Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 851: Which antipsychotic drug is approved for the management of psychosis in Parkinsonian patients?

A. risperidone
B. clozapine (Correct Answer)
C. olanzapine
D. haloperidol

Explanation: ***Correct: Clozapine*** - **Clozapine** is the only antipsychotic extensively studied and approved for the treatment of **psychosis in Parkinson's disease (PDP)** due to its low propensity to exacerbate motor symptoms. - Its unique pharmacological profile, including lower **D2 receptor blockade** compared to other antipsychotics, makes it suitable for this vulnerable population. - Clozapine has the strongest evidence base for efficacy without worsening motor function in PDP. *Incorrect: Olanzapine* - **Olanzapine** has a significant **risk of worsening motor symptoms** in Parkinson's patients due to its potent **D2 receptor antagonism**. - It is generally contraindicated for treating psychosis in Parkinson's disease. *Incorrect: Haloperidol* - **Haloperidol** is a high-potency typical antipsychotic with strong **D2 receptor blockade**, which can severely **worsen Parkinsonian motor symptoms** (e.g., rigidity, bradykinesia). - Its use is strictly avoided in patients with Parkinson's disease. *Incorrect: Risperidone* - **Risperidone** also carries a considerable risk of **exacerbating motor symptoms** in Parkinson's disease due to its **D2 receptor antagonism**, although less severe than haloperidol. - It is generally not recommended as a first-line treatment for PDP.

Question 852: Which antiemetic phenothiazine has labyrinthine suppressant activity and is used for vertigo?

A. Prochlorperazine
B. Promethazine (Correct Answer)
C. Cinnarizine
D. Hyoscine

Explanation: ***Promethazine*** - Promethazine is a **phenothiazine derivative** with strong **antihistaminic (H1)** properties, making it highly effective for **labyrinthine suppression** and treatment of vertigo. - It is widely used for **motion sickness, vertigo, and nausea** associated with vestibular disturbances. - Its mechanism combines **dopamine D2 receptor antagonism** (phenothiazine effect) with potent **antihistaminic** and **anticholinergic** actions that specifically suppress vestibular function. - The antihistaminic component is particularly important for labyrinthine suppressant activity. *Prochlorperazine* - While prochlorperazine is a **phenothiazine antiemetic**, it is primarily used for severe nausea and vomiting (migraine, postoperative, chemotherapy-induced). - It has predominantly **dopamine D2 antagonist** activity at the chemoreceptor trigger zone (CTZ) but weaker antihistaminic properties compared to promethazine. - Less commonly used specifically for vertigo compared to promethazine due to weaker vestibular suppressant effects. *Cinnarizine* - While effective for vertigo, cinnarizine is an **antihistamine** and **calcium channel blocker**, not a phenothiazine. - It acts on the **vestibular system** by inhibiting calcium influx into vestibular sensory cells. *Hyoscine* - Hyoscine (**scopolamine**) is an **anticholinergic drug** (not a phenothiazine) effective for motion sickness and some forms of vertigo. - Works by blocking **muscarinic acetylcholine receptors** in the vestibular nuclei.

Question 853: Which of the following drugs has the maximum chances of causing hyperprolactinemia?

A. Clozapine
B. Olanzapine
C. Ziprasidone
D. Risperidone (Correct Answer)

Explanation: ***Risperidone*** - **Risperidone** has a higher propensity to cause **hyperprolactinemia** compared to other atypical antipsychotics due to its strong **dopamine D2 receptor antagonism**, which disinhibits prolactin secretion [1]. - This side effect can lead to symptoms like **galactorrhea**, **amenorrhea**, **gynecomastia**, and **sexual dysfunction** [1]. *Clozapine* - **Clozapine** generally has a **low risk of hyperprolactinemia** because it has a relatively weak affinity for **dopamine D2 receptors** and also acts as a **serotonin 5-HT2A antagonist**, which can counteract prolactin elevation [1]. - While other severe side effects like **agranulocytosis** are associated with clozapine, hyperprolactinemia is not a prominent concern. *Olanzapine* - **Olanzapine** has a moderate potential for elevating **prolactin levels**, often less than risperidone but more than aripiprazole or quetiapine. - Its effects on prolactin are attributable to its **dopamine D2 receptor antagonism**, but other pharmacological properties can modulate this effect. *Ziprasidone* - **Ziprasidone** is known for its **low risk of hyperprolactinemia**, similar to aripiprazole [1]. - This is partly due to its **less potent D2 receptor antagonism** and its additional actions as a serotonin 5-HT1A agonist, which can actually decrease prolactin release.

Question 854: Which of the following is the shortest-acting competitive neuromuscular blocking agent?

A. Atracurium
B. Rocuronium
C. Mivacurium (Correct Answer)
D. Cisatracurium

Explanation: ***Mivacurium*** - Mivacurium is characterized by its **rapid onset** and **ultrashort duration** of action, primarily due to its hydrolysis by plasma pseudocholinesterase [3]. - This rapid metabolism makes it highly suitable for procedures requiring **brief neuromuscular blockade** or when rapid recovery is desirable. *Atracurium* - Atracurium has an **intermediate duration** of action and is primarily metabolized by **Hofmann elimination**, a non-enzymatic chemical degradation, and ester hydrolysis [3]. - While it's useful in patients with renal or hepatic dysfunction, its duration is significantly longer than mivacurium [4]. *Rocuronium* - Rocuronium is an **intermediate-acting** neuromuscular blocking agent known for its **rapid onset** of action, making it a common choice for **rapid sequence induction** [1]. - Its duration of action is longer than mivacurium and it is primarily eliminated by the kidneys and liver [2]. *Cisatracurium* - Cisatracurium is an **intermediate-acting** neuromuscular blocker that is an isomer of atracurium [3]. - It also undergoes **Hofmann elimination**, but it is more potent and produces fewer histamine release issues than atracurium, yet its duration is still longer than mivacurium [3].

Question 855: Shortest-acting non-depolarizing muscle relaxant is:

A. Mivacurium (Correct Answer)
B. Atracurium
C. Succinylcholine
D. Vecuronium

Explanation: ***Mivacurium*** - **Mivacurium** is an intermediate-acting **non-depolarizing** neuromuscular blocker due to its rapid metabolism by **plasma cholinesterases**, making it the shortest-acting among the non-depolarizing agents available [1, 2]. - Its short duration of action (12-18 minutes) allows for quicker recovery of muscle function, which can be advantageous for **short surgical procedures** or for rapid control of muscle relaxation when precise timing is crucial [2]. *Succinylcholine* - **Succinylcholine** is a **depolarizing** neuromuscular blocker, not non-depolarizing, and has a very rapid onset and ultra-short duration of action (5-10 minutes) but acts through a different mechanism by mimicking acetylcholine. - Its use is associated with several side effects, including **malignant hyperthermia**, **hyperkalemia**, and **muscle pain**, which differ from those of non-depolarizing agents. *Atracurium* - **Atracurium** is an intermediate-acting non-depolarizing muscle relaxant that undergoes **Hofmann elimination** and **ester hydrolysis** for metabolism, giving it a duration of action of approximately 20-35 minutes, which is longer than mivacurium [1]. - While suitable for patients with renal or hepatic impairment due to its unique metabolism, it can cause **histamine release**, leading to hypotension or bronchospasm [2]. *Vecuronium* - **Vecuronium** is an intermediate-acting non-depolarizing muscle relaxant with a duration of action of about 25-40 minutes and is primarily eliminated by the liver and kidneys. - It is known for its **cardiovascular stability** as it does not cause histamine release or significant hemodynamic changes, but its longer duration makes it less ideal when very short-acting relaxation is needed.

Question 856: Which drug selectively acts on GABA-A receptors to induce sleep with minimal effects on sleep architecture?

A. Zolpidem (Correct Answer)
B. Phenobarbitone
C. Buspirone
D. Diazepam

Explanation: ***Zolpidem*** - **Zolpidem** is a non-benzodiazepine hypnotic that selectively binds to the **omega-1 subtype of GABA-A receptors**, primarily mediating sedation. - This selective action results in sleep induction with **minimal disruption of normal sleep architecture**, making it preferable for insomnia. *Phenobarbitone* - **Phenobarbitone** is a barbiturate that non-selectively enhances GABA-A receptor activity, leading to global CNS depression. - It significantly **disturbs sleep architecture**, reducing REM sleep and slow-wave sleep, and carries a higher risk of dependence and overdose. *Buspirone* - **Buspirone** is an anxiolytic that acts as a partial agonist at **5-HT1A serotonin receptors** and has no direct activity at GABA-A receptors. - It treats generalized anxiety disorder but does **not induce sleep** and is not used as a hypnotic. *Diazepam* - **Diazepam** is a benzodiazepine that non-selectively binds to various subunits of the GABA-A receptor, enhancing GABAergic transmission. - While it induces sleep, it also **significantly alters sleep architecture** (reducing REM and slow-wave sleep) and has a longer half-life, increasing the risk of daytime sedation.

Question 857: Which of the following synthetic opioids is known for its rapid onset, short duration of action due to high lipid solubility, but does not have local anesthetic effects?

A. Meperidine
B. Tramadol
C. Fentanyl (Correct Answer)
D. Morphine

Explanation: ***Fentanyl*** - **Fentanyl** is a potent **synthetic opioid** known for its **rapid onset and short duration of action**, primarily due to its **high lipid solubility**. - It works by agonizing μ-opioid receptors but **lacks local anesthetic properties**, unlike some other opioids with structural similarities to local anesthetics. - Its high lipophilicity allows rapid penetration of the blood-brain barrier, contributing to its quick onset of action. *Tramadol* - **Tramadol** is an atypical synthetic opioid that acts as a weak μ-opioid receptor agonist and also inhibits the reuptake of norepinephrine and serotonin. - It exhibits **some local anesthetic-like properties** due to its interaction with neuronal sodium channels, which contributes to its analgesic effect. *Meperidine* - **Meperidine** has a chemical structure similar to local anesthetics and possesses significant **local anesthetic properties**, in addition to its μ-opioid receptor agonist activity. - Its mechanism involves blocking fast sodium channels, which can contribute to local anesthesia, particularly at high concentrations. *Morphine* - **Morphine** is a **naturally-derived opioid** (not synthetic) that primarily acts as a potent agonist at μ-opioid receptors. - While it does not possess significant local anesthetic properties, it differs from fentanyl in being a natural opioid alkaloid with different pharmacokinetic properties (slower onset, longer duration, lower lipid solubility).

Question 858: Anti-vertigo drug which modulates calcium channels and has a prominent labyrinthine suppressant property is:

A. Cyproheptadine
B. Cinnarizine (Correct Answer)
C. Clemastine
D. Cetirizine

Explanation: ***Cinnarizine*** - It is a **selective peripheral vestibular suppressant** that works by inhibiting calcium influx into the vestibular sensory cells. - Its **calcium channel blocking** properties help to reduce the excitability of vestibular organs, thereby alleviating vertigo symptoms. *Cyproheptadine* - This is a **first-generation antihistamine** with anticholinergic and antiserotonergic properties, primarily used for allergy and appetite stimulation. - It does not primarily act as a calcium channel modulator or have significant direct labyrinthine suppressant effects for vertigo. *Clemastine* - This is another **first-generation antihistamine** with anticholinergic effects, primarily used for allergic reactions [1]. - Its main action is blocking histamine H1 receptors, and it lacks the specific calcium channel modulating and vestibular suppressant properties relevant for vertigo treatment. *Cetirizine* - This is a **second-generation antihistamine** that selectively blocks H1 receptors and has minimal sedative effects [2]. - While it can be used for allergic conditions, it does not possess the calcium channel blocking or potent labyrinthine suppressant action required for effective vertigo management.

Question 859: The mechanism of action of botulinum toxin primarily involves disruption of:

A. Muscle transmission
B. Non-neuromuscular transmission
C. Neuromuscular transmission (Correct Answer)
D. Neural transmission

Explanation: ***Neuromuscular transmission*** - **Botulinum toxin** acts at the **neuromuscular junction**, specifically targeting proteins involved in **neurotransmitter** (acetylcholine) release. - It cleaves **SNARE proteins** (SNAP-25, synaptobrevin, syntaxin), thereby preventing the fusion of synaptic vesicles with the presynaptic membrane and the subsequent release of **acetylcholine**, leading to muscle paralysis. - This is the primary and most specific mechanism of action of botulinum toxin produced by *Clostridium botulinum*. *Muscle transmission* - This option is too general; while muscle function is affected, the primary disruption is at the **junction between nerves and muscles**, not directly within the muscle fiber itself. - The toxin's action is on the **presynaptic nerve terminal**, preventing the signal from reaching the muscle, rather than interfering with the muscle's internal contraction mechanism. *Non-neuromuscular transmission* - This is incorrect as **botulinum toxin** specifically targets and disrupts the process of **neuromuscular transmission**, not non-neuromuscular pathways. - Its effects are localized to the **cholinergic nerve terminals**, which are abundant at neuromuscular junctions. *Neural transmission* - While it affects parts of the nervous system, stating "neural transmission" is too broad. The toxin is highly specific to the **peripheral cholinergic nerve terminals** at the neuromuscular junction, not general neural transmission throughout the central or peripheral nervous system. - It does not disrupt the conduction of action potentials along the nerve axon but rather the **release of neurotransmitters** at the synapse.

Question 860: In a clinical scenario where a patient presents with flaccid paralysis, which of the following toxins is most likely responsible?

A. Botulism (Correct Answer)
B. Tetanus
C. Diphtheria
D. Cholera

Explanation: ***Correct Option: Botulism*** - **Botulinum toxin** blocks the release of **acetylcholine** at the neuromuscular junction, leading to **flaccid paralysis**. - This paralysis typically progresses symmetrically and can affect ocular, bulbar, and peripheral muscles. *Incorrect Option: Tetanus* - **Tetanus toxin** inhibits the release of **inhibitory neurotransmitters** (**GABA** and **glycine**) in the central nervous system. - This leads to uncontrolled muscle contractions, presenting as **spastic paralysis** and **lockjaw**. *Incorrect Option: Diphtheria* - **Diphtheria toxin** causes local inflammation and can lead to systemic effects, including **myocarditis** and **neuropathy**. - The neuropathy can cause weakness, but it is typically a **delayed polyneuropathy** rather than acute flaccid paralysis. *Incorrect Option: Cholera* - **Cholera toxin** activates adenylyl cyclase in intestinal cells, leading to excessive fluid and electrolyte secretion. - The primary symptom is **severe watery diarrhea** and dehydration, not paralysis.

Practice by Chapter

General Anesthetics

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Local Anesthetics

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Sedative-Hypnotics

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Antiepileptic Drugs

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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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