Central Nervous System Pharmacology Practice Questions

Q: Tetrabenazine acts by inhibiting which of the following?

Vesicular monoamine transporter. **Explanation:** **Tetrabenazine** is a reversible inhibitor of the **Vesicular Monoamine Transporter type 2 (VMAT2)**. 1. **Mechanism of Action (Why B is correct):** VMAT2 is responsible for transporting monoamines (Dopamine, Serotonin, Norepinephrine) from the cytosol into synaptic vesicles for storage. By inhibiting VMAT2, Tetrabenazine prevents the packaging of these neurotransmitters, leading to their degradation by cytosolic MAO. This results in the **depletion of monoamine stores**, particularly dopamine, in the nerve terminals. This reduction in dopamine levels is clinically useful in treating hyperkinetic movement disorders. 2. **Why other options are incorrect:** * **MAO-B (A):** Inhibitors like Selegiline or Rasagiline prevent the breakdown of dopamine; Tetrabenazine actually promotes its depletion. * **Dopamine D2 receptors (C):** While Tetrabenazine has a weak affinity for D2 receptors, its primary and potent mechanism is VMAT2 inhibition. Direct D2 blockers are typical/atypical antipsychotics (e.g., Haloperidol). * **COMT (D):** COMT inhibitors (e.g., Entacapone) are used in Parkinson’s disease to prevent the peripheral breakdown of Levodopa. **Clinical Pearls for NEET-PG:** * **Indications:** Primarily used for **Huntington’s Chorea** and other hyperkinetic disorders like Tardive Dyskinesia or Tourette syndrome. * **Side Effects:** Due to monoamine depletion, it can cause **depression**, sedation, and secondary Parkinsonism. * **Deutetrabenazine:** A newer, deuterated form of Tetrabenazine with a longer half-life and better tolerability. * **Valbenazine:** A highly selective VMAT2 inhibitor specifically approved for Tardive Dyskinesia.

Q: Which local anesthetic can cause Methaemoglobinemia?

Prilocaine. ### Explanation **Correct Answer: B. Prilocaine** **1. Why Prilocaine is the correct answer:** Prilocaine is an amide-type local anesthetic that is metabolized in the liver into **o-toluidine** (ortho-toluidine). This specific metabolite is a potent oxidizing agent that converts ferrous iron ($Fe^{2+}$) in hemoglobin to ferric iron ($Fe^{3+}$), forming **methemoglobin**. Unlike normal hemoglobin, methemoglobin cannot bind oxygen and causes a "left shift" in the dissociation curve, leading to tissue hypoxia and characteristic "chocolate-colored blood" or cyanosis that does not improve with oxygen. **2. Analysis of incorrect options:** * **A. Procaine:** This is an ester-type local anesthetic. While it is metabolized into para-aminobenzoic acid (PABA)—which is associated with allergic reactions—it does not produce metabolites that cause significant oxidative stress to hemoglobin. * **C & D:** Since only Prilocaine (and its metabolite o-toluidine) is classically associated with this side effect among the options provided, these choices are incorrect. **3. Clinical Pearls for NEET-PG:** * **The "Other" Culprit:** Apart from Prilocaine, **Benzocaine** (often used as a topical spray for endoscopy) is the other major local anesthetic frequently implicated in causing methemoglobinemia. * **Threshold:** Methemoglobinemia typically occurs when the dose of Prilocaine exceeds **600 mg**. * **Antidote:** The definitive treatment is **Methylene Blue** (1–2 mg/kg IV over 5 minutes). It acts as a cofactor for the enzyme NADPH-methemoglobin reductase to reduce ferric iron back to its functional ferrous state. * **High-Yield Association:** Patients with **G6PD deficiency** are at a higher risk and should be treated cautiously, as Methylene Blue may be ineffective or cause hemolysis in these individuals.

Q: The selective MAO-B inhibitor among the following is

Selegiline. **Explanation:** Monoamine oxidase (MAO) is an enzyme responsible for the oxidative deamination of biogenic amines. It exists in two isoforms: **MAO-A** (preferentially degrades serotonin, norepinephrine, and dopamine) and **MAO-B** (preferentially degrades dopamine). **1. Why Selegiline is Correct:** **Selegiline** is a selective, irreversible inhibitor of **MAO-B**. By inhibiting the breakdown of dopamine in the striatum, it increases dopamine levels without significantly affecting systemic norepinephrine or serotonin. This selectivity makes it highly effective in the management of **Parkinson’s disease** (often as an adjunct to Levodopa) and, at higher doses, for depression. **2. Analysis of Incorrect Options:** * **Clorgyline:** This is a selective and irreversible inhibitor of **MAO-A**. It is primarily used in research and is not a standard clinical treatment for Parkinson's. * **Moclobemide:** This is a **RIMA** (Reversible Inhibitor of MAO-A). It is used as an antidepressant and is safer than older MAOIs because it carries a lower risk of the "cheese reaction." * **Tranylcypromine:** This is a **non-selective**, irreversible inhibitor of both MAO-A and MAO-B. It is an older antidepressant associated with significant dietary restrictions. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cheese Reaction (Hypertensive Crisis):** Occurs when patients on non-selective MAOIs or MAO-A inhibitors consume tyramine-rich food (aged cheese, wine). Tyramine displaces NE, leading to massive sympathetic discharge. * **Selectivity Loss:** Selegiline loses its MAO-B selectivity at higher doses (>10 mg/day), increasing the risk of hypertensive crisis. * **Rasagiline:** Another potent, irreversible MAO-B inhibitor used in Parkinson’s, often preferred over Selegiline as it is not metabolized into amphetamine derivatives. * **Drug Interaction:** Never combine MAOIs with SSRIs/SNRIs due to the risk of **Serotonin Syndrome**.

Q: A 22-year-old female on antiepileptic therapy got married. When should folic acid supplementation be advised to this female?

All women who could become pregnant. **Explanation:** The correct answer is **B. All women who could become pregnant.** **1. Why Option B is Correct:** Antiepileptic drugs (AEDs), particularly enzyme inducers (like Carbamazepine, Phenytoin) and Valproate, interfere with folate metabolism. Low folate levels are strongly associated with **Neural Tube Defects (NTDs)** like spina bifida. Since the neural tube closes by the **28th day of gestation**—often before a woman even realizes she is pregnant—supplementation must be started preemptively. For women on AEDs, the risk of malformations is 2-3 times higher than the general population; therefore, continuous supplementation is recommended for any woman of childbearing age who is sexually active. **2. Why Other Options are Incorrect:** * **Option A:** While starting 3 months prior is ideal for planned pregnancies, many pregnancies are unplanned. Waiting for a "pre-conception window" leaves many women unprotected. * **Option C:** By the time pregnancy is confirmed (usually week 5-6), the neural tube has already closed. Supplementation at this stage is too late to prevent NTDs. * **Option D:** Post-delivery supplementation does not address the teratogenic risks associated with AEDs during organogenesis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Dosage:** While 0.4 mg is standard for the general population, women on AEDs are often prescribed a higher dose (**5 mg/day**) of folic acid. * **Valproate:** Carries the highest risk of NTDs and cognitive impairment; it should be avoided in women of childbearing age if alternatives exist. * **Drug of Choice:** Levetiracetam and Lamotrigine are generally considered the safest AEDs during pregnancy. * **Vitamin K:** Enzyme-inducing AEDs can cause Vitamin K deficiency in the newborn; 1 mg of Vitamin K should be administered to the neonate at birth to prevent hemorrhagic disease.

Q: A patient on therapy for a Central Nervous System illness develops an abnormality. What is the possible cause?

Antipsychotics. ***Antipsychotics*** - **Thioridazine** and other antipsychotics are well-known to cause **retinal pigmentary changes** and **bull's eye maculopathy**, especially with prolonged use. - The **phenothiazine class** antipsychotics have particular **retinal toxicity** due to their affinity for melanin-containing tissues in the eye. *Antidepressants* - Antidepressants do **not typically cause retinopathy** or significant ocular pigmentary changes. - Common side effects include **dry mouth**, **sedation**, and **anticholinergic effects**, but not retinal abnormalities. *Antiepileptics* - **Vigabatrin** can cause **bilateral concentric visual field defects**, but this presents as **peripheral field loss** rather than bull's eye maculopathy. - Other antiepileptics like **phenytoin** cause **gingival hyperplasia** and **hirsutism**, not retinal pigmentary changes. *Anti-Parkinsonian drugs* - These medications primarily cause **dyskinesias**, **hallucinations**, and **orthostatic hypotension** but do not cause retinopathy. - **Levodopa** and **dopamine agonists** affect motor function and behavior, not retinal pigmentation.

Q: Which of the following anesthetic drugs produces powerful stimulation of the cerebral cortex?

Cocaine. ### Explanation **Correct Option: A (Cocaine)** Cocaine is unique among local anesthetics because it is the only one that acts as a **powerful CNS stimulant** at therapeutic doses. While most local anesthetics (LAs) initially cause CNS depression (or excitation only as a sign of toxicity), cocaine inhibits the reuptake of catecholamines (norepinephrine, dopamine, and serotonin) at nerve terminals. The increased concentration of dopamine in the CNS leads to the characteristic stimulation of the cerebral cortex, resulting in euphoria, increased alertness, and psychomotor agitation. **Incorrect Options:** * **B, C, and D (Procaine, Lidocaine, Tetracaine):** These are synthetic local anesthetics. Unlike cocaine, they do not inhibit catecholamine reuptake. At therapeutic doses, they have no stimulant effect on the cortex. In cases of **systemic toxicity (LAST)**, they may cause "apparent" stimulation (tremors or seizures) by inhibiting inhibitory pathways in the brain, but their primary pharmacological profile is that of a CNS depressant. **High-Yield Clinical Pearls for NEET-PG:** * **Vasoconstriction:** Cocaine is the only local anesthetic that causes **vasoconstriction** (due to inhibition of NE reuptake). All other LAs (except ropivacaine/levobupivacaine at low doses) are vasodilators. * **Metabolism:** Cocaine is an ester but is metabolized primarily by **liver esterases**, whereas other esters (like Procaine) are metabolized by **pseudocholinesterase** in the plasma. * **Cardiotoxicity:** Cocaine is highly cardiotoxic; it can cause hypertension, arrhythmias, and myocardial infarction due to its sympathomimetic effects. * **Clinical Use:** Today, it is primarily used topically in ENT surgeries for its combined anesthetic and vasoconstrictive properties.

Q: Strychnine acts by inhibiting which of the following neurotransmitters?

Glycine. **Explanation:** **Strychnine** is a potent alkaloid and a competitive antagonist of **Glycine**, which is the primary inhibitory neurotransmitter in the spinal cord. 1. **Mechanism of Action (Why B is correct):** Glycine normally binds to its receptors on motor neurons in the spinal cord to cause hyperpolarization (inhibition). Strychnine competitively blocks these glycine receptors. By inhibiting the "inhibitor," strychnine causes disinhibition of motor neurons, leading to unchecked sensory stimuli and powerful, symmetric muscle spasms (opisthotonus). 2. **Why other options are incorrect:** * **GABA (A):** While GABA is the major inhibitory neurotransmitter in the brain, its receptors are primarily targeted by drugs like benzodiazepines or toxins like **Picrotoxin** and **Bicuculline**, not strychnine. * **Acetylcholine (C):** This is the primary excitatory neurotransmitter at the neuromuscular junction. Drugs affecting it include organophosphates or botulinum toxin. * **Dopamine (D):** This is involved in the reward pathway and motor control in the basal ganglia. Its inhibition is associated with Parkinsonism or antipsychotic drug action. **High-Yield Clinical Pearls for NEET-PG:** * **Renshaw Cells:** These are inhibitory interneurons in the spinal cord that release glycine. Strychnine acts specifically at these sites. * **Clinical Presentation:** Strychnine poisoning presents with "spinal convulsions," characterized by a conscious patient experiencing generalized tonic-clonic seizures and a classic **"Risus Sardonicus"** (grimace) and **Opisthotonus** (archback), similar to Tetanus. * **Tetanus Toxin vs. Strychnine:** While both cause similar spasms, Tetanus toxin prevents the *release* of glycine, whereas Strychnine blocks the *receptor*.

Q: The primary site of action for addictive drugs is:

Nucleus accumbens. ### Explanation **1. Why Nucleus Accumbens is Correct:** The **Nucleus Accumbens (NAc)** is the central component of the brain’s **reward circuitry** (the mesolimbic pathway) [1]. Most addictive drugs (e.g., cocaine, amphetamines, opioids, nicotine) exert their reinforcing effects by increasing the concentration of **dopamine** in the NAc [1, 2]. This dopamine surge originates from the Ventral Tegmental Area (VTA) and signals "reward," leading to the compulsive drug-seeking behavior characteristic of addiction [1]. **2. Why the Other Options are Incorrect:** * **Option A: Nucleus Raphe Magnus:** This is a major serotonergic nucleus located in the medulla. It is primarily involved in the **descending inhibition of pain** (antinociception) rather than the reward pathway. * **Option C: Kolliker-Fuse Nucleus:** Located in the pons, this nucleus is part of the **parabrachial complex** and plays a critical role in regulating the respiratory rhythm and the transition between inspiration and expiration. * **Option D: Nucleus Parabrachialis:** This area acts as a relay station for visceral sensations (like taste and pain) and autonomic control. While it has connections to the amygdala, it is not the primary site for drug addiction. **3. High-Yield Clinical Pearls for NEET-PG:** * **The Mesolimbic Pathway:** Connects the **VTA to the Nucleus Accumbens**. This is the "pleasure center" of the brain [1, 2]. * **Dopamine (D2) Receptors:** Chronic drug abuse often leads to the downregulation of D2 receptors in the NAc, contributing to tolerance and anhedonia. * **Cocaine Mechanism:** Specifically inhibits the reuptake of dopamine in the NAc by blocking the dopamine transporter (DAT). * **Opioids:** Act by inhibiting GABAergic interneurons in the VTA, which disinhibits (activates) dopaminergic neurons projecting to the NAc.

Q: Flibanserin is used in the treatment of:

Female hypoactive sexual desire disorder. **Explanation:** **Flibanserin** is the first FDA-approved medication specifically indicated for the treatment of **Hypoactive Sexual Desire Disorder (HSDD)** in premenopausal women. HSDD is characterized by a persistent or recurrent deficiency of sexual fantasies and desire for sexual activity that causes marked distress. **Mechanism of Action:** Flibanserin is a **multifunctional serotonin agonist-antagonist (MSAA)**. It acts as a **5-HT1A receptor agonist** and a **5-HT2A receptor antagonist**. By modulating these receptors, it decreases serotonin (which inhibits sexual desire) and increases dopamine and norepinephrine (which promote sexual excitation) in the prefrontal cortex. **Analysis of Incorrect Options:** * **B. Erectile dysfunction:** This is primarily treated with Phosphodiesterase-5 (PDE-5) inhibitors like Sildenafil or Tadalafil, which act on the nitric oxide pathway. * **C. Anorgasmia:** While sometimes associated with HSDD, anorgasmia is a separate orgasmic disorder. There is currently no FDA-approved drug specifically for anorgasmia. * **D. Dyspareunia:** Painful intercourse in postmenopausal women is typically treated with lubricants, local estrogen therapy, or **Ospemifene** (a selective estrogen receptor modulator). **High-Yield Clinical Pearls for NEET-PG:** * **Trade Name:** Addyi (often called the "Female Viagra," though its mechanism is central, not peripheral). * **Dosing:** It must be taken **daily at bedtime** to mitigate side effects like somnolence and dizziness. * **Black Box Warning:** Significant risk of **severe hypotension and syncope** when taken with **alcohol**. It is also contraindicated with strong CYP3A4 inhibitors. * **Bremelanotide:** Another drug for HSDD, but unlike Flibanserin, it is a melanocortin receptor agonist administered via subcutaneous injection on an as-needed basis.

Question 1

Tetrabenazine acts by inhibiting which of the following?

Accepted Answer

Vesicular monoamine transporter

Answer

MAO-B

Answer

Dopamine D2 receptors

Answer

COMT

Question 2

Which local anesthetic can cause Methaemoglobinemia?

Accepted Answer

Prilocaine

Answer

Procaine

Answer

Both Procaine and Prilocaine

Answer

None of the above

Question 3

The selective MAO-B inhibitor among the following is

Accepted Answer

Selegiline

Answer

Clorgyline

Answer

Moclobemide

Answer

Tranylcypromine

Question 4

A 22-year-old female on antiepileptic therapy got married. When should folic acid supplementation be advised to this female?

Accepted Answer

All women who could become pregnant

Answer

3 months before pregnancy

Answer

As soon as pregnancy is confirmed

Answer

After delivery

Question 5

A patient on therapy for a Central Nervous System illness develops an abnormality. What is the possible cause?

Accepted Answer

Antipsychotics

Answer

Antidepressants

Answer

Antiepileptics

Answer

Anti-Parkinsonian drugs

Question 6

Which of the following anesthetic drugs produces powerful stimulation of the cerebral cortex?

Accepted Answer

Cocaine

Answer

Procaine

Answer

Lidocaine

Answer

Tetracaine

Question 7

Strychnine acts by inhibiting which of the following neurotransmitters?

Accepted Answer

Glycine

Answer

GABA

Answer

Acetylcholine

Answer

Dopamine

Question 8

The primary site of action for addictive drugs is:

Accepted Answer

Nucleus accumbens

Answer

Nucleus raphe magnus

Answer

Kolliker-Fusenucleus

Answer

Nucleus parabrachialis

Question 9

Flibanserin is used in the treatment of:

Accepted Answer

Female hypoactive sexual desire disorder

Answer

Erectile dysfunction

Answer

Anorgasmia

Answer

Dyspareunia

Question 10

Local anesthetic is not effective in inflamed tissue because:

Accepted Answer

The pH is more acidic, rendering the local anesthetic ineffective

Answer

All impulses generated cannot be blocked

Answer

The myelin sheath is inflamed and does not absorb the solution

Answer

All of the above

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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