Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 841: All of the following are correct about ketamine, EXCEPT which of the following?

A. It increases arterial blood pressure
B. It inhibits polysynaptic reflexes in the spinal cord
C. It functionally "dissociates" the thalamus
D. It is a potent bronchoconstrictor (Correct Answer)

Explanation: ***It is a potent bronchoconstrictor*** - **Ketamine** is known for its **bronchodilatory properties**, making it a suitable anesthetic for patients with asthma or reactive airway disease, rather than a bronchoconstrictor [1]. - Its ability to relax bronchial smooth muscle is mediated, in part, by its indirect sympathetic stimulation and direct effects on airways. *It functionally "dissociates" the thalamus* - Ketamine's mechanism of action involves **N-methyl-D-aspartate (NMDA) receptor antagonism**, which leads to a "dissociative" state [2]. - This results in a functional separation between the **thalamoneocortical** and **limbic systems**, explaining its unique anesthetic effects. *It increases arterial blood pressure* - Ketamine typically causes an **increase in heart rate** and **arterial blood pressure** due to its sympathomimetic effects. - This is achieved through the release of **endogenous catecholamines**, which stimulate the cardiovascular system. *It inhibits polysynaptic reflexes in the spinal cord* - Ketamine acts as a powerful **analgesic** by inhibiting ascending **polysynaptic reflexes** in the spinal cord. - This contributes to its ability to provide profound **pain relief** separate from its anesthetic effects [2].

Question 842: Most commonly abused opioid -

A. Morphine
B. Diacetylmorphine (Correct Answer)
C. Oxycodone
D. Buprenorphine

Explanation: ***Diacetylmorphine*** - **Diacetylmorphine**, commonly known as **heroin**, is synthetically derived from **morphine** but is significantly more potent and lipid-soluble, allowing it to cross the **blood-brain barrier** rapidly [1, 3]. - Its rapid onset of action and intense euphoric effects contribute to its high potential for **abuse** and addiction, making it one of the most commonly abused opioids globally, particularly through intravenous injection [1]. *Morphine* - While **morphine** is a potent opioid and has a high potential for abuse, it is often prescribed in clinical settings for severe pain. - Its slower onset and less intense "rush" compared to **heroin** make it less frequently the **primary opioid of abuse** in illicit street drug markets [1]. *Oxycodone* - **Oxycodone** is a highly abused prescription opioid, especially in the form of controlled-release formulations like **OxyContin**, but its abuse is primarily linked to prescription drug diversion rather than being the most common illicitly manufactured opioid of abuse. - While it contributes significantly to the opioid crisis, **heroin** (diacetylmorphine) remains the most commonly abused opioid in the illicit market due to its widespread availability and potency [1]. *Buprenorphine* - **Buprenorphine** is a **partial opioid agonist** used in the treatment of opioid dependence (opioid replacement therapy) due to its ceiling effect on respiratory depression and ability to block the effects of other opioids. - Although it can be abused, particularly in combination with naloxone (Suboxone) via intravenous injection, its primary role is in **medication-assisted treatment**, making it less commonly abused as a standalone illicit opioid compared to **heroin**.

Question 843: What is a key difference between fosphenytoin and phenytoin?

A. Can be used in absence seizures
B. Can be mixed with saline (Correct Answer)
C. Can be given orally
D. It is the drug of choice for myoclonic seizures

Explanation: **Can be mixed with saline** - **Fosphenytoin** is a water-soluble prodrug that is converted to phenytoin in the body; its solubility allows it to be **mixed with saline** solutions for intravenous administration, minimizing the risk of precipitation. - Unlike phenytoin, fosphenytoin's formulation avoids the need for propylene glycol, which is associated with adverse cardiovascular effects and makes phenytoin incompatible with saline. *Can be used in absence seizures* - Neither **fosphenytoin nor phenytoin** is effective for treating **absence seizures**, and they can sometimes worsen them. - **Ethosuximide** or **valproic acid** are the drugs of choice for absence seizures. *Can be given orally* - While **phenytoin** is commonly available in oral forms (capsules, chewable tablets, suspension), **fosphenytoin** is primarily designed for **parenteral administration** (intravenous or intramuscular). - Fosphenytoin is a prodrug that is rapidly converted to phenytoin *in vivo*, but it is not typically available or indicated for direct oral administration. *It is the drug of choice for myoclonic seizures* - Neither **fosphenytoin nor phenytoin** is the drug of choice for **myoclonic seizures**; they can exacerbate this type of seizure. - **Valproic acid** and **levetiracetam** are preferred treatments for myoclonic seizures due to their broader spectrum of activity.

Question 844: Extrapyramidal syndrome-like side effects are seen in which of the following medications?

A. Haloperidol (Correct Answer)
B. Clozapine
C. Tetracycline
D. Ketoconazole

Explanation: ***Haloperidol*** - **Haloperidol** is a **typical antipsychotic** known for its potent **dopamine D2 receptor blockade**. - This strong blockade in the **nigrostriatal pathway** often leads to **extrapyramidal symptoms (EPS)** such as dystonia, akathisia, and parkinsonism. *Clozapine* - **Clozapine** is an **atypical antipsychotic** that has a lower propensity for causing **extrapyramidal symptoms (EPS)** due to its weaker D2 receptor antagonism and potent serotonin 5-HT2A receptor blockade. - While it can cause other severe side effects, such as **agranulocytosis** and **myocarditis**, EPS are less common compared to typical antipsychotics. *Tetracycline* - **Tetracycline** is an **antibiotic** primarily used to treat bacterial infections. - Its mechanism of action involves inhibiting bacterial protein synthesis, and it is not associated with **neurological side effects** like **extrapyramidal symptoms**. *Ketoconazole* - **Ketoconazole** is an **antifungal medication** that works by inhibiting ergosterol synthesis in fungi. - It is known for potential **hepatotoxicity** and **endocrine dysfunction**, but not for causing **extrapyramidal symptoms**.

Question 845: Which of the following is the mechanism of action of tetanospasmin ?

A. Inhibition of release of GABA and glycine (Correct Answer)
B. Inhibition of Ach release from synapse
C. Inhibition of protein synthesis
D. Activation of adenylyl cyclase

Explanation: ***Inhibition of release of GABA and glycine*** - **Tetanospasmin** is a potent neurotoxin produced by *Clostridium tetani* that acts by blocking the release of inhibitory neurotransmitters, specifically **GABA (gamma-aminobutyric acid)** and **glycine**, from presynaptic terminals in the spinal cord and brainstem. - This inhibition leads to **uncontrolled muscle spasms**, rigidity, and convulsions, characteristic of tetanus, due to the lack of inhibitory signals to motor neurons. *Inhibition of Ach release from synapse* - This mechanism is characteristic of **botulinum toxin** (produced by *Clostridium botulinum*), not tetanospasmin. - Botulinum toxin inhibits the release of **acetylcholine (ACh)** at the neuromuscular junction, leading to flaccid paralysis. *Inhibition of protein synthesis* - This mechanism is associated with toxins like **diphtheria toxin** and **exotoxin A** from *Pseudomonas aeruginosa*. - These toxins inactivate elongation factor-2 (EF-2), thereby blocking protein synthesis and causing cell death. *Activation of adenylyl cyclase* - Toxins such as **cholera toxin** and **pertussis toxin** act by activating adenylyl cyclase, leading to an increase in intracellular cAMP levels. - This mechanism causes effects like severe diarrhea in cholera and respiratory symptoms in whooping cough.

Question 846: What is the primary therapeutic use of 5-HT1B/1D agonists?

A. Anti-anxiety medications
B. Acute migraine treatment (Correct Answer)
C. Anti-nausea medications for chemotherapy
D. Drugs for gastroesophageal reflux disease (GERD)

Explanation: ***Acute migraine treatment*** - 5-HT1B/1D agonists, such as **triptans**, primarily work by causing **vasoconstriction of intracranial blood vessels** and inhibiting the release of pro-inflammatory neuropeptides. - This action directly alleviates the pain and associated symptoms of **acute migraine attacks**. *Anti-anxiety medications* - Anti-anxiety medications typically target neurotransmitter systems like **GABA** (e.g., benzodiazepines) or **serotonin reuptake** (e.g., SSRIs), not the 5-HT1B/1D receptors in this context. - While serotonin plays a role in anxiety, specific 5-HT1B/1D agonism does not lead to anxiolytic effects. *Anti-nausea medications for chemotherapy* - Anti-nausea medications used for chemotherapy-induced nausea and vomiting often target **5-HT3 receptors** (e.g., ondansetron) to block their pro-emetic effects. - 5-HT1B/1D agonists do not have primary anti-emetic properties useful in this setting. *Drugs for gastroesophageal reflux disease (GERD)* - GERD medications primarily focus on reducing stomach acid production (e.g., **proton pump inhibitors**, H2 blockers) or neutralizing it (antacids). - 5-HT1B/1D agonists do not directly influence gastric acid secretion or esophageal motility in a way beneficial for GERD.

Question 847: Which of the following is not a peripherally acting muscle relaxant?

A. Mivacurium
B. Atracurium
C. Chlorzoxazone (Correct Answer)
D. Dantrolene

Explanation: ***Chlorzoxazone*** - **Chlorzoxazone** is a **centrally acting muscle relaxant** that works by inhibiting polysynaptic reflex arcs in the central nervous system, rather than acting directly on the neuromuscular junction. - Its primary site of action is the **spinal cord** and **subcortical areas** of the brain, leading to generalized muscle relaxation. *Mivacurium* - **Mivacurium** is a **short-acting, non-depolarizing neuromuscular blocker** that acts peripherally by competing with acetylcholine for binding sites on nicotinic receptors at the motor end plate. - It causes muscle relaxation by preventing acetylcholine from depolarizing the muscle fiber, thus inhibiting muscle contraction. *Atracurium* - **Atracurium** is an **intermediate-acting, non-depolarizing neuromuscular blocker** that also acts peripherally at the neuromuscular junction. - It binds to **nicotinic acetylcholine receptors** on the motor end plate, blocking the action of acetylcholine and preventing muscle contraction. *Dantrolene* - **Dantrolene** is a **peripherally acting muscle relaxant** that directly interferes with muscle contraction by inhibiting calcium release from the sarcoplasmic reticulum. - Its unique mechanism of action is directly on the **skeletal muscle fiber**, making it effective in conditions like malignant hyperthermia.

Question 848: Anandamide is a natural ligand for which of the following receptors?

A. Opioid receptors
B. Dopamine D2 receptors
C. Cannabinoid receptors (Correct Answer)
D. GABA receptors

Explanation: ***Cannabinoid receptors*** - **Anandamide** (N-arachidonoylethanolamine) is an **endocannabinoid**, which means it is an endogenous ligand for the **cannabinoid receptors (CB1 and CB2)** in the body. - Its discovery was crucial in understanding the **endocannabinoid system**, which plays a role in pain modulation, mood regulation, appetite, memory, and neuroprotection. - CB1 receptors are predominantly found in the CNS, while CB2 receptors are more abundant in peripheral tissues and immune cells. *Opioid receptors* - Opioid receptors bind **endogenous opioids** (like endorphins, enkephalins, and dynorphins) and **exogenous opioids** (like morphine), mediating analgesia and other effects. - Anandamide does not bind to opioid receptors; its mechanism of action is distinct and involves the cannabinoid system. *GABA receptors* - **GABA receptors (GABA-A and GABA-B)** are the primary inhibitory neurotransmitter receptors in the CNS, mediating the effects of gamma-aminobutyric acid. - While both the GABAergic and endocannabinoid systems can modulate neuronal excitability, anandamide does not directly bind to GABA receptors. *Dopamine D2 receptors* - **Dopamine D2 receptors** are part of the dopaminergic system, primarily mediating the effects of the neurotransmitter **dopamine** on motor control, reward pathways, and cognition. - While the endocannabinoid and dopaminergic systems can interact functionally, anandamide itself does not directly bind to dopamine D2 receptors.

Question 849: Which of the following drugs is approved for treatment of both relapsing-remitting AND primary progressive multiple sclerosis?

A. Fingolimod
B. Omalizumab
C. Ocrelizumab (Correct Answer)
D. Natalizumab

Explanation: ***Ocrelizumab*** - This **anti-CD20 monoclonal antibody** is uniquely approved for both **relapsing-remitting MS (RRMS)** and **primary progressive MS (PPMS)**. - It targets **CD20-expressing B cells**, providing comprehensive disease modification across different MS phenotypes. *Fingolimod* - This **sphingosine 1-phosphate receptor modulator** is approved only for **relapsing-remitting MS**, not primary progressive MS. - While effective for RRMS, it lacks the **dual indication** that makes Ocrelizumab the most comprehensive treatment option. *Omalizumab* - This **anti-IgE monoclonal antibody** is used for **severe allergic asthma** and **chronic idiopathic urticaria**. - It has **no role in multiple sclerosis treatment** and works through IgE-mediated allergic pathways unrelated to MS pathophysiology. *Natalizumab* - This **integrin receptor antagonist** is used for MS but is typically reserved as **second-line therapy** due to **PML risk**. - Unlike Ocrelizumab, it is **not approved for primary progressive MS** and requires careful monitoring for serious complications.

Question 850: Which of the following is granted orphan drug status for the treatment of Dravet's syndrome?

A. Stiripentol (Correct Answer)
B. Icatibant
C. Pitolisant
D. Tafamidis

Explanation: ***Stiripentol*** - **Stiripentol** is an anti-epileptic drug that has been granted **orphan drug status** for its use in treating **Dravet syndrome**. - It is used as an adjunctive therapy, often with clobazam and valproate, to reduce the frequency and severity of seizures in patients with this severe form of epilepsy. *Icatibant* - **Icatibant** is a bradykinin B2 receptor antagonist primarily used for the treatment of acute attacks of **hereditary angioedema (HAE)**. - It is not indicated for epilepsy or Dravet syndrome. *Pitolisant* - **Pitolisant** is a selective histamine H3 receptor antagonist/inverse agonist used to treat **narcolepsy with or without cataplexy**. - Its mechanism of action involves increasing histamine release in the brain to promote wakefulness, which is unrelated to seizure management in Dravet syndrome. *Tafamidis* - **Tafamidis** is a transthyretin stabilizer indicated for the treatment of **transthyretin amyloidosis (ATTR)**, a rare genetic or age-related disease affecting the heart and nerves. - It does not have any approved use or orphan drug status for the treatment of Dravet syndrome.

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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