What is the drug of choice for a classical angina attack?
Which calcium channel blocker has the shortest duration of action?
Which of the following is NOT a beta-2 agonist?
Which of the following is a renin inhibitor?
In which of the following conditions is Verapamil not typically used?
Which drug is used for sympathectomy in experimental animals?
Which of the following is NOT a side effect of digitalis?
Nesiritide causes vasodilation through?
Which of the following medications is most likely to cause reflex tachycardia?
Aminophylline inhibits which of the following enzymes?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 31: 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 32: 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 33: 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 34: 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 35: In which of the following conditions is Verapamil not typically used?
- A. Angina pectoris
- B. Atrial fibrillation
- C. Ventricular tachycardia (Correct Answer)
- D. Hypertension
Explanation: ***Ventricular tachycardia*** - Verapamil, a **non-dihydropyridine calcium channel blocker**, can worsen hemodynamics in patients with **ventricular tachycardia (VT)** by causing profound hypotension or precipitating cardiac arrest. - VT often requires prompt treatment with **antiarrhythmics like amiodarone** or **electrical cardioversion**, as it can be life-threatening. - Verapamil is **contraindicated in VT** due to its negative inotropic effects and risk of hemodynamic collapse. *Angina pectoris* - Verapamil is effectively used to treat angina pectoris by **decreasing myocardial oxygen demand** through negative chronotropic and inotropic effects, and by causing **coronary vasodilation**, improving blood flow. - Its effects help to reduce the frequency and severity of anginal episodes, particularly in **stable angina**. *Atrial fibrillation* - Verapamil is commonly used for **rate control in atrial fibrillation** by **slowing conduction through the AV node**, which decreases the ventricular response rate. - It helps to manage symptoms and prevent complications related to rapid heart rates in this arrhythmia. *Hypertension* - Verapamil is used in the treatment of **hypertension** through its vasodilatory effects and reduction in peripheral vascular resistance. - It is particularly useful in patients who cannot tolerate other antihypertensive agents or as part of combination therapy.
Question 36: 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 37: Which of the following is NOT a side effect of digitalis?
- A. Nausea and vomiting
- B. Ventricular Bigeminy
- C. Vasodilatation (Correct Answer)
- D. Ventricular tachycardia
Explanation: **Vasodilatation** - **Digitalis**, primarily digoxin, is known for its **positive inotropic effect**, increasing myocardial contractility, and for its **vasoconstrictive properties** at higher doses due to sympathetic activation and direct smooth muscle effects, not vasodilatation. - While it can indirectly improve cardiac output and thus tissue perfusion, its direct vascular effects do not typically include widespread vasodilatation. *Ventricular tachycardia* - **Digitalis toxicity** can lead to various arrhythmias, including **ventricular tachycardia**, which is a potentially life-threatening side effect. - This occurs due to increased automaticity and delayed afterdepolarizations in ventricular myocytes. *Nausea and vomiting* - **Gastrointestinal symptoms** such as **nausea and vomiting** are common early signs of digitalis toxicity. - These effects are thought to be mediated by the drug's action on the chemoreceptor trigger zone in the brainstem. *Ventricular Bigeminy* - **Ventricular bigeminy**, characterized by alternating normal and premature ventricular beats, is another classic manifestation of **digitalis toxicity**. - This arrhythmia results from enhanced automaticity and altered conduction properties in the ventricles.
Question 38: Nesiritide causes vasodilation through?
- A. ATP
- B. Cyclic adenosine monophosphate (cAMP)
- C. K+ ions
- D. Guanosine 3',5'-cyclic monophosphate (cGMP) (Correct Answer)
Explanation: ***Guanosine 3',5'-cyclic monophosphate (cGMP)*** - **Nesiritide** is a synthetic **B-type natriuretic peptide (BNP)** that acts as a potent vasodilator [2]. - It works by binding to **guanylyl cyclase receptors**, leading to an increase in intracellular **cGMP**, which promotes smooth muscle relaxation [1], [2]. *Cyclic adenosine monophosphate (cAMP)* - While **cAMP** is a crucial second messenger in various cellular processes and can mediate some forms of vasodilation, it is primarily associated with **beta-adrenergic receptor activation**, not the mechanism of action of nesiritide. - Nesiritide's pathway is distinct from those involving **cAMP-mediated** relaxation, which often involves different kinases and protein phosphorylation. *ATP* - **ATP** (adenosine triphosphate) is the primary **energy currency** of the cell and is involved in numerous cellular functions, including muscle contraction and relaxation, but it is not a direct mediator of nesiritide's vasodilatory effects. - Though ATP can be broken down to produce **adenosine**, which has vasodilatory properties, this is not the specific mechanism through which nesiritide causes vasodilation. *K+ ions* - Changes in **potassium ion (K+)** flux across cell membranes are essential for regulating vascular tone, as K+ channel activation can lead to hyperpolarization and relaxation of smooth muscle. - However, **nesiritide's primary mechanism** of action does not involve direct modulation of K+ channels; its vasodilatory effects are mediated by the **cGMP pathway** [2].
Question 39: 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 40: 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.