NEET-PG 2013 - Pharmacology Practice Questions

Q: Botulinum toxin acts on

Synapse. ***Synapse*** - **Botulinum toxin** acts by inhibiting the release of **acetylcholine** at the **neuromuscular junction**, which is a type of synapse. - This blockade of neurotransmitter release at the **presynaptic terminal** prevents muscle contraction, leading to paralysis. *Smooth muscle of intestine* - While botulinum toxin can affect smooth muscle indirectly by paralyzing the motor nerves innervating them, its primary site of action is the **synapse** itself, not directly on the muscle fibers. - The toxin primarily targets the nerve endings, rather than the mechanical contractility of the muscle cell. *Central nervous system* - **Botulinum toxin** does not readily cross the **blood-brain barrier**, meaning its primary effects are peripheral. - Its therapeutic and toxic effects are localized to the **peripheral nervous system** and neuromuscular junctions. *Sensory nerves* - **Botulinum toxin** specifically targets **motor nerve endings** to inhibit acetylcholine release, leading to muscle paralysis. - It does not directly affect the function of **sensory nerve transmission** or pain perception in the same way.

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: Which drug is contraindicated in G6PD deficiency?

Primaquine. ***Primaquine*** - **Primaquine** is an antimalarial drug that generates **severe oxidative stress** in red blood cells. - It is **definitively contraindicated** in **G6PD deficiency** as it consistently causes **acute hemolytic anemia**. - Among antimalarials, primaquine poses the **highest risk** and should **never be used** in G6PD-deficient patients. - It is used for radical cure of P. vivax and P. ovale malaria, but alternative regimens must be used in G6PD deficiency. *Chloroquine* - **Chloroquine** can cause hemolysis in **G6PD deficiency**, though the risk is **lower than primaquine**. - It is **not considered fully safe** and should be used with **caution** in G6PD-deficient patients. - At standard doses, the risk is moderate, but hemolysis can occur, especially in certain G6PD variants. - However, it is not absolutely contraindicated and may be used when benefits outweigh risks with close monitoring. *Quinine* - **Quinine** can also cause **hemolysis** in patients with **G6PD deficiency**. - The risk varies with G6PD variant severity and dosage. - In **severe G6PD deficiency**, quinine should be avoided when alternatives are available. - While less consistently problematic than primaquine, it still requires caution and monitoring. *All of the options* - This option is incorrect in the context of this question because **primaquine** is the **most consistently and severely contraindicated** drug. - While chloroquine and quinine can cause hemolysis, they have **variable risk profiles** and may be used cautiously in some situations, unlike primaquine which is **absolutely contraindicated**. - The question asks for "which drug" (singular), indicating primaquine as the primary answer due to its consistent and severe risk.

Q: Which of the following anticoagulants is given orally?

Rivaroxaban. ***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.

Q: Which of the following statements about lamotrigine is correct?

Has a half-life of approximately 24 hours.. ***Has a half-life of approximately 24 hours.*** - Lamotrigine's **half-life** is typically around **24 to 33 hours** in adults, which allows for once or twice-daily dosing. - This relatively long half-life is advantageous for maintaining **stable plasma concentrations** and improving patient adherence. *Is the first choice for absence seizures.* - **Ethosuximide** or **valproate** are generally considered first-line treatments for **absence seizures**. - Lamotrigine is not the preferred initial therapy due to its **slower titration** and occasional lack of efficacy in this seizure type. *Is not significantly metabolized in the liver.* - Lamotrigine is **significantly metabolized** in the liver, primarily through **glucuronidation** by the **UGT1A4 enzyme**. - This hepatic metabolism explains many of its **drug interactions**, particularly with other antiepileptic drugs affecting UGT enzymes. *Has decreased efficacy in treating depressive episodes.* - Lamotrigine is known for its **mood-stabilizing properties** and is effective in treating and preventing **depressive episodes**, particularly in **bipolar disorder**. - Its efficacy in depression is a key distinguishing feature, making it a valuable option for patients with comorbid mood disorders.

Q: Which of the following antiretroviral drugs is not associated with peripheral neuropathy?

Indinavir. ***Indinavir*** - **Indinavir** is a **protease inhibitor** that can cause side effects such as **nephrolithiasis** (kidney stones) and **hyperbilirubinemia**, but it is generally *not associated with peripheral neuropathy*. - It works by blocking the viral protease enzyme, preventing the cleavage of viral polyproteins into functional proteins, which disrupts viral replication. *Stavudine* - **Stavudine** is a **nucleoside reverse transcriptase inhibitor (NRTI)** notorious for causing dose-dependent **peripheral neuropathy**. - This toxicity is due to its interference with **mitochondrial DNA synthesis**, leading to nerve damage. *Zalcitabine* - **Zalcitabine** (ddC) is another **NRTI** strongly associated with a high incidence of **peripheral neuropathy**. - Its mechanism of action and side effect profile are similar to those of stavudine in causing **mitochondrial toxicity**. *Didanosine* - **Didanosine** (ddI) is an **NRTI** known to cause several adverse effects, including **peripheral neuropathy**, particularly at higher doses. - Like other dideoxynucleoside analogs, its toxicity is linked to **mitochondrial dysfunction**.

Q: Which of the following medications is known to cause peripheral neuropathy?

Vincristine. ***Vincristine*** - **Vincristine** is a **vinca alkaloid chemotherapeutic agent** that is **notorious** for causing **peripheral neuropathy** as its **dose-limiting toxicity**. - It interferes with **microtubule function** during mitosis, leading to **axonal damage** and predominantly **sensorimotor neuropathy**. - Peripheral neuropathy occurs in **virtually all patients** receiving vincristine and typically manifests as **distal paresthesias**, **loss of deep tendon reflexes**, and **motor weakness**. - This is the **most characteristic adverse effect** of vincristine. *Paclitaxel* - **Paclitaxel** is a **taxane chemotherapeutic agent** that also causes **peripheral neuropathy** as a significant adverse effect. - It stabilizes **microtubules**, preventing their depolymerization, leading to neurotoxicity. - While peripheral neuropathy is common with paclitaxel, it shares prominence with other major toxicities like **myelosuppression** and **hypersensitivity reactions**. *Sulfonamide* - **Sulfonamide antibiotics** are primarily associated with **hypersensitivity reactions**, **crystalluria**, **skin rashes**, and **hematologic abnormalities**. - Peripheral neuropathy is not a recognized or common adverse effect of sulfonamides. *Amiodarone* - **Amiodarone** is an **antiarrhythmic drug** with multiple adverse effects including **pulmonary fibrosis**, **thyroid dysfunction**, **corneal deposits**, and **hepatotoxicity**. - While rare cases of **peripheral neuropathy** have been reported, it is **not a characteristic or common adverse effect** of amiodarone.

Q: Mechanism of action of tranexamic acid is

Prevents fibrinolysis. ***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.

Q: Which second generation antihistaminic does not produce an active metabolite?

Cetirizine. ***Cetirizine*** - Cetirizine is unique among second-generation antihistamines as it is an **active metabolite** of hydroxyzine and **does not undergo further significant metabolism** to an active compound. - This characteristic contributes to its relatively **predictable pharmacokinetics** and reduced potential for drug interactions related to metabolism. *Loratadine* - Loratadine is a **prodrug** that is extensively metabolized in the liver by **CYP3A4 and CYP2D6** to its active metabolite, **desloratadine**. - Desloratadine is responsible for most of the **antihistaminic effects** of loratadine. *Terfenadine* - Terfenadine is a **prodrug** that is extensively metabolized by **CYP3A4** to its active metabolite, **fexofenadine**. - Due to its **cardiotoxicity** (QT prolongation) when its metabolism was inhibited, terfenadine was withdrawn from the market, and fexofenadine was developed as a safer alternative. *None of the options* - This option is incorrect because **cetirizine** does not produce an active metabolite, making it a valid answer for the question.

Q: Visual field monitoring is important before starting which of the following drugs for epilepsy treatment?

Vigabatrin. ***Vigabatrin*** - **Vigabatrin** is known to cause **irreversible concentric visual field constriction** (peripheral vision loss) due to retinal toxicity. - Regular **ophthalmological monitoring**, including **visual field testing**, is crucial before and during treatment to detect and manage this adverse effect early. *Topiramate* - Topiramate can cause **acute angle-closure glaucoma** and **myopia**, which affect vision, but regular visual field monitoring is not a primary requirement for this specific side effect. - Its main concerns often relate to cognitive side effects and kidney stones, rather than progressive visual field loss requiring baseline and ongoing field testing. *Valproic acid* - Valproic acid is not typically associated with specific visual field defects requiring routine monitoring. - Its major side effects often involve **hepatotoxicity**, **pancreatitis**, and **teratogenicity**. *Carbamazepine* - Carbamazepine's notable side effects include **aplastic anemia**, **hyponatremia**, and **Stevens-Johnson syndrome**. - While it can cause some ocular side effects like **diplopia** or **nystagmus**, it does not typically lead to the progressive and irreversible visual field constriction seen with vigabatrin, which necessitates strict monitoring.

Question 1

Botulinum toxin acts on

Accepted Answer

Synapse

Answer

Smooth muscle of intestine

Answer

Central nervous system

Answer

Sensory nerves

Question 2

Which of the following is an antitussive opioid?

Accepted Answer

Ethylmorphine

Answer

Pethidine

Answer

Methadone

Answer

Buprenorphine

Question 3

Which drug is contraindicated in G6PD deficiency?

Accepted Answer

Primaquine

Answer

Chloroquine

Answer

Quinine

Answer

All of the options

Question 4

Which of the following anticoagulants is given orally?

Accepted Answer

Rivaroxaban

Answer

Argatraban

Answer

Alteplase

Answer

Fondaparinux

Question 5

Which of the following statements about lamotrigine is correct?

Accepted Answer

Has a half-life of approximately 24 hours.

Answer

Is the first choice for absence seizures.

Answer

Is not significantly metabolized in the liver.

Answer

Has decreased efficacy in treating depressive episodes.

Question 6

Which of the following antiretroviral drugs is not associated with peripheral neuropathy?

Accepted Answer

Indinavir

Answer

Stavudine

Answer

Zalcitabine

Answer

Didanosine

Question 7

Which of the following medications is known to cause peripheral neuropathy?

Accepted Answer

Vincristine

Answer

Sulfonamide

Answer

Amiodarone

Answer

Paclitaxel

Question 8

Mechanism of action of tranexamic acid is

Accepted Answer

Prevents fibrinolysis

Answer

Decrease vascular permeability

Answer

Smooth muscle contraction

Answer

Activates Plasmin formation

Question 9

Which second generation antihistaminic does not produce an active metabolite?

Accepted Answer

Cetirizine

Answer

Loratadine

Answer

Terfenadine

Answer

None of the options

Question 10

Visual field monitoring is important before starting which of the following drugs for epilepsy treatment?

Accepted Answer

Vigabatrin

Answer

Topiramate

Answer

Valproic acid

Answer

Carbamazepine

NEET-PG 2013 — Pharmacology