Which of the following is a tricyclic antidepressant?
Which of the following is NOT a beta-2 agonist?
Beta2-agonists cause all except:
Which of the following is a mineralocorticoid antagonist?
Which of the following is a renin inhibitor?
Which of the following is a metabolite of hydroxyzine?
Which of the following medications is most likely to cause reflex tachycardia?
Aminophylline inhibits which of the following enzymes?
Which calcium channel blocker has the shortest duration of action?
What is the mechanism of action of Abatacept?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 41: Which of the following is a tricyclic antidepressant?
- A. Fluoxetine
- B. Citalopram
- C. Doxepin (Correct Answer)
- D. Venlafaxine
Explanation: ***Doxepin*** - **Doxepin** is a **tricyclic antidepressant (TCA)** that inhibits the reuptake of **serotonin** and **norepinephrine**, and also has significant **histaminergic** and **cholinergic** blocking effects. - TCAs, including doxepin, are commonly used for treating **depression**, **anxiety**, and certain pain conditions. *Venlafaxine* - **Venlafaxine** is a **serotonin-norepinephrine reuptake inhibitor (SNRI)**, not a tricyclic antidepressant. - SNRIs selectively block the reuptake of both **serotonin** and **norepinephrine**, but lack the broad receptor affinity of TCAs. *Fluoxetine* - **Fluoxetine** is a **selective serotonin reuptake inhibitor (SSRI)**, which specifically targets serotonin reuptake. - SSRIs are generally considered a first-line treatment for depression due to a more favorable side effect profile compared to TCAs. *Citalopram* - **Citalopram** is also a **selective serotonin reuptake inhibitor (SSRI)**, much like fluoxetine. - It works by increasing the levels of **serotonin** in the brain by blocking its reuptake, differentiating it from tricyclic antidepressants.
Question 42: Which of the following is NOT a beta-2 agonist?
- A. Ketotifen (Correct Answer)
- B. Terbutaline
- C. Salbutamol
- D. Bambuterol
Explanation: ***Ketotifen*** - **Ketotifen** is an **oral anti-allergic drug** that acts as a **mast cell stabilizer** and **H1-antihistamine**, not a beta-2 agonist. - It is used for **prophylactic treatment** of asthma and allergic conditions, working through different mechanisms than bronchodilators. *Terbutaline* - **Terbutaline** is a **short-acting beta-2 agonist (SABA)** used for bronchodilation in asthma and COPD [2]. - Available in **oral, inhaled, and injectable forms** for rapid relief of bronchospasm. *Salbutamol* - **Salbutamol** (also known as albuterol) is a **short-acting beta-2 agonist (SABA)** and the most widely used rescue inhaler for asthma [1], [2]. - Provides **rapid bronchodilation** by stimulating beta-2 receptors in airway smooth muscles [3]. *Bambuterol* - **Bambuterol** is a **long-acting beta-2 agonist (LABA)** that is a prodrug of **terbutaline**. - It is slowly converted to the active form in the body, providing **sustained bronchodilation** for maintenance therapy.
Question 43: Beta2-agonists cause all except:
- A. Hyperkalemia (Correct Answer)
- B. Hyperglycemia
- C. Tremor
- D. Palpitation
Explanation: ***Hyperkalemia*** - Beta2-agonists actually cause **hypokalemia**, not hyperkalemia, by promoting the intracellular shift of potassium. - This effect is due to the stimulation of the **Na+/K+-ATPase pump** by beta-2 adrenergic receptors. *Hyperglycemia* - Beta2-agonists can lead to **hyperglycemia** by promoting glycogenolysis and gluconeogenesis in the liver. - They also decrease **insulin secretion** and increase insulin resistance. *Tremor* - **Tremor** is a common side effect of beta2-agonists, particularly in the hands, due to direct stimulation of beta2 receptors on skeletal muscle. - This muscle stimulation leads to increased muscle twitching and a fine tremor. *Palpitation* - **Palpitations** can occur due to the systemic absorption of beta2-agonists, leading to activation of beta1 receptors in the heart. - This can cause **tachycardia** and a sensation of a racing heart.
Question 44: Which of the following is a mineralocorticoid antagonist?
- A. Spironolactone (Correct Answer)
- B. Inamrinone
- C. Nicorandil
- D. Ketorolac
Explanation: ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that acts as a competitive antagonist of **aldosterone** at the mineralocorticoid receptors in the renal tubules [1], [2]. - Its primary use is in conditions like **heart failure**, **cirrhosis with ascites**, and **primary hyperaldosteronism** (Conn's syndrome) [2]. *Inamrinone* - **Inamrinone** is a **phosphodiesterase-3 inhibitor** (PDE3 inhibitor) and is classified as an **inotropic agent**. - It increases **intracellular cAMP** in cardiac cells, leading to increased **contractility** and **vasodilation**, and is used in severe heart failure. *Nicorandil* - **Nicorandil** is a **potassium channel opener** and a **nitrate-like drug** that causes both venous and arterial vasodilation. - It is primarily used as an **antianginal agent** due to its ability to reduce cardiac workload and improve coronary blood flow. *Ketorolac* - **Ketorolac** is a **nonsteroidal anti-inflammatory drug (NSAID)** that primarily inhibits **cyclooxygenase (COX) enzymes**. - It is used for **short-term management of acute moderate to severe pain** and has no direct activity on mineralocorticoid receptors.
Question 45: Which of the following is a renin inhibitor?
- A. Losartan
- B. Benazepril
- C. Remikiren (Correct Answer)
- D. Imidapril
Explanation: **Remikiren** - **Remikiren** is a direct **renin inhibitor** that acts by binding to the active site of renin, preventing its interaction with angiotensinogen. - This inhibition reduces the formation of **angiotensin I** and subsequently **angiotensin II**, leading to decreased blood pressure. *Losartan* - **Losartan** is an **Angiotensin II Receptor Blocker (ARB)**, meaning it blocks AT1 receptors, preventing angiotensin II from binding. - It does not inhibit renin activity directly but rather acts downstream in the **renin-angiotensin-aldosterone system (RAAS)**. *Benazepril* - **Benazepril** is an **Angiotensin-Converting Enzyme (ACE) inhibitor**, which blocks the enzyme responsible for converting **angiotensin I** to **angiotensin II**. - It does not directly inhibit renin production or activity. *Imidapril* - **Imidapril** is also an **Angiotensin-Converting Enzyme (ACE) inhibitor**, similar to benazepril. - Its mechanism of action involves inhibiting ACE, thereby reducing **angiotensin II** levels, rather than directly inhibiting renin.
Question 46: 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 47: 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.
Question 48: Aminophylline inhibits which of the following enzymes?
- A. MAO
- B. Alcohol dehydrogenase
- C. Cytochrome P450
- D. Phosphodiesterase (Correct Answer)
Explanation: ***Phosphodiesterase*** - **Aminophylline** is a methylxanthine derivative that primarily acts as a **phosphodiesterase (PDE) inhibitor** [1], [2]. - By inhibiting PDE, aminophylline increases intracellular levels of **cAMP** and **cGMP**, leading to **bronchodilation** and other effects [2], [3]. *MAO* - **MAO (monoamine oxidase)** inhibitors are antidepressants that prevent the breakdown of neurotransmitters like serotonin, norepinephrine, and dopamine. - Aminophylline does not significantly inhibit MAO. *Alcohol dehydrogenase* - **Alcohol dehydrogenase** is an enzyme responsible for metabolizing alcohol (ethanol) in the liver. - Aminophylline has no direct inhibitory effect on alcohol dehydrogenase. *Cytochrome P450* - **Cytochrome P450 (CYP450)** enzymes are a group of enzymes primarily involved in the metabolism of drugs and other xenobiotics in the liver [4]. - While aminophylline (and its active metabolite theophylline) can be metabolized by and *affect* certain **CYP450** isoenzymes (e.g., CYP1A2), it does not act as a general inhibitor of the entire CYP450 system; its primary therapeutic action is not through CYP450 inhibition.
Question 49: 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 50: 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.