Central Nervous System Pharmacology Practice Questions

Q: Which of the following is a central nervous system stimulant?

Cocaine. **Explanation:** **Correct Answer: A. Cocaine** Cocaine is a potent **indirect-acting sympathomimetic** and a classic CNS stimulant. Its primary mechanism involves the inhibition of the reuptake of monoamines—specifically **Dopamine, Norepinephrine, and Serotonin**—at the synaptic cleft. By blocking the dopamine transporter (DAT), it increases dopamine concentration in the nucleus accumbens, leading to euphoria, increased alertness, and psychomotor agitation. **Analysis of Incorrect Options:** * **B. Alcohol:** Ethanol is a **CNS depressant**. It enhances the inhibitory effect of GABA at GABA-A receptors and inhibits excitatory NMDA glutamate receptors, leading to sedation and decreased cognitive function. * **C. Nicotine:** While nicotine has complex effects (biphasic), it is primarily classified as a **ganglionic stimulant**. In the CNS, it acts on nicotinic acetylcholine receptors (nAChRs). While it has mild alerting effects, in the context of standard pharmacology classification for competitive exams, Cocaine is the definitive "stimulant" compared to the others. * **D. Cannabis:** Marijuana is classified as a **hallucinogen or psychotomimetic**. Its active component, THC, acts on CB1 receptors. It typically produces a "dream-like" state, altered perception, and sedation rather than pure CNS stimulation. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Cocaine blocks the **NET (Norepinephrine Transporter)**, leading to excessive sympathetic activity. * **Clinical Presentation:** Mydriasis, tachycardia, hypertension, and potential myocardial infarction (due to coronary vasospasm). * **Treatment of Toxicity:** **Benzodiazepines** are the first-line treatment for cocaine-induced agitation and cardiovascular toxicity. * **Contraindication:** **Beta-blockers** should be avoided in cocaine toxicity as they can lead to "unopposed alpha-stimulation," worsening hypertension.

Q: Which drug is used for smoking cessation?

Varenicline. **Explanation:** **Varenicline** is the correct answer. It is a **selective partial agonist at the α4β2 nicotinic acetylcholine receptors (nAChR)** in the brain. Its mechanism of action is twofold: 1. **Agonist Effect:** It provides a low-level release of dopamine, which helps mitigate the symptoms of nicotine withdrawal. 2. **Antagonist Effect:** By binding to the receptor with high affinity, it prevents inhaled nicotine from binding. This reduces the "reward" or reinforcement associated with smoking, making a relapse less satisfying. **Analysis of Incorrect Options:** * **Theophylline (Option A):** A methylxanthine used as a bronchodilator in asthma and COPD. It acts primarily by inhibiting phosphodiesterase (PDE) and antagonizing adenosine receptors. * **Bicalutamide (Option B):** A non-steroidal anti-androgen used in the management of prostate cancer. * **Salmeterol (Option C):** A Long-Acting Beta-2 Agonist (LABA) used for the maintenance treatment of asthma and COPD; it has no role in addiction medicine. **High-Yield Clinical Pearls for NEET-PG:** * **First-line agents** for smoking cessation include Varenicline, Bupropion (an atypical antidepressant), and Nicotine Replacement Therapy (NRT). * **Varenicline Side Effects:** The most common side effect is **nausea**. It is also associated with **neuropsychiatric symptoms** (vivid dreams, depression, suicidal ideation) and should be used cautiously in patients with pre-existing psychiatric illness. * **Bupropion** is specifically preferred in smokers who are concerned about weight gain or have comorbid depression, but it is contraindicated in patients with a history of seizures.

Q: Tolerance is seen in all, except?

Cocaine. The correct answer is **Cocaine**. In pharmacology, tolerance refers to the requirement of higher doses of a drug to achieve the same effect previously produced by a lower dose. **Why Cocaine is the correct answer:** Cocaine is a unique CNS stimulant because it primarily exhibits **reverse tolerance (sensitization)** rather than traditional tolerance [1]. With repeated use, the user may become *more* sensitive to its effects, particularly its psychomotor and convulsant actions. While some tolerance can develop to its euphoric effects, the lack of significant physiological tolerance to its dangerous side effects (like seizures and cardiac arrhythmias) distinguishes it from the other options [3]. **Analysis of Incorrect Options:** * **Morphine (Opioids):** Exhibits profound tolerance to most effects (analgesia, euphoria, respiratory depression) except for **miosis and constipation**, which are high-yield "no-tolerance" exceptions [2]. * **Amphetamine:** Rapid tolerance (tachyphylaxis) develops to its anorectic and pressor effects due to the depletion of neuronal norepinephrine stores. * **Barbiturates:** These induce hepatic microsomal enzymes (pharmacokinetic tolerance) and cause CNS adaptation (pharmacodynamic tolerance). **High-Yield NEET-PG Pearls:** 1. **Miosis and Constipation:** Remember these two effects of Morphine never show tolerance. 2. **Tachyphylaxis:** This is a form of rapid-onset tolerance seen with Ephedrine, Tyramine, and Amphetamines. 3. **Cross-tolerance:** Often occurs between drugs of the same class (e.g., between different Benzodiazepines or between Alcohol and Barbiturates). 4. **Cocaine Mechanism:** It acts by blocking the reuptake of Dopamine, Norepinephrine, and Serotonin (NET, DAT, and SERT inhibitors) [3].

Q: Which antidepressant is relatively contraindicated in young men secondary to its side effect of priapism?

Trazodone. **Explanation:** **Trazodone** is a SARI (Serotonin Antagonist and Reuptake Inhibitor) primarily used for insomnia and depression. The correct answer is Trazodone because it is notorious for causing **priapism** (a painful, persistent erection lasting >4 hours), which is considered a urological emergency. * **Mechanism:** This side effect is attributed to its potent **$\alpha_1$-adrenergic receptor antagonism**. Blockade of these receptors in the corpora cavernosa prevents the sympathetic-mediated vasoconstriction required for detumescence, leading to "trapped" blood flow. Due to this association, it is often humorously referred to as **"Trazobone."** **Analysis of Incorrect Options:** * **Sertraline (SSRI):** The most common sexual side effect of SSRIs is **delayed ejaculation** or erectile dysfunction, not priapism. In fact, SSRIs are sometimes used therapeutically to treat premature ejaculation. * **Imipramine & Amitriptyline (TCAs):** These Tricyclic Antidepressants are more commonly associated with **anticholinergic side effects** (dry mouth, blurred vision, urinary retention) and cardiac arrhythmias. While they can cause sexual dysfunction, priapism is extremely rare compared to Trazodone. **High-Yield Clinical Pearls for NEET-PG:** * **Management of Priapism:** If Trazodone-induced priapism occurs, the immediate treatment involves intracavernosal injection of an $\alpha$-agonist like **Phenylephrine**. * **Other Side Effects:** Trazodone is highly sedating (due to $H_1$ blockade) and can cause postural hypotension (due to $\alpha_1$ blockade). * **Drug of Choice:** Trazodone is frequently used "off-label" as a hypnotic for patients with depression-associated insomnia because it lacks the addictive potential of benzodiazepines.

Q: True about phenytoin?

Causes nystagmus and ataxia. **Explanation:** Phenytoin is a high-yield hydantoin derivative used primarily for focal and generalized tonic-clonic seizures. Its mechanism involves the blockade of voltage-gated sodium channels in their inactivated state. **Why Option D is Correct:** Nystagmus and ataxia are the hallmark signs of **dose-dependent cerebellar-vestibular toxicity**. At therapeutic levels (10–20 µg/mL), mild nystagmus may appear. As levels exceed 20–30 µg/mL, ataxia, slurred speech, and incoordination develop. This occurs because phenytoin follows **zero-order kinetics** (saturation kinetics) at higher doses; a small increase in dose leads to a disproportionately large increase in plasma concentration, rapidly reaching toxic levels. **Analysis of Incorrect Options:** * **Option A:** Phenytoin has high oral bioavailability (~90%) and does **not** undergo significant first-pass metabolism. It is metabolized by hepatic CYP2C9/2C19 enzymes. * **Option B:** Phenytoin is highly **teratogenic**. It causes **Fetal Hydantoin Syndrome**, characterized by craniofacial anomalies (cleft lip/palate), microcephaly, and hypoplastic phalanges/nails. * **Option C:** Phenytoin is **ineffective** in absence seizures and may even exacerbate them. The drug of choice for absence seizures is **Ethosuximide** (or Valproate). **High-Yield Clinical Pearls for NEET-PG:** * **Non-dose dependent side effects (Mnemonic: P-H-E-N-Y-T-O-I-N):** **P**-450 induction, **H**irsutism, **E**nlarged gums (Gingival hyperplasia due to PDGF), **N**ystagmus, **Y**ellow-brown skin (pigmentation), **T**eratogenicity, **O**steomalacia (Vitamin D deficiency), **I**nterference with B12/Folate (Megaloblastic anemia), **N**europathy. * **Fosphenytoin:** A water-soluble prodrug of phenytoin used IV to avoid the local irritation and "Purple Glove Syndrome" associated with phenytoin.

Q: Naltrexone is used to maintain abstinence following opioid withdrawal in addicts. It blocks all of the following features of opioid use, except:

Craving for opioids. **Explanation:** **Naltrexone** is a long-acting, competitive **opioid receptor antagonist** with high affinity for $\mu$ (mu) receptors. Its primary role in addiction medicine is to block the pharmacological effects of exogenous opioids, thereby preventing the "high" if a patient relapses. **Why "Craving" is the correct answer:** While Naltrexone effectively blocks the physical and psychological effects of opioids (like euphoria), it **does not directly suppress the psychological craving** for opioids. In fact, because it induces a state of receptor blockade without providing any agonistic "reward," it can sometimes exacerbate cravings or lead to poor compliance. This is a key clinical distinction from **Methadone** or **Buprenorphine**, which are agonists/partial agonists that satisfy cravings by stimulating the receptors. **Analysis of Incorrect Options:** * **A. Euphoriant effects:** Naltrexone occupies the $\mu$-receptors, preventing opioids from binding and triggering the dopamine release in the reward pathway. * **C & D. Miosis and Respiratory depression:** These are classic pharmacological actions of opioids mediated by $\mu$ and $\kappa$ receptors. As a competitive antagonist, Naltrexone prevents these physiological effects by blocking receptor activation. **High-Yield NEET-PG Pearls:** 1. **Prerequisite:** Naltrexone should only be started after a patient is **opioid-free for 7–10 days**. Administering it earlier will precipitate **acute withdrawal syndrome**. 2. **Alcoholism:** Naltrexone is also FDA-approved for **Alcohol Dependence**; it reduces the "reward" of drinking by blocking endogenous opioid release. 3. **Naloxone vs. Naltrexone:** Remember **Naloxone** is for acute toxicity (short-acting, IV), while **Naltrexone** is for maintenance/abstinence (long-acting, Oral/Depot). 4. **Vivitrol:** This is the monthly injectable depot formulation of Naltrexone used to improve compliance.

Q: Which of the following antiepileptic drugs acts by affecting the levels of GABA?

Sodium valproate. **Explanation:** The correct answer is **Sodium valproate**. This drug is a broad-spectrum antiepileptic that exerts its effects through multiple mechanisms, primarily by increasing the levels of **GABA** (Gamma-Aminobutyric Acid), the brain's chief inhibitory neurotransmitter. It achieves this by: 1. Inhibiting **GABA transaminase** (the enzyme responsible for GABA degradation). 2. Stimulating **Glutamic Acid Decarboxylase (GAD)** (the enzyme responsible for GABA synthesis). 3. Blocking voltage-gated sodium channels and T-type calcium channels. **Analysis of Incorrect Options:** * **Ethosuximide:** Its primary mechanism is the inhibition of **T-type Calcium channels** in thalamic neurons. It is the drug of choice for Absence seizures but does not significantly affect GABA levels. * **Phenytoin sodium:** It acts by blocking **voltage-gated Sodium channels** in their inactive state, preventing high-frequency repetitive firing of action potentials. * **Carbamazepine:** Similar to phenytoin, it primarily works by stabilizing the inactivated state of **voltage-gated Sodium channels**. **High-Yield Clinical Pearls for NEET-PG:** * **Valproate** is the drug of choice for **Myoclonic seizures** and generalized tonic-clonic seizures (GTCS). * It is highly **teratogenic**, specifically associated with **Neural Tube Defects** (Spina Bifida); hence, folic acid supplementation is mandatory if used in pregnancy. * Other GABA-modulating drugs include **Vigabatrin** (irreversible inhibitor of GABA transaminase) and **Tiagabine** (GABA uptake inhibitor/GAT-1 blocker). * Common side effects of Valproate: Weight gain, Alopecia (curling of hair), Hepatotoxicity, and Pancreatitis.

Q: What is the primary pharmacological action of Flumazenil?

Benzodiazepine antagonist. **Explanation:** **1. Why Option A is correct:** Flumazenil is a competitive **benzodiazepine (BZD) receptor antagonist**. It binds with high affinity to the specific BZD binding site on the **GABA-A receptor** complex, effectively displacing benzodiazepines and reversing their effects. It is primarily used for the reversal of BZD-induced sedation and the management of BZD overdose. **2. Why the other options are incorrect:** * **Option B (Benzodiazepine agonist):** These are drugs like Diazepam or Alprazolam that facilitate GABAergic transmission by increasing the *frequency* of chloride channel opening. Flumazenil blocks these effects. * **Option C (Melatonin receptor agonist):** This describes drugs like **Ramelteon** and Tasimelteon, which are used for insomnia but act on MT1 and MT2 receptors in the suprachiasmatic nucleus, not the GABA receptor. * **Option D (GABA analogue):** This refers to drugs like **Gabapentin** or Pregabalin. Despite their name, they do not act directly on GABA receptors; they primarily bind to voltage-gated calcium channels ($\alpha_2\delta$ subunit). **3. High-Yield Clinical Pearls for NEET-PG:** * **Short Half-life:** Flumazenil has a very short half-life (~1 hour). Since most BZDs last longer, **resedation** can occur, requiring repeated doses or an infusion. * **Seizure Risk:** The most serious side effect is **precipitating seizures**, especially in patients with long-term BZD dependence or those who have co-ingested TCAs (Tricyclic Antidepressants). * **Specific Action:** Flumazenil reverses BZDs and "Z-drugs" (Zolpidem, Zaleplon), but it **cannot** reverse the effects of Barbiturates or Alcohol.

Q: All of the following drugs are non-depolarizing neuromuscular blocking agents except?

Succinylcholine. Neuromuscular blocking agents (NMBAs) are classified into two main categories based on their mechanism of action at the nicotinic acetylcholine receptors (Nm) of the motor endplate: **Non-depolarizing (Competitive)** and **Depolarizing (Non-competitive)** blockers [1]. **Why Succinylcholine is the correct answer:** Succinylcholine (Suxamethonium) is the **only** clinically used **depolarizing** neuromuscular blocker [2]. It acts as an agonist at the Nm receptors, causing persistent depolarization of the motor endplate. This results in initial muscle twitching (fasciculations) followed by flaccid paralysis because the membrane cannot repolarize to respond to subsequent stimuli [1, 2]. **Analysis of Incorrect Options:** * **A. D-tubocurarine:** The prototype non-depolarizing blocker derived from curare. It competes with acetylcholine for the Nm receptor without activating it [3]. * **B. Gallamine triethiodide:** A synthetic non-depolarizing agent. It is rarely used now due to its significant vagolytic effect (tachycardia). * **C. Pancuronium bromide:** A long-acting steroid-based non-depolarizing blocker [1]. Like others in this class, its effects can be reversed by acetylcholinesterase inhibitors like Neostigmine. **High-Yield Clinical Pearls for NEET-PG:** * **Metabolism:** Succinylcholine is rapidly hydrolyzed by **pseudocholinesterase** (plasma cholinesterase) [1]. Deficiency of this enzyme leads to prolonged apnea. * **Side Effects of Succinylcholine:** Hyperkalemia (dangerous in burn/trauma patients), malignant hyperthermia (treated with **Dantrolene**), and muscle soreness. * **Phase II Block:** Prolonged exposure to succinylcholine can transition from a depolarizing block to a block that resembles non-depolarizing agents [1]. * **Hoffman Elimination:** Remember that **Atracurium** and **Cisatracurium** undergo spontaneous degradation (Hoffman elimination), making them safe in liver and kidney failure [1].

Q: A 15-year-old boy with epilepsy, treated with a combination of valproate and phenytoin, has good seizure control. Levels of both drugs are within the therapeutic range. All of the following adverse effects can be attributed to valproate except?

Lymphadenopathy. **Explanation:** The correct answer is **Lymphadenopathy**, as it is a classic side effect associated with **Phenytoin**, not Sodium Valproate. Phenytoin can cause "Pseudolymphoma syndrome," characterized by lymph node enlargement, fever, and rash. **Analysis of Options:** * **Weight gain (Option A):** Valproate is notorious for causing significant weight gain (often >5-10 kg) due to increased appetite and metabolic changes. This is a common reason for non-compliance. * **Elevated ALT (Option B):** Hepatotoxicity is a serious adverse effect of Valproate. Asymptomatic elevation of liver enzymes (ALT/AST) occurs in up to 20% of patients. It is particularly dangerous in children under 2 years of age (Reye’s-like syndrome). * **Hyperammonemia (Option C):** Valproate interferes with the urea cycle (inhibiting carbamoyl phosphate synthetase I), leading to increased serum ammonia levels. This can occur even in the presence of normal liver function tests and may lead to encephalopathy. **High-Yield Clinical Pearls for NEET-PG:** * **Valproate Mnemonic (VALPROATE):** **V**omiting, **A**lopecia (curly hair), **L**iver toxicity, **P**ancreatitis/PCOS, **R**etention of fat (Weight gain), **O**edema, **A**norexia (rarely), **T**remors/Teratogenicity (Neural tube defects), **E**nzyme inhibitor. * **Phenytoin Specifics:** Remember **"HOT MALARIA"** for Phenytoin: **H**irsutism, **O**steomalacia, **T**eratogenicity (Fetal Hydantoin Syndrome), **M**egaloblastic anemia, **A**taxia, **L**ymphadenopathy, **I**nsulin inhibition, **R**ash, **I**nducer of CYP450, **A**lveolar hyperplasia (Gingival hyperplasia). * Valproate is a broad-spectrum anti-epileptic and is the drug of choice for Generalized Tonic-Clonic Seizures (GTCS), Myoclonic, and Absence seizures.

Question 1

Which of the following is a central nervous system stimulant?

Accepted Answer

Cocaine

Answer

Alcohol

Answer

Nicotine

Answer

Cannabis

Question 2

Which drug is used for smoking cessation?

Accepted Answer

Varenicline

Answer

Theophylline

Answer

Biclutamide

Answer

Salmeterol

Question 3

Tolerance is seen in all, except?

Accepted Answer

Cocaine

Answer

Morphine

Answer

Amphetamine

Answer

Barbiturates

Question 4

Which antidepressant is relatively contraindicated in young men secondary to its side effect of priapism?

Accepted Answer

Trazodone

Answer

Sertraline

Answer

Imipramine

Answer

Amitriptyline

Question 5

True about phenytoin?

Accepted Answer

Causes nystagmus and ataxia

Answer

Undergoes first-pass metabolism

Answer

Is not teratogenic

Answer

Is the drug of choice for absence seizures

Question 6

Naltrexone is used to maintain abstinence following opioid withdrawal in addicts. It blocks all of the following features of opioid use, except:

Accepted Answer

Craving for opioids

Answer

Euphoriant effects of opioids

Answer

Miosis

Answer

Respiratory depression

Question 7

Which of the following antiepileptic drugs acts by affecting the levels of GABA?

Accepted Answer

Sodium valproate

Answer

Ethosuximide

Answer

Phenytoin sodium

Answer

Carbamazepine

Question 8

What is the primary pharmacological action of Flumazenil?

Accepted Answer

Benzodiazepine antagonist

Answer

Benzodiazepine agonist

Answer

Melatonin receptor agonist

Answer

GABA analogue

Question 9

All of the following drugs are non-depolarizing neuromuscular blocking agents except?

Accepted Answer

Succinylcholine

Answer

D-tubocurarine

Answer

Gallamine triethiodide

Answer

Pancuronium bromide

Question 10

A 15-year-old boy with epilepsy, treated with a combination of valproate and phenytoin, has good seizure control. Levels of both drugs are within the therapeutic range. All of the following adverse effects can be attributed to valproate except?

Accepted Answer

Lymphadenopathy

Answer

Weight gain of 5 kg

Answer

Serum alanine aminotransferase 150 IU/L

Answer

Rise in serum ammonia level by 20 µmol/L

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

On this page

Practice by Chapter

Want unlimited practice?