Depression US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Depression. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Depression US Medical PG Question 1: Which of the following neuroanatomical areas is/are considered to be involved in the etiology of depression?
- A. Striatum
- B. Amygdala
- C. Hippocampus
- D. All of the options (Correct Answer)
Depression Explanation: ***All of the options***
- The **amygdala**, **hippocampus**, and **striatum** are all part of complex neural circuits that have been implicated in the pathophysiology of depression.
- Dysregulation in these areas can lead to emotional processing deficits, memory impairments, and anhedonia, which are core symptoms of depression.
*Amygdala*
- The **amygdala** is primarily involved in processing emotions, particularly fear and anxiety, and shows increased activity in depressed individuals, contributing to negative mood.
- While significant, it is just one component of a broader network involved in depression.
*Hippocampus*
- The **hippocampus** plays a crucial role in memory and mood regulation, and studies often show reduced volume and function in depressed patients, affecting learning and emotional context.
- Although it is significantly affected, depression involves multiple brain regions, not solely the hippocampus.
*Striatum*
- The **striatum**, particularly the **ventral striatum**, is vital for reward processing, motivation, and motor control, and its dysfunction can contribute to anhedonia and lack of motivation in depression.
- While critical for reward pathways, the striatum is part of a larger interconnected system implicated in this condition.
Depression US Medical PG Question 2: A 38-year-old professor with depression requests you to prescribe an antidepressant that would be least likely to cause sexual dysfunction. Which of the following drugs would you prescribe?
- A. Bupropion (Correct Answer)
- B. Venlafaxine
- C. Fluoxetine
- D. Escitalopram
Depression Explanation: ***Bupropion***- Bupropion is a **norepinephrine-dopamine reuptake inhibitor (NDRI)** that differs structurally and mechanically from SSRIs and SNRIs. - It is known for its relatively neutral effect on sexual function, often having the **lowest incidence** of sexual side effects among commonly prescribed antidepressants, and is sometimes used to treat SSRI-induced sexual dysfunction.*Escitalopram*- As a **selective serotonin reuptake inhibitor (SSRI)**, escitalopram frequently causes sexual side effects such as decreased libido, delayed orgasm, and anorgasmia.- This class of drugs elevates **serotonin levels**, which is strongly implicated in causing sexual dysfunction.*Venlafaxine*- Venlafaxine is a **serotonin-norepinephrine reuptake inhibitor (SNRI)**, and its serotonergic component carries a medium-to-high risk of causing sexual dysfunction.- The common sexual side effects include **erectile dysfunction** in men and reduced arousal in women.*Fluoxetine*- Fluoxetine is a commonly prescribed **SSRI** with a significant association with sexual side effects, including inhibited orgasm and reduced libido.- Its long half-life means that these adverse effects, if they occur, can persist following **discontinuation**.
Depression US Medical PG Question 3: All are required to diagnose major depression except?
- A. Depressed mood
- B. Decreased concentration
- C. Nihilistic ideas (Correct Answer)
- D. Insomnia
Depression Explanation: ***Nihilistic ideas***
- While nihilistic ideas (e.g., belief that life is meaningless or that nothing matters) can occur in severe depression, they are **not a mandatory diagnostic criterion** for major depressive disorder (MDD).
- The diagnosis of MDD requires a specific number of core symptoms, and nihilistic ideation is not listed as one of them in diagnostic manuals like the DSM-5.
*Depressed mood*
- A **depressed mood** for most of the day, nearly every day, is one of the two **cardinal symptoms** required for a diagnosis of major depressive disorder.
- The other cardinal symptom is anhedonia (loss of interest or pleasure).
*Insomnia*
- **Insomnia** (difficulty falling or staying asleep) or hypersomnia (sleeping excessively) is a common neurovegetative symptom of major depressive disorder and is one of the **nine diagnostic criteria**.
- At least 5 of these 9 criteria must be present for a diagnosis, including at least one of the two cardinal symptoms.
*Decreased concentration*
- **Diminished ability to think or concentrate**, or indecisiveness, is another of the **nine diagnostic criteria** for major depressive disorder.
- This cognitive symptom highlights the impact of depression on mental function beyond mood.
Depression US Medical PG Question 4: A 33-year-old man visits his psychiatrist with feelings of sadness on most days of the week for the past 4 weeks. He says that he is unable to participate in his daily activities and finds it hard to get out of bed on most days. If he has nothing scheduled for the day, he sometimes sleeps for 10–12 hours at a stretch. He has also noticed that on certain days, his legs feel heavy and he finds it difficult to walk, as though there are bricks tied to his feet. However, he is still able to attend social events and also enjoys playing with his children when he comes home from work. Other than these simple pleasures, he has lost interest in most of the activities he previously enjoyed. Another troubling fact is that he had gained weight over the past month, mainly because he eats so much when overcome by these feelings of depression. His is prescribed a medication to treat his symptoms. Which of the following is the mechanism of action of the drug he was most likely prescribed?
- A. Activates the γ-aminobutyric acid receptors
- B. Inhibit the uptake of serotonin and norepinephrine at the presynaptic cleft (Correct Answer)
- C. Works as an antagonist at the dopamine and serotonin receptors
- D. Non-selectively inhibits monoamine oxidase A and B
- E. Stimulates the release of norepinephrine and dopamine in the presynaptic cleft
Depression Explanation: ***Inhibit the uptake of serotonin and norepinephrine at the presynaptic cleft***
- The patient presents with symptoms characteristic of **atypical depression**, including increased sleep (**hypersomnia**), increased appetite leading to weight gain, **leaden paralysis** (heavy feelings in the limbs), and **mood reactivity** (enjoying social events/playing with children).
- For initial treatment of atypical depression, **SSRIs** (e.g., fluoxetine, sertraline) and **SNRIs** (e.g., venlafaxine, duloxetine) are considered **first-line therapies** due to their favorable safety profile and efficacy.
- **SNRIs** address both serotonin and norepinephrine imbalances and are effective for atypical depression, particularly when there is significant fatigue or pain.
*Activates the γ-aminobutyric acid receptors*
- This mechanism describes **benzodiazepines** or other GABAergic drugs, which are typically used for anxiety, insomnia, or acute agitation.
- While they can provide symptomatic relief for anxiety associated with depression, they do not target the core depressive symptoms, lack antidepressant efficacy, and carry risk of dependence.
*Works as an antagonist at the dopamine and serotonin receptors*
- This mechanism describes **second-generation antipsychotics** (e.g., quetiapine, aripiprazole), which are primarily used to treat psychotic disorders or as adjuncts in severe depression with psychotic features or treatment-resistant depression.
- The patient's symptoms do not suggest psychotic features, and antipsychotics are not first-line treatment for uncomplicated atypical depression.
*Non-selectively inhibits monoamine oxidase A and B*
- This describes **non-selective MAOIs** (e.g., phenelzine, tranylcypromine), which are considered the **most effective** antidepressants for atypical depression based on clinical trials.
- However, MAOIs are typically reserved for **treatment-resistant depression** due to their significant side effect profile, dietary restrictions (tyramine-free diet to prevent **hypertensive crisis**), and drug interaction risks.
- Given this is an initial presentation without treatment failure, MAOIs would not be the first-line choice despite their superior efficacy.
*Stimulates the release of norepinephrine and dopamine in the presynaptic cleft*
- This mechanism could describe **amphetamines** or certain **wake-promoting agents**, which are not standard antidepressant treatments.
- **Bupropion** (an antidepressant) inhibits reuptake of norepinephrine and dopamine but does not directly stimulate their release.
- Stimulants are occasionally used as adjuncts for treatment-resistant depression but are not first-line monotherapy due to abuse potential and limited evidence for long-term efficacy in depression.
Depression US Medical PG Question 5: A 60-year-old woman with treatment-resistant depression has been referred for electroconvulsive therapy (ECT) after failing adequate trials of four different antidepressants including augmentation strategies. She has severe depression with psychomotor retardation, significant weight loss, and pervasive guilt. Her family is concerned about potential cognitive side effects of ECT. They ask about factors that might be modified to minimise cognitive adverse effects while maintaining treatment efficacy. Which modification would most effectively reduce cognitive side effects while preserving antidepressant efficacy?
- A. Using unilateral electrode placement on the non-dominant hemisphere rather than bilateral placement (Correct Answer)
- B. Reducing the electrical dose to just above seizure threshold regardless of electrode placement
- C. Extending the interval between treatments from twice weekly to once weekly throughout the course
- D. Using ultra-brief pulse width stimulation with bilateral electrode placement
- E. Limiting the total number of ECT sessions to a maximum of 6 treatments
Depression Explanation: ***Using unilateral electrode placement on the non-dominant hemisphere rather than bilateral placement***
- **Right-unilateral (RUL) ECT** is consistently associated with significantly fewer **cognitive adverse effects**, particularly regarding verbal memory and orientation, compared to **bilateral ECT**.
- While bilateral placement is generally faster-acting, RUL ECT maintains comparable **antidepressant efficacy** provided the electrical dose is sufficiently higher (typically 6 times) than the **seizure threshold**.
*Reducing the electrical dose to just above seizure threshold regardless of electrode placement*
- While lower doses minimize cognitive side effects, using a dose just above the **seizure threshold** in unilateral ECT is often **ineffective** for treating depression.
- To ensure efficacy in RUL placement, the dose must be significantly above threshold; therefore, reducing it too low risks a non-therapeutic response.
*Extending the interval between treatments from twice weekly to once weekly throughout the course*
- Reducing treatment frequency to **once weekly** may slow the rate of cognitive decline but significantly delays the **speed of remission** and clinical improvement.
- **Twice-weekly sessions** are the standard of care to balance clinical response time with the risk of cumulative cognitive impairment.
*Using ultra-brief pulse width stimulation with bilateral electrode placement*
- **Ultra-brief pulse (0.3ms)** stimulation reduces cognitive side effects compared to standard brief pulse, but the benefits are most established when combined with **unilateral placement**.
- Combining ultra-brief pulses with **bilateral placement** still poses a higher risk of cognitive deficits compared to the unilateral alternative.
*Limiting the total number of ECT sessions to a maximum of 6 treatments*
- Arbitrarily limiting sessions may result in **incomplete remission** or early relapse, as many patients require 8 to 12 sessions for a full therapeutic response.
- Treatment course length should be determined by **clinical response** and recovery from symptoms like psychomotor retardation, rather than a fixed number of treatments.
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