Central Nervous System Pharmacology Practice Questions

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

Miosis. **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.

Q: Droperidol is used as:

All of the above. **Explanation:** Droperidol is a butyrophenone derivative, chemically related to Haloperidol. Its pharmacological profile allows it to be used across multiple clinical scenarios: 1. **Antipsychotic:** Like other butyrophenones, Droperidol is a potent central **D2 receptor antagonist**. While primarily used in anesthesia today, it was originally developed as an antipsychotic medication. 2. **Antiemetic:** It acts on the Chemoreceptor Trigger Zone (CTZ) in the area postrema of the medulla. It is highly effective in preventing and treating **Postoperative Nausea and Vomiting (PONV)**, even in sub-therapeutic doses. 3. **Neurolept Analgesia:** This is a state of quiescence, altered consciousness, and indifference to surroundings. It is achieved by combining a neuroleptic (Droperidol) with a potent opioid analgesic (Fentanyl). The fixed-dose combination (50:1 ratio) is known as **Innovar**. If nitrous oxide is added to this combination, it becomes **Neurolept Anesthesia**. **Why "All of the above" is correct:** Since Droperidol possesses sedative/antipsychotic properties, potent antiemetic effects, and is a core component of neurolept analgesia, all three individual options are clinically accurate descriptions of its use. **High-Yield Clinical Pearls for NEET-PG:** * **Black Box Warning:** The FDA issued a warning for Droperidol regarding **QT interval prolongation** and potential Torsades de Pointes. ECG monitoring is recommended. * **Side Effects:** Can cause extrapyramidal symptoms (dystonia) due to dopamine blockade. * **Contraindication:** Avoid in patients with Parkinson’s disease. * **Innovar Composition:** 2.5 mg Droperidol + 0.05 mg Fentanyl per mL.

Q: Which drug should be avoided in a patient with non-ketotic hyperglycemia presenting with seizure?

Phenytoin. **Explanation:** **Phenytoin** is the correct answer because it is uniquely contraindicated in seizures associated with **Non-Ketotic Hyperglycemic (NKH)** states. 1. **Mechanism of Contraindication:** Phenytoin inhibits the release of insulin from pancreatic beta cells (by stabilizing membranes and reducing calcium influx). In a patient already suffering from severe hyperglycemia, Phenytoin can further elevate blood glucose levels, exacerbating the underlying metabolic derangement. Furthermore, clinical studies have shown that Phenytoin is often ineffective in controlling seizures caused by NKH; the definitive treatment is aggressive hydration and insulin therapy, not anticonvulsants. 2. **Analysis of Incorrect Options:** * **Carbamazepine (A):** While it acts on sodium channels like Phenytoin, it does not significantly interfere with insulin secretion or glucose metabolism. * **Valproate (B):** Valproate is a broad-spectrum AED. While it can cause weight gain and metabolic syndrome over long-term use, it does not acutely worsen hyperglycemia in an emergency NKH setting. * **Clobazam (D):** As a benzodiazepine, it is used for acute seizure control and has no adverse effect on glycemic control. **Clinical Pearls for NEET-PG:** * **Drug of Choice for NKH Seizures:** Fluid resuscitation (Normal Saline) and Insulin. * **Phenytoin Side Effects (High Yield):** Remember the mnemonic **HOT MALAI** (Hirsutism, Osteomalacia, Teratogenicity, Megaloblastic anemia, Ataxia, Lymphadenopathy, **Insulin inhibition**, and Gum Hyperplasia). * **Zero-order Kinetics:** Phenytoin follows capacity-limited elimination, making its plasma levels highly sensitive to small dose changes.

Q: What is the drug of choice for treating drug-induced parkinsonism caused by phenothiazines?

Benzhexol. **Explanation:** The correct answer is **Benzhexol** (also known as Trihexyphenidyl). **Mechanism and Rationale:** Drug-induced parkinsonism (DIP) is a common extrapyramidal side effect of antipsychotics like phenothiazines. These drugs work by blocking **D2 receptors** in the nigrostriatal pathway. In the striatum, there is a functional balance between **Dopamine (inhibitory)** and **Acetylcholine (excitatory)**. When phenothiazines block dopamine receptors, it leads to a relative cholinergic overactivity. To treat this, we use **centrally acting anticholinergics** like Benzhexol, Benztropine, or Procyclidine. They restore the balance by reducing cholinergic tone. **Why other options are incorrect:** * **Levodopa (A) & Benserazide (B):** These are used for idiopathic Parkinson’s disease. In DIP, dopamine receptors are already blocked by the offending drug; therefore, increasing dopamine levels with Levodopa is ineffective and can worsen the underlying psychosis. * **Selegiline (D):** This is a MAO-B inhibitor used as an adjuvant in idiopathic Parkinson’s. It does not address the acute cholinergic-dopaminergic imbalance caused by receptor blockade. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** For drug-induced parkinsonism and acute muscular dystonia, the DOC is a central anticholinergic (Benzhexol/Benztropine) or an antihistamine with strong anticholinergic properties (Promethazine). * **Avoid Levodopa:** Never use Levodopa in DIP as it can precipitate or worsen psychosis. * **Tardive Dyskinesia:** Unlike other extrapyramidal symptoms, anticholinergics **worsen** tardive dyskinesia. The DOC for tardive dyskinesia is Valbenazine or Deutetrabenazine (VMAT2 inhibitors).

Q: In a child with infantile spasms and visual defects, which highly effective drug is generally avoided?

Vigabatrin. **Explanation:** **Vigabatrin** is a structural analog of GABA that irreversibly inhibits GABA-transaminase. While it is highly effective for infantile spasms (West Syndrome)—and is the first-line treatment for cases associated with Tuberous Sclerosis—it is notorious for causing **permanent peripheral visual field constriction** (retinal toxicity) in up to 30-50% of patients. In a child who already has pre-existing visual defects, adding a drug with a high risk of permanent visual loss is contraindicated or generally avoided to prevent further morbidity. **Analysis of Incorrect Options:** * **A. Lamotrigine:** This is an anticonvulsant used for various seizure types (like Lennox-Gastaut syndrome) but is not a primary treatment for infantile spasms and does not carry a specific risk of permanent visual field loss. * **B. Topiramate:** While it can cause ocular side effects like acute myopia or secondary angle-closure glaucoma, it is not the "highly effective" drug typically associated with the specific management dilemma of infantile spasms and chronic visual field defects. * **C. ACTH:** Adrenocorticotropic hormone is the overall first-line treatment for idiopathic infantile spasms. It has significant systemic side effects (hypertension, immunosuppression, Cushingoid features) but does not cause visual field defects. **Clinical Pearls for NEET-PG:** * **West Syndrome Triad:** Infantile spasms, Hypsarrhythmia on EEG, and Mental retardation. * **Drug of Choice (DOC):** ACTH is the DOC for most cases; **Vigabatrin** is the DOC specifically if **Tuberous Sclerosis** is the underlying cause. * **Monitoring:** Patients on Vigabatrin require baseline and periodic ophthalmologic screening (e.g., perimetry or electroretinogram).

Q: Parkinsonism is induced by all drugs except?

Amantadine. **Explanation:** The pathophysiology of Parkinsonism involves a deficiency of dopamine in the nigrostriatal pathway. Therefore, any drug that reduces dopamine levels or blocks dopamine receptors can induce **Drug-Induced Parkinsonism (DIP)**. **Why Amantadine is the Correct Answer:** Amantadine is an **anti-parkinsonian drug**, not a cause of it. Its mechanism involves increasing dopamine release from presynaptic terminals, inhibiting dopamine reuptake, and acting as an NMDA receptor antagonist. It is clinically used to treat early Parkinson’s disease and to reduce levodopa-induced dyskinesias. **Analysis of Incorrect Options (Drugs that cause Parkinsonism):** * **Reserpine:** It is a vesicular monoamine transporter (VMAT) inhibitor. It depletes presynaptic stores of dopamine, leading to a functional deficiency. * **Metoclopramide:** A potent central **D2 receptor antagonist** used as an antiemetic. It crosses the blood-brain barrier and is a common cause of extrapyramidal symptoms (EPS) in clinical practice. * **Chlorpromazine:** A typical (first-generation) antipsychotic that works by blocking D2 receptors in the mesolimbic and nigrostriatal pathways. Nigrostriatal blockade directly results in Parkinsonian symptoms (tremor, rigidity, bradykinesia). **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of DIP:** Antipsychotics (Haloperidol, Chlorpromazine). * **Other causative agents:** Valproate, Flunarizine (calcium channel blocker used for migraine), and Tetrabenazine. * **Treatment of choice for DIP:** Centrally acting anticholinergics like **Trihexyphenidyl (Benzhexol)** or **Benztropine**. Levodopa is usually ineffective because the receptors are blocked. * **Amantadine Side Effect:** Look for **Livedo Reticularis** (purplish lace-like skin discoloration) and ankle edema in exam vignettes.

Q: The dose of which of the following local anesthetics does NOT need to be decreased in patients with deranged liver function?

Procaine. **Explanation:** The metabolism of local anesthetics (LAs) depends entirely on their chemical structure, specifically the linkage between the aromatic ring and the hydrocarbon chain. **1. Why Procaine is Correct:** Local anesthetics are classified into two groups: **Amides** and **Esters**. * **Esters** (e.g., Procaine, Chloroprocaine, Tetracaine) are metabolized by **pseudocholinesterase (plasma cholinesterase)** enzymes in the blood. * Since their metabolism occurs primarily in the plasma and not the liver, their clearance is largely independent of hepatic function. Therefore, the dose of Procaine does not need to be adjusted in patients with liver disease. **2. Why the Other Options are Incorrect:** * **Lignocaine and Bupivacaine (Amides):** Amide LAs (identified by having two "i"s in their name) are metabolized primarily by **hepatic microsomal enzymes** (Cytochrome P450). In patients with deranged liver function or reduced hepatic blood flow (e.g., CHF, cirrhosis), the half-life of these drugs is significantly prolonged, increasing the risk of Systemic Toxicity (LAST). Thus, doses must be decreased. * **Cocaine:** Although an ester, cocaine is unique because it undergoes significant metabolism by **hepatic carboxylesterase** in addition to plasma cholinesterase. Therefore, its clearance can still be affected by liver dysfunction. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** Am**i**des have two "i"s (L**i**doca**i**ne, Bup**i**vaca**i**ne, Pr**i**loca**i**ne, Rop**i**vaca**i**ne). Esters have one "i" (Proca**i**ne, Coca**i**ne, Benzoca**i**ne). * **Prilocaine** is associated with **Methemoglobinemia** (due to its metabolite o-toluidine). * **Bupivacaine** is the most **cardiotoxic** LA; Intralipid (20% lipid emulsion) is the specific antidote for toxicity. * **Chloroprocaine** has the shortest duration of action and fastest metabolism among esters.

Q: What is the drug of choice for generalized tonic-clonic status epilepticus?

Lorazepam. **Explanation:** **Status Epilepticus (SE)** is a medical emergency defined as a continuous seizure lasting more than 5 minutes or recurrent seizures without recovery of consciousness between episodes. **Why Lorazepam is the Correct Answer:** Benzodiazepines are the first-line treatment for terminating active seizures due to their rapid onset of action and high affinity for GABA-A receptors, which enhances inhibitory neurotransmission. **Lorazepam** is the preferred drug of choice (DOC) over Diazepam because it is less lipid-soluble; it remains in the vascular compartment longer, providing a more sustained anticonvulsant effect (6–12 hours) compared to the rapid redistribution of Diazepam. **Analysis of Incorrect Options:** * **A. Ethosuximide:** This is the DOC for **Absence seizures** only. It works by blocking T-type calcium channels and has no role in managing status epilepticus or tonic-clonic seizures. * **B. Sodium Valproate:** While a broad-spectrum anticonvulsant used for maintenance therapy in GTCS, it is considered a second-line agent in SE (used if benzodiazepines fail). * **C. Lamotrigine:** This is used for long-term prophylaxis of various seizures and bipolar disorder. It is not available in a rapid-acting intravenous formulation suitable for emergency seizure termination. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence of Management in SE:** 1. **1st Line:** Lorazepam (IV) or Midazolam (IM/Buccal if IV access is unavailable). 2. **2nd Line:** Phenytoin/Fosphenytoin, Levetiracetam, or Valproate. 3. **3rd Line (Refractory):** Phenobarbital, Propofol, or Thiopental (requires intubation). * **Drug of Choice for Febrile Seizures:** Diazepam (Rectal/IV). * **Drug of Choice for Absence Seizures:** Ethosuximide (Valproate if associated with GTCS).

Q: Which mood stabilizer is used in the management of temporal lobe epilepsy?

Carbamazepine. **Explanation:** **Carbamazepine** is the drug of choice for the management of **Temporal Lobe Epilepsy (TLE)**, also known as focal seizures with impaired awareness. While it is primarily an anticonvulsant, it is a potent mood stabilizer used in Psychiatry for the treatment of Acute Mania and Prophylaxis of Bipolar Disorder, especially in patients who are non-responsive to Lithium. Its mechanism involves blocking voltage-gated sodium channels, which stabilizes hyperexcitable neuronal membranes. **Analysis of Options:** * **Valproate (Option B):** While Valproate is a broad-spectrum antiepileptic and a first-line mood stabilizer, it is typically the drug of choice for generalized tonic-clonic seizures and myoclonic seizures rather than specifically for TLE. * **Lamotrigine (Option C):** This is used primarily for the maintenance phase of Bipolar Disorder (preventing depressive episodes) and focal seizures. However, it is not the traditional "gold standard" for TLE compared to Carbamazepine. * **Lithium (Option D):** Lithium is the "gold standard" for Bipolar Affective Disorder (BPAD) but has **no anticonvulsant properties**. In fact, Lithium can lower the seizure threshold in high doses. **High-Yield Clinical Pearls for NEET-PG:** * **DOC for TLE:** Carbamazepine. * **Side Effects:** Agranulocytosis, Aplastic anemia, and **Stevens-Johnson Syndrome** (associated with the HLA-B*1502 allele). * **Enzyme Induction:** Carbamazepine is a potent **cytochrome P450 inducer**, leading to many drug-drug interactions (e.g., reducing the efficacy of oral contraceptives). * **SIADH:** It can cause hyponatremia by increasing ADH sensitivity.

Question 1

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

Accepted Answer

Miosis

Answer

Muscle aches and body pain

Answer

Yawning

Answer

Rhinorrhoea

Question 2

A patient with Parkinsonism experienced a decreased therapeutic effect of levodopa when a specific drug was co-administered. However, no such interaction was observed when the patient switched to a levodopa-carbidopa combination. What is the likely identity of the drug prescribed by the physician?

Accepted Answer

Vitamin B complex

Answer

Metoclopramide

Answer

Chlorpromazine

Answer

Isoniazid

Question 3

Droperidol is used as:

Accepted Answer

All of the above

Answer

Antipsychotic

Answer

Antiemetic

Answer

Neurolept analgesia

Question 4

Which drug should be avoided in a patient with non-ketotic hyperglycemia presenting with seizure?

Accepted Answer

Phenytoin

Answer

Carbamazepine

Answer

Valproate

Answer

Clobazam

Question 5

What is the drug of choice for treating drug-induced parkinsonism caused by phenothiazines?

Accepted Answer

Benzhexol

Answer

Levodopa

Answer

Benserazide

Answer

Selegiline

Question 6

In a child with infantile spasms and visual defects, which highly effective drug is generally avoided?

Accepted Answer

Vigabatrin

Answer

Lamotrigine

Answer

Topiramate

Answer

ACTH

Question 7

Parkinsonism is induced by all drugs except?

Accepted Answer

Amantadine

Answer

Reserpine

Answer

Metoclopramide

Answer

Chlorpromazine

Question 8

The dose of which of the following local anesthetics does NOT need to be decreased in patients with deranged liver function?

Accepted Answer

Procaine

Answer

Lignocaine

Answer

Bupivacaine

Answer

Cocaine

Question 9

What is the drug of choice for generalized tonic-clonic status epilepticus?

Accepted Answer

Lorazepam

Answer

Ethosuxamide

Answer

Sodium valproate

Answer

Lamotrigene

Question 10

Which mood stabilizer is used in the management of temporal lobe epilepsy?

Accepted Answer

Carbamazepine

Answer

Valproate

Answer

Lamotrigine

Answer

Lithium

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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