NEET-PG 2020 — Pharmacology
26 Previous Year Questions with Answers & Explanations
Which of the following antiarrhythmic drugs is contraindicated in a patient with interstitial lung disease?
Patient with pulmonary fibrosis. Which antiarrhythmic drug is contraindicated?
A patient on lithium therapy developed hypertension and was started on a thiazide diuretic. After a few days, he developed coarse tremors and other symptoms suggestive of lithium toxicity. What is the probable mechanism of interaction between thiazide diuretics and lithium?
Which of the following is not considered a prokinetic agent?
Misoprostol used in the induction of labour is an analogue of which of the following type of prostaglandin?
A patient diagnosed with Rheumatoid arthritis was on medications. After 2 years, he developed a blurring vision and was found to have corneal opacity. Which drug is most likely to cause this?
A person was given a muscle relaxant that competitively blocks nicotinic receptors. Which of the following drugs is used for reversal of muscle relaxation after surgery?
What is the Drug of Choice (DOC) for Onychomycosis?
Which of the following drugs can be given in patients of primary pulmonary hypertension?
Which of the following vitamins, when taken at higher doses, can cause cystoid macular edema?
NEET-PG 2020 - Pharmacology NEET-PG Practice Questions and MCQs
Question 1: Which of the following antiarrhythmic drugs is contraindicated in a patient with interstitial lung disease?
- A. Amiodarone (Correct Answer)
- B. Lignocaine
- C. Sotalol
- D. Quinidine
Explanation: ***Amiodarone*** - **Amiodarone** is contraindicated in patients with interstitial lung disease due to its well-known and potentially severe pulmonary toxicity, which can exacerbate or induce **pulmonary fibrosis**. - Its long half-life means that drug accumulation and persistent adverse effects, including **ILD exacerbation**, are significant concerns. *Sotalol* - **Sotalol** primarily carries risks of **prolonged QT interval** and **torsades de pointes** because it has both beta-blocking and Class III antiarrhythmic properties. - While it has cardiac and minor non-cardiac side effects, it is not specifically known to cause or worsen **interstitial lung disease**. *Lignocaine* - **Lignocaine** (lidocaine) is a Class Ib antiarrhythmic primarily used for **ventricular arrhythmias**, especially in acute settings. - Its adverse effects are mainly **neurological** (e.g., dizziness, seizures at high doses) and **cardiovascular** (e.g., hypotension, bradycardia), with no significant association with lung disease. *Quinidine* - **Quinidine** is a Class Ia antiarrhythmic that can cause a variety of side effects, including **gastrointestinal upset**, **cinchonism** (tinnitus, blurred vision), and **cardiac rhythm disturbances**. - While it can rarely cause a hypersensitivity pneumonitis, it is not a primary concern or contraindication in existing **interstitial lung disease** compared to amiodarone.
Question 2: Patient with pulmonary fibrosis. Which antiarrhythmic drug is contraindicated?
- A. Amiodarone (Correct Answer)
- B. Flecainide
- C. Lidocaine
- D. IV ibutilide
Explanation: Amiodarone - **Amiodarone** is contraindicated in patients with pulmonary fibrosis due to its well-known and potentially severe pulmonary toxicity, which can exacerbate existing lung conditions or induce new ones like **interstitial lung disease**. Dose-related pulmonary toxicity is the most important adverse effect, and potentially fatal pulmonary fibrosis can be observed even at low doses [1]. - Its long half-life means that its toxic effects, including **pulmonary toxicity**, can persist for an extended period even after discontinuation [1], [2]. *Flecainide* - **Flecainide** is a Class IC antiarrhythmic drug primarily associated with cardiac side effects and is generally not contraindicated in patients with pulmonary fibrosis. - Its main risks include **proarrhythmia**, especially in patients with structural heart disease, but not pulmonary issues [3]. *IV ibutilide* - **IV ibutilide** is a Class III antiarrhythmic agent used for rapid conversion of atrial fibrillation/flutter and is not specifically contraindicated in pulmonary fibrosis. - Its primary concern is the risk of **QT prolongation** and **Torsades de Pointes**, rather than pulmonary complications. *Lidocaine* - **Lidocaine** is a Class IB antiarrhythmic typically used for ventricular arrhythmias, especially in the setting of acute myocardial infarction. It is not contraindicated in pulmonary fibrosis. - Its main side effects are **neurological (e.g., seizures, paresthesias)** at higher doses, not pulmonary complications.
Question 3: A patient on lithium therapy developed hypertension and was started on a thiazide diuretic. After a few days, he developed coarse tremors and other symptoms suggestive of lithium toxicity. What is the probable mechanism of interaction between thiazide diuretics and lithium?
- A. Thiazide increases the tubular reabsorption of lithium (Correct Answer)
- B. Thiazide inhibits the metabolism of lithium
- C. Thiazides act as an add-on drug to lithium
- D. None of the above
Explanation: ***Thiazide increases the tubular reabsorption of lithium*** - Thiazide diuretics cause a decrease in sodium reabsorption in the distal convoluted tubule, leading to increased sodium excretion in urine. - The kidneys, in an attempt to conserve sodium, increase reabsorption in the proximal tubule. Because **lithium** is reabsorbed similarly to sodium in the proximal tubule, this increased reabsorption also affects lithium, leading to a rise in its plasma concentration and toxicity. *Thiazide inhibits the metabolism of lithium* - Lithium is primarily excreted by the kidneys and is not significantly metabolized in the body. - Thiazide diuretics do not affect enzyme systems responsible for drug metabolism. *Thiazides act as an add on the drug to lithium* - This statement is vague and does not explain a mechanism of interaction leading to toxicity. - While both drugs might be prescribed concurrently for different conditions, "add on" does not describe a pharmacological interaction causing altered drug levels. *None of the above* - This option is incorrect because a clear and well-understood mechanism for the interaction between thiazide diuretics and lithium exists.
Question 4: Which of the following is not considered a prokinetic agent?
- A. Dopamine antagonist
- B. 5HT4 agonist
- C. Macrolides
- D. Diphenylmethane (Correct Answer)
Explanation: Diphenylmethane derivatives (e.g., bisacodyl, sodium picosulfate) are stimulant laxatives, not prokinetic agents. While they do increase colonic motility, they work by direct stimulation of the colonic mucosa and myenteric plexus, causing increased water secretion and peristalsis [3]. Prokinetic agents specifically enhance coordinated gastrointestinal motility through modulation of neurotransmitters (acetylcholine, dopamine, serotonin, motilin), whereas laxatives work through different mechanisms (osmotic effects, stimulation, bulk formation). Therefore, diphenylmethane derivatives are classified as laxatives, not prokinetics. Dopamine antagonist - Dopamine antagonists like metoclopramide and domperidone block D2 receptors in the chemoreceptor trigger zone and GI tract, enhancing acetylcholine release and promoting gastric emptying [2]. - They are commonly used as prokinetic agents and antiemetics [2]. 5HT4 agonist - 5HT4 agonists (e.g., cisapride, prucalopride) stimulate serotonin receptors in the enteric nervous system, increasing acetylcholine release and enhancing colonic motility [1]. - They are effective prokinetic agents for conditions like chronic constipation and gastroparesis [1]. Macrolides - Certain macrolide antibiotics, such as erythromycin, act as motilin receptor agonists at sub-antibiotic doses. - By mimicking motilin, they stimulate gastric and intestinal contractions (phase III of migrating motor complex), functioning as prokinetic agents.
Question 5: Misoprostol used in the induction of labour is an analogue of which of the following type of prostaglandin?
- A. PG E1 (Correct Answer)
- B. PG E2
- C. PG I2
- D. PG F2alpha
Explanation: ***PG E1*** - **Misoprostol** is a synthetic analogue of **prostaglandin E1 (PGE1)**, which is used for cervical ripening and uterine contractions in labor induction. - PGE1 analogues help to soften the cervix, increase its compliance, and stimulate uterine smooth muscle contraction. *PG E2* - **Dinoprostone** is a synthetic analogue of **prostaglandin E2 (PGE2)**, commonly used for cervical ripening and induction of labor. - While PGE2 also induces labor, misoprostol specifically mimics the actions of PGE1. *PG I2* - **Prostacyclin (PGI2)** is primarily known for its role in inhibiting platelet aggregation and causing vasodilation. - It is not routinely used for labor induction due to its primary vascular effects and lack of direct uterine contractile properties at relevant doses. *PG F2alpha* - **Prostaglandin F2-alpha (PGF2α)**, such as **carboprost**, is used for postpartum hemorrhage to cause strong uterine contractions. - While it causes uterine contractions, its primary obstetric use is not for labor induction but rather for stimulating aggressive uterine contraction to stop bleeding.
Question 6: A patient diagnosed with Rheumatoid arthritis was on medications. After 2 years, he developed a blurring vision and was found to have corneal opacity. Which drug is most likely to cause this?
- A. Sulfasalazine
- B. Leflunomide
- C. Chloroquine (Correct Answer)
- D. Methotrexate
Explanation: ***Chloroquine*** - **Chloroquine (and hydroxychloroquine)** can accumulate in the **cornea**, leading to **corneal opacity** (vortex keratopathy or cornea verticillata) and **retinopathy**, manifesting as blurring vision. - While corneal changes are usually reversible upon discontinuation, the retinal toxicity, particularly **maculopathy** (bull's eye maculopathy), can be permanent and severe. *Sulfasalazine* - Common side effects include **gastrointestinal upset**, headache, skin rash, and **bone marrow suppression**. - It is not typically associated with **corneal opacity** or significant ocular toxicity. *Leflunomide* - Known for side effects such as **hepatotoxicity**, gastrointestinal issues (diarrhea), **alopecia**, and **hypertension**. - **Ocular side effects** like corneal opacity are not characteristic of leflunomide use. *Methotrexate* - Primary side effects include **bone marrow suppression**, **hepatotoxicity**, **mucositis**, and **pulmonary fibrosis**. - Although it can cause ocular side effects like **conjunctivitis**, it is not a common cause of **corneal opacity**.
Question 7: A person was given a muscle relaxant that competitively blocks nicotinic receptors. Which of the following drugs is used for reversal of muscle relaxation after surgery?
- A. Carbachol
- B. Succinylcholine
- C. Physostigmine
- D. Neostigmine (Correct Answer)
Explanation: ***Neostigmine*** - **Neostigmine** is an **acetylcholinesterase inhibitor** that increases the amount of acetylcholine at the neuromuscular junction, thereby overcoming the competitive block at nicotinic receptors [1], [4]. - This increase in acetylcholine effectively reverses the paralysis caused by **nondepolarizing muscle relaxants**, making it useful for post-surgical recovery [2]. *Carbachol* - **Carbachol** is a **direct-acting cholinergic agonist** that stimulates both muscarinic and nicotinic receptors and is not typically used for reversing competitive neuromuscular blockade. - Its primary use is for glaucoma and to stimulate the bladder or bowels, not to counteract muscle relaxants. *Succinylcholine* - **Succinylcholine** is a **depolarizing muscle relaxant** and would prolong, rather than reverse, muscle blockade if administered after a competitive blocker [3]. - It works by initially causing depolarization and then preventing further muscle contraction, leading to paralysis. *Physostigmine* - **Physostigmine** is an **acetylcholinesterase inhibitor** that crosses the blood-brain barrier, making it more suitable for treating central anticholinergic toxicity rather than peripheral neuromuscular blockade. - While it inhibits acetylcholinesterase, its central effects and potential for seizures limit its use for reversing surgical muscle relaxation.
Question 8: What is the Drug of Choice (DOC) for Onychomycosis?
- A. Terbinafine (Correct Answer)
- B. Fluconazole
- C. Itraconazole
- D. Nystatin
Explanation: ***Terbinafine*** - **Terbinafine** is considered the **drug of choice** for **onychomycosis** due to its potent fungicidal activity against **dermatophytes**, which are the most common cause of nail infections [1]. - It accumulates in the nail plate at therapeutic levels, leading to high cure rates and a relatively good safety profile [2]. *Fluconazole* - While effective against some fungi, **fluconazole** is primarily fungistatic and generally less effective against dermatophytes compared to terbinafine for onychomycosis, resulting in lower cure rates [1]. - It is often preferred for **mucocutaneous candidiasis** and other systemic fungal infections [1]. *Itraconazole* - **Itraconazole** is an alternative for onychomycosis, often administered in pulse doses, but it can have more significant drug interactions and a higher risk of hepatic toxicity compared to terbinafine [1]. - Its efficacy against dermatophytes is comparable to terbinafine, but its side effect profile makes it a second-line option [1]. *Nystatin* - **Nystatin** is a topical antifungal effective primarily against **Candida species**, and is not effective against **dermatophytes**, which are the main pathogens in onychomycosis. - It is typically used for mucocutaneous candidiasis, such as oral thrush or vaginal yeast infections, and is not absorbed systemically.
Question 9: Which of the following drugs can be given in patients of primary pulmonary hypertension?
- A. Icatibant
- B. Bosentan (Correct Answer)
- C. Sodium nitroprusside
- D. Labetalol
Explanation: ***Bosentan*** - **Bosentan** is an **endothelin receptor antagonist** that blocks the vasoconstrictive and proliferative effects of endothelin-1, a key mediator in the pathogenesis of **pulmonary hypertension**. - It is an FDA-approved medication specifically used for the treatment of **pulmonary arterial hypertension (PAH)**, improving exercise capacity and delaying clinical worsening. *Icatibant* - **Icatibant** is a **bradykinin B2 receptor antagonist** used in the treatment of **hereditary angioedema**. - It has no known role or efficacy in the management of **primary pulmonary hypertension**. *Labetalol* - **Labetalol** is a **beta-blocker** with **alpha-1 adrenergic blocking activity** used primarily for systemic **hypertension** and **hypertensive emergencies**. - Beta-blockers are generally **contraindicated** in pulmonary hypertension as they can worsen right heart function and lead to clinical deterioration. *Sodium nitroprusside* - **Sodium nitroprusside** is a **direct arterial and venous vasodilator** used in hypertensive crises and severe heart failure by reducing both preload and afterload. - While it can lower systemic blood pressure, its use in pulmonary hypertension is **limited** due to the risk of **systemic hypotension** and the lack of selective pulmonary vasodilation compared to other agents.
Question 10: Which of the following vitamins, when taken at higher doses, can cause cystoid macular edema?
- A. Niacin (Correct Answer)
- B. Vitamin A
- C. Vitamin D
- D. Vitamin E
Explanation: ***Niacin*** - High doses of **niacin (nicotinic acid)**, particularly the extended-release forms used for lipid management, are known to cause **cystoid macular edema (CME)**. - The mechanism is thought to involve **vasodilation** and metabolic changes in the retinal pigment epithelium. *Vitamin A* - While essential for vision, **excessive vitamin A** intake (hypervitaminosis A) can lead to symptoms like **headache**, **blurred vision**, and skin changes, but not typically cystoid macular edema. - Deficiency of vitamin A can cause **night blindness** and xerophthalmia. *Vitamin D* - High doses of vitamin D can lead to **hypercalcemia**, causing symptoms such as nausea, vomiting, and kidney stones. - It does not directly cause **cystoid macular edema**. *Vitamin E* - **Excessive vitamin E** intake can interfere with **blood clotting** and increase the risk of bleeding, especially in individuals on anticoagulants. - There is no established link between high-dose vitamin E and **cystoid macular edema**.