• Questions 1-56: No answers provided (need to answer these)
• Questions 57-79+: Answers already provided in the document

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Answers to All Neuropharmacology Questions

Questions 1-56 (Answers Provided Below)

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• A is wrong: Benzodiazepines do NOT directly open Cl- channels - they bind to the GABA-A receptor and enhance the frequency of Cl- channel opening in response to GABA.
• B is wrong: Benzodiazepines have no analgesic action.
• C is wrong: Anxiety improvement occurs within days to 1 week, not 2-4 weeks (that timeline applies to antidepressants).
• D is correct: All benzodiazepines produce some degree of sedation.
• E is wrong: Unlike barbiturates, benzodiazepines do NOT produce general anesthesia even in high doses (a key safety advantage).

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• Triazolam has a very short half-life (~2-5 hours), making it useful as a hypnotic for sleep onset.
• Phenobarbital (A) is long-acting.
• Diazepam (B) is long-acting (~20-70 hours).
• Chlordiazepoxide (C) is long-acting.
• Flurazepam (E) is long-acting (active metabolites last 40-250 hours).

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• A is wrong: Phenobarbital has no analgesic properties.
• B is wrong: Diazepam does NOT induce cytochrome P450; phenobarbital does, but diazepam does not.
• C is wrong: Phenobarbital is absolutely contraindicated in acute intermittent porphyria (it induces ALA synthase and worsens the condition).
• D is correct: Phenobarbital causes dose-dependent respiratory depression, and ethanol synergistically enhances this CNS/respiratory depression.
• E is wrong: Buspirone acts on 5-HT1A receptors and has a completely different mechanism from benzodiazepines - it has no cross-tolerance with them.

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• It is intermediate-acting and reliable IM/IV absorption.
• It prevents and treats withdrawal seizures.
• Pentobarbital (C) is not first-line.
• Phenytoin (D) is ineffective for alcohol withdrawal seizures.
• Buspirone (E) is for chronic anxiety, not acute withdrawal.

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• Sexual dysfunction (anorgasmia, decreased libido) is a common SSRI side effect.
• Mirtazapine (NaSSA) has low rates of sexual dysfunction and can actually counter SSRI-induced sexual dysfunction.
• Fluvoxamine (A), Sertraline (B), Citalopram (C) are all SSRIs and would perpetuate the same problem.
• Lithium (E) is for bipolar/augmentation, not appropriate here.

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• Tricyclic antidepressants (TCAs) like amitriptyline have potent anticholinergic effects that cause mydriasis (pupil dilation), which can precipitate acute angle-closure glaucoma in susceptible patients.
• SSRIs (sertraline, fluvoxamine) and bupropion are safer options.

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• SSRIs are first-line for OCD. Fluvoxamine is specifically FDA-approved for OCD.
• Imipramine (A) and amitriptyline (C) are TCAs - not first-line for OCD.
• Tranylcypromine (D) is an MAOI - not appropriate first-line.
• Lithium (E) is for bipolar disorder.

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• Risperidone (atypical/second-generation antipsychotic) has demonstrated benefit for negative symptoms.
• Chlorpromazine (A), Fluphenazine (B), Haloperidol (C), and Thioridazine (E) are all typical antipsychotics - they treat positive symptoms but have little benefit for negative symptoms.

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• Aripiprazole is unique as a D2 partial agonist - it acts as an agonist when dopamine is low and as a functional antagonist when dopamine is high.
• All other listed agents (clozapine, haloperidol, risperidone, thioridazine) are pure D2 antagonists.

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• The patient is experiencing acute dystonia (extrapyramidal side effect) from pimozide (a D2 blocker).
• Benztropine is a centrally-acting anticholinergic that counteracts the dopamine-acetylcholine imbalance in the striatum caused by dopamine blockade.
• (This is confirmed in the document's answer to Q77 - the repeat version.)

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• Chlorpromazine is a low-potency typical antipsychotic with strong sedative (antihistamine) properties, making it useful when insomnia is a major complaint.
• (Confirmed in document's answer to Q78.)

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• Classic absence seizures: sudden brief staring, behavioral arrest, no aura, no post-ictal confusion, abrupt offset.
• The prolonged recovery time described in Q14 suggests complex partial (see Q14 below).

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• Key distinguishing feature: prolonged post-ictal recovery (minutes) is characteristic of complex partial seizures, NOT absence seizures.
• Absence seizures have no post-ictal phase and recovery is instantaneous.

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• Carbamazepine is first-line for focal (partial) seizures including complex partial.
• Ethosuximide (A) is for absence seizures only, not effective for partial seizures.
• Diazepam (C) is for acute seizure termination, not maintenance.

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• Levetiracetam has minimal protein binding, no hepatic CYP induction/inhibition, and is renally excreted unchanged - making it the drug with the least pharmacokinetic interaction with carbamazepine.
• Carbamazepine is a potent CYP3A4 inducer and will lower levels of lamotrigine (D), topiramate (A), tiagabine (B), and zonisamide (E).

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• A is wrong: Active metabolites matter for some (e.g., thioridazine → mesoridazine), but this is not universally "important to action."
• B is correct: Haloperidol has ~40-75% bioavailability; chlorpromazine and thioridazine have extensive first-pass metabolism (~30% bioavailability).
• C is wrong: Elimination half-lives of antipsychotics are typically 20-40 hours, not 3-6 hours.
• D is wrong: Clinical duration of action is long (often weeks), not short.
• E is wrong: Clozapine is a dibenzodiazepine, not a dihydroindolone. Molindone is the dihydroindolone.

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• Thioridazine blocks cardiac potassium channels (hERG), prolongs the QTc interval, and can cause fatal ventricular arrhythmias (torsades de pointes). This is why it is now restricted to treatment-resistant cases only.
• Chlorpromazine (A) has some QT effects but less severe.
• Haloperidol (D) also has some QT effects but thioridazine is the classic answer.

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• During pregnancy: Renal clearance of lithium INCREASES, so lithium levels FALL (less toxic risk during pregnancy; dose may need to be increased).
• Post-partum: Renal clearance returns to normal suddenly, lithium levels RISE and toxicity risk increases.
• Thiazides (B): Reduce lithium excretion → toxicity.
• Dehydration (C): Reduces renal clearance → toxicity.
• NSAIDs (D): Reduce renal lithium clearance → toxicity.

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• A is correct: TCAs, SSRIs, and SNRIs are highly protein bound (>90%).
• B is wrong: Fluoxetine is well absorbed orally (~72% bioavailability).
• C is wrong: Tricyclics are extensively metabolized hepatically; little is excreted unchanged in urine.
• D is wrong: Half-lives are typically 12-36 hours for most antidepressants (fluoxetine is days to weeks).
• E is wrong: The older MAOIs (phenelzine, tranylcypromine) bind irreversibly to MAO, so their clinical duration extends far beyond their pharmacokinetic half-life; half-life does NOT govern dosing intervals.

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• Amoxapine is a tetracyclic antidepressant that can cause seizures and severe cardiotoxicity in overdose, making single-drug overdose dangerous.
• Moclobemide (A) is a reversible MAOI with a wide safety margin in overdose.
• SSRIs like paroxetine (B) and sertraline (C) are relatively safe in overdose.
• Trazodone (D) is generally safer than TCAs in overdose (priapism is its main concern).

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• Diazepam is approximately 98-99% protein bound to albumin.
• Gentamicin (A): <10% protein bound.
• Theophylline (B): ~40-60% bound.
• Carbamazepine (C): ~75% bound.
• Atenolol (D): <10% protein bound.

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• Barbiturates are the classic trigger for acute porphyria - they induce ALA synthase (the rate-limiting enzyme in heme synthesis), dramatically increasing porphyrin precursor accumulation.
• Zolpidem (A), chloral hydrate (B), and diazepam (E) also carry some risk, but phenobarbitone is the absolute contraindication.
• Buspirone (C) is considered relatively safe.

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• A is wrong: Lignocaine (lidocaine) is a Class IB antiarrhythmic, not Class IA (Class IA includes quinidine, procainamide).
• B is wrong: At normal physiological pH (7.4), most local anaesthetics (pKa ~8-9) exist predominantly in the ionized (charged) form - the uncharged form is the minority but is what crosses the membrane.
• C is wrong: Bupivacaine can cause methemoglobinemia - that's prilocaine. Bupivacaine causes cardiac toxicity.
• D is wrong: Procaine is an ester metabolized by plasma pseudocholinesterase, not the liver, so liver disease does not prolong its duration.
• E is correct: Small, lightly myelinated A-delta fibers (pain/temperature) are blocked before large myelinated motor fibers - this is the basis for differential nerve block.

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• A is wrong: Ketamine is CONTRAINDICATED in head injury (it raises intracranial pressure).
• B is wrong: Propofol has a rapid onset AND rapid offset due to high lipid solubility and redistribution.
• C is wrong: Etomidate is notable for causing LESS cardiovascular depression/hypotension than thiopentone - not more.
• D is correct: Neuroleptanalgesia combines an opioid (fentanyl) with a butyrophenone neuroleptic (droperidol) to produce a state of analgesia and reduced anxiety without full unconsciousness.
• E is wrong: Thiopentone is metabolised at only about 10-15% per hour, not 40-50%.

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• A is wrong: Suxamethonium (succinylcholine) is a DEPOLARISING neuromuscular blocker, not non-depolarising.
• B is wrong: It is contraindicated in penetrating eye injuries specifically (raises intraocular pressure), but not ALL eye operations.
• C is correct: Suxamethonium mimics acetylcholine at all cholinergic receptors including cardiac muscarinic (causing bradycardia) and nicotinic autonomic ganglia.
• D is correct in mechanism, but the question is "which statement is correct" - C is more specifically accurate.
• E is wrong: Suxamethonium causes HYPERkalaemia (not hypercalcaemia) in burns >24 hours old, due to upregulation of extrajunctional acetylcholine receptors.

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• A is correct: Isoflurane provides coronary vasodilation and is commonly used in cardiac surgery; however, it can cause "coronary steal." Sevoflurane is actually now preferred, but among the options listed, isoflurane is the traditional answer for IHD.
• B is wrong: Nitrous oxide is teratogenic (inhibits methionine synthase/folate pathway) and is contraindicated in the first trimester.
• C is wrong: Halothane's MAC is ~0.75%, not 75%. Desflurane's MAC is ~6-7%, making halothane MORE potent than desflurane (lower MAC = higher potency).
• D is wrong: Desflurane undergoes minimal hepatic metabolism (<0.02%), making it one of the safest in terms of hepatotoxicity.

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• A is wrong: Phenytoin is ~90% protein bound to albumin, not 20-30%.
• B is wrong: Ethosuximide (or valproate) is the drug of choice for absence seizures, not phenytoin (which can worsen absence seizures).
• C is wrong: Phenytoin undergoes capacity-limited (zero-order/Michaelis-Menten) elimination, not flow-limited elimination.
• D is correct: Because phenytoin follows non-linear (zero-order) kinetics at therapeutic doses, small dose increases can produce disproportionately large increases in plasma concentration - this is clinically very important.
• E is wrong: Phenytoin preferentially binds to the INACTIVATED state of sodium channels (not activated state). This is what gives it selectivity for rapidly firing neurons.

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• A is wrong: Ketamine is structurally related to phencyclidine (PCP), not psilocybin.
• B is correct: LSD is a potent serotonin (5-HT2A) agonist; it also acts on other 5-HT subtypes.
• C is wrong: Marijuana causes MYDriasis (pupil dilation) - wait, actually marijuana typically causes CONJUNCTIVAL INJECTION (redness) and may cause mild miosis or no change in pupil size; the word in the document says "conjunctival infection" but the correct term is "conjunctival injection." Mydriasis is associated with stimulants. This option is partially misleading.
• D is wrong: Cocaine has a SHORT plasma half-life (~1 hour).
• E is wrong: Amphetamines SUPPRESS appetite (anorexigenic), not stimulate it.

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• A is wrong: Flumazenil is cleared hepatically, not renally.
• B is wrong: Flumazenil does NOT predictably reverse benzodiazepine-induced respiratory depression - reversal is variable, and the benzodiazepine effect may outlast flumazenil.
• C is wrong: Flumazenil antagonizes benzodiazepines, NOT opioids (naloxone/naltrexone is for opioids).
• D is correct: In patients chronically dependent on benzodiazepines or with mixed overdose (e.g., benzodiazepine + TCA), flumazenil can precipitate seizures by unmasking TCA toxicity or triggering benzodiazepine withdrawal.
• E is wrong: Flumazenil has a very short half-life of approximately 1 hour (not 10 hours), which is why re-sedation occurs.

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• A is correct: Pancuronium is predominantly renally excreted (~80%) and must be used with caution in renal failure.
• B is wrong: Rocuronium is an AMINOSTEROID derivative, not an isoquinolone. (Isoquinolines include atracurium, cisatracurium, mivacurium.)
• C is wrong: Rocuronium does NOT undergo Hofmann elimination - atracurium and cisatracurium do.
• D is wrong: Vecuronium is eliminated predominantly via the BILIARY/HEPATIC route (~50% biliary), with some renal excretion.
• E is wrong: Atracurium undergoes Hofmann elimination (spontaneous chemical degradation at body pH and temperature) AND ester hydrolysis - NOT plasma pseudocholinesterase. Mivacurium is hydrolyzed by pseudocholinesterase.

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• Sumatriptan is a 5-HT1B/1D receptor agonist used in acute migraine treatment.
• Fluoxetine (A) blocks serotonin reuptake (indirect increase in serotonin).
• Amitriptyline (B) blocks serotonin and norepinephrine reuptake (TCA).
• Moclobemide (C) inhibits MAO-A, reducing serotonin breakdown (indirect).
• Ondansetron (D) is a 5-HT3 antagonist (antiemetic), not an agonist.

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• Pethidine is metabolized to norpethidine (normeperidine), which accumulates in renal failure and is a potent CNS stimulant that causes tremors, myoclonus, and seizures.
• Morphine (A) accumulates toxic metabolite morphine-6-glucuronide in renal failure (causes respiratory depression, not seizures).

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• A is correct: Ethanol is lipid soluble (small, amphipathic molecule), allowing it to cross the blood-brain barrier rapidly.
• B is wrong: The MEOS system is activated at HIGHER blood concentrations (>100 mg/dL); at lower levels, alcohol dehydrogenase (ADH) is the primary pathway.
• C is also correct: Ethanol causes peripheral vasodilation (flushing, warmth sensation), though it does NOT raise core temperature.
• D is wrong: The most common neurological complication of chronic alcoholism is a SYMMETRICAL peripheral neuropathy, predominantly affecting the lower limbs (not asymmetrical, not hands specifically).
• E is wrong: Alcohol is estimated to contribute to approximately 5-7% (sometimes cited as up to 16%) of hypertension cases - "10%" is plausible but the classic figure is closer to 5-7%.

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• Esters: Procaine, cocaine, tetracaine, benzocaine, chloroprocaine (metabolized by plasma pseudocholinesterase).
• Amides: Bupivacaine (A), ropivacaine (B), prilocaine (C), lignocaine/lidocaine (E), mepivacaine (all metabolized hepatically).
• Memory aid: amides have two "i"s in the generic name (lIdocaIne, bupIvacaIne), esters have one.

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• Opioid tolerance develops via receptor desensitization/downregulation, not "rapid receptor disintegration."

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• A is wrong: Lignocaine penetrates the axon in its UNCHARGED (neutral) form, then re-ionizes inside the axon to block the channel from the intracellular side.
• B is wrong: Bupivacaine is more potent than lignocaine (longer duration, higher lipid solubility).
• C is correct: Local anesthetics bind preferentially to open (activated) and inactivated sodium channels rather than resting channels - this is the basis of use-dependent (frequency-dependent) block.
• D is wrong: Lignocaine is a WEAK BASE (pKa ~7.9), not a weak acid.
• E is wrong: Local anesthetics block sodium channels at their INTRACELLULAR end (cytoplasmic side).

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• A is wrong: Post-operative nausea/vomiting is actually REDUCED with propofol (it has antiemetic properties - a major advantage).
• B is wrong: Propofol causes HYPOTENSION, not hypertension.
• C is correct: "Propofol infusion syndrome" (PRIS) - a rare but life-threatening complication involving severe metabolic acidosis, rhabdomyolysis, cardiac failure, and renal failure. Risk is highest with prolonged high-dose infusions in critically ill children (especially those with respiratory infections).
• D is wrong: Propofol is negatively inotropic (causes myocardial depression and vasodilation).
• E is wrong: Tremor is not a common side effect; excitatory movements (myoclonus) can occur during induction.

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• A is wrong: Volatile agents decrease MAP in a dose-dependent fashion but not always "in direct proportion."
• B is wrong: Nitrous oxide has a relatively HIGH MAC (~105%), meaning it is a weak anesthetic (you would need more than 1 atmosphere to anesthetize with N2O alone).
• C is wrong: Halogenated agents have a HIGHER brain:blood partition coefficient (they accumulate in the brain) - actually the brain:blood coefficient for volatile agents is close to 1.
• D is correct: All inhaled anesthetics cause respiratory depression - they decrease tidal volume and increase respiratory rate (rapid, shallow breathing pattern).
• E is wrong: They decrease cerebral metabolic rate but INCREASE cerebral blood flow (vasodilation) - these effects are dissociated.

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• A is wrong: Local anesthetics block Na+ channels, not K+ channels.
• B is wrong: They prevent DEPOLARIZATION (block inward Na+ current), not repolarization.
• C is wrong: Local anesthetics are used WITH VASOCONSTRICTORS (epinephrine) to prolong their local action (not vasodilators).
• D is correct: High extracellular K+ depolarizes the membrane, causing more Na+ channels to remain in the inactivated state, which is the state local anesthetics bind with highest affinity - thus enhancing their activity.
• E is wrong: High extracellular Ca2+ stabilizes the membrane (hyperpolarizes threshold), REDUCING local anesthetic activity.

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• Phenytoin (A) - gum hypertrophy (gingival hyperplasia): CORRECT side effect.
• Ethosuximide (B) - hirsutism: WRONG - hirsutism is a side effect of phenytoin, not ethosuximide. Ethosuximide causes GI symptoms, drowsiness, blood dyscrasias.
• Phenobarbital (C) - enzyme induction: CORRECT.
• Carbamazepine (D) - ataxia: CORRECT.
• Valproate (E) - idiosyncratic hepatic toxicity: CORRECT.

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• Benztropine is a centrally-acting anticholinergic (muscarinic antagonist) used in Parkinsonism and drug-induced EPS.
• Its main side effects are anticholinergic: dry mouth, urinary retention, constipation, blurred vision, and centrally - confusion/cognitive impairment (especially in the elderly).
• Miosis (A) is wrong - anticholinergics cause mydriasis (pupil dilation).
• Diarrhoea (C) is wrong - causes constipation.
• GIT haemorrhage (D) is not a benztropine side effect.
• Bronchorrhoea (E) is wrong - causes bronchodilation/reduced secretions.

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• A is wrong: Thiopentone IS highly lipid soluble (this enables its rapid CNS penetration).
• B is wrong: Thiopentone is only given IV (not IM) - it causes severe tissue necrosis if given perivascularly or IM due to its high alkalinity (pH 10.5).
• C is wrong: Thiopentone has NO analgesic properties; it may even have anti-analgesic (hyperalgesic) effects at subanaesthetic doses.
• D is correct: Excitatory phenomena including tremor, muscle twitching, and convulsive movements can occur, particularly during induction.
• E is also correct: The brief duration of action after a single induction dose of thiopentone is due to redistribution from the highly vascularized CNS to muscle and fat.

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• A is correct: N2O/O2 mixtures are standard carrier gases for volatile agents like halothane.
• B is wrong: Nitrous oxide has GOOD analgesic properties (used as Entonox - 50% N2O/O2 - for labor and procedural pain).
• Nitrous oxide does NOT cause hepatotoxicity (that's halothane).
• N2O can diffuse into air-filled cavities (bowel, pneumothorax, middle ear) - this is a known concern.

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Summary Table for Questions 1-56

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Answers Already Provided in Document (Q57 onwards)