Which of the following is a metabolite of hydroxyzine?
Which second generation antihistaminic does not produce an active metabolite?
Which of the following is NOT a function of Prostaglandin E1 (PGE1)?
What is a common side effect of salmeterol?
What is the mechanism of action of Abatacept?
Which drug is used for sympathectomy in experimental animals?
Which calcium channel blocker has the shortest duration of action?
What is the drug of choice for a classical angina attack?
What are the primary mechanisms behind cardiac toxicity associated with Tricyclic antidepressants?
Which of the following medications is most likely to cause reflex tachycardia?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 41: Which of the following is a metabolite of hydroxyzine?
- A. Fexofenadine
- B. Terfenadine
- C. Cetirizine (Correct Answer)
- D. Azelastine
Explanation: ***Cetirizine*** - **Cetirizine** is the principal active metabolite of **hydroxyzine**, formed through the oxidation of the primary alcohol group of hydroxyzine [2]. - Both hydroxyzine and cetirizine are **H1-receptor antagonists**, but cetirizine is a **second-generation antihistamine** known for being less sedating due to its limited ability to cross the blood-brain barrier [2]. *Fexofenadine* - **Fexofenadine** is an active metabolite of **terfenadine**, not hydroxyzine [2]. - **Fexofenadine** is a second-generation antihistamine used to treat allergies, known for its non-sedating properties [3]. *Terfenadine* - **Terfenadine** is a second-generation antihistamine that was withdrawn from the market due to its cardiotoxicity, particularly the risk of **QT prolongation** and **Torsades de Pointes**. - Its active metabolite is **fexofenadine**, which does not cause similar cardiac issues [2]. *Azelastine* - **Azelastine** is an antihistamine primarily available as a **nasal spray** for the treatment of allergic rhinitis and conjunctivitis [1], [3]. - It is not a metabolite of hydroxyzine but a distinct therapeutic compound.
Question 42: Which second generation antihistaminic does not produce an active metabolite?
- A. Loratadine
- B. Terfenadine
- C. Cetirizine (Correct Answer)
- D. None of the options
Explanation: ***Cetirizine*** - Cetirizine is unique among second-generation antihistamines as it is an **active metabolite** of hydroxyzine and **does not undergo further significant metabolism** to an active compound. - This characteristic contributes to its relatively **predictable pharmacokinetics** and reduced potential for drug interactions related to metabolism. *Loratadine* - Loratadine is a **prodrug** that is extensively metabolized in the liver by **CYP3A4 and CYP2D6** to its active metabolite, **desloratadine**. - Desloratadine is responsible for most of the **antihistaminic effects** of loratadine. *Terfenadine* - Terfenadine is a **prodrug** that is extensively metabolized by **CYP3A4** to its active metabolite, **fexofenadine**. - Due to its **cardiotoxicity** (QT prolongation) when its metabolism was inhibited, terfenadine was withdrawn from the market, and fexofenadine was developed as a safer alternative. *None of the options* - This option is incorrect because **cetirizine** does not produce an active metabolite, making it a valid answer for the question.
Question 43: Which of the following is NOT a function of Prostaglandin E1 (PGE1)?
- A. Plays a role in initiating puberty (Correct Answer)
- B. Modulates inflammatory responses
- C. Used in the management of erectile dysfunction
- D. Maintains the patency of the ductus arteriosus
Explanation: ***Plays a role in initiating puberty*** - **Prostaglandin E1 (PGE1)** is primarily involved in smooth muscle relaxation, vasodilation, and inflammation, and does not have a direct role in initiating **puberty**. - The initiation of puberty is mainly controlled by the **hypothalamic-pituitary-gonadal (HPG) axis** and surge of **gonadotropin-releasing hormone (GnRH)**. *Used in the management of erectile dysfunction* - **PGE1 formulations** (alprostadil) are used as a topical or intracavernosal injection to treat **erectile dysfunction** by inducing vasodilation in the penis. - Its vasodilatory effects increase blood flow to the corpora cavernosa, leading to **penile erection**. *Modulates inflammatory responses* - **PGE1** is involved in **inflammatory processes**, often exerting both pro- and anti-inflammatory effects depending on the context and specific receptors activated. - It can help to **reduce inflammation** and pain, as well as influencing immune cell function. *Maintains the patency of the ductus arteriosus* - In newborns with **congenital heart defects**, **PGE1** is administered to maintain the **patency of the ductus arteriosus**, allowing for blood flow between the aorta and pulmonary artery. - This is crucial for conditions where pulmonary or systemic blood flow is dependent on a patent ductus, bridging the infant to surgery or other interventions.
Question 44: What is a common side effect of salmeterol?
- A. Tremors (Correct Answer)
- B. Seizures
- C. Hypertension
- D. Hyperkalemia
Explanation: ***Tremors*** - **Salmeterol** is a **long-acting beta-2 adrenergic agonist (LABA)** that can stimulate beta-2 receptors in skeletal muscle, leading to **fine muscle tremors**. - This side effect is dose-dependent and more common with higher doses or in patients sensitive to sympathomimetic effects. *Seizures* - **Seizures** are a rare and atypical side effect of **salmeterol** and other beta-2 agonists; they are not considered a common adverse event. - While systemic absorption can occur, the central nervous system effects leading to seizures are not frequently observed. *Hypertension* - While beta-2 agonists can cause a slight increase in **heart rate** due to systemic absorption, **hypertension** is not a common side effect of inhaled salmeterol. - Other cardiovascular effects like palpitations can occur, but significant or sustained hypertension is rare. *Hyperkalemia* - **Hyperkalemia** (elevated potassium) is not a side effect of **salmeterol**; in fact, beta-2 agonists commonly cause the **opposite effect - hypokalemia** (decreased serum potassium). - Beta-2 receptor stimulation activates Na⁺-K⁺-ATPase pumps, driving potassium from serum into cells, causing transient hypokalemia. - This effect is clinically relevant and requires monitoring, especially when combined with other medications that lower potassium.
Question 45: What is the mechanism of action of Abatacept?
- A. Tumor necrosis factor (TNF) alpha inhibitor
- B. Monoclonal antibody against interleukin-6 (IL-6) receptor
- C. Interleukin-1 (IL-1) receptor antagonist
- D. Inhibitor of co-stimulation of T cells (Correct Answer)
Explanation: ***Inhibitor of co-stimulation of T cells*** - Abatacept is a **fusion protein** that blocks the **CD28-CD80/86 co-stimulatory pathway**, which is crucial for full T-cell activation. - By binding to **CD80** and **CD86** on antigen-presenting cells, it prevents their interaction with **CD28** on T cells, thus inhibiting T-cell proliferation and cytokine production. *Tumor necrosis factor (TNF) alpha inhibitor* - TNF alpha inhibitors (e.g., **adalimumab**, **infliximab**, **etanercept**) bind to and neutralize **TNF alpha**, a pro-inflammatory cytokine. - While used in similar conditions, their mechanism is distinct from Abatacept's T-cell co-stimulation blockade. *Monoclonal antibody against interleukin-6 (IL-6) receptor* - Drugs like **tocilizumab** target the **IL-6 receptor**, blocking the signaling of **IL-6**, another important inflammatory cytokine. - This mechanism primarily affects cytokine signaling rather than directly inhibiting T-cell activation in the same way as abatacept. *Interleukin-1 (IL-1) receptor antagonist* - **Anakinra** is an example of an **IL-1 receptor antagonist**, which competes with IL-1 for binding to its receptor, thereby blocking its pro-inflammatory effects. - This mechanism focuses on inhibiting the action of IL-1, unlike Abatacept's role in T-cell activation.
Question 46: Which drug is used for sympathectomy in experimental animals?
- A. Guanethidine (Correct Answer)
- B. Atropine
- C. Diazoxide
- D. Thebaine
Explanation: ***Guanethidine*** - **Guanethidine** is a potent **adrenergic neuron blocking drug** that is taken up by noradrenergic neurons and prevents the release of norepinephrine, leading to a chemical sympathectomy. - In experimental animal models, it is used to induce a **pharmacological sympathectomy** to study the effects of sympathetic nervous system blockade on various physiological processes. *Atropine* - **Atropine** is a **muscarinic acetylcholine receptor antagonist** that blocks the effects of acetylcholine at parasympathetic postganglionic terminals. - It is primarily used to block **parasympathetic responses**, not sympathetic ones, and therefore would not induce a sympathectomy. *Diazoxide* - **Diazoxide** is a direct **arteriolar vasodilator** that works by opening potassium channels in vascular smooth muscle. - It is used to quickly reduce blood pressure in **hypertensive emergencies** and for treating hypoglycemia due to insulin oversecretion, and does not cause sympathectomy. *Thebaine* - **Thebaine** is an **opioid alkaloid** found in opium, structurally similar to morphine and codeine, but with primarily stimulatory rather than depressant effects. - It acts as a **convulsant** and is used as a precursor in the synthesis of other opioids, but has no role in causing sympathectomy.
Question 47: Which calcium channel blocker has the shortest duration of action?
- A. Diltiazem
- B. Amlodipine
- C. Nimodipine (Correct Answer)
- D. Verapamil
Explanation: ***Nimodipine*** - Nimodipine is a **dihydropyridine calcium channel blocker** specifically formulated for cerebral vasodilation and used in conditions like **subarachnoid hemorrhage**. - It has a relatively **short half-life** and rapid onset, making its duration of action shorter compared to other commonly used calcium channel blockers. *Amlodipine* - Amlodipine is known for its **long duration of action** and once-daily dosing due to its slow absorption and high bioavailability. - Its prolonged action is beneficial for conditions like **hypertension and angina**, where sustained vasodilation is desired. *Diltiazem* - Diltiazem's duration of action is **intermediate** compared to other calcium channel blockers, often requiring BID to TID dosing for immediate-release formulations. - It's a **non-dihydropyridine calcium channel blocker** with effects on both vascular smooth muscle and cardiac conduction. *Verapamil* - Verapamil also has an **intermediate duration of action**, similar to diltiazem, with immediate-release forms requiring multiple daily doses. - As a **non-dihydropyridine calcium channel blocker**, it has significant effects on myocardial contractility and AV nodal conduction.
Question 48: What is the drug of choice for a classical angina attack?
- A. CCBs
- B. β-blocker
- C. GTN (Correct Answer)
- D. Prazosin
Explanation: ***GTN*** - **Glyceryl trinitrate (GTN)** is the drug of choice for immediate relief of a classical angina attack because it rapidly dilates coronary arteries and peripheral blood vessels, reducing **myocardial oxygen demand** and improving blood flow [2]. - Its **nitric oxide** mediated vasodilatory effects quickly alleviate chest pain by decreasing **preload** and afterload [2], [3]. *CCBs* - **Calcium channel blockers (CCBs)** are used for long-term prevention of angina by reducing myocardial oxygen demand, but they are not the first-line treatment for acute relief due to their slower onset of action [1]. - While they can dilate coronary arteries and reduce heart rate/contractility, their role is more in **prophylaxis** rather than acute symptom management [1]. *β-blocker* - **Beta-blockers** are primarily used for chronic management and prevention of angina by reducing heart rate, contractility, and blood pressure, thereby decreasing myocardial oxygen demand. - They are generally avoided for acute angina attacks as they do not provide rapid symptomatic relief and can potentially worsen symptoms in some acute ischemic conditions. *Prazocin* - **Prazosin** is an **alpha-1 adrenergic blocker** primarily used to treat hypertension and benign prostatic hyperplasia. - It causes vasodilation but is not indicated for the treatment of acute angina, as its mechanism of action and onset of effect are not suitable for rapid relief of myocardial ischemia.
Question 49: What are the primary mechanisms behind cardiac toxicity associated with Tricyclic antidepressants?
- A. Norepinephrine reuptake inhibition only
- B. Anticholinergic effects on the heart
- C. Both norepinephrine reuptake inhibition and anticholinergic effects on the heart (Correct Answer)
- D. Direct membrane stabilizing effects only
Explanation: ***Both norepinephrine reuptake inhibition and anticholinergic effects on the heart*** - **Tricyclic antidepressants (TCAs)** block the reuptake of **norepinephrine**, which can lead to increased sympathetic tone on the heart and potentially **tachyarrhythmias** or other cardiac complications. - TCAs also have potent **anticholinergic effects**, blocking muscarinic receptors in the heart; this can increase **heart rate** and affect cardiovascular stability. - While **direct membrane stabilizing effects** (sodium channel blockade) are critical for **QRS widening and conduction delays**, the combination of norepinephrine reuptake inhibition and anticholinergic effects accounts for the broader spectrum of **TCA-induced cardiac toxicity** including tachycardia and hemodynamic instability. *Norepinephrine reuptake inhibition only* - While TCAs do inhibit norepinephrine reuptake contributing to tachycardia and increased sympathetic tone, this mechanism alone does not fully explain the breadth of cardiac effects seen with these drugs. - The **anticholinergic effects** play a significant additional role in altering cardiac function. *Anticholinergic effects on the heart* - While TCAs do exert anticholinergic effects that can impact heart rate and cardiovascular function, this mechanism alone fails to account for the additional contributions from **norepinephrine reuptake inhibition** to the overall cardiac toxicity. - The combination of both mechanisms is necessary for a complete understanding of **TCA-induced cardiac effects**. *Direct membrane stabilizing effects only* - This option refers to the **quinidine-like action** of TCAs, which involves blocking myocardial fast sodium channels, leading to a **prolonged QRS interval** and increased risk of **ventricular arrhythmias** and **conduction defects**. - While direct membrane stabilization is the **primary mechanism of TCA-induced conduction abnormalities** (QRS widening, heart blocks), the question asks for mechanisms of broader **cardiac toxicity**, which includes the combined effects of norepinephrine reuptake inhibition and anticholinergic actions on heart rate and hemodynamics.
Question 50: Which of the following medications is most likely to cause reflex tachycardia?
- A. Nifedipine (Correct Answer)
- B. Verapamil
- C. Propranolol
- D. Amlodipine
Explanation: ***Nifedipine*** - Nifedipine is a **dihydropyridine calcium channel blocker** that causes significant peripheral vasodilation, leading to a rapid drop in blood pressure. - This sudden drop in blood pressure triggers a **baroreflex response**, compensatory increase in heart rate. *Verapamil* - Verapamil is a **non-dihydropyridine calcium channel blocker** that primarily acts on the cardiac pacemaker cells and slows AV nodal conduction. - While it can cause vasodilation, its direct negative chronotropic effect on the heart often **blunts or prevents reflex tachycardia**. *Propranolol* - Propranolol is a **non-selective beta-blocker** that blocks beta-1 and beta-2 adrenergic receptors. - It directly **decreases heart rate and myocardial contractility**, thereby preventing reflex tachycardia. *Amlodipine* - Amlodipine is a **dihydropyridine calcium channel blocker**, similar to nifedipine, but it has a **slower onset of action and a longer half-life**. - Its more gradual onset of vasodilation often results in a significantly **less pronounced or absent reflex tachycardia** compared to nifedipine.