NEET-PG 2013 - Pharmacology Practice Questions

Q: What conditions is Metformin primarily used to treat?

Both Type 2 Diabetes and Polycystic Ovary Syndrome (PCOS). ***Both Type 2 Diabetes and Polycystic Ovary Syndrome (PCOS)*** - **Metformin** is a first-line treatment for **Type 2 Diabetes** due to its ability to decrease hepatic glucose production and improve insulin sensitivity [1], [2]. - It is also commonly used off-label for **PCOS** to improve insulin resistance, ovulation, and reduce androgen levels. *Only Type 2 Diabetes* - While Metformin is a cornerstone for **Type 2 Diabetes** treatment, stating "only" is incorrect as it has other significant therapeutic uses [2]. - Its benefits extend beyond diabetes management, particularly in conditions involving **insulin resistance**. *Only Polycystic Ovary Syndrome (PCOS)* - Metformin is used in **PCOS**, but it is not the sole condition it treats, and its primary indication remains **Type 2 Diabetes** [2]. - This option incorrectly limits its application to just one condition, overlooking its major role in diabetes. *Pregnancy Induced Hypertension* - **Metformin** is not indicated for the treatment of **pregnancy-induced hypertension** (gestational hypertension). - Treatment for pregnancy-induced hypertension typically involves medications like **labetalol**, **methyldopa**, or **nifedipine**, with delivery being the definitive management for severe cases.

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 the longest acting glucocorticoid?

Dexamethasone. ***Correct: Dexamethasone*** - **Dexamethasone** is a long-acting glucocorticoid with a **biological half-life of 36–72 hours**, making it the longest acting among the options provided - Its prolonged action is due to its **high affinity for the glucocorticoid receptor** and relatively slow metabolism - Provides sustained anti-inflammatory and immunosuppressive effects *Incorrect: Prednisone* - **Prednisone** is an intermediate-acting glucocorticoid with a biological half-life of 12-36 hours - Requires metabolism in the liver to its active form, prednisolone - Duration of action is significantly shorter than dexamethasone *Incorrect: Prednisolone* - **Prednisolone** is the active form of prednisone, with a similar intermediate duration of action (12-36 hours) - Primarily used when liver conversion of prednisone is impaired - Does not possess the extended duration of action characteristic of dexamethasone *Incorrect: Cortisone* - **Cortisone** is a short-acting glucocorticoid with a biological half-life of 8-12 hours - It is a prodrug that needs to be converted to **hydrocortisone** (cortisol) in the liver to become active - Has the shortest duration among all options

Q: Which of the following is the most potent topical corticosteroid?

Clobetasol propionate. ***Clobetasol propionate*** - **Clobetasol propionate** is recognized as one of the most potent **Class I topical corticosteroids**, used for severe inflammatory skin conditions. - Its high potency allows for effective suppression of severe inflammation and pruritus, but also carries a greater risk of **adverse effects** with prolonged use. *Triamcinolone acetonide* - **Triamcinolone acetonide** is a **medium-potency** topical corticosteroid (Class IV-V), less potent than clobetasol propionate. - It is commonly used for moderate inflammatory skin conditions, such as eczema and psoriasis, but not for severe cases requiring maximum potency. *Hydrocortisone acetate* - **Hydrocortisone acetate** is a **low-potency** topical corticosteroid (Class VII), making it the least potent option listed. - It's often used for mild inflammatory conditions, sensitive areas like the face, or for less severe conditions requiring minimal corticosteroid strength. *Betamethasone valerate* - **Betamethasone valerate** is a **medium-to-high potency** topical corticosteroid (Class III-V), placing it among stronger corticosteroids but still less potent than clobetasol propionate. - It is effective for moderate to severe inflammatory skin conditions but does not reach the highest level of potency demonstrated by clobetasol.

Q: Which of the following reduces the efficacy of oral contraceptives?

Griseofulvin. ***Griseofulvin*** - **Griseofulvin** is an antifungal agent known to induce liver enzymes, specifically the **cytochrome P450 system**. - Enzyme induction accelerates the metabolism and clearance of **oral contraceptives**, leading to lower plasma concentrations and reduced efficacy. *Erythromycin* - **Erythromycin** is a macrolide antibiotic that typically inhibits liver enzymes rather than inducing them. - While it can interfere with the metabolism of some drugs, it usually **increases** rather than decreases the plasma levels of co-administered medications, and is not known to reduce oral contraceptive efficacy. *Disulfiram* - **Disulfiram** is used to treat chronic alcoholism and inhibits aldehyde dehydrogenase. - It does not significantly interact with the metabolism of **oral contraceptives** via the cytochrome P450 system or other mechanisms that would reduce their efficacy. *Cimetidine* - **Cimetidine** is an H2 receptor antagonist that is known to inhibit cytochrome P450 enzymes. - This inhibition would likely **increase** the plasma concentration of drugs metabolized by these enzymes, such as oral contraceptives, rather than reducing their efficacy.

Q: What is the best drug for control of acute esophageal variceal bleeding?

Octreotide. ***Octreotide*** - **Octreotide** is a somatostatin analog that causes **splanchnic vasoconstriction**, reducing portal venous inflow and pressure, which is crucial in controlling **esophageal variceal bleeding**. - Its mechanism involves inhibiting the release of **vasodilatory hormones** like glucagon, leading to a decrease in portal pressure without significant systemic side effects. *Vasopressin* - **Vasopressin** is a potent vasoconstrictor that can reduce portal pressure but has significant systemic side effects such as **myocardial ischemia** and **bowel ischemia** due to widespread vasoconstriction. - It is generally no longer considered the first-line pharmacological treatment for variceal bleeding due to its **adverse effect profile**. *GnRH* - **GnRH** (Gonadotropin-releasing hormone) plays a role in regulating the reproductive system by controlling the release of FSH and LH from the pituitary. - It has **no direct role** in the management or control of esophageal bleeding. *Propranolol* - **Propranolol** is a non-selective beta-blocker primarily used for **prophylaxis** of variceal bleeding by reducing portal pressure chronically. - It works by reducing cardiac output and causing splanchnic vasoconstriction, but it is **not used for acute control** of active bleeding.

Q: What is the drug of choice for pheochromocytoma?

Phenoxybenzamine. ***Phenoxybenzamine*** - This is an **irreversible, non-selective alpha-adrenergic blocker**, which is the drug of choice for preparing patients for surgical removal of a pheochromocytoma. - It effectively controls **hypertension** by blocking the effects of catecholamines on blood vessels, preventing a hypertensive crisis during surgery. *Propranolol* - **Beta-blockers** like propranolol should **not be used as monotherapy** in pheochromocytoma because blocking beta-2 receptors without prior alpha blockade can lead to unopposed alpha-adrenergic vasoconstriction and precipitate a **hypertensive crisis**. - It can be added **after adequate alpha-blockade** to control tachycardia. *Prazosin* - Prazosin is a **reversible, selective alpha-1 adrenergic blocker**, which is not preferred over phenoxybenzamine due to its shorter duration of action and reversibility. - While it can lower blood pressure, its efficacy in preventing hypertensive crises during surgery for pheochromocytoma is **less robust** compared to phenoxybenzamine. *Nitroprusside* - Sodium nitroprusside is a **potent vasodilator** often used for **hypertensive emergencies**, but it is not the drug of choice for long-term management or preoperative preparation in pheochromocytoma. - Its use in pheochromocytoma is typically reserved for **acute hypertensive crises** when other agents are insufficient, rather than initial management.

Q: The best agent for increasing HDL cholesterol is?

Nicotinic acid. ***Nicotinic acid*** - **Nicotinic acid** (niacin) is known to significantly increase **high-density lipoprotein (HDL) cholesterol** levels by reducing its catabolism. - It also has beneficial effects on other lipid parameters, such as lowering **triglycerides** and **LDL cholesterol**. *Statin* - **Statins** (HMG-CoA reductase inhibitors) are highly effective at lowering **LDL cholesterol** and moderately lowering triglycerides. - While they can cause a modest increase in HDL cholesterol, their primary role is not HDL elevation. *Gugulipids* - **Gugulipids**, derived from the gum resin of the _Commiphora mukul_ tree, have been used in traditional medicine to lower cholesterol. - Evidence for their efficacy in significantly increasing HDL cholesterol is weak and not clinically recommended. *Fibrates* - **Fibrates** primarily work to lower **triglyceride levels** and can modestly increase HDL cholesterol. - Their effect on HDL is generally less pronounced compared to nicotinic acid.

Q: All of the following are adverse effects of nicotinic acid except:

Pancreatitis. ***Pancreatitis*** - **Pancreatitis** is not a commonly reported adverse effect of nicotinic acid (niacin) therapy. - While other gastrointestinal side effects like nausea and vomiting can occur, pancreatic inflammation is not characteristic. *Vasodilation* - **Cutaneous flushing** and **vasodilation** are very common adverse effects of nicotinic acid, mediated by prostaglandin release. - This effect can cause a sensation of warmth, redness, and itching, especially at the start of therapy. *Liver dysfunction* - **Liver dysfunction**, including elevated liver enzymes and rare cases of **hepatotoxicity**, can occur with high doses of nicotinic acid. - Regular monitoring of liver function tests is recommended for patients on niacin therapy. *Hyperpigmentation* - **Hyperpigmentation**, particularly **acanthosis nigricans**, is a known cutaneous side effect of nicotinic acid. - This typically presents as dark, velvety patches on the skin, especially in skin fold areas.

Question 1

What conditions is Metformin primarily used to treat?

Accepted Answer

Both Type 2 Diabetes and Polycystic Ovary Syndrome (PCOS)

Answer

Only Type 2 Diabetes

Answer

Only Polycystic Ovary Syndrome (PCOS)

Answer

Pregnancy Induced Hypertension

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 is the longest acting glucocorticoid?

Accepted Answer

Dexamethasone

Answer

Prednisone

Answer

Prednisolone

Answer

Cortisone

Question 4

Which of the following is the most potent topical corticosteroid?

Accepted Answer

Clobetasol propionate

Answer

Triamcinolone acetonide

Answer

Hydrocortisone acetate

Answer

Betamethasone valerate

Question 5

Which of the following reduces the efficacy of oral contraceptives?

Accepted Answer

Griseofulvin

Answer

Disulfiram

Answer

Erythromycin

Answer

Cimetidine

Question 6

What is the best drug for control of acute esophageal variceal bleeding?

Accepted Answer

Octreotide

Answer

Vasopressin

Answer

GnRH

Answer

Propranolol

Question 7

What is the drug of choice for pheochromocytoma?

Accepted Answer

Phenoxybenzamine

Answer

Propranolol

Answer

Prazosin

Answer

Nitroprusside

Question 8

The best agent for increasing HDL cholesterol is?

Accepted Answer

Nicotinic acid

Answer

Statin

Answer

Gugulipids

Answer

Fibrates

Question 9

All of the following are adverse effects of nicotinic acid except:

Accepted Answer

Pancreatitis

Answer

Liver dysfunction

Answer

Vasodilation

Answer

Hyperpigmentation

Question 10

What is the mechanism of action of clofibrate in lipid metabolism?

Accepted Answer

Increases lipoprotein lipase activity through PPAR alpha, leading to enhanced lipolysis of triglycerides.

Answer

Inhibits lipolysis in adipose tissue.

Answer

Inhibits HMG CoA reductase.

Answer

Binds bile acids and bile salts in the small intestine.

NEET-PG 2013 — Pharmacology