NEET-PG 2023 - Pharmacology PYQs Practice Questions

Q: Claviceps purpurea produces which of the following toxins?

Ergot alkaloids. ***Ergot alkaloids*** - **Claviceps purpurea** is a fungus that infects cereals, particularly rye, and produces a group of toxic compounds known as **ergot alkaloids**. - These alkaloids can cause a condition called **ergotism**, which includes symptoms like hallucinations, gangrene, and severe vasoconstriction. *Aflatoxins* - **Aflatoxins** are produced by species of **Aspergillus fungi**, such as *A. flavus* and *A. parasiticus*, not *Claviceps purpurea*. - They are potent **carcinogens** and are commonly found in contaminated crops like peanuts and maize. *Sanguinarine alkaloid* - **Sanguinarine** is an alkaloid derived from plants like **bloodroot (Sanguinaria canadensis)**, not *Claviceps purpurea*. - It has been linked to **glaucoma** and liver toxicity. *Pyrazolidone drug* - **Pyrazolidone** is a classification of synthetic drugs, often used as **non-steroidal anti-inflammatory drugs (NSAIDs)**, such as phenylbutazone. - This is a pharmaceutical compound and not naturally derived from *Claviceps purpurea* or any fungus. [Practice more Pharmacology PYQs on OnCourse]

Q: A patient on atracurium develops seizures due to accumulation of which substance?

Laudanosine. ***Laudanosine*** - Atracurium is metabolized into **laudanosine**, a **neurotoxic metabolite** that can accumulate, particularly in patients with renal or hepatic dysfunction, leading to **seizures** and central nervous system excitation. - Due to its potential for neurotoxicity, atracurium is often replaced by **cisatracurium**, which produces less laudanosine. *Cisatracurium* - **Cisatracurium** is an isomer of atracurium that is also metabolized via **Hofmann elimination** but produces significantly **less laudanosine**. - It is preferred in patients with **renal or hepatic impairment** due to its reduced potential for metabolite accumulation and neurotoxicity. *Atracurium acid* - Atracurium acid is one of the **inactive metabolites** of atracurium, along with laudanosine. - Unlike laudanosine, atracurium acid is **not neurotoxic** and does not contribute to seizure activity. *Histamine* - Atracurium can cause an **immediate release of histamine**, leading to transient hypotension, flushing, and bronchospasm, especially with rapid bolus injection. - While histamine release is an adverse effect of atracurium, it is **not directly responsible for seizure activity**. [Practice more Pharmacology PYQs on OnCourse]

Q: A child presented with a history of ingestion of an unknown plant and developed mydriasis, tachycardia, dry mouth, warm skin, and delirium. Which of the following groups of drugs is likely to be responsible for the symptoms of this child?

Anticholinergic. ***Anticholinergic*** - The constellation of mydriasis, tachycardia, dry mouth, warm skin, and delirium is classic for **anticholinergic toxicity**, often described as "hot as a hare, blind as a bat, dry as a bone, red as a beet, and mad as a hatter." - This toxidrome is caused by the blockade of **muscarinic acetylcholine receptors**, leading to widespread inhibition of parasympathetic nervous system functions. - Common plant sources include **Datura** (jimsonweed) and **Atropa belladonna** (deadly nightshade). *Sympathomimetic* - While **mydriasis** and **tachycardia** can be present, sympathomimetic toxicity typically causes **diaphoresis (sweating)** and **hypertension**, not dry skin and mouth. - Patients often present with agitation, paranoia, and potentially seizures, but the key differentiating factor is the presence of profuse sweating. *Opioid* - Opioid overdose is characterized by the classic triad of **miosis (pinpoint pupils)**, **respiratory depression**, and **CNS depression (coma)**, none of which are present in this case. - Other common symptoms include bradycardia, hypotension, and hypothermia, which are contrary to the child's presentation. *Benzodiazepine* - Benzodiazepine overdose typically causes **CNS depression** including drowsiness, ataxia, and slurred speech, but usually spares vital signs unless combined with other depressants. - **Mydriasis**, **tachycardia**, and **dry mouth** are not characteristic symptoms of benzodiazepine toxicity; pupils are typically normal or slightly dilated due to hypoxia in severe cases. [Practice more Pharmacology PYQs on OnCourse]

Q: Which of the following drugs inhibits the activation of plasminogen?

Aminocaproic acid. ***Correct Option: Aminocaproic acid*** - **Aminocaproic acid** is an antifibrinolytic drug that acts by competitively inhibiting the activation of **plasminogen** to plasmin. - By preventing the formation of plasmin, it stabilizes blood clots and is used to treat excessive bleeding. *Incorrect Option: Streptokinase* - **Streptokinase** is a **thrombolytic agent** that forms a complex with plasminogen, converting uncomplexed plasminogen into plasmin. - This action promotes the degradation of fibrin clots, making it a **fibrinolytic drug**, not an inhibitor of plasminogen activation. *Incorrect Option: Reteplase* - **Reteplase** is a **recombinant tissue plasminogen activator (tPA)** that directly converts plasminogen to plasmin. - This drug actively promotes **fibrinolysis** and clot breakdown, making it a thrombolytic agent. *Incorrect Option: Clopidogrel* - **Clopidogrel** is an **antiplatelet drug** that inhibits platelet aggregation by irreversibly blocking the P2Y12 adenosine diphosphate (ADP) receptor on platelets. - Its mechanism of action is focused on **platelet function**, not on the plasminogen-plasmin system. [Practice more Pharmacology PYQs on OnCourse]

Q: Which of the following clotting factors in a patient on Warfarin therapy would show the earliest decrease in functional activity?

Factor VII. ***Factor VII*** - Factor VII has the **shortest half-life** (approximately 6 hours) among the vitamin K-dependent clotting factors, meaning its functional activity decreases **most rapidly** after starting warfarin therapy. - Warfarin inhibits vitamin K epoxide reductase, preventing gamma-carboxylation of **all vitamin K-dependent factors** (II, VII, IX, X). However, Factor VII's short half-life means pre-existing functional Factor VII is depleted first. - This is why **PT/INR** (which measures the extrinsic pathway dependent on Factor VII) rises before aPTT in warfarin therapy. - Reduced gamma-carboxylation impairs Factor VII's ability to bind calcium and phospholipids, essential for its activation in the extrinsic coagulation pathway. *Factor IX* - Factor IX is a **vitamin K-dependent factor** affected by warfarin, but its longer half-life (approximately 24 hours) means functional activity decreases more slowly than Factor VII. - It plays a key role in the **intrinsic coagulation pathway**. *Factor X* - Factor X is a **vitamin K-dependent clotting factor** whose gamma-carboxylation is inhibited by warfarin. - Its half-life (approximately 40 hours) is longer than Factor VII, resulting in a **slower decline in functional activity**. *Prothrombin (Factor II)* - Prothrombin (Factor II) is a **vitamin K-dependent factor** affected by warfarin. - It has the **longest half-life** (60-72 hours) among vitamin K-dependent factors, meaning its functional levels decrease most slowly after initiating warfarin therapy. [Practice more Pharmacology PYQs on OnCourse]

Question 1

Claviceps purpurea produces which of the following toxins?

Accepted Answer

Ergot alkaloids

Answer

Aflatoxins

Answer

Sanguinarine alkaloid

Answer

Pyrazolidone drug

Question 2

A patient on atracurium develops seizures due to accumulation of which substance?

Accepted Answer

Laudanosine

Answer

Atracurium acid

Answer

Cisatracurium

Answer

Histamine

Question 3

A child presented with a history of ingestion of an unknown plant and developed mydriasis, tachycardia, dry mouth, warm skin, and delirium. Which of the following groups of drugs is likely to be responsible for the symptoms of this child?

Accepted Answer

Anticholinergic

Answer

Sympathomimetic

Answer

Opioid

Answer

Benzodiazepine

Question 4

Which of the following drugs inhibits the activation of plasminogen?

Accepted Answer

Aminocaproic acid

Answer

Streptokinase

Answer

Reteplase

Answer

Clopidogrel

Question 5

Which of the following clotting factors in a patient on Warfarin therapy would show the earliest decrease in functional activity?

Accepted Answer

Factor VII

Answer

Factor IX

Answer

Factor X

Answer

Prothrombin (Factor 2)

Question 6

A patient with a malignancy is undergoing chemotherapy. The platelet counts were reduced after the previous cycle of chemotherapy. Which of the following drugs can be used to treat this patient?

Accepted Answer

Oprelvekin (IL-11) - stimulates platelet production

Answer

Filgrastim - stimulates white blood cell production

Answer

Amifostine - protects against chemotherapy toxicity

Answer

Erythropoietin - stimulates red blood cell production

Question 7

A patient who is a known case of hypertension on multiple anti-hypertensive medications came to OPD. His ECG finding is given below. Which of the following drugs is responsible for the ECG finding? (Image of ECG finding)

Accepted Answer

Spironolactone

Answer

Prazosin

Answer

Metoprolol

Answer

Hydrochlorothiazide

Question 8

A 3-week-old infant presents with a cough and sore throat. The mother reports that the infant develops a paroxysm of cough followed by apnea. The total leucocyte count is >50,000 cells/μL. Based on these symptoms, which of the following drugs is the most appropriate treatment for this patient?

Accepted Answer

Azithromycin

Answer

Amoxicillin

Answer

Cotrimoxazole

Answer

Erythromycin

Question 9

A patient with recurrent gout attacks was started on a drug that inhibits uric acid synthesis. His symptoms were reduced after therapy. Which drug was he started on?

Accepted Answer

Allopurinol

Answer

Probenecid

Answer

Colchicine

Answer

Diclofenac

Question 10

A patient given digoxin started having side effects like nausea and vomiting. The serum concentration of digoxin was 4 ng/mL. The plasma therapeutic range is 1-2 ng/mL. If the half-life of digoxin is 40 hours, how long should one wait before resuming the treatment?

Accepted Answer

80 hours

Answer

120 hours

Answer

140-180 hours

Answer

1 half-life (40 hours)

NEET-PG 2023 — Pharmacology