Central Nervous System Pharmacology Practice Questions

Q: Which of the following local anesthetics is safer for surface and infiltrating anesthesia?

Lignocaine. **Explanation:** **Lignocaine (Lidocaine)** is the most widely used local anesthetic (LA) because it is an all-rounder. It is the correct answer because it is effective both topically (surface) and via injection (infiltration). It has a rapid onset, intermediate duration of action, and a high therapeutic index, making it significantly safer than its counterparts for routine clinical use. **Analysis of Options:** * **Procaine (Option A):** An ester-linked LA with low potency and poor lipid solubility. It has **virtually no surface anesthetic activity**, making it unsuitable for topical application. * **Cocaine (Option B):** While an excellent surface anesthetic with intrinsic vasoconstrictive properties, it is **highly toxic** and has significant potential for addiction and CNS stimulation. It is never used for infiltration due to its tissue toxicity and systemic side effects. * **Amethocaine/Tetracaine (Option D):** A very potent ester LA used primarily for surface (ophthalmic) and spinal anesthesia. However, it is **more toxic** than Lignocaine and is generally avoided for infiltration anesthesia due to the risk of systemic toxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Lignocaine works by blocking voltage-gated $Na^+$ channels from the intracellular side. * **Metabolism:** Lignocaine is an **Amide**, metabolized in the **Liver** (mnemonic: Amides have two 'i's in their name: L**i**doca**i**ne). * **Drug of Choice:** Lignocaine is the DOC for ventricular arrhythmias (Class Ib antiarrhythmic). * **Maximum Dose:** 4 mg/kg (plain) and 7 mg/kg (with Adrenaline). * **Safety:** Prilocaine is the safest (least toxic) amide, but Lignocaine remains the gold standard for combined surface and infiltration use.

Q: All of the following agents are used for prophylaxis of migraine, except?

Ethosuximide. **Explanation:** The correct answer is **Ethosuximide** because it has no clinical role in migraine prophylaxis. Its mechanism of action involves blocking **T-type calcium channels** in the thalamus, making it the drug of choice specifically for **Absence Seizures (Petit Mal)**, but it does not affect the neurovascular pathways involved in migraine. **Analysis of Options:** * **Propranolol (Option A):** A non-selective beta-blocker and the **first-line agent** for migraine prophylaxis. It works by stabilizing vascular tone and reducing central sympathetic excitability. * **Valproate (Option B):** An antiepileptic that increases GABA levels and modulates glutamate. It is highly effective for preventing migraine attacks, though contraindicated in pregnancy due to teratogenicity (neural tube defects). * **Topiramate (Option C):** An antiepileptic that blocks sodium channels and antagonizes glutamate receptors. It is a first-line prophylactic agent, especially useful in patients who are overweight, as it causes weight loss. **High-Yield Clinical Pearls for NEET-PG:** * **Prophylaxis Criteria:** Indicated if attacks occur >2–3 times/month or are severe/disabling. * **First-line Prophylactic Agents:** Beta-blockers (Propranolol, Timolol), Anticonvulsants (Topiramate, Valproate), and Calcium Channel Blockers (Flunarizine). * **Newer Agents:** CGRP antagonists (e.g., Erenumab) are used for refractory cases. * **Acute Treatment:** Triptans (5-HT 1B/1D agonists) are the gold standard for aborting an acute attack, but they are **not** used for prophylaxis. * **Amitriptyline:** A TCA often used for prophylaxis when the patient also has comorbid depression or insomnia.

Q: Buprenorphine is:

Partial agonist at mu receptor. **Explanation:** Buprenorphine is a semi-synthetic highly lipophilic opioid. Its pharmacological profile is unique and high-yield for NEET-PG: 1. **Why Option A is Correct:** Buprenorphine acts as a **partial agonist at the $\mu$ (mu) opioid receptor**. It has a very high affinity for the receptor but low intrinsic activity. This results in a "ceiling effect" for respiratory depression, making it safer in overdose compared to full agonists like morphine. It also has a slow dissociation rate from the $\mu$ receptor, leading to a long duration of action. 2. **Why Options B & D are Incorrect:** Buprenorphine is actually an **antagonist at the $\kappa$ (kappa) receptor**, not an agonist. This $\kappa$-antagonism is thought to contribute to its antidepressant effects and lack of dysphoria. 3. **Why Option C is Incorrect:** Full $\mu$ agonists (e.g., Morphine, Fentanyl, Methadone) have high intrinsic activity without a ceiling effect. Buprenorphine can actually antagonize the effects of full agonists if administered concurrently, potentially precipitating withdrawal in opioid-dependent individuals. **High-Yield Clinical Pearls for NEET-PG:** * **Mixed Action:** It is a $\mu$ partial agonist and $\kappa$ antagonist. * **Ceiling Effect:** Increasing the dose beyond a certain point does not increase the analgesic effect or respiratory depression. * **Clinical Use:** Used in opioid substitution therapy (detoxification) and chronic pain management. * **Naloxone Interaction:** Because it binds so tightly to $\mu$ receptors, buprenorphine-induced respiratory depression is difficult to reverse with standard doses of Naloxone.

Q: Which antihistamine is used in motion sickness?

Diphenhydramine. **Explanation:** The correct answer is **Diphenhydramine**. **1. Why Diphenhydramine is correct:** Motion sickness occurs due to overstimulation of the vestibular apparatus in the inner ear. To be effective in motion sickness, an antihistamine must possess two key properties: it must be a **first-generation H1 blocker** (lipophilic enough to cross the blood-brain barrier) and it must have significant **anticholinergic (antimuscarinic) activity**. Diphenhydramine fulfills both criteria. It acts on the vestibular nuclei and the vomiting center in the brain to suppress the nausea and vertigo associated with motion. **2. Why other options are incorrect:** * **Cetirizine (A) and Fexofenadine (D):** These are **second-generation antihistamines**. They are highly ionized and do not cross the blood-brain barrier significantly. Furthermore, they lack the potent anticholinergic activity required to suppress the vestibular system. Therefore, they are ineffective for motion sickness. * **Meclizine (B):** While Meclizine is indeed used for motion sickness (especially for longer durations due to its 24-hour half-life), in the context of this specific question, Diphenhydramine is the classic prototype often tested. *Note: If both were options, Meclizine is often preferred clinically for less sedation, but Diphenhydramine remains a standard correct answer for its potent central action.* **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** For the *prevention* of motion sickness, the most potent drug is **Hyoscine (Scopolamine)**, administered via a transdermal patch. * **Timing:** Antihistamines must be taken **30–60 minutes before** the journey to be effective. * **Other First-Gen Drugs:** Promethazine, Cyclizine, and Dimenhydrinate are also used for motion sickness. * **Side Effect Profile:** The main limiting side effect of these drugs is **sedation** and dry mouth (due to anticholinergic action).

Q: What is the drug of choice for intractable hiccups?

Chlorpromazine. **Chlorpromazine** is the only FDA-approved medication specifically indicated for the treatment of intractable hiccups (singultus). Intractable hiccups are defined as those lasting more than one month. **Why Chlorpromazine is the Correct Choice:** The pathophysiology of hiccups involves a reflex arc consisting of the vagus nerve, phrenic nerve, and sympathetic chain (T6–T12), coordinated by a "hiccup center" in the brainstem. Chlorpromazine, a typical antipsychotic of the low-potency phenothiazine class, acts as a potent **dopamine (D2) receptor antagonist** in the hypothalamus and brainstem. It effectively interrupts the hiccup reflex arc through its central sedative and antagonistic effects. **Analysis of Incorrect Options:** * **Metoclopramide (A):** While it is a prokinetic and D2 antagonist used as a second-line agent (especially if the cause is gastric stasis), it is not the primary drug of choice. * **Haloperidol (B):** This is a high-potency antipsychotic that has been used off-label for hiccups, but it lacks the formal approval and historical clinical preference established for Chlorpromazine. * **Thioridazine (C):** Although it is a phenothiazine like chlorpromazine, it is not used for hiccups due to its significant side-effect profile, including the risk of QTc prolongation. **High-Yield Clinical Pearls for NEET-PG:** * **First-line for Intractable Hiccups:** Chlorpromazine (Oral or IV). * **Alternative/Second-line agents:** Baclofen (GABA-B agonist), Gabapentin, or Metoclopramide. * **Non-pharmacological trigger:** Gastric distension is the most common trigger for acute hiccups. * **Side effect to watch:** When using Chlorpromazine, monitor for hypotension and extrapyramidal symptoms (EPS).

Q: Which of the following antiepileptic agents acts on the GABAergic system to decrease the uptake of GABA into neurons and glial cells?

Tiagabine. ### Explanation **Correct Answer: D. Tiagabine** **Mechanism of Action:** Tiagabine is a selective inhibitor of the **GAT-1 (GABA Transporter-1)**. Under normal physiological conditions, GABA is cleared from the synaptic cleft into neurons and surrounding glial cells (astrocytes) via these transporters. By blocking GAT-1, Tiagabine prevents the reuptake of GABA, thereby increasing its concentration and prolonging its inhibitory action at the synaptic cleft. **Analysis of Incorrect Options:** * **A. Vigabatrin:** It acts on the GABAergic system but through a different mechanism. It is an irreversible inhibitor of **GABA-transaminase (GABA-T)**, the enzyme responsible for the degradation of GABA. This leads to increased intracellular levels of GABA. * **B. Progabide:** This is a **GABA receptor agonist** (acting on both GABA-A and GABA-B receptors) and a prodrug of GABA. It does not inhibit uptake. * **C. Gabapentin:** Despite its name, it does not act directly on GABA receptors or transporters. Its primary mechanism is the inhibition of **voltage-gated calcium channels (α2δ-1 subunit)**, which reduces the release of excitatory neurotransmitters like glutamate. **High-Yield NEET-PG Pearls:** * **Tiagabine:** Think "T" for **T**ransporter inhibitor. * **Vigabatrin:** Associated with a high-yield side effect: **Permanent bilateral visual field constriction** (requires periodic perimetry). It is the drug of choice for **Infantile Spasms** associated with Tuberous Sclerosis. * **GAT-1 vs. GABA-T:** Do not confuse reuptake (GAT-1/Tiagabine) with metabolism (GABA-T/Vigabatrin). * **Valproate:** Also affects GABA by inhibiting GABA-T and stimulating Glutamic Acid Decarboxylase (GAD), the enzyme that synthesizes GABA.

Q: All are adverse effects of phenytoin except?

Hypertension. **Explanation:** Phenytoin is a widely used hydantoin derivative for epilepsy, known for its narrow therapeutic index and a distinct profile of adverse effects. **Why Hypertension is the Correct Answer:** Phenytoin does **not** cause hypertension. In fact, when administered intravenously (especially if given too rapidly), phenytoin can cause **hypotension** and cardiac arrhythmias. This is primarily due to the solvent propylene glycol used in the formulation and the drug’s stabilizing effect on sodium channels in the myocardium. **Analysis of Incorrect Options:** * **Hypertrophy of Gums (Gingival Hyperplasia):** This is a classic side effect occurring in about 20% of patients. It is due to the overgrowth of gingival collagen fibers, stimulated by an increase in platelet-derived growth factor (PDGF). * **Hirsutism:** Phenytoin often causes excessive hair growth on the face and body, making it a less desirable choice for young female patients. * **Hypersensitivity:** Phenytoin can trigger various immune-mediated reactions, ranging from simple skin rashes to life-threatening conditions like **Stevens-Johnson Syndrome (SJS)** or **DRESS syndrome**, particularly in individuals with the HLA-B*1502 allele. **NEET-PG High-Yield Pearls:** To remember Phenytoin’s side effects, use the mnemonic **"PHENYTOIN"**: * **P**- P450 Inducer * **H**- Hypertrophy of gums / Hirsutism * **E**- Embryopathy (Fetal Hydantoin Syndrome: cleft lip/palate, microcephaly) * **N**- Neuropathy (Peripheral) * **Y**- Yields Vitamin D deficiency (Osteomalacia) * **T**- Teratogenicity * **O**- Osteomalacia * **I**- Interference with B12/Folate metabolism (Megaloblastic anemia) * **N**- Nystagmus (earliest sign of toxicity)

Q: Which of the following statements about phenytoin is FALSE?

Does not require drug dosage monitoring. Phenytoin is a high-yield topic in NEET-PG due to its complex pharmacokinetics and distinct side-effect profile. **Explanation for the Correct Option:** Option D is the false statement because Phenytoin **requires frequent Therapeutic Drug Monitoring (TDM)**. This is primarily due to its **zero-order (non-linear/saturation) kinetics** at therapeutic concentrations. Small increases in dose can lead to disproportionately large increases in plasma levels, rapidly reaching toxic ranges. Additionally, it has a **narrow therapeutic index** (10–20 µg/mL), making monitoring essential for safety and efficacy. **Analysis of Incorrect Options:** * **A. Causes hirsutism:** This is a well-known side effect. Phenytoin causes an overgrowth of body hair (hirsutism) and **gingival hyperplasia** (due to increased expression of platelet-derived growth factor). * **B. Has teratogenic effects:** Phenytoin is a known teratogen. It causes **Fetal Hydantoin Syndrome**, characterized by craniofacial anomalies (cleft lip/palate), microcephaly, and hypoplastic phalanges/nails. * **C. Has a narrow therapeutic index:** This is true. The margin between the effective dose and the toxic dose is very small, necessitating the TDM mentioned above. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Blocks voltage-gated sodium channels in the inactive state. * **Metabolism:** It is a potent **CYP450 inducer**, leading to numerous drug interactions (e.g., decreasing the efficacy of oral contraceptives and warfarin). * **Adverse Effects Mnemonic (P-H-E-N-Y-T-O-I-N):** **P**-450 induction, **H**irsutism, **E**nlarged gums, **N**ystagmus (earliest sign of toxicity), **Y**ellow-brown skin, **T**eratogenicity, **O**steomalacia (Vitamin D interference), **I**nterference with B12/Folate (Megaloblastic anemia), **N**europathy. * **Zero-order kinetics** is also followed by Aspirin (at high doses), Warfarin, and Ethanol.

Question 1

Which of the following local anesthetics is safer for surface and infiltrating anesthesia?

Accepted Answer

Lignocaine

Answer

Procaine

Answer

Cocaine

Answer

Amethocaine

Question 2

All of the following agents are used for prophylaxis of migraine, except?

Accepted Answer

Ethosuximide

Answer

Propranolol

Answer

Valproate

Answer

Topiramate

Question 3

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

Accepted Answer

Sedation

Answer

Osteomalacia

Answer

Maculopapular rash

Answer

Megaloblastic anaemia

Question 4

Buprenorphine is:

Accepted Answer

Partial agonist at mu receptor

Answer

Partial agonist at kappa receptor

Answer

Full agonist at mu receptor

Answer

Full agonist at kappa receptor

Question 5

A patient with recent-onset primary generalized epilepsy develops a drug reaction with a skin rash due to Phenytoin sodium. What is the most appropriate course of action?

Accepted Answer

Shift to sodium valproate

Answer

Shift to clonazepam

Answer

Restart phenytoin sodium after 2 weeks

Answer

Shift to Ethosuximide

Question 6

Which antihistamine is used in motion sickness?

Accepted Answer

Diphenhydramine

Answer

Cetirizine

Answer

Meclizine

Answer

Fexofenadine

Question 7

What is the drug of choice for intractable hiccups?

Accepted Answer

Chlorpromazine

Answer

Metoclopramide

Answer

Haloperidol

Answer

Thioridazine

Question 8

Which of the following antiepileptic agents acts on the GABAergic system to decrease the uptake of GABA into neurons and glial cells?

Accepted Answer

Tiagabine

Answer

Vigabatrin

Answer

Progabide

Answer

Gabapentin

Question 9

All are adverse effects of phenytoin except?

Accepted Answer

Hypertension

Answer

Hypertrophy of gums

Answer

Hirsutism

Answer

Hypersensitivity

Question 10

Which of the following statements about phenytoin is FALSE?

Accepted Answer

Does not require drug dosage monitoring

Answer

Causes hirsutism

Answer

Has teratogenic effects

Answer

Has a narrow therapeutic index

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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