NEET-PG 2015 - Pharmacology PYQs Practice Questions

Q: Adverse effects of phenytoin include the following EXCEPT:

Hypercalcemia. ***Hypercalcemia*** - Phenytoin can actually lead to **hypocalcemia** due to its effect on vitamin D metabolism, increasing its degradation and leading to osteomalacia or rickets [1]. - Therefore, **hypercalcemia** is not an expected adverse effect of phenytoin use. *Lymphadenopathy* - **Generalized lymphadenopathy** is a known, though less common, adverse effect of phenytoin, sometimes mimicking lymphoma. - It's part of a broader hypersensitivity reaction that can occur with the drug. *Ataxia* - **Ataxia** is a common dose-dependent adverse effect of phenytoin, especially at higher therapeutic or toxic levels [1], [2]. - It manifests as impaired coordination and balance due to cerebellar dysfunction [1]. *Hirsutism* - **Hirsutism**, or excessive hair growth, is a well-known chronic side effect of phenytoin [1]. - This effect is more aesthetically concerning than medically dangerous and is particularly common in young women [1]. [Practice more Pharmacology PYQs on OnCourse]

Q: Drug not used in pulmonary hypertension is:

Alpha blocker. ***Alpha blocker*** - Alpha-blockers primarily cause **systemic vasodilation** [1] and are not indicated for the specific pulmonary vascular remodeling and vasoconstriction seen in pulmonary hypertension. [2] - Their use could lead to an undesirable drop in **systemic blood pressure** [3] without adequately addressing the pulmonary arterial pressure. *Calcium channel blocker* - **Calcium channel blockers** (namely **dihydropyridines** like nifedipine and amlodipine) are used in a small subset of pulmonary hypertension patients who are **vasoreactive** on acute testing. - They work by relaxing pulmonary arterial smooth muscle, reducing **pulmonary vascular resistance**. *Endothelin receptor antagonist* - **Endothelin receptor antagonists** (e.g., bosentan, ambrisentan) block the effects of **endothelin-1**, a potent vasoconstrictor and smooth muscle proliferator involved in pulmonary hypertension. - They improve hemodynamics, exercise capacity, and clinical outcomes by preventing **vasoconstriction** and **vascular remodeling**. *Prostacyclin* - **Prostacyclin analogs** (e.g., epoprostenol, treprostinil) are potent **vasodilators** and inhibitors of platelet aggregation. - They are highly effective in treating severe pulmonary hypertension by relaxing pulmonary arteries and preventing **thrombosis**. [Practice more Pharmacology PYQs on OnCourse]

Q: What is the cause of cough and angioedema in a patient receiving ACE inhibitors?

Bradykinin accumulation. ***Bradykinin accumulation*** - **ACE inhibitors** block the enzyme **angiotensin-converting enzyme (ACE)**, which is responsible for degrading **bradykinin**. - The resulting **accumulation of bradykinin** is a potent vasodilator and increases capillary permeability, leading to **cough** (5-20% of patients) and **angioedema** (0.1-0.7%). - This is the most **precise answer** as it specifies the mechanism: impaired degradation leading to accumulation. *Bradykinin (alone)* - While **bradykinin** is the mediator involved, this option is **less precise** than "bradykinin accumulation." - **Bradykinin** is naturally present in the body; the problem with ACE inhibitors is specifically the **accumulation** due to impaired degradation. - The correct answer requires understanding that it's the **excess levels**, not just the presence, that causes symptoms. *Increased renin levels* - **ACE inhibitors** block the conversion of **angiotensin I to angiotensin II**, leading to reduced negative feedback. - This causes **compensatory increase in renin secretion** from the juxtaglomerular apparatus. - However, increased renin is **not responsible** for cough or angioedema—these are bradykinin-mediated effects. *Increased angiotensin-II levels* - **ACE inhibitors** actually **decrease angiotensin-II levels**, which is their primary **antihypertensive mechanism**. - This option is **incorrect** as ACE inhibitors reduce (not increase) angiotensin-II. - The reduction in angiotensin-II does not cause cough or angioedema. [Practice more Pharmacology PYQs on OnCourse]

Q: What is the mechanism of action of ticagrelor?

P2Y12 receptor antagonist. ***P2Y12 receptor antagonist*** - **Ticagrelor** is an **oral antiplatelet drug** that reversibly binds to the **P2Y12 ADP receptor** on platelet surfaces. - By blocking this receptor, it prevents **ADP-mediated platelet activation** and subsequent aggregation, reducing the risk of thrombotic events. *Cox inhibition* - **COX inhibitors** like **aspirin** prevent the synthesis of **thromboxane A2**, a powerful platelet aggregator. - This mechanism is characteristic of **NSAIDs** and **aspirin**, not ticagrelor. *GPIIB/IIIA inhibition* - **GPIIb/IIIa inhibitors** (e.g., abciximab, eptifibatide, tirofiban) directly block the final common pathway for platelet aggregation by preventing **fibrinogen binding** to the GPIIb/IIIa receptor. - While also an antiplatelet mechanism, this is distinct from ticagrelor's action on the P2Y12 receptor. *Inhibition of thromboxane synthase* - Inhibition of **thromboxane synthase** would reduce the production of **thromboxane A2**, similar to the effect of COX inhibition. - This is not the primary mechanism of action for ticagrelor; drugs like **dazoxiben** or **picotamide** act through this pathway. [Practice more Pharmacology PYQs on OnCourse]

Q: What was the first oral direct thrombin inhibitor to be developed and approved for clinical use?

Ximelagatran. ***Ximelagatran*** - **Ximelagatran** was the **first oral direct thrombin inhibitor** to be developed and approved for clinical use. - Despite its initial approval, it was later withdrawn due to concerns about **drug-induced liver injury**. *Indraparinux* - **Indraparinux** is a **synthetic heparin analog** and an **indirect Factor Xa inhibitor**, not a direct thrombin inhibitor. - It was developed as a long-acting anticoagulant but did not achieve widespread clinical adoption. *Dabigatran* - **Dabigatran** is currently a widely used **oral direct thrombin inhibitor**, but it was approved **after ximelagatran**. - It is often cited as the first of the modern non-vitamin K antagonist oral anticoagulants (**NOACs**) to be widely marketed, but not the very first to be developed and approved for clinical use. *Fondaparinux* - **Fondaparinux** is a synthetic **selective Factor Xa inhibitor**, structurally similar to the antithrombin-binding region of heparin. - It works indirectly by enhancing antithrombin's activity against Factor Xa, and is not a direct thrombin inhibitor. [Practice more Pharmacology PYQs on OnCourse]

Question 1

Adverse effects of phenytoin include the following EXCEPT:

Accepted Answer

Hypercalcemia

Answer

Ataxia

Answer

Hirsutism

Answer

Lymphadenopathy

Question 2

Drug not used in pulmonary hypertension is:

Accepted Answer

Alpha blocker

Answer

Endothelin receptor antagonist

Answer

Prostacyclin

Answer

Calcium channel blocker

Question 3

What is the cause of cough and angioedema in a patient receiving ACE inhibitors?

Accepted Answer

Bradykinin accumulation

Answer

Bradykinin

Answer

Increased renin levels

Answer

Increased angiotensin-II levels

Question 4

What is the mechanism of action of ticagrelor?

Accepted Answer

P2Y12 receptor antagonist

Answer

Cox inhibition

Answer

Inhibition of thromboxane synthase

Answer

GPIIb/IIIa inhibition

Question 5

What was the first oral direct thrombin inhibitor to be developed and approved for clinical use?

Accepted Answer

Ximelagatran

Answer

Indraparinux

Answer

Fondaparinux

Answer

Dabigatran

Question 6

Which of the following antidiabetic drugs is NOT an insulin secretagogue?

Accepted Answer

Pramlintide

Answer

Glinides

Answer

Exenatide

Answer

Sulfonylureas

Question 7

Which dopamine receptor is known for its inhibitory action in the central nervous system?

Accepted Answer

Dopamine Receptor D2

Answer

Dopamine Receptor D5

Answer

No inhibitory dopamine receptor present

Answer

Dopamine Receptor D1

Question 8

High volume of distribution is primarily determined by:

Accepted Answer

High lipid solubility

Answer

High plasma protein binding

Answer

Elimination rate

Answer

Half-life of the drug

Question 9

Volume of distribution of a drug is 500 ml and target concentration of drug in blood is 5 g/L. 20% of administered drug is reached to systemic circulation. What will be the loading dose of that drug -

Accepted Answer

12.5 gm

Answer

1 gm

Answer

5 gm

Answer

25 gm

Question 10

Permission from DCGI [Drug controller general, India] is needed before which phase of drug trial?

Accepted Answer

Phase 3

Answer

Phase 1

Answer

Phase 2

Answer

Phase 4

NEET-PG 2015 — Pharmacology