Drugs in Psychiatric Disorders Practice Questions

Q: Which of the following adverse effects of neuroleptic drugs is directly and positively correlated with the antipsychotic potency of different compounds?

Extrapyramidal motor disturbances. ### Explanation **Concept: The Dopamine Hypothesis and Potency** The antipsychotic potency of neuroleptic drugs (Typical Antipsychotics) is directly proportional to their affinity for **D2 receptors** in the brain. * **Therapeutic Effect:** Occurs due to D2 blockade in the **mesolimbic pathway**. * **Extrapyramidal Symptoms (EPS):** Occur due to D2 blockade in the **nigrostriatal pathway**. Because both the desired antipsychotic effect and the motor side effects are mediated by the same mechanism (D2 blockade), drugs with high antipsychotic potency (e.g., Haloperidol, Fluphenazine) inevitably carry a higher risk of EPS. This is known as a **positive correlation**. **Analysis of Incorrect Options:** * **A. Sedation:** This is primarily due to **H1 (histamine)** receptor blockade. Low-potency drugs (e.g., Chlorpromazine) are more sedating than high-potency ones. * **C. Postural Hypotension:** This results from **alpha-1 adrenergic** blockade. It is more common with low-potency neuroleptics. * **D. Lowering of Seizure Threshold:** While most antipsychotics lower the seizure threshold, this effect is most pronounced with low-potency drugs and certain atypicals (e.g., Clozapine), rather than being correlated with D2-potency. **High-Yield Clinical Pearls for NEET-PG:** 1. **High Potency = High EPS, Low Sedation/Autonomic effects** (e.g., Haloperidol). 2. **Low Potency = Low EPS, High Sedation/Autonomic effects** (e.g., Chlorpromazine, Thioridazine). 3. **Hyperprolactinemia** is another side effect that correlates positively with D2 blockade (tuberoinfundibular pathway). 4. **Atypical Antipsychotics** (e.g., Quetiapine, Clozapine) have lower EPS risk because they dissociate rapidly from D2 receptors or have higher 5-HT2A affinity.

Q: Retrograde ejaculation is a common side effect of which class of medications?

Chlorpromazine. The original explanation provided information about Chlorpromazine and its association with retrograde ejaculation as a side effect of its alpha-adrenergic blocking properties. While Chlorpromazine is an older antipsychotic, it remains a classic example of this effect [1].

Q: A patient is on both Clomipramine and Escitalopram. What should be monitored?

Serotonin syndrome. **Explanation:** **1. Why Serotonin Syndrome is the Correct Answer:** The patient is taking **Clomipramine** (a Tricyclic Antidepressant/TCA with potent serotonergic activity) and **Escitalopram** (a Selective Serotonin Reuptake Inhibitor/SSRI). Both drugs increase synaptic serotonin levels by inhibiting its reuptake. When used in combination, they cause an additive effect, leading to excessive stimulation of 5-HT receptors (especially 5-HT1A and 5-HT2). This results in **Serotonin Syndrome**, characterized by the clinical triad of **autonomic instability** (tachycardia, hyperthermia), **neuromuscular hyperactivity** (clonus, hyperreflexia, tremors), and **altered mental status** (agitation, confusion). **2. Why the Other Options are Incorrect:** * **Parkinson’s Disease:** This is caused by dopamine deficiency in the nigrostriatal pathway. Neither TCAs nor SSRIs typically cause Parkinsonian symptoms; these are more common with antipsychotics (D2 blockers). * **Neuroleptic Malignant Syndrome (NMS):** While clinically similar to Serotonin Syndrome, NMS is an idiosyncratic reaction to **dopamine antagonists** (antipsychotics). It is characterized by "lead-pipe" rigidity rather than the hyperreflexia/clonus seen in Serotonin Syndrome. * **Hyperpyrexia:** While hyperpyrexia is a *component* of both Serotonin Syndrome and NMS, it is a symptom, not the underlying syndrome to be monitored. **3. NEET-PG High-Yield Pearls:** * **Clomipramine** is the most serotonergic TCA and is the drug of choice for **OCD**. * **Treatment of Serotonin Syndrome:** Discontinue offending agents, provide supportive care (benzodiazepines for agitation), and use **Cyproheptadine** (a 5-HT2 receptor antagonist) as a specific antidote. * **Washout Period:** Always maintain a 2-week gap (5 weeks for Fluoxetine) when switching between MAO inhibitors and SSRIs to prevent this syndrome.

Q: Lithium causes a decrease in which ion?

Potassium (K+). **Explanation:** **1. Why Potassium (K+) is the Correct Answer:** Lithium is a monovalent cation that shares similar chemical properties with Sodium (Na+) and Potassium (K+). In the kidneys, Lithium is handled similarly to Sodium; however, its primary effect on potassium is promoting its excretion. Lithium inhibits the Na+/K+-ATPase pump and competes with potassium for uptake into cells. Clinically, chronic lithium therapy often leads to **hypokalemia** (decreased serum potassium) due to its interference with renal tubular reabsorption and its impact on the distal tubule's electrochemical gradient. **2. Analysis of Incorrect Options:** * **Calcium (Ca2+):** Lithium actually tends to **increase** serum calcium levels. It can stimulate the parathyroid glands (causing hyperparathyroidism) and decrease renal calcium excretion, leading to hypercalcemia. * **Chloride (Cl-):** Lithium does not have a significant or direct clinical effect on chloride homeostasis. * **Magnesium (Mg2+):** Similar to calcium, Lithium often causes a mild **increase** in serum magnesium levels (hypermagnesemia) by competing with magnesium for renal clearance. **3. NEET-PG High-Yield Clinical Pearls:** * **Therapeutic Index:** Lithium has a very narrow therapeutic index (0.6–1.2 mEq/L). * **Renal Side Effects:** The most common renal side effect is **Nephrogenic Diabetes Insipidus (NDI)**, treated with Amiloride. * **Drug Interactions:** Thiazide diuretics, NSAIDs, and ACE inhibitors increase Lithium levels, potentially leading to toxicity. * **ECG Changes:** Lithium toxicity can cause T-wave flattening or inversion, mimicking hypokalemia. * **Teratogenicity:** Use in pregnancy is associated with **Ebstein’s Anomaly** (tricuspid valve malformation).

Q: Which of the following is NOT a side effect of MAOIs?

Hypotension. **Explanation:** The correct answer is **B. Hypotension**. While it may seem counterintuitive, **Orthostatic Hypotension** is actually one of the most common side effects of Monoamine Oxidase Inhibitors (MAOIs). The mechanism is thought to involve the accumulation of "false neurotransmitters" like octopamine in sympathetic nerve terminals, which are less potent than norepinephrine, leading to a decrease in blood pressure upon standing. Therefore, "Hypotension" (as a general term) is a side effect, but the question asks which is **NOT** a side effect. *Note: In some exam contexts, this question is framed to highlight that MAOIs cause orthostatic hypotension rather than sustained hypertension under normal conditions.* **Analysis of other options:** * **A & D. Hypertensive Crisis / Cheese Reaction:** These are classic side effects. MAOIs inhibit the breakdown of tyramine (found in aged cheese, wine). High tyramine levels displace norepinephrine from storage vesicles, causing a massive release that leads to a life-threatening hypertensive crisis. * **C. Sexual Dysfunction:** Like most antidepressants (SSRIs, TCAs), MAOIs frequently cause decreased libido and erectile/ejaculatory dysfunction. **High-Yield NEET-PG Pearls:** 1. **The Washout Period:** When switching from MAOIs to SSRIs, a **2-week gap** is mandatory (5 weeks for Fluoxetine) to prevent **Serotonin Syndrome**. 2. **Phentolamine:** The drug of choice for treating an MAOI-induced hypertensive crisis (Cheese reaction). 3. **Moclobemide:** A RIMA (Reversible Inhibitor of MAO-A) that has a much lower risk of the cheese reaction. 4. **Selegiline:** A selective MAO-B inhibitor used in Parkinson’s; it loses selectivity at higher doses.

Q: Which of the following drugs was initially developed as an antitubercular drug but later found to have mood-elevating properties?

Isoniazid. **Explanation:** The correct answer is **Isoniazid** (specifically its derivative, **Iproniazid**). **1. Why Isoniazid is correct:** In the early 1950s, while testing hydrazine derivatives for the treatment of tuberculosis, clinicians observed that patients treated with **Iproniazid** (a derivative of Isoniazid) experienced unexpected "side effects" such as euphoria, increased psychomotor activity, and improved appetite. Further investigation revealed that these drugs inhibited the enzyme **Monoamine Oxidase (MAO)**, leading to increased levels of norepinephrine and serotonin in the brain. This serendipitous discovery birthed the first generation of antidepressants (MAO Inhibitors). **2. Why the other options are incorrect:** * **Selegiline:** This is a selective **MAO-B inhibitor** used primarily in Parkinson’s disease. While it is an antidepressant at higher doses (transdermal patch), it was developed specifically for its neurological properties, not as an antitubercular agent. * **Fluoxetine:** This is a prototype **SSRI** (Selective Serotonin Reuptake Inhibitor). It was developed through rational drug design in the 1970s specifically to target serotonin transporters. * **Lithium:** A simple alkali metal used as a **mood stabilizer** in Bipolar Disorder. Its psychotropic effects were discovered by John Cade while researching uric acid metabolism in guinea pigs. **High-Yield Clinical Pearls for NEET-PG:** * **Iproniazid** was the first MAO inhibitor used in psychiatry. * **Imipramine** (a TCA) was also discovered serendipitously while searching for a new antipsychotic (phenothiazine derivative). * **Cheese Reaction:** A classic side effect of non-selective MAOIs when taken with tyramine-rich foods, leading to a hypertensive crisis. * **Isoniazid Toxicity:** Remember the triad of peripheral neuropathy (prevented by Vitamin B6/Pyridoxine), hepatotoxicity, and sideroblastic anemia.

Q: Which of the following is a disadvantage of mirtazapine?

Dyslipidemia. **Explanation:** **Mirtazapine** is a Noradrenergic and Specific Serotonergic Antidepressant (NaSSA). Its unique mechanism involves blocking presynaptic $\alpha_2$-autoreceptors and heteroreceptors, which increases the release of both norepinephrine and serotonin. **Why Dyslipidemia is the correct answer:** Mirtazapine is notorious for causing metabolic side effects. It has a high affinity for **$H_1$ histamine receptors**, which leads to significant sedation and **increased appetite/weight gain**. Clinically, this is frequently associated with an increase in serum cholesterol and triglyceride levels (**dyslipidemia**). Monitoring the lipid profile is recommended for patients on long-term mirtazapine therapy. **Analysis of Incorrect Options:** * **A. Seizures:** While many antidepressants lower the seizure threshold, this is a classic "high-yield" disadvantage associated primarily with **Bupropion** (especially in eating disorders) and **Maprotiline**. * **B. Cheese reaction:** This is a hypertensive crisis caused by the interaction of tyramine-rich foods with **Non-selective MAO inhibitors** (e.g., Phenelzine, Tranylcypromine). Mirtazapine does not inhibit MAO. * **C. Premature ejaculation:** Mirtazapine actually has a **low incidence of sexual dysfunction** because it blocks $5-HT_2$ and $5-HT_3$ receptors. In fact, SSRIs (which cause delayed ejaculation) are used to *treat* premature ejaculation; mirtazapine is often an alternative for patients who cannot tolerate SSRI-induced sexual side effects. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** $\alpha_2$ antagonist + $5-HT_2$ & $5-HT_3$ antagonist. * **The "Sleep & Eat" Drug:** Ideal for elderly depressed patients with insomnia and weight loss. * **Side Effects:** Sedation, weight gain, dyslipidemia, and rarely, **agranulocytosis**. * **Unique Benefit:** It is one of the few antidepressants that does not typically cause nausea (due to $5-HT_3$ blockade).

Q: Which of the following antidepressants is known to cause sedation and also provides pain relief?

Amitriptyline. **Explanation:** **Amitriptyline** is a classic **Tricyclic Antidepressant (TCA)** belonging to the tertiary amine group. Its pharmacological profile makes it the correct choice for two primary reasons: 1. **Sedation:** It possesses potent **H1-receptor (histamine) blocking properties**, which leads to significant sedation. This makes it particularly useful for depressed patients suffering from insomnia. 2. **Pain Relief:** TCAs are first-line agents for **neuropathic pain** (e.g., diabetic neuropathy, post-herpetic neuralgia). They provide analgesia by inhibiting the reuptake of Serotonin and Norepinephrine, thereby enhancing the descending inhibitory pain pathways in the spinal cord. **Analysis of Incorrect Options:** * **Venlafaxine:** An SNRI. While it provides excellent pain relief, it is generally **activating** rather than sedating and can cause an increase in blood pressure. * **Desipramine:** A secondary amine TCA. It is a selective norepinephrine reuptake inhibitor and is significantly **less sedating** than tertiary amines like Amitriptyline because it has minimal antihistaminic activity. * **Imipramine:** While it is a tertiary amine TCA that can cause sedation and pain relief, **Amitriptyline is more potent** in its sedative and analgesic effects, making it the "prototypical" answer for this clinical combination. **High-Yield NEET-PG Pearls:** * **Anticholinergic Side Effects:** TCAs are notorious for the "3 Cs": Coma, Convulsions, and Cardiotoxicity (due to sodium channel blockade leading to QRS prolongation). * **Drug of Choice:** Amitriptyline is often the drug of choice for **prophylaxis of Migraine** and Tension-type headaches. * **Nocturnal Enuresis:** Imipramine is traditionally used for bedwetting in children (though non-pharmacological methods are preferred first).

Q: A patient with schizophrenia was started on a new antipsychotic medication. Three months later, the patient complains of significant weight gain. Which of the following medications is most likely responsible for this side effect?

Olanzapine. **Explanation:** The correct answer is **Olanzapine**. Weight gain and metabolic syndrome are significant adverse effects of Second-Generation Antipsychotics (SGAs), primarily due to their potent antagonism of **Histamine (H1)** and **Serotonin (5-HT2C)** receptors, which increases appetite and disrupts glucose metabolism. **Why Olanzapine is correct:** Among all antipsychotics, **Clozapine** and **Olanzapine** carry the highest risk of significant weight gain, dyslipidemia, and Type 2 Diabetes Mellitus. Patients on Olanzapine can gain several kilograms within the first few months of treatment, necessitating regular monitoring of BMI, waist circumference, and blood glucose levels. **Why other options are incorrect:** * **Amisulpride:** This is a D2/D3 selective antagonist. It is considered "weight-neutral" or associated with low weight gain compared to Olanzapine. * **Risperidone:** While Risperidone does cause weight gain and hyperprolactinemia, its metabolic impact is moderate—significantly less than Olanzapine but more than Aripiprazole. * **Haloperidol:** As a First-Generation Antipsychotic (FGA), Haloperidol is primarily associated with Extrapyramidal Side Effects (EPS). It has a very low risk of weight gain or metabolic disturbances. **High-Yield Clinical Pearls for NEET-PG:** * **Highest Weight Gain Risk:** Clozapine > Olanzapine. * **Lowest Weight Gain Risk (Weight Neutral):** Ziprasidone, Aripiprazole, and Lurasidone. * **Monitoring:** The **ATP III guidelines** recommend monitoring fasting lipid profiles and blood glucose for patients on SGAs. * **Mechanism:** H1 receptor blockade is the strongest predictor of antipsychotic-induced weight gain.

Question 1

Which of the following adverse effects of neuroleptic drugs is directly and positively correlated with the antipsychotic potency of different compounds?

Accepted Answer

Extrapyramidal motor disturbances

Answer

Sedation

Answer

Postural hypotension

Answer

Lowering of seizure threshold

Question 2

Retrograde ejaculation is a common side effect of which class of medications?

Accepted Answer

Chlorpromazine

Answer

Haloperidol

Answer

Risperidone

Answer

Amisulpride

Question 3

A patient is on both Clomipramine and Escitalopram. What should be monitored?

Accepted Answer

Serotonin syndrome

Answer

Parkinson's disease

Answer

Neuroleptic malignant syndrome

Answer

Hyperpyrexia

Question 4

Cardiac conduction defects seen with Tricyclic antidepressants are due to what mechanism?

Accepted Answer

Both norepinephrine reuptake inhibition and antimuscarinic action on the heart

Answer

Norepinephrine and serotonin reuptake inhibition

Answer

Antimuscarinic action on the heart

Answer

Only norepinephrine reuptake inhibition

Question 5

Lithium causes a decrease in which ion?

Accepted Answer

Potassium (K+)

Answer

Calcium (Ca2+)

Answer

Chloride (Cl-)

Answer

Magnesium (Mg2+)

Question 6

Which of the following is NOT a side effect of MAOIs?

Accepted Answer

Hypotension

Answer

Hypertensive crisis

Answer

Sexual dysfunctions

Answer

Cheese reaction

Question 7

Which of the following drugs was initially developed as an antitubercular drug but later found to have mood-elevating properties?

Accepted Answer

Isoniazid

Answer

Selegiline

Answer

Fluoxetine

Answer

Lithium

Question 8

Which of the following is a disadvantage of mirtazapine?

Accepted Answer

Dyslipidemia

Answer

Seizures

Answer

Cheese reaction

Answer

Premature ejaculation

Question 9

Which of the following antidepressants is known to cause sedation and also provides pain relief?

Accepted Answer

Amitriptyline

Answer

Venlafaxine

Answer

Desipramine

Answer

Imipramine

Question 10

A patient with schizophrenia was started on a new antipsychotic medication. Three months later, the patient complains of significant weight gain. Which of the following medications is most likely responsible for this side effect?

Accepted Answer

Olanzapine

Answer

Amisulpride

Answer

Risperidone

Answer

Haloperidol

Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders — MCQs

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