Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 261: Which of the following medications is NOT used for the treatment of anxiety?

A. Propranolol
B. Alprazolam
C. Buspirone
D. Haloperidol (Correct Answer)

Explanation: **Explanation:** The correct answer is **Haloperidol**. **Why Haloperidol is the correct choice:** Haloperidol is a high-potency **typical antipsychotic** that acts primarily by blocking Dopamine (D2) receptors in the mesolimbic pathway. It is indicated for schizophrenia, acute psychosis, and Tourette syndrome. It is **not** an anxiolytic; in fact, it can sometimes cause restlessness (akathisia) as an extrapyramidal side effect, which may mimic or worsen the feeling of agitation. **Analysis of other options:** * **Propranolol:** A non-selective beta-blocker used to treat the **peripheral autonomic symptoms** of anxiety (tachycardia, tremors, sweating). It is particularly high-yield for "performance anxiety" or stage fright. * **Alprazolam:** A Benzodiazepine (BZD) that enhances GABA-A receptor activity. It is a first-line agent for the acute management of **Panic Disorder** and Generalized Anxiety Disorder (GAD) due to its rapid onset. * **Buspirone:** A selective **5-HT1A partial agonist**. It is used for chronic GAD. Unlike BZDs, it lacks sedative, hypnotic, or muscle relaxant properties and has no abuse potential, but it takes 2–4 weeks to show effects. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of choice for GAD:** SSRIs (Long-term); Benzodiazepines (Acute). * **Buspirone Advantage:** No "hangover" effect, no interaction with alcohol, and no withdrawal symptoms. * **Performance Anxiety:** Propranolol is the drug of choice, taken 30–60 minutes before the event. * **Haloperidol Side Effects:** Highly associated with Extrapyramidal Symptoms (EPS) and Neuroleptic Malignant Syndrome (NMS).

Question 262: Which of the following drugs is useful in the acute attack of migraine?

A. Bromocriptine
B. Cinnarizine
C. Sumatriptan (Correct Answer)
D. Ondansetron

Explanation: **Explanation:** **Sumatriptan (Option C)** is the correct answer because it is a selective **5-HT$_{1B/1D}$ receptor agonist**. These receptors are located on cranial blood vessels and trigeminal nerve endings. Activation leads to: 1. **Vasoconstriction** of dilated intracranial extracerebral vessels. 2. **Inhibition of neuropeptide release** (like CGRP and Substance P) from trigeminal nerve terminals, which reduces neurogenic inflammation. Triptans are considered the "gold standard" for the **abortive (acute) treatment** of moderate-to-severe migraine attacks. **Analysis of Incorrect Options:** * **Bromocriptine (A):** A dopamine (D2) agonist used primarily in Prolactinoma and Parkinson’s disease. It has no role in migraine management. * **Cinnarizine (B):** A calcium channel blocker with antihistaminic properties. It is used for **prophylaxis** of migraine and control of vertigo, but it is ineffective during an acute attack. * **Ondansetron (D):** A 5-HT$_3$ antagonist used as an antiemetic. While it may help manage the nausea associated with migraine, it does not treat the underlying pathophysiology of the headache itself. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** For mild-to-moderate acute attacks, NSAIDs (like Naproxen) are first-line. For severe attacks, **Triptans** are the DOC. * **Contraindications for Triptans:** Due to their vasoconstrictive action, they are strictly contraindicated in patients with **Ischemic Heart Disease (IHD)**, Prinzmetal angina, and uncontrolled hypertension. * **Prophylaxis Drugs:** Remember the mnemonic **"V-B-A-T"** (Valproate, Beta-blockers like Propranolol, Amitriptyline, Topiramate/Flunarizine).

Question 263: Which of the following is a nonsedative anxiolytic?

A. Buspirone (Correct Answer)
B. Hydroxyzine
C. Chlorpromazine
D. Alprazolam

Explanation: ### Explanation **Correct Answer: A. Buspirone** **Mechanism and Rationale:** Buspirone is a unique anxiolytic that acts as a **selective partial agonist at the 5-HT1A receptors**. Unlike Benzodiazepines, it does not interact with the GABA-A receptor complex. Its primary clinical advantage is that it provides relief from anxiety **without causing sedation**, hypnosis, muscle relaxation, or anticonvulsant effects. It also lacks the potential for abuse or physical dependence, making it ideal for chronic generalized anxiety disorder (GAD). However, it has a slow onset of action (taking 1–2 weeks to show effects) and is ineffective for acute anxiety or panic attacks. **Analysis of Incorrect Options:** * **B. Hydroxyzine:** An H1-receptor antagonist (antihistamine) with significant sedative properties. It is used for acute situational anxiety but causes marked drowsiness. * **C. Chlorpromazine:** A typical antipsychotic (low potency). While it has calming effects, it is primarily used for psychosis and is highly sedative due to its alpha-1 and H1 blocking actions. * **D. Alprazolam:** A Benzodiazepine. While highly effective for anxiety and panic disorders, its primary side effect is **sedation** and psychomotor impairment. It also carries a high risk of dependence. **High-Yield Clinical Pearls for NEET-PG:** * **"Driving Safety":** Buspirone is the preferred anxiolytic for patients whose occupations require mental alertness (e.g., pilots, drivers). * **No Interaction with Alcohol:** Unlike Benzodiazepines, Buspirone does not potentiate the CNS depressant effects of alcohol. * **Metabolism:** It is metabolized by **CYP3A4**; its levels can increase significantly if taken with grapefruit juice or erythromycin. * **Rule Out:** Buspirone is **not** effective in treating Benzodiazepine withdrawal.

Question 264: A 30-year-old epileptic female on Phenytoin therapy developed weakness and fatigue. Blood examination revealed Hb= 4.6 gm, MCV=102 fL, and MCH =40 pg/dL. What is the most probable diagnosis?

A. Heart failure
B. Iron deficiency anemia
C. Phenytoin-induced agranulocytosis
D. Megaloblastic anemia (Correct Answer)

Explanation: **Explanation:** The patient presents with symptoms of anemia (weakness, fatigue) and a low hemoglobin (4.6 gm/dL). The key diagnostic clues are the **elevated MCV (102 fL)** and **elevated MCH (40 pg/dL)**, which indicate a **macrocytic anemia**. **Why Megaloblastic Anemia is correct:** Phenytoin is a well-known inducer of **folate deficiency**. It interferes with folate metabolism by inhibiting the intestinal enzyme *folate conjugase*, thereby reducing the absorption of dietary folic acid. Chronic phenytoin therapy leads to impaired DNA synthesis in red blood cell precursors, resulting in megaloblastic (macrocytic) anemia. **Analysis of Incorrect Options:** * **Heart failure:** While severe anemia can lead to high-output heart failure, it does not explain the macrocytic blood indices (high MCV/MCH). * **Iron deficiency anemia:** This typically presents as **microcytic hypochromic** anemia (Low MCV, Low MCH), which contradicts the laboratory findings provided. * **Phenytoin-induced agranulocytosis:** This refers to a severe reduction in white blood cell count (granulocytes), not red blood cells. While phenytoin can cause blood dyscrasias, the high MCV specifically points toward a maturation defect like megaloblastic anemia. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Phenytoin decreases folate absorption and increases its catabolism. * **Management:** Supplementation with **Folic Acid** can reverse the anemia. However, be cautious: high doses of folic acid can lower phenytoin levels by increasing its metabolism, potentially precipitating seizures. * **Other Phenytoin Side Effects (Mnemonic: HOT MALAR):** **H**irsutism, **O**steomalacia, **T**eratogenicity (Fetal Hydantoin Syndrome), **M**egaloblastic anemia, **A**taxia, **L**ymphadenopathy, **A**rrhythmias, **R**igidity (Gingival Hyperplasia).

Question 265: Which anti-epileptic drug can be safely used in pregnancy?

A. Valproic acid
B. Phenytoin
C. Carbamazepine
D. Lamotrigine (Correct Answer)

Explanation: The management of epilepsy in pregnancy requires balancing maternal seizure control with the risk of teratogenicity. **Lamotrigine** is considered one of the safest anti-epileptic drugs (AEDs) during pregnancy [1] because it has a significantly lower risk of major congenital malformations (approx. 2–3%) compared to older AEDs. It is not associated with a specific "syndrome" of defects, though clinicians must monitor serum levels closely as clearance increases during pregnancy. **Analysis of Incorrect Options:** * **Valproic acid (Option A):** This is the **most teratogenic** AED. It is associated with a high risk of neural tube defects (e.g., spina bifida) and impaired cognitive development (lower IQ) in the offspring [1]. It is strictly avoided in pregnancy unless no other drug works. * **Phenytoin (Option B):** Causes **Fetal Hydantoin Syndrome**, characterized by craniofacial dysmorphism (cleft lip/palate), hypoplastic phalanges/nails, and microcephaly. * **Carbamazepine (Option C):** Associated with an increased risk of neural tube defects and craniofacial abnormalities, though the risk is lower than with Valproate. **NEET-PG High-Yield Pearls:** * **Safest AEDs in pregnancy:** Lamotrigine and Levetiracetam. * **Drug of choice for seizures in pregnancy:** If a patient is already well-controlled on a drug (except Valproate), it is usually continued at the lowest effective dose. * **Folic Acid Supplementation:** All pregnant women on AEDs should take high-dose folic acid (5 mg/day) to reduce the risk of neural tube defects. * **Vitamin K:** Enzyme-inducing AEDs (Phenytoin, Carbamazepine, Phenobarbital) can cause neonatal hemorrhage; Vitamin K is administered to the mother in the last month of pregnancy and to the newborn at birth [1].

Question 266: All of the following adverse effects are associated with carbamazepine except?

A. Teratogenicity
B. Neurotoxicity
C. Decrease in antidiuretic hormone (Correct Answer)
D. Hypersensitivity

Explanation: **Explanation:** The correct answer is **C (Decrease in antidiuretic hormone)** because Carbamazepine actually causes an **increase** in the action of Antidiuretic Hormone (ADH). **1. Why Option C is correct:** Carbamazepine acts as an ADH enhancer by increasing the sensitivity of renal tubules to ADH and stimulating its release. This leads to water retention and **dilutional hyponatremia** (SIADH-like picture). Therefore, saying it causes a "decrease" in ADH is physiologically incorrect. **2. Why other options are incorrect:** * **A. Teratogenicity:** Carbamazepine is a known teratogen associated with **neural tube defects** (e.g., spina bifida) due to interference with folate metabolism. * **B. Neurotoxicity:** Dose-related neurotoxicity is common, manifesting as diplopia, ataxia, vertigo, and sedation. * **C. Hypersensitivity:** It can cause various skin reactions, ranging from mild rashes to life-threatening **Stevens-Johnson Syndrome (SJS)** or Toxic Epidermal Necrolysis (TEN), particularly in patients with the **HLA-B*1502** allele. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Blocks voltage-gated sodium channels in the inactivated state. * **Drug of Choice (DOC):** It remains the DOC for **Trigeminal Neuralgia**. * **Auto-induction:** Carbamazepine induces its own metabolism (CYP3A4 inducer), meaning the half-life decreases after chronic administration. * **Hematological Side Effect:** It can cause rare but serious **aplastic anemia** and agranulocytosis; baseline CBC is often recommended. * **Mnemonic (ADVERSE):** **A**taxia, **D**iplopia/Dizziness, **V**ertigo, **E**nzyme induction, **R**ash, **S**IADH, **E**pigenetic (Teratogenic).

Question 267: Gingival hypertrophy and hirsutism are known side effects associated with the use of which of the following antiepileptic drugs?

A. Diazepam
B. Primidone
C. Carbamazepine
D. Diphenylhydantoin (Correct Answer)

Explanation: **Explanation:** **Diphenylhydantoin (Phenytoin)** is the correct answer. It is a first-line antiepileptic drug that acts by blocking voltage-gated sodium channels in their inactive state. The side effect profile of Phenytoin is a high-yield topic for NEET-PG, often remembered by the mnemonic **"P-H-E-N-Y-T-O-I-N"**: * **P:** P-450 induction * **H:** **Hirsutism** and **Hypertrophy of gums** (Gingival hyperplasia occurs due to increased expression of platelet-derived growth factor (PDGF) stimulating fibroblast proliferation). * **E:** Enlarged lymph nodes (Pseudolymphoma) * **N:** Nystagmus (earliest sign of toxicity) * **Y:** Yellow-brown skin pigmentation * **T:** Teratogenicity (Fetal Hydantoin Syndrome) * **O:** Osteomalacia (due to Vitamin D interference) * **I:** Interference with B12/Folate metabolism (Megaloblastic anemia) * **N:** Neuropathy (Peripheral) **Analysis of Incorrect Options:** * **A. Diazepam:** A Benzodiazepine primarily used for Status Epilepticus. Common side effects include sedation, ataxia, and respiratory depression, but not gingival changes. * **B. Primidone:** A prodrug converted to Phenobarbital. It causes sedation, cognitive impairment, and megaloblastic anemia, but is not associated with hirsutism. * **C. Carbamazepine:** Known for causing diplopia, ataxia, SIADH (hyponatremia), and serious skin reactions like Stevens-Johnson Syndrome (SJS), especially in patients with the HLA-B*1502 allele. **Clinical Pearls for NEET-PG:** 1. **Zero-order kinetics:** Phenytoin follows saturation kinetics at therapeutic doses; a small dose increase can lead to a disproportionate rise in plasma levels. 2. **Fetal Hydantoin Syndrome:** Characterized by cleft lip/palate, microcephaly, and hypoplastic phalanges. 3. **Fosphenytoin:** A water-soluble prodrug of phenytoin used IV to avoid the "Purple Glove Syndrome" and local irritation associated with phenytoin.

Question 268: What is the drug of choice for drug-induced Parkinsonism?

A. Levodopa
B. Benserazide
C. Benzhexol (Correct Answer)
D. Selegiline

Explanation: **Explanation:** **Mechanism of Drug-Induced Parkinsonism (DIP):** Drug-induced Parkinsonism is primarily caused by the use of **D2 receptor antagonists**, such as typical antipsychotics (e.g., Haloperidol) or antiemetics (e.g., Metoclopramide). These drugs block dopamine receptors in the striatum, leading to a relative **cholinergic overactivity**. **Why Benzhexol is the Correct Choice:** Since the underlying pathology is an excess of acetylcholine rather than a primary deficiency of dopamine (as seen in idiopathic Parkinson’s disease), the treatment of choice is a **centrally acting anticholinergic** drug. **Benzhexol** (also known as Trihexyphenidyl) and Benztropine restore the dopaminergic-cholinergic balance by blocking muscarinic receptors in the CNS. **Analysis of Incorrect Options:** * **Levodopa (A) & Benserazide (B):** Levodopa is the gold standard for idiopathic Parkinson’s disease. However, in DIP, dopamine receptors are already blocked by the offending drug. Adding more dopamine is ineffective and can potentially worsen the underlying psychiatric condition for which the antipsychotic was originally prescribed. * **Selegiline (D):** This is a MAO-B inhibitor used as an adjunct in idiopathic Parkinson’s. It does not address the acute cholinergic surge seen in DIP. **High-Yield Clinical Pearls for NEET-PG:** * **Prophylaxis:** Anticholinergics are often co-prescribed with high-potency antipsychotics to prevent Extrapyramidal Side Effects (EPS). * **Contraindication:** Avoid anticholinergics in elderly patients with DIP if possible, as they can precipitate **delirium, urinary retention, or narrow-angle glaucoma**. * **Amantadine:** Can be used as an alternative if anticholinergics are contraindicated. * **Key Distinction:** DIP is a reversible cause of Parkinsonism; the first step in management is usually withdrawing the offending agent.

Question 269: Which dopamine agonist is used in the treatment of Parkinsonism?

A. Ropinirole
B. Pramipexole
C. Bromocriptine
D. All of the above (Correct Answer)

Explanation: **Explanation:** In Parkinson’s disease, the primary pathology is the progressive loss of dopaminergic neurons in the substantia nigra. **Dopamine agonists** act by directly stimulating post-synaptic dopamine receptors (primarily $D_2$ and $D_3$) in the striatum, bypassing the need for presynaptic conversion (unlike Levodopa). **Breakdown of Options:** * **Bromocriptine (Option C):** This is an older, **Ergot-derived** dopamine agonist. While effective, its use has declined due to side effects like pulmonary and retroperitoneal fibrosis and heart valve erythromelalgia. * **Ropinirole (Option A) & Pramipexole (Option B):** These are **Non-Ergot** dopamine agonists. They are currently preferred over Bromocriptine because they have a better safety profile (no risk of fibrosis) and are highly selective for $D_2$ and $D_3$ receptors. Since all three drugs function as dopamine agonists used to manage motor symptoms in Parkinsonism, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug of Choice:** Non-ergot agonists (Pramipexole/Ropinirole) are often preferred in younger patients to delay the initiation of Levodopa and minimize motor fluctuations. 2. **Apomorphine:** A potent dopamine agonist used as "rescue therapy" for acute "off" episodes via subcutaneous injection. 3. **Rotigotine:** A dopamine agonist available as a **transdermal patch**, providing continuous drug delivery. 4. **Side Effects:** Common side effects include nausea, orthostatic hypotension, and **impulse control disorders** (pathological gambling, hypersexuality) due to $D_3$ stimulation in the mesolimbic pathway.

Question 270: Extrapyramidal symptoms are a known complication of treatment with which class of drugs?

A. Antipsychotics (Correct Answer)
B. Anti-anxiety drugs
C. Antidepressants
D. Antimalarial drugs

Explanation: **Explanation:** **1. Why Antipsychotics is Correct:** Extrapyramidal symptoms (EPS) are primarily caused by the **blockade of Dopamine (D2) receptors** in the **Nigrostriatal pathway** of the brain. Typical antipsychotics (First Generation), such as Haloperidol and Chlorpromazine, have a high affinity for D2 receptors. When dopamine is inhibited in the basal ganglia, it leads to an imbalance between dopamine and acetylcholine, resulting in movement disorders. EPS includes acute dystonia, akathisia, parkinsonism, and tardive dyskinesia. **2. Why Other Options are Incorrect:** * **Anti-anxiety drugs:** Most (like Benzodiazepines) act via GABA-A receptors. They cause sedation and muscle relaxation rather than motor side effects. * **Antidepressants:** SSRIs and TCAs primarily affect Serotonin and Norepinephrine. While SSRIs can rarely cause akathisia, they are not classically associated with the EPS profile seen with dopamine antagonists. * **Antimalarial drugs:** These (e.g., Chloroquine) are associated with retinal toxicity or hemolysis in G6PD deficiency, not dopamine blockade. **3. NEET-PG High-Yield Clinical Pearls:** * **Drug of choice for Acute Dystonia:** Central anticholinergics like **Promethazine** or **Benztropine**. * **Drug of choice for Akathisia:** **Propranolol** (Beta-blocker). * **Tardive Dyskinesia:** Occurs due to "dopamine receptor supersensitivity" after long-term use. Treatment involves switching to **Clozapine** or using VMAT-2 inhibitors (Valbenazine). * **Atypical Antipsychotics:** (e.g., Quetiapine, Clozapine) have a lower risk of EPS because they dissociate rapidly from D2 receptors and also block 5HT-2A receptors.

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General Anesthetics

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Local Anesthetics

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Drugs of Abuse and Addiction

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Psychostimulants

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Hallucinogens

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CNS Stimulants and Cognitive Enhancers

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