Central Nervous System Pharmacology Practice Questions

Q: Adrenaline is added to Lignocaine injection for what purpose?

All of the above. Lignocaine is a medium-acting local anesthetic (LA) with vasodilator properties. When combined with Adrenaline (usually in a 1:200,000 concentration), it produces several clinical benefits based on the principle of **vasoconstriction**. **Explanation of Options:** * **A. Less bleeding at the site:** Adrenaline acts on $\alpha_1$ receptors in the local blood vessels, causing vasoconstriction. This reduces surgical site bleeding, providing a clearer operative field. * **B. Higher doses can be given:** By constricting local vessels, Adrenaline slows the systemic absorption of Lignocaine. This reduces the peak plasma concentration and the risk of systemic toxicity (LAST), allowing the maximum safe dose to be increased (e.g., from 5 mg/kg to 7 mg/kg). * **C. Prolonged duration of action:** Slower absorption means the drug remains in contact with the nerve fibers for a longer period, significantly extending the duration of the block. Since all three mechanisms occur simultaneously, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Maximum Doses:** Lignocaine plain = 5 mg/kg; Lignocaine with Adrenaline = 7 mg/kg. * **Contraindications:** Adrenaline-containing LAs must **never** be used in areas supplied by end-arteries (fingers, toes, nose, ears, and penis) due to the risk of ischemia and gangrene. * **pH Effect:** Adrenaline is stable only in acidic solutions. Therefore, commercial Lignocaine with Adrenaline has a lower pH, which can cause more "sting" on injection compared to plain Lignocaine. * **Bupivacaine:** Adrenaline does not significantly prolong the duration of Bupivacaine as much as it does for Lignocaine, because Bupivacaine is already highly protein-bound and long-acting.

Q: What is the drug of choice for myoclonic seizures?

Valproic acid. **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.

Q: Which drug is NOT used in the management of Alzheimer Disease?

Ropinirole. 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).

Q: Which anti-epileptic drug is not contraindicated during pregnancy?

Carbamazepine. **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.

Q: Which of the following agents does not cause an increase in serotonin levels?

LSD. **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.

Q: Eteplirsen has been recently FDA approved for the treatment of which condition?

Duchenne muscular dystrophy. **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.

Q: A 30-year-old epileptic female on Phenytoin therapy developed weakness and fatigue. Blood examination revealed Hb= 4.6 gm, MCV=102 fL, and MCH =40 pg/dL. What is the most probable diagnosis?

Megaloblastic anemia. **Explanation:** The patient presents with symptoms of anemia (weakness, fatigue) and a low hemoglobin (4.6 gm/dL). The key diagnostic clues are the **elevated MCV (102 fL)** and **elevated MCH (40 pg/dL)**, which indicate a **macrocytic anemia**. **Why Megaloblastic Anemia is correct:** Phenytoin is a well-known inducer of **folate deficiency**. It interferes with folate metabolism by inhibiting the intestinal enzyme *folate conjugase*, thereby reducing the absorption of dietary folic acid. Chronic phenytoin therapy leads to impaired DNA synthesis in red blood cell precursors, resulting in megaloblastic (macrocytic) anemia. **Analysis of Incorrect Options:** * **Heart failure:** While severe anemia can lead to high-output heart failure, it does not explain the macrocytic blood indices (high MCV/MCH). * **Iron deficiency anemia:** This typically presents as **microcytic hypochromic** anemia (Low MCV, Low MCH), which contradicts the laboratory findings provided. * **Phenytoin-induced agranulocytosis:** This refers to a severe reduction in white blood cell count (granulocytes), not red blood cells. While phenytoin can cause blood dyscrasias, the high MCV specifically points toward a maturation defect like megaloblastic anemia. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Phenytoin decreases folate absorption and increases its catabolism. * **Management:** Supplementation with **Folic Acid** can reverse the anemia. However, be cautious: high doses of folic acid can lower phenytoin levels by increasing its metabolism, potentially precipitating seizures. * **Other Phenytoin Side Effects (Mnemonic: HOT MALAR):** **H**irsutism, **O**steomalacia, **T**eratogenicity (Fetal Hydantoin Syndrome), **M**egaloblastic anemia, **A**taxia, **L**ymphadenopathy, **A**rrhythmias, **R**igidity (Gingival Hyperplasia).

Q: Which anti-epileptic drug can be safely used in pregnancy?

Lamotrigine. The management of epilepsy in pregnancy requires balancing maternal seizure control with the risk of teratogenicity. **Lamotrigine** is considered one of the safest anti-epileptic drugs (AEDs) during pregnancy [1] because it has a significantly lower risk of major congenital malformations (approx. 2–3%) compared to older AEDs. It is not associated with a specific "syndrome" of defects, though clinicians must monitor serum levels closely as clearance increases during pregnancy. **Analysis of Incorrect Options:** * **Valproic acid (Option A):** This is the **most teratogenic** AED. It is associated with a high risk of neural tube defects (e.g., spina bifida) and impaired cognitive development (lower IQ) in the offspring [1]. It is strictly avoided in pregnancy unless no other drug works. * **Phenytoin (Option B):** Causes **Fetal Hydantoin Syndrome**, characterized by craniofacial dysmorphism (cleft lip/palate), hypoplastic phalanges/nails, and microcephaly. * **Carbamazepine (Option C):** Associated with an increased risk of neural tube defects and craniofacial abnormalities, though the risk is lower than with Valproate. **NEET-PG High-Yield Pearls:** * **Safest AEDs in pregnancy:** Lamotrigine and Levetiracetam. * **Drug of choice for seizures in pregnancy:** If a patient is already well-controlled on a drug (except Valproate), it is usually continued at the lowest effective dose. * **Folic Acid Supplementation:** All pregnant women on AEDs should take high-dose folic acid (5 mg/day) to reduce the risk of neural tube defects. * **Vitamin K:** Enzyme-inducing AEDs (Phenytoin, Carbamazepine, Phenobarbital) can cause neonatal hemorrhage; Vitamin K is administered to the mother in the last month of pregnancy and to the newborn at birth [1].

Q: All of the following adverse effects are associated with carbamazepine except?

Decrease in antidiuretic hormone. **Explanation:** The correct answer is **C (Decrease in antidiuretic hormone)** because Carbamazepine actually causes an **increase** in the action of Antidiuretic Hormone (ADH). **1. Why Option C is correct:** Carbamazepine acts as an ADH enhancer by increasing the sensitivity of renal tubules to ADH and stimulating its release. This leads to water retention and **dilutional hyponatremia** (SIADH-like picture). Therefore, saying it causes a "decrease" in ADH is physiologically incorrect. **2. Why other options are incorrect:** * **A. Teratogenicity:** Carbamazepine is a known teratogen associated with **neural tube defects** (e.g., spina bifida) due to interference with folate metabolism. * **B. Neurotoxicity:** Dose-related neurotoxicity is common, manifesting as diplopia, ataxia, vertigo, and sedation. * **C. Hypersensitivity:** It can cause various skin reactions, ranging from mild rashes to life-threatening **Stevens-Johnson Syndrome (SJS)** or Toxic Epidermal Necrolysis (TEN), particularly in patients with the **HLA-B*1502** allele. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Blocks voltage-gated sodium channels in the inactivated state. * **Drug of Choice (DOC):** It remains the DOC for **Trigeminal Neuralgia**. * **Auto-induction:** Carbamazepine induces its own metabolism (CYP3A4 inducer), meaning the half-life decreases after chronic administration. * **Hematological Side Effect:** It can cause rare but serious **aplastic anemia** and agranulocytosis; baseline CBC is often recommended. * **Mnemonic (ADVERSE):** **A**taxia, **D**iplopia/Dizziness, **V**ertigo, **E**nzyme induction, **R**ash, **S**IADH, **E**pigenetic (Teratogenic).

Q: Which drug is primarily used in the management of Alzheimer's disease?

Rivastigmine. **Explanation:** **Rivastigmine** is the correct answer because it is a centrally acting, reversible acetylcholinesterase inhibitor (AChEI) that effectively crosses the blood-brain barrier. In Alzheimer’s disease, there is a progressive loss of cholinergic neurons in the nucleus basalis of Meynert. By inhibiting the breakdown of acetylcholine in the synaptic cleft, Rivastigmine enhances cholinergic neurotransmission, thereby improving cognitive function and slowing the progression of symptoms. **Analysis of Options:** * **Tacrine (A):** Although it was the first AChEI approved for Alzheimer’s, it is no longer used clinically due to significant **hepatotoxicity** and the requirement for frequent dosing. * **Pyridostigmine (C):** This is a quaternary ammonium compound that does not cross the blood-brain barrier. It is primarily used in the management of **Myasthenia Gravis** due to its longer duration of action compared to Neostigmine. * **Neostigmine (D):** Like Pyridostigmine, it is a polar quaternary amine with poor CNS penetration. It is used for reversing neuromuscular blockade (post-surgery), Myasthenia Gravis, and paralytic ileus. **Clinical Pearls for NEET-PG:** * **Rivastigmine Unique Feature:** It is the only AChEI available as a **transdermal patch**, which reduces gastrointestinal side effects (nausea/vomiting) and improves patient compliance. * **Other Alzheimer’s Drugs:** Donepezil and Galantamine are other AChEIs used. **Memantine** (an NMDA receptor antagonist) is used for moderate-to-severe cases. * **Side Effects:** Common side effects of these drugs are cholinergic in nature: diarrhea, urination, miosis, bradycardia, and salivation (DUMBELS).

Question 1

Adrenaline is added to Lignocaine injection for what purpose?

Accepted Answer

All of the above

Answer

Less bleeding at the site

Answer

Higher doses can be given

Answer

Prolonged duration of action

Question 2

What is the drug of choice for myoclonic seizures?

Accepted Answer

Valproic acid

Answer

Phenytoin

Answer

Ethosuximide

Answer

Carbamazepine

Question 3

Which drug is NOT used in the management of Alzheimer Disease?

Accepted Answer

Ropinirole

Answer

Memantine

Answer

Galantamine

Answer

Donepezil

Question 4

Which anti-epileptic drug is not contraindicated during pregnancy?

Accepted Answer

Carbamazepine

Answer

Ethosuximide

Answer

Phenytoin

Answer

Valproate

Question 5

Which of the following agents does not cause an increase in serotonin levels?

Accepted Answer

LSD

Answer

MDMA

Answer

Amphetamine

Answer

Fluoxetine

Question 6

Eteplirsen has been recently FDA approved for the treatment of which condition?

Accepted Answer

Duchenne muscular dystrophy

Answer

Spinal muscular atrophy

Answer

Subacute sclerosing panencephalitis

Answer

Acute myeloid leukemia

Question 7

A 30-year-old epileptic female on Phenytoin therapy developed weakness and fatigue. Blood examination revealed Hb= 4.6 gm, MCV=102 fL, and MCH =40 pg/dL. What is the most probable diagnosis?

Accepted Answer

Megaloblastic anemia

Answer

Heart failure

Answer

Iron deficiency anemia

Answer

Phenytoin-induced agranulocytosis

Question 8

Which anti-epileptic drug can be safely used in pregnancy?

Accepted Answer

Lamotrigine

Answer

Valproic acid

Answer

Phenytoin

Answer

Carbamazepine

Question 9

All of the following adverse effects are associated with carbamazepine except?

Accepted Answer

Decrease in antidiuretic hormone

Answer

Teratogenicity

Answer

Neurotoxicity

Answer

Hypersensitivity

Question 10

Which drug is primarily used in the management of Alzheimer's disease?

Accepted Answer

Rivastigmine

Answer

Tacrine

Answer

Pyridostigmine

Answer

Neostigmine

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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