NEET-PG 2024 - Pharmacology Practice Questions

Q: Why is atropine mixed with diphenoxylate in combination medications?

To prevent abuse of diphenoxylate. ***To prevent abuse of diphenoxylate*** - **Diphenoxylate** is an opioid derivative with potential for abuse due to its CNS effects at high doses. - Adding **atropine** discourages abuse by producing unpleasant anticholinergic side effects (e.g., dry mouth, blurred vision, urinary retention) if high doses are ingested. *Atropine decreases the adverse effects of diphenoxylate* - **Atropine** does not decrease the adverse effects of diphenoxylate; rather, it introduces its own set of **anticholinergic** side effects. - The combination is designed to make recreational use unpleasant, not to mitigate side effects of diphenoxylate itself. *To enhance the antidiarrheal effect* - While atropine has some anticholinergic properties that can reduce gut motility, its primary purpose in this combination is **not to enhance the antidiarrheal effect**. - **Diphenoxylate** is the primary antidiarrheal agent, and the amount of atropine included is typically subtherapeutic for significant antidiarrheal action. *Atropine produces direct spasmolytic action* - Although **atropine** does have **spasmolytic** effects by blocking muscarinic receptors in the gut, this is not the main reason for its addition to diphenoxylate. - The dosage of atropine in the combination is usually low enough to cause unpleasant systemic effects but not necessarily to significantly contribute to the antispasmodic action at therapeutic doses of diphenoxylate. *Atropine increases the bioavailability of diphenoxylate* - **Atropine** does not affect the **pharmacokinetics** or **bioavailability** of diphenoxylate. - The two drugs are combined for abuse deterrence purposes, not for any pharmacokinetic interaction or enhancement of drug absorption.

Q: A patient presents with symptoms of tachycardia, tachypnea, hypertension, and hypocalcemia after consuming an unknown substance. The patient also has high anion gap metabolic acidosis. Which of the following substances was most likely consumed?

Ethylene glycol. ***Ethylene glycol*** - Ethylene glycol poisoning is characterized by **tachycardia**, **tachypnea**, **hypertension**, **hypocalcemia**, and a **high anion gap metabolic acidosis** due to the accumulation of toxic metabolites like oxalic and glycolic acids. - The formation of **calcium oxalate crystals** in the kidneys contributes to hypocalcemia and acute kidney injury, a hallmark of severe ethylene glycol toxicity. *Iron* - Iron overdose typically presents with **gastrointestinal symptoms** (vomiting, diarrhea, abdominal pain), shock, and metabolic acidosis, but not specifically with hypocalcemia or the characteristic crystal formation seen with ethylene glycol. - While it can cause metabolic acidosis, the absence of **hypocalcemia** and specific renal effects pointing to oxalate crystals differentiates it from ethylene glycol. *Methanol* - Methanol poisoning causes a **high anion gap metabolic acidosis**, visual disturbances (e.g., "snowstorm" vision), and central nervous system depression. - It does not typically lead to **hypocalcemia** or the kidney damage associated with calcium oxalate crystal formation. *Isopropanol* - Isopropanol (rubbing alcohol) poisoning causes **CNS depression**, **hypotension**, and an **osmolar gap** without significant anion gap metabolic acidosis. - It does not cause **hypocalcemia** or the high anion gap metabolic acidosis characteristic of ethylene glycol toxicity. *Digoxin* - Digoxin toxicity primarily affects the **cardiac system**, causing bradycardia, arrhythmias (e.g., ventricular fibrillation, heart block), and **gastrointestinal symptoms**. - It does not cause a high anion gap metabolic acidosis, hypocalcemia, or the other systemic sympathetic effects described in the scenario.

Q: In which phase of clinical trials is drug dosing typically determined?

Phase 1. ***Phase 1*** - This phase involves a small group of **healthy volunteers** to assess the drug's safety, **pharmacokinetics (PK)**, and establish an initial dosing range. - The primary goal is to determine a **safe dosage level**, establish the **maximum tolerated dose (MTD)**, and identify potential side effects. - This is where drug dosing is **typically determined**. *Phase 0* - This is an exploratory phase involving **microdosing** studies with subtherapeutic doses. - The goal is to gather preliminary PK/PD data, but **not to determine therapeutic dosing**. *Phase 2* - This phase involves a larger group of **patients** with the condition to be treated. - The main goal is to evaluate the drug's **effectiveness** and further assess safety, but not primarily to determine initial dosing. *Phase 3* - This phase involves a large number of patients across multiple sites to confirm the drug's **efficacy** and monitor side effects in a broader population. - Dosing strategies have generally been established in earlier phases, and this phase primarily validates them. *Phase 4* - This phase occurs **after a drug has been approved** and marketed. - It involves ongoing surveillance to monitor long-term effects, collect additional information on safety, and identify new uses, but not initial dose determination.

Q: A patient with HIV who is currently on antiretroviral therapy consisting of zidovudine, lamivudine, and nevirapine is diagnosed with tuberculosis. Considering potential drug interactions, which of the following TB drugs should be changed in this patient?

Rifampicin. **Rifampicin** - **Rifampicin** is a potent **CYP450 enzyme inducer**, which significantly increases the metabolism of **nevirapine**, a non-nucleoside reverse transcriptase inhibitor (NNRTI), leading to subtherapeutic levels and potential treatment failure. - In patients on **nevirapine-based ART**, **rifampicin** is typically avoided or replaced with other rifamycins (like **rifabutin**), or the antiretroviral regimen is switched to one that is less affected by enzyme induction. *Isoniazid* - **Isoniazid** does not have significant, clinically problematic interactions with the antiretroviral regimen mentioned (zidovudine, lamivudine, nevirapine), and is generally well-tolerated. - It is a cornerstone of TB treatment and is usually continued without dose adjustment or substitution in this scenario. *Pyrazinamide* - **Pyrazinamide** is part of the standard first-line TB treatment regimen and does not have clinically significant drug interactions with zidovudine, lamivudine, or nevirapine. - It can be safely continued without dose adjustment in patients on this ART regimen. *Ethambutol* - **Ethambutol** primarily causes **optic neuritis** as a side effect and does not have significant pharmacokinetic interactions with the antiretroviral drugs listed. - Its use in TB treatment alongside this ART regimen is generally safe and does not require a change. *Streptomycin* - **Streptomycin** is an **aminoglycoside antibiotic** primarily used for multi-drug resistant TB or in specific situations, and its main toxicity is **ototoxicity** and **nephrotoxicity**. - It does not have known significant drug interactions with zidovudine, lamivudine, or nevirapine that would necessitate a change.

Q: Which of the following is commonly used for maintenance therapy in opioid abuse?

Buprenorphine. ***Buprenorphine*** - **Buprenorphine** is a **partial opioid agonist** commonly used for the maintenance treatment of **opioid use disorder** due to its ability to reduce cravings and prevent withdrawal symptoms. - It has a "ceiling effect," meaning that its opioid effects level off at higher doses, which contributes to its **safety profile** and lower risk of overdose compared to full agonists. - Preferred over methadone in many settings due to its **superior safety profile**, lower abuse potential, and ability to be prescribed in office-based settings. *Clonidine* - **Clonidine** is an **alpha-2 adrenergic agonist** primarily used to manage **autonomic symptoms** of opioid withdrawal (e.g., sweating, hypertension), but it does not address cravings or provide opioid effects. - It is not considered a primary maintenance therapy for opioid use disorder. *Butorphanol* - **Butorphanol** is a **mixed opioid agonist-antagonist** often used for pain relief, but its partial agonist activity and potential for withdrawal in opioid-dependent individuals make it unsuitable for maintenance therapy in opioid abuse. - It can precipitate **opioid withdrawal** in patients who are opioid-dependent. *Naloxone* - **Naloxone** is an **opioid antagonist** used to rapidly reverse the effects of opioid overdose by blocking opioid receptors. - While critical in overdose situations, it is not used for maintenance therapy as it would induce immediate and severe opioid withdrawal symptoms. *Methadone* - **Methadone** is a **full opioid agonist** that is also used for maintenance therapy in opioid use disorder, particularly in specialized opioid treatment programs. - However, it requires **daily supervised dosing** in most jurisdictions, has a higher risk of overdose, respiratory depression, and QT prolongation, making buprenorphine often the **preferred first-line agent** for maintenance therapy.

Q: Caffeine is a widely used stimulant that promotes wakefulness. Which of the following mechanisms is responsible for this effect?

Adenosine antagonism. ***Adenosine antagonism*** - Caffeine acts as a **competitive antagonist** at **adenosine receptors** (primarily A1 and A2A) in the brain. - **Adenosine** is an inhibitory neurotransmitter that promotes drowsiness and reduces neuronal activity; by blocking its receptors, caffeine prevents this sedation and promotes wakefulness. - This is the **primary mechanism** responsible for caffeine's stimulant effects at typical dietary doses. *Increased discharge of norepinephrine from the locus ceruleus* - While increased **norepinephrine** can promote wakefulness, it is not the primary direct mechanism by which caffeine exerts its stimulant effects. - Caffeine may indirectly affect norepinephrine release as a downstream consequence of adenosine receptor blockade, but this is a secondary effect. *Release of histamine* - **Histamine** is indeed a neurotransmitter involved in wakefulness and arousal, but caffeine does not primarily promote wakefulness by directly causing histamine release. - Some antihistamines cause drowsiness by blocking central histamine receptors, but caffeine's mechanism is distinct from the histaminergic system. *Inhibition of phosphodiesterase* - Caffeine does inhibit **phosphodiesterase (PDE)** enzymes, leading to increased intracellular **cAMP** levels. - However, PDE inhibition occurs at significantly **higher concentrations** than those required for adenosine receptor antagonism, making it a less important mechanism for caffeine's typical stimulant effects at common dietary doses (1-3 cups of coffee). *Dopamine reuptake inhibition* - While some CNS stimulants (e.g., **methylphenidate**, **cocaine**) work primarily through dopamine reuptake inhibition, this is **not** caffeine's primary mechanism. - Caffeine may have minor indirect effects on dopamine neurotransmission through its adenosine receptor antagonism, but direct dopamine reuptake inhibition is not a significant mechanism of action.

Q: A 65-year-old patient presents with symptoms of bone pain, anemia, hypercalcemia, and renal impairment. A bone marrow biopsy confirms the diagnosis of multiple myeloma. The patient is started on a treatment regimen. Which of the following treatments is most likely associated with the reactivation of herpes zoster?

Bortezomib. ***Bortezomib*** - **Bortezomib**, a **proteasome inhibitor**, is known to increase the risk of herpes zoster reactivation in patients with multiple myeloma due to its immunosuppressive effects. - Prophylaxis with antiviral agents (e.g., acyclovir) is often recommended during bortezomib treatment to prevent this complication. - Studies show herpes zoster incidence of 10-15% in bortezomib-treated patients without prophylaxis. *Lenalidomide* - While lenalidomide is an **immunomodulatory drug** used in multiple myeloma, it is generally associated with a lower risk of herpes zoster reactivation compared to proteasome inhibitors. - It primarily acts by inhibiting angiogenesis and stimulating T-cell and natural killer cell activity. *Daratumumab* - **Daratumumab** is a **monoclonal antibody** targeting CD38 on myeloma cells, leading to their destruction. - Although it has immunosuppressive effects, it is less commonly associated with herpes zoster reactivation than bortezomib. *Melphalan* - **Melphalan** is an **alkylating agent** used in chemotherapy for multiple myeloma, particularly in conditioning regimens for stem cell transplantation. - While it causes myelosuppression and general immunosuppression, the direct association with herpes zoster reactivation is not as prominent or specific as with bortezomib. *Dexamethasone* - **Dexamethasone** is a **corticosteroid** commonly used in combination regimens for multiple myeloma (e.g., RVD, VCD). - While corticosteroids cause immunosuppression and can increase infection risk, the specific association with herpes zoster reactivation is less pronounced than with bortezomib.

Q: Which of the following growth hormone analogues is not used for the treatment of GH deficiency but is used in the treatment of HIV associated lipodystrophy?

Tesamorelin. ***Tesamorelin*** - **Tesamorelin** is a **growth hormone-releasing hormone (GHRH) analogue** approved specifically for the treatment of **HIV-associated lipodystrophy**. - It works by stimulating the natural production and release of endogenous growth hormone, which helps reduce **visceral adipose tissue** observed in this condition. - **Key distinction:** NOT used for GH deficiency, but specifically for lipodystrophy. *Sermorelin* - **Sermorelin** is also a **GHRH analogue**, but it is primarily used to diagnose and treat **growth hormone deficiency** in children. - It is not approved for lipodystrophy and works by stimulating the pituitary to secrete growth hormone. *Somatropin* - **Somatropin** is the recombinant form of **human growth hormone (GH)** itself, used to treat **growth hormone deficiency** in both children and adults. - While it can affect body composition, its primary indication is not HIV-associated lipodystrophy. *Mecasermin* - **Mecasermin** is recombinant **insulin-like growth factor-1 (IGF-1)** used to treat severe primary IGF-1 deficiency. - It is used for growth failure in children with GH gene deletion or GH receptor defects, not for HIV-associated lipodystrophy. *Pegvisomant* - **Pegvisomant** is a **growth hormone receptor antagonist** used to treat **acromegaly**, a condition caused by excessive growth hormone. - It works by blocking the action of growth hormone at its receptor, directly opposing the therapeutic goal for lipodystrophy.

Question 1

Why is atropine mixed with diphenoxylate in combination medications?

Accepted Answer

To prevent abuse of diphenoxylate

Answer

Atropine decreases the adverse effects of diphenoxylate

Answer

To enhance the antidiarrheal effect

Answer

Atropine produces direct spasmolytic action

Answer

Atropine increases the bioavailability of diphenoxylate

Question 2

A patient presents with symptoms of tachycardia, tachypnea, hypertension, and hypocalcemia after consuming an unknown substance. The patient also has high anion gap metabolic acidosis. Which of the following substances was most likely consumed?

Accepted Answer

Ethylene glycol

Answer

Iron

Answer

Methanol

Answer

Digoxin

Answer

Isopropanol

Question 3

In which phase of clinical trials is drug dosing typically determined?

Accepted Answer

Phase 1

Answer

Phase 2

Answer

Phase 3

Answer

Phase 4

Answer

Phase 0

Question 4

A patient with HIV who is currently on antiretroviral therapy consisting of zidovudine, lamivudine, and nevirapine is diagnosed with tuberculosis. Considering potential drug interactions, which of the following TB drugs should be changed in this patient?

Accepted Answer

Rifampicin

Answer

Isoniazid

Answer

Ethambutol

Answer

Streptomycin

Answer

Pyrazinamide

Question 5

Which of the following is commonly used for maintenance therapy in opioid abuse?

Accepted Answer

Buprenorphine

Answer

Clonidine

Answer

Butorphanol

Answer

Naloxone

Answer

Methadone

Question 6

Caffeine is a widely used stimulant that promotes wakefulness. Which of the following mechanisms is responsible for this effect?

Accepted Answer

Adenosine antagonism

Answer

Increased discharge of norepinephrine from the locus ceruleus

Answer

Release of histamine

Answer

Inhibition of phosphodiesterase

Answer

Dopamine reuptake inhibition

Question 7

A 65-year-old patient presents with symptoms of bone pain, anemia, hypercalcemia, and renal impairment. A bone marrow biopsy confirms the diagnosis of multiple myeloma. The patient is started on a treatment regimen. Which of the following treatments is most likely associated with the reactivation of herpes zoster?

Accepted Answer

Bortezomib

Answer

Lenalidomide

Answer

Daratumumab

Answer

Melphalan

Answer

Dexamethasone

Question 8

Which of the following is a selective norepinephrine reuptake inhibitor that can be used for the treatment of ADHD?

Accepted Answer

Atomoxetine

Answer

Reboxetine

Answer

Methylphenidate

Answer

Guanfacine

Answer

Modafinil

Question 9

An 18-year-old boy from Rajasthan weighing 50 kg is diagnosed with mixed P . vivax and P . falciparum malaria. What is the appropriate treatment regimen on day 2?

Accepted Answer

Artesunate 50 mg (4 tablets) + Sulfadoxine/ pyrimethamine ( 750/37.5 mg ) (2 tablets) + Primaquine 2.5 mg ( 6 tablets)

Answer

Artesunate 50 mg (4 tablets) + Primaquine 2.5 mg ( 6 tablets)

Answer

Artesunate 50 mg (4 tablets) + Primaquine 7.5 mg (6 tablets)

Answer

Artesunate 50 mg (4 tablets) + Sulfadoxine/ pyrimethamine ( 750/37.5 mg ) (2 tablets) + Primaquine 7.5 mg ( 6 tablets)

Answer

Artesunate 50 mg (4 tablets) only

Question 10

Which of the following growth hormone analogues is not used for the treatment of GH deficiency but is used in the treatment of HIV associated lipodystrophy?

Accepted Answer

Tesamorelin

Answer

Sermorelin

Answer

Somatropin

Answer

Pegvisomant

Answer

Mecasermin

NEET-PG 2024 — Pharmacology