Central Nervous System Pharmacology Practice Questions

Q: Which of the following drugs are used in the management of generalized anxiety disorder?

All of the above. **Explanation:** The management of Generalized Anxiety Disorder (GAD) involves both acute symptom control and long-term maintenance therapy. The correct answer is **All of the above** because each drug class represented plays a specific role in the treatment algorithm. 1. **Paroxetine (Option B):** Selective Serotonin Reuptake Inhibitors (SSRIs) like Paroxetine and Escitalopram are considered **first-line agents** for the long-term management of GAD. They are preferred due to their efficacy and lower side-effect profile compared to older agents. 2. **Venlafaxine (Option C):** Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) are also **first-line treatments**. Venlafaxine (especially the extended-release formulation) is highly effective for patients who may not respond fully to SSRIs. 3. **Alprazolam (Option D):** Benzodiazepines (BZDs) provide **rapid symptomatic relief**. While not recommended for long-term monotherapy due to the risk of dependence and tolerance, they are frequently used as "bridge therapy" during the first 2–4 weeks of SSRI/SNRI treatment (as antidepressants have a delayed onset of action). **Why other options are "wrong":** In this "All of the above" format, no single option is incorrect. Each drug is FDA-approved or clinically indicated for GAD. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** SSRIs (e.g., Escitalopram, Paroxetine) are the DOC for long-term GAD management. * **Buspirone:** A 5-HT1A partial agonist specifically used for GAD; it lacks sedative, anticonvulsant, or muscle relaxant properties and has no abuse potential. * **Onset of Action:** SSRIs/SNRIs take 2–4 weeks to work; BZDs work instantly. * **Pregabalin/Gabapentin:** These are considered second-line alternatives for GAD in some international guidelines.

Q: Dilantin causes which of the following deficiencies?

Folic acid deficiency. **Explanation:** **Dilantin (Phenytoin)** is a widely used hydantoin-derivative antiepileptic drug. The correct answer is **Folic acid deficiency** because Phenytoin interferes with folate metabolism through several mechanisms: 1. **Inhibition of Intestinal Absorption:** It inhibits the enzyme *folate conjugase*, preventing the breakdown of polyglutamates into absorbable monoglutamates. 2. **Induction of Microsomal Enzymes:** Phenytoin induces hepatic enzymes, leading to increased utilization and depletion of folate stores [1]. 3. **Competitive Inhibition:** It may interfere with the uptake of folate by the intestinal mucosa. **Analysis of Incorrect Options:** * **B, C, and D (Thiamine, Nicotinamide, Riboflavin):** These are B-complex vitamins (B1, B3, and B2, respectively). While certain drugs like Isoniazid (B6) or Alcohol (B1) affect these vitamins, Phenytoin has no documented clinical association with their deficiency. **Clinical Pearls for NEET-PG:** * **Megaloblastic Anemia:** Chronic Phenytoin therapy can lead to macrocytosis and megaloblastic anemia due to folate depletion [1]. * **Teratogenicity:** Folate deficiency is a contributing factor to **Fetal Hydantoin Syndrome** (cleft lip/palate, microcephaly, and digital hypoplasia). Supplementation with 5mg folic acid is recommended for pregnant women on Phenytoin. * **Gingival Hyperplasia:** This is another high-yield side effect of Phenytoin, often linked to altered collagen metabolism and local folate deficiency in gingival tissues [1]. * **Zero-Order Kinetics:** Phenytoin follows saturation kinetics, making its plasma levels highly sensitive to dose changes [1].

Q: Which of the following is a skeletal muscle relaxant that acts as a central a2 adrenergic agonist?

Tizanidine. **Explanation:** **Tizanidine** is a centrally acting skeletal muscle relaxant that exerts its effect as a **selective $\alpha_2$-adrenergic agonist** [1, 4]. It acts primarily in the spinal cord, where it stimulates presynaptic $\alpha_2$ receptors [1]. This leads to a decrease in the release of excitatory amino acids (like glutamate and aspartate) from spinal interneurons, thereby inhibiting spinal polysynaptic reflex arcs and reducing muscle spasticity [2]. **Analysis of Options:** * **Brimonidine (Option B):** While it is also a selective $\alpha_2$ agonist, it is used topically in ophthalmology to reduce intraocular pressure in **glaucoma**. It does not have a clinical role as a skeletal muscle relaxant. * **Chlormezanone (Option C):** This is an older, centrally acting muscle relaxant and antianxiety agent. Its mechanism is non-specific (sedative-like) and does not involve $\alpha_2$ agonism. It has been withdrawn in many countries due to the risk of Stevens-Johnson Syndrome. * **Quinine (Option D):** It is an antimalarial drug that is sometimes used for nocturnal leg cramps. It acts directly on the muscle fiber by increasing the refractory period and decreasing the excitability of the motor end-plate, rather than acting centrally. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Use:** Tizanidine is preferred in patients with multiple sclerosis or spinal cord injury because it causes **less muscle weakness** compared to Baclofen or Diazepam [3]. * **Side Effects:** Common side effects include drowsiness, xerostomia (dry mouth), and hypotension (due to its structural similarity to clonidine). * **Comparison:** Unlike **Baclofen** (GABA$_B$ agonist) [1] or **Dantrolene** (Ryanodine receptor antagonist) [4], Tizanidine’s primary mechanism is $\alpha_2$ agonism.

Q: GABA reuptake is inhibited by which of the following medications?

Tiagabine. **Explanation:** **Tiagabine** is the correct answer because it specifically inhibits the **GAT-1 (GABA transporter-1)**, which is responsible for the reuptake of GABA from the synaptic cleft into neurons and glial cells. By blocking this transporter, Tiagabine increases the duration and concentration of GABA in the synaptic space, thereby enhancing inhibitory neurotransmission. This mechanism makes it an effective adjunctive treatment for focal (partial) seizures. **Analysis of Incorrect Options:** * **Topiramate:** This is a broad-spectrum anti-epileptic with multiple mechanisms, including blocking voltage-gated sodium channels, antagonizing AMPA/kainate receptors, and enhancing GABA-A receptor activity. It does **not** inhibit GABA reuptake. * **Felbamate:** Primarily acts by blocking NMDA receptors and modulating GABA-A receptors. It is rarely used due to the risk of aplastic anemia and hepatic failure. * **Perampanel:** This is a first-in-class selective, non-competitive antagonist of **AMPA receptors** (glutamate receptors). It acts on the post-synaptic excitatory pathway rather than the GABAergic inhibitory pathway. **NEET-PG High-Yield Pearls:** * **Vigabatrin vs. Tiagabine:** Do not confuse them. **Vigabatrin** inhibits **GABA-transaminase (GABA-T)**, the enzyme that degrades GABA, while **Tiagabine** inhibits the **GAT-1 transporter** (reuptake). * **Side Effect Alert:** Tiagabine can occasionally induce non-convulsive status epilepticus in patients without epilepsy. * **Vigabatrin Side Effect:** Classically associated with **permanent visual field defects** (concentric contraction).

Q: Which of the following are endogenous opioid peptides?

All of the above. The correct answer is **D. All of the above.**Endogenous opioid peptides are naturally occurring molecules in the body that act on opioid receptors to modulate pain, reward, and addictive behaviors [1]. These peptides are derived from three distinct large precursor proteins:1. **Enkephalins (Option A):** Derived from **Pro-enkephalin**. The two primary forms are Leu-enkephalin and Met-enkephalin. They have a high affinity for **delta (δ) receptors** [2] and are widely distributed in the CNS and interneurons involved in pain gating.2. **Endorphins (Option B):** Derived from **Pro-opiomelanocortin (POMC)**. The most significant is **β-endorphin**, which is primarily found in the pituitary gland and hypothalamus. It has a high affinity for **mu (μ) receptors** [2].3. **Dynorphins (Option C):** Derived from **Pro-dynorphin**. These peptides (Dynorphin A and B) have a high affinity for **kappa (κ) receptors** [2] and are involved in spinal cord pain processing and dysphoria.Why other options are incorrect:Options A, B, and C are all correct sub-types of endogenous opioids; therefore, selecting any single one would be incomplete. "All of the above" is the most accurate choice.High-Yield Clinical Pearls for NEET-PG:* **Precursor Mnemonic:** **P**OMC → **E**ndorphins; **P**ro-enkephalin → **E**nkephalins; **P**ro-dynorphin → **D**ynorphins.* **Receptor Selectivity:** * **μ (Mu):** Endorphins > Enkephalins > Dynorphins (Main receptor for analgesia and respiratory depression) [2].* **δ (Delta):** Enkephalins > Endorphins > Dynorphins [2].* **κ (Kappa):** Dynorphins >> Endorphins/Enkephalins (Associated with miosis and dysphoria) [2].* **Nociceptin/Orphanin FQ:** This is a fourth, more recently identified endogenous ligand that acts on the NOP (ORL-1) receptor.

Q: What are the treatments for increased intracranial pressure?

All of the above. **Explanation:** The management of increased intracranial pressure (ICP) involves a multi-modal approach aimed at reducing the volume of the brain parenchyma, cerebrospinal fluid (CSF), or intracranial blood. 1. **Mannitol (Osmotic Diuretic):** This is the gold standard pharmacological treatment. It works via two mechanisms: an immediate **rheological effect** (reducing blood viscosity, which causes reflex vasoconstriction) and a delayed **osmotic effect** (drawing water out of the brain parenchyma into the intravascular space). 2. **Loop Diuretics (e.g., Furosemide):** These are often used as adjuncts to Mannitol. They reduce ICP by decreasing CSF production at the choroid plexus and inducing systemic diuresis, which helps lower overall intravascular volume and potentiates the osmotic gradient created by Mannitol. 3. **Ventriculostomy Catheter (External Ventricular Drain - EVD):** This is the most effective method for immediate ICP reduction. It allows for both the **monitoring** of ICP and the **therapeutic drainage** of CSF to rapidly decrease intracranial volume. **Why "All of the above" is correct:** Effective ICP management requires both medical (Mannitol, Loop diuretics) and surgical/interventional (Ventriculostomy) strategies to stabilize the patient and prevent brain herniation. **High-Yield NEET-PG Pearls:** * **Mannitol Contraindications:** Acute pulmonary edema, severe heart failure, and established anuria. * **Hypertonic Saline (3%):** An increasingly popular alternative to Mannitol, especially in hemodynamically unstable patients. * **Cushing’s Triad (Sign of high ICP):** Hypertension, Bradycardia, and Irregular respirations. * **Positioning:** Head of the bed should be elevated to **30–45 degrees** to facilitate venous drainage.

Q: What is the drug of choice for intractable hiccups?

Chlorpromazine. **Explanation:** **Chlorpromazine (Option D)** is the only FDA-approved medication for the treatment of intractable hiccups (singultus). Intractable hiccups are defined as those lasting more than one month. While the exact pathophysiology of hiccups involves a complex reflex arc (vagus nerve, phrenic nerve, and sympathetic chain), Chlorpromazine is thought to work by antagonizing dopamine (D2) receptors in the hypothalamus and the medullary vomiting center, effectively inhibiting the reflex arc. **Analysis of Incorrect Options:** * **Metoclopramide (Option A):** While sometimes used off-label for hiccups (especially those related to gastric stasis or GERD) due to its prokinetic and central dopamine antagonist properties, it is not the primary drug of choice compared to Chlorpromazine. * **Fluoxetine (Option B):** This is an SSRI used for depression and anxiety. It has no established role in the acute or chronic management of hiccups. * **Selegiline (Option C):** This is a selective MAO-B inhibitor used in Parkinson’s disease. It does not influence the hiccup reflex arc. **High-Yield Clinical Pearls for NEET-PG:** * **First-line for Intractable Hiccups:** Chlorpromazine (Typical Antipsychotic). * **Alternative/Off-label options:** Baclofen (GABA-B agonist) and Gabapentin are frequently used if Chlorpromazine is ineffective or contraindicated. * **Mechanism:** Chlorpromazine belongs to the **Aliphatic Phenothiazine** class, known for high sedation and significant alpha-blocking properties. * **Side Effect Note:** When using Chlorpromazine, clinicians must monitor for hypotension and extrapyramidal symptoms (EPS).

Question 1

Which of the following drugs are used in the management of generalized anxiety disorder?

Accepted Answer

All of the above

Answer

Alprazolam

Answer

Paroxetine

Answer

Venlafaxine

Question 2

Dilantin causes which of the following deficiencies?

Accepted Answer

Folic acid deficiency

Answer

Thiamine deficiency

Answer

Nicotinamide deficiency

Answer

Riboflavin deficiency

Question 3

A patient diagnosed with schizophrenia was prescribed haloperidol for violent behaviour and agitation. On the third day, the patient developed rigidity and was unable to move their neck, with a fixed stare to one side. Which of the following drugs can be used for the treatment of this patient?

Accepted Answer

Promethazine

Answer

Increase dose of haloperidol

Answer

Risperidone

Answer

Diazepam

Question 4

Which of the following is a skeletal muscle relaxant that acts as a central a2 adrenergic agonist?

Accepted Answer

Tizanidine

Answer

Brimonidine

Answer

Chlormezanone

Answer

Quinine

Question 5

GABA reuptake is inhibited by which of the following medications?

Accepted Answer

Tiagabine

Answer

Topiramate

Answer

Felbamate

Answer

Perampanel

Question 6

Regarding phenytoin, all are true except?

Accepted Answer

At lower concentrations, it follows zero-order kinetics

Answer

Potent microsomal enzyme inducer

Answer

Highly protein bound

Answer

With increasing dose, the Vmax increases.

Question 7

Which of the following are endogenous opioid peptides?

Accepted Answer

All of the above

Answer

Enkephalins

Answer

Endorphins

Answer

Dynorphins

Question 8

What are the treatments for increased intracranial pressure?

Accepted Answer

All of the above

Answer

Loop diuretics

Answer

Mannitol

Answer

Ventriculostomy catheter

Question 9

What are the common side effects of fluoxetine?

Accepted Answer

Urinary retention

Answer

Weight gain

Answer

Sweating

Answer

Diarrhoea

Question 10

What is the drug of choice for intractable hiccups?

Accepted Answer

Chlorpromazine

Answer

Metoclopramide

Answer

Fluoxetine

Answer

Selegiline

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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