NEET-PG 2021 - Pharmacology PYQs Practice Questions

Q: Beta 2 receptors act via which of the following secondary messenger systems

Adenylate Cyclase. ***Adenylate Cyclase*** - **Beta-2 adrenergic receptors** are G-protein coupled receptors that primarily activate the **Gs protein**. - Activation of Gs protein leads to the stimulation of **adenylate cyclase**, which converts ATP to **cAMP**, a crucial secondary messenger for various cellular responses. *Phospholipase C* - **Phospholipase C** is typically activated by **Gq protein-coupled receptors**, such as alpha-1 adrenergic receptors or M1/M3 muscarinic receptors. - Its activation leads to the production of **IP3** and **DAG**, which then trigger intracellular calcium release and protein kinase C activation, respectively. *Guanylate Cyclase* - **Guanylate cyclase** produces **cGMP** as a secondary messenger and is primarily associated with **nitric oxide signaling** (soluble guanylate cyclase) or **natriuretic peptide receptors** (particulate guanylate cyclase). - This system is distinct from the adrenergic receptor pathways. *Direct ion channel activation* - **Direct ion channel activation** occurs in **ligand-gated ion channels**, where the binding of a neurotransmitter directly opens an ion pore without the involvement of G-proteins or secondary messengers. - Examples include nicotinic acetylcholine receptors and GABA-A receptors, which are functionally different from the G-protein coupled **beta-2 receptors**. *Tyrosine Kinase* - **Tyrosine kinase** signaling is characteristic of **receptor tyrosine kinases (RTKs)**, such as insulin receptors and growth factor receptors (e.g., EGF, PDGF receptors). - These receptors undergo autophosphorylation and initiate signaling cascades independent of G-proteins, making them distinct from **beta-2 adrenergic receptors**. [Practice more Pharmacology PYQs on OnCourse]

Q: A child accidentally ingested a fruit from a tree while playing. After the ingestion, he presented with symptoms of restlessness, painful swallowing, photophobia, dry skin, urinary retention, and elevated body temperature. What is the most likely cause of poisoning, and what is the appropriate antidote for it?

Datura poisoning & Physostigmine. ***Datura poisoning & Physostigmine*** - The symptoms of **restlessness, painful swallowing, photophobia, dry skin, urinary retention, and elevated body temperature** are classic signs of **anticholinergic toxicity**, which is characteristic of **Datura poisoning**. - **Physostigmine** is an **acetylcholinesterase inhibitor** that increases acetylcholine levels, effectively reversing the anticholinergic effects of Datura. *Yellow Oleander poisoning & Atropine* - **Yellow Oleander poisoning** primarily causes **cardiac effects** (e.g., bradycardia, arrhythmias) due to cardiac glycosides, not the anticholinergic symptoms described. - **Atropine** is an **anticholinergic agent** and would worsen the symptoms of Datura poisoning rather than being an antidote for it. *Datura poisoning & Pralidoxime* - While **Datura poisoning** is correct given the symptoms, **Pralidoxime** is an antidote for **organophosphate poisoning**, acting as a cholinesterase reactivator, and has no efficacy in anticholinergic toxicity. *Organophosphate poisoning & Pralidoxime* - **Organophosphate poisoning** presents with **cholinergic symptoms** (e.g., salivation, lacrimation, urination, defecation, GI upset, emesis, miosis, bronchospasm, bradycardia), which are opposite to the anticholinergic signs seen here. - Although **Pralidoxime** is a correct antidote for organophosphate poisoning, the clinical picture does not support this diagnosis. *Mushroom (Amanita) poisoning & Atropine* - **Certain mushroom poisonings** (e.g., muscarine-containing mushrooms like *Inocybe* and *Clitocybe* species) cause **cholinergic symptoms** (salivation, sweating, miosis, bradycardia), not anticholinergic symptoms. - While **Atropine** would be the correct antidote for muscarinic mushroom poisoning, the clinical presentation here shows anticholinergic toxicity, not cholinergic excess. [Practice more Pharmacology PYQs on OnCourse]

Q: What is the mechanism of action of Tocilizumab?

Inhibits binding of IL-6 to its receptor IL-6R. ***Inhibits binding of IL-6 to its receptor IL-6R*** - **Tocilizumab** is a **monoclonal antibody** that specifically targets the **interleukin-6 (IL-6) receptor**. - By blocking IL-6 from binding to its receptor, Tocilizumab **inhibits IL-6 mediated signaling**, thereby reducing inflammation and immune responses. *TNF Alpha inhibition* - **TNF-alpha inhibitors** (e.g., adalimumab, infliximab) target **tumor necrosis factor-alpha**, a different pro-inflammatory cytokine. - While both TNF-alpha and IL-6 are involved in inflammatory diseases, their signaling pathways and therapeutic targets are distinct. *IL-18 inhibition* - **IL-18** is another pro-inflammatory cytokine, but Tocilizumab does **not directly target** or inhibit its activity. - Drugs that target IL-18 or its pathways are distinct from those targeting IL-6. *IL-17 inhibition* - **IL-17 inhibitors** (e.g., secukinumab, ixekizumab) are biologics that target **interleukin-17**, particularly useful in psoriasis and ankylosing spondylitis. - Tocilizumab's mechanism is specific to **IL-6**, not IL-17. *Inhibits binding of IL-1* - **Interleukin-1 (IL-1)** is a key mediator of inflammation, but specific **IL-1 inhibitors** (e.g., anakinra, canakinumab) act by blocking IL-1 or its receptor. - Tocilizumab's mechanism is specific to the **IL-6 cytokine-receptor interaction**, not IL-1. [Practice more Pharmacology PYQs on OnCourse]

Q: What is the mechanism of action of Methotrexate?

Inhibition of Dihydrofolate reductase. ***Inhibition of Dihydrofolate reductase*** - **Methotrexate** is a **folate analog** that competitively inhibits **dihydrofolate reductase (DHFR)**, an enzyme essential for converting **dihydrofolate** to **tetrahydrofolate**. - This inhibition blocks the synthesis of **purines** and **pyrimidines**, thereby preventing DNA and RNA synthesis and ultimately inhibiting cell proliferation. *Inhibits pyrimidine synthesis* - While methotrexate ultimately inhibits pyrimidine synthesis by depleting tetrahydrofolate, its direct mechanism is not the inhibition of the pyrimidine synthesis pathway enzymes themselves. - Its primary action is upstream, by inhibiting DHFR. *Inhibits cell replication by acting on G phase of cell cycle* - Methotrexate primarily inhibits cells in the **S-phase** of the cell cycle, as it interferes with DNA synthesis. - It does not specifically target the G phase; rather, it affects cells that are actively attempting to replicate their DNA. *Inhibits Thymidylate synthase* - **Thymidylate synthase** is inhibited by drugs like **5-fluorouracil**, which directly blocks the conversion of **deoxyuridine monophosphate (dUMP)** to **deoxythymidine monophosphate (dTMP)**. - Methotrexate's effect on thymidylate synthesis is indirect, mediated by the depletion of the cofactor **N5,N10-methylene-tetrahydrofolate** due to DHFR inhibition. *Inhibits RNA polymerase* - **RNA polymerase** inhibition is the mechanism of drugs like **rifampin** (bacterial RNA polymerase) and **α-amanitin** (eukaryotic RNA polymerase). - Methotrexate does not directly inhibit RNA polymerase; its effects on RNA synthesis are secondary to depletion of nucleotide precursors through DHFR inhibition. [Practice more Pharmacology PYQs on OnCourse]

Q: Which antitubercular drug reduces the efficacy of oral contraceptive pills (OCPs)?

Rifampicin. ***Rifampicin*** - **Rifampicin** is a potent inducer of **cytochrome P450 enzymes**, particularly CYP3A4, which metabolize oral contraceptive pills (OCPs). - This increased metabolism leads to lower systemic levels of contraceptive hormones, reducing their efficacy and increasing the risk of **unintended pregnancy**. - Women on Rifampicin should use **additional barrier contraception** or alternative contraceptive methods. *Isoniazid* - **Isoniazid** is primarily metabolized by N-acetyltransferase and cytochrome P450, but it is not a significant enzyme inducer. - It does not typically interfere with the effectiveness of **oral contraceptive pills**. *Ethambutol* - **Ethambutol** is eliminated largely unchanged via renal excretion and is not a significant inducer or inhibitor of cytochrome P450 enzymes. - It does not interact with **oral contraceptive pills**. *Pyrazinamide* - **Pyrazinamide** is metabolized by the liver, but it does not significantly induce or inhibit the cytochrome P450 system involved in OCP metabolism. - It is not known to reduce the effectiveness of **oral contraceptive pills**. *Streptomycin* - **Streptomycin** is an aminoglycoside antibiotic that is not metabolized by the liver and does not affect cytochrome P450 enzymes. - It has no interaction with **oral contraceptive pills**. [Practice more Pharmacology PYQs on OnCourse]

Question 1

Beta 2 receptors act via which of the following secondary messenger systems

Accepted Answer

Adenylate Cyclase

Answer

Phospholipase C

Answer

Guanylate Cyclase

Answer

Direct ion channel activation

Answer

Tyrosine Kinase

Question 2

A child accidentally ingested a fruit from a tree while playing. After the ingestion, he presented with symptoms of restlessness, painful swallowing, photophobia, dry skin, urinary retention, and elevated body temperature. What is the most likely cause of poisoning, and what is the appropriate antidote for it?

Accepted Answer

Datura poisoning & Physostigmine

Answer

Yellow Oleander poisoning & Atropine

Answer

Datura poisoning & Pralidoxime

Answer

Organophosphate poisoning & Pralidoxime

Answer

Mushroom (Amanita) poisoning & Atropine

Question 3

What is the mechanism of action of Tocilizumab?

Accepted Answer

Inhibits binding of IL-6 to its receptor IL-6R

Answer

TNF Alpha inhibition

Answer

IL-18 inhibition

Answer

Inhibits binding of IL-1

Answer

IL-17 inhibition

Question 4

What is the mechanism of action of Methotrexate?

Accepted Answer

Inhibition of Dihydrofolate reductase

Answer

Inhibits pyrimidine synthesis

Answer

Inhibits cell replication by acting on G phase of cell cycle

Answer

Inhibits Thymidylate synthase

Answer

Inhibits RNA polymerase

Question 5

Which antitubercular drug reduces the efficacy of oral contraceptive pills (OCPs)?

Accepted Answer

Rifampicin

Answer

Isoniazid

Answer

Ethambutol

Answer

Pyrazinamide

Answer

Streptomycin

Question 6

A patient on digoxin therapy presents with atrial fibrillation and controlled ventricular rate. Upon evaluation, the patient's serum digoxin levels are elevated compared to previous values. Which of the following concomitant medications is most likely to have contributed to the enhanced digoxin toxicity?

Accepted Answer

Clarithromycin

Answer

Triamterene

Answer

KCL

Answer

Atenolol

Answer

Amiodarone

Question 7

A patient is taking metronidazole for anaerobic infection. Which of the following should be avoided during this period

Accepted Answer

Alcohol

Answer

Colchicine

Answer

Rifampicin

Answer

Ciprofloxacin

Answer

Warfarin

Question 8

Topiramate is used in

Accepted Answer

Management of Seizures in Lennox-Gastaut Syndrome

Answer

1st Line Treatment of ADHD

Answer

Treatment of Acute Migraine

Answer

Treatment of Dementia

Answer

Treatment of Bipolar Disorder

Question 9

Which of the following drugs is used for the long term management of obesity

Accepted Answer

Liraglutide

Answer

Fenfluramine

Answer

Sibutramine

Answer

Metformin

Answer

Orlistat

Question 10

A 30-year-old male presents with a history of consuming an unknown substance. On examination, the patient has diaphoresis, headache, and features resembling acute coronary spasm. Which of the following clinical features is least likely to be present in this patient?

Accepted Answer

Bradycardia

Answer

Hypertension

Answer

Tachycardia

Answer

Hyperthermia

Answer

Mydriasis

NEET-PG 2021 — Pharmacology