Central Nervous System Pharmacology Practice Questions

Q: Which of the following antiepileptic drugs can be used to treat neonatal jaundice?

Phenobarbital. **Explanation:** **Phenobarbital** is the correct answer because of its potent ability to act as a **microsomal enzyme inducer**. In the context of neonatal jaundice, it induces the hepatic enzyme **UDP-glucuronosyltransferase (UGT1A1)**. This enzyme is responsible for the conjugation of free (unconjugated) bilirubin with glucuronic acid, making it water-soluble and excretable. By increasing the synthesis of this enzyme and Y-binding proteins (ligandin), phenobarbital enhances the clearance of bilirubin, particularly in conditions like **Crigler-Najjar Syndrome Type II** and occasionally in severe physiological jaundice. **Incorrect Options:** * **Phenytoin:** While it is a hepatic enzyme inducer, it does not significantly target the UGT1A1 pathway required for bilirubin conjugation and is associated with potential toxicity in neonates. * **Sodium Valproate:** This drug is an **enzyme inhibitor**. It would theoretically worsen jaundice by inhibiting metabolic pathways and carries a high risk of hepatotoxicity. * **Vigabatrin:** This drug acts by irreversibly inhibiting GABA transaminase. It has no significant effect on hepatic microsomal enzymes or bilirubin metabolism. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Phenobarbital remains the first-line drug for **Neonatal Seizures**. * **Crigler-Najjar Syndrome:** Phenobarbital is effective in **Type II** (partial enzyme deficiency) but ineffective in **Type I** (total enzyme deficiency). * **Adverse Effect:** A key side effect in children is **hyperactivity/behavioral changes**, whereas in adults, it causes sedation. * **Metabolism:** It follows first-order kinetics (unlike Phenytoin, which follows zero-order at high doses).

Q: What is the drug of choice for myoclonic epilepsy in pregnancy?

Sodium valproate. **Explanation:** The drug of choice for **Myoclonic Epilepsy** (such as Juvenile Myoclonic Epilepsy) is **Sodium Valproate**. It is a broad-spectrum antiepileptic drug (AED) that acts by increasing GABA levels, blocking voltage-gated sodium channels, and inhibiting T-type calcium channels. It is uniquely effective against myoclonic jerks, whereas many other AEDs can actually exacerbate them. **Why Sodium Valproate is the answer despite the pregnancy context:** In clinical practice, Valproate is generally avoided in pregnancy due to its high teratogenic potential (Neural Tube Defects) [1]. However, for **Myoclonic Epilepsy**, it remains the most effective agent. If a patient’s seizures are only controlled by Valproate, it is continued at the lowest effective dose with folic acid supplementation, as uncontrolled seizures pose a greater risk to the fetus than the drug itself [1]. (Note: Levetiracetam is often a preferred alternative in pregnancy, but among the given options, Valproate is the gold standard for myoclonus). **Analysis of Incorrect Options:** * **A. Carbamazepine:** Primarily used for focal seizures. It is contraindicated in myoclonic epilepsy as it can **worsen** myoclonic jerks. * **C. Phenobarbitone:** An enzyme inducer used in neonatal seizures; however, it is not the first-line for myoclonic patterns and carries significant sedative side effects. * **D. Phenytoin:** Like Carbamazepine, it is a sodium channel blocker that can aggravate myoclonic and absence seizures. **High-Yield NEET-PG Pearls:** * **Teratogenicity:** Valproate is associated with **Neural Tube Defects** (e.g., Spina Bifida). Screen with Alpha-fetoprotein and Level II Ultrasound. * **Drug of Choice (DOC):** Valproate is the DOC for all generalized seizures (Absence, Myoclonic, Tonic-Clonic). * **Avoid in Myoclonus:** Carbamazepine, Phenytoin, and Gabapentin.

Q: All of the following are therapeutic effects for which cannabinoids are commonly used, except?

Weight loss. **Explanation:** The correct answer is **D. Weight loss**. Cannabinoids, specifically those acting on **CB1 receptors** in the hypothalamus and mesolimbic system, are potent **appetite stimulants** (orexigenic effect). This leads to increased food intake and weight gain, often referred to as "the munchies." In clinical practice, synthetic cannabinoids like **Dronabinol** are FDA-approved to treat anorexia and weight loss associated with AIDS. Conversely, CB1 receptor *antagonists* (e.g., Rimonabant) were once studied for weight loss but were withdrawn due to psychiatric side effects. **Analysis of Incorrect Options:** * **A. Decreased intraocular pressure:** Cannabinoids effectively lower intraocular pressure (IOP) by increasing aqueous humor outflow and potentially decreasing production. While not first-line due to systemic side effects, this is a recognized pharmacological effect. * **B. Reduced muscle spasticity:** Cannabinoids (e.g., **Nabiximols**) are used as adjunctive therapy for symptomatic relief of spasticity in patients with **Multiple Sclerosis** who have not responded to other anti-spasticity medications. * **C. Relief of nausea and vomiting:** Cannabinoids possess significant antiemetic properties. Dronabinol and Nabilone are used specifically for **Chemotherapy-Induced Nausea and Vomiting (CINV)** in patients who fail to respond to conventional antiemetics. **High-Yield Clinical Pearls for NEET-PG:** * **Receptors:** CB1 (mainly CNS/Presynaptic inhibition) and CB2 (mainly Peripheral/Immune cells). * **Dronabinol:** Synthetic Δ9-THC used for CINV and AIDS-related cachexia. * **Nabiximols (Sativex):** 1:1 ratio of THC:CBD, used for MS spasticity. * **Epidiolex:** Purified CBD used for refractory pediatric seizures (Lennox-Gastaut and Dravet syndromes).

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

Ketamine. **Explanation:** The correct answer is **Ketamine**. The primary mechanism of action for Ketamine is the non-competitive antagonism of **NMDA (N-methyl-D-aspartate) receptors**, which are excitatory glutamate receptors. Unlike most other intravenous anesthetics, Ketamine does not act through the GABAergic system; instead, it produces "dissociative anesthesia" by interrupting transmission between the thalamocortical and limbic systems. **Analysis of Options:** * **Thiopentone (Option A):** A barbiturate that acts by increasing the **duration** of GABA-A receptor channel opening. At higher doses, it can directly activate the receptor (GABA-mimetic). * **Propofol (Option B):** Acts primarily by facilitating inhibitory neurotransmission through **GABA-A receptors**. It increases the binding affinity of GABA and, at high concentrations, directly activates the chloride channel. * **Zolpidem (Option C):** A non-benzodiazepine hypnotic ("Z-drug") that selectively binds to the **α1 subunit of the GABA-A receptor** (BZ1 site), mediating its sedative-hypnotic effects. **High-Yield Clinical Pearls for NEET-PG:** * **Ketamine "Triple High":** It is unique because it increases **BP (sympathomimetic)**, **Heart Rate**, and **Intracranial Pressure (ICP)**. It is the induction agent of choice in hypovolemic shock but contraindicated in head injuries. * **Dissociative Anesthesia:** Characterized by catalepsy, amnesia, and profound analgesia while the patient appears awake (eyes open). * **Emergence Delirium:** A common side effect of Ketamine, which can be prevented by pre-medication with Benzodiazepines (e.g., Midazolam).

Q: A patient develops nausea, vomiting, tingling and numbness on the tip of a finger that also turns blue after taking a drug for an acute attack of migraine. Which of the following is the most likely drug implicated in causing these findings?

Dihydroergotamine. ### Explanation **Correct Option: A. Dihydroergotamine** The patient is presenting with symptoms of **Ergotism** (St. Anthony’s Fire). Dihydroergotamine (DHE) and Ergotamine are non-selective 5-HT$_{1}$ receptor agonists used for acute migraine. Their primary side effect profile stems from **potent, long-lasting peripheral vasoconstriction** mediated by alpha-adrenergic receptors. The "blue finger" (cyanosis), tingling, and numbness are signs of **peripheral ischemia** and vasospasm. If left untreated, this can progress to gangrene. Nausea and vomiting are also common due to the stimulation of the Chemoreceptor Trigger Zone (CTZ). **Why Incorrect Options are Wrong:** * **B. Sumatriptan:** While triptans are selective 5-HT$_{1B/1D}$ agonists that cause vasoconstriction, they primarily affect cranial vessels. While they can cause "chest tightness" (coronary vasospasm), they rarely cause the severe peripheral ischemia/cyanosis characteristic of ergots. * **C. Aspirin:** An NSAID used for mild-to-moderate migraine. Its primary side effects are gastric irritation, peptic ulcers, and antiplatelet effects, not peripheral vasospasm. * **D. Butorphanol:** An opioid agonist-antagonist used as a nasal spray for migraine. It causes sedation, dizziness, and potential dependence, but does not cause vasoconstriction. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Ergotism:** Intense vasoconstriction + endothelial damage $\rightarrow$ thrombosis $\rightarrow$ gangrene. * **Contraindications for Ergots:** Coronary artery disease, peripheral vascular disease (Raynaud's), pregnancy, and uncontrolled hypertension. * **Drug Interaction:** Ergots should **not** be used within 24 hours of Triptans due to the risk of additive vasospastic reactions. * **Treatment of Ergotism:** Vasodilators like **Sodium Nitroprusside** or Nitroglycerin.

Q: Pethidine differs from morphine in producing which of the following effect?

Tachycardia. ### Explanation The correct answer is **Tachycardia**. **1. Why Tachycardia is the correct answer:** Morphine and most other opioids typically cause **bradycardia** due to central vagal stimulation. However, **Pethidine (Meperidine)** is unique because its chemical structure is related to **Atropine**. Due to this inherent antimuscarinic (atropine-like) activity, pethidine causes **tachycardia** instead of bradycardia. This is a classic "exception" frequently tested in pharmacology. **2. Why other options are incorrect:** * **Sedation (A):** Both morphine and pethidine are CNS depressants that produce significant sedation. While pethidine is sometimes perceived as "less sedating" in clinical practice, it is not a point of pharmacological difference in terms of the effect produced. * **Euphoria (C):** Both drugs act on $\mu$-opioid receptors in the brain to produce euphoria, which contributes to their high abuse potential. * **All of the above (D):** Since sedation and euphoria are common to both drugs, this option is incorrect. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mydriasis:** Unlike morphine (which causes "pinpoint pupils" via Edinger-Westphal nucleus stimulation), pethidine can cause **mydriasis** (pupillary dilation) due to its atropine-like action. * **Seizures:** Pethidine is metabolized to **norpethidine**, which is a CNS stimulant. In patients with renal failure or chronic use, norpethidine accumulation can lead to tremors and **seizures**. * **Smooth Muscle:** Pethidine has less inhibitory effect on the Sphincter of Oddi compared to morphine, making it traditionally preferred (though still controversial) in biliary colic. * **Interaction:** Pethidine is contraindicated with **MAO inhibitors** as it can precipitate a life-threatening "Serotonin Syndrome" (hyperpyrexia, coma, and convulsions).

Q: Carbamazepine is NOT used in which of the following conditions?

Migraine. Explanation: **Carbamazepine** is a sodium channel blocker that stabilizes hyperexcitable neuronal membranes [1], [4]. While it is a versatile drug in neurology and psychiatry, it has no established role in the acute treatment or prophylaxis of **Migraine** [2]. **Why Migraine is the Correct Answer:** The first-line drugs for migraine prophylaxis include Beta-blockers (Propranolol), Anticonvulsants (Topiramate, Valproate), Tricyclic Antidepressants (Amitriptyline), and Calcium Channel Blockers (Flunarizine) [2]. Carbamazepine is not effective for migraine and may even exacerbate headaches in some patients. **Analysis of Incorrect Options:** * **Mania:** Carbamazepine is a recognized **mood stabilizer** [5]. It is used as a second-line agent in Acute Mania and Prophylaxis of Bipolar Disorder, especially in patients who do not respond to Lithium [3]. * **Partial Seizure:** It is a **drug of choice (DOC)** for Focal (Partial) seizures and Generalized Tonic-Clonic Seizures (GTCS) [3]. It works by prolonging the inactivated state of voltage-gated sodium channels [5]. * **Trigeminal Neuralgia:** Carbamazepine is the **DOC** for Trigeminal Neuralgia [1]. It effectively reduces the paroxysmal neuropathic pain associated with this condition. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Blocks voltage-gated $Na^+$ channels [4]. * **Pharmacokinetics:** It is a potent **enzyme inducer** and exhibits **auto-induction** (induces its own metabolism). * **Side Effects:** Most common is diplopia/ataxia. Most serious include **Aplastic Anemia** and **Stevens-Johnson Syndrome** (associated with HLA-B*1502 allele). * **Other Uses:** Glossopharyngeal neuralgia and Diabetic Neuropathy. * **Contraindication:** It can **worsen Absence and Myoclonic seizures**.

Q: Which of the following causes vasoconstriction in blood vessels?

Cocaine. **Explanation:** **1. Why Cocaine is Correct:** Most local anesthetics (LAs) are naturally **vasodilators**. Cocaine is the unique exception. It causes potent **vasoconstriction** by inhibiting the reuptake of norepinephrine (NE) at the sympathetic nerve endings. This increased concentration of NE in the synaptic cleft leads to prolonged stimulation of alpha-adrenergic receptors on blood vessels. Clinically, this property makes cocaine useful for topical anesthesia in ENT procedures (e.g., nasal surgery) as it reduces bleeding and shrinks mucosal membranes. **2. Why the Other Options are Incorrect:** * **Lignocaine (Lidocaine):** A standard amide LA that causes significant vasodilation. This is why it is often combined with Adrenaline (epinephrine) to prolong its duration of action and reduce systemic toxicity. * **Prilocaine:** Also a vasodilator, though slightly less so than lignocaine. It is notable for causing methemoglobinemia at high doses. * **Bupivacaine:** A potent, long-acting amide LA that causes vasodilation. It is particularly known for its cardiotoxicity. **3. High-Yield Clinical Pearls for NEET-PG:** * **The "Exceptions" Rule:** While almost all LAs are vasodilators, **Cocaine** (potent vasoconstrictor) and **Ropivacaine/Levobupivacaine** (mild vasoconstrictive properties at clinical doses) are the exceptions. * **Adrenaline Ratios:** When adding adrenaline to LAs like Lignocaine, the standard concentration used is **1:200,000**. * **Contraindications:** Never use LAs with adrenaline in "end-artery" areas (fingers, toes, tip of the nose, penis, or ear lobes) to avoid ischemic necrosis. * **Ester vs. Amide:** Cocaine is an **Ester**, while Lignocaine, Prilocaine, and Bupivacaine are **Amides** (Tip: Amides have two "i"s in their name).

Question 1

Which of the following antiepileptic drugs can be used to treat neonatal jaundice?

Accepted Answer

Phenobarbital

Answer

Phenytoin

Answer

Sodium valproate

Answer

Vigabatrin

Question 2

What is the drug of choice for myoclonic epilepsy in pregnancy?

Accepted Answer

Sodium valproate

Answer

Carbamazepine

Answer

Phenobarbitone

Answer

Phenytoin

Question 3

All of the following are therapeutic effects for which cannabinoids are commonly used, except?

Accepted Answer

Weight loss

Answer

Decreased intraocular pressure

Answer

Reduced muscle spasticity

Answer

Relief of nausea and vomiting

Question 4

All of the following act on the GABA receptor except?

Accepted Answer

Ketamine

Answer

Thiopentone

Answer

Propofol

Answer

Zolpidem

Question 5

All of the following statements about lignocaine are true EXCEPT?

Accepted Answer

It is given orally for the treatment of cardiac arrhythmias.

Answer

It blocks active sodium channels with more affinity than resting sodium channels.

Answer

It can cause cardiotoxicity.

Answer

Adrenaline increases the duration of action of lignocaine when used for infiltration anesthesia.

Question 6

A patient develops nausea, vomiting, tingling and numbness on the tip of a finger that also turns blue after taking a drug for an acute attack of migraine. Which of the following is the most likely drug implicated in causing these findings?

Accepted Answer

Dihydroergotamine

Answer

Sumatriptan

Answer

Aspirin

Answer

Butorphanol

Question 7

Pethidine differs from morphine in producing which of the following effect?

Accepted Answer

Tachycardia

Answer

Sedation

Answer

Euphoria

Answer

All of the above

Question 8

Carbamazepine is NOT used in which of the following conditions?

Accepted Answer

Migraine

Answer

Mania

Answer

Partial seizure

Answer

Trigeminal neuralgia

Question 9

Which of the following causes vasoconstriction in blood vessels?

Accepted Answer

Cocaine

Answer

Lignocaine

Answer

Prilocaine

Answer

Bupivacaine

Question 10

The effect of local anesthesia can be increased by the addition of which substance?

Accepted Answer

Adrenaline

Answer

Isoprenaline

Answer

Dopamine

Answer

Felypressin (synthetic vasopressin)

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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