Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 781: Ketamine acts on which of the following?

A. NMDA receptor (Correct Answer)
B. Glycine receptor
C. GABAa receptor
D. Ach receptor

Explanation: ***NMDA receptor*** - **Ketamine** primarily acts as an **N-methyl-D-aspartate (NMDA) receptor antagonist**, blocking the effects of **glutamate**. - This action leads to its **dissociative anesthetic** effects, including analgesia, amnesia, and a cataleptic state. *Glycine receptor* - The **glycine receptor** is an inhibitory ionotropic receptor, primarily found in the **spinal cord** and brainstem. - Its activation leads to **hyperpolarization** and a decrease in neuronal excitability, a mechanism distinct from ketamine's action. *GABAa receptor* - The **GABAa receptor** is the primary inhibitory neurotransmitter receptor in the brain, and drugs like **benzodiazepines** and **barbiturates** act on it to produce sedation. - While ketamine has some indirect GABAergic effects at high doses, its primary mechanism of action is not through direct binding to GABAa receptors. *Ach receptor* - The **acetylcholine (Ach) receptor** is involved in various functions, including muscle contraction (nicotinic receptors) and parasympathetic responses (muscarinic receptors). - Drugs like **atropine** and **neostigmine** target these receptors, which are not the primary site of action for **ketamine**.

Question 782: Which antiepileptic drug is used for neuropathic pain and works by inhibiting voltage-gated calcium channels?

A. Carbamazepine
B. Levetiracetam
C. Gabapentin (Correct Answer)
D. Lamotrigine

Explanation: ***Gabapentin*** - **Gabapentin** is a commonly used antiepileptic drug that primarily acts by binding to the **alpha-2-delta subunit of voltage-gated calcium channels**, reducing calcium influx and subsequent neurotransmitter release. - This mechanism is particularly effective in treating **neuropathic pain**, such as diabetic neuropathy and postherpetic neuralgia. *Carbamazepine* - **Carbamazepine** works primarily by blocking **voltage-gated sodium channels**, thereby stabilizing neuronal membranes and inhibiting repetitive neuronal firing. - While effective for certain types of pain, like **trigeminal neuralgia**, its primary mechanism and widespread use for general neuropathic pain differ from gabapentin. *Levetiracetam* - **Levetiracetam's** precise mechanism of action is not fully understood, but it is thought to involve binding to the **synaptic vesicle protein 2A (SV2A)**, modulating neurotransmitter release. - It is primarily used as an antiepileptic for various seizure types and is generally **not a first-line treatment for neuropathic pain**. *Lamotrigine* - **Lamotrigine** works by blocking **voltage-gated sodium channels** and, to a lesser extent, **calcium channels**, thereby stabilizing neuronal membranes and inhibiting excitatory neurotransmitter release. - While it has some efficacy in neuropathic pain, its primary mechanism and therapeutic profile are distinct from gabapentin's selective action on voltage-gated calcium channels.

Question 783: A patient with epilepsy is given a drug that enhances GABA activity to prevent seizure activity. Which drug is appropriate?

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

Explanation: ***Valproic acid*** - **Valproic acid** primarily enhances **GABAergic activity** by inhibiting GABA transaminase, increasing GABA synthesis, and reducing GABA reuptake, which collectively help to stabilize neuronal activity and prevent seizures. - It is a **broad-spectrum anticonvulsant** effective against various seizure types, including generalized tonic-clonic, absence, and myoclonic seizures. *Phenytoin* - **Phenytoin** works by **blocking voltage-gated sodium channels**, thereby stabilizing neuronal membranes and preventing repetitive firing of action potentials. - It is effective for **focal (partial) seizures** and generalized tonic-clonic seizures, but its primary mechanism is not direct GABA potentiation. *Gabapentin* - **Gabapentin** modulates the **voltage-gated calcium channels** (specifically the α₂δ subunit), reducing the release of excitatory neurotransmitters. - While it has broad-spectrum effects that can reduce seizure activity, its direct mechanism of action is not primarily through enhancing GABA activity. *Lamotrigine* - **Lamotrigine** stabilizes neuronal membranes by **blocking voltage-gated sodium channels** and, to a lesser extent, inhibiting voltage-gated calcium channels. - It also reduces the release of excitatory neurotransmitters like glutamate, but it does not directly enhance GABAergic transmission.

Question 784: A patient presents with a rapid onset of muscle weakness after starting a new medication. Which physiological mechanism should be primarily investigated?

A. Sodium channel blocking
B. Potassium channel activation
C. Calcium channel enhancement
D. Acetylcholine receptor blocking (Correct Answer)

Explanation: **Acetylcholine receptor blocking** ✓ - Many medications can block **postsynaptic acetylcholine receptors** at the neuromuscular junction, causing **rapid-onset muscle weakness** or paralysis [3], [4]. - **Neuromuscular blockers** (e.g., rocuronium, succinylcholine) directly block ACh receptors, preventing muscle contraction [2], [4]. - **Aminoglycoside antibiotics** (e.g., gentamicin, tobramycin) can interfere with neuromuscular transmission, especially in patients with renal impairment or myasthenia gravis [1]. - This mechanism explains **acute flaccid paralysis** with preserved consciousness and sensation. - **Key clinical point:** This is the PRIMARY mechanism to investigate for medication-induced rapid-onset muscle weakness. *Potassium channel activation* - Activating potassium channels causes **hyperpolarization** of the cell membrane, making it less excitable. - While theoretically possible, **rapid-onset severe muscle weakness** from medications is NOT commonly mediated through this mechanism. - Conditions like **hypokalemic periodic paralysis** involve potassium channel dysfunction, but this is not the typical drug-induced scenario. *Sodium channel blocking* - Blocking sodium channels reduces the ability of muscle cells to **depolarize** and generate action potentials. - **Local anesthetics** and certain **antiarrhythmics** block sodium channels, but these typically cause localized or cardiac effects. - **Rapid-onset widespread skeletal muscle weakness** is NOT the primary manifestation of sodium channel blockers. - These drugs more commonly affect cardiac conduction or cause local numbness. *Calcium channel enhancement* - **Enhancing** calcium channel activity would increase intracellular calcium, promoting muscle contraction (NOT weakness). - Medications that **block** calcium channels (e.g., verapamil, diltiazem) primarily affect vascular smooth muscle and cardiac muscle. - Calcium channel blockers do NOT typically cause acute skeletal muscle weakness as their primary effect. - This option represents the opposite mechanism of what would cause weakness.

Question 785: What are the possible CNS effects of local anesthetic agents?

A. Convulsions
B. All of the options (Correct Answer)
C. Perioral numbness
D. Depression

Explanation: ***All of the options*** - **All three listed effects are genuine CNS manifestations** of local anesthetic systemic toxicity (LAST). - Local anesthetics produce a **biphasic CNS effect**: initial excitatory symptoms (perioral numbness, seizures) followed by depressive symptoms at higher concentrations. - Since the question asks for "**possible** CNS effects" (not the most severe or primary effect), all listed options are medically accurate answers. **CNS Effects of Local Anesthetics:** **Early/Excitatory Phase:** - *Perioral numbness* - Often the first CNS sign, indicating rising plasma levels; numbness and tingling around the mouth and tongue - *Convulsions/Seizures* - Result from blockade of inhibitory neurons, causing uninhibited excitatory activity; a serious manifestation requiring immediate treatment **Late/Depressive Phase:** - *Depression* - Occurs at very high toxic concentrations; includes CNS depression, loss of consciousness, respiratory depression, and potentially coma - This follows the excitatory phase as local anesthetics depress all neuronal activity at extremely high doses *Convulsions alone* - While convulsions are a serious and characteristic CNS effect, they represent only one possible manifestation, not all possible effects. *Perioral numbness alone* - This is an early warning sign of LAST but not the only CNS effect possible. *Depression alone* - This is a late-stage effect but not the only CNS manifestation possible.

Question 786: Which of the following drugs is useful in the prophylaxis of migraine?

A. Propranolol (Correct Answer)
B. Sumatriptan
C. Domperidone
D. Ergotamine

Explanation: ***Propranolol*** - **Propranolol** is a **beta-blocker** commonly used for **migraine prophylaxis** by reducing the frequency and severity of attacks. - It works by modulating **serotonergic pathways** and reducing the body's **fight-or-flight response**, which can be a trigger for migraines. *Sumatriptan* - **Sumatriptan** is a **serotonin (5-HT1B/1D) receptor agonist** used for the **acute treatment** of migraine attacks, not for prophylaxis. - It works by causing **vasoconstriction** of cranial blood vessels and inhibiting the release of **pro-inflammatory neuropeptides**. *Domperidone* - **Domperidone** is a **dopamine antagonist** used as an **antiemetic** to relieve nausea and vomiting, which can be associated with migraine attacks. - It does not have a role in the **prophylactic treatment** of migraine itself. *Ergotamine* - **Ergotamine** is an **ergot alkaloid** used for the **acute treatment** of moderate to severe migraines. - Due to its potential for **vasoconstriction** and **drug-induced headache** (medication overuse headache), it is not recommended for routine prophylaxis.

Question 787: Oculogyric crisis is known to be produced by all of the following drugs except:

A. Perphenazine
B. Atropine (Correct Answer)
C. Prochlorperazine
D. Trifluoperazine

Explanation: ***Atropine*** - **Atropine** is an **anticholinergic drug** that primarily causes mydriasis (pupil dilation) and cycloplegia (paralysis of ciliary muscle), but it is not known to cause oculogyric crisis. - Oculogyric crisis is a form of **acute dystonia**, which is typically associated with dopamine antagonists. *Prochlorperazine* - **Prochlorperazine** is a **dopamine receptor antagonist** and a typical antipsychotic, commonly used as an antiemetic. - It is known to produce **extrapyramidal symptoms**, including **acute dystonias** like oculogyric crisis, due to its dopamine-blocking effects. *Perphenazine* - **Perphenazine** is a **first-generation (typical) antipsychotic** with potent dopamine-blocking activity. - Similar to other typical antipsychotics, it can cause **extrapyramidal side effects**, including **oculogyric crisis**. *Trifluoperazine* - **Trifluoperazine** is a **high-potency typical antipsychotic** that strongly blocks dopamine D2 receptors. - Its strong dopamine antagonism makes it highly prone to causing **extrapyramidal symptoms**, such as **acute dystonias** like oculogyric crisis.

Question 788: Which of the following is true about barbiturates?

A. Limbic system is most sensitive to the depressive action of barbiturates to CNS
B. Shows GABA facilitatory action (Correct Answer)
C. Enhances GABAergic activity by mimicking GABA's effects
D. Primarily acts by blocking voltage gated Na+ and K+ channels

Explanation: ***Shows GABA facilitatory action*** - Barbiturates enhance the effect of **GABA** (gamma-aminobutyric acid), the primary inhibitory neurotransmitter in the central nervous system, by increasing the **duration** of chloride channel opening. - This facilitatory action leads to **hyperpolarization** of neurons, making them less excitable and resulting in CNS depression. - This is the **primary mechanism** of action of barbiturates at therapeutic doses. *Enhances GABAergic activity by mimicking GABA's effects* - While barbiturates enhance GABAergic activity, they do not **mimic GABA's effects** in the same direct way that full agonists do. - Instead of acting as direct agonists, barbiturates **allosterically modulate** the GABA<sub>A</sub> receptor, increasing the receptor's affinity for GABA and prolonging the opening time of the associated chloride channel. *Limbic system is most sensitive to the depressive action of barbiturates to CNS* - The **reticular activating system (RAS)** in the brainstem, which plays a crucial role in regulating wakefulness and arousal, is generally considered the most sensitive area to the depressive effects of barbiturates. - While the limbic system is affected, its sensitivity is not uniquely highest compared to other CNS regions like the RAS, which is critical for the sedative and hypnotic effects observed. *Primarily acts by blocking voltage gated Na+ and K+ channels* - This is **incorrect**. The primary mechanism of barbiturates is through **GABA<sub>A</sub> receptor modulation**, not by blocking voltage-gated ion channels. - While barbiturates can have non-specific membrane effects on voltage-gated channels at very high (toxic) concentrations, this is not their primary or therapeutic mechanism of action.

Question 789: Which of the following statements about the anti-Parkinson drug levodopa is true?

A. Levodopa is an active metabolite of dopamine.
B. About 50% of administered levodopa is peripherally converted to dopamine.
C. Only a small percentage of administered levodopa crosses the blood-brain barrier (approximately 2%). (Correct Answer)
D. Levodopa is not used in the management of hepatic coma.

Explanation: ***Only a small percentage of administered levodopa crosses the blood-brain barrier (approximately 2%).*** - This is the **correct statement**. Only about **1-5%** (approximately 2%) of orally administered levodopa crosses the **blood-brain barrier** to reach the brain where it is converted to dopamine. - The majority is metabolized peripherally by aromatic L-amino acid decarboxylase (AADC), which emphasizes the need to co-administer levodopa with a **peripheral decarboxylase inhibitor** like **carbidopa** or **benserazide** to increase CNS availability. - This poor bioavailability to the CNS is a fundamental pharmacokinetic challenge in levodopa therapy. *Levodopa is not used in the management of hepatic coma.* - While this statement is technically true (levodopa has no indication for hepatic coma), it is not the best answer as it simply states what levodopa is NOT used for rather than describing its pharmacological properties. - Hepatic coma is managed with lactulose, rifaximin, and measures to reduce ammonia, not anti-Parkinson drugs. *Levodopa is an active metabolite of dopamine.* - This is **incorrect** - the relationship is reversed. **Levodopa** is a **precursor to dopamine**, not a metabolite of it. - Levodopa is converted TO dopamine by decarboxylase enzymes, making dopamine the metabolite of levodopa. - Dopamine itself cannot effectively cross the **blood-brain barrier**, which is why its precursor levodopa must be administered. *About 50% of administered levodopa is peripherally converted to dopamine.* - This is **incorrect**. A much **higher percentage** (approximately **90-95%**) of administered levodopa is peripherally converted to dopamine when given alone without a **peripheral decarboxylase inhibitor**. - This extensive peripheral conversion leads to systemic side effects like nausea, vomiting, and cardiac arrhythmias, while reducing the amount of levodopa reaching the brain.

Question 790: What is the drug of choice for aborting the acute attack of migraine?

A. NSAIDs such as indomethacin
B. Opioids such as morphine
C. Triptans such as sumatriptan (Correct Answer)
D. Glucocorticoids

Explanation: ***Triptans such as sumatriptan*** - **Triptans** are **serotonin 5-HT1B/1D receptor agonists** that cause **vasoconstriction** of intracranial blood vessels and inhibit pronociceptive neuropeptide release, making them highly effective for acute migraine attacks. - They are considered the **first-line specific treatment** for moderate to severe migraine pain or when NSAIDs are ineffective. *NSAIDs such as indomethacin* - **NSAIDs** are effective for mild to moderate migraine attacks but are generally **less effective** than triptans for severe attacks. - While they can reduce inflammation and pain, their mechanism of action is **non-specific** compared to triptans in targeting migraine pathology. *Opioids such as morphine* - **Opioids** are generally **not recommended** for acute migraine treatment due to their potential for **abuse, dependence**, and lack of specific anti-migraine effects. - They can also worsen migraine outcomes over time and contribute to **medication overuse headache**. *Glucocorticoids* - **Glucocorticoids** like dexamethasone may be used as **adjunctive therapy** to prevent migraine recurrence, particularly in status migrainosus. - However, they are **not the primary drug of choice** for aborting an acute attack due to their slower onset of action and broad side effect profile.

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

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