NEET-PG 2013 - Pharmacology Practice Questions

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.

Q: Drug that binds bile acids in the intestine and prevents their return to liver via the enterohepatic circulation?

Cholestyramine. ***Cholestyramine*** - **Cholestyramine** is a **bile acid-binding resin** that sequesters bile acids in the intestine, preventing their reabsorption. - This interruption of the **enterohepatic circulation** leads to increased synthesis of new bile acids from cholesterol in the liver, thus lowering plasma LDL cholesterol. *Niacin* - **Niacin (nicotinic acid)** reduces the hepatic synthesis and secretion of **VLDL**, which in turn lowers LDL and triglyceride levels. - It works primarily through mechanisms related to fat metabolism in the liver and adipose tissue, not direct bile acid binding in the intestine. *Fenofibrate* - **Fenofibrate** is a **PPAR-α agonist** that primarily reduces triglyceride levels by increasing fatty acid oxidation and lipoprotein lipase activity, and secondarily increases HDL. - Its main action is on lipid metabolism in the liver and peripheral tissues, not by binding bile acids in the gut. *Gugulipid* - **Gugulipid** is a phytosterol derived from the guggul tree, sometimes used in traditional medicine for cholesterol management. - Its purported mechanism involves increasing **bile acid excretion** and inhibiting cholesterol biosynthesis, but it does not directly bind bile acids in the same manner as resins like cholestyramine.

Q: Which of the following is an antitussive opioid?

Ethylmorphine. ***Ethylmorphine*** - **Ethylmorphine** (also known as dionin) is an opioid derivative with significant **antitussive properties**, meaning it suppresses coughing. - It works by acting on opioid receptors in the **medulla oblongata**, reducing the cough reflex. *Pethidine* - **Pethidine** (also known as meperidine) is a synthetic opioid primarily used for **moderate to severe pain relief**. - While it has some central nervous system effects, its main therapeutic use is as an **analgesic**, not an antitussive. *Methadone* - **Methadone** is a synthetic opioid used for treating **opioid dependence** and for **chronic severe pain**. - Its main application is in addiction treatment and pain management, not specifically as a cough suppressant. *Buprenorphine* - **Buprenorphine** is a **partial opioid agonist** used for pain management and **opioid dependence**. - It has a high affinity for opioid receptors but produces a limited effect, making it less likely to be used solely as an antitussive and more for its analgesic or anti-addictive properties.

Q: Drug of choice for familial hypercholesterolemia?

Lovastatin. ***Lovastatin*** - **Statins** (HMG-CoA reductase inhibitors) are the **first-line therapy** for familial hypercholesterolemia as they effectively lower **LDL cholesterol** levels by inhibiting cholesterol synthesis [1]. - While other agents can be used adjunctively, statins like lovastatin are the cornerstone for managing this genetic condition [2]. *Nicotinic acid* - **Nicotinic acid** (niacin) primarily lowers **triglycerides** and increases **HDL cholesterol**, but it is less potent than statins for reducing LDL-C, especially in familial hypercholesterolemia [1]. - Its use is often limited by significant **side effects** like flushing. *Cholestyramine* - **Cholestyramine** is a **bile acid sequestrant** that binds to bile acids in the intestine, preventing their reabsorption and mildly lowering LDL cholesterol. - It is less effective than statins and often causes **gastrointestinal side effects** such as constipation and bloating. *Gemfibrozil* - **Gemfibrozil** is a **fibrate**, primarily used to lower **triglyceride levels** and increase HDL cholesterol. - It has minimal impact on LDL cholesterol compared to statins and is not the primary treatment for familial hypercholesterolemia [2].

Q: Which of the following is a parenteral direct thrombin inhibitor?

Argatroban. ***Argatroban*** - **Argatroban** is a **synthetic direct thrombin inhibitor** administered exclusively via **intravenous infusion**, making it a parenteral drug. - It does not require antithrombin for its action and is primarily used in patients with **heparin-induced thrombocytopenia (HIT)**. *Ximelagatran* - **Ximelagatran** was an **oral direct thrombin inhibitor** but was withdrawn from the market due to concerns about severe **liver toxicity**. - As an oral drug, it is not a parenteral medication. *Dabigatran* - **Dabigatran** is a **direct thrombin inhibitor** that is administered **orally** in capsule form (as dabigatran etexilate, a prodrug). - Therefore, it is not a parenteral medication. *Heparin* - **Heparin** is an **indirect thrombin inhibitor** because it requires binding to **antithrombin** to exert its anticoagulant effect. - Although administered parenterally, its mechanism of action is indirect.

Q: Which of the following drugs inhibits the activation of plasminogen?

Aminocaproic acid. ***Correct Option: Aminocaproic acid*** - **Aminocaproic acid** is an antifibrinolytic drug that acts by competitively inhibiting the activation of **plasminogen** to plasmin. - By preventing the formation of plasmin, it stabilizes blood clots and is used to treat excessive bleeding. *Incorrect Option: Streptokinase* - **Streptokinase** is a **thrombolytic agent** that forms a complex with plasminogen, converting uncomplexed plasminogen into plasmin. - This action promotes the degradation of fibrin clots, making it a **fibrinolytic drug**, not an inhibitor of plasminogen activation. *Incorrect Option: Reteplase* - **Reteplase** is a **recombinant tissue plasminogen activator (tPA)** that directly converts plasminogen to plasmin. - This drug actively promotes **fibrinolysis** and clot breakdown, making it a thrombolytic agent. *Incorrect Option: Clopidogrel* - **Clopidogrel** is an **antiplatelet drug** that inhibits platelet aggregation by irreversibly blocking the P2Y12 adenosine diphosphate (ADP) receptor on platelets. - Its mechanism of action is focused on **platelet function**, not on the plasminogen-plasmin system.

Question 1

What is the drug of choice for pheochromocytoma?

Accepted Answer

Phenoxybenzamine

Answer

Propranolol

Answer

Prazosin

Answer

Nitroprusside

Question 2

The best agent for increasing HDL cholesterol is?

Accepted Answer

Nicotinic acid

Answer

Statin

Answer

Gugulipids

Answer

Fibrates

Question 3

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

Accepted Answer

Pancreatitis

Answer

Liver dysfunction

Answer

Vasodilation

Answer

Hyperpigmentation

Question 4

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.

Question 5

Drug that binds bile acids in the intestine and prevents their return to liver via the enterohepatic circulation?

Accepted Answer

Cholestyramine

Answer

Niacin

Answer

Fenofibrate

Answer

Gugulipid

Question 6

Which of the following is an antitussive opioid?

Accepted Answer

Ethylmorphine

Answer

Pethidine

Answer

Methadone

Answer

Buprenorphine

Question 7

Drug of choice for familial hypercholesterolemia?

Accepted Answer

Lovastatin

Answer

Nicotinic acid

Answer

Cholestyramine

Answer

Gemfibrozil

Question 8

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 9

Which of the following is a parenteral direct thrombin inhibitor?

Accepted Answer

Argatroban

Answer

Ximelagatran

Answer

Dabigatran

Answer

Heparin

Question 10

Which of the following drugs inhibits the activation of plasminogen?

Accepted Answer

Aminocaproic acid

Answer

Streptokinase

Answer

Reteplase

Answer

Clopidogrel

NEET-PG 2013 — Pharmacology