Drug that binds bile acids in the intestine and prevents their return to liver via the enterohepatic circulation?
Which of the following is an antitussive opioid?
Drug of choice for familial hypercholesterolemia?
Which of the following statements about hypolipidemic drugs is false?
Which of the following is a parenteral direct thrombin inhibitor?
Which of the following drugs inhibits the activation of plasminogen?
Mechanism of action of tranexamic acid is
What is the mechanism of action of Warfarin?
Which of the following anticoagulants is given orally?
What is Hydroxyethyl starch?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 101: Drug that binds bile acids in the intestine and prevents their return to liver via the enterohepatic circulation?
- A. Niacin
- B. Fenofibrate
- C. Cholestyramine (Correct Answer)
- D. Gugulipid
Explanation: ***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.
Question 102: Which of the following is an antitussive opioid?
- A. Pethidine
- B. Methadone
- C. Buprenorphine
- D. Ethylmorphine (Correct Answer)
Explanation: ***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.
Question 103: Drug of choice for familial hypercholesterolemia?
- A. Nicotinic acid
- B. Lovastatin (Correct Answer)
- C. Cholestyramine
- D. Gemfibrozil
Explanation: ***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].
Question 104: Which of the following statements about hypolipidemic drugs is false?
- A. Gemfibrozil causes myopathy
- B. Gemfibrozil can increase myopathy caused by statins
- C. Lovastatin can cause hepatic dysfunction
- D. Cholesterol reducing drugs are contraindicated in child less than 8 years (Correct Answer)
Explanation: ***Cholesterol reducing drugs are contraindicated in child less than 8 years*** - While cholesterol-lowering drugs are generally avoided in young children, there are specific **genetic dyslipidemias** where treatment may be initiated earlier under specialist supervision [1]. - The statement is **false** because some genetic conditions may necessitate earlier treatment, making a blanket contraindication for all children under 8 inaccurate [1]. *Gemfibrozil causes myopathy* - **Gemfibrozil** (a fibric acid derivative) can indeed cause **myopathy**, especially when used alone or in combination with other lipid-lowering agents [2]. - This adverse effect is thought to be due to its mechanism of action affecting fatty acid metabolism and muscle integrity. *Gemfibrozil can increase myopathy caused by statins* - The co-administration of **gemfibrozil** with **statins** significantly increases the risk of **myopathy** and **rhabdomyolysis** [2]. - This is primarily due to gemfibrozil inhibiting the **glucuronidation** of statins, which increases statin plasma concentrations [2]. *Lovastatin can cause hepatic dysfunction* - **Statins**, including **lovastatin**, can cause **elevations in liver transaminases** and, in rare cases, lead to **drug-induced liver injury** [1]. - Regular monitoring of liver function tests is recommended when initiating statin therapy and during follow-up [2].
Question 105: Which of the following is a parenteral direct thrombin inhibitor?
- A. Ximelagatran
- B. Dabigatran
- C. Argatroban (Correct Answer)
- D. Heparin
Explanation: ***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.
Question 106: Which of the following drugs inhibits the activation of plasminogen?
- A. Streptokinase
- B. Aminocaproic acid (Correct Answer)
- C. Reteplase
- D. Clopidogrel
Explanation: ***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 107: Mechanism of action of tranexamic acid is
- A. Decrease vascular permeability
- B. Smooth muscle contraction
- C. Activates Plasmin formation
- D. Prevents fibrinolysis (Correct Answer)
Explanation: ***Correct: Prevents fibrinolysis*** - Tranexamic acid is an **antifibrinolytic agent** that works by inhibiting the activation of plasminogen to plasmin. - By preventing the formation of plasmin, it stabilizes **fibrin clots** and reduces bleeding. *Incorrect: Decrease vascular permeability* - This is primarily the mechanism of action of drugs like antihistamines or corticosteroids, which work on **inflammation** and **allergic reactions**. - Tranexamic acid does not directly target vascular permeability; its primary role is in **hemostasis**. *Incorrect: Smooth muscle contraction* - This describes the action of drugs like **vasoconstrictors** (e.g., epinephrine) or agents that promote uterine contractions (e.g., oxytocin). - Tranexamic acid has no direct effect on **smooth muscle contraction**. *Incorrect: Activates Plasmin formation* - This is the opposite of tranexamic acid's action; drugs that activate plasmin, such as **tissue plasminogen activators (tPAs)**, are used to break down clots. - Tranexamic acid specifically **inhibits plasminogen activation**, thereby preventing plasmin formation.
Question 108: What is the mechanism of action of Warfarin?
- A. Inhibition of Vitamin K epoxide reductase (Correct Answer)
- B. Inhibition of gamma glutamyl carboxylase
- C. Activation of Vitamin K epoxide reductase
- D. Activation of gamma glutamyl carboxylase
Explanation: ***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**.
Question 109: Which of the following anticoagulants is given orally?
- A. Argatraban
- B. Alteplase
- C. Rivaroxaban (Correct Answer)
- D. Fondaparinux
Explanation: ***Rivaroxaban*** - Rivaroxaban is a **direct oral anticoagulant (DOAC)** that specifically inhibits **Factor Xa**. - It is administered orally and does not require routine coagulation monitoring. *Argatraban* - Argatroban is a **direct thrombin inhibitor (DTI)** primarily used intravenously, especially in patients with **heparin-induced thrombocytopenia (HIT)**. - It is not an orally administered anticoagulant. *Alteplase* - Alteplase is a **thrombolytic agent** (clot buster), not an anticoagulant, that works by converting **plasminogen to plasmin**. - It is administered intravenously to dissolve existing clots. *Fondaparinux* - Fondaparinux is a **synthetic pentasaccharide** that selectively inhibits **Factor Xa** by binding to antithrombin. - It is administered **subcutaneously**, not orally.
Question 110: What is Hydroxyethyl starch?
- A. Vasodilator
- B. Inotrope
- C. Plasma expander (Correct Answer)
- D. Diuretic
Explanation: ***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.