Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 171: Which antihistamine is used in motion sickness?

A. Cetirizine
B. Meclizine
C. Diphenhydramine (Correct Answer)
D. Fexofenadine

Explanation: **Explanation:** The correct answer is **Diphenhydramine**. **1. Why Diphenhydramine is correct:** Motion sickness occurs due to overstimulation of the vestibular apparatus in the inner ear. To be effective in motion sickness, an antihistamine must possess two key properties: it must be a **first-generation H1 blocker** (lipophilic enough to cross the blood-brain barrier) and it must have significant **anticholinergic (antimuscarinic) activity**. Diphenhydramine fulfills both criteria. It acts on the vestibular nuclei and the vomiting center in the brain to suppress the nausea and vertigo associated with motion. **2. Why other options are incorrect:** * **Cetirizine (A) and Fexofenadine (D):** These are **second-generation antihistamines**. They are highly ionized and do not cross the blood-brain barrier significantly. Furthermore, they lack the potent anticholinergic activity required to suppress the vestibular system. Therefore, they are ineffective for motion sickness. * **Meclizine (B):** While Meclizine is indeed used for motion sickness (especially for longer durations due to its 24-hour half-life), in the context of this specific question, Diphenhydramine is the classic prototype often tested. *Note: If both were options, Meclizine is often preferred clinically for less sedation, but Diphenhydramine remains a standard correct answer for its potent central action.* **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** For the *prevention* of motion sickness, the most potent drug is **Hyoscine (Scopolamine)**, administered via a transdermal patch. * **Timing:** Antihistamines must be taken **30–60 minutes before** the journey to be effective. * **Other First-Gen Drugs:** Promethazine, Cyclizine, and Dimenhydrinate are also used for motion sickness. * **Side Effect Profile:** The main limiting side effect of these drugs is **sedation** and dry mouth (due to anticholinergic action).

Question 172: Which of the following is the earliest and shortest acting skeletal muscle relaxant?

A. Rocuronium
B. Vecuronium
C. Atracurium
D. Suxamethonium (Correct Answer)

Explanation: **Explanation:** **Suxamethonium (Succinylcholine)** is the correct answer because it is the only **depolarizing neuromuscular blocker** in clinical use. Its unique mechanism and metabolism account for its rapid profile: * **Earliest Onset:** It has the fastest onset of action (approx. 30–60 seconds) because it is a small, highly flexible molecule that rapidly reaches the motor endplate. * **Shortest Duration:** It has the shortest duration of action (approx. 5–10 minutes) because it is rapidly hydrolyzed by **pseudocholinesterase (plasma cholinesterase)** in the blood. **Analysis of Incorrect Options:** * **Rocuronium (Option A):** An aminosteroid non-depolarizing blocker. While it has the fastest onset among non-depolarizing agents (60–90 seconds), its duration is intermediate (30–40 minutes). * **Vecuronium (Option B):** An intermediate-acting non-depolarizing blocker with an onset of 2–3 minutes and a duration of 30–40 minutes. * **Atracurium (Option C):** An intermediate-acting benzylisoquinolinium agent. It is notable for **Hofmann elimination**, but its onset (2–3 minutes) and duration (20–35 minutes) are significantly longer than Suxamethonium. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Suxamethonium is the gold standard for **Rapid Sequence Induction (RSI)** due to its fast onset. * **Side Effects:** Watch for muscle fasciculations, hyperkalemia (avoid in burn/trauma patients), and it is a known trigger for **Malignant Hyperthermia**. * **Phase II Block:** Prolonged exposure to Suxamethonium can lead to a Phase II block, where the membrane repolarizes but becomes desensitized. * **Scumbeline Apnea:** Occurs in patients with genetic deficiency or atypical pseudocholinesterase.

Question 173: Which of the following antiparkinsonian drugs can be administered as a transdermal patch?

A. Oxybutynin
B. Selegiline (Correct Answer)
C. Ropinirole
D. Amantidine

Explanation: **Explanation:** **Selegiline** is a selective, irreversible inhibitor of Monoamine Oxidase-B (MAO-B). While it is commonly administered orally, it is also available as a **transdermal patch**. The transdermal route is particularly advantageous because it bypasses first-pass hepatic metabolism, providing more stable plasma concentrations. Interestingly, at higher doses delivered via the patch, selegiline loses its MAO-B selectivity and inhibits MAO-A as well, making it effective for Major Depressive Disorder in addition to Parkinson’s disease. **Analysis of Incorrect Options:** * **Oxybutynin (A):** While available as a transdermal patch, it is an anticholinergic used for **overactive bladder**, not an antiparkinsonian drug. * **Ropinirole (C):** A non-ergot dopamine agonist used in Parkinson’s, but it is administered **orally**. Note: A similar dopamine agonist, **Rotigotine**, is the one famously administered via a transdermal patch. * **Amantadine (D):** An antiviral drug that increases dopamine release; it is administered **orally** (capsules/syrup). **NEET-PG High-Yield Pearls:** 1. **Rotigotine vs. Selegiline:** Both are antiparkinsonian drugs available as patches. If both appear in options, look for the specific context (Dopamine agonist vs. MAO-B inhibitor). 2. **Cheese Reaction:** Oral selegiline (at low doses) usually doesn't require dietary restrictions. However, the transdermal patch at high doses (12mg) may require avoiding tyramine-rich foods. 3. **Metabolism:** Selegiline is metabolized into **L-amphetamine and L-methamphetamine**, which may cause insomnia if taken late in the day.

Question 174: Which of the following antiepileptic agents acts on the GABAergic system to decrease the uptake of GABA into neurons and glial cells?

A. Vigabatrin
B. Progabide
C. Gabapentin
D. Tiagabine (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Tiagabine** **Mechanism of Action:** Tiagabine is a selective inhibitor of the **GAT-1 (GABA Transporter-1)**. Under normal physiological conditions, GABA is cleared from the synaptic cleft into neurons and surrounding glial cells (astrocytes) via these transporters. By blocking GAT-1, Tiagabine prevents the reuptake of GABA, thereby increasing its concentration and prolonging its inhibitory action at the synaptic cleft. **Analysis of Incorrect Options:** * **A. Vigabatrin:** It acts on the GABAergic system but through a different mechanism. It is an irreversible inhibitor of **GABA-transaminase (GABA-T)**, the enzyme responsible for the degradation of GABA. This leads to increased intracellular levels of GABA. * **B. Progabide:** This is a **GABA receptor agonist** (acting on both GABA-A and GABA-B receptors) and a prodrug of GABA. It does not inhibit uptake. * **C. Gabapentin:** Despite its name, it does not act directly on GABA receptors or transporters. Its primary mechanism is the inhibition of **voltage-gated calcium channels (α2δ-1 subunit)**, which reduces the release of excitatory neurotransmitters like glutamate. **High-Yield NEET-PG Pearls:** * **Tiagabine:** Think "T" for **T**ransporter inhibitor. * **Vigabatrin:** Associated with a high-yield side effect: **Permanent bilateral visual field constriction** (requires periodic perimetry). It is the drug of choice for **Infantile Spasms** associated with Tuberous Sclerosis. * **GAT-1 vs. GABA-T:** Do not confuse reuptake (GAT-1/Tiagabine) with metabolism (GABA-T/Vigabatrin). * **Valproate:** Also affects GABA by inhibiting GABA-T and stimulating Glutamic Acid Decarboxylase (GAD), the enzyme that synthesizes GABA.

Question 175: Which of the following is the drug of choice for febrile seizures?

A. Carbamazepine
B. Rectal diazepam (Correct Answer)
C. Valproic acid
D. Magnesium sulphate

Explanation: **Explanation:** **Febrile seizures** are the most common seizure disorder in childhood, typically occurring between 6 months and 5 years of age. The management is divided into acute termination and prophylaxis. 1. **Why Rectal Diazepam is correct:** For an acute episode of febrile seizures lasting more than 5 minutes, the primary goal is rapid termination. **Rectal diazepam (0.5 mg/kg)** is the drug of choice because it is highly lipid-soluble, ensuring rapid onset of action, and the rectal route is preferred in a convulsing child where intravenous access is difficult to establish. In a hospital setting, IV Lorazepam is often preferred, but Rectal Diazepam remains the classic textbook answer for emergency management. 2. **Why other options are incorrect:** * **Carbamazepine:** It is used for focal seizures and may actually worsen certain generalized seizure types. It has no role in the acute management of febrile seizures. * **Valproic acid:** While effective for long-term prophylaxis of atypical or recurrent febrile seizures, it is not used for acute termination due to its slower onset compared to benzodiazepines. * **Magnesium sulphate:** This is the drug of choice for **Eclampsia** (seizures in pregnancy), not febrile seizures. **High-Yield Clinical Pearls for NEET-PG:** * **Simple Febrile Seizure:** Generalized, lasts <15 mins, does not recur within 24 hours. * **Complex Febrile Seizure:** Focal, lasts >15 mins, or recurs within 24 hours. * **Prophylaxis:** Routine long-term prophylaxis is generally **not recommended** due to side effects. If necessary, **Intermittent Prophylaxis** (oral diazepam started at the onset of fever) is preferred. * **Drug of Choice for Status Epilepticus:** IV Lorazepam.

Question 176: All are adverse effects of phenytoin except?

A. Hypertrophy of gums
B. Hirsutism
C. Hypertension (Correct Answer)
D. Hypersensitivity

Explanation: **Explanation:** Phenytoin is a widely used hydantoin derivative for epilepsy, known for its narrow therapeutic index and a distinct profile of adverse effects. **Why Hypertension is the Correct Answer:** Phenytoin does **not** cause hypertension. In fact, when administered intravenously (especially if given too rapidly), phenytoin can cause **hypotension** and cardiac arrhythmias. This is primarily due to the solvent propylene glycol used in the formulation and the drug’s stabilizing effect on sodium channels in the myocardium. **Analysis of Incorrect Options:** * **Hypertrophy of Gums (Gingival Hyperplasia):** This is a classic side effect occurring in about 20% of patients. It is due to the overgrowth of gingival collagen fibers, stimulated by an increase in platelet-derived growth factor (PDGF). * **Hirsutism:** Phenytoin often causes excessive hair growth on the face and body, making it a less desirable choice for young female patients. * **Hypersensitivity:** Phenytoin can trigger various immune-mediated reactions, ranging from simple skin rashes to life-threatening conditions like **Stevens-Johnson Syndrome (SJS)** or **DRESS syndrome**, particularly in individuals with the HLA-B*1502 allele. **NEET-PG High-Yield Pearls:** To remember Phenytoin’s side effects, use the mnemonic **"PHENYTOIN"**: * **P**- P450 Inducer * **H**- Hypertrophy of gums / Hirsutism * **E**- Embryopathy (Fetal Hydantoin Syndrome: cleft lip/palate, microcephaly) * **N**- Neuropathy (Peripheral) * **Y**- Yields Vitamin D deficiency (Osteomalacia) * **T**- Teratogenicity * **O**- Osteomalacia * **I**- Interference with B12/Folate metabolism (Megaloblastic anemia) * **N**- Nystagmus (earliest sign of toxicity)

Question 177: Which of the following drugs is used for painful diabetic neuropathy?

A. Duloxetine
B. Pregabalin
C. Amitriptyline
D. All of the above (Correct Answer)

Explanation: **Explanation:** The management of painful diabetic neuropathy (PDN) involves targeting the central and peripheral sensitization of pain pathways. The correct answer is **All of the above** because these three drugs represent the first-line pharmacological classes recommended by international guidelines (ADA, AAN). 1. **Duloxetine (Option A):** A Serotonin-Norepinephrine Reuptake Inhibitor (SNRI). It increases the levels of norepinephrine and serotonin in the descending inhibitory pain pathways of the spinal cord, effectively "dampening" pain signals. It is often preferred when comorbid depression is present. 2. **Pregabalin (Option B):** A Gabapentinoid. It binds to the **α2-δ subunit of voltage-gated calcium channels** in the CNS. This reduces the influx of calcium into nerve terminals, thereby decreasing the release of excitatory neurotransmitters like glutamate and substance P. 3. **Amitriptyline (Option C):** A Tricyclic Antidepressant (TCA). It works via multiple mechanisms, including inhibition of norepinephrine/serotonin reuptake and blockade of sodium channels. While highly effective, its use is often limited by anticholinergic side effects (dry mouth, sedation, urinary retention). **High-Yield Clinical Pearls for NEET-PG:** * **First-line agents:** Pregabalin, Duloxetine, and TCAs (Amitriptyline). * **Pregabalin vs. Gabapentin:** Pregabalin has more predictable pharmacokinetics and higher bioavailability. * **Side Effect Profile:** Avoid TCAs in elderly patients due to the risk of arrhythmias (QT prolongation) and orthostatic hypotension. * **FDA Approval:** Duloxetine and Pregabalin are specifically FDA-approved for PDN, whereas Amitriptyline is used off-label but remains a gold standard in clinical practice.

Question 178: Which of the following statements about phenytoin is FALSE?

A. Causes hirsutism
B. Has teratogenic effects
C. Has a narrow therapeutic index
D. Does not require drug dosage monitoring (Correct Answer)

Explanation: Phenytoin is a high-yield topic in NEET-PG due to its complex pharmacokinetics and distinct side-effect profile. **Explanation for the Correct Option:** Option D is the false statement because Phenytoin **requires frequent Therapeutic Drug Monitoring (TDM)**. This is primarily due to its **zero-order (non-linear/saturation) kinetics** at therapeutic concentrations. Small increases in dose can lead to disproportionately large increases in plasma levels, rapidly reaching toxic ranges. Additionally, it has a **narrow therapeutic index** (10–20 µg/mL), making monitoring essential for safety and efficacy. **Analysis of Incorrect Options:** * **A. Causes hirsutism:** This is a well-known side effect. Phenytoin causes an overgrowth of body hair (hirsutism) and **gingival hyperplasia** (due to increased expression of platelet-derived growth factor). * **B. Has teratogenic effects:** Phenytoin is a known teratogen. It causes **Fetal Hydantoin Syndrome**, characterized by craniofacial anomalies (cleft lip/palate), microcephaly, and hypoplastic phalanges/nails. * **C. Has a narrow therapeutic index:** This is true. The margin between the effective dose and the toxic dose is very small, necessitating the TDM mentioned above. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Blocks voltage-gated sodium channels in the inactive state. * **Metabolism:** It is a potent **CYP450 inducer**, leading to numerous drug interactions (e.g., decreasing the efficacy of oral contraceptives and warfarin). * **Adverse Effects Mnemonic (P-H-E-N-Y-T-O-I-N):** **P**-450 induction, **H**irsutism, **E**nlarged gums, **N**ystagmus (earliest sign of toxicity), **Y**ellow-brown skin, **T**eratogenicity, **O**steomalacia (Vitamin D interference), **I**nterference with B12/Folate (Megaloblastic anemia), **N**europathy. * **Zero-order kinetics** is also followed by Aspirin (at high doses), Warfarin, and Ethanol.

Question 179: Morphine withdrawal is characterized by all of the following symptoms except:

A. Miosis (Correct Answer)
B. Muscle aches and body pain
C. Yawning
D. Rhinorrhoea

Explanation: **Explanation:** The correct answer is **A. Miosis**. **1. Why Miosis is the correct answer:** Morphine withdrawal symptoms are generally the **physiological opposite** of the drug’s acute effects. Acute opioid use causes miosis (pinpoint pupils) due to stimulation of the Edinger-Westphal nucleus. Conversely, **mydriasis (pupillary dilation)** is a hallmark sign of opioid withdrawal. Therefore, miosis is not a feature of withdrawal; it is a feature of acute intoxication. **2. Analysis of incorrect options:** * **B. Muscle aches and body pain:** Opioids are potent analgesics. During withdrawal, the pain threshold drops significantly, leading to characteristic myalgia, bone pain, and abdominal cramps. * **C & D. Yawning and Rhinorrhoea:** These are "wet" symptoms caused by autonomic hyperactivity. Early signs of morphine withdrawal include the "flu-like" triad of **yawning, rhinorrhoea, and lacrimation**, along with diaphoresis (sweating). **3. NEET-PG High-Yield Pearls:** * **The "Rule of Opposites":** If the drug causes constipation, withdrawal causes diarrhea. If the drug causes sedation, withdrawal causes insomnia and agitation. * **Piloerection:** The appearance of "gooseflesh" (cold turkey) is a highly specific sign of severe opioid withdrawal. * **Miosis Exception:** While most opioids cause miosis, **Meperidine (Pethidine)** is an exception; it can cause mydriasis due to its atropine-like (anticholinergic) action. * **Management:** Clonidine (α2 agonist) is used to reduce autonomic hyperactivity, while Methadone or Buprenorphine are used for detoxification and maintenance.

Question 180: Flumazenil is:

A. Antianginal drug
B. Opiate antagonist
C. Benzodiazepine antagonist (Correct Answer)
D. Opiate agonist

Explanation: **Explanation:** **Flumazenil** is a specific **competitive antagonist** at the benzodiazepine (BZD) binding site on the GABA-A receptor complex. It effectively reverses the sedative, psychomotor, and cognitive effects of benzodiazepines but does not reverse the effects of drugs acting at other sites (like barbiturates or alcohol). **Analysis of Options:** * **Option C (Correct):** Flumazenil has a high affinity for the BZD receptor. It is used clinically to reverse BZD-induced sedation for procedures and in the management of BZD overdose. * **Option B & D (Incorrect):** **Naloxone** and **Naltrexone** are the prototypical opiate antagonists. Opiate agonists include drugs like Morphine or Fentanyl. Flumazenil has no activity at opioid receptors. * **Option A (Incorrect):** Antianginal drugs include Nitrates, Beta-blockers, or Calcium Channel Blockers. Flumazenil has no cardiovascular or anti-ischemic properties. **High-Yield Clinical Pearls for NEET-PG:** 1. **Short Half-life:** Flumazenil has a very short duration of action (~1 hour). Since most benzodiazepines (e.g., Diazepam) last longer, **resedation** can occur, requiring repeated doses or an infusion. 2. **Seizure Risk:** The most serious side effect is the precipitation of **seizures**, especially in patients with long-term BZD dependence or those who have co-ingested tricyclic antidepressants (TCAs). 3. **Z-drugs:** Flumazenil also reverses the effects of "Z-drugs" (Zolpidem, Zaleplon, and Eszopiclone) as they also bind to the BZD site. 4. **Route:** It is administered intravenously (IV) only.

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

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