Central Nervous System Pharmacology Practice Questions

Q: Which drug is NOT used for analgesia in a patient with head injury?

Morphine. **Explanation:** The correct answer is **Morphine**. In patients with head injuries, opioids like Morphine are generally contraindicated or used with extreme caution due to three primary reasons: 1. **Respiratory Depression & ICP:** Morphine causes respiratory depression, leading to CO₂ retention (hypercapnia). CO₂ is a potent cerebral vasodilator, which increases cerebral blood flow and subsequently elevates **Intracranial Pressure (ICP)**, risking brain herniation. 2. **Pupillary Changes:** Morphine causes miosis (pinpoint pupils). This masks the pupillary pupillary dilation (mydriasis) that serves as a critical clinical sign of neurological deterioration or uncal herniation. 3. **Sedation:** It induces drowsiness and mental clouding, making it difficult for clinicians to perform accurate neurological assessments (GCS monitoring). **Why other options are incorrect:** * **NSAIDs (e.g., Ibuprofen) & Rofecoxib (COX-2 Inhibitor):** These provide effective analgesia without affecting the respiratory center or pupillary size. While non-selective NSAIDs are sometimes avoided acutely due to anti-platelet effects (risk of bleed), they do not carry the specific neurological contraindications of opioids. * **Acetaminophen (Paracetamol):** This is the drug of choice for mild-to-moderate pain in head injuries as it has no effect on ICP, respiration, or neurological monitoring. **High-Yield Clinical Pearls for NEET-PG:** * **DOC for Head Injury Pain:** Acetaminophen is preferred. * **Opioid of choice (if essential):** Fentanyl is sometimes preferred over Morphine in ICU settings due to its shorter half-life and less effect on histamine release, but the general rule for exams remains: **Avoid Morphine in Head Injury.** * **Other Contraindications for Morphine:** Bronchial asthma, Undiagnosed abdominal pain, Biliary colic, and Hypertrophy of the prostate.

Q: Thiopentone does not cause which of the following effects?

Decreased stage 2 of sleep. **Explanation:** Thiopentone sodium is an ultra-short-acting barbiturate used for the induction of anesthesia. Understanding its effects on the CNS and sleep architecture is crucial for NEET-PG. **Why Option D is correct:** Barbiturates, including Thiopentone, significantly alter the sleep cycle. They **increase Stage 2 (NREM)** sleep while **decreasing Stage 3 and 4 (deep/slow-wave sleep)** and **decreasing REM sleep**. Therefore, the statement that it "decreases Stage 2" is incorrect, making it the right answer for this "except" type question. **Why other options are incorrect:** * **Options A, B, and C:** Thiopentone is a potent cerebral vasoconstrictor. It leads to a significant **reduction in Cerebral Blood Flow (CBF)**, **Cerebral Metabolic Rate of Oxygen (CMRO2)**, and **Intracranial Pressure (ICP)**. These properties make it a drug of choice for induction in patients with head injuries or space-occupying lesions (SOL) where intracranial tension is elevated. **High-Yield Clinical Pearls for NEET-PG:** * **Cerebral Protection:** Thiopentone provides "barbiturate coma" which protects the brain during focal ischemia by reducing metabolic demand. * **Respiratory Effect:** It is a potent respiratory depressant and can cause laryngospasm (ensure adequate depth or use of muscle relaxants). * **Cardiovascular Effect:** It causes peripheral vasodilation and can lead to hypotension; use with caution in hypovolemic patients. * **Contraindication:** Absolutely contraindicated in **Acute Intermittent Porphyria** (induces ALA synthetase). * **Redistribution:** The short duration of action is due to **redistribution** from the brain to skeletal muscle and fat, not due to rapid metabolism.

Q: Non-depolarizing neuromuscular blockade is potentiated by which of the following?

Quinidine. **Explanation:** The potentiation of non-depolarizing neuromuscular blockers (NDNMBs) occurs through mechanisms that either decrease acetylcholine (ACh) release or stabilize the post-junctional membrane. **Why Quinidine is Correct:** **Quinidine** (a Class IA antiarrhythmic) potentiates NDNMBs by acting at both pre-junctional and post-junctional sites. It reduces the release of ACh from the motor nerve terminal and decreases the sensitivity of the motor end-plate to ACh. It also has a direct depressant effect on the muscle fiber itself. **Analysis of Incorrect Options:** * **Hyperkalemia (A):** High extracellular potassium causes partial depolarization of the resting membrane, making it easier for ACh to trigger an action potential. This **antagonizes** (reverses) the effect of NDNMBs. Conversely, **hypokalemia** potentiates the blockade. * **Hypomagnesemia (B):** Magnesium acts as a physiological calcium channel blocker at the nerve terminal. **Hypermagnesemia** inhibits ACh release and potentiates blockade. Therefore, hypomagnesemia would theoretically antagonize the block. * **Chronic Phenytoin Therapy (C):** Long-term use of phenytoin (and carbamazepine) leads to **resistance** to NDNMBs due to the up-regulation of acetylcholine receptors and increased metabolism of the blockers. (Note: Acute administration may potentiate the block, but chronic therapy antagonizes it). **High-Yield Clinical Pearls for NEET-PG:** * **Drugs that Potentiate NDNMBs:** Aminoglycosides (e.g., Gentamicin), Tetracyclines, Calcium channel blockers, Volatile anesthetics (Isoflurane > Halothane), and Lithium. * **Electrolyte Abnormalities that Potentiate NDNMBs:** Hypokalemia, Hypermagnesemia, Hypocalcemia, and Respiratory Acidosis. * **Myasthenia Gravis:** Patients are extremely sensitive to NDNMBs; even small doses can cause prolonged paralysis.

Q: Ketamine acts on which receptors?

NMDA. **Explanation:** **Ketamine** is a unique intravenous anesthetic agent that primarily acts as a non-competitive antagonist at the **NMDA (N-methyl-D-aspartate) receptors**. These receptors are a subtype of glutamate receptors located in the brain and spinal cord. By blocking these receptors, ketamine inhibits the excitatory neurotransmitter glutamate, leading to a state of **"Dissociative Anesthesia."** This state is characterized by profound analgesia, amnesia, and a cataleptic appearance where the patient’s eyes remain open with a slow nystagmic gaze, yet they are disconnected from their surroundings. **Analysis of Incorrect Options:** * **GABA (Option A):** Most intravenous anesthetics (like Propofol, Etomidate, and Thiopental) and Benzodiazepines act by enhancing GABA-A receptors. Ketamine is a notable exception as it does not primarily act on the GABA system. * **Muscarinic (Option B):** Ketamine actually possesses mild anticholinergic properties (which can lead to bronchodilation), but this is not its primary mechanism for anesthesia. * **5-HT4 (Option C):** These are serotonin receptors primarily involved in gastrointestinal motility and have no role in the anesthetic action of Ketamine. **High-Yield Clinical Pearls for NEET-PG:** 1. **Sympathomimetic Action:** Unlike other induction agents, Ketamine increases HR, BP, and CO, making it the **induction agent of choice for patients in hypovolemic shock.** 2. **Bronchodilation:** It is the drug of choice for induction in **asthmatic patients.** 3. **Emergence Delirium:** A common side effect characterized by hallucinations and vivid dreams; it can be prevented by co-administration of **Benzodiazepines (Midazolam).** 4. **Contraindications:** Avoid in patients with increased Intracranial Pressure (ICP) or Intraocular Pressure (IOP), and in those with Ischemic Heart Disease (due to increased myocardial oxygen demand).

Q: Which drug is used to prevent alcohol withdrawal syndrome?

Diazepam. **Explanation:** **1. Why Diazepam is the Correct Answer:** Benzodiazepines (BZDs) like **Diazepam** are the **gold standard and first-line treatment** for preventing and managing Alcohol Withdrawal Syndrome (AWS). Chronic alcohol consumption causes down-regulation of GABA receptors and up-regulation of NMDA receptors. Sudden cessation leads to a state of CNS hyperexcitability. Diazepam, a long-acting BZD, acts as a GABA-A agonist, providing **cross-tolerance** with alcohol. It effectively prevents seizures, delirium tremens, and stabilizes vital signs due to its long half-life and active metabolites. **2. Why Other Options are Incorrect:** * **Clonidine (B):** An alpha-2 agonist that helps reduce autonomic overactivity (tachycardia, hypertension) but **does not prevent seizures or delirium**, which are the most dangerous complications of withdrawal. * **Propranolol (C):** A beta-blocker used symptomatically to control tremors and tachycardia. Like clonidine, it lacks anti-epileptic properties and can mask the early signs of withdrawal. * **Methadone (D):** A mu-opioid receptor agonist used specifically for **Opioid withdrawal** and maintenance therapy, not for alcohol withdrawal. **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Chlordiazepoxide or Diazepam are preferred due to their long half-life (self-tapering effect). * **Liver Failure Exception:** In patients with cirrhosis or liver failure, use **LOT** drugs (**L**orazepam, **O**xazepam, **T**emazepam) as they do not require hepatic oxidation and have no active metabolites. * **Wernicke’s Encephalopathy:** Always administer **Thiamine (B1)** before glucose to prevent precipitating Wernicke’s. * **Disulfiram:** Used for aversion therapy (maintenance of abstinence), never for acute withdrawal.

Q: Which local anesthetic is commonly used in wound or ulcer management?

Benzocaine. **Explanation:** **Benzocaine** is the correct answer because it is a unique ester-linked local anesthetic characterized by its **very low solubility in water**. Due to this property, it is absorbed too slowly to be given by injection but is highly effective for **topical application** on mucous membranes and denuded skin surfaces (wounds or ulcers). It provides prolonged surface anesthesia without significant systemic toxicity, making it the drug of choice for treating painful skin conditions, mouth ulcers, and as a throat spray before endoscopy. **Analysis of Incorrect Options:** * **Prilocaine (A):** An amide local anesthetic primarily used for infiltration and regional blocks. It is a component of EMLA cream but is not used alone for open wound management. Its major side effect is methemoglobinemia. * **Chloroprocaine (B):** An ester anesthetic with a very short duration of action due to rapid hydrolysis by plasma cholinesterase. It is primarily used for infiltration and epidural anesthesia, not topical wound care. * **Bupivacaine (D):** A potent, long-acting amide anesthetic. It is highly cardiotoxic if absorbed systemically and is used for infiltration, spinal, and epidural anesthesia, but lacks effective topical activity on intact skin or ulcers. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Benzocaine acts by blocking voltage-gated sodium channels, but unlike others, it exists almost entirely in the **unionized form** at physiological pH. * **Side Effect:** Like prilocaine, benzocaine can cause **methemoglobinemia** if used in excessive quantities topically. * **EMLA Cream:** A eutectic mixture of **Lidocaine (2.5%) and Prilocaine (2.5%)** used to anesthetize intact skin before venipuncture. * **Cocaine:** The only local anesthetic with intrinsic **vasoconstrictive** properties; all others are vasodilators (except ropivacaine/levobupivacaine which have mild vasoconstriction).

Question 1

All of the following are true about cocaine except one?

Accepted Answer

Produces para-aminobenzoic acid as a metabolite

Answer

Is an ester of benzoic acid

Answer

Is metabolized by the liver

Answer

Is a vasoconstrictor

Question 2

What is true regarding tolerance occurring in regular opium abusers?

Accepted Answer

No tolerance occurs to constipating and miotic actions of morphine.

Answer

Tolerance develops to all actions of morphine.

Answer

No tolerance occurs to euphoric and sedative actions of morphine.

Answer

The lethal dose of morphine is not significantly increased.

Question 3

Which drug is NOT used for analgesia in a patient with head injury?

Accepted Answer

Morphine

Answer

NSAIDs

Answer

Rofecoxib

Answer

Acetaminophen

Question 4

Thiopentone does not cause which of the following effects?

Accepted Answer

Decreased stage 2 of sleep

Answer

Fall in intracranial tension

Answer

Decreased oxygen consumption of brain

Answer

Decreased metabolic rate of brain

Question 5

Non-depolarizing neuromuscular blockade is potentiated by which of the following?

Accepted Answer

Quinidine

Answer

Hyperkalemia

Answer

Hypomagnesemia

Answer

Chronic phenytoin therapy

Question 6

Ketamine acts on which receptors?

Accepted Answer

NMDA

Answer

GABA

Answer

Muscarinic

Answer

5-HT4

Question 7

Which of the following factors markedly increases the risk of valproate-induced liver toxicity?

Accepted Answer

Age younger than 2 years

Answer

Allergic reactions to phenobarbital

Answer

Male gender

Answer

Family history of epilepsy

Question 8

An acute syndrome of abnormal involuntary movements resembling tardive dyskinesia is associated with excessive dosage of which of the following medications?

Accepted Answer

Reserpine

Answer

Propranolol

Answer

Clonidine

Answer

Levodopa

Question 9

Which drug is used to prevent alcohol withdrawal syndrome?

Accepted Answer

Diazepam

Answer

Clonidine

Answer

Propranolol

Answer

Methadone

Question 10

Which local anesthetic is commonly used in wound or ulcer management?

Accepted Answer

Benzocaine

Answer

Prilocaine

Answer

Chloroprocaine

Answer

Bupivacaine

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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