Cardiovascular Drugs Practice Questions

Q: A 65-year-old retired school teacher presents with chest pain of 6 hours duration with dyspnea grade III. On examination RR $=24 / \mathrm{min}$ with use of accessory muscles of respiration, elevated pulsatile JVP, pulse rate of 120 bpm and $\mathrm{BP}=150 / 90$. Troponin I is $0.08 \mathrm{ng} / \mathrm{dL}$ and ECG is shown below. Which of these drugs will not be useful for this patient?

β-blocker. ***β-blocker*** - The ECG shows significant **ST elevation** in leads V1-V4, indicating an **anterior ST-elevation myocardial infarction (STEMI)**. The patient also has signs of **acute decompensated heart failure** (dyspnea, elevated JVP, tachypnea, accessory muscle use). - β-blockers are **contraindicated** in patients with **acute heart failure** or **cardiogenic shock** because they can worsen cardiac output by reducing contractility and heart rate. *Aspirin* - **Aspirin** is an essential antiplatelet agent used in the acute management of **STEMI** to prevent further thrombus formation and reduce mortality. - It works by irreversibly inhibiting cyclooxygenase-1 (COX-1) in platelets, thereby reducing thromboxane A2 production and platelet aggregation. *Heparin* - **Heparin**, specifically unfractionated or low molecular weight heparin, is indicated in **STEMI** to prevent further clot propagation and to maintain patency of the infarct-related artery, especially during and after percutaneous coronary intervention (PCI). - It acts as an anticoagulant by enhancing the activity of antithrombin, thereby inhibiting various coagulation factors. *Morphine* - **Morphine** is commonly used in **STEMI** for pain relief, which can also help reduce myocardial oxygen demand and alleviate anxiety. - While it can be useful, caution is advised in patients with heart failure due to potential for vasodilation and hypotension, but it is not absolutely contraindicated like β-blockers in acute heart failure.

Q: Prescription of which of the following drugs can lead to periorbital edema of non-pitting variety?

Aliskiren. ***Aliskiren***- **Aliskiren**, a **direct renin inhibitor**, can lead to **angioedema**, which often manifests as **non-pitting periorbital edema**. This occurs due to its effect on the **renin-angiotensin-aldosterone system (RAAS)** and bradykinin metabolism.- The angioedema caused by aliskiren is similar to that caused by **ACE inhibitors**, involving an increase in **bradykinin** levels, leading to increased vascular permeability and fluid leakage into tissues [1, 2].*COX-1 inhibitor*- **COX-1 inhibitors**, such as NSAIDs, can cause **fluid retention** and **edema** through various mechanisms, including effects on kidney function and prostaglandin synthesis.- However, the edema typically caused by COX-1 inhibitors is usually **pitting edema** and is not primarily characterized as isolated non-pitting periorbital swelling, which is more typical of angioedema.*Recombinant C1 INH*- **Recombinant C1 esterase inhibitor (C1 INH)** is used to **treat** angioedema, particularly in cases of hereditary angioedema, by replacing deficient or dysfunctional C1 INH.- Therefore, prescribing this drug would act to **resolve** or prevent angioedema, not cause it.*Icatibant*- **Icatibant** is a **bradykinin B2 receptor antagonist** used to treat acute attacks of **hereditary angioedema**.- Its mechanism of action involves **blocking the effects of bradykinin**, which is responsible for the increased vascular permeability and edema in angioedema; thus, it would **alleviate** rather than cause this type of edema.

Q: A 50-year-old patient with premature atherosclerosis has deranged lipid profile. On examination there is development of plane xanthomas in palmar creases. All are useful for this patient except:

Colestipol. ***Colestipol*** - The patient has **premature atherosclerosis** and **plane xanthomas in palmar creases**, which is suggestive of a genetic lipid disorder like **Familial Dysbetalipoproteinemia** (Type III Hyperlipoproteinemia). This condition primarily involves elevated **chylomicron remnants** and **VLDL remnants**. [1] - **Colestipol** is a **bile acid sequestrant**. It primarily lowers LDL cholesterol by binding bile acids in the intestine, leading to increased hepatic synthesis of bile acids from cholesterol. It is generally not effective for reducing the remnants in this specific disorder and can sometimes even worsen hypertriglyceridemia, which is characteristic of Type III. [1] *Diet control* - **Diet modification**, particularly reducing fat and simple carbohydrates, is a cornerstone of management for all dyslipidemias, including Familial Dysbetalipoproteinemia. [1] - It helps to lower **chylomicron and VLDL remnants**, which are the primary lipid abnormalities in this condition. [1] *Niacin* - **Niacin** (nicotinic acid) is very effective in lowering **VLDL** and **triglycerides**, and raising **HDL cholesterol**. [1] - It is considered a particularly beneficial treatment for **Familial Dysbetalipoproteinemia** due to its impact on remnant lipoproteins. [1] *Fenofibrate* - **Fibrates**, like fenofibrate, are highly effective in reducing **triglycerides** and increasing **HDL cholesterol** by activating PPAR-alpha. [1] - They are specifically indicated and very useful in the treatment of **Familial Dysbetalipoproteinemia** as they promote the catabolism of VLDL and chylomicron remnants. [1]

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**.

Question 1

A 65-year-old retired school teacher presents with chest pain of 6 hours duration with dyspnea grade III. On examination RR $=24 / \mathrm{min}$ with use of accessory muscles of respiration, elevated pulsatile JVP, pulse rate of 120 bpm and $\mathrm{BP}=150 / 90$. Troponin I is $0.08 \mathrm{ng} / \mathrm{dL}$ and ECG is shown below. Which of these drugs will not be useful for this patient?

Accepted Answer

β-blocker

Answer

Aspirin

Answer

Heparin

Answer

Morphine

Question 2

Prescription of which of the following drugs can lead to periorbital edema of non-pitting variety?

Accepted Answer

Aliskiren

Answer

COX-1 inhibitor

Answer

Recombinant C1 INH

Answer

Icatibant

Question 3

A 50-year-old patient with premature atherosclerosis has deranged lipid profile. On examination there is development of plane xanthomas in palmar creases. All are useful for this patient except:

Accepted Answer

Colestipol

Answer

Diet control

Answer

Niacin

Answer

Fenofibrate

Question 4

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 5

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 6

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 7

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 8

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 9

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 10

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

Cardiovascular Drugs — MCQs

Cardiovascular Drugs — MCQs

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