Central Nervous System Pharmacology — MCQs
On this page
Which of the following is the only clinically available depolarizing muscle relaxant?
What is the preferred medication for treating severe cases of rheumatic chorea that do not respond to standard treatments?
Suxamethonium primarily acts on which type of receptors?
Which of the following metal ions is associated with secondary Parkinsonisms?
In the context of pharmacology, what is the term 'Mickey Finn' commonly associated with?
Buprenorphine is a partial agonist at which opioid receptor?
What effect does morphine have on muscle tone?
Antidepressant drug used in nocturnal enuresis is:
Where is the benzodiazepine binding site located on GABA receptors?
Which anti-cholinesterase drug is known for its central nervous system activity?
Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs
Question 821: Which of the following is the only clinically available depolarizing muscle relaxant?
- A. Decamethonium
- B. Suxamethonium (Correct Answer)
- C. Mivacurium
- D. None of the options
Explanation: ***Suxamethonium*** - **Suxamethonium** (also known as succinylcholine) is currently the **only depolarizing neuromuscular blocker** available for clinical use. - It works by mimicking acetylcholine, binding to and activating nicotinic acetylcholine receptors at the **neuromuscular junction**, causing initial muscle fasciculations followed by relaxation. *Decamethonium* - **Decamethonium** is a depolarizing neuromuscular blocker but is **no longer clinically available** due to its prolonged action and side effects. - It also acts by opening nicotinic acetylcholine receptor channels, leading to depolarization and muscle paralysis. *Mivacurium* - **Mivacurium** is a **nondepolarizing neuromuscular blocker**, meaning it acts as a competitive antagonist at the acetylcholine receptor. - It is known for its **short duration of action** due to rapid hydrolysis by plasma cholinesterases but is not depolarizing. *None of the options* - This option is incorrect because suxamethonium is indeed a clinically available depolarizing muscle relaxant. - The question specifically asks for the *only* clinically available one, which suxamethonium fulfills.
Question 822: What is the preferred medication for treating severe cases of rheumatic chorea that do not respond to standard treatments?
- A. Diazepam
- B. Probenecid
- C. Valproate
- D. Haloperidol (Correct Answer)
Explanation: **Haloperidol** - **Haloperidol**, a **dopamine receptor antagonist**, is a highly effective medication for severe rheumatic chorea that is refractory to standard treatments like carbamazepine or valproate. - Its mechanism of action involves blocking dopamine receptors in the brain, thereby reducing the **hyperkinetic movements** characteristic of chorea. *Valproate* - **Valproate** is a commonly used antiepileptic drug that can be effective for managing chorea, especially in milder cases. - However, it is generally considered a second-line agent for severe, refractory cases of **rheumatic chorea** compared to haloperidol. *Diazepam* - **Diazepam** is a benzodiazepine, primarily used for its **anxiolytic** and **sedative** properties due to its effect on GABA receptors. - While it can help alleviate some motor restlessness, it is not a first-line treatment for the involuntary movements of **chorea** and lacks the specific anti-chorea efficacy of antipsychotics. *Probenecid* - **Probenecid** is a uricosuric drug used to treat **gout** by increasing the excretion of uric acid. - It has no known role or efficacy in the management of **rheumatic chorea**.
Question 823: Suxamethonium primarily acts on which type of receptors?
- A. Nicotinic acetylcholine receptors (Correct Answer)
- B. Potassium channels
- C. Calcium channels
- D. Chloride channels
Explanation: ***Nicotinic acetylcholine receptors*** - **Suxamethonium** is a depolarizing muscle relaxant that acts as an **agonist at nicotinic acetylcholine receptors** at the neuromuscular junction. - This initial activation leads to muscle fasciculations followed by prolonged depolarization, causing **flaccid paralysis**. *Potassium channels* - While some drugs may affect potassium channels to alter neuronal excitability, suxamethonium's primary mechanism of action is not on these channels. - Blocking potassium channels is characteristic of drugs like **certain antiarrhythmics** or **sulfonylureas**. *Calcium channels* - **Calcium channels** play a role in muscle contraction, but they are not the primary target of suxamethonium. - Drugs like **dihydropyridines** (e.g., nifedipine) target calcium channels for their antihypertensive effects. *Chloride channels* - Chloride channels are involved in maintaining resting membrane potential and inhibitory neurotransmission. - Drugs such as **benzodiazepines** indirectly enhance GABA-mediated chloride influx, which is distinct from suxamethonium's action.
Question 824: Which of the following metal ions is associated with secondary Parkinsonisms?
- A. Magnesium (Mg)
- B. Selenium (Se)
- C. Manganese (Mn) (Correct Answer)
- D. Molybdenum (Mo)
Explanation: ***Manganese (Mn)*** - Chronic exposure to high levels of **manganese** can lead to **manganism**, a neurological disorder characterized by **Parkinsonian-like symptoms**, including bradykinesia, rigidity, and gait disturbances [1]. - This is due to manganese accumulation in the **basal ganglia**, particularly the **globus pallidus**, affecting dopaminergic pathways. *Magnesium (Mg)* - **Magnesium** is an essential mineral vital for numerous bodily functions, including nerve and muscle function. - While imbalances can cause neurological issues (e.g., tremors with hypomagnesemia), it is not directly associated with **secondary parkinsonism**. *Selenium (Se)* - **Selenium** is a trace element with antioxidant properties, important for thyroid hormone metabolism and immune function. - Both deficiency and toxicity can cause various health problems, but it is not known to cause **secondary parkinsonism**. *Molybdenum (Mo)* - **Molybdenum** is an essential trace element that functions as a cofactor for several enzymes. - No known association exists between molybdenum exposure, deficiency, or toxicity and the development of **secondary parkinsonism**.
Question 825: In the context of pharmacology, what is the term 'Mickey Finn' commonly associated with?
- A. Chloroform
- B. Methyl alcohol
- C. Chloral hydrate (Correct Answer)
- D. Ethylene glycol
Explanation: ***Chloral hydrate*** - A "Mickey Finn" is a slang term for a drink **laced with a psychoactive drug or incapacitating agent** given to an unsuspecting person. - Historically, **chloral hydrate** was a common substance used for this purpose due to its rapid sedative-hypnotic effects. *Chloroform* - While chloroform is a potent anesthetic and sedative, it is primarily used as an **inhalant** and is not typically administered orally in drinks. - Ingesting chloroform in large quantities can be **fatal due to severe hepatotoxicity and neurotoxicity**. *Methyl alcohol* - **Methyl alcohol (methanol)** is highly toxic and causes severe metabolic acidosis, blindness, and death, even in small amounts. - It does not induce the quick, incapacitating sedative effects associated with a "Mickey Finn" but rather a **delayed, severe poisoning syndrome**. *Ethylene glycol* - **Ethylene glycol** is an antifreeze agent that is also highly toxic, causing kidney failure and metabolic derangements. - Similar to methanol, its effects are **delayed and severe**, not the immediate incapacitating sedation implied by the term "Mickey Finn."
Question 826: Buprenorphine is a partial agonist at which opioid receptor?
- A. Mu (Correct Answer)
- B. Kappa
- C. Delta
- D. ORL-1
Explanation: ***Mu*** - Buprenorphine primarily acts as a **partial agonist** at the **mu opioid receptor**, providing analgesic effects with a ceiling effect on respiratory depression. - Its partial agonism at the mu receptor contributes to its lower potential for respiratory depression and overdose compared to full mu agonists. *Kappa* - While buprenorphine has some antagonist activity at the kappa receptor, its primary therapeutic action is not at this receptor. - **Kappa receptor agonists** like pentazocine can produce dysphoria and psychotomimetic effects. *Delta* - The delta opioid receptor is involved in analgesia and emotional responses, but buprenorphine has very low affinity and activity at this receptor. - **Delta receptor agonists** are not widely used clinically due to limited efficacy and side effects. *ORL-1* - The ORL-1 (Opioid Receptor-like 1) receptor, also known as the nociceptin receptor, is distinct from classical opioid receptors. - Buprenorphine has **no significant activity** at the ORL-1 receptor, which primarily mediates pain, anxiety, and learning.
Question 827: What effect does morphine have on muscle tone?
- A. Increased muscle tone (Correct Answer)
- B. Respiratory stimulation
- C. Decreased muscle tone
- D. Mydriasis
Explanation: ***Increased muscle tone*** - Morphine **increases skeletal muscle tone** and can cause muscle rigidity, particularly with rapid IV administration (truncal rigidity). - It significantly increases **smooth muscle tone** in various organs including the sphincter of Oddi (causing biliary colic), bladder sphincter (causing urinary retention), and GI tract (causing constipation). - This increased tone in sphincters and smooth muscle is a well-documented effect mediated through **opioid receptor activation**. *Bradycardia (not increased heart rate)* - Morphine typically causes **bradycardia** (decreased heart rate) due to vagal stimulation and central effects, not tachycardia. - Increased heart rate would be atypical and not a primary pharmacological effect of morphine. *Miosis (not mydriasis)* - Morphine characteristically causes **miosis** (pinpoint pupils) due to stimulation of the Edinger-Westphal nucleus of the oculomotor nerve. - Mydriasis (dilated pupils) is seen with anticholinergics or sympathomimetics, not opioids. *Respiratory depression (not stimulation)* - Morphine causes **respiratory depression**, not stimulation, by reducing the responsiveness of brainstem respiratory centers to CO2. - This is one of the most dangerous adverse effects and the primary cause of death in opioid overdose.
Question 828: Antidepressant drug used in nocturnal enuresis is:
- A. Imipramine (Correct Answer)
- B. Fluoxetine
- C. Trazodone
- D. Sertraline
Explanation: ***Imipramine*** - **Imipramine**, a **tricyclic antidepressant (TCA)**, is frequently used off-label for **nocturnal enuresis** in children [1]. - Its mechanism of action in enuresis is thought to involve a combination of anticholinergic effects (which relax the bladder detrusor muscle) and central nervous system effects (which may increase bladder capacity and arousal from sleep) [1]. *Fluoxetine* - **Fluoxetine** is a **selective serotonin reuptake inhibitor (SSRI)** and is primarily used for depression, anxiety disorders, and OCD [2]. - It is not indicated for the treatment of nocturnal enuresis and does not have the same bladder-relaxing or arousal-modulating properties as imipramine in this context. *Trazodone* - **Trazodone** is a **serotonin antagonist and reuptake inhibitor (SARI)**, commonly prescribed for depression and insomnia due to its prominent sedative effects. - It is not used for nocturnal enuresis and its mechanism of action does not confer benefits for bladder control. *Sertraline* - **Sertraline** is another **selective serotonin reuptake inhibitor (SSRI)** used for a wide range of psychiatric conditions, including depression, anxiety, and panic disorder [2]. - Like fluoxetine, it is not an appropriate treatment for nocturnal enuresis and lacks the specific known effects beneficial for this condition.
Question 829: Where is the benzodiazepine binding site located on GABA receptors?
- A. β-subunit
- B. δ-subunit
- C. γ-subunit (Correct Answer)
- D. α-subunit
Explanation: ***γ-subunit*** - The **benzodiazepine binding site** is located at the interface between the **α and γ subunits** of the GABA-A receptor, with the **γ-subunit (especially γ2) being essential** for benzodiazepine sensitivity. - The presence of the **γ2 subunit** is **mandatory** for benzodiazepine binding - receptors lacking this subunit are **insensitive to benzodiazepines**. - Benzodiazepines bind to this site and act as **positive allosteric modulators**, increasing the frequency of **chloride channel opening** in response to GABA. - This is the **standard answer** for NEET-PG and medical PG examinations in India. *α-subunit* - The **α-subunit** contributes to forming the benzodiazepine binding pocket at the α-γ interface. - Different **α-subunit isoforms** (α1, α2, α3, α5) determine the pharmacological profile and tissue distribution of benzodiazepine effects. - However, the **α-subunit alone** cannot bind benzodiazepines without the γ-subunit. *β-subunit* - The **β-subunit** contains the primary binding site for **GABA** itself. - It does not participate in benzodiazepine binding but is crucial for the receptor's overall function and GABAergic signaling. *δ-subunit* - The **δ-subunit** replaces the γ-subunit in certain GABA-A receptor subtypes that mediate **tonic inhibition**. - Receptors containing **δ-subunits** are **insensitive to benzodiazepines** but sensitive to neurosteroids and certain general anesthetics. - This is a key distinguishing feature between phasic (γ-containing) and tonic (δ-containing) GABA-A receptors.
Question 830: Which anti-cholinesterase drug is known for its central nervous system activity?
- A. Physostigmine (Correct Answer)
- B. Edrophonium
- C. Pyridostigmine
- D. Neostigmine
Explanation: ***Physostigmine*** - Unlike most other anti-cholinesterases, **physostigmine** is a **tertiary amine** and is relatively lipid-soluble, allowing it to cross the **blood-brain barrier**. [2] - Its ability to increase acetylcholine in the CNS makes it useful in treating anticholinergic toxicity (e.g., atropine overdose). [2] *Pyridostigmine* - **Pyridostigmine** is a **quaternary amine** and does not readily cross the blood-brain barrier, primarily acting peripherally. - It is mainly used in the long-term management of **myasthenia gravis**. *Edrophonium* - **Edrophonium** is a very short-acting **quaternary amine** that does not cross the blood-brain barrier. [1] - It is primarily used for the **diagnosis of myasthenia gravis** (Tensilon test) due to its rapid onset and short duration of action. [1] *Neostigmine* - **Neostigmine** is also a **quaternary amine** with poor lipid solubility, meaning it has minimal central nervous system activity. [2] - It is commonly used to reverse the effects of **non-depolarizing neuromuscular blockers** and in the treatment of **myasthenia gravis**.
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
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free