Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 321: What is the mechanism of action of buspirone?

A. Antagonism at the 5-HT1B receptor.
B. Antagonism at the 5-HT2C receptor.
C. Partial agonism at the 5-HT1B receptor.
D. Partial agonism at the 5-HT1A receptor. (Correct Answer)

Explanation: ***Partial agonism at the 5-HT1A receptor.*** - Buspirone is known to act primarily as a **partial agonist** at the **serotonin 5-HT1A receptor**, which is responsible for its anxiolytic effects. - This action helps to modulate serotonin neurotransmission, leading to a reduction in anxiety symptoms without significant sedative or addictive properties. *Antagonism at the 5-HT1B receptor.* - While 5-HT1B receptors are involved in serotonin regulation, buspirone's primary anxiolytic effect is not mediated through **antagonism** at these receptors. - Antagonism at 5-HT1B receptors is not a prominent mechanism for typical anxiolytic medications like buspirone. *Antagonism at the 5-HT2C receptor.* - **Antagonism at the 5-HT2C receptor** is sometimes associated with **atypical antipsychotics** and their metabolic side effects, but it is not the primary mechanism of action for buspirone. - Buspirone is not generally considered an antipsychotic and its effects are distinct from those driven by 5-HT2C antagonism. *Partial agonism at the 5-HT1B receptor.* - Buspirone's main anxiolytic action is distinctly linked to the **5-HT1A receptor**, not the 5-HT1B receptor. - Although serotonin receptors are numerous and complex, buspirone's specific therapeutic profile arises from its interaction with 5-HT1A.

Question 322: Which of the following typical antipsychotic drugs is least commonly used in depot form?

A. Haloperidol
B. Fluphenazine
C. Chlorpromazine (Correct Answer)
D. Trifluoperazine

Explanation: ***Chlorpromazine*** - Chlorpromazine is a **typical antipsychotic** that is **NOT available in depot form** for clinical use. - It is available only in **oral** and **short-acting injectable** formulations, making it the **least commonly used in depot form** among the options listed. - Its high sedative properties, orthostatic hypotension risk, and pharmacokinetic profile make it unsuitable for long-acting depot formulation. *Haloperidol* - **Haloperidol decanoate** is one of the **most widely used depot formulations** of typical antipsychotics. - Administered intramuscularly every **3-4 weeks**, it is highly effective for **long-term maintenance treatment** in schizophrenia. - Its favorable pharmacokinetic profile makes it ideal for depot preparation. *Fluphenazine* - **Fluphenazine decanoate** and **fluphenazine enanthate** are **well-established depot preparations** with decades of clinical use. - These formulations allow for dosing every **2-4 weeks**, significantly improving **medication adherence** in chronic psychotic disorders. - Fluphenazine depot is a first-line option for long-acting injectable antipsychotic therapy. *Trifluoperazine* - Trifluoperazine is primarily available and used as an **oral medication** for maintenance therapy. - While some limited depot formulations have been reported in older literature, they are **not commonly used in clinical practice**. - However, it is still more available in depot form than chlorpromazine, which has essentially **no depot use**.

Question 323: Which drug is not considered a mood stabilizer?

A. Lithium
B. Lamotrigine
C. Imipramine (Correct Answer)
D. Carbamazepine

Explanation: ***Imipramine*** - Imipramine is a **tricyclic antidepressant (TCA)**, primarily used to treat depression, not to stabilize mood in bipolar disorder. - TCAs can sometimes induce **mania** or hypomania in individuals with bipolar disorder, thus they are generally not used as monotherapy for mood stabilization. *Lithium* - **Lithium** is considered the gold standard and one of the oldest and most effective **mood stabilizers** for bipolar disorder. - It works by modulating **neurotransmitter systems** and second messenger pathways in the brain. *Lamotrigine* - **Lamotrigine** is an **anticonvulsant** medication that is also recognized as an effective **mood stabilizer**, particularly for preventing depressive episodes in bipolar disorder. - Its mechanism involves stabilizing neuronal membranes by blocking **voltage-gated sodium channels**. *Carbamazepine* - **Carbamazepine** is an **anticonvulsant** medication often used as a **mood stabilizer** for the treatment of acute manic and mixed episodes in bipolar disorder. - It works by reducing the excitability of nerve impulses through blocking **voltage-sensitive sodium channels**.

Question 324: Which of the following actions is NOT associated with tricyclic antidepressants?

A. Block 5-HT or NE reuptake
B. Anticholinergic action
C. MAO inhibition (Correct Answer)
D. Causes sedation

Explanation: ***MAO inhibition*** - Tricyclic antidepressants (TCAs) primarily exert their effects by inhibiting the reuptake of **norepinephrine** and **serotonin**, not by inhibiting monoamine oxidase (MAO). - **MAO inhibitors** are a distinct class of antidepressants with a different mechanism of action and side effect profile. *Anticholinergic action* - Many TCAs have significant **anticholinergic effects**, blocking muscarinic receptors and leading to side effects like dry mouth, constipation, and blurred vision. - These effects contribute to the **adverse event profile** of TCAs, especially in elderly patients. *Block 5-HT or NE reuptake* - The primary mechanism of action of TCAs involves the **inhibition of serotonin (5-HT)** and **norepinephrine (NE) reuptake** into presynaptic neurons. - This action increases the concentration of these neurotransmitters in the **synaptic cleft**, thereby potentiating their effects. *Causes sedation* - TCAs frequently cause **sedation**, particularly the more histaminergic ones (e.g., amitriptyline, doxepin), due to their **histamine H1 receptor antagonism**. - This side effect can be beneficial for patients with insomnia but can be problematic for daytime functioning.

Question 325: What is the mechanism of action of duloxetine?

A. Selective serotonin reuptake inhibition
B. Selective norepinephrine reuptake inhibition
C. Inhibition of both serotonin and norepinephrine reuptake (Correct Answer)
D. No effect on neurotransmitter reuptake

Explanation: ***Inhibition of both serotonin and norepinephrine reuptake*** - **Duloxetine** is a **serotonin-norepinephrine reuptake inhibitor (SNRI)**, meaning it blocks the reuptake of both neurotransmitters, increasing their concentrations in the synaptic cleft [2]. - This dual action contributes to its efficacy in treating **depression**, **anxiety disorders**, and **neuropathic pain** [2], [3]. *Selective serotonin reuptake inhibition* - This describes the mechanism of **SSRIs (Selective Serotonin Reuptake Inhibitors)**, such as fluoxetine or sertraline, which primarily target serotonin [1]. - Duloxetine's mechanism is broader, affecting both serotonin and norepinephrine [2]. *Selective norepinephrine reuptake inhibition* - This mechanism is characteristic of medications like **atomoxetine**, used for ADHD, which primarily targets norepinephrine. - Duloxetine has a dual action, not selective to norepinephrine alone. *No effect on neurotransmitter reuptake* - Medications with no effect on neurotransmitter reuptake would not typically be effective as antidepressants or treatments for neuropathic pain. - Duloxetine's therapeutic effects are directly linked to its inhibition of reuptake for both serotonin and norepinephrine [2], [4].

Question 326: Most common renal sequela of lithium toxicity is?

A. Renal tubular acidosis
B. Glycosuria
C. MPGN
D. Nephrogenic Diabetes Insipidus (Correct Answer)

Explanation: ***Nephrogenic Diabetes Insipidus*** - **Lithium** interferes with the action of **ADH** on the renal tubules, specifically at the **collecting ducts**, leading to an inability to concentrate urine. - This results in **polyuria** (excessive urination) and **polydipsia** (excessive thirst), characteristic symptoms of **nephrogenic diabetes insipidus**. *Renal tubular acidosis* - While lithium can affect tubular function, **renal tubular acidosis** is less common than nephrogenic diabetes insipidus. - RTA involves impaired acid excretion or bicarbonate reabsorption, leading to **metabolic acidosis**. *Glycosuria* - **Glycosuria** (glucose in urine) is primarily associated with **diabetes mellitus** or other conditions affecting glucose reabsorption in the proximal tubule. - Lithium toxicity does not typically cause glycosuria. *MPGN* - **Membranoproliferative glomerulonephritis (MPGN)** is a type of glomerular injury characterized by specific changes in the glomerulus. - MPGN is not directly caused by **lithium toxicity**; lithium primarily affects tubular function rather than glomerular structure.

Question 327: Which of the following is the most characteristic sexual side effect of SSRIs?

A. Retrograde ejaculation
B. Erectile dysfunction
C. Delayed ejaculation (Correct Answer)
D. Anxiety

Explanation: ***Delayed ejaculation*** - **Delayed ejaculation** is a common and characteristic sexual side effect of SSRIs due to their impact on serotonin pathways involved in sexual response. - This effect can lead to significant distress and non-adherence to treatment, and often requires dose adjustment or switching to an alternative antidepressant. *Erectile dysfunction* - While **erectile dysfunction** can occur with SSRIs, it is a less specific and less consistently reported sexual side effect compared to ejaculatory dysfunction. - Many factors, including underlying mood disorder and comorbidities, can contribute to erectile dysfunction, making it less characteristic of SSRI use alone. *Retrograde ejaculation* - **Retrograde ejaculation** is a condition where semen enters the bladder during orgasm, and while it can be a side effect of some medications (e.g., alpha-blockers), it is not a hallmark sexual side effect of SSRIs. - SSRIs primarily affect the process of emission and expulsion, leading more commonly to delayed or absent ejaculation rather than retrograde flow. *Anxiety* - **Anxiety** is generally a *primary symptom* of the conditions SSRIs are prescribed to treat, such as depression or anxiety disorders, not a sexual side effect of the medication itself. - Although SSRIs can initially cause or worsen anxiety in some patients before therapeutic effects are seen, this is a systemic side effect, not a sexual one.

Question 328: At which receptor is the primary action of antipsychotic medications required?

A. M, muscarinic
B. 5HT4 serotonergic
C. D1 dopaminergic
D. D2 dopaminergic (Correct Answer)

Explanation: ***D2 dopaminergic*** - The **antipsychotic effects** of typical (first-generation) antipsychotics are primarily mediated through **D2 receptor blockade** [1]. - Blocking D2 receptors in the **mesolimbic pathway** helps reduce positive symptoms of psychosis like hallucinations and delusions [2]. *M, muscarinic* - **Muscarinic receptor blockade** is a common adverse effect of some antipsychotics, leading to anticholinergic side effects such as **dry mouth** and **blurred vision**, rather than their primary therapeutic action. - This action does not directly contribute to the antipsychotic effect. *D1 dopaminergic* - While D1 receptors are involved in dopamine signaling, they are **not the primary target** for the antipsychotic action of most drugs [1]. - Some atypical antipsychotics may affect D1 receptors, but it's secondary to their D2 antagonism and serotonin modulation. *5HT4 serotonergic* - **Serotonin receptors (5HT)**, particularly 5HT2A, are important targets for atypical (second-generation) antipsychotics. - However, 5HT4 receptors are **not a primary target** for the antipsychotic effects, and 5HT2A blockade modulates dopamine release, which is still connected to the D2 hypothesis.

Question 329: Which of the following is a classic tricyclic antidepressant (TCA) commonly used as the prototype for the class?

A. Amitriptyline (Correct Answer)
B. Citalopram
C. Venlafaxine
D. Nortriptyline

Explanation: ***Amitriptyline*** - **Amitriptyline** is a classic tricyclic antidepressant (TCA) and is widely recognized for its use in treating depression, neuropathic pain, and migraine prophylaxis. Its characteristic side effect profile, including **anticholinergic effects** and **sedation**, is well-known. - It is one of the **oldest and most frequently prescribed TCAs**, making it a common reference point in pharmacology and clinical practice. *Citalopram* - **Citalopram** is an **SSRI** (selective serotonin reuptake inhibitor), not a TCA. It works by selectively inhibiting the reuptake of serotonin. - It has a different side effect profile compared to TCAs, generally with fewer anticholinergic and cardiovascular effects. *Venlafaxine* - **Venlafaxine** is an **SNRI** (serotonin-norepinephrine reuptake inhibitor), not a TCA. It inhibits the reuptake of both serotonin and norepinephrine. - It has efficacy in treating depression and anxiety disorders, but its mechanism of action is distinct from TCAs. *Nortriptyline* - **Nortriptyline** is indeed a TCA, specifically a **secondary amine TCA**, which is an active metabolite of amitriptyline. - While it is a TCA, amitriptyline is generally more broadly recognized and used as the prototype for the class, with nortriptyline often being highlighted for its slightly better tolerability profile (e.g., less sedation, less orthostatic hypotension) compared to tertiary amine TCAs like amitriptyline.

Question 330: Lithium directly affects which ion ?

A. Sodium (Correct Answer)
B. Potassium
C. Magnesium
D. Calcium

Explanation: ***Sodium*** - Lithium directly interferes with **sodium ion transport** across cell membranes, particularly by inhibiting the **Na+/K+-ATPase** pump. - This interference alters intracellular sodium concentrations and affects neural excitability, contributing to its **mood-stabilizing** effects. *Potassium* - While potassium transport is linked to the **Na+/K+-ATPase pump**, lithium primarily acts through its effect on **sodium transport**, rather than directly mimicking or significantly altering potassium. - Changes in potassium levels due to lithium are largely secondary to its primary impact on sodium. *Magnesium* - Lithium has a more direct impact on **sodium channels** and transporters, contrasting with its less direct or significant interaction with magnesium metabolism. - Though magnesium is crucial for numerous cellular processes, it is not the primary ion directly affected by lithium's therapeutic actions. *Calcium* - Lithium does not directly affect **calcium channels** or calcium signaling pathways in the same way it impacts sodium. - While lithium may indirectly influence calcium-dependent processes, its primary direct target for therapeutic effects is not calcium.

Practice by Chapter

Antipsychotics: Typical and Atypical

Practice Questions

Antidepressants: SSRIs and SNRIs

Practice Questions

Tricyclic Antidepressants

Practice Questions

MAO Inhibitors

Practice Questions

Mood Stabilizers

Practice Questions

Anxiolytics

Practice Questions

Drugs for ADHD

Practice Questions

Drugs for Sleep Disorders

Practice Questions

Drugs for Dementia

Practice Questions

Drug-Induced Psychiatric Symptoms

Practice Questions

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