Central Nervous System Pharmacology Practice Questions

Q: Which of the following is an advantage of adding adrenaline to lignocaine for local anesthetic injection?

All of the above. **Explanation:** The addition of **Adrenaline (Epinephrine)** to local anesthetics like Lignocaine is a classic pharmacological strategy based on its **vasoconstrictive properties** (via $\alpha_1$ receptors). 1. **Prolonged Duration of Action (Option C):** By causing local vasoconstriction, adrenaline reduces the rate of drug removal from the injection site by the bloodstream. This keeps the Lignocaine in contact with the nerve fibers for a longer period, significantly extending the duration of anesthesia. 2. **Decreased Systemic Toxicity (Option A):** Slower absorption into the systemic circulation results in lower peak plasma concentrations of the anesthetic. This reduces the risk of systemic side effects, particularly Central Nervous System (CNS) and Cardiovascular toxicity. 3. **Higher Permissible Doses (Option B):** Because systemic absorption is delayed, the body can metabolize the drug more effectively as it enters the blood slowly. This allows the clinician to safely administer a higher total dose. For Lignocaine, the maximum dose increases from **3 mg/kg (plain)** to **7 mg/kg (with adrenaline)**. **High-Yield Clinical Pearls for NEET-PG:** * **Concentration:** Adrenaline is typically added in a concentration of **1:200,000** (5 µg/mL). * **Contraindications:** Never use adrenaline-containing local anesthetics in areas supplied by **end-arteries** (e.g., fingers, toes, tip of the nose, ears, and penis) due to the risk of ischemia and gangrene. * **pH Effect:** Adrenaline is stable only in acidic solutions. Adding it lowers the pH of the anesthetic solution, which may increase the "sting" upon injection. * **Marker of Intravascular Injection:** Adrenaline acts as a marker; if accidentally injected into a vessel, it causes immediate tachycardia and hypertension, alerting the anesthesiologist.

Q: Which of the following is the longest acting local anesthetic?

Dibucaine. **Explanation:** The duration of action of a local anesthetic (LA) is primarily determined by its **protein binding capacity** and **lipid solubility**. **Dibucaine (Option C)** is an amide-linked local anesthetic that is the most potent, most toxic, and longest-acting among the options provided. It has an exceptionally high affinity for plasma proteins and high lipid solubility, giving it a duration of action significantly longer than bupivacaine. While its clinical use is limited today (primarily used for the "Dibucaine Number" to detect atypical pseudocholinesterase), it remains the correct answer in the context of pharmacological duration. **Analysis of Incorrect Options:** * **Bupivacaine (Option A):** A potent, long-acting amide LA commonly used for spinal and epidural anesthesia. While it is long-acting (3–6 hours), it is shorter-acting than Dibucaine. * **Ropivacaine (Option B):** An S-enantiomer of bupivacaine with a similar duration of action but slightly less cardiotoxicity. Its duration is comparable to or slightly less than bupivacaine. * **Tetracaine (Option D):** An ester-linked anesthetic used mainly for spinal and topical anesthesia. It is long-acting for an ester but does not exceed the duration of Dibucaine. **High-Yield Clinical Pearls for NEET-PG:** * **Dibucaine Number:** A measure of the quality of pseudocholinesterase. Normal = 80 (Dibucaine inhibits 80% of the enzyme); Atypical = 20. It helps diagnose prolonged apnea after Succinylcholine administration. * **Potency & Duration:** Lipid solubility determines **potency**, while protein binding determines **duration of action**. * **Cardiotoxicity:** Bupivacaine is the most cardiotoxic (binds strongly to sodium channels during diastole). Intralipid 20% is the antidote for Local Anesthetic Systemic Toxicity (LAST).

Q: Osteomalacia is an adverse effect of which of the following drugs?

Phenytoin. **Explanation:** **Phenytoin** is a classic cause of **osteomalacia** (in adults) and rickets (in children) due to its effect on Vitamin D metabolism. **Mechanism:** Phenytoin is a potent **inducer of Cytochrome P450 (CYP) enzymes** in the liver. This induction accelerates the catabolism of Vitamin D into inactive metabolites. Consequently, there is a decrease in intestinal calcium absorption, leading to hypocalcemia. This triggers a secondary rise in Parathyroid Hormone (PTH), which mobilizes calcium from the bones, resulting in decreased bone mineral density and osteomalacia. **Analysis of Options:** * **A. Primidone:** While Primidone is an enzyme inducer and can theoretically cause bone loss, Phenytoin is the most classically associated and frequently tested drug for this specific adverse effect in competitive exams. * **C. Carbamazepine:** Like Phenytoin, it is an enzyme inducer and can cause bone loss, but Phenytoin has a more profound and well-documented clinical association with overt osteomalacia. * **D. Valproic Acid:** It is an enzyme **inhibitor**. While it can cause bone loss through different mechanisms (e.g., direct effect on osteoblasts), it is not the primary answer for classical enzyme-induction-mediated osteomalacia. **Clinical Pearls for NEET-PG:** * **Gingival Hyperplasia:** Another high-yield side effect of Phenytoin (due to increased PDGF). * **Fetal Hydantoin Syndrome:** Characterized by hypoplastic phalanges, cleft lip/palate, and microcephaly. * **Zero-order Kinetics:** Phenytoin follows saturation kinetics at therapeutic/higher doses. * **Prophylaxis:** Patients on long-term Phenytoin should be monitored for Vitamin D levels and may require Calcium and Vitamin D supplementation.

Q: Lorazepam can be safely used as a preanesthetic medication in a patient undergoing liver transplantation without fear of excessive CNS depression because the drug is:

conjugated extrahepatically. **Explanation:** The correct answer is **C. conjugated extrahepatically.** **Concept:** Benzodiazepines (BZDs) are primarily metabolized in the liver via two pathways: 1. **Phase I (Oxidation):** Carried out by Cytochrome P450 enzymes. This process is significantly impaired in liver disease and often produces active metabolites with long half-lives (e.g., Diazepam). 2. **Phase II (Conjugation):** Glucuronidation converts the drug into inactive, water-soluble metabolites. Crucially, glucuronidation is relatively preserved in hepatic failure and can also occur **extrahepatically** (e.g., in the kidneys). Lorazepam, along with Oxazepam and Temazepam (remembered by the mnemonic **LOT**), undergoes direct Phase II conjugation without requiring Phase I oxidation. Therefore, even in a patient undergoing liver transplantation (severe hepatic impairment), Lorazepam does not accumulate to toxic levels, making it safer than other BZDs. **Analysis of Incorrect Options:** * **Option A:** Most BZDs are highly lipid-soluble and must be metabolized to water-soluble forms before excretion; they are not excreted unchanged. * **Option B:** BZDs are primarily excreted via the renal route after conjugation, not through active GI secretion. * **Option C:** Lorazepam is a potent CNS depressant. While it is used as an anxiolytic, it can cause significant sedation and respiratory depression at higher doses. **NEET-PG High-Yield Pearls:** * **LOT Drugs:** **L**orazepam, **O**xazepam, and **T**emazepam are the BZDs of choice in elderly patients and those with liver cirrhosis/failure. * **Midazolam:** Commonly used as a preanesthetic due to its short half-life and prominent **anterograde amnesia**, but it requires Phase I oxidation and is less safe in liver failure than Lorazepam. * **Flumazenil:** The specific antidote for BZD overdose (competitive antagonist at the GABA-A receptor).

Q: Cleft lip is caused by which of the following drugs?

Phenytoin. Phenytoin is the correct answer because it is classically associated with Fetal Hydantoin Syndrome. This syndrome occurs due to the production of epoxide metabolites during phenytoin metabolism, which are teratogenic. The hallmark features include cleft lip and cleft palate, microcephaly, digital hypoplasia (hypoplastic nails/phalanges), and cardiac defects.Analysis of Options:Sodium Valproate (Option C): While highly teratogenic, it is most specifically associated with Neural Tube Defects (e.g., Spina Bifida) [1] due to its interference with folate metabolism. It can cause "Fetal Valproate Syndrome" (craniofacial dysmorphism), but cleft lip is more classically linked to Phenytoin in exams.Phenobarbitone (Option D): This drug is associated with cardiac defects and hemorrhage in the newborn (due to Vitamin K deficiency), but it is not the primary drug linked to isolated cleft lip/palate.Levetiracetam (Option A): This is considered one of the safest antiepileptic drugs during pregnancy, along with Lamotrigine. It has a much lower risk of major congenital malformations.High-Yield NEET-PG Pearls:Drug of Choice (DOC) for Epilepsy in Pregnancy: Levetiracetam or Lamotrigine.Folate Supplementation: All women on AEDs should take high-dose Folic acid (5mg) to reduce the risk of neural tube defects.Enzyme Induction: Phenytoin, Phenobarbitone, and Carbamazepine are enzyme inducers that can decrease Vitamin K levels; thus, Vitamin K prophylaxis is given to the mother in the last month of pregnancy to prevent neonatal hemorrhage.

Q: Which of the following statements regarding drugs used in Parkinsonism is true?

COMT inhibitors prolong the action of Levodopa.. **Explanation:** **1. Why Option C is Correct:** Levodopa is metabolized in the periphery by two main enzymes: Dopa decarboxylase (DDC) and **Catechol-O-methyltransferase (COMT)**. While DDC inhibitors (Carbidopa) are routinely used, COMT still converts Levodopa into 3-O-methyldopa, reducing its availability to the brain. **COMT inhibitors** (e.g., Entacapone, Tolcapone) block this pathway, decreasing the peripheral degradation of Levodopa. This increases its plasma half-life and ensures a more sustained delivery to the CNS, thereby **prolonging its duration of action** and helping manage "wearing-off" phenomena. **2. Why Other Options are Incorrect:** * **Option A:** Amantadine is an **antiviral** drug that acts as a **dopaminergic** agent (increasing dopamine release and inhibiting reuptake) and an NMDA antagonist. It is not a cholinergic drug; in fact, it possesses mild anticholinergic properties. * **Option B:** Vitamin B6 (Pyridoxine) is a cofactor for the enzyme Dopa decarboxylase. It **accelerates the peripheral metabolism** of Levodopa into Dopamine. Since Dopamine cannot cross the blood-brain barrier, Vitamin B6 actually **decreases** the effectiveness of Levodopa (unless a DDC inhibitor like Carbidopa is also used). **3. High-Yield Clinical Pearls for NEET-PG:** * **Entacapone** acts only peripherally, while **Tolcapone** acts both peripherally and centrally (but is associated with hepatotoxicity). * **Amantadine** is the drug of choice for Levodopa-induced dyskinesias and can cause **Livedo Reticularis** (mottled skin discoloration). * **"On-off" phenomenon** is a long-term complication of Levodopa therapy characterized by fluctuations in motor performance. * **Bromocriptine** is an Ergot-derived dopamine agonist, whereas **Pramipexole and Ropinirole** are non-ergot derivatives (preferred due to fewer side effects like pulmonary fibrosis).

Q: Dexmedetomidine acts on which receptor for its analgesic action?

a2A. **Explanation:** **1. Why Option C is Correct:** Dexmedetomidine is a highly selective **alpha-2 ($\alpha_2$) adrenergic agonist**. Its analgesic properties are primarily mediated through the **$\alpha_{2A}$ subtype receptors** located in the **dorsal horn of the spinal cord** [1]. Activation of these receptors inhibits the release of nociceptive neurotransmitters (like Substance P and glutamate) and hyperpolarizes post-synaptic neurons, effectively "closing the gate" on pain signals. It is approximately 8 times more selective for $\alpha_2$ receptors than clonidine. **2. Why Other Options are Incorrect:** * **Option A (5HT2A):** These are serotonin receptors. While serotonin plays a role in descending pain modulation, dexmedetomidine does not have significant affinity for these receptors. 5HT2A antagonists are more relevant in treating psychosis or migraine. * **Option B & D (D2 & D5):** These are dopamine receptors. D2 receptors are targets for antipsychotics and anti-emetics, while D5 is a D1-like receptor. Dexmedetomidine does not act via the dopaminergic system for its primary clinical effects. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Sedation:** Dexmedetomidine produces "conscious sedation" (arousable sedation) by acting on the **locus coeruleus** in the brainstem [1]. * **Unique Feature:** It provides sedation **without significant respiratory depression**, making it ideal for ICU weaning and awake fiberoptic intubation. * **Side Effects:** The most common side effects are **bradycardia** and **hypotension** (due to central sympatholytic action) [1]. * **Comparison:** Unlike clonidine (non-selective $\alpha_2$ agonist), dexmedetomidine has a much higher $\alpha_2:\alpha_1$ selectivity ratio (1600:1).

Q: Central muscle relaxants act by:

Inhibiting spinal polysynaptic reflexes. **Explanation:** Central muscle relaxants (e.g., Diazepam, Baclofen, Tizanidine, and Mephenesin congeners) reduce skeletal muscle tone by acting primarily on the **spinal cord and subcortical levels** of the Central Nervous System (CNS). **Why Option B is Correct:** The primary mechanism of these drugs is the **selective inhibition of polysynaptic reflexes** in the spinal cord. They increase the activity of inhibitory neurotransmitters (like GABA) or inhibit excitatory interneurons. By depressing these polysynaptic pathways, they reduce the excitatory input to alpha-motor neurons, thereby decreasing muscle spasticity without significantly affecting voluntary muscle strength. **Why Other Options are Incorrect:** * **Option A:** Decreased nerve conduction is the mechanism of **Local Anesthetics**, which block voltage-gated sodium channels. * **Option C:** Blocking conduction across the neuromuscular junction (NMJ) is the mechanism of **Peripheral Muscle Relaxants** (e.g., Succinylcholine, Vecuronium). These act on nicotinic receptors ($N_m$), not the CNS. * **Option D:** While many central muscle relaxants cause sedation as a side effect, "CNS depression" is a generalized effect of hypnotics/anesthetics. The specific therapeutic action for muscle relaxation is the targeted inhibition of spinal reflexes. **High-Yield Clinical Pearls for NEET-PG:** * **Baclofen:** A $GABA_B$ agonist; the drug of choice for spasticity in Multiple Sclerosis. * **Tizanidine:** An $\alpha_2$ adrenergic agonist (similar to Clonidine) that reduces spasticity with less muscle weakness than Baclofen. * **Diazepam:** Acts via $GABA_A$ receptors to increase chloride conductance. * **Dantrolene:** Often confused with central relaxants, but it is a **directly acting** muscle relaxant that inhibits calcium release from the sarcoplasmic reticulum (used in Malignant Hyperthermia).

Question 1

Which of the following is a short-acting benzodiazepine?

Accepted Answer

Lorazepam

Answer

Diazepam

Answer

Flurazepam

Answer

Chlordiazepoxide

Question 2

Which of the following is an advantage of adding adrenaline to lignocaine for local anesthetic injection?

Accepted Answer

All of the above

Answer

Decreases the systemic toxicity

Answer

Higher doses can be given

Answer

Duration of action can be prolonged

Question 3

Which of the following statements is NOT true of local anesthetics?

Accepted Answer

The local anesthetic binds to its receptor mainly when the Na+ channel is in the resting state.

Answer

The local anesthetic is required in the unionized form for penetrating the neuronal membrane.

Answer

The local anesthetic approaches its receptor only from the intraneuronal face of the Na+ channel.

Answer

The local anesthetic combines with its receptor in the ionized cationic form.

Question 4

Which of the following is the longest acting local anesthetic?

Accepted Answer

Dibucaine

Answer

Bupivacaine

Answer

Ropivacaine

Answer

Tetracaine

Question 5

Osteomalacia is an adverse effect of which of the following drugs?

Accepted Answer

Phenytoin

Answer

Primidone

Answer

Carbamazepine

Answer

Valproic acid

Question 6

Lorazepam can be safely used as a preanesthetic medication in a patient undergoing liver transplantation without fear of excessive CNS depression because the drug is:

Accepted Answer

conjugated extrahepatically

Answer

excreted in unchanged form

Answer

actively secreted into the GI tract

Answer

a selective anxiolytic devoid of CNS depressant actions

Question 7

Cleft lip is caused by which of the following drugs?

Accepted Answer

Phenytoin

Answer

Levetiracetam

Answer

Sodium valproate

Answer

Phenobarbitone

Question 8

Which of the following statements regarding drugs used in Parkinsonism is true?

Accepted Answer

COMT inhibitors prolong the action of Levodopa.

Answer

Amantadine is a cholinergic drug.

Answer

Vitamin B6 enhances the action of Levodopa.

Answer

None of the above.

Question 9

Dexmedetomidine acts on which receptor for its analgesic action?

Accepted Answer

a2A

Answer

5HT2A

Answer

D2

Answer

D5

Question 10

Central muscle relaxants act by:

Accepted Answer

Inhibiting spinal polysynaptic reflexes

Answer

Decreased nerve conduction

Answer

Blocking conduction across the neuromuscular junction

Answer

Central nervous system depression

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

On this page

Practice by Chapter

Want unlimited practice?