Central Nervous System Pharmacology Practice Questions

Q: What condition results from the increased sensitivity of dopamine receptors following chronic dopamine receptor blockade?

Dyskinesia. ***Tardive Dyskinesia*** - **Chronic dopamine receptor blockade**, often observed with long-term use of **antipsychotics**, leads to an **upregulation** of dopamine receptors. - This **increased sensitivity** to dopamine can result in **involuntary movements** such as **tardive dyskinesia** when dopamine levels fluctuate or the blockade is partially overcome. *Hyperphagia* - This refers to abnormally **increased appetite or consumption of food**, which is a general symptom and not specifically linked to the mechanism described. - While some medications affecting dopamine can influence appetite, **hyperphagia** is not the direct result of increased dopamine receptor sensitivity post-blockade. *Hyperpathia* - This describes an **abnormally painful reaction to a stimulus**, especially a repetitive one, and an elevated pain threshold. - It is a **neuropathic pain syndrome** and is not directly related to changes in dopamine receptor sensitivity. *Hypomania* - Hypomania is a **mood state** characterized by persistent elevated, expansive, or irritable mood, and increased activity or energy, less severe than mania. - While dopamine pathways are involved in mood regulation, **hypomania** is not a direct consequence of increased sensitivity of dopamine receptors following chronic blockade.

Q: Which of the following is not a use of Thiopentone?

As antidepressant. As antidepressant - **Thiopentone** is a short-acting **barbiturate** and a potent central nervous system depressant, with no known antidepressant properties. [1] - Its mechanism of action involves enhancing **GABAergic inhibition**, leading to sedation and anesthesia, not mood elevation. *Induction of anesthesia* - **Thiopentone** is a classic intravenous anesthetic, often used for **rapid induction of general anesthesia** due to its fast onset of action. [2], [4] - It quickly crosses the **blood-brain barrier** to produce unconsciousness, making it effective for this purpose. [4] *Medically induced coma* - **Thiopentone** can be used to induce and maintain a **medically induced coma**, particularly in cases of severe head injury or status epilepticus, to reduce metabolic demand and cerebral edema. [3] - Its ability to significantly suppress brain activity makes it suitable for **neuroprotection** in critical care settings. [3] *As truth serum* - Historically, **thiopentone** (often referred to as **sodium pentothal**) has been colloquially known as a **"truth serum"** due to its ability to lower inhibitions and make subjects more loquacious. - While it can facilitate questioning by making individuals less guarded, its effectiveness as a reliable truth serum is largely unsubstantiated and ethically controversial.

Q: Which among the following is a depolarising muscle relaxant?

Decamethonium. **Correct: Decamethonium** - **Decamethonium** is a **depolarizing neuromuscular blocker** that mimics acetylcholine at the neuromuscular junction, leading to initial muscle fasciculations followed by paralysis. - It binds to and activates **nicotinic acetylcholine receptors**, causing persistent depolarization and preventing further muscle contraction. - While historically important, it is rarely used clinically today compared to succinylcholine. *Incorrect: D-tubocurarine* - **D-tubocurarine** is a **non-depolarizing neuromuscular blocker** that acts as a competitive antagonist at the nicotinic acetylcholine receptors. - It prevents acetylcholine from binding, thereby inhibiting muscle contraction without initial depolarization. *Incorrect: Doxacurium* - **Doxacurium** is a **non-depolarizing neuromuscular blocker** of the long-acting benzylisoquinolinium class. - It functions by competitively blocking acetylcholine at the neuromuscular junction, leading to muscle relaxation. *Incorrect: Atracurium* - **Atracurium** is an **intermediate-acting, non-depolarizing neuromuscular blocker** also of the benzylisoquinolinium class. - It undergoes unique elimination pathways, including **Hofmann elimination** and ester hydrolysis, making it suitable for patients with renal or hepatic impairment.

Q: Which drug is the first-line treatment for absence seizures?

Ethosuximide. ***Ethosuximide*** - **Ethosuximide** is the **first-line drug** of choice for treating **absence seizures** due to its specific mechanism of action in inhibiting **T-type calcium channels** in the thalamus. - Its efficacy is highly specific to **absence seizures**, meaning it is primarily effective for this type of seizure and generally not for other seizure types. *Lamotrigine* - While effective for various seizure types, including **generalized tonic-clonic seizures** and **focal seizures**, **lamotrigine** is considered a **second-line agent** for absence seizures. - It is often used when **ethosuximide** or **valproic acid** is not tolerated or ineffective, or when there are co-existing seizure types. *Carbamazepine* - **Carbamazepine** is a first-line treatment for **focal seizures** and **generalized tonic-clonic seizures**, but it is generally **contraindicated** for absence seizures. - In some cases, **carbamazepine** can paradoxically **worsen absence seizures** or precipitate them due to its distinct mechanism of action involving **sodium channel blockade**. *Phenytoin* - **Phenytoin** is primarily used for **focal seizures** and **generalized tonic-clonic seizures** by stabilizing neuronal membranes and reducing neuronal excitability via **sodium channel blockade**. - It is **not effective** for absence seizures and, like carbamazepine, can sometimes **exacerbate** them or has no beneficial effect.

Q: Which drug is used in amytrophic lateral sclerosis?

Riluzole. ***Riluzole*** - **Riluzole** is an **NMDA receptor antagonist** that is approved for the treatment of **amyotrophic lateral sclerosis (ALS)**. - It works by reducing **glutamate-mediated excitotoxicity**, which is thought to contribute to neuronal damage in ALS, thereby extending survival time and delaying the need for tracheostomy. *Glatiramer acetate* - **Glatiramer acetate** is an immunomodulating drug used in the treatment of **multiple sclerosis (MS)**. - It is believed to work by inducing and activating **T-suppressor cells** specific for myelin basic protein, thus reducing the frequency of relapses in MS. *Tacrine* - **Tacrine** is an **acetylcholinesterase inhibitor** that was previously used for the treatment of **mild to moderate Alzheimer's disease**. - Its use has largely been replaced by newer, better-tolerated drugs due to its significant **hepatotoxicity** and frequent dosing schedule. *Olanzapine* - **Olanzapine** is an **atypical antipsychotic** medication used to treat conditions such as **schizophrenia** and **bipolar disorder**. - It primarily exerts its effects by blocking **dopamine D2** and **serotonin 5-HT2A** receptors.

Q: Which of the following does not release histamine?

Pancuronium. ***Pancuronium*** - **Pancuronium** is a **non-depolarizing neuromuscular blocker** that does **not cause histamine release** [1], [2], and therefore has minimal effects on blood pressure and heart rate. - This characteristic makes it a suitable choice for patients where **hemodynamic stability** is crucial. *D- Tubocurarine (D-TC)* - **D-Tubocurarine** is a historical **non-depolarizing neuromuscular blocker** known to cause significant **histamine release** [1], [2]. - Histamine release can lead to **hypotension, bronchospasm**, and other allergic-type reactions [1], [2]. *Succinylcholine* - **Succinylcholine** is a **depolarizing neuromuscular blocker** that can cause **histamine release**, particularly with rapid injection or high doses [1]. - Histamine release can result in **flushing, hypotension**, and **tachycardia**. *Mivacurium* - **Mivacurium** is a **short-acting non-depolarizing neuromuscular blocker** well-known for causing **histamine release** [2]. - The histamine release observed with Mivacurium is often described as **dose-dependent** and can lead to cutaneous flushing and hypotension.

Q: What is the classification of Rotigotine?

Dopamine agonist. ***Dopamine agonist*** - Rotigotine is classified as a **non-ergoline dopamine agonist**, meaning it directly stimulates dopamine receptors in the brain. - It is used in the treatment of **Parkinson's disease** and **restless legs syndrome** by mimicking the effects of dopamine. *Dopamine antagonist* - **Dopamine antagonists** block dopamine receptors and are typically used as antipsychotics or antiemetics. - This classification would have opposite pharmacological effects to what is seen with rotigotine. *GABA agonist* - **GABA agonists** enhance the effects of the inhibitory neurotransmitter GABA, leading to sedation or seizure control. - This mechanism of action is unrelated to rotigotine's primary effects on dopamine pathways. *GABA antagonist* - **GABA antagonists** block GABA receptors, which can lead to increased neuronal excitability and seizures. - This is not the mechanism of action for rotigotine, which targets the dopaminergic system.

Q: Which of the following drugs does not potentiate the effect of NMDA at NMDA receptors?

Ketamine. ***Ketamine*** - **Ketamine** is an **NMDA receptor antagonist**, meaning it blocks the activity of NMDA receptors rather than potentiating it. - It binds to a site within the **NMDA receptor channel**, preventing ion flow and neuronal excitation. - Used clinically as a dissociative anesthetic and for treatment-resistant depression. *Aspartic acid* - **Aspartic acid** functions as an **excitatory neurotransmitter** and is an **agonist** at NMDA receptors. - It readily activates these receptors by binding to the glutamate-binding site, thereby potentiating their effects. *D-serine* - **D-serine** acts as an **endogenous co-agonist** at the NMDA receptor by binding to the **glycine regulatory site** (also called the glycine-B site). - Its binding is essential for the full activation and potentiation of NMDA receptor activity. - Along with glycine, it is one of the primary physiological co-agonists required for NMDA receptor function. *Homocysteic acid* - **Homocysteic acid** is an **endogenous excitatory amino acid** that acts as an **agonist** at NMDA receptors. - It directly binds to and activates NMDA receptors at the glutamate-binding site, thus potentiating their effects.

Q: Patient on treatment with carbidopa + levodopa for 10 years now has wearing-off effect. What should be added to restore action?

Tolcapone. ***Tolcapone*** - **Tolcapone** is a **catechol-O-methyltransferase (COMT) inhibitor** that prevents the peripheral breakdown of levodopa, increasing its availability to the brain. - Adding a COMT inhibitor is the **primary strategy** to mitigate the **wearing-off effect** in patients receiving chronic levodopa therapy by prolonging levodopa's half-life and duration of action. - COMT inhibitors directly extend the duration of each levodopa dose, making them first-line adjuncts for wearing-off phenomenon. *Rasagiline* - **Rasagiline** is a **monoamine oxidase-B (MAO-B) inhibitor** used in Parkinson's disease to reduce the breakdown of dopamine in the brain. - It is also effective as an adjunct in treating **wearing-off** and can reduce daily off-time, though COMT inhibitors are typically preferred as first-line agents for this specific indication. - MAO-B inhibitors work by increasing central dopamine levels rather than directly extending levodopa's duration. *Benzhexol* - **Benzhexol** (also known as trihexyphenidyl) is an **anticholinergic agent** primarily used to treat tremor and dystonia in Parkinson's disease, especially in younger patients. - It does not address the aetiology of the **wearing-off phenomenon**, which is due to fluctuating levodopa levels and dopamine deficiency. *Amantadine* - **Amantadine** is an **NMDA receptor antagonist** used primarily to reduce **dyskinesias** associated with long-term levodopa therapy in Parkinson's disease. - While it has some efficacy in early Parkinson's and improving motor fluctuations, it is not the primary intervention for the **wearing-off effect** where reduced duration of benefit from levodopa is the main issue.

Q: A patient with treatment-resistant schizophrenia presents with excessive salivation, increased blood glucose, and hyperlipidemia after switching from haloperidol and thioridazine. Which antipsychotic medication is most likely responsible for these side effects?

Clozapine. ***Clozapine*** - Clozapine is a highly effective antipsychotic for **treatment-resistant schizophrenia** but is known for significant metabolic side effects including **hyperglycemia**, **dyslipidemia**, and dose-dependent **sialorrhea** (excessive salivation). - The combination of **excessive salivation**, **increased blood glucose**, and **hyperlipidemia** after a switch in antipsychotics strongly points to clozapine. *Ziprasidone* - Ziprasidone is considered to have a relatively **favorable metabolic profile**, with a low risk of weight gain, hyperglycemia, and hyperlipidemia. - It is not typically associated with prominent **sialorrhea**. *Risperidone* - Risperidone can cause **weight gain** and some metabolic disturbances, but it is less commonly associated with the severe metabolic dysregulation and sialorrhea seen with clozapine. - While it can cause elevated prolactin, **sialorrhea** and significant **hyperglycemia** and **hyperlipidemia** are not its most defining or severe side effects compared to clozapine. *Aripiprazole* - Aripiprazole is a **partial dopamine agonist** and generally has a **low risk of metabolic side effects**, including minimal impact on blood glucose and lipids. - It is also not typically associated with **sialorrhea**.

Question 1

What condition results from the increased sensitivity of dopamine receptors following chronic dopamine receptor blockade?

Accepted Answer

Dyskinesia

Answer

Hyperphagia

Answer

Hyperpathia

Answer

Hypomania

Question 2

Which of the following is not a use of Thiopentone?

Accepted Answer

As antidepressant

Answer

Induction of anesthesia

Answer

Medically induced coma

Answer

As truth serum

Question 3

Which among the following is a depolarising muscle relaxant?

Accepted Answer

Decamethonium

Answer

D-tubocurarine

Answer

Doxacurium

Answer

Atracurium

Question 4

Which drug is the first-line treatment for absence seizures?

Accepted Answer

Ethosuximide

Answer

Carbamazepine

Answer

Phenytoin

Answer

Lamotrigine

Question 5

Which drug is used in amytrophic lateral sclerosis?

Accepted Answer

Riluzole

Answer

Tacrine

Answer

Olanzapine

Answer

Glatiramer acetate

Question 6

Which of the following does not release histamine?

Accepted Answer

Pancuronium

Answer

d-Tubocurarine

Answer

Succinylcholine

Answer

Mivacurium

Question 7

What is the classification of Rotigotine?

Accepted Answer

Dopamine agonist

Answer

Dopamine antagonist

Answer

GABA agonist

Answer

GABA antagonist

Question 8

Which of the following drugs does not potentiate the effect of NMDA at NMDA receptors?

Accepted Answer

Ketamine

Answer

Aspartic acid

Answer

D-serine

Answer

Homocysteic acid

Question 9

Patient on treatment with carbidopa + levodopa for 10 years now has wearing-off effect. What should be added to restore action?

Accepted Answer

Tolcapone

Answer

Benzhexol

Answer

Rasagiline

Answer

Amantadine

Question 10

A patient with treatment-resistant schizophrenia presents with excessive salivation, increased blood glucose, and hyperlipidemia after switching from haloperidol and thioridazine. Which antipsychotic medication is most likely responsible for these side effects?

Accepted Answer

Clozapine

Answer

Ziprasidone

Answer

Risperidone

Answer

Aripiprazole

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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