Anxiolytics — MCQs
Antidote for benzodiazepine poisoning: FMGE 10, 13; NEET 14
Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?
A patient on SSRI sertraline was also prescribed amitriptyline and subsequently developed serotonin toxicity. What is the likely treatment for serotonin toxicity?
What is the primary therapeutic use of 5-HT1B/1D agonists?
What is the drug of choice for rapid relief of an acute panic attack?
Match the following: Column A: a. Beta 1 b. Beta 2 c. Beta 3 Column B: 1. Mirabegron 2. Betaxolol 3. Salbutamol
Which anti-epileptic drug marked X will act at the site shown?
Atropine is not an antidote in:
Which of the following is the most characteristic sexual side effect of SSRIs?
Which of the following antidepressants is least likely to have sexual side effects?
Anxiolytics Indian Medical PG Practice Questions and MCQs
Question 1: Antidote for benzodiazepine poisoning: FMGE 10, 13; NEET 14
- A. Flumazenil (Correct Answer)
- B. Naloxone
- C. Atropine
- D. N-acetyl-cysteine
Explanation: ***Flumazenil*** - **Flumazenil** is a competitive **benzodiazepine receptor antagonist** that can reverse the sedative and other central nervous system effects of benzodiazepines. - It works by blocking benzodiazepines from binding to their receptor sites on the **GABA-A receptor complex**. *Naloxone* - **Naloxone** is a competitive **opioid receptor antagonist** used to reverse opioid overdose. - It has no effect on **benzodiazepine toxicity** as it targets different receptor systems. *Atropine* - **Atropine** is an **anticholinergic drug** used to reverse the effects of **cholinergic poisoning** (e.g., from organophosphates, carbamates) or symptomatic bradycardia. - It works on muscarinic acetylcholine receptors and is not involved in benzodiazepine metabolism or action. *N-acetyl-cysteine* - **N-acetyl-cysteine (NAC)** is primarily used as an antidote for **acetaminophen (paracetamol) poisoning**, where it replenishes glutathione. - It is also used in some cases of mucolysis but has no role in reversing benzodiazepine toxicity.
Question 2: Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?
- A. Diazepam
- B. Zolpidem
- C. Phenobarbitone
- D. Buspirone (Correct Answer)
Explanation: ***Buspirone*** - **Buspirone** is a unique anxiolytic that primarily acts as a **partial agonist at 5-HT1A receptors**. - Unlike benzodiazepines, it lacks significant **anticonvulsant**, **muscle relaxant**, or **sedative-hypnotic properties** and does not lead to physical dependence or withdrawal. *Diazepam* - **Diazepam** is a **benzodiazepine** that acts by enhancing the effect of **GABA** at GABA-A receptors, leading to significant anxiolytic, sedative, muscle relaxant, and anticonvulsant effects. - It does not primarily act via **5-HT1A receptor partial agonism**. *Zolpidem* - **Zolpidem** is a **non-benzodiazepine hypnotic** that selectively binds to the **GABA-A receptor** subunit, primarily mediating sedative effects. - While it's used for insomnia, it doesn't primarily act as a **5-HT1A partial agonist** and is not typically used for its anxiolytic properties in the same way as buspirone. *Phenobarbitone* - **Phenobarbitone** is a **barbiturate** that acts by prolonging the opening of **chloride channels** associated with GABA-A receptors, leading to strong sedative, hypnotic, and anticonvulsant effects. - Its mechanism of action is distinct from **5-HT1A receptor partial agonism**, and it carries a high risk of dependence and overdose.
Question 3: A patient on SSRI sertraline was also prescribed amitriptyline and subsequently developed serotonin toxicity. What is the likely treatment for serotonin toxicity?
- A. Flumazenil
- B. Cyproheptadine (Correct Answer)
- C. L-Carnitine
- D. Leucovorin
- E. Naloxone
Explanation: ***Cyproheptadine*** - **Cyproheptadine** is a serotonin antagonist that can help reverse the effects of excessive serotonin in the central nervous system. - It works by blocking **serotonin 5-HT2A receptors**, which are implicated in the pathophysiology of serotonin toxicity. *Flumazenil* - **Flumazenil** is a benzodiazepine receptor antagonist used to reverse the effects of benzodiazepine overdose. - It has no role in the treatment of **serotonin toxicity**, as it does not affect serotonin pathways. *L-Carnitine* - **L-Carnitine** is a mitochondrial co-factor used in fatty acid metabolism, sometimes supplemented for certain metabolic disorders or muscle pain. - It does not have any direct action on **serotonin receptors** or the serotonin system, making it ineffective for serotonin toxicity. *Leucovorin* - **Leucovorin** (folinic acid) is used to counteract the effects of methotrexate toxicity or to enhance the effects of fluorouracil in chemotherapy. - It is not involved in modulating **neurotransmitter levels** or reversing the symptoms of serotonin toxicity. *Naloxone* - **Naloxone** is an opioid receptor antagonist used to reverse opioid overdose. - It has no effect on **serotonin receptors** or serotonergic pathways, making it ineffective for treating serotonin toxicity.
Question 4: What is the primary therapeutic use of 5-HT1B/1D agonists?
- A. Anti-anxiety medications
- B. Acute migraine treatment (Correct Answer)
- C. Anti-nausea medications for chemotherapy
- D. Drugs for gastroesophageal reflux disease (GERD)
Explanation: ***Acute migraine treatment*** - 5-HT1B/1D agonists, such as **triptans**, primarily work by causing **vasoconstriction of intracranial blood vessels** and inhibiting the release of pro-inflammatory neuropeptides. - This action directly alleviates the pain and associated symptoms of **acute migraine attacks**. *Anti-anxiety medications* - Anti-anxiety medications typically target neurotransmitter systems like **GABA** (e.g., benzodiazepines) or **serotonin reuptake** (e.g., SSRIs), not the 5-HT1B/1D receptors in this context. - While serotonin plays a role in anxiety, specific 5-HT1B/1D agonism does not lead to anxiolytic effects. *Anti-nausea medications for chemotherapy* - Anti-nausea medications used for chemotherapy-induced nausea and vomiting often target **5-HT3 receptors** (e.g., ondansetron) to block their pro-emetic effects. - 5-HT1B/1D agonists do not have primary anti-emetic properties useful in this setting. *Drugs for gastroesophageal reflux disease (GERD)* - GERD medications primarily focus on reducing stomach acid production (e.g., **proton pump inhibitors**, H2 blockers) or neutralizing it (antacids). - 5-HT1B/1D agonists do not directly influence gastric acid secretion or esophageal motility in a way beneficial for GERD.
Question 5: What is the drug of choice for rapid relief of an acute panic attack?
- A. Benzodiazepines (rapid anxiolytic action) (Correct Answer)
- B. Neuroleptics (antipsychotic agents)
- C. Beta-blockers (manage physical symptoms)
- D. Tricyclic Antidepressants (long-term management)
Explanation: ***Benzodiazepines (rapid anxiolytic action)*** - **Benzodiazepines** are used for **rapid symptomatic relief** of acute panic attacks due to their **fast onset of action** (within 30-60 minutes) and potent anxiolytic effects. - They work by enhancing the effect of **GABA**, an inhibitory neurotransmitter, leading to CNS depression and reduced anxiety. - **Important note:** While effective for acute relief, benzodiazepines are recommended only for **short-term use** (2-4 weeks) due to risks of dependence, tolerance, and withdrawal. - **First-line long-term treatment** for panic disorder is **SSRIs** (not benzodiazepines). *Beta-blockers (manage physical symptoms)* - **Beta-blockers** can help manage **physical symptoms** of anxiety such as palpitations and tremors, but they do not address the core psychological component of a panic attack. - They are often used as an adjunct or in performance anxiety situations, but not for acute panic attack relief. *Neuroleptics (antipsychotic agents)* - **Neuroleptics** (antipsychotic agents) are primarily used for treating **psychotic disorders** like schizophrenia, not panic attacks. - Their side effect profile and mechanism of action make them unsuitable for acute anxiety or panic. *Tricyclic Antidepressants (long-term management)* - **Tricyclic Antidepressants (TCAs)** like imipramine and clomipramine can be used for **long-term management** of panic disorder. - However, their onset of action is slow (2-4 weeks), making them unsuitable for acute panic attack relief. - **SSRIs are preferred over TCAs** for long-term management due to better tolerability.
Question 6: Match the following: Column A: a. Beta 1 b. Beta 2 c. Beta 3 Column B: 1. Mirabegron 2. Betaxolol 3. Salbutamol
- A. a-2, b-3 ,c-1 (Correct Answer)
- B. a-2, b-1, c-3
- C. a-3, b-2, c-1
- D. a-3, b-1, c-2
Explanation: ***a-2, b-3, c-1*** - This pairing correctly matches **Betaxolol** with **Beta 1 selective** antagonism, **Salbutamol** with **Beta 2 selective** agonism, and **Mirabegron** with **Beta 3 selective** agonism. - **Betaxolol** is a beta-1 selective adrenergic receptor antagonist, primarily used in ophthalmology to reduce intraocular pressure and as an antihypertensive. **Salbutamol** is a selective beta-2 adrenergic agonist used as a bronchodilator in asthma and COPD, causing relaxation of bronchial smooth muscle. **Mirabegron** is a selective beta-3 adrenergic agonist used to treat overactive bladder by relaxing the detrusor muscle. *a-2, b-1, c-3* - This option incorrectly assigns **Mirabegron** to Beta 2. Mirabegron is a **Beta 3 selective agonist**. - It also incorrectly assigns **Salbutamol** to Beta 3. Salbutamol is a **Beta 2 selective agonist**. *a-3, b-2, c-1* - This option incorrectly assigns **Salbutamol** to Beta 1. Salbutamol is a **Beta 2 selective agonist**. - It also incorrectly assigns **Betaxolol** to Beta 2. Betaxolol is a **Beta 1 selective antagonist**. *a-3, b-1, c-2* - This option incorrectly assigns **Salbutamol** to Beta 1 and **Betaxolol** to Beta 3. - **Salbutamol** is a Beta 2 selective agonist, and **Betaxolol** is a Beta 1 selective antagonist.
Question 7: Which anti-epileptic drug marked X will act at the site shown?
- A. Tiagabine (Correct Answer)
- B. Vigabatrin
- C. Gabapentin
- D. Rufinamide
Explanation: ***Tiagabine*** - The image shows site 'X' as a **GABA reuptake transporter** that actively removes GABA from the synaptic cleft back into the presynaptic neuron or glial cells - **Tiagabine** specifically inhibits **GABA reuptake transporters (GAT-1)**, thereby increasing GABA concentration in the synaptic cleft and enhancing its inhibitory effect - This is the mechanism directly targeting the site shown in the diagram *Vigabatrin* - Irreversible inhibitor of **GABA transaminase (GABA-T)**, the enzyme responsible for catabolizing GABA - Acts intracellularly to prevent GABA breakdown, not at the synaptic reuptake transporter shown - Different mechanism from the site depicted *Gabapentin* - GABA analog but does not bind to GABA receptors or interfere with GABA reuptake - Primary mechanism involves modulating **voltage-gated calcium channels (α2δ subunit)**, reducing excitatory neurotransmitter release - Does not act at GABA transporters *Rufinamide* - Prolongs the inactive state of **voltage-dependent sodium channels**, reducing neuronal excitability - Mechanism is distinct from GABA reuptake or metabolism - Does not act at the site shown in the diagram
Question 8: Atropine is not an antidote in:
- A. Baygon
- B. Parathion
- C. Endrin (Correct Answer)
- D. Tik 20
Explanation: ***Endrin*** - Endrin is an **organochlorine insecticide**, and its toxicity is primarily mediated through the central nervous system, causing seizures and neurological symptoms. - Atropine is an **anticholinergic drug** and is ineffective because organochlorines do not act on cholinergic receptors; therefore, it is not an antidote for endrin poisoning. *Baygon* - Baygon is a **carbamate insecticide**, which inhibits acetylcholinesterase, leading to cholinergic crisis. - Atropine is an appropriate antidote for Baygon poisoning, as it blocks the effects of excess acetylcholine at muscarinic receptors. *Parathion* - Parathion is an **organophosphate insecticide**, known for irreversible inhibition of acetylcholinesterase, resulting in severe cholinergic toxicity. - Atropine is a crucial antidote for parathion poisoning, used to counteract the muscarinic effects of acetylcholine accumulation. *Tik 20* - Tik 20 typically contains **organophosphate compounds** such as malathion or parathion, which are acetylcholinesterase inhibitors. - As an effective anticholinergic, atropine is indicated in the treatment of poisoning by organophosphates found in products like Tik 20.
Question 9: 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 10: Which of the following antidepressants is least likely to have sexual side effects?
- A. Amitriptyline
- B. Fluoxetine
- C. Venlafaxine
- D. Mirtazapine (Correct Answer)
Explanation: ***Mirtazapine*** - **Mirtazapine** is an atypical antidepressant (NaSSA - Noradrenergic and Specific Serotonergic Antidepressant) that works by blocking alpha-2 adrenergic receptors, enhancing serotonin and norepinephrine release [1]. - It has the **lowest incidence of sexual side effects** among antidepressants because it blocks 5-HT2 and 5-HT3 receptors while avoiding significant 5-HT1A stimulation, which is responsible for sexual dysfunction with SSRIs [1]. - It may even **improve libido** in some cases due to its unique receptor profile and histamine antagonism that can enhance sleep quality. *Amitriptyline* - **Amitriptyline** is a tricyclic antidepressant (TCA) with broad receptor actions, including anticholinergic and antihistaminic effects. - TCAs like amitriptyline can cause **sexual dysfunction** (including erectile dysfunction and decreased libido) due to their anticholinergic properties and effects on multiple neurotransmitter systems, though typically less severe than SSRIs. *Fluoxetine* - **Fluoxetine** is a selective serotonin reuptake inhibitor (SSRI), and while effective for depression, it is associated with a **high incidence of sexual side effects** (30-70% of patients) [2]. - These side effects include **decreased libido**, **anorgasmia**, and **erectile dysfunction**, caused by increased serotonergic activity at 5-HT2 receptors in areas regulating sexual function [2]. *Venlafaxine* - **Venlafaxine** is a serotonin-norepinephrine reuptake inhibitor (SNRI), increasing both serotonin and norepinephrine levels in the brain [1]. - Like SSRIs, SNRIs such as venlafaxine frequently cause **sexual dysfunction**, with common complaints including reduced libido and difficulty achieving orgasm due to enhanced serotonergic neurotransmission [1].
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