Central Nervous System Pharmacology Practice Questions

Q: All of the following are true regarding lidocaine except:

It is the most cardiotoxic local anesthetic.. **Explanation:** **Why Option B is the correct answer (The "Except" statement):** Lidocaine is actually known for its relatively low cardiotoxicity compared to other local anesthetics. **Bupivacaine** is the most cardiotoxic local anesthetic; it binds more tightly to sodium channels during diastole ("slow-in, slow-out" kinetics), making resuscitation from bupivacaine-induced cardiac arrest extremely difficult. Lidocaine, conversely, dissociates rapidly from the channels. **Analysis of other options:** * **Option A:** Local anesthetics like lidocaine follow the "state-dependent blockade" principle. They have a higher affinity for sodium channels in the **active** (open) and **inactive** (refractory) states rather than the resting state. * **Option C:** Lidocaine is a **Class IB anti-arrhythmic**. It is administered intravenously to treat ventricular arrhythmias, particularly those associated with acute myocardial infarction or cardiac surgery. * **Option D:** Lidocaine undergoes **extensive first-pass metabolism** in the liver (extraction ratio >0.7). Therefore, it cannot be administered orally for systemic effects and requires parenteral administration. **NEET-PG High-Yield Pearls:** * **Drug of Choice:** Lidocaine is the most widely used local anesthetic due to its rapid onset and intermediate duration of action. * **Bupivacaine Toxicity:** If bupivacaine toxicity occurs, the antidote is **Intravenous Lipid Emulsion (20% Intralipid)**. * **Metabolism:** Lidocaine is metabolized by hepatic CYP1A2 to active metabolites (MEGX and glycine xylidide), which can contribute to toxicity (seizures). * **Adrenaline Co-administration:** Often added to lidocaine to cause vasoconstriction, which decreases systemic absorption, reduces toxicity, and prolongs the duration of the block.

Q: Which of the following drugs is used for smoking cessation?

Bupropion. **Explanation:** **Bupropion (Option A)** is the correct answer. It is an atypical antidepressant that acts as a **Norepinephrine-Dopamine Reuptake Inhibitor (NDRI)**. In the context of smoking cessation, it works by increasing dopamine levels in the nucleus accumbens, which mimics the reward pathway of nicotine and reduces withdrawal symptoms and the urge to smoke. It is FDA-approved for this purpose and is often started 1–2 weeks before the "quit date." **Why the other options are incorrect:** * **Buspirone (Option B):** A selective 5-HT1A partial agonist used primarily as an **anxiolytic** for Generalized Anxiety Disorder (GAD). It has no proven efficacy in smoking cessation. * **Venlafaxine (Option C):** A Serotonin-Norepinephrine Reuptake Inhibitor (SNRI) used for major depression and panic disorders. While it affects neurotransmitters, it is not a first-line agent for nicotine addiction. * **Fluoxetine (Option D):** A Selective Serotonin Reuptake Inhibitor (SSRI). Although it treats depression (which can be comorbid with nicotine dependence), clinical trials have shown it is not effective for smoking cessation. **High-Yield Clinical Pearls for NEET-PG:** * **Varenicline** (a nicotinic α4β2 partial agonist) is currently considered the most effective monotherapy for smoking cessation. * **Contraindication:** Bupropion is strictly contraindicated in patients with **seizure disorders** or **eating disorders** (bulimia/anorexia) as it lowers the seizure threshold. * **Weight Gain:** Bupropion is a preferred choice for smokers concerned about post-cessation weight gain, as it tends to delay weight increase.

Q: Which drug is contraindicated for use along with local anaesthetics?

Noradrenaline. ### Explanation **Core Concept: Vasoconstriction and Tissue Necrosis** Local anesthetics (LAs) are often combined with vasoconstrictors (like Adrenaline) to prolong the duration of action, decrease systemic toxicity, and provide a bloodless surgical field. However, **Noradrenaline** is contraindicated for this purpose. **Why Noradrenaline is the Correct Answer:** Noradrenaline is a potent **alpha-1 adrenergic agonist** with minimal beta-2 activity. When injected locally, it causes intense, prolonged vasoconstriction. This can lead to severe localized ischemia, tissue hypoxia, and subsequent **tissue necrosis or sloughing** at the injection site. Unlike adrenaline, which has balanced alpha and beta effects (causing some vasodilation in skeletal muscle), noradrenaline’s vasoconstriction is too aggressive for safe local infiltration. **Analysis of Incorrect Options:** * **Adrenaline (Option C):** This is the **gold standard** vasoconstrictor used with LAs (usually in a 1:200,000 concentration). It effectively delays absorption without the extreme ischemic risk associated with noradrenaline. * **Dopamine & Dobutamine (Options A & B):** These are primarily used as inotropic/vasopressor agents in critical care (e.g., shock or heart failure). They are not used as adjuncts to local anesthesia, but they are not specifically "contraindicated" in the same pharmacological context as noradrenaline regarding local tissue necrosis. **High-Yield Clinical Pearls for NEET-PG:** * **The "End-Artery" Rule:** Even with Adrenaline, avoid use in areas supplied by end-arteries (fingers, toes, nose, ears, and penis) to prevent gangrene. * **Maximum Dose:** The addition of Adrenaline increases the maximum safe dose of Lignocaine from **3 mg/kg to 7 mg/kg**. * **Felypressin:** A synthetic vasopressin derivative used as an alternative to adrenaline in dental anesthesia, especially for patients where catecholamines are risky (e.g., hyperthyroidism).

Q: Which of the following drugs, proposed for the management of opioid addiction, blocks the action of injected heroin for up to 48 hours with a single dose, and does not activate opioid receptors?

Naltrexone. **Explanation:** The correct answer is **Naltrexone**. **Why Naltrexone is correct:** Naltrexone is a long-acting, competitive **opioid antagonist**. Unlike agonists, it has no intrinsic activity and does not activate opioid receptors (it has zero efficacy). By binding to the $\mu$-opioid receptors with high affinity, it competitively blocks the effects of exogenous opioids like heroin. Its primary clinical advantage in addiction management is its long half-life; a single oral dose can effectively block the "high" of heroin for **48 to 72 hours**, thereby aiding in the prevention of relapse in highly motivated patients. **Why the other options are incorrect:** * **Amphetamine (A):** This is a CNS stimulant that increases synaptic dopamine and norepinephrine. It has no role in blocking opioid receptors and is itself a drug of abuse. * **Buspirone (B):** An anxiolytic that acts as a partial agonist at 5-HT1A receptors. It is used for Generalized Anxiety Disorder (GAD) and does not interact with the opioid system. * **Methadone (C):** While used in opioid addiction, methadone is a **long-acting $\mu$-opioid agonist**. It *does* activate receptors (providing "substitution therapy") to prevent withdrawal symptoms. It does not block heroin via antagonism but rather through cross-tolerance. **High-Yield Clinical Pearls for NEET-PG:** * **Naltrexone vs. Naloxone:** Naloxone is short-acting (30–90 mins) and used for **acute opioid overdose** (IV). Naltrexone is long-acting and used for **maintenance/relapse prevention** and **alcohol dependence** (reduces craving). * **Prerequisite:** Naltrexone must only be started after a patient is opioid-free for 7–10 days to avoid precipitating severe **acute withdrawal syndrome**. * **Vivitrol:** This is the injectable, extended-release formulation of naltrexone administered once monthly.

Q: Administration of which antiepileptic drug is associated with the development of hyperldnesia in children?

Phenobarbitone. **Explanation:** The correct answer is **Phenobarbitone**. **Mechanism and Rationale:** Phenobarbitone is a long-acting barbiturate that acts as a GABA-A receptor agonist, increasing the duration of chloride channel opening. While it is an effective anticonvulsant, it has a paradoxical effect on the behavior of children. Instead of sedation, it frequently causes **behavioral disturbances**, specifically **hyperkinesia** (hyperactivity), irritability, and decreased cognitive performance. This "paradoxical excitement" is a classic side effect often tested in exams. **Analysis of Incorrect Options:** * **Phenytoin sodium:** Primarily associated with gingival hyperplasia, hirsutism, and osteomalacia. In children, it can cause coarsening of facial features but not typically hyperkinesia. * **Sodium valproate:** Known for weight gain, alopecia, and hepatotoxicity. It is generally sedating rather than activating. * **Carbamazepine:** Common side effects include diplopia, ataxia, and hyponatremia (SIADH). It is rarely associated with hyperactivity in children. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Phenobarbitone remains the DOC for **Neonatal Seizures**. * **Paradoxical Effect:** While it causes sedation in adults, it causes **hyperactivity/irritability in children** and **confusion/agitation in the elderly**. * **Metabolism:** It is a potent **microsomal enzyme inducer**, leading to numerous drug-drug interactions (e.g., reducing the efficacy of oral contraceptives or warfarin). * **Contraindication:** It is strictly contraindicated in patients with **Acute Intermittent Porphyria** as it induces ALA synthase.

Q: Which drug is effective in the treatment of Tardive dyskinesia?

Tetrabenazine. **Explanation:** **Tardive Dyskinesia (TD)** is a late-onset extrapyramidal side effect caused by chronic use of dopamine receptor blockers (antipsychotics). It is characterized by involuntary, repetitive movements (e.g., lip-smacking, tongue protrusion) due to **dopamine receptor supersensitivity** in the nigrostriatal pathway. **Why Tetrabenazine is correct:** Tetrabenazine is a reversible inhibitor of the **Vesicular Monoamine Transporter 2 (VMAT2)**. By inhibiting VMAT2, it prevents the storage of dopamine in presynaptic vesicles, leading to dopamine depletion in the synaptic cleft. Reducing the amount of dopamine available to stimulate the supersensitive receptors effectively alleviates the involuntary movements of TD. (Note: Valbenazine and Deutetrabenazine are newer, more selective VMAT2 inhibitors). **Why the other options are incorrect:** * **A. Central anticholinergics (e.g., Benztropine, Trihexyphenidyl):** These are used to treat *acute* extrapyramidal symptoms like dystonia or parkinsonism. However, in TD, they can actually **worsen** symptoms by further shifting the dopamine-acetylcholine balance. * **B. Dantrolene:** This is a peripherally acting muscle relaxant (ryanodine receptor antagonist) used primarily for **Malignant Hyperthermia** and Neuroleptic Malignant Syndrome (NMS). * **C. Succinylcholine:** This is a depolarizing neuromuscular blocker used for rapid sequence induction in anesthesia; it has no role in chronic movement disorders. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for TD:** VMAT2 inhibitors (Tetrabenazine/Valbenazine). * **Paradoxical Management:** The first step in TD management is often reducing the dose of the offending antipsychotic or switching to **Clozapine** (the antipsychotic with the lowest risk of TD). * **Tetrabenazine Side Effect:** It can cause significant depression and suicidality due to systemic depletion of serotonin and norepinephrine.

Q: All of the following drugs are used in the treatment of dementia except?

Duloxetine. **Explanation:** The treatment of dementia, particularly Alzheimer’s disease, focuses on enhancing cholinergic transmission or modulating glutamatergic excitability. **Why Duloxetine is the correct answer:** **Duloxetine** is a **Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)**. It is primarily used as an antidepressant, anxiolytic, and for the management of chronic pain conditions like diabetic peripheral neuropathy and fibromyalgia. It has **no established role** in the cognitive enhancement or pathophysiology of dementia. **Analysis of incorrect options:** * **Donepezil & Galantamine (Options C & D):** These are **Reversible Acetylcholinesterase Inhibitors (AChEIs)**. By inhibiting the breakdown of acetylcholine in the synaptic cleft, they compensate for the cholinergic deficit seen in Alzheimer’s. They are first-line treatments for mild-to-moderate dementia. (Note: Rivastigmine is another drug in this class). * **Memantine (Option A):** This is an **NMDA receptor antagonist**. It works by blocking pathological "noise" from excessive glutamate stimulation, which prevents excitotoxicity. It is typically used for moderate-to-severe Alzheimer’s, often in combination with Donepezil. **High-Yield Clinical Pearls for NEET-PG:** * **Rivastigmine** is the only AChEI available as a **transdermal patch**, which improves compliance and reduces GI side effects. * **Common Side Effects of AChEIs:** Diarrhea, nausea, and bradycardia (SLUDGE effects). * **Newer Drug:** **Aducanumab** and **Lecanemab** are monoclonal antibodies targeting amyloid-beta plaques, recently approved for early-stage Alzheimer's. * **Vascular Dementia:** Management focuses on controlling risk factors (Aspirin, Statins) rather than specific cognitive enhancers.

Q: Which of the following is NOT a side effect of fenfluramine?

Dizziness. **Explanation:** Fenfluramine is a sympathomimetic amine that was primarily used as an appetite suppressant (anorectic). Its mechanism involves the release of serotonin (5-HT) and inhibition of its reuptake. **Why Dizziness is the correct answer:** While fenfluramine can cause central nervous system effects, **dizziness** is not a characteristic or hallmark side effect associated with its clinical profile or its withdrawal from the market. In fact, unlike other amphetamine derivatives, fenfluramine often causes **sedation** or drowsiness rather than stimulation or dizziness. **Analysis of Incorrect Options:** * **Pulmonary Hypertension:** Fenfluramine is notorious for causing primary pulmonary hypertension (PPH). This occurs due to increased circulating serotonin levels, which cause vasoconstriction and smooth muscle proliferation in the pulmonary vasculature. * **Valvular Defects:** The drug was famously withdrawn from the market (along with dexfenfluramine) because it caused **cardiac valvulopathy** (specifically thickening of the mitral and aortic valves). This is mediated by the activation of **5-HT2B receptors** located on cardiac valves. * **Sudden Deaths:** Due to the severity of pulmonary hypertension and cardiac valvular damage, several cases of sudden cardiac death were reported, leading to its ban by the FDA in 1997. **High-Yield Clinical Pearls for NEET-PG:** * **"Fen-Phen" Combination:** The combination of Fenfluramine and Phentermine was popular for weight loss but led to the "epidemic" of valvular heart disease. * **Current Use:** Low-dose fenfluramine has recently been repurposed and FDA-approved for the treatment of seizures associated with **Dravet syndrome** and **Lennox-Gastaut syndrome**. * **Key Receptor:** Always associate **5-HT2B receptor agonism** with drug-induced valvular heart disease (also seen with Ergotamine and Pergolide).

Q: Selective decrease in IgA is seen with administration of which of the following drugs?

Phenytoin. **Explanation:** **Phenytoin** is a classic hydantoin anticonvulsant known for a unique side effect profile. The selective decrease in **Serum IgA** levels occurs in approximately 20–25% of patients treated with Phenytoin. The underlying mechanism involves the inhibition of B-cell differentiation into IgA-secreting plasma cells. While often asymptomatic, this can occasionally lead to an increased frequency of upper respiratory tract infections or contribute to the development of gingival hyperplasia. **Analysis of Options:** * **Phenytoin (Correct):** It is the only drug among the options consistently associated with selective IgA deficiency. It also causes other immunological effects like the DRESS syndrome and Stevens-Johnson Syndrome (SJS). * **Diazepam & Clonazepam (Incorrect):** These are Benzodiazepines (BZDs) that act via GABA-A receptors. They do not have significant effects on immunoglobulin levels or the humoral immune system. * **Phenobarbitone (Incorrect):** While it is a long-acting barbiturate used for epilepsy, it is not associated with selective IgA deficiency. Its primary side effects include sedation, cognitive impairment, and osteomalacia. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Phenytoin Side Effects (HOT MALAI):** **H**irsutism, **O**steomalacia, **T**eratogenicity (Fetal Hydantoin Syndrome), **M**egaloblastic anemia (due to folate deficiency), **A**taxia, **L**ymphadenopathy, **A**rrhythmias (on rapid IV), **I**nsulin inhibition (hyperglycemia), and **Gingival Hyperplasia**. * Phenytoin follows **Zero-order kinetics** (Capacity-limited elimination) at therapeutic or high concentrations. * It is a potent **Inducer** of Cytochrome P450 enzymes.

Question 1

All of the following are true regarding lidocaine except:

Accepted Answer

It is the most cardiotoxic local anesthetic.

Answer

It acts on sodium channels in both active and inactive states.

Answer

It is given intravenously for cardiac arrhythmias.

Answer

It undergoes extensive first-pass metabolism.

Question 2

Which of the following drugs is used for smoking cessation?

Accepted Answer

Bupropion

Answer

Buspirone

Answer

Venlafaxine

Answer

Fluoxetine

Question 3

Which drug is contraindicated for use along with local anaesthetics?

Accepted Answer

Noradrenaline

Answer

Dopamine

Answer

Dobutamine

Answer

Adrenaline

Question 4

What is the mechanism of action of valproic acid?

Accepted Answer

Inhibition of 'T' type Ca+2 current

Answer

Inhibition of Na+ channel inactivation

Answer

Inhibition of GABA

Answer

Opening of K+ channels

Question 5

Which of the following drugs, proposed for the management of opioid addiction, blocks the action of injected heroin for up to 48 hours with a single dose, and does not activate opioid receptors?

Accepted Answer

Naltrexone

Answer

Amphetamine

Answer

Buspirone

Answer

Methadone

Question 6

Administration of which antiepileptic drug is associated with the development of hyperldnesia in children?

Accepted Answer

Phenobarbitone

Answer

Phenytoin sodium

Answer

Sodium valproate

Answer

Carbamazepine

Question 7

Which drug is effective in the treatment of Tardive dyskinesia?

Accepted Answer

Tetrabenazine

Answer

Central anticholinergic

Answer

Dantrolene

Answer

Succinylcholine

Question 8

All of the following drugs are used in the treatment of dementia except?

Accepted Answer

Duloxetine

Answer

Memantine

Answer

Galantamine

Answer

Donepezil

Question 9

Which of the following is NOT a side effect of fenfluramine?

Accepted Answer

Dizziness

Answer

Pulmonary hypertension

Answer

Valvular defects

Answer

Sudden deaths

Question 10

Selective decrease in IgA is seen with administration of which of the following drugs?

Accepted Answer

Phenytoin

Answer

Diazepam

Answer

Clonazepam

Answer

Phenobarbitone

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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