Central Nervous System Pharmacology — MCQs
On this page
In the liver, which of the following is responsible for the metabolism of alcohol?
Which neurotransmitter is primarily responsible for the action of Barbiturates?
All of the following act through GABA except?
Which of the following is an antagonist of benzodiazepines?
Dryness of mouth caused by antipsychotic drugs is primarily due to the blockade of which type of receptors?
Which antiepileptic drug can cause folate deficiency anemia?
Which of the following antiepileptic drugs is not associated with congenital malformations when used in pregnant women?
Which of the following is an aminoneurotransmitter?
Which of the following agents enhances the bioavailability of levodopa in patients with Parkinson's disease?
Which of the following drugs is known to cause aplastic anemia as a side effect?
Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs
Question 371: In the liver, which of the following is responsible for the metabolism of alcohol?
- A. Alcohol dehydrogenase (ADH)
- B. Aldehyde dehydrogenase (ALDH)
- C. Microsomal ethanol-oxidizing system (MEOS)
- D. All of the above (Correct Answer)
Explanation: Alcohol metabolism in the liver is a multi-pathway process involving several enzyme systems. While Alcohol Dehydrogenase is the primary pathway, the other systems play critical roles depending on the concentration and frequency of alcohol intake [1, 2]. **Explanation of the Correct Answer:** Alcohol is metabolized in the liver via three main pathways, making **Option D** the correct choice: 1. **Alcohol Dehydrogenase (ADH):** This is the **major pathway** for ethanol metabolism. Located in the cytosol, ADH converts ethanol to acetaldehyde. It follows zero-order kinetics at typical blood alcohol levels [1]. 2. **Microsomal Ethanol-Oxidizing System (MEOS):** This pathway involves the **CYP2E1** enzyme (part of the Cytochrome P450 system) in the endoplasmic reticulum. It becomes significantly active at high blood alcohol concentrations or in chronic drinkers [2]. 3. **Aldehyde Dehydrogenase (ALDH):** This mitochondrial enzyme is responsible for the second step of metabolism, converting the toxic intermediate **acetaldehyde into acetate**. Without ALDH, the metabolic cycle cannot be completed [2]. **Why individual options are incomplete:** Options A, B, and C are all correct components of the metabolic process. Selecting only one would ignore the integrated nature of hepatic ethanol clearance. **High-Yield Clinical Pearls for NEET-PG:** * **Disulfiram:** Inhibits **ALDH**, leading to acetaldehyde accumulation, which causes the "disulfiram-like reaction" (flushing, tachycardia, nausea) [2]. * **Fomepizole:** Inhibits **ADH**; it is the antidote of choice for Methanol and Ethylene Glycol poisoning [2]. * **MEOS Induction:** Chronic alcohol consumption induces CYP2E1, which can increase the hepatotoxicity of drugs like **Acetaminophen (Paracetamol)** due to increased production of the toxic metabolite NAPQI [2]. * **Kinetics:** Alcohol metabolism follows **zero-order kinetics** (a constant amount is metabolized per unit time), except at very low concentrations [1].
Question 372: Which neurotransmitter is primarily responsible for the action of Barbiturates?
- A. Glutamate
- B. Glycine
- C. Aspartate
- D. GABA (Correct Answer)
Explanation: **Explanation:** **1. Why GABA is correct:** Barbiturates act as positive allosteric modulators of the **GABA-A receptor** complex. They bind to a specific site on the chloride channel, distinct from the benzodiazepine binding site. Their primary mechanism involves **increasing the duration** of chloride channel opening (mnemonic: *Barbi-DUR-ate* for duration). At higher concentrations, barbiturates can also act as **GABA-mimetics**, directly activating the receptor even in the absence of GABA, which contributes to their lower therapeutic index and higher risk of fatal overdose compared to benzodiazepines. **2. Why the other options are incorrect:** * **Glutamate & Aspartate:** These are the primary **excitatory** neurotransmitters in the CNS. While barbiturates do inhibit glutamate receptors (specifically AMPA receptors) at high doses, this is a secondary effect. Their sedative-hypnotic action is fundamentally mediated through GABA. * **Glycine:** This is the major inhibitory neurotransmitter in the **spinal cord** and brainstem. Barbiturates do not primarily target glycine receptors to exert their central sedative effects. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism Difference:** Benzodiazepines increase the **frequency** of channel opening, whereas Barbiturates increase the **duration**. * **Enzyme Induction:** Barbiturates are potent **CYP450 enzyme inducers**, leading to numerous drug interactions (e.g., decreasing the efficacy of Warfarin or Oral Contraceptives). * **Contraindication:** They are strictly contraindicated in **Acute Intermittent Porphyria** because they induce ALA synthase, the rate-limiting enzyme in porphyrin synthesis. * **Antidote:** Unlike benzodiazepines (Flumazenil), there is **no specific antidote** for barbiturate poisoning; management is purely supportive (alkalinization of urine for Phenobarbital).
Question 373: All of the following act through GABA except?
- A. Phenobarbitone
- B. Carbamazepine (Correct Answer)
- C. Zopiclone
- D. Muscimol
Explanation: **Explanation:** The question tests the understanding of the mechanisms of action of various CNS drugs, specifically focusing on the GABAergic system. **Why Carbamazepine is the correct answer:** Carbamazepine is an anticonvulsant that primarily acts by **blocking voltage-gated sodium channels** in their inactivated state. This stabilizes neuronal membranes and inhibits repetitive firing. It does **not** have a direct or indirect effect on the GABA receptor complex. **Analysis of incorrect options:** * **Phenobarbitone:** This is a barbiturate that acts as a positive allosteric modulator of the **GABA-A receptor**. It increases the **duration** of chloride channel opening and, at higher doses, can directly mimic GABA (GABA-mimetic). * **Zopiclone:** This is a "Z-drug" (non-benzodiazepine hypnotic). It acts selectively on the **α1 subunit of the GABA-A receptor** to enhance the inhibitory effects of GABA, similar to benzodiazepines but with a different chemical structure. * **Muscimol:** This is a potent, selective **GABA-A receptor agonist** derived from the mushroom *Amanita muscaria*. It binds directly to the same site as the endogenous neurotransmitter GABA. **High-Yield Clinical Pearls for NEET-PG:** * **Barbiturates vs. Benzodiazepines:** Barbiturates increase the *duration* of Cl- channel opening, while Benzodiazepines increase the *frequency* (Mnemonic: **Ben**zodiazepines = **Fr**equency; **Bar**biturates = **Dur**ation). * **Carbamazepine** is the drug of choice for **Trigeminal Neuralgia**. * **Zopiclone/Zolpidem** are preferred for insomnia because they cause less disruption of sleep architecture and have a lower potential for dependence compared to benzodiazepines. * **GABA-B Agonist:** Remember that **Baclofen** acts on GABA-B receptors (G-protein coupled) to treat spasticity.
Question 374: Which of the following is an antagonist of benzodiazepines?
- A. Nalorphine
- B. Carbamazepine
- C. Naloxone
- D. Flumazenil (Correct Answer)
Explanation: ### Explanation **Correct Option: D. Flumazenil** Flumazenil is a competitive antagonist at the **GABA-A receptor** benzodiazepine (BZD) binding site. It specifically reverses the sedative, psychomotor, and anticonvulsant effects of benzodiazepines and "Z-drugs" (Zolpidem, Zopiclone). It is the drug of choice for managing BZD overdose and reversing anesthesia induced by midazolam. **Analysis of Incorrect Options:** * **A. Nalorphine:** This is a mixed opioid agonist-antagonist. While it can antagonize opioid effects, it is rarely used today due to its psychotomimetic side effects. * **B. Carbamazepine:** This is an anticonvulsant and mood stabilizer that works primarily by blocking **voltage-gated sodium channels**. It has no antagonistic activity at the BZD receptor. * **C. Naloxone:** This is a pure **opioid receptor antagonist**. It is the specific antidote for opioid overdose (e.g., morphine, heroin) but has no effect on BZD-induced respiratory depression. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Flumazenil has a high affinity for the BZD site but lacks intrinsic activity (neutral antagonist). * **Duration of Action:** Flumazenil has a very **short half-life** (~1 hour). Since most BZDs (like Diazepam) last longer, "re-sedation" can occur, necessitating repeated doses or an infusion. * **Contraindication:** Avoid flumazenil in patients with long-term BZD dependence or those who have co-ingested TCAs, as it can precipitate **acute withdrawal seizures**. * **Z-drugs:** Remember that Flumazenil also reverses non-benzodiazepine hypnotics like **Zolpidem and Zaleplon**.
Question 375: Dryness of mouth caused by antipsychotic drugs is primarily due to the blockade of which type of receptors?
- A. Muscarinic acetylcholine receptors (Correct Answer)
- B. GABA receptors
- C. Serotonergic receptors
- D. Dopaminergic receptors
Explanation: **Explanation:** The dryness of mouth (xerostomia) associated with antipsychotic drugs is a classic **anticholinergic side effect**. Many antipsychotics, particularly low-potency typical antipsychotics (e.g., Chlorpromazine) and certain atypicals (e.g., Clozapine, Olanzapine), have a high affinity for **Muscarinic (M1) receptors**. Blockade of these receptors in the salivary glands inhibits parasympathetic stimulation, leading to reduced salivary secretion. **Analysis of Options:** * **Option A (Correct):** Muscarinic blockade prevents the action of acetylcholine on salivary glands. This "atropine-like" effect also causes blurred vision, constipation, and urinary retention. * **Option B (Incorrect):** GABA is the primary inhibitory neurotransmitter. Drugs affecting GABA (like benzodiazepines) cause sedation and anxiolysis, not dry mouth. * **Option C (Incorrect):** Serotonergic (5-HT2A) blockade is a hallmark of atypical antipsychotics and helps reduce extrapyramidal symptoms (EPS), but it does not cause xerostomia. * **Option D (Incorrect):** Dopaminergic (D2) blockade in the mesolimbic pathway is the primary mechanism for the *antipsychotic* effect. Blockade in the nigrostriatal pathway leads to EPS (Parkinsonism), not dry mouth. **High-Yield NEET-PG Pearls:** * **Mnemonic for Anticholinergic Toxicity:** "Dry as a bone (dry mouth/skin), Red as a beet (flushing), Hot as a hare (hyperthermia), Blind as a bat (mydriasis), Mad as a hatter (delirium)." * **Thioridazine and Chlorpromazine** are the typical antipsychotics with the strongest anticholinergic profiles. * **Clozapine Paradox:** Despite being a potent muscarinic antagonist, Clozapine often causes **sialorrhea** (excessive salivation) instead of dry mouth, likely due to its agonist activity at M4 receptors or inhibition of the swallowing reflex.
Question 376: Which antiepileptic drug can cause folate deficiency anemia?
- A. Valproate
- B. Phenytoin (Correct Answer)
- C. Phenobarbitone
- D. Carbamazepine
Explanation: **Explanation:** **Phenytoin** is the correct answer because it is a well-known inducer of **folate deficiency**, which can lead to **megaloblastic anemia**. The underlying mechanism involves Phenytoin’s ability to interfere with the intestinal absorption of dietary folates and increase the hepatic metabolism of folate by inducing microsomal enzymes. Chronic use leads to depleted folate stores, resulting in impaired DNA synthesis in red blood cell precursors. **Analysis of Options:** * **Valproate (A):** While Valproate is associated with bone marrow suppression (thrombocytopenia) and is highly teratogenic (neural tube defects due to folate interference in pregnancy), it is not the classic cause of megaloblastic anemia in routine clinical practice compared to Phenytoin. * **Phenobarbitone (C) & Carbamazepine (D):** Both are enzyme inducers and can occasionally lower folate levels, but they are significantly less likely to cause clinically symptomatic megaloblastic anemia than Phenytoin. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Phenytoin Side Effects (PHENYTOIN):** **P**-P450 induction, **H**-Hirsutism, **E**-Enlarged gums (Gingival hyperplasia), **N**-Nystagmus, **Y**-Yellow-brown skin (pigmentation), **T**-Teratogenicity (Fetal Hydantoin Syndrome), **O**-Osteomalacia (Vitamin D interference), **I**-Interference with B9 (Megaloblastic Anemia), **N**-Neuropathy. * **Management:** Patients on long-term Phenytoin therapy should be monitored for macrocytosis and often require supplemental **Folic Acid**. * **Gum Hyperplasia:** This occurs due to increased expression of Platelet-Derived Growth Factor (PDGF).
Question 377: Which of the following antiepileptic drugs is not associated with congenital malformations when used in pregnant women?
- A. Phenytoin
- B. Valproic acid
- C. Carbamazepine
- D. Phenobarbitone (Correct Answer)
Explanation: **Explanation:** The management of epilepsy during pregnancy is a high-yield NEET-PG topic. The core concept is that while almost all older-generation antiepileptic drugs (AEDs) carry some teratogenic risk, the question asks to identify the drug **least** associated with specific major malformations compared to the others in the list, or the one traditionally considered "safer" in specific clinical contexts. **1. Why Phenobarbitone is the Correct Answer:** Among the options provided, **Phenobarbitone** is often cited in classical pharmacology textbooks as having a lower incidence of major structural malformations compared to Valproate or Phenytoin. While it is not "risk-free" (it can cause neonatal hemorrhage due to Vitamin K deficiency and minor craniofacial defects), it is frequently used in resource-limited settings and has a long safety record regarding gross structural defects compared to the high-risk profile of Valproate. **2. Analysis of Incorrect Options:** * **Valproic acid (Option B):** This is the **most teratogenic** AED. It is strongly associated with **Neural Tube Defects (Spina Bifida)** due to interference with folate metabolism. It also causes "Fetal Valproate Syndrome." * **Phenytoin (Option A):** Associated with **Fetal Hydantoin Syndrome**, characterized by hypoplastic phalanges, nail dysplasia, cleft lip/palate, and microcephaly. * **Carbamazepine (Option C):** Known to cause neural tube defects and craniofacial anomalies, though the risk is lower than Valproate. **Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** For epilepsy in pregnancy, **Levetiracetam** and **Lamotrigine** are currently considered the safest (lowest teratogenic risk). * **Folic Acid:** All pregnant women on AEDs should receive high-dose folic acid (5 mg/day) to reduce the risk of neural tube defects. * **Vitamin K:** Enzyme-inducing AEDs (Phenytoin, Phenobarbitone) can cause neonatal bleeding; Vitamin K prophylaxis is essential for the newborn.
Question 378: Which of the following is an aminoneurotransmitter?
- A. Acetylcholine
- B. GABA (Correct Answer)
- C. Lignocaine
- D. Epinephrine
Explanation: Neurotransmitters are chemically classified into three main categories: **Amino acids**, **Amines** (Biogenic amines), and **Peptides**. Why GABA is correct: **GABA (Gamma-aminobutyric acid)** is the primary inhibitory neurotransmitter in the CNS [1] and belongs to the **Amino Acid** group. Other members of this group include Glutamate (the primary excitatory neurotransmitter), Glycine, and Aspartate. These are simple amino acids that act directly on receptors to mediate fast synaptic transmission. Analysis of Incorrect Options: * **A. Acetylcholine:** While a major neurotransmitter, it is chemically an **ester** of choline and acetic acid, not an amino acid or a simple amine. * **C. Lignocaine:** This is a **Local Anesthetic** drug that acts by blocking voltage-gated sodium channels. It is not an endogenous neurotransmitter. * **D. Epinephrine:** This belongs to the **Biogenic Amines** (specifically Catecholamines) category. While derived from the amino acid tyrosine, it is chemically classified as an amine, not an "amino acid neurotransmitter." High-Yield Clinical Pearls for NEET-PG: * **GABA-A Receptors:** Ionotropic receptors (ligand-gated $Cl^-$ channels) [1]. Target for Benzodiazepines, Barbiturates, and Alcohol. * **GABA-B Receptors:** Metabotropic receptors (G-protein coupled) [1]. Target for **Baclofen** (used in spasticity). * **Glycine:** The major inhibitory neurotransmitter in the **spinal cord** [1]. Its action is antagonized by **Strychnine**. * **Glutamate:** The most common excitatory neurotransmitter; excess levels are associated with excitotoxicity (e.g., in stroke).
Question 379: Which of the following agents enhances the bioavailability of levodopa in patients with Parkinson's disease?
- A. Amantadine
- B. Ropinirole
- C. Entacapone (Correct Answer)
- D. Selegiline
Explanation: **Explanation:** The correct answer is **Entacapone**. **Why Entacapone is correct:** Levodopa is the precursor to dopamine. When administered orally, it is rapidly metabolized in the periphery by two enzymes: **DOPA decarboxylase (DDC)** and **Catechol-O-methyltransferase (COMT)**. While Carbidopa inhibits DDC, it leads to a compensatory increase in COMT activity, which converts levodopa into 3-O-methyldopa. **Entacapone** is a selective, reversible **peripheral COMT inhibitor**. By blocking this pathway, it prevents the peripheral degradation of levodopa, thereby increasing its plasma half-life and **bioavailability** to the brain. This helps reduce "off" periods in patients with motor fluctuations. **Why the other options are incorrect:** * **Amantadine (A):** An antiviral drug that acts by increasing dopamine release and blocking NMDA receptors. It does not affect levodopa metabolism. * **Ropinirole (B):** A non-ergot **Dopamine Agonist** that acts directly on postsynaptic D2/D3 receptors. It mimics dopamine but does not alter levodopa levels. * **Selegiline (D):** A selective **MAO-B inhibitor**. It acts primarily within the **Central Nervous System** to prevent the breakdown of dopamine already formed in the brain. It does not significantly enhance the peripheral bioavailability of levodopa. **High-Yield Clinical Pearls for NEET-PG:** * **Tolcapone vs. Entacapone:** Entacapone acts only peripherally, whereas Tolcapone acts both peripherally and centrally. However, Tolcapone is rarely used due to **hepatotoxicity** (requires LFT monitoring). * **Orange Discoloration:** Entacapone can cause harmless orange discoloration of urine. * **Stalevo:** A fixed-dose combination of Levodopa + Carbidopa + Entacapone.
Question 380: Which of the following drugs is known to cause aplastic anemia as a side effect?
- A. Valproate
- B. Carbamazepine (Correct Answer)
- C. Lamotrigine
- D. Lithium
Explanation: **Explanation:** **Carbamazepine** is a first-line antiepileptic drug for focal seizures and trigeminal neuralgia [1]. Its association with **aplastic anemia** and agranulocytosis is a classic, high-yield side effect. While rare (occurring in approximately 2–5 per million patients per year), it is a serious idiosyncratic reaction involving bone marrow suppression. This necessitates baseline and periodic complete blood counts (CBC) during treatment. **Analysis of Incorrect Options:** * **A. Valproate:** Most commonly associated with **hepatotoxicity** (especially in children <2 years), weight gain, alopecia, and **thrombocytopenia** (low platelets), rather than global aplastic anemia. It is also highly teratogenic (neural tube defects). * **C. Lamotrigine:** The most significant life-threatening side effect is **Stevens-Johnson Syndrome (SJS)** or Toxic Epidermal Necrolysis (TEN). It does not typically cause bone marrow failure. * **D. Lithium:** Known for causing **leukocytosis** (an increase in white blood cell count), which is sometimes used therapeutically in Felty’s syndrome. Other side effects include nephrogenic diabetes insipidus, tremors, and hypothyroidism. **Clinical Pearls for NEET-PG:** * **HLA-B*1502 Link:** In patients of Asian descent, this allele significantly increases the risk of SJS/TEN when taking Carbamazepine. * **Enzyme Induction:** Carbamazepine is a potent **CYP450 inducer**, leading to many drug-drug interactions (e.g., decreasing the efficacy of oral contraceptives). * **Other drugs causing Aplastic Anemia:** Chloramphenicol, Phenylbutazone, Gold salts, and Felbamate [2].
Practice by Chapter
General Anesthetics
Practice Questions
Local Anesthetics
Practice Questions
Sedative-Hypnotics
Practice Questions
Antiepileptic Drugs
Practice Questions
Antiparkinsonian Drugs
Practice Questions
Opioid Analgesics
Practice Questions
Drugs of Abuse and Addiction
Practice Questions
Psychostimulants
Practice Questions
Hallucinogens
Practice Questions
CNS Stimulants and Cognitive Enhancers
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free