NEET-PG 2013 - Pharmacology Practice Questions

Q: Which drug is used for sympathectomy in experimental animals?

Guanethidine. ***Guanethidine*** - **Guanethidine** is a potent **adrenergic neuron blocking drug** that is taken up by noradrenergic neurons and prevents the release of norepinephrine, leading to a chemical sympathectomy. - In experimental animal models, it is used to induce a **pharmacological sympathectomy** to study the effects of sympathetic nervous system blockade on various physiological processes. *Atropine* - **Atropine** is a **muscarinic acetylcholine receptor antagonist** that blocks the effects of acetylcholine at parasympathetic postganglionic terminals. - It is primarily used to block **parasympathetic responses**, not sympathetic ones, and therefore would not induce a sympathectomy. *Diazoxide* - **Diazoxide** is a direct **arteriolar vasodilator** that works by opening potassium channels in vascular smooth muscle. - It is used to quickly reduce blood pressure in **hypertensive emergencies** and for treating hypoglycemia due to insulin oversecretion, and does not cause sympathectomy. *Thebaine* - **Thebaine** is an **opioid alkaloid** found in opium, structurally similar to morphine and codeine, but with primarily stimulatory rather than depressant effects. - It acts as a **convulsant** and is used as a precursor in the synthesis of other opioids, but has no role in causing sympathectomy.

Q: Which of the following is a mineralocorticoid antagonist?

Spironolactone. ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that acts as a competitive antagonist of **aldosterone** at the mineralocorticoid receptors in the renal tubules [1], [2]. - Its primary use is in conditions like **heart failure**, **cirrhosis with ascites**, and **primary hyperaldosteronism** (Conn's syndrome) [2]. *Inamrinone* - **Inamrinone** is a **phosphodiesterase-3 inhibitor** (PDE3 inhibitor) and is classified as an **inotropic agent**. - It increases **intracellular cAMP** in cardiac cells, leading to increased **contractility** and **vasodilation**, and is used in severe heart failure. *Nicorandil* - **Nicorandil** is a **potassium channel opener** and a **nitrate-like drug** that causes both venous and arterial vasodilation. - It is primarily used as an **antianginal agent** due to its ability to reduce cardiac workload and improve coronary blood flow. *Ketorolac* - **Ketorolac** is a **nonsteroidal anti-inflammatory drug (NSAID)** that primarily inhibits **cyclooxygenase (COX) enzymes**. - It is used for **short-term management of acute moderate to severe pain** and has no direct activity on mineralocorticoid receptors.

Q: Which of the following is NOT a function of Prostaglandin E1 (PGE1)?

Plays a role in initiating puberty. ***Plays a role in initiating puberty*** - **Prostaglandin E1 (PGE1)** is primarily involved in smooth muscle relaxation, vasodilation, and inflammation, and does not have a direct role in initiating **puberty**. - The initiation of puberty is mainly controlled by the **hypothalamic-pituitary-gonadal (HPG) axis** and surge of **gonadotropin-releasing hormone (GnRH)**. *Used in the management of erectile dysfunction* - **PGE1 formulations** (alprostadil) are used as a topical or intracavernosal injection to treat **erectile dysfunction** by inducing vasodilation in the penis. - Its vasodilatory effects increase blood flow to the corpora cavernosa, leading to **penile erection**. *Modulates inflammatory responses* - **PGE1** is involved in **inflammatory processes**, often exerting both pro- and anti-inflammatory effects depending on the context and specific receptors activated. - It can help to **reduce inflammation** and pain, as well as influencing immune cell function. *Maintains the patency of the ductus arteriosus* - In newborns with **congenital heart defects**, **PGE1** is administered to maintain the **patency of the ductus arteriosus**, allowing for blood flow between the aorta and pulmonary artery. - This is crucial for conditions where pulmonary or systemic blood flow is dependent on a patent ductus, bridging the infant to surgery or other interventions.

Q: Most clinically significant side effect of topiramate requiring immediate medical attention?

Visual impairment. ***Visual impairment*** - Topiramate can cause **acute angle-closure glaucoma**, a medical emergency that typically occurs within the **first month of therapy**. - Mechanism: Topiramate causes **ciliary body swelling** and **uveal effusion**, leading to anterior rotation of the iris-lens diaphragm and angle closure. - Clinical presentation: Rapid-onset **blurred vision**, **eye pain**, **headache**, **redness**, and may progress to permanent vision loss if untreated. - Management: **Immediate discontinuation** of topiramate and urgent **ophthalmology referral** for intraocular pressure management. *Weight loss* - Weight loss is a common and often desired side effect of topiramate, related to its effect on **appetite suppression** and enhanced satiety. - While it can be significant, it does not typically require immediate medical attention unless it becomes excessive or leads to nutritional deficiencies. - This side effect is sometimes therapeutically exploited in migraine prophylaxis. *Insomnia* - Insomnia is a known side effect of topiramate and can impact quality of life but is generally not life-threatening or an immediate medical emergency. - Management often involves adjusting the dosage, timing of administration (dosing earlier in the day), or prescribing sleep aids. *Hemolysis* - Hemolysis is **not a recognized side effect** of topiramate. - Topiramate is not known to directly cause the destruction of red blood cells. - Other serious side effects of topiramate include metabolic acidosis, kidney stones, and cognitive impairment, but not hemolysis.

Q: Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?

Buspirone. ***Buspirone*** - **Buspirone** is a unique anxiolytic that primarily acts as a **partial agonist at 5-HT1A receptors**. - Unlike benzodiazepines, it lacks significant **anticonvulsant**, **muscle relaxant**, or **sedative-hypnotic properties** and does not lead to physical dependence or withdrawal. *Diazepam* - **Diazepam** is a **benzodiazepine** that acts by enhancing the effect of **GABA** at GABA-A receptors, leading to significant anxiolytic, sedative, muscle relaxant, and anticonvulsant effects. - It does not primarily act via **5-HT1A receptor partial agonism**. *Zolpidem* - **Zolpidem** is a **non-benzodiazepine hypnotic** that selectively binds to the **GABA-A receptor** subunit, primarily mediating sedative effects. - While it's used for insomnia, it doesn't primarily act as a **5-HT1A partial agonist** and is not typically used for its anxiolytic properties in the same way as buspirone. *Phenobarbitone* - **Phenobarbitone** is a **barbiturate** that acts by prolonging the opening of **chloride channels** associated with GABA-A receptors, leading to strong sedative, hypnotic, and anticonvulsant effects. - Its mechanism of action is distinct from **5-HT1A receptor partial agonism**, and it carries a high risk of dependence and overdose.

Q: Which of the following is an antipsychotic drug?

Flupenthixol. ***Flupenthixol*** - **Flupenthixol** is a **first-generation (typical) antipsychotic** used primarily for managing **schizophrenia** and other psychotic disorders. - It acts by blocking **dopamine D2 receptors** in the brain, reducing positive symptoms like **hallucinations and delusions**. *Rasagiline* - **Rasagiline** is a **monoamine oxidase-B (MAO-B) inhibitor** used in the treatment of **Parkinson's disease**. - It works by preventing the breakdown of **dopamine** in the brain, thereby improving motor symptoms, and is not an antipsychotic. *Clobazam* - **Clobazam** is a **benzodiazepine** primarily indicated for the treatment of **epilepsy** (specifically Lennox-Gastaut syndrome) and **anxiety**. - Its mechanism involves enhancing the effect of **GABA** in the brain, producing sedative and anticonvulsant effects, distinct from antipsychotic action. *Divalproex* - **Divalproex** is a combination product of **valproic acid** and **sodium valproate**, typically used as a **mood stabilizer** for **bipolar disorder**, an **antiepileptic**, and for **migraine prophylaxis**. - It modulates **GABAergic** transmission and sodium channels, but it is not classified as an antipsychotic drug.

Q: What is the primary indication for the use of Erlotinib?

NSCLC. ***NSCLC (Non-Small Cell Lung Cancer)*** - **Erlotinib** is primarily indicated for patients with advanced **non-small cell lung cancer (NSCLC)**, particularly those with activating mutations in the **epidermal growth factor receptor (EGFR)**. - It functions as an **EGFR tyrosine kinase inhibitor**, blocking the signaling pathways essential for cancer cell growth and survival. - This is the **FDA-approved primary indication** and where Erlotinib shows the most significant clinical benefit. *Pancreatic cancer* - While Erlotinib has been used in combination with gemcitabine for **locally advanced, unresectable or metastatic pancreatic cancer**, it is not its primary or most prominent indication. - Its efficacy in pancreatic cancer is generally modest and overshadowed by its dramatic impact in EGFR-mutated NSCLC. *Colon cancer* - **Erlotinib** is **not a primary treatment** for **colon cancer**. - Other targeted therapies (such as anti-EGFR monoclonal antibodies like cetuximab) or chemotherapy regimens are typically used for colorectal cancer. *Gall bladder cancer* - **Erlotinib** is generally **not indicated** for the treatment of **gallbladder cancer**. - Treatment often involves surgery, chemotherapy, or radiation, with targeted therapies being less established for this malignancy.

Q: What is the initial loading dose of chloroquine base for treating uncomplicated malaria in children?

10 mg/kg (maximum 600 mg). ***10 mg/kg (maximum 600 mg)*** - The standard **initial loading dose** of chloroquine base for uncomplicated malaria in children is **10 mg/kg body weight**, with a maximum cap of **600 mg** to prevent toxicity. - This is followed by **5 mg/kg** at 6 hours, 24 hours, and 48 hours (total course of 25 mg/kg over 3 days). - This represents **WHO-recommended** weight-based dosing for pediatric malaria treatment. *5 mg/kg* - **5 mg/kg** is the dose for the **subsequent doses** (at 6, 24, and 48 hours after the initial dose), not the initial loading dose. - The initial dose must be higher (10 mg/kg) to rapidly achieve therapeutic blood levels. *15 mg/kg* - **15 mg/kg** exceeds the recommended initial dose and increases the risk of **chloroquine toxicity**. - Chloroquine has a narrow therapeutic index, and overdosing can cause serious **cardiovascular** (arrhythmias, hypotension) and **neurological** effects (seizures, visual disturbances). *25 mg/kg* - **25 mg/kg** represents the **total cumulative dose** over the entire 3-day treatment course, not the initial single dose. - Giving this amount as a single dose would result in severe toxicity and is contraindicated.

Q: Which is a GABA transaminase inhibitor?

Valproate. ***Valproate*** - Valproate is known to inhibit **GABA transaminase**, an enzyme responsible for the breakdown of **gamma-aminobutyric acid (GABA)**. - By inhibiting this enzyme, valproate increases the concentration of **GABA** in the brain, enhancing its inhibitory effects and contributing to its anticonvulsant properties. *TCA* - **Tricyclic antidepressants (TCAs)** primarily work by inhibiting the reuptake of **norepinephrine** and **serotonin** in the brain. - They do not directly inhibit GABA transaminase but rather modulate monoamine neurotransmission. *Sertraline* - **Sertraline** is a **selective serotonin reuptake inhibitor (SSRI)** that works by blocking the reabsorption of **serotonin** into presynaptic neurons. - Its primary mechanism of action is focused on serotonin pathways, not on GABA metabolism. *Gabapentin* - **Gabapentin** is an anticonvulsant that is thought to exert its effects by modulating **calcium channels** and increasing **GABA synthesis**, but it is not a direct inhibitor of GABA transaminase. - Its mechanism of action is distinct from directly preventing GABA breakdown.

Q: Nesiritide causes vasodilation through?

Guanosine 3',5'-cyclic monophosphate (cGMP). ***Guanosine 3',5'-cyclic monophosphate (cGMP)*** - **Nesiritide** is a synthetic **B-type natriuretic peptide (BNP)** that acts as a potent vasodilator [2]. - It works by binding to **guanylyl cyclase receptors**, leading to an increase in intracellular **cGMP**, which promotes smooth muscle relaxation [1], [2]. *Cyclic adenosine monophosphate (cAMP)* - While **cAMP** is a crucial second messenger in various cellular processes and can mediate some forms of vasodilation, it is primarily associated with **beta-adrenergic receptor activation**, not the mechanism of action of nesiritide. - Nesiritide's pathway is distinct from those involving **cAMP-mediated** relaxation, which often involves different kinases and protein phosphorylation. *ATP* - **ATP** (adenosine triphosphate) is the primary **energy currency** of the cell and is involved in numerous cellular functions, including muscle contraction and relaxation, but it is not a direct mediator of nesiritide's vasodilatory effects. - Though ATP can be broken down to produce **adenosine**, which has vasodilatory properties, this is not the specific mechanism through which nesiritide causes vasodilation. *K+ ions* - Changes in **potassium ion (K+)** flux across cell membranes are essential for regulating vascular tone, as K+ channel activation can lead to hyperpolarization and relaxation of smooth muscle. - However, **nesiritide's primary mechanism** of action does not involve direct modulation of K+ channels; its vasodilatory effects are mediated by the **cGMP pathway** [2].

Question 1

Which drug is used for sympathectomy in experimental animals?

Accepted Answer

Guanethidine

Answer

Atropine

Answer

Diazoxide

Answer

Thebaine

Question 2

Which of the following is a mineralocorticoid antagonist?

Accepted Answer

Spironolactone

Answer

Inamrinone

Answer

Nicorandil

Answer

Ketorolac

Question 3

Which of the following is NOT a function of Prostaglandin E1 (PGE1)?

Accepted Answer

Plays a role in initiating puberty

Answer

Modulates inflammatory responses

Answer

Used in the management of erectile dysfunction

Answer

Maintains the patency of the ductus arteriosus

Question 4

Most clinically significant side effect of topiramate requiring immediate medical attention?

Accepted Answer

Visual impairment

Answer

Weight loss

Answer

Insomnia

Answer

Hemolysis

Question 5

Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?

Accepted Answer

Buspirone

Answer

Diazepam

Answer

Zolpidem

Answer

Phenobarbitone

Question 6

Which of the following is an antipsychotic drug?

Accepted Answer

Flupenthixol

Answer

Rasagiline

Answer

Clobazam

Answer

Divalproex

Question 7

What is the primary indication for the use of Erlotinib?

Accepted Answer

NSCLC

Answer

Colon cancer

Answer

Gall bladder cancer

Answer

Pancreatic cancer

Question 8

What is the initial loading dose of chloroquine base for treating uncomplicated malaria in children?

Accepted Answer

10 mg/kg (maximum 600 mg)

Answer

5 mg/kg

Answer

15 mg/kg

Answer

25 mg/kg

Question 9

Which is a GABA transaminase inhibitor?

Accepted Answer

Valproate

Answer

TCA

Answer

Gabapentin

Answer

Sertraline

Question 10

Nesiritide causes vasodilation through?

Accepted Answer

Guanosine 3',5'-cyclic monophosphate (cGMP)

Answer

ATP

Answer

Cyclic adenosine monophosphate (cAMP)

Answer

K+ ions

NEET-PG 2013 — Pharmacology