Central Nervous System Pharmacology Practice Questions

Q: All of the following act on the GABA receptor except?

Dexmedetomidine. **Explanation:** The correct answer is **Dexmedetomidine** because its mechanism of action is entirely independent of the GABAergic system. **1. Why Dexmedetomidine is the correct answer:** Dexmedetomidine is a highly selective **central alpha-2 ($\alpha_2$) adrenergic agonist**. It acts primarily on the locus coeruleus in the brainstem to induce sedation and analgesia. Unlike most intravenous anesthetics, it produces "conscious sedation" (the patient remains easily arousable) and does not cause significant respiratory depression. **2. Why the other options are incorrect:** * **Propofol:** Acts by facilitating inhibitory neurotransmission through **GABA-A receptors**. It increases the duration of chloride channel opening. * **Thiopentone (Barbiturates):** Acts on the **GABA-A receptor** at a site distinct from benzodiazepines. At low doses, it increases the duration of chloride channel opening; at high doses, it can directly mimic GABA (GABA-mimetic action). * **Etomidate:** A carboxylated imidazole derivative that acts as a potent and selective **GABA-A receptor** modulator, specifically enhancing the effects of GABA. **High-Yield Clinical Pearls for NEET-PG:** * **Dexmedetomidine:** Known for its "analgesic-sparing effect" and is the drug of choice for sedation in the ICU for non-intubated patients. A common side effect is bradycardia. * **Etomidate:** Best for hemodynamically unstable patients (cardiovascular stability) but can cause **adrenocortical suppression** by inhibiting the enzyme 11-beta-hydroxylase. * **Propofol:** Drug of choice for Day Care Surgery due to rapid recovery and anti-emetic properties. * **Ketamine:** Unlike the others, this acts on **NMDA receptors** (antagonist) and is the only induction agent that stimulates the sympathetic nervous system.

Q: Which of the following is a vasoconstrictor?

None of the above. **Explanation:** The fundamental pharmacological property of almost all local anesthetics (LAs) is **vasodilation**. They achieve this by relaxing the vascular smooth muscle. This vasodilation increases the rate of systemic absorption, shortens the duration of the block, and increases the risk of systemic toxicity. **Why "None of the above" is correct:** Options A, B, and C (Bupivacaine, Procaine, and Lidocaine) are all potent vasodilators. Therefore, none of them act as vasoconstrictors. In clinical practice, a vasoconstrictor like **Adrenaline (Epinephrine)** is often added to these drugs to counteract their vasodilatory effects, thereby prolonging the duration of action and reducing surgical bleeding. **Analysis of Options:** * **Bupivacaine:** A long-acting amide LA. It is a potent vasodilator and is notably the most cardiotoxic LA. * **Procaine:** An ester-linked LA. It is a very strong vasodilator with a short duration of action. * **Lidocaine:** The most commonly used amide LA. It causes significant vasodilation, which is why it is frequently formulated with adrenaline (1:200,000). **High-Yield NEET-PG Pearls:** 1. **The Exceptions:** **Cocaine** is the only naturally occurring LA that is a potent **vasoconstrictor** (it inhibits norepinephrine reuptake). 2. **Modern Exceptions:** Among synthetic LAs, **Ropivacaine** and **Levobupivacaine** possess mild intrinsic vasoconstrictive properties at lower concentrations. 3. **Adrenaline Addition:** Adding adrenaline to LAs is contraindicated in "end-artery" areas (fingers, toes, penis, nose, and earlobes) due to the risk of ischemic necrosis. 4. **Prilocaine:** Another amide LA that has minimal vasodilatory effects compared to lidocaine.

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.

Question 1

All of the following act on the GABA receptor except?

Accepted Answer

Dexmedetomidine

Answer

Propofol

Answer

Thiopentone

Answer

Etomidate

Question 2

Regarding phenytoin, all are true except?

Accepted Answer

At lower concentrations, it follows zero-order kinetics

Answer

Potent microsomal enzyme inducer

Answer

Highly protein bound

Answer

With increasing dose, the Vmax increases.

Question 3

Which of the following is a vasoconstrictor?

Accepted Answer

None of the above

Answer

Bupivacaine

Answer

Procaine

Answer

Lidocaine

Question 4

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 5

Which of the following drugs is used for smoking cessation?

Accepted Answer

Bupropion

Answer

Buspirone

Answer

Venlafaxine

Answer

Fluoxetine

Question 6

Which drug is contraindicated for use along with local anaesthetics?

Accepted Answer

Noradrenaline

Answer

Dopamine

Answer

Dobutamine

Answer

Adrenaline

Question 7

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 8

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 9

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 10

Which drug is effective in the treatment of Tardive dyskinesia?

Accepted Answer

Tetrabenazine

Answer

Central anticholinergic

Answer

Dantrolene

Answer

Succinylcholine

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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