NEET-PG 2022 — Pharmacology
10 Previous Year Questions with Answers & Explanations
Which of the following anticancer drugs is MOST characteristically associated with pulmonary fibrosis?
Which of the following is NOT a mechanism of action of theophylline in bronchial asthma?
A female patient presents to you with a unilateral headache. It is associated with nausea, photophobia, and phonophobia. What is the drug of choice for acute management?
A patient presents to the emergency department with a history of ingestion of ten tablets of paracetamol. He has developed oliguria and liver function tests show deranged values. In the context of paracetamol overdose, which of the following can be used in the management of this condition?
A patient comes with a history of asthma and sinusitis. On looking into his medical records, you notice this has been attributed to Samter’s triad. Which drug should be avoided in this patient due to its potential to exacerbate respiratory symptoms?
A middle-aged male patient presents with protrusion of the chin, excessive sweating, impaired glucose tolerance, and enlargement of hands and feet. Which of the following is a growth hormone receptor antagonist used to treat this condition?
A woman presenting with symptoms of urinary tract infection was prescribed a drug that causes tendon rupture and arthropathy. What is the mechanism of action of the drug?
Multidrug-resistant (MDR) tuberculosis shows resistance to which of the following drugs?
A 55-year-old woman is undergoing chemotherapy for breast cancer and experiences severe nausea and vomiting. Which antiemetic, recognized for its minimal extrapyramidal side effects, would be appropriate for her condition?
The mechanism of action of botulinum toxin A is best described by:
NEET-PG 2022 - Pharmacology NEET-PG Practice Questions and MCQs
Question 1: Which of the following anticancer drugs is MOST characteristically associated with pulmonary fibrosis?
- A. Mercaptopurine
- B. Busulfan (Correct Answer)
- C. Methotrexate
- D. Cyclophosphamide
Explanation: ***Busulfan*** - **Busulfan** is an **alkylating agent** that is **MOST characteristically** associated with **pulmonary fibrosis** among the given options. - Causes **"Busulfan lung"** - a distinctive chronic interstitial pulmonary fibrosis that can occur in **4-6% of patients**. - Typically develops **insidiously** after prolonged therapy with **cumulative dose-related toxicity**. - Presents with **progressive dyspnea, dry cough**, and restrictive lung pattern on pulmonary function tests. - This is a **classic association** emphasized in medical examinations. *Cyclophosphamide* - **Cyclophosphamide** can also cause **pulmonary fibrosis**, particularly with high cumulative doses. - However, it is **less characteristically** associated with this complication compared to busulfan. - Pulmonary toxicity is more **variable and less predictable** in severity. *Methotrexate* - **Methotrexate** can cause lung toxicity, most commonly as **acute methotrexate pneumonitis** (hypersensitivity reaction). - While **chronic fibrosis can occur**, it is less frequent than the acute inflammatory process. - Not the **most characteristic** association for pulmonary fibrosis. *Mercaptopurine* - **Mercaptopurine** is an **antimetabolite** primarily associated with **hepatotoxicity** and **myelosuppression**. - **Not associated** with pulmonary fibrosis.
Question 2: Which of the following is NOT a mechanism of action of theophylline in bronchial asthma?
- A. Adenosine receptor antagonism
- B. Increased histone deacetylation
- C. Phosphodiesterase inhibition
- D. Beta-2 receptor stimulation (Correct Answer)
Explanation: ***Beta-2 receptor stimulation*** - Theophylline is a **non-selective phosphodiesterase inhibitor** and an **adenosine receptor antagonist**, but it does not directly stimulate beta-2 receptors. - **Beta-2 receptor agonists** like salbutamol or formoterol are the medications that work by stimulating these receptors to cause bronchodilation. *Phosphodiesterase inhibition* - Theophylline inhibits **phosphodiesterase enzymes**, leading to an increase in intracellular **cAMP** levels. - This increase in **cAMP** promotes bronchodilation by relaxing airway smooth muscle. *Adenosine receptor antagonism* - Theophylline acts as an antagonist at **adenosine receptors**, particularly A1 and A2B. - Antagonism of adenosine receptors can reduce bronchoconstriction and inflammatory mediator release, contributing to its anti-asthmatic effects. *Increased histone deacetylation* - Theophylline, particularly at lower concentrations, increases the activity of **histone deacetylase (HDAC)**. - This action helps to **repress inflammatory gene expression**, which is a unique anti-inflammatory mechanism separate from its bronchodilatory effects.
Question 3: A female patient presents to you with a unilateral headache. It is associated with nausea, photophobia, and phonophobia. What is the drug of choice for acute management?
- A. Flunarizine
- B. Sumatriptan (Correct Answer)
- C. Propranolol
- D. Topiramate
Explanation: ***Sumatriptan*** - **Sumatriptan**, a **triptan**, is an effective abortive therapy for **acute migraine attacks** due to its selective serotonin 5-HT1B/1D receptor agonist action, leading to vasoconstriction and inhibition of neurogenic inflammation. - The symptoms described—**unilateral headache**, nausea, **photophobia**, and **phonophobia**—are classic features of migraine. *Flunarizine* - **Flunarizine** is a **calcium channel blocker** used for migraine **prophylaxis**, not for acute treatment. - It is typically prescribed for patients experiencing frequent or severe migraine attacks to reduce their incidence. *Propranolol* - **Propranolol** is a **beta-blocker** primarily used for migraine **prophylaxis**. - It helps prevent migraine attacks by modulating cerebral blood flow and neuronal excitability, but it is not effective for acute pain relief during an attack. *Topiramate* - **Topiramate** is an **antiepileptic drug** often used for migraine **prophylaxis**. - It works by various mechanisms, including altering neurotransmitter activity, but it does not provide acute symptomatic relief for an ongoing migraine attack.
Question 4: A patient presents to the emergency department with a history of ingestion of ten tablets of paracetamol. He has developed oliguria and liver function tests show deranged values. In the context of paracetamol overdose, which of the following can be used in the management of this condition?
- A. N-acetylcysteine (Correct Answer)
- B. Dopamine
- C. Ursodeoxycholic acid
- D. Furosemide
Explanation: **Correct: N-acetylcysteine** - **N-acetylcysteine (NAC)** is the specific antidote for **paracetamol overdose**, working by replenishing **glutathione** stores in the liver. - Replenishing **glutathione** helps detoxify the toxic metabolite **N-acetyl-p-benzoquinone imine (NAPQI)**, preventing further **hepatic damage** and facilitating recovery in cases of **liver failure** and potential **renal damage** (oliguria). - Most effective when given within **8 hours** of ingestion, but remains beneficial even with **established hepatotoxicity** (as in this case with deranged LFTs). *Incorrect: Dopamine* - **Dopamine** is a **vasopressor** primarily used to increase **blood pressure** and **cardiac output** in conditions like **shock**. - While it might be used to support circulation in severe overdose complications, it does not directly treat the **paracetamol toxicity** itself. *Incorrect: Ursodeoxycholic acid* - **Ursodeoxycholic acid (UDCA)** is a **cholagogue** used in the management of **cholestatic liver diseases** (e.g., primary biliary cholangitis) by improving bile flow. - It has no role in the direct management of **acute liver failure** due to **paracetamol overdose**. *Incorrect: Furosemide* - **Furosemide** is a **loop diuretic** used to increase **urine output** in conditions like **fluid overload** or **heart failure**. - While **oliguria** is present, it is often a sign of **acute kidney injury** requiring supportive care, and furosemide would not address the underlying **toxic mechanism** of paracetamol.
Question 5: A patient comes with a history of asthma and sinusitis. On looking into his medical records, you notice this has been attributed to Samter’s triad. Which drug should be avoided in this patient due to its potential to exacerbate respiratory symptoms?
- A. Cotrimoxazole
- B. Co-amoxiclav
- C. Chloramphenicol
- D. Aspirin (Correct Answer)
Explanation: ***Aspirin (Correct Answer)*** - Samter's triad, or **aspirin-exacerbated respiratory disease (AERD)**, is characterized by **asthma**, **nasal polyps with chronic rhinosinusitis**, and a severe reaction to **aspirin** and other **NSAIDs**. - **Aspirin** inhibits COX-1, leading to an overproduction of **leukotrienes**, which causes bronchoconstriction and exacerbates respiratory symptoms in susceptible individuals. - This is the drug that **must be avoided** in patients with Samter's triad. *Cotrimoxazole (Incorrect)* - **Cotrimoxazole** (trimethoprim-sulfamethoxazole) is an antibiotic not directly involved in the cyclooxygenase pathway. - While allergic reactions can occur, it is **not specifically contraindicated** in Samter's triad. *Co-amoxiclav (Incorrect)* - **Co-amoxiclav** (amoxicillin/clavulanic acid) is a penicillin-class antibiotic, and its mechanism of action does not involve prostaglandin synthesis. - It does not pose a specific risk for exacerbating respiratory symptoms in patients with **Samter's triad**. *Chloramphenicol (Incorrect)* - **Chloramphenicol** is an antibiotic that inhibits bacterial protein synthesis and is not associated with the pathogenesis of Samter's triad. - It does not impact the **cyclooxygenase or lipoxygenase pathways** that are central to AERD.
Question 6: A middle-aged male patient presents with protrusion of the chin, excessive sweating, impaired glucose tolerance, and enlargement of hands and feet. Which of the following is a growth hormone receptor antagonist used to treat this condition?
- A. Pegvisomant (Correct Answer)
- B. Olcegepant
- C. Cabergoline
- D. Octreotide
Explanation: ***Pegvisomant*** - **Pegvisomant** is a **growth hormone receptor antagonist** that binds to growth hormone receptors, preventing endogenous growth hormone from signaling and reducing IGF-1 levels. - It is specifically used in the treatment of **acromegaly**, a condition characterized by excessive growth hormone secretion, which aligns with the patient's symptoms of chin protrusion, excessive sweating, impaired glucose tolerance, and enlarged hands and feet. *Octreotide* - **Octreotide** is a **somatostatin analog** that works by inhibiting growth hormone secretion from the pituitary gland. - While used in acromegaly, it is not a growth hormone receptor antagonist, but rather reduces the production of growth hormone itself. *Cabergoline* - **Cabergoline** is a **dopamine agonist** primarily used to treat hyperprolactinemia by inhibiting prolactin secretion. - It can sometimes be used in acromegaly for patients with co-secretion of prolactin or those who are sensitive to its effects on growth hormone, but it is not a direct growth hormone receptor antagonist. *Olcegepant* - **Olcegepant** is a **calcitonin gene-related peptide (CGRP) receptor antagonist** developed for the treatment of migraine. - It has no known therapeutic role in the management of acromegaly or growth hormone-related disorders.
Question 7: A woman presenting with symptoms of urinary tract infection was prescribed a drug that causes tendon rupture and arthropathy. What is the mechanism of action of the drug?
- A. Ribosomal inhibition
- B. Cell wall synthesis
- C. Inhibition of folic acid synthesis
- D. DNA gyrase inhibition (Correct Answer)
Explanation: ***DNA gyrase inhibition*** - The description of a drug causing **tendon rupture** and **arthropathy** in the context of a urinary tract infection (UTI) suggests a **fluoroquinolone**. - Fluoroquinolones exert their bactericidal effect by inhibiting **bacterial DNA gyrase** (also known as topoisomerase II) and **topoisomerase IV**, thereby preventing DNA replication and repair. *Ribosomal inhibition* - This mechanism is characteristic of antibiotics like **aminoglycosides**, **tetracyclines**, and **macrolides**. - While some of these can treat UTIs, they are not typically associated with **tendon rupture** or **arthropathy** as major side effects. *Cell wall synthesis* - This is the mechanism of action for **beta-lactam antibiotics** (e.g., penicillins, cephalosporins) and **vancomycin**. - These drugs are common for UTIs but do not cause **tendon rupture** or **arthropathy**. *Inhibition of folic acid synthesis* - This mechanism is used by **sulfonamides** and **trimethoprim**, often combined as trimethoprim-sulfamethoxazole. - While effective for UTIs, these drugs are not known to cause **tendon rupture** or **arthropathy**.
Question 8: Multidrug-resistant (MDR) tuberculosis shows resistance to which of the following drugs?
- A. Isoniazid, rifampicin, and fluoroquinolone
- B. Fluoroquinolone
- C. Isoniazid, rifampicin, and kanamycin
- D. Isoniazid and rifampicin only (Correct Answer)
Explanation: ***Isoniazid and rifampicin only*** - **Multidrug-resistant (MDR) tuberculosis** is specifically defined by resistance to both **isoniazid** and **rifampicin**. - These two drugs are considered the most effective first-line anti-TB medications, making resistance to both a significant treatment challenge. *Isoniazid, rifampicin, and fluoroquinolone* - Resistance to **isoniazid**, **rifampicin**, and *any* fluoroquinolone defines **pre-extensively drug-resistant (pre-XDR) TB**, not MDR-TB. - Adding resistance to a fluoroquinolone indicates a more severe and harder-to-treat form of tuberculosis. *Fluoroquinolone* - Resistance to **fluoroquinolone** alone does not define MDR-TB; it is only one component of resistance that, when combined with resistance to isoniazid and rifampicin, signifies pre-XDR or XDR-TB. - While fluoroquinolones are important second-line drugs, their resistance in isolation does not meet the criteria for MDR-TB. *Isoniazid, rifampicin, and kanamycin* - Resistance to **isoniazid**, **rifampicin**, and *any* second-line injectable agent (like **kanamycin**, capreomycin, or amikacin) defines **extensively drug-resistant (XDR) TB**, not MDR-TB. - XDR-TB represents an even more complex and difficult form of the disease to treat, requiring highly specialized regimens.
Question 9: A 55-year-old woman is undergoing chemotherapy for breast cancer and experiences severe nausea and vomiting. Which antiemetic, recognized for its minimal extrapyramidal side effects, would be appropriate for her condition?
- A. Metoclopramide
- B. Ondansetron (Correct Answer)
- C. Promethazine
- D. Prochlorperazine
Explanation: ***Ondansetron*** - **Ondansetron** is a 5-HT3 receptor antagonist, highly effective against chemotherapy-induced nausea and vomiting (CINV) due to its action on serotonin receptors in the **chemoreceptor trigger zone** and **gastrointestinal tract**. - It is known for its favorable side effect profile, with **minimal to no extrapyramidal symptoms**, making it a preferred choice in patients where such effects are a concern. *Metoclopramide* - While effective against nausea and vomiting, **metoclopramide** (a D2 receptor antagonist) can cause **extrapyramidal symptoms** such as **dystonia** and **tardive dyskinesia**, especially with prolonged use or higher doses. - Its mechanism of action includes both prokinetic effects and central antiemetic action, but its side effect profile makes it less ideal when avoiding extrapyramidal symptoms is a priority. *Promethazine* - **Promethazine** is a first-generation antihistamine with antiemetic properties, but it can cause significant **sedation** and has some **anticholinergic side effects**. - Although its extrapyramidal risk is lower than some other drugs, it's not the primary choice for chemotherapy-induced nausea due to its sedative effects and generally less potent antiemetic action for CINV compared to 5-HT3 antagonists. *Prochlorperazine* - **Prochlorperazine** is a phenothiazine antipsychotic with strong antiemetic effects, acting primarily as a **dopamine receptor antagonist**. - It carries a significant risk of **extrapyramidal side effects**, including **acute dystonia** and **parkinsonism**, making it less suitable when such side effects must be strictly avoided.
Question 10: The mechanism of action of botulinum toxin A is best described by:
- A. Slowing of myelinated nerve fiber transmission
- B. Postsynaptic receptor blockade
- C. Acetylcholinesterase inhibition
- D. Presynaptic blockade of acetylcholine release (Correct Answer)
Explanation: ***Presynaptic blockade of acetylcholine release*** - **Botulinum toxin A** acts by cleaving specific proteins (**SNARE proteins** like SNAP-25, synaptobrevin, and syntaxin) essential for the fusion of **acetylcholine-containing vesicles** with the presynaptic membrane. - This prevents the release of acetylcholine into the **neuromuscular junction**, leading to muscle paralysis. *Slowing of myelinated nerve fiber transmission* - This describes the action of agents that affect **myelin sheaths** (e.g., demyelinating diseases) or ion channels involved in action potential propagation, not the mechanism of botulinum toxin. - Botulinum toxin specifically targets the **synaptic transmission**, not the speed of nerve conduction itself. *Postsynaptic receptor blockade* - This mechanism is seen with drugs like **curare** or **neuromuscular blockers** (e.g., rocuronium, vecuronium), which compete with acetylcholine for binding to **nicotinic acetylcholine receptors** on the muscle endplate. - Botulinum toxin does not affect the postsynaptic receptors directly; its action is entirely presynaptic. *Acetylcholinesterase inhibition* - **Acetylcholinesterase inhibitors** (e.g., neostigmine, pyridostigmine) prevent the breakdown of acetylcholine in the synaptic cleft, increasing its concentration and prolonging its action. - This mechanism would enhance, rather than block, muscle contraction, which is opposite to the effect of botulinum toxin.