Central Nervous System Pharmacology — MCQs
On this page
Which of the following is an antipsychotic drug?
Which of the following drugs can prevent or delay the onset of Alzheimer's disease?
Levodopa can aggravate which of the following malignancies?
Which of the following drugs has teratogenic potential?
What is the drug of choice for myoclonic seizures?
Which drug is NOT used in the management of Alzheimer Disease?
Which of the following drugs is a serotonin-norepinephrine reuptake inhibitor?
Which anti-epileptic drug is not contraindicated during pregnancy?
Which of the following agents does not cause an increase in serotonin levels?
Eteplirsen has been recently FDA approved for the treatment of which condition?
Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs
Question 251: Which of the following is an antipsychotic drug?
- A. Doxepine
- B. Fluoxetine
- C. Clozapine (Correct Answer)
- D. All
Explanation: **Explanation:** **Clozapine (Option C)** is the correct answer. It is a prototypical **Atypical Antipsychotic** (Second Generation Antipsychotic). Unlike typical antipsychotics that primarily block $D_2$ receptors, Clozapine has a high affinity for $5-HT_{2A}$ receptors and a relatively lower affinity for $D_2$ receptors. This profile reduces the risk of Extrapyramidal Side Effects (EPS). **Analysis of Incorrect Options:** * **Doxepin (Option A):** This is a **Tricyclic Antidepressant (TCA)**. It primarily inhibits the reuptake of Norepinephrine and Serotonin. It is also used for its potent antihistaminic properties in dermatology and for insomnia. * **Fluoxetine (Option B):** This is a **Selective Serotonin Reuptake Inhibitor (SSRI)**. It is the first-line treatment for depression, OCD, and panic disorders. It is not classified as an antipsychotic. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for Resistant Schizophrenia:** Clozapine is the drug of choice for treatment-resistant schizophrenia (failure of two or more antipsychotics). * **Adverse Effects:** The most feared complication is **Agranulocytosis** (requires mandatory WBC monitoring). Other side effects include **seizures** (dose-dependent), **sialorrhea** (excessive salivation), and significant weight gain/metabolic syndrome. * **Suicide Prevention:** Clozapine is the only antipsychotic proven to reduce the risk of suicidal behavior in patients with schizophrenia. * **EPS Profile:** It has the lowest risk of Extrapyramidal Side Effects and does not cause a rise in Prolactin levels.
Question 252: Which of the following drugs can prevent or delay the onset of Alzheimer's disease?
- A. Tacrine
- B. NSAID (Correct Answer)
- C. Donepezil
- D. None of the above
Explanation: ### Explanation **Correct Answer: B. NSAID** **Why NSAIDs are the correct choice:** The pathogenesis of Alzheimer’s Disease (AD) involves chronic neuroinflammation characterized by microglial activation and the release of pro-inflammatory cytokines around amyloid-beta (Aβ) plaques. Epidemiological studies have shown that long-term use of **Non-Steroidal Anti-inflammatory Drugs (NSAIDs)**, particularly non-selective COX inhibitors like Ibuprofen or Indomethacin, is associated with a **reduced risk and delayed onset** of AD. They work by inhibiting neuroinflammation and, in some cases, directly modulating γ-secretase activity to reduce the production of amyloidogenic Aβ42 peptides. However, it is crucial to note that while they may *prevent* or *delay* onset, they are ineffective once clinical symptoms are established. **Why other options are incorrect:** * **A. Tacrine & C. Donepezil:** These are **Centrally acting Cholinesterase Inhibitors (ChEIs)**. They are used for the **symptomatic management** of mild-to-moderate AD by increasing acetylcholine levels in the synaptic cleft. They improve cognitive function and quality of life but **do not** alter the underlying disease pathology, prevent the disease, or delay its eventual onset. (Note: Tacrine is now obsolete due to hepatotoxicity). **High-Yield Clinical Pearls for NEET-PG:** * **First-line treatment for AD:** Donepezil, Rivastigmine, or Galantamine (ChEIs). * **NMDA Receptor Antagonist:** Memantine is used for moderate-to-severe AD; it is neuroprotective by preventing glutamate-induced excitotoxicity. * **Disease-Modifying Therapy:** Aducanumab and Lecanemab (monoclonal antibodies against Aβ) are the newer agents aimed at clearing plaques. * **Vitamin E & Selegiline:** Sometimes used for their antioxidant properties to slow progression, though evidence is limited. * **Estrogen:** Like NSAIDs, observational studies suggest a protective role in postmenopausal women, but it is not used for treatment.
Question 253: Levodopa can aggravate which of the following malignancies?
- A. Squamous cell cancer
- B. Pleomorphic adenoma
- C. Basal cell carcinoma
- D. Malignant melanoma (Correct Answer)
Explanation: **Explanation:** **Correct Answer: D. Malignant Melanoma** The correct answer is **Malignant Melanoma**. This association is based on the biochemical pathway shared by dopamine and melanin. Both substances are synthesized from the common precursor amino acid, **L-Tyrosine**. L-Tyrosine is converted to **L-Dopa** by the enzyme tyrosine hydroxylase. In the brain, L-Dopa is converted to dopamine; however, in melanocytes, L-Dopa is a crucial intermediate in the synthesis of melanin. It is hypothesized that exogenous administration of Levodopa may stimulate the activity of melanocytes or provide the substrate necessary for the rapid proliferation of malignant melanocytic cells. Consequently, Levodopa is strictly contraindicated in patients with a history of undiagnosed skin lesions or a known history of melanoma. **Analysis of Incorrect Options:** * **A, B, and C:** Squamous cell cancer, Pleomorphic adenoma, and Basal cell carcinoma do not involve the melanocytic pathway or the metabolic intermediates of catecholamine synthesis. There is no clinical or pharmacological evidence suggesting that Levodopa influences the progression of these specific tumors. **High-Yield Clinical Pearls for NEET-PG:** * **Pre-treatment screening:** Always perform a thorough skin examination before initiating Levodopa therapy in elderly patients. * **Vitamin B6 (Pyridoxine) Interaction:** Pyridoxine enhances the peripheral decarboxylation of Levodopa, reducing its availability to the CNS (unless given with Carbidopa). * **Dietary Interaction:** High-protein meals interfere with Levodopa absorption due to competition with aromatic amino acids for transport across the blood-brain barrier. * **Psychiatric Side Effects:** Levodopa can trigger visual hallucinations and psychosis due to increased dopaminergic activity in the mesolimbic pathway.
Question 254: Which of the following drugs has teratogenic potential?
- A. Carbamazepine (Correct Answer)
- B. Clonazepam
- C. Risperidone
- D. Olanzapine
Explanation: **Explanation:** **Carbamazepine (Option A)** is the correct answer because it is a well-documented teratogen. It is associated with a 1% risk of **Neural Tube Defects (NTDs)**, specifically spina bifida, due to its interference with folate metabolism. Additionally, it can cause "Fetal Carbamazepine Syndrome," characterized by craniofacial defects, fingernail hypoplasia, and developmental delays. **Analysis of Incorrect Options:** * **Clonazepam (Option B):** While benzodiazepines were historically linked to cleft lip/palate, recent large-scale studies show that the absolute risk is very low. They are generally considered safer than older anticonvulsants like Valproate or Carbamazepine. * **Risperidone & Olanzapine (Options C & D):** These are atypical antipsychotics. Current evidence suggests they do not significantly increase the risk of major congenital malformations, though they may be associated with neonatal withdrawal symptoms or metabolic issues if used late in pregnancy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Valproate** is the most teratogenic antiepileptic, causing the highest incidence of NTDs (up to 2–5%). 2. **Phenytoin** causes **Fetal Hydantoin Syndrome** (cleft lip/palate, microcephaly, and digital hypoplasia). 3. **Drug of Choice:** For a pregnant woman with epilepsy, **Levetiracetam** or **Lamotrigine** are preferred due to their superior safety profiles. 4. **Prevention:** All women on enzyme-inducing AEDs (like Carbamazepine) should receive **high-dose Folic Acid (5 mg/day)** pre-conceptionally to reduce NTD risk.
Question 255: What is the drug of choice for myoclonic seizures?
- A. Valproic acid (Correct Answer)
- B. Phenytoin
- C. Ethosuximide
- D. Carbamazepine
Explanation: **Explanation:** **Valproic acid** is the drug of choice (DOC) for **myoclonic seizures** because of its broad-spectrum mechanism of action. It acts by increasing GABA levels (inhibiting GABA transaminase), blocking voltage-gated sodium channels, and inhibiting T-type calcium channels. This multi-modal action makes it highly effective for generalized epilepsies, including myoclonic, tonic-clonic, and absence seizures. **Analysis of Incorrect Options:** * **Phenytoin (B):** This is a narrow-spectrum anticonvulsant that blocks sodium channels. It is ineffective for myoclonic seizures and may actually **exacerbate** them. * **Ethosuximide (C):** This is the DOC specifically for **Absence seizures** (petit mal). It works by blocking T-type calcium channels in the thalamus but lacks efficacy against myoclonic or tonic-clonic seizures. * **Carbamazepine (D):** Similar to phenytoin, it is a narrow-spectrum drug used for focal and generalized tonic-clonic seizures. It is contraindicated in myoclonic and absence seizures as it can worsen the condition. **High-Yield Clinical Pearls for NEET-PG:** * **Broad Spectrum:** Valproate is the DOC for most idiopathic generalized epilepsies (GTCS, Myoclonic, Atonic). * **Teratogenicity:** It is highly associated with **Neural Tube Defects** (Spina Bifida); hence, it is avoided in pregnancy (Levetiracetam is often preferred). * **Side Effects:** Remember the mnemonic **VALPROATE**: **V**omit, **A**lopecia, **L**iver toxicity (Hepatotoxicity), **P**ancreatitis, **R**etained fat (Weight gain), **O**edema, **A**norexia, **T**remors, **E**nzyme inhibitor. * **Alternative:** **Levetiracetam** is an increasingly popular alternative for myoclonic seizures due to a better safety profile.
Question 256: Which drug is NOT used in the management of Alzheimer Disease?
- A. Memantine
- B. Galantamine
- C. Ropinirole (Correct Answer)
- D. Donepezil
Explanation: The management of Alzheimer’s Disease (AD) primarily focuses on addressing the cholinergic deficit and glutamatergic excitotoxicity associated with cognitive decline [2, 1]. **Why Ropinirole is the correct answer:** **Ropinirole** is a **D2/D3 dopamine receptor agonist**. It is used in the management of **Parkinson’s Disease** and Restless Legs Syndrome [3]. It has no role in Alzheimer’s Disease; in fact, dopaminergic drugs can sometimes worsen hallucinations or confusion in elderly patients with dementia. **Why the other options are incorrect:** * **Donepezil & Galantamine (Options B & D):** These are **reversible Acetylcholinesterase Inhibitors (AChEIs)** [1, 2]. By inhibiting the breakdown of acetylcholine in the synaptic cleft, they enhance cholinergic transmission, which helps improve memory and cognitive function in mild-to-moderate AD [2]. (Note: Rivastigmine is another drug in this class [2]). * **Memantine (Option A):** This is an **NMDA receptor antagonist** [1, 2]. It works by blocking pathological levels of glutamate, preventing neurotoxicity [1]. It is typically used for moderate-to-severe AD [1, 2], often in combination with Donepezil [1]. **High-Yield Clinical Pearls for NEET-PG:** 1. **First-line for Mild AD:** Donepezil (long half-life, once-daily dosing). 2. **Rivastigmine:** Available as a transdermal patch; useful for patients with swallowing difficulties. 3. **Side Effects of AChEIs:** Primarily GI-related (nausea, diarrhea) and bradycardia (due to increased vagal tone). 4. **Aducanumab/Donanemab:** Newer monoclonal antibodies targeting amyloid-beta plaques (recently FDA-approved, high-yield for recent updates).
Question 257: Which of the following drugs is a serotonin-norepinephrine reuptake inhibitor?
- A. Venlafaxine (Correct Answer)
- B. Amphetamine
- C. Doxepin
- D. Mianserin
Explanation: **Explanation:** **1. Why Venlafaxine is Correct:** Venlafaxine is a prototype **Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)**. It works by inhibiting the reuptake transporters for both serotonin (5-HT) and norepinephrine (NE) in the synaptic cleft, thereby increasing their availability. At lower doses, it primarily affects serotonin reuptake, while at higher doses, its effect on norepinephrine becomes more pronounced. It is commonly used for Major Depressive Disorder, Generalized Anxiety Disorder, and neuropathic pain. **2. Analysis of Incorrect Options:** * **Amphetamine:** This is a CNS stimulant that acts as an **indirect-acting sympathomimetic**. It primarily works by increasing the release of stored catecholamines (Dopamine and NE) from nerve terminals and inhibiting their reuptake. * **Doxepin:** This is a **Tricyclic Antidepressant (TCA)**. While TCAs also inhibit 5-HT and NE reuptake, they are classified separately because they also block muscarinic, histaminergic (H1), and alpha-adrenergic receptors, leading to a broader side-effect profile compared to SNRIs. * **Mianserin:** This is an **Atypical Antidepressant** (specifically a tetracyclic). It acts primarily as an antagonist at presynaptic **alpha-2 adrenoceptors**, which increases the release of norepinephrine; it does not act as a reuptake inhibitor. **3. High-Yield Clinical Pearls for NEET-PG:** * **SNRIs vs. TCAs:** SNRIs (Venlafaxine, Duloxetine, Desvenlafaxine) are preferred over TCAs because they lack the "3 C's" of TCA toxicity: Coma, Convulsions, and Cardiotoxicity (arrhythmias). * **Side Effects:** A unique side effect of Venlafaxine (especially at high doses) is **dose-dependent hypertension** due to increased norepinephrine levels. * **Duloxetine:** Another SNRI frequently tested; it is the drug of choice for **Diabetic Neuropathy** and Fibromyalgia.
Question 258: Which anti-epileptic drug is not contraindicated during pregnancy?
- A. Ethosuximide
- B. Carbamazepine (Correct Answer)
- C. Phenytoin
- D. Valproate
Explanation: **Explanation:** The management of epilepsy during pregnancy requires balancing maternal seizure control with the risk of teratogenicity [1]. While almost all older anti-epileptic drugs (AEDs) carry some risk, **Carbamazepine** is considered relatively safer compared to the other options listed and is **not strictly contraindicated**, although it is associated with a small risk of neural tube defects (approx. 0.5–1%). **Why the other options are incorrect:** * **Valproate (Option D):** This is the **most teratogenic** AED. It is highly contraindicated due to a high incidence (up to 10%) of **Neural Tube Defects (Spina Bifida)**, craniofacial anomalies, and impaired cognitive development (lower IQ). * **Phenytoin (Option C):** Associated with **Fetal Hydantoin Syndrome**, characterized by craniofacial dysmorphism, hypoplastic phalanges/nails, and microcephaly. * **Ethosuximide (Option A):** While primarily used for absence seizures, it is associated with a risk of "Ethosuximide Syndrome," which includes patent ductus arteriosus and other structural malformations. **NEET-PG High-Yield Pearls:** 1. **Drug of Choice:** For a pregnant woman with epilepsy, **Levetiracetam** or **Lamotrigine** are currently the preferred first-line agents due to the lowest teratogenic potential. 2. **Folic Acid:** All women of childbearing age on AEDs should receive high-dose folic acid (5 mg/day) to reduce the risk of neural tube defects. 3. **Vitamin K:** Enzyme-inducing AEDs (Phenytoin, Carbamazepine, Phenobarbital) can cause neonatal hemorrhage; Vitamin K prophylaxis is given to the mother in the last month of pregnancy and to the newborn [1]. 4. **Monotherapy:** The clinical goal is to maintain the patient on the lowest effective dose of a single drug (monotherapy) to minimize fetal risk.
Question 259: Which of the following agents does not cause an increase in serotonin levels?
- A. MDMA
- B. Amphetamine
- C. Fluoxetine
- D. LSD (Correct Answer)
Explanation: **Explanation:** The correct answer is **LSD (Lysergic acid diethylamide)**. The fundamental concept here is the difference between a **serotonin agonist** and a **serotonin-releasing/reuptake-inhibiting agent**. **Why LSD is the correct answer:** LSD is a potent hallucinogen that acts primarily as a **partial agonist at 5-HT₂A receptors** in the prefrontal cortex. It mimics the action of serotonin at the receptor site rather than increasing the actual concentration of serotonin in the synaptic cleft. Therefore, it does not "increase serotonin levels." **Analysis of Incorrect Options:** * **MDMA (Ecstasy):** This is a potent serotonin releaser. It reverses the direction of the serotonin transporter (SERT), pumping massive amounts of stored serotonin into the synapse. * **Amphetamine:** While primarily known for increasing dopamine and norepinephrine, amphetamines also stimulate the release of serotonin from presynaptic vesicles, thereby increasing its levels. * **Fluoxetine:** As a Selective Serotonin Reuptake Inhibitor (SSRI), it blocks the SERT protein. By preventing the reabsorption of serotonin, it directly increases the concentration of serotonin available in the synaptic cleft. **NEET-PG High-Yield Pearls:** * **Serotonin Syndrome:** Be wary of combining drugs that increase serotonin levels (e.g., SSRIs + MAOIs or MDMA), as this can lead to life-threatening Serotonin Syndrome (hyperthermia, muscle rigidity, and autonomic instability). * **LSD Mechanism:** Remember that LSD-induced hallucinations are specifically linked to **5-HT₂A** agonism. * **Fenfluramine:** Another high-yield serotonin releaser (formerly used for obesity) that was withdrawn due to cardiac valvulopathy.
Question 260: Eteplirsen has been recently FDA approved for the treatment of which condition?
- A. Duchenne muscular dystrophy (Correct Answer)
- B. Spinal muscular atrophy
- C. Subacute sclerosing panencephalitis
- D. Acute myeloid leukemia
Explanation: **Explanation:** **Eteplirsen** is a pioneering drug that utilizes **Exon-skipping technology**. It is specifically FDA-approved for the treatment of **Duchenne Muscular Dystrophy (DMD)** in patients who have a confirmed mutation of the dystrophin gene amenable to **exon 51 skipping**. 1. **Why the correct answer is right:** DMD is caused by mutations (mostly deletions) in the *DMD* gene that disrupt the reading frame, leading to a complete absence of the protein **dystrophin**. Eteplirsen is an **antisense oligonucleotide (morpholino)** that binds to exon 51 of the dystrophin pre-mRNA. This "skips" the mutated exon during splicing, restoring the reading frame and allowing the production of a shorter but functional dystrophin protein (converting a severe DMD phenotype into a milder Becker-like phenotype). 2. **Why incorrect options are wrong:** * **Spinal Muscular Atrophy (SMA):** Treated with **Nusinersen** (an antisense oligonucleotide targeting *SMN2* gene) or **Onasemnogene abeparvovec** (gene therapy). * **Subacute Sclerosing Panencephalitis (SSPE):** A late complication of Measles; managed with intrathecal Interferon-alpha and Ribavirin, though prognosis remains poor. * **Acute Myeloid Leukemia (AML):** Treated with chemotherapy (e.g., Cytarabine, Anthracyclines) or targeted therapies like Midostaurin or Enasidenib. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Exon-skipping (Antisense Oligonucleotide). * **Route:** Intravenous infusion. * **Other DMD Drugs:** **Golodirsen** and **Viltolarsen** (target Exon 53); **Casimersen** (targets Exon 45). * **Deflazacort:** A corticosteroid specifically used to improve muscle strength in DMD patients.
Practice by Chapter
General Anesthetics
Practice Questions
Local Anesthetics
Practice Questions
Sedative-Hypnotics
Practice Questions
Antiepileptic Drugs
Practice Questions
Antiparkinsonian Drugs
Practice Questions
Opioid Analgesics
Practice Questions
Drugs of Abuse and Addiction
Practice Questions
Psychostimulants
Practice Questions
Hallucinogens
Practice Questions
CNS Stimulants and Cognitive Enhancers
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free