Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 71: Neuroleptics cause hyperprolactinemia by blocking the effect of which neurotransmitter on pituitary lactotropes?

A. Dopamine (Correct Answer)
B. Glycine
C. Acetylcholine
D. Serotonin

Explanation: **Explanation:** The correct answer is **Dopamine**. **Mechanism of Action:** In the normal physiological state, dopamine acts as the primary **Prolactin Inhibiting Factor (PIF)**. It is secreted by the tuberoinfundibular pathway of the hypothalamus and acts on **D2 receptors** located on the pituitary lactotropes to tonicly inhibit prolactin secretion. Neuroleptics (antipsychotics) work by blocking D2 receptors. When these drugs block D2 receptors in the tuberoinfundibular pathway, the inhibitory effect of dopamine is lost, leading to disinhibition of lactotropes and a subsequent rise in serum prolactin levels (**Hyperprolactinemia**). **Analysis of Incorrect Options:** * **Glycine:** An inhibitory neurotransmitter primarily found in the spinal cord and brainstem; it does not regulate prolactin. * **Acetylcholine:** While involved in various central pathways, it does not play a primary role in the tonic inhibition of prolactin. * **Serotonin:** Generally has a stimulatory effect on prolactin release (via 5-HT receptors), but it is not the neurotransmitter blocked by neuroleptics to cause this specific side effect. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Features:** Hyperprolactinemia manifests as galactorrhea, gynecomastia, amenorrhea, and infertility. * **Drug Specifics:** Typical antipsychotics (e.g., Haloperidol) and the atypical antipsychotic **Risperidone** are most notorious for causing hyperprolactinemia. * **Exceptions:** **Aripiprazole** (a partial D2 agonist) and **Quetiapine** are less likely to cause significant prolactin elevation. * **Treatment:** If a drug must be used to treat hyperprolactinemia, dopamine agonists like **Cabergoline** or Bromocriptine are preferred.

Question 72: Which of the following psychiatric disorders, apart from depression, are selectively treated with serotonin reuptake inhibitors?

A. Phobias
B. Obsessive compulsive disorder
C. Post-traumatic stress disorder
D. All of the above (Correct Answer)

Explanation: Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line pharmacological treatment for a wide spectrum of psychiatric conditions beyond Major Depressive Disorder. Their primary mechanism involves inhibiting the presynaptic reuptake of serotonin (5-HT), thereby increasing its availability in the synaptic cleft and modulating downstream neural circuits involved in anxiety and impulse control. **Explanation of Options:** * **Obsessive-Compulsive Disorder (OCD):** SSRIs (e.g., Fluoxetine, Fluvoxamine, Sertraline) are the gold standard treatment. They typically require higher doses and a longer duration (10–12 weeks) to show efficacy compared to depression. * **Phobias:** SSRIs are highly effective for **Social Anxiety Disorder (Social Phobia)** and Panic Disorder with or without agoraphobia. They help desensitize the "fear circuitry" in the amygdala. * **Post-Traumatic Stress Disorder (PTSD):** SSRIs (specifically Sertraline and Paroxetine) are FDA-approved first-line agents that help manage the core symptoms of re-experiencing, avoidance, and hyperarousal. Since SSRIs are the treatment of choice for all three conditions, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **DOC (Drug of Choice):** SSRIs are the DOC for OCD, PTSD, Panic Disorder, Social Phobia, GAD, and Premenstrual Dysphoric Disorder (PMDD). * **OCD Exception:** While SSRIs are first-line, **Clomipramine** (a TCA) is the most potent drug for OCD but is reserved for second-line due to its side-effect profile. * **Side Effects:** Remember the "S" mnemonic: **S**exual dysfunction (most common long-term side effect), **S**leep disturbances, and **S**tomach upset (nausea/diarrhea). * **Fluoxetine** has the longest half-life, making it least likely to cause withdrawal symptoms.

Question 73: A patient in the emergency department exhibits psychosis. Pharmacological intervention to decrease psychosis would most likely involve which of the following mechanisms?

A. Blockade of dopaminergic neurotransmission (Correct Answer)
B. Stimulation of dopaminergic neurotransmission
C. Blockade of nitrergic neurotransmission
D. Stimulation of nitrergic neurotransmission

Explanation: ### Explanation **1. Why Option A is Correct:** The primary pharmacological management of psychosis is based on the **Dopamine Hypothesis of Schizophrenia**. This hypothesis suggests that psychosis results from overactivity of dopaminergic neurons in the **mesolimbic pathway** of the brain. Antipsychotic drugs (Neuroleptics) work by blocking postsynaptic **D2 receptors**, thereby reducing dopaminergic neurotransmission. Both typical (e.g., Haloperidol) and atypical antipsychotics (e.g., Risperidone) share this fundamental mechanism of D2 receptor antagonism to alleviate positive symptoms like hallucinations and delusions. **2. Why Other Options are Incorrect:** * **Option B:** Stimulating dopaminergic neurotransmission (e.g., using Levodopa or Amphetamines) actually **induces or worsens** psychosis. This is a common side effect seen in Parkinson’s patients treated with dopamine agonists. * **Options C & D:** Nitrergic neurotransmission involves Nitric Oxide (NO). While research is ongoing regarding the role of NO in NMDA receptor signaling and its potential link to schizophrenia, it is **not** the established target for standard emergency pharmacological intervention in psychosis. **3. NEET-PG High-Yield Pearls:** * **Mesolimbic Pathway:** Blockade here leads to the **therapeutic effect** (reduction of positive symptoms). * **Nigrostriatal Pathway:** Blockade here leads to **Extrapyramidal Side Effects (EPS)** like dystonia and parkinsonism. * **Tuberoinfundibular Pathway:** Blockade here leads to **Hyperprolactinemia** (galactorrhea, gynecomastia). * **Mesocortical Pathway:** Low dopamine here is linked to **negative symptoms** (apathy, withdrawal); traditional blockers may worsen these. * **Atypical Antipsychotics:** These also block **5-HT2A receptors**, which helps reduce EPS and improve negative symptoms.

Question 74: Which of the following is NOT a side effect of depression?

A. Propranolol
B. Oral contraceptives
C. L-dopa
D. Flupenthixol (Correct Answer)

Explanation: **Explanation:** The question asks which drug is **NOT** associated with causing depression as a side effect. **1. Why Flupenthixol is the correct answer:** Flupenthixol is a thioxanthene neuroleptic (antipsychotic). While high doses are used to treat schizophrenia, **low doses (0.5–3 mg/day)** have a unique **antidepressant and anxiolytic effect**. Unlike many other antipsychotics that can cause "neuroleptic-induced deficit syndrome" (mimicking depression), low-dose flupenthixol is specifically indicated for the management of psychogenic depression and depressive neurosis. Therefore, it is a treatment for, rather than a cause of, depression. **2. Analysis of Incorrect Options (Drugs that cause depression):** * **Propranolol:** Beta-blockers, particularly lipophilic ones like propranolol, can cross the blood-brain barrier and are well-documented to cause depressive symptoms, fatigue, and sleep disturbances. * **Oral Contraceptives (OCPs):** Hormonal fluctuations caused by OCPs (specifically the progestogen component) are associated with mood swings and clinical depression in susceptible individuals due to interference with tryptophan metabolism. * **L-dopa:** While used for Parkinson’s disease, L-dopa can cause a wide range of psychiatric side effects, including depression, anxiety, and psychosis, as it alters dopamine levels in the mesolimbic pathway. **NEET-PG High-Yield Pearls:** * **Other drugs causing depression:** Reserpine (depletes monoamines), Interferon-alpha, Isotretinoin, and Corticosteroids. * **Reserpine** is the classic historical example used to support the "Monoamine Hypothesis" of depression. * **Flupenthixol** is often used in clinical practice for "masked depression" or depression with psychosomatic symptoms.

Question 75: Which drug can act as an antagonist of Haloperidol?

A. Ropinirole (Correct Answer)
B. Clozapine
C. Imipramine
D. Pimozide

Explanation: ### Explanation **Correct Option: A. Ropinirole** The core concept here is the **Dopaminergic-Antidopaminergic balance**. * **Haloperidol** is a high-potency, first-generation (typical) antipsychotic that acts as a potent **Dopamine D2 receptor antagonist**. It works by blocking dopamine receptors in the brain. * **Ropinirole** is a non-ergoline **Dopamine D2/D3 receptor agonist** [1]. Because they have opposing actions at the same receptor site (one blocks, the other stimulates), Ropinirole acts as a functional and pharmacological antagonist to the effects of Haloperidol. In clinical practice, dopamine agonists are sometimes used to manage the Extrapyramidal Side Effects (EPS) caused by Haloperidol [1]. **Why the other options are incorrect:** * **B. Clozapine:** This is an atypical antipsychotic [2]. While it has a lower affinity for D2 receptors than Haloperidol, it is still a dopamine antagonist (primarily D4 and 5-HT2A). It would synergize with, rather than antagonize, the antipsychotic effects [2]. * **C. Imipramine:** A Tricyclic Antidepressant (TCA) that primarily inhibits the reuptake of Norepinephrine and Serotonin. It does not have a direct antagonistic relationship with Haloperidol’s dopaminergic blockade. * **D. Pimozide:** Like Haloperidol, Pimozide is a typical antipsychotic (diphenylbutylpiperidine class) that blocks D2 receptors. It would enhance the effects of Haloperidol rather than antagonize them. **High-Yield Clinical Pearls for NEET-PG:** * **Drug-Induced Parkinsonism:** Haloperidol-induced rigidity is treated with central anticholinergics (e.g., Benztropine, Trihexyphenidyl) or dopamine agonists (e.g., Amantadine). * **Bromocriptine:** Another dopamine agonist frequently tested as the treatment of choice for **Neuroleptic Malignant Syndrome (NMS)**, a life-threatening reaction to Haloperidol. * **Inverse Relationship:** Remember that drugs used to treat Schizophrenia (antagonists) can cause Parkinsonian symptoms, while drugs used to treat Parkinson’s (agonists like Ropinirole) can cause psychosis.

Question 76: What is the mechanism of action of Selective Serotonin Reuptake Inhibitors (SSRIs)?

A. Inhibit the reuptake of norepinephrine
B. Inhibit the reuptake of norepinephrine and serotonin
C. Inhibit the reuptake of dopamine
D. Inhibit the reuptake of serotonin (Correct Answer)

Explanation: **Explanation:** **Mechanism of Action:** Selective Serotonin Reuptake Inhibitors (SSRIs) work by specifically inhibiting the **Serotonin Transporter (SERT)** located on the presynaptic neuronal membrane. By blocking this transporter, SSRIs prevent the re-entry of serotonin (5-HT) into the presynaptic terminal, thereby increasing the concentration of serotonin available in the synaptic cleft. This enhanced serotonergic neurotransmission is the primary mechanism for their antidepressant and anxiolytic effects. **Analysis of Incorrect Options:** * **Option A:** Inhibition of norepinephrine reuptake is the primary mechanism of **Selective Norepinephrine Reuptake Inhibitors (SNRIs)** like Reboxetine or Atomoxetine. * **Option B:** Inhibition of both norepinephrine and serotonin reuptake is the mechanism of **Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)** (e.g., Venlafaxine, Duloxetine) and **Tricyclic Antidepressants (TCAs)** (e.g., Amitriptyline). * **Option C:** Inhibition of dopamine reuptake is a characteristic of drugs like **Bupropion** (an NDRI) or stimulants like Methylphenidate. **High-Yield Clinical Pearls for NEET-PG:** * **First-line Treatment:** SSRIs are the first-line drugs for Depression, OCD, Panic Disorder, Social Phobia, and PTSD. * **Prototype Drugs:** Fluoxetine (longest half-life), Sertraline, Paroxetine, Fluvoxamine, Citalopram, and Escitalopram (most potent/selective). * **Side Effects:** Most common are GI upset (nausea/diarrhea) and **sexual dysfunction** (delayed ejaculation). * **Serotonin Syndrome:** A dangerous interaction when SSRIs are combined with MAO inhibitors, characterized by hyperthermia, muscle rigidity, and cardiovascular collapse. * **Lag Period:** Clinical improvement typically takes 2–4 weeks despite immediate biochemical effects.

Question 77: Which of the following is a feature of serotonin syndrome associated with SSRIs and MAOIs?

A. Tremors (Correct Answer)
B. Agitation
C. Cardiovascular collapse
D. Hypothermia

Explanation: **Explanation:** Serotonin Syndrome is a potentially life-threatening condition caused by excessive serotonergic activity in the CNS, typically occurring when **SSRIs** are combined with **MAOIs**, TCAs, or Linezolid. It is characterized by a clinical triad of cognitive-behavioral changes, autonomic instability, and neuromuscular excitability. **1. Why Tremors is the correct answer:** Neuromuscular hyperactivity is a hallmark of serotonin syndrome. **Tremors**, along with **clonus** (spontaneous, inducible, or ocular) and **hyperreflexia**, are classic diagnostic features. These symptoms are often more pronounced in the lower extremities. **2. Analysis of Incorrect Options:** * **Agitation:** While agitation is a common symptom of serotonin syndrome, it is a non-specific behavioral change. In the context of standardized exams like NEET-PG, **neuromuscular signs (Tremors/Clonus)** are considered more pathognomonic and specific for identifying the syndrome compared to general agitation. * **Cardiovascular collapse:** This is a terminal complication of severe, untreated cases rather than a primary diagnostic feature. The initial autonomic sign is usually tachycardia or hypertension. * **Hypothermia:** This is incorrect because serotonin syndrome causes **Hyperthermia** (often >41°C in severe cases) due to excessive muscular activity. **High-Yield Clinical Pearls for NEET-PG:** * **Hunter’s Criteria:** The most sensitive diagnostic tool; it emphasizes **Clonus** (spontaneous, inducible, or ocular) as the most important sign. * **Drug of Choice:** Management involves stopping the offending agents and administering **Cyproheptadine** (a 5-HT2A antagonist). * **Differential Diagnosis:** Unlike Neuroleptic Malignant Syndrome (NMS), which presents with "lead-pipe" rigidity and bradyreflexia, Serotonin Syndrome presents with **hyperreflexia and clonus**.

Question 78: Which among the following is not an antipsychotic?

A. Risperidone
B. Haloperidol
C. Fluoxetine (Correct Answer)
D. Clozapine

Explanation: ### Explanation The correct answer is **Fluoxetine** because it belongs to the class of **Selective Serotonin Reuptake Inhibitors (SSRIs)**, which are primarily used as **antidepressants**, not antipsychotics. #### Why Fluoxetine is the Correct Choice: Fluoxetine works by inhibiting the reuptake of serotonin (5-HT) at the presynaptic terminal, increasing serotonin levels in the synaptic cleft. It is a first-line treatment for Major Depressive Disorder (MDD), Obsessive-Compulsive Disorder (OCD), and Panic Disorder. It does not possess the dopamine (D2) receptor antagonism required to treat psychosis. #### Why the Other Options are Incorrect: * **Risperidone (Option A):** An **Atypical (Second-generation) Antipsychotic**. It blocks both D2 and 5-HT2A receptors. It is commonly used for schizophrenia and bipolar mania. * **Haloperidol (Option B):** A **Typical (First-generation) Antipsychotic**. It is a potent D2 receptor antagonist. It is highly effective for positive symptoms of schizophrenia but carries a high risk of Extrapyramidal Side Effects (EPS). * **Clozapine (Option D):** An **Atypical Antipsychotic**. It is the "gold standard" for **treatment-resistant schizophrenia**. It has a low affinity for D2 receptors but acts on various other receptors (D4, 5-HT2A, Alpha, Histamine). #### High-Yield Clinical Pearls for NEET-PG: * **Fluoxetine** has the longest half-life among SSRIs (due to its active metabolite, norfluoxetine), making it the least likely to cause withdrawal syndrome. * **Clozapine** is associated with **agranulocytosis** (requires mandatory WBC monitoring) and lowers the seizure threshold. * **Hyperprolactinemia** is a common side effect of Risperidone and Haloperidol due to D2 blockade in the tuberoinfundibular pathway. * **Drug of choice for OCD:** SSRIs (like Fluoxetine), but in higher doses than used for depression.

Question 79: Cardiac conduction defects seen with Tricyclic antidepressants are due to which mechanism?

A. Norepinephrine and serotonin reuptake inhibition
B. Antimuscarinic action on the heart
C. Only norepinephrine reuptake inhibition
D. Both norepinephrine reuptake inhibition and antimuscarinic action on the heart (Correct Answer)

Explanation: ### Explanation Tricyclic Antidepressants (TCAs) like Amitriptyline and Imipramine have a complex pharmacological profile that affects multiple neurotransmitter systems, leading to significant cardiovascular side effects. **Why Option D is Correct:** The cardiac conduction defects (such as tachycardia and arrhythmias) are a result of a **dual mechanism**: 1. **Norepinephrine (NE) Reuptake Inhibition:** By blocking the NET transporter, TCAs increase the concentration of NE at the cardiac sympathetic synapses. This leads to increased stimulation of $\beta_1$-adrenergic receptors, causing **tachycardia**. 2. **Antimuscarinic Action:** TCAs act as potent antagonists at $M_2$ receptors in the heart. This inhibits the parasympathetic (vagal) "braking" effect on the SA node, further contributing to tachycardia and altered conduction. **Why Other Options are Incorrect:** * **Option A:** While TCAs do inhibit serotonin (5-HT) reuptake, this mechanism is primarily responsible for their antidepressant effect and does not directly contribute to cardiac conduction defects. * **Option B & C:** These are incomplete. The cardiotoxicity of TCAs is synergistic; focusing on only one mechanism ignores the significant contribution of the other. **High-Yield Clinical Pearls for NEET-PG:** * **The "3 C’s" of TCA Overdose:** **C**oma, **C**onvulsions, and **C**ardiotoxicity. * **ECG Changes:** The most characteristic ECG finding in TCA toxicity is **QRS widening** (>100 ms) and **QT prolongation**. This is primarily due to their "Quinidine-like" effect (blockade of fast sodium channels). * **Antidote:** The drug of choice for TCA-induced arrhythmias is **Intravenous Sodium Bicarbonate**, which increases extracellular sodium and blood pH, helping to displace the drug from sodium channels.

Question 80: Venlafaxine inhibits the reuptake of which neurotransmitters?

A. Norepinephrine
B. Norepinephrine and serotonin (Correct Answer)
C. Serotonin
D. None of the above

Explanation: **Explanation:** Venlafaxine is the prototype drug of the **Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)** class. Its primary mechanism of action involves the potent inhibition of the neuronal reuptake of both **serotonin (5-HT)** and **norepinephrine (NE)**. By blocking these transporters (SERT and NET), venlafaxine increases the synaptic concentration of these neurotransmitters, leading to enhanced neurotransmission. * **Why Option B is Correct:** Venlafaxine has a dual mechanism. At lower doses, it primarily inhibits serotonin reuptake (similar to SSRIs), but as the dose increases, its inhibitory effect on norepinephrine reuptake becomes clinically significant. At very high doses, it also weakly inhibits dopamine reuptake. * **Why Option A is Incorrect:** While it does inhibit NE reuptake, selecting only NE ignores its potent effect on serotonin. Pure norepinephrine reuptake inhibitors (NRIs) include drugs like **Reboxetine**. * **Why Option C is Incorrect:** This describes **SSRIs** (e.g., Fluoxetine, Sertraline). While Venlafaxine acts on serotonin, its classification and clinical utility depend on its additional effect on norepinephrine. **High-Yield Clinical Pearls for NEET-PG:** 1. **Dose-Dependent Blood Pressure:** A unique side effect of Venlafaxine (due to its NE effect) is **dose-dependent hypertension**. Regular BP monitoring is mandatory at higher doses. 2. **Indications:** Apart from Major Depressive Disorder, SNRIs are first-line for **Generalized Anxiety Disorder (GAD)** and chronic pain conditions like **Diabetic Neuropathy** and **Fibromyalgia** (especially Duloxetine). 3. **Desvenlafaxine:** This is the active metabolite of venlafaxine and is also used clinically. 4. **Withdrawal:** Venlafaxine is notorious for a severe "discontinuation syndrome" if stopped abruptly due to its short half-life.

Practice by Chapter

Antipsychotics: Typical and Atypical

Practice Questions

Antidepressants: SSRIs and SNRIs

Practice Questions

Tricyclic Antidepressants

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MAO Inhibitors

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Mood Stabilizers

Practice Questions

Anxiolytics

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Drugs for ADHD

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Drugs for Sleep Disorders

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Drugs for Dementia

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Drug-Induced Psychiatric Symptoms

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