Central Nervous System Pharmacology Practice Questions

Q: Which of the following drugs is used for Smoking Cessation?

Bupropion. ***Bupropion*** - **Bupropion** is an antidepressant that is also approved as a smoking cessation aid. It works by inhibiting the reuptake of **dopamine** and **norepinephrine**, which can help reduce nicotine cravings and withdrawal symptoms. - It is often prescribed as a first-line pharmacotherapy for smoking cessation, with a typical treatment duration of 7-12 weeks. *Buprenorphine* - **Buprenorphine** is a partial opioid agonist primarily used to treat opioid addiction. It is not indicated for smoking cessation. - While it can help manage withdrawal symptoms from opioids, it has no direct mechanism of action that would reduce nicotine dependence or cravings. *Methadone* - **Methadone** is a full opioid agonist primarily used for the treatment of opioid use disorder (OUD) and chronic pain management. It is not used for smoking cessation. - Its mechanism involves binding to opioid receptors to prevent withdrawal symptoms and reduce cravings for other opioids. *Naltrexone* - **Naltrexone** is an opioid antagonist used primarily for the treatment of alcohol dependence and opioid use disorder. It is not indicated for smoking cessation. - It blocks the effects of opioids and reduces alcohol cravings, but does not affect nicotine pathways or dependence.

Q: Most commonly abused opioid -

Diacetylmorphine. ***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**.

Q: Which local anesthetic is known for its vasoconstrictive properties?

Cocaine. ***Cocaine*** - Cocaine is unique among local anesthetics for its inherent **sympathomimetic** properties, leading to **vasoconstriction**. - This vasoconstriction is due to its ability to block the reuptake of **norepinephrine** and other catecholamines at adrenergic nerve terminals. *Procaine* - Procaine is an **ester-type** local anesthetic that typically causes **vasodilation**, which can lead to rapid systemic absorption and a shorter duration of action. - It does not possess any inherent vasoconstrictive properties. *Lidocaine* - Lidocaine, an **amide-type** local anesthetic, generally causes **vasodilation** at clinical concentrations. - Due to this vasodilatory effect, **epinephrine** is often added to lidocaine preparations to prolong its action and reduce systemic absorption. *Chlorprocaine* - Chlorprocaine is another **ester-type** local anesthetic known for its rapid onset and short duration of action. - It primarily causes **vasodilation**, similar to procaine, and has no intrinsic vasoconstrictive effects.

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

It is a potent bronchoconstrictor. ***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].

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

Acute migraine treatment. ***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.

Q: What is a key difference between fosphenytoin and phenytoin?

Can be mixed with saline. **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.

Q: Which of the following antiepileptic drugs is most classically associated with causing hirsutism?

Phenytoin. ***Phenytoin*** - **Phenytoin** is the **most classically associated** antiepileptic drug with **hirsutism**, which is abnormal/excessive growth of hair [1]. - The mechanism involves changes in **androgen metabolism** and stimulation of hair follicle growth. - Other cosmetic side effects include **gingival hyperplasia** and **coarsening of facial features** [1].*Valproate* - Valproate can paradoxically cause both **hair loss (alopecia)** and **hirsutism**, particularly in women and children. - However, phenytoin has a **stronger and more classical association** with hirsutism. - Valproate is also known for **weight gain**, **hepatotoxicity**, **pancreatitis**, and **teratogenicity**.*Carbamazepine* - Carbamazepine's common side effects include **drowsiness**, **dizziness**, **diplopia**, and **hyponatremia**. - It is not classically linked to **hirsutism** as a prominent adverse effect. - Can cause **agranulocytosis** and **Stevens-Johnson syndrome** in rare cases.*Phenobarbitone* - Phenobarbitone is an older antiepileptic drug associated with **sedation**, **cognitive impairment**, and **dependence**. - It does not commonly cause **hirsutism**. - Also causes **enzyme induction** leading to multiple drug interactions.

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

Chlorzoxazone. ***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.

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

Cannabinoid receptors. ***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.

Q: What is the maximum dose of plain lignocaine (in mg) for adults?

300. ***300 mg*** - The maximum recommended dose of **plain lidocaine** (without epinephrine) for adults is typically **300 mg** or 4.5 mg/kg, whichever is less. - Exceeding this dose can increase the risk of **systemic toxicity**, including central nervous system and cardiovascular effects. *500 mg* - This dose is generally considered the maximum for **lidocaine with epinephrine** in adults, as **epinephrine** causes vasoconstriction and delays systemic absorption of lidocaine. - For **plain lidocaine**, 500 mg would be an overdose and significantly increase the risk of toxicity. *700 mg* - This is well above the recommended maximum dose for both plain lidocaine and lidocaine with epinephrine, posing a **severe risk of toxicity**. - Such a high dose could lead to **seizures**, cardiac arrhythmias, and even **cardiac arrest**. *1000 mg* - This dose is extremely dangerous and far exceeds any recommended maximum for lidocaine, regardless of whether it contains epinephrine. - Administration of 1000 mg of lidocaine would almost certainly result in **severe and potentially fatal toxicity**.

Question 1

Which of the following drugs is used for Smoking Cessation?

Accepted Answer

Bupropion

Answer

Methadone

Answer

Buprenorphine

Answer

Naltrexone

Question 2

Most commonly abused opioid -

Accepted Answer

Diacetylmorphine

Answer

Morphine

Answer

Oxycodone

Answer

Buprenorphine

Question 3

Which local anesthetic is known for its vasoconstrictive properties?

Accepted Answer

Cocaine

Answer

Lidocaine

Answer

Chlorprocaine

Answer

Procaine

Question 4

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

Accepted Answer

It is a potent bronchoconstrictor

Answer

It increases arterial blood pressure

Answer

It inhibits polysynaptic reflexes in the spinal cord

Answer

It functionally "dissociates" the thalamus

Question 5

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

Accepted Answer

Acute migraine treatment

Answer

Anti-anxiety medications

Answer

Anti-nausea medications for chemotherapy

Answer

Drugs for gastroesophageal reflux disease (GERD)

Question 6

What is a key difference between fosphenytoin and phenytoin?

Accepted Answer

Can be mixed with saline

Answer

Can be used in absence seizures

Answer

Can be given orally

Answer

It is the drug of choice for myoclonic seizures

Question 7

Which of the following antiepileptic drugs is most classically associated with causing hirsutism?

Accepted Answer

Phenytoin

Answer

Valproate

Answer

Carbamazepine

Answer

Phenobarbitone

Question 8

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

Accepted Answer

Chlorzoxazone

Answer

Mivacurium

Answer

Atracurium

Answer

Dantrolene

Question 9

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

Accepted Answer

Cannabinoid receptors

Answer

Opioid receptors

Answer

Dopamine D2 receptors

Answer

GABA receptors

Question 10

What is the maximum dose of plain lignocaine (in mg) for adults?

Accepted Answer

300

Answer

500

Answer

700

Answer

1000

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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