Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 881: Which of the following drugs causes extrapyramidal symptoms?

A. Antibiotics
B. Salicylates
C. Barbiturates
D. Phenothiazines (Correct Answer)

Explanation: ***Phenothiazines*** - Phenothiazines are a class of **antipsychotics** that block **dopamine D2 receptors** in the brain. - This blockade, especially in the **nigrostriatal pathway**, can lead to extrapyramidal symptoms such as **dystonia**, **akathisia**, **parkinsonism**, and **tardive dyskinesia**. *Antibiotics* - While some antibiotics (e.g., fluoroquinolones) can cause central nervous system side effects like seizures or confusion, they are **not typically associated** with extrapyramidal symptoms. - Their primary mechanism of action is **antibacterial**, not affecting dopamine pathways in a way that induces these motor side effects. *Salicylates* - Salicylates, such as aspirin, are primarily used for their **anti-inflammatory, analgesic, and antipyretic** effects. - Their side effects mainly involve the **gastrointestinal tract** (e.g., irritation, ulcers) and **bleeding disturbances**, but not extrapyramidal symptoms. *Barbiturates* - Barbiturates are **CNS depressants** that enhance the effects of **GABA**, leading to sedation, hypnosis, and anticonvulsant actions. - Their main side effects include **sedation**, **respiratory depression**, and **tolerance/dependence**, with no direct link to extrapyramidal motor dysfunction.

Question 882: The drug of choice for absence attacks is

A. Phenytoin
B. Primidone
C. Ethosuximide (Correct Answer)
D. Phenobarbitone

Explanation: ***Ethosuximide*** - **Ethosuximide** is the most effective and preferred drug for treating **absence seizures** due to its selective mechanism of action. - It works by blocking **T-type calcium channels** in the thalamus, which are crucial for generating the characteristic 3-Hz spike-and-wave discharges of absence seizures. *Phenytoin* - **Phenytoin** is primarily used for **tonic-clonic seizures** and **focal seizures**, but it is generally ineffective for absence seizures and can even worsen them. - Its mechanism of action involves stabilizing neuronal membranes by **blocking voltage-gated sodium channels**, which is not the primary pathophysiology of absence seizures. *Primidone* - **Primidone** is an anticonvulsant that is metabolized to **phenobarbital** and **phenylethylmalonamide (PEMA)**. It is effective for **generalized tonic-clonic** and **focal seizures**. - It is not considered a first-line treatment for **absence seizures** and may not be effective. *Phenobarbitone* - **Phenobarbitone** (phenobarbital) is a barbiturate effective against **generalized tonic-clonic** and **focal seizures** but is not a drug of choice for absence seizures. - While it has broad-spectrum anticonvulsant activity by enhancing **GABAergic inhibition**, it is less effective and has more prominent sedative side effects compared to ethosuximide for absence epilepsy.

Question 883: Which of the following drugs is least preferred for the treatment of multiple sclerosis?

A. Interferon beta-1b
B. Mycophenolate (Correct Answer)
C. Interferon beta-1a
D. Glatiramer acetate

Explanation: ***Mycophenolate*** - **Mycophenolate mofetil** is an immunosuppressant typically used to prevent **organ transplant rejection** and in autoimmune diseases like **lupus nephritis**. - While it has immunosuppressive properties, it is **not approved** or considered a first-line or even second-line treatment for **multiple sclerosis (MS)** due to a lack of robust evidence of efficacy and a less favorable risk-benefit profile compared to other established MS therapies. *Interferon beta-1a* - **Interferon beta-1a** is a **disease-modifying therapy (DMT)** widely used for **relapsing-remitting multiple sclerosis (RRMS)**, reducing relapse rates and slowing disease progression. - It works by modulating the **immune response** to decrease inflammation and demyelination in the central nervous system. *Interferon beta-1b* - Similar to interferon beta-1a, **interferon beta-1b** is an established **DMT** for **RRMS** and some forms of **secondary progressive MS**. - It also functions through **immunomodulation**, helping to reduce the frequency and severity of relapses. *Glatiramer acetate* - **Glatiramer acetate** is an **immunomodulator** approved for the treatment of **RRMS**, working by mimicking myelin basic protein and inducing T-cell tolerance. - It effectively **reduces relapse rates** and is considered a safe and well-tolerated option for long-term use in MS patients.

Question 884: The drug used in an ameliorative test for myasthenia gravis is

A. Physostigmine
B. Edrophonium (Correct Answer)
C. Tacrine
D. Pyridostigmine

Explanation: ***Edrophonium*** - **Edrophonium** is a **short-acting acetylcholinesterase inhibitor** used in the **Tensilon test** for diagnosing myasthenia gravis. - Its rapid onset and brief duration of action (5-10 minutes) allow for quick assessment of symptomatic improvement in patients with the disease. *Physostigmine* - **Physostigmine** is an **acetylcholinesterase inhibitor** that can cross the **blood-brain barrier**, making it useful for treating anticholinergic toxicity. - It has a longer duration of action than edrophonium and is not typically used for the acute diagnostic test of myasthenia gravis. *Tacrine* - **Tacrine** is an **acetylcholinesterase inhibitor** primarily used in the management of **Alzheimer's disease** to improve cognitive function. - It is not used for the diagnosis or short-term ameliorative testing of myasthenia gravis. *Pyridostigmine* - **Pyridostigmine** is an **intermediate-acting acetylcholinesterase inhibitor** used for the chronic symptomatic treatment of myasthenia gravis. - While it improves muscle strength, its longer duration of action (3-6 hours) makes it unsuitable for the rapid diagnostic "Tensilon test."

Question 885: Diplopia and ataxia are the adverse effects of which of the following drugs?

A. Phenytoin and carbamazepine (Correct Answer)
B. Gabapentin and carbamazepine
C. Gabapentin with phenytoin
D. Valproate and topiramate

Explanation: ***Phenytoin and carbamazepine*** - Both **phenytoin** and **carbamazepine** are well-known to cause **diplopia** (double vision) and **ataxia** (impaired coordination) as dose-related adverse effects, especially at higher therapeutic levels. - These neurological side effects occur due to their impact on the **central nervous system**, affecting motor control and ocular movements. *Gabapentin and carbamazepine* - While **carbamazepine** can cause diplopia and ataxia, **gabapentin** primarily causes dizziness, drowsiness, and fatigue, but less commonly diplopia or significant ataxia at therapeutic doses. - Gabapentin's mechanism of action differs from carbamazepine, leading to a distinct adverse effect profile. *Gabapentin with phenytoin* - **Phenytoin** is associated with diplopia and ataxia, but **gabapentin** is less likely to cause these specific effects compared to phenytoin. - The combination would not be the primary answer for both drugs specifically causing prominent diplopia and ataxia. *Valproate and topiramate* - **Valproate** can cause tremor and sedation but is less commonly associated with prominent diplopia and ataxia. - **Topiramate** frequently causes cognitive slowing, word-finding difficulties, and paresthesias, but diplopia and ataxia are not its most characteristic adverse effects.

Question 886: Which of the following is FALSE about ropivacaine?

A. More cardiotoxic than lignocaine
B. Contains only R enantiomer (Correct Answer)
C. Less cardiotoxic than bupivacaine
D. Onset of action is faster than bupivacaine

Explanation: ***Contains only R enantiomer*** - Ropivacaine is a **pure S-enantiomer** (S-(-)-enantiomer) preparation, NOT the R-enantiomer. - This single enantiomer formulation contributes to its **reduced cardiotoxicity** and improved safety profile compared to racemic bupivacaine. - The statement "contains only R enantiomer" is **FALSE** - this is the correct answer. *Less cardiotoxic than bupivacaine* - Ropivacaine has **lower lipid solubility** and faster dissociation from cardiac sodium channels compared to bupivacaine. - This results in **significantly reduced cardiotoxicity**, making it safer for large-volume regional blocks. - This statement is **TRUE**. *More cardiotoxic than lignocaine* - Ropivacaine is indeed **more cardiotoxic than lidocaine** due to its greater potency and longer duration of action. - Amide local anesthetics with higher potency (bupivacaine > ropivacaine > lidocaine) carry greater cardiac risk. - This statement is **TRUE**. *Onset of action is faster than bupivacaine* - Ropivacaine and bupivacaine have **similar onset times** (10-15 minutes for epidural/nerve blocks). - Both have similar pKa values (ropivacaine 8.1, bupivacaine 8.1), resulting in comparable onset characteristics. - While ropivacaine may have marginally faster onset in some contexts, clinically they are considered equivalent. - This statement is generally **FALSE or equivocal**, making it potentially the second-best answer, but the R-enantiomer statement is definitively false.

Question 887: Which ergot-derived dopamine receptor agonist is known to cause cardiac valvular fibrosis?

A. Levodopa
B. Ropinrole
C. Pramipexole
D. Pergolide & cabergoline (Correct Answer)

Explanation: ***Pergolide & cabergoline*** - Both **Pergolide** and **Cabergoline** are **ergot-derived dopamine agonists** [1], [2], [3] that have been associated with **cardiac valvular fibrosis** [1], [2]. - This adverse effect is mediated by their agonistic activity on **5-HT2B serotonin receptors** located on heart valve fibroblasts [2]. *Levodopa* - **Levodopa** is a precursor to dopamine and is used to treat Parkinson's disease, but it is not an ergot derivative [1]. - It does not directly cause cardiac valvular fibrosis; its main side effects are related to motor complications and gastrointestinal issues. *Ropinrole* - **Ropinrole** is a **non-ergot dopamine agonist** used for Parkinson's disease and restless legs syndrome [1]. - Unlike ergot-derived agonists, it has a lower affinity for 5-HT2B receptors and is not significantly associated with cardiac valvular fibrosis. *Pramipexole* - **Pramipexole** is another **non-ergot dopamine agonist** with a similar safety profile to ropinirole regarding cardiac health [1]. - It does not cause cardiac valvular fibrosis and is generally preferred over ergot derivatives due to their cardiovascular side effects.

Question 888: A 56-year-old woman has nausea due to chemotherapy for breast cancer. Droperidol is effective in reducing nausea because it blocks which of the following?

A. Glucocorticoid receptors in the vomiting center
B. Dopamine receptors in the CTZ (Correct Answer)
C. ACh receptors in the periphery
D. 5-HT3 receptors in the CTZ

Explanation: **Dopamine receptors in the CTZ** - Droperidol is a **butyrophenone antipsychotic** that acts as an **antidopaminergic agent**, primarily targeting **D2 dopamine receptors**. - Its antiemetic effect is mainly due to blocking these **dopamine receptors in the chemoreceptor trigger zone (CTZ)**, which is involved in initiating the vomiting reflex. *Glucocorticoid receptors in the vomiting center* - **Glucocorticoids** like dexamethasone are used as antiemetics, but they act via **glucocorticoid receptors**, not through dopamine receptor blockade. - Their mechanism involves inhibiting prostaglandin synthesis and inflammation, reducing the release of serotonin. *ACh receptors in the periphery* - Drugs that block **acetylcholine (ACh) receptors** (e.g., scopolamine) are used for motion sickness, but they are not the primary mechanism of action for droperidol. - **Anticholinergics** typically exert their effects on the vestibular system and peripheral muscarinic receptors. *5-HT 2 receptors in the CTZ* - While some antiemetics (e.g., **ondansetron**) block **serotonin (5-HT3) receptors**, droperidol's primary action is not on **5-HT2 receptors**. - **Serotonin antagonists** are particularly effective for chemotherapy-induced nausea and vomiting as chemotherapy often releases serotonin from enterochromaffin cells.

Question 889: The drug of choice for infantile spasms in a patient with tuberous sclerosis is:

A. Lamotrigine
B. Levetiracetam
C. Vigabatrin (Correct Answer)
D. Tiagabine

Explanation: ***Vigabatrin*** - **Vigabatrin** is considered the **first-line treatment** for **infantile spasms** associated with **tuberous sclerosis complex (TSC)**. - Its mechanism of action involves **irreversibly inhibiting GABA transaminase**, thereby increasing GABA levels in the brain. - It has shown **superior efficacy** in TSC-related infantile spasms compared to other antiepileptic drugs, with response rates of 70-95% in this specific population. - While ACTH (adrenocorticotropic hormone) is an alternative first-line agent for non-TSC infantile spasms, vigabatrin is specifically preferred in TSC due to its effectiveness and the underlying pathophysiology. *Lamotrigine* - While an effective **antiepileptic drug** for various seizure types, **lamotrigine** is not the primary choice for infantile spasms, especially in the context of TSC. - It works by blocking **voltage-gated sodium channels** and modulating calcium channels, but its efficacy for infantile spasms is generally lower than first-line options. - Lamotrigine is more commonly used for focal seizures and generalized tonic-clonic seizures. *Levetiracetam* - **Levetiracetam** is a broad-spectrum antiepileptic drug, but it is typically used as a **second-line or adjunctive therapy** for infantile spasms. - Its primary mechanism involves binding to the **synaptic vesicle protein 2A (SV2A)**, modulating neurotransmitter release. - While well-tolerated, it has not demonstrated the same level of efficacy as vigabatrin or ACTH for infantile spasms. *Tiagabine* - **Tiagabine** works by blocking the reuptake of **GABA** through GABA transporter 1 (GAT-1), thereby increasing GABAergic transmission. - It is **not indicated for infantile spasms** and is primarily used for focal seizures. - Tiagabine can sometimes precipitate or worsen non-convulsive status epilepticus and spike-wave stupor, making it inappropriate for this condition.

Question 890: In cases of spasticity, which drug is least likely to be used?

A. Baclofen
B. Tizanidine
C. Amitriptyline (Correct Answer)
D. Diazepam

Explanation: ***Amitriptyline*** - **Amitriptyline** is a **tricyclic antidepressant** primarily used for treating depression, neuropathic pain, and migraines. - While it has sedative effects, it does not directly act on the mechanisms that reduce muscle tone in spasticity. *Baclofen* - **Baclofen** is a **GABA-B receptor agonist** that reduces the release of excitatory neurotransmitters, effectively decreasing muscle spasticity. - It is one of the most commonly prescribed drugs for spasticity, available in oral and intrathecal forms. *Tizanidine* - **Tizanidine** is an **alpha-2 adrenergic agonist** that works by increasing presynaptic inhibition of motor neurons, thereby reducing muscle tone. - It is frequently used for spasticity associated with multiple sclerosis or spinal cord injury. *Diazepam* - **Diazepam** is a **benzodiazepine** that acts as a GABA-A receptor agonist, enhancing GABA's inhibitory effects on the central nervous system. - It reduces spasticity by causing generalized muscle relaxation, though its sedative properties can be a limiting side effect.

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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