flecainide is actually **used to treat WPW syndrome** as it slows conduction through both pathways and increases the refractory period of the accessory pathway. - It is one of the **recommended drugs** for preventing recurrent arrhythmias in symptomatic WPW patients. *Metoprolol* - **Beta-blockers** can be used cautiously in WPW for rate control, but are **relatively contraindicated** if there is atrial fibrillation with rapid ventricular response via the accessory pathway. - They primarily slow AV nodal conduction and may paradoxically increase ventricular rate if AF develops. - However, they are not as absolutely contraindicated as adenosine in the acute setting. *None* - This is incorrect because there are specific drugs that are absolutely contraindicated in WPW syndrome, particularly **adenosine, digoxin, verapamil, and diltiazem** when there is risk of pre-excited atrial fibrillation.

Q: Which of the following drugs will act on the phase of cardiac action potential marked as $X$ ?

Ivabradine. ***Ivabradine*** - Phase X in the image refers to the **funny current (If)**, which is responsible for the **spontaneous depolarization** of pacemaker cells in the heart. - **Ivabradine** selectively inhibits the funny current, thereby reducing heart rate without affecting contractility or blood pressure significantly. *Verapamil* - Verapamil is a **calcium channel blocker** that primarily acts on L-type calcium channels. - Its effects are mainly on the **depolarization phase (phase 0 in nodal cells, phase 2 in ventricular myocytes)** and plateau phase, not the funny current. *Lidocaine* - Lidocaine is a **sodium channel blocker** (Class IB antiarrhythmic). - It primarily acts on phase 0 of the action potential in ventricular myocytes by **reducing sodium influx**, which is not the phase indicated by X. *Flecainide* - Flecainide is a **sodium channel blocker** (Class IC antiarrhythmic). - It primarily affects the **depolarization (phase 0) of cardiac myocytes** by blocking fast sodium channels, which is distinct from the funny current (Phase X).

Q: The synaptic cleft shown is from the sympathetic outflow system. The following anti-hypertensive drug $X$ acts via the mechanism shown below:

Reserpine. ***Reserpine*** - The image indicates that drug X acts on the **neurotransmitter re-uptake pump** located on the synaptic vesicles within the axon terminal. - **Reserpine** inhibits the **vesicular monoamine transporter (VMAT)**, which is responsible for packaging neurotransmitters like norepinephrine, dopamine, and serotonin into synaptic vesicles for release. - This depletes neurotransmitter stores and reduces sympathetic activity, leading to anti-hypertensive effect. *Clonidine* - **Clonidine** is an **alpha-2 adrenergic agonist** that acts pre-synaptically on autoreceptors to reduce the release of norepinephrine. - Its mechanism does not involve directly blocking the re-uptake pump as depicted in the image. *Trimethaphan* - **Trimethaphan** is a **ganglionic blocker** that acts by interfering with nicotinic receptors at autonomic ganglia. - It does not directly affect neurotransmitter re-uptake or storage within the presynaptic terminal as shown in the diagram. *Guanethidine* - **Guanethidine** is an adrenergic neuron blocker that inhibits the **release** of norepinephrine from nerve terminals. - Unlike reserpine, it does not block VMAT or affect vesicular storage of neurotransmitters as depicted in the mechanism shown.

Q: Which of the anti-arrhythmic drug actions shown below will have high predisposition to development of Torsades de pointes?

A. ***A*** - This graph shows significant **QT prolongation** due to inhibition of delayed rectifier potassium channels (**IKr**), characteristic of **Class III antiarrhythmic drugs** like sotalol and amiodarone. - The prolonged repolarization increases risk of **early afterdepolarizations (EADs)**, which can trigger **Torsades de pointes** arrhythmias. *B* - This graph shows **decreased phase 0 slope** of depolarization with minimal change in action potential duration, characteristic of **Class IC antiarrhythmics** like flecainide. - Class IC drugs primarily block **fast sodium channels** causing conduction slowing, but have **low predisposition** to Torsades de pointes due to minimal QT prolongation. *C* - This graph shows **shortened action potential duration** with changes in phase 4 and phase 0, characteristic of **Class I/II antiarrhythmic combinations**. - **No significant QT prolongation** is observed compared to baseline, therefore the predisposition to **Torsades de pointes is minimal**. *D* - This graph shows **rate slowing effects** with prolonged cycle length, characteristic of **Class II antiarrhythmics** (beta-blockers) like propranolol. - Beta-blockers have **protective effects** against arrhythmias and do not cause QT prolongation, thus having **very low Torsades de pointes risk**.

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.

Question 1

A 50-year-old patient with type IIA hyperlipoproteinemia is started on intestinal cholesterol absorption inhibitor. Which drug and its receptor combination is correct?

Accepted Answer

X = Ezetimibe, Y = NPC1L1 receptor

Answer

X = Ezetimibe, Y = PPAR alpha receptor

Answer

X = Mipomersen, Y = LDL receptor

Answer

X = Mipomersen, Y = ABCD1 receptor

Question 2

A 1-year-old child with moderate VSD is scheduled for surgery next month. For control of symptoms of CHF, a drug $X$ was given. The uneducated parents gave double the dose of drug resulting in the child developing listlessness and poor feeding. Based on the ECG shown, what is the drug prescribed and its side effect?

Accepted Answer

Digoxin toxicity, ventricular bigeminy

Answer

Spironolactone, hypokalemia

Answer

Furosemide, hypokalemia

Answer

Beta blocker, third-degree heart block

Question 3

Telmisartan acts on the following receptors for its action. Name X and Y? (Recent NEET Pattern 2016-17)

Accepted Answer

AT1 and AT2

Answer

V1 and V2

Answer

ENaC and ROMK

Answer

All of these

Question 4

A young air force pilot complains of palpitations and recurrent pre-syncope like condition during training exercises. He passed out in the cockpit in last training exercise after which he is grounded and sent for medical examination. ECG was done. Which of the following drugs is absolutely contraindicated in this condition?

Accepted Answer

Adenosine

Answer

Metoprolol

Answer

Flecainide

Answer

None

Question 5

Which of the following drugs will act on the phase of cardiac action potential marked as $X$ ?

Accepted Answer

Ivabradine

Answer

Verapamil

Answer

Lidocaine

Answer

Flecainide

Question 6

The synaptic cleft shown is from the sympathetic outflow system. The following anti-hypertensive drug $X$ acts via the mechanism shown below:

Accepted Answer

Reserpine

Answer

Clonidine

Answer

Trimethaphan

Answer

Guanethidine

Question 7

Which of the anti-arrhythmic drug actions shown below will have high predisposition to development of Torsades de pointes?

Accepted Answer

A

Answer

B

Answer

C

Answer

D

Question 8

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 9

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 10

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

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

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