NEET-PG 2013 - Pharmacology Practice Questions

Q: Nesiritide causes vasodilation through?

Guanosine 3',5'-cyclic monophosphate (cGMP). ***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].

Q: Which of the antithyroid drugs inhibits iodine trapping?

Thiocyanates. ***Thiocyanates*** - **Thiocyanates** are competitive inhibitors of the **sodium-iodide symporter (NIS)**, which is responsible for actively transporting iodide into thyroid follicular cells (iodine trapping) [1]. - By blocking NIS, thiocyanates prevent the thyroid gland from accumulating iodide, thereby inhibiting thyroid hormone synthesis [1]. *Radioactive iodine* - **Radioactive iodine (RAI)** primarily works by being taken up by thyroid cells and emitting **beta particles**, which destroy the thyroid tissue [3]. - It does not inhibit iodine trapping, but rather uses the trapping mechanism to concentrate in the thyroid and exert its destructive effect [3]. *Iodides* - **Iodides** (e.g., Lugol's solution) paradoxically inhibit organification and hormone release from the thyroid gland, an effect known as the **Wolff-Chaikoff effect** [2]. - They also decrease the vascularity and size of the thyroid gland, making them useful in preparing patients for thyroidectomy, but do not directly inhibit iodine trapping [2]. *Methimazole* - **Methimazole** is a **thionamide** drug that primarily inhibits the enzyme **thyroid peroxidase**. - This prevents the **organification of iodide** (incorporation of iodine into tyrosine residues) and the **coupling of iodotyrosines** (forming T3 and T4), not the initial trapping of iodine.

Q: Which of the following is NOT a beta-2 agonist?

Ketotifen. ***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.

Q: What is Hydroxyethyl starch?

Plasma expander. ***Plasma expander*** - **Hydroxyethyl starch** is a **colloid solution** used intravenously to increase plasma volume and maintain oncotic pressure. - It is often used in situations of **hypovolemia** or shock to support circulation. *Vasodilator* - A **vasodilator** is a medication that widens blood vessels, typically used to lower blood pressure or improve blood flow. - Hydroxyethyl starch does not directly cause **vasodilation** as its primary mechanism of action. *Inotrope* - An **inotrope** is an agent that alters the force or energy of muscular contractions, mainly affecting the heart's contractility. - Hydroxyethyl starch has no direct effect on **myocardial contractility**. *Diuretic* - A **diuretic** is a substance that promotes increased production of urine, thereby increasing the excretion of water from the body. - While fluid administration can temporarily increase urine output, hydroxyethyl starch is not classified as a **diuretic agent** itself.

Q: What is the mechanism of action of Warfarin?

Inhibition of Vitamin K epoxide reductase. ***Inhibition of Vitamin K epoxide reductase*** - Warfarin blocks **Vitamin K epoxide reductase (VKORC1)** [1, 2, 3], an enzyme essential for recycling oxidized vitamin K into its active reduced form [1, 3]. - This reduction prevents the activation of **vitamin K-dependent clotting factors** (II, VII, IX, X), leading to anticoagulation [1, 3]. *Inhibition of gamma glutamyl carboxylase* - **Gamma-glutamyl carboxylase** uses reduced vitamin K as a cofactor to carboxylate specific glutamic acid residues on clotting factors [1, 3]. - While essential for clotting factor activation, this enzyme itself is **not directly inhibited by warfarin** [1, 3]. *Activation of Vitamin K epoxide reductase* - Activating **VKORC1** would increase the production of reduced vitamin K, thereby **promoting coagulation** rather than inhibiting it [1, 2]. - This is the opposite of warfarin's intended therapeutic effect. *Activation of gamma glutamyl carboxylase* - Activating **gamma-glutamyl carboxylase** would enhance the carboxylation and activation of **clotting factors**, leading to procoagulant effects [1, 3]. - This mechanism contradicts warfarin's role as an **anticoagulant**.

Q: Which drug is primarily used in the treatment of breast cancer?

Tamoxifen. ***Tamoxifen*** - **Tamoxifen** is a **selective estrogen receptor modulator (SERM)** primarily used to treat and prevent **estrogen receptor (ER)-positive breast cancer**. - It works by blocking estrogen from binding to receptors in breast cancer cells, thereby inhibiting their growth. *Cyproterone* - **Cyproterone** is an **anti-androgen** and **progestogen** primarily used to treat conditions like **prostate cancer**, **acne**, and **hirsutism** in women. - Its main mechanism involves blocking androgen receptors and reducing androgen production, which is not the primary pathway for breast cancer. *Testosterone* - **Testosterone** is an **androgen** (male sex hormone) and is **not used** in the primary treatment of breast cancer. - In certain rare cases of severe metastatic breast cancer, androgens like high-dose testosterone have been historically used for palliation, but this is not standard therapy. *Chlorambucil* - **Chlorambucil** is an **alkylating agent** used primarily in the treatment of **chronic lymphocytic leukemia (CLL)** and certain **lymphomas**. - It works by interfering with DNA replication and transcription, but it is not a first-line or primary agent for breast cancer.

Q: Beta2-agonists cause all except:

Hyperkalemia. ***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.

Q: Which one of the following agents has been associated with hemorrhagic stroke?

Phenylpropanolamine. ***Phenylpropanolamine*** - **Phenylpropanolamine (PPA)** is a sympathomimetic agent that was formerly used as a nasal decongestant and anorectic. - Its use has been linked to an increased risk of **hemorrhagic stroke**, particularly in young women, due to its **vasoconstrictive effects** and potential to cause a sudden, severe rise in blood pressure. *Terfenadine* - **Terfenadine** is a second-generation antihistamine that was voluntarily withdrawn from the market due to its association with severe **cardiac arrhythmias (QT prolongation and Torsades de Pointes)**, not hemorrhagic stroke. - It works by blocking H1 histamine receptors but also had effects on cardiac potassium channels. *Quinidine* - **Quinidine** is an antiarrhythmic drug (Class Ia) primarily used to treat supraventricular and ventricular arrhythmias. - Its main side effects include **gastrointestinal disturbances**, **cinchonism**, and the risk of **QT prolongation** leading to Torsades de Pointes; it is not typically associated with hemorrhagic stroke. *Fenfluramine* - **Fenfluramine** was an anorectic drug used in the treatment of obesity, often in combination with phentermine. - It was withdrawn from the market due to its association with **pulmonary hypertension** and **cardiac valvulopathy**, not hemorrhagic stroke.

Q: Which of the following medications is most likely to cause reflex tachycardia?

Nifedipine. ***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 1

Nesiritide causes vasodilation through?

Accepted Answer

Guanosine 3',5'-cyclic monophosphate (cGMP)

Answer

ATP

Answer

Cyclic adenosine monophosphate (cAMP)

Answer

K+ ions

Question 2

Which of the antithyroid drugs inhibits iodine trapping?

Accepted Answer

Thiocyanates

Answer

Radioactive iodine

Answer

Iodides

Answer

Methimazole

Question 3

Which of the following statements about hypolipidemic drugs is false?

Accepted Answer

Cholesterol reducing drugs are contraindicated in child less than 8 years

Answer

Gemfibrozil causes myopathy

Answer

Gemfibrozil can increase myopathy caused by statins

Answer

Lovastatin can cause hepatic dysfunction

Question 4

Which of the following is NOT a beta-2 agonist?

Accepted Answer

Ketotifen

Answer

Terbutaline

Answer

Salbutamol

Answer

Bambuterol

Question 5

What is Hydroxyethyl starch?

Accepted Answer

Plasma expander

Answer

Vasodilator

Answer

Inotrope

Answer

Diuretic

Question 6

What is the mechanism of action of Warfarin?

Accepted Answer

Inhibition of Vitamin K epoxide reductase

Answer

Inhibition of gamma glutamyl carboxylase

Answer

Activation of Vitamin K epoxide reductase

Answer

Activation of gamma glutamyl carboxylase

Question 7

Which drug is primarily used in the treatment of breast cancer?

Accepted Answer

Tamoxifen

Answer

Cyproterone

Answer

Testosterone

Answer

Chlorambucil

Question 8

Beta2-agonists cause all except:

Accepted Answer

Hyperkalemia

Answer

Hyperglycemia

Answer

Tremor

Answer

Palpitation

Question 9

Which one of the following agents has been associated with hemorrhagic stroke?

Accepted Answer

Phenylpropanolamine

Answer

Terfenadine

Answer

Quinidine

Answer

Fenfluramine

Question 10

Which of the following medications is most likely to cause reflex tachycardia?

Accepted Answer

Nifedipine

Answer

Verapamil

Answer

Propranolol

Answer

Amlodipine

NEET-PG 2013 — Pharmacology