NEET-PG 2024 - Pharmacology PYQs Practice Questions

Q: Which of the following is correct about the EMLA patch shown in the image below?

Eutectic mixture is used. ***Eutectic mixture is used*** - EMLA stands for **Eutectic Mixture of Local Anesthetics**, indicating that it uses a mixture of lidocaine and prilocaine to lower their melting points, allowing them to remain liquid at room temperature. - This liquid form enhances skin penetration, providing more effective topical anesthesia compared to individual agents. *Adverse effect is methemoglobinemia* - While methemoglobinemia is a potential side effect of **prilocaine**, which is part of the EMLA cream, it is usually only seen with **excessive doses** or in susceptible individuals (e.g., infants). - Given its topical application and typical dosing, it is not the most common or direct feature associated with correct use of the EMLA patch. *Contains bupivacaine & lignocaine* - The EMLA patch contains **lidocaine (lignocaine)** and **prilocaine**, not bupivacaine. - Bupivacaine is another local anesthetic, but it is not a component of the EMLA formulation. *0.5% concentration of lignocaine has 50 mg in 1 gm is used* - The EMLA patch typically contains a 2.5% concentration of **lidocaine** and 2.5% of **prilocaine**, meaning 25 mg of each per gram of cream. - A 0.5% concentration would be 5 mg per gram, so the stated concentration and amount are incorrect for the EMLA formulation. *Requires application for at least 15 minutes for adequate anesthesia* - EMLA requires a **minimum of 60 minutes** of application time for adequate dermal anesthesia, not 15 minutes. - For procedures on intact skin, the recommended application time is **60-120 minutes** to achieve optimal anesthetic effect. [Practice more Pharmacology PYQs on OnCourse]

Q: A Myasthenia Gravis patient on mycophenolate and pyridostigmine presents with hypercalcemia. Apart from the obvious drug-related cause, what other condition could be associated with hypercalcemia in this patient?

Non-Small Cell Lung Cancer (NSCLC). ***Non-Small Cell Lung Cancer (NSCLC)*** - **Hypercalcemia of malignancy** is a common paraneoplastic syndrome in NSCLC, particularly squamous cell carcinoma, due to the production of **parathyroid hormone-related protein (PTHrP)**. - Patients with myasthenia gravis, especially those with thymoma, have an increased risk of developing other malignancies, including lung cancer, making this an important consideration. *Drug induced* - While certain medications can cause hypercalcemia, the question specifically asks for a condition **apart from the obvious drug-related cause**. - Medications like **thiazide diuretics**, **lithium**, or excessive **vitamin D** supplementation are known causes of hypercalcemia. *Parathyroid adenoma* - A parathyroid adenoma causes **primary hyperparathyroidism**, characterized by elevated PTH and hypercalcemia. - While possible, the association with myasthenia gravis and the increased risk of malignancy make **paraneoplastic syndrome** a more contextual answer here given the prompt. *Small Cell Lung Cancer (SCLC)* - SCLC is more commonly associated with other paraneoplastic syndromes like **SIADH (syndrome of inappropriate antidiuretic hormone secretion)** due to ectopic ADH production, or **Cushing's syndrome** due to ectopic ACTH production. - While hypercalcemia can rarely occur, it is **less common** and typically not due to PTHrP in SCLC compared to NSCLC. *Sarcoidosis* - Sarcoidosis can cause hypercalcemia through increased production of **1,25-dihydroxyvitamin D** by activated macrophages in granulomas, leading to enhanced intestinal calcium absorption. - However, in the context of a myasthenia gravis patient with the clinical scenario described, **malignancy-associated hypercalcemia** (particularly NSCLC) is a more likely and clinically relevant consideration. [Practice more Pharmacology PYQs on OnCourse]

Q: Caffeine impairs sleep by which of the following mechanisms?

Blocks adenosine action and promotes wakefulness. ***Blocks adenosine action and promotes wakefulness*** - Caffeine functions as a competitive **adenosine receptor antagonist**, primarily at A1 and A2A receptors in the brain. - By blocking adenosine, which is an endogenous sleep-promoting neurochemical, caffeine reduces its inhibitory effects on wakefulness centers, thus **promoting alertness** and delaying sleep onset. *Activates locus coeruleus & promotes wakefulness* - While caffeine indirectly influences brain regions that promote wakefulness, its primary mechanism is not direct activation of the **locus coeruleus**. - Its effects on wakefulness are mediated more broadly through antagonism of **adenosine receptors.** *No role in maintaining wakefulness* - This statement is incorrect; caffeine is well-known for its **psychoactive properties** and its ability to increase alertness and reduce fatigue. - Its widespread consumption is largely attributed to its role in **promoting wakefulness** and improving cognitive function. *Activates histamine release and prevents sleep* - Caffeine does not significantly activate **histamine release** as a primary mechanism for its wake-promoting effects. - The wake-promoting effects of histamine are mediated via H1 receptors, but this is a separate pathway not directly targeted by caffeine. *Inhibits phosphodiesterase and increases cAMP levels* - While caffeine does inhibit **phosphodiesterase enzymes** (particularly at higher concentrations), this is not the primary mechanism for its wake-promoting effects. - The concentrations required for significant phosphodiesterase inhibition are much higher than those achieved with typical caffeine consumption; **adenosine receptor antagonism** occurs at much lower doses and is the dominant mechanism for its effects on sleep and alertness. [Practice more Pharmacology PYQs on OnCourse]

Q: Phenobarbitone exerts its therapeutic effect primarily through which mechanism?

Enhancement of GABA-A receptor function. ***Enhancement of GABA-A receptor function*** - **Phenobarbitone** (phenobarbital) is a barbiturate that acts primarily by **enhancing GABA-A receptor activity** - It binds to a distinct **barbiturate binding site** on the GABA-A receptor complex - This binding **prolongs the duration of chloride channel opening** in response to GABA - Results in increased **chloride ion influx**, neuronal **hyperpolarization**, and **decreased neuronal excitability** - This mechanism underlies its **anticonvulsant** and **sedative-hypnotic** properties *NMDA receptor antagonism* - While some anticonvulsants work through NMDA receptor antagonism (e.g., ketamine, felbamate), this is **not the primary mechanism** of phenobarbitone *Voltage-gated sodium channel blockade* - Sodium channel blockade is the mechanism of action for drugs like **phenytoin, carbamazepine**, and **lamotrigine** - Phenobarbitone does not significantly block sodium channels at therapeutic concentrations *Voltage-gated calcium channel blockade* - Calcium channel blockers like **ethosuximide** (T-type) and **gabapentin** (α2δ subunit) work through this mechanism - This is not the primary mechanism for phenobarbitone *Potassium channel opening* - Potassium channel openers like **retigabine** increase potassium conductance - Phenobarbitone does not primarily work through this mechanism [Practice more Pharmacology PYQs on OnCourse]

Q: Which of the following are toxic metabolites associated with methanol poisoning?

Formic acid + Lactic acid. ***Formic acid + Lactic acid*** - **Methanol** is metabolized in the body into **formaldehyde** and then to **formic acid**, which is primarily responsible for its toxicity. - While not a direct derivative, **lactic acid** levels often rise significantly in severe methanol poisoning due to **hypoxia** and **metabolic acidosis** caused by formic acid-induced mitochondrial dysfunction. *Formic acid + Oxalic acid* - **Formic acid** is indeed a toxic metabolite of methanol, but **oxalic acid** is not. - **Oxalic acid** is a toxic metabolite of **ethylene glycol** poisoning, not methanol. *Glycolic acid + Oxalic acid* - Neither **glycolic acid** nor **oxalic acid** are toxic metabolites of methanol. - Both **glycolic acid** and **oxalic acid** are associated with **ethylene glycol** poisoning. *Oxalic acid + Lactic acid* - **Oxalic acid** is not a derivative of methanol poisoning. - While **lactic acid** can be elevated in methanol poisoning, its combination with oxalic acid is incorrect for methanol metabolites. *Hippuric acid + Formic acid* - **Formic acid** is correct, but **hippuric acid** is not a metabolite of methanol. - **Hippuric acid** is a metabolite of **toluene** and is used as a urinary marker for toluene exposure. [Practice more Pharmacology PYQs on OnCourse]

Question 1

Which of the following is correct about the EMLA patch shown in the image below?

Accepted Answer

Eutectic mixture is used

Answer

Adverse effect is methemoglobinemia

Answer

Contains bupivacaine & lignocaine

Answer

0.5% concentration of lignocaine has 50 mg in 1 gm is used

Answer

Requires application for at least 15 minutes for adequate anesthesia

Question 2

A Myasthenia Gravis patient on mycophenolate and pyridostigmine presents with hypercalcemia. Apart from the obvious drug-related cause, what other condition could be associated with hypercalcemia in this patient?

Accepted Answer

Non-Small Cell Lung Cancer (NSCLC)

Answer

Drug induced

Answer

Parathyroid adenoma

Answer

Small Cell Lung Cancer (SCLC)

Answer

Sarcoidosis

Question 3

Caffeine impairs sleep by which of the following mechanisms?

Accepted Answer

Blocks adenosine action and promotes wakefulness

Answer

Activates locus coeruleus & promotes wakefulness

Answer

No role in maintaining wakefulness

Answer

Activates histamine release and prevents sleep

Answer

Inhibits phosphodiesterase and increases cAMP levels

Question 4

Phenobarbitone exerts its therapeutic effect primarily through which mechanism?

Accepted Answer

Enhancement of GABA-A receptor function

Answer

Voltage-gated sodium channel blockade

Answer

Voltage-gated calcium channel blockade

Answer

Potassium channel opening

Answer

NMDA receptor antagonism

Question 5

Which of the following are toxic metabolites associated with methanol poisoning?

Accepted Answer

Formic acid + Lactic acid

Answer

Formic acid + Oxalic acid

Answer

Glycolic acid + Oxalic acid

Answer

Oxalic acid + Lactic acid

Answer

Hippuric acid + Formic acid

Question 6

A patient with a history of binge alcohol intake presented to the emergency department with convulsions, altered sensorium, and a plasma glucose level of $45 \mathrm{mg} / \mathrm{dL}$. Which of the following treatments is needed?

Accepted Answer

Thiamine followed by Dextrose

Answer

Thiamine

Answer

$25 \% $ Dextrose

Answer

Fomepizole

Answer

Glucagon

Question 7

Methotrexate use causes reduced synthesis of which of the following?

Accepted Answer

TMP

Answer

CMP

Answer

GMP

Answer

AMP

Answer

UMP

Question 8

Which of the following cardioselective betablockers has been shown to decrease mortality in patients with congestive heart failure?

Accepted Answer

Bisoprolol

Answer

Propranolol

Answer

Labetalol

Answer

Pindolol

Answer

Atenolol

Question 9

Aprepitant is a drug used in the treatment of some cases of chemotherapy-induced nausea and vomiting. What is the mechanism of action of this drug?

Accepted Answer

NK1 antagonist

Answer

NK3 antagonist

Answer

NK1 agonist

Answer

NK2 agonist

Answer

NK2 antagonist

Question 10

Which of the following is an inclusion criterion for the shorter bedaquiline regimen in the treatment of tuberculosis?

Accepted Answer

Rifampicin-resistant but fluoroquinolone-sensitive TB

Answer

Extrapulmonary TB like Tubercular meningitis

Answer

Rifampicin resistance with both KatG and inhA mutation

Answer

Rifampicin-sensitive TB

Answer

Extensively drug-resistant TB (XDR-TB)

NEET-PG 2024 — Pharmacology