Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 871: Secobarbital is what type of barbiturate?

A. Long acting barbiturate
B. Intermediate acting barbiturate
C. Short acting barbiturate (Correct Answer)
D. Ultra short acting barbiturate

Explanation: ***Short acting barbiturate*** - **Secobarbital** is classified as a short-acting barbiturate, with an onset of action of 15-30 minutes and a duration of 3-6 hours. - Due to its rapid onset and relatively short duration, it has been used as a **sedative-hypnotic** for inducing sleep. *Long acting barbiturate* - **Long-acting barbiturates** like **phenobarbital** have a prolonged duration of action, typically lasting 10-16 hours. - They are primarily used as **antiepileptics** due to their sustained effects. *Intermediate acting barbiturate* - **Intermediate-acting barbiturates** such as **amobarbital** have durations of action between 6-10 hours. - They were historically used for insomnia, but their use has declined due to safer alternatives. *Ultra short acting barbiturate* - **Ultra-short-acting barbiturates** like **thiopental** have an extremely rapid onset (seconds) and very short duration (minutes). - They are mainly used for **induction of anesthesia** due to their quick action and rapid redistribution.

Question 872: Muscle rigidity due to opioids is primarily caused by their effect on which receptor?

A. mu (Correct Answer)
B. kappa
C. sigma
D. delta

Explanation: ***mu*** - Opioids, by activating **mu-opioid receptors**, particularly in the **brainstem** and **spinal cord**, can cause a phenomenon known as "wooden chest syndrome" or muscle rigidity. - This effect results from increased dopamine turnover in the **nigrostriatal pathway** and is pronounced with rapid intravenous administration of potent opioids like **fentanyl**. *kappa* - **Kappa-opioid receptors** are primarily associated with effects like **dysphoria** [1], **sedation**, and **diuresis**. - While they contribute to some opioid effects, they are not the primary mediators of **muscle rigidity**. *sigma* - The **sigma receptor** is not considered a classical opioid receptor and is not directly involved in the analgesic effects of opioids. - Activation of **sigma receptors** is associated with effects like **dysphoria**, hallucinations, and motor incoordination, but not the specific muscle rigidity caused by opioids. *delta* - **Delta-opioid receptors** play a role in **analgesia** [1], **mood regulation**, and **epileptic seizures**. - They are not directly implicated in the mechanism of **opioid-induced muscle rigidity**.

Question 873: Entacapone acts by inhibiting which of the following enzyme?

A. COMT (Correct Answer)
B. MAO-A
C. MAO-B
D. Decarboxylase

Explanation: ***Correct: COMT*** - **Entacapone** is a selective, reversible **COMT (Catechol-O-Methyltransferase) inhibitor** [1], [2] - Acts **peripherally** (does not cross blood-brain barrier) [1], [2] - Used as **adjunct to levodopa/carbidopa** in Parkinson's disease [2] - **Mechanism:** Prevents peripheral conversion of levodopa to 3-O-methyldopa, thereby **increasing levodopa bioavailability** and prolonging its duration of action [1], [2] - Reduces "wearing-off" phenomenon in Parkinson's patients [2] *Incorrect: MAO-A* - Monoamine oxidase-A metabolizes dopamine, norepinephrine, and serotonin - **Moclobemide** is a reversible MAO-A inhibitor (antidepressant) - Not the mechanism of entacapone *Incorrect: MAO-B* - Monoamine oxidase-B preferentially metabolizes dopamine in the CNS - **Selegiline and rasagiline** are MAO-B inhibitors used in Parkinson's disease [2] - These work centrally, unlike entacapone which is peripheral [2] *Incorrect: Decarboxylase* - DOPA decarboxylase converts levodopa to dopamine - **Carbidopa and benserazide** are decarboxylase inhibitors (given with levodopa) [2] - Entacapone works downstream by inhibiting COMT, not decarboxylase

Question 874: A patient has frequent migraine attacks. Which of the following drugs is recommended for prophylaxis?

A. None of the options
B. Propranolol (Correct Answer)
C. Pindolol
D. Ergotamine

Explanation: **Correct: Propranolol** - Propranolol is a **beta-blocker** commonly used for **migraine prophylaxis** [1] - It is **FDA-approved** and considered a **first-line agent** for preventing migraine attacks [1] - It works by reducing the frequency and severity of migraine attacks through its effects on vascular tone and neuronal excitability [1] *Incorrect: Pindolol* - Pindolol is a beta-blocker but is **less effective for migraine prophylaxis** compared to propranolol - It has **intrinsic sympathomimetic activity (ISA)**, which reduces its efficacy in preventing migraines - Not a preferred agent for migraine prevention *Incorrect: Ergotamine* - Ergotamine is used for **acute treatment** of migraine attacks, **not for prophylaxis** [2] - It works by constricting blood vessels and is a vasoconstrictor [2] - **Not suitable for daily preventive use** due to potential side effects, risk of ergotism, and medication overuse headaches (rebound headaches) [2] *Incorrect: None of the options* - This option is incorrect because **propranolol** is a well-established and recommended drug for migraine prophylaxis according to current guidelines

Question 875: The mechanism of action of haloperidol is the blockade of

A. Serotonin receptor
B. GABA receptor
C. Dopamine receptor (Correct Answer)
D. Adrenergic receptor

Explanation: ***Dopamine receptor*** - Haloperidol is a **first-generation antipsychotic** that primarily acts as a potent **D2 dopamine receptor antagonist**. - Its therapeutic effects in treating psychosis are largely due to blocking **dopamine D2 receptors** in the mesolimbic pathway, which helps reduce positive symptoms like hallucinations and delusions. *Serotonin receptor* - While some atypical (second-generation) antipsychotics block serotonin receptors (e.g., 5-HT2A), **haloperidol's primary mechanism of action is not serotonin receptor blockade**. - Serotonin receptor antagonism is more associated with the mechanism of action of newer antipsychotics, which also exhibit D2 antagonism but with a different receptor profile. *GABA receptor* - **Haloperidol does not primarily act on GABA receptors**; drugs like benzodiazepines are known for their GABAergic effects. - GABA (gamma-aminobutyric acid) is the main inhibitory neurotransmitter in the brain, and drugs targeting its receptors are typically anxiolytics or sedatives. *Adrenergic receptor* - Although haloperidol can have some weak alpha-1 adrenergic receptor blocking activity, this is a **secondary effect** and not its primary mechanism of action. - Its antipsychotic efficacy is overwhelmingly attributed to its potent **dopamine receptor blockade**.

Question 876: Symptomatic treatment is only required in withdrawal syndrome caused by:

A. Alcohol
B. Cocaine
C. Morphine
D. Cannabis (Correct Answer)

Explanation: ***Cannabis*** - **Cannabis withdrawal syndrome** is generally mild and non-life-threatening, **requiring only symptomatic management** for symptoms such as irritability, anxiety, sleep disturbances, and cravings. - Unlike withdrawal from opioids or alcohol, cannabis withdrawal does not present with severe physiological complications, seizures, or significant psychological distress requiring pharmacotherapy. - **Supportive care alone is sufficient** with reassurance, hydration, and rest. *Morphine* - **Opioid withdrawal** (e.g., from morphine) can be very distressing and painful, involving severe gastrointestinal symptoms, myalgia, and intense cravings. - **Requires pharmacological intervention** with medications like **methadone**, **buprenorphine**, or **clonidine** for symptom control and to prevent relapse. - Not merely symptomatic treatment. *Alcohol* - **Alcohol withdrawal syndrome** can be severe and life-threatening, potentially progressing to **delirium tremens** and seizures. - **Necessitates pharmacological treatment** with **benzodiazepines** (e.g., lorazepam, diazepam) to prevent serious complications. - Symptomatic treatment alone is inadequate and dangerous. *Cocaine* - **Cocaine withdrawal** is characterized by **dysphoria**, fatigue, hypersomnia, and intense cravings with high relapse risk. - While primarily managed with supportive care, **severe cases often require pharmacological intervention** for depression (antidepressants) and intense cravings. - Unlike cannabis, the psychological severity often necessitates more than just symptomatic management.

Question 877: Which of the following drugs is primarily used for the treatment of Parkinson's disease?

A. Mazindol
B. Benserazide
C. Levodopa (Correct Answer)
D. Bromocriptine

Explanation: ***Levodopa*** - Levodopa is a **dopamine precursor** that crosses the blood-brain barrier and is converted to dopamine in the brain, replacing the depleted dopamine in Parkinson's disease [1], [2]. - It is considered the **most effective drug** for managing the motor symptoms of Parkinson's disease, particularly in the early and moderate stages [2], [4]. *Mazindol* - **Mazindol** is an appetite suppressant used for obesity and acts primarily as a norepinephrine-dopamine reuptake inhibitor. - It is **not indicated** for the treatment of Parkinson's disease. *Benserazide* - **Benserazide** is a **peripheral DOPA decarboxylase inhibitor** that does not cross the blood-brain barrier [1]. - It is used in combination with levodopa (e.g., in co-beneldopa) to prevent the peripheral metabolism of levodopa, increasing its availability to the brain, but it is **not used alone** to treat Parkinson's disease [1]. *Bromocriptine* - **Bromocriptine** is a **dopamine agonist** that directly stimulates dopamine receptors in the brain [3]. - While used in Parkinson's disease, it is generally considered a **second-line treatment** or used as an adjunct to levodopa, and not the primary drug [3].

Question 878: Administration of which of the following will reverse respiratory depression caused by opioids?

A. Naloxone (Correct Answer)
B. Kappa receptor blocker
C. Delta receptor blocker
D. Adrenergic receptor stimulator

Explanation: ***Naloxone*** - **Naloxone** is a pure **opioid receptor antagonist** that rapidly reverses all effects of opioid overdose, including respiratory depression - It has high affinity for **mu-opioid receptors**, which mediate both respiratory depression and analgesia - Naloxone is the **gold standard antidote** for opioid overdose and life-threatening respiratory depression - It reverses opioid effects within 1-2 minutes when given intravenously *Kappa receptor blocker* - **Kappa receptors** primarily mediate dysphoria, sedation, and some analgesia - The life-threatening **respiratory depression** from opioid overdose is primarily mediated by **mu receptors**, not kappa receptors - Selective kappa blockade would not effectively reverse mu-opioid induced respiratory depression *Delta receptor blocker* - **Delta opioid receptors** are primarily involved in modulating pain perception and emotional responses - They have minimal direct involvement in **respiratory depression** compared to mu receptors - Blocking delta receptors would not effectively counteract respiratory depression induced by **mu-opioid agonists** like morphine, fentanyl, or heroin *Adrenergic receptor stimulator* - **Adrenergic stimulators** (e.g., epinephrine) act on the sympathetic nervous system and may cause bronchodilation - They do not reverse the **central mechanism** of opioid-induced respiratory depression, which occurs at the brainstem respiratory centers via opioid receptors - While they might provide some cardiovascular support, they do not address the underlying **CNS depression** and are not appropriate antidotes for opioid toxicity

Question 879: Which of the following is a non-cholinergic agent?

A. Galantamine
B. Donepezil
C. Tacrine
D. Memantine (Correct Answer)

Explanation: ***Memantine*** - Memantine is an **NMDA receptor antagonist** and works by blocking the effects of excessive **glutamate**, a neurotransmitter that can contribute to neuronal damage in Alzheimer's disease. - Unlike the other options, it does not directly interfere with the **acetylcholine** system but rather modulates glutamatergic neurotransmission. *Galantamine* - Galantamine is an **acetylcholinesterase inhibitor** and an allosteric modulator of nicotinic acetylcholine receptors. - It increases the availability of **acetylcholine** in the synaptic cleft, making it a cholinergic agent. *Donepezil* - Donepezil is a **reversible acetylcholinesterase inhibitor** used in the treatment of Alzheimer's disease. - Its mechanism of action involves increasing the concentration of **acetylcholine** in the brain, thus it is a cholinergic agent. *Tacrine* - Tacrine was one of the first **acetylcholinesterase inhibitors** approved for Alzheimer's disease. - It works by preventing the breakdown of **acetylcholine**, thereby increasing its levels in the brain and is considered a cholinergic agent.

Question 880: What is the drug used in uncomplicated alcohol withdrawal?

A. Diazepam (Correct Answer)
B. Clonidine
C. Methadone
D. Propranolol

Explanation: ***Diazepam***- **Benzodiazepines** like diazepam are the cornerstone of treatment for alcohol withdrawal due to their ability to mitigate severe symptoms such as **seizures** and **delirium tremens** [1].- Diazepam, with its **long half-life**, provides a sustained therapeutic effect, helping to prevent symptom re-emergence.*Clonidine*- While clonidine can alleviate **autonomic symptoms** like elevated heart rate and blood pressure, it does not prevent **seizures or delirium**, which are critical concerns in alcohol withdrawal.- It is often used as an **adjunct** but not as monotherapy for uncomplicated withdrawal.*Methadone*- Methadone is an **opioid agonist** primarily used in the treatment of **opioid addiction**, not alcohol withdrawal.- It has no role in directly managing symptoms of alcohol withdrawal and could be dangerous if misused in this context.*Propranolol*- Propranolol is a **beta-blocker** that can help reduce some **autonomic symptoms** such as **tremors** and **tachycardia**.- Similar to clonidine, it does not address the risk of **seizures** or **delirium tremens**, making it unsuitable as a primary treatment.

Practice by Chapter

General Anesthetics

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Local Anesthetics

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Antiparkinsonian Drugs

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Opioid Analgesics

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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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