GC164 I Am Depressed Mood Disorders
Mood disorders are a category of mental health conditions—including major depressive disorder, persistent depressive disorder, and bipolar disorder—characterized by significant disturbances in emotional state that impair daily functioning.
I Am Depressed: Mood Disorders
This lecture by Dr. Wai-chi Chan (GC 164) covers the entire clinical landscape of major depressive disorder (MDD) — from distinguishing normal sadness from pathological depression, through epidemiology, DSM-5 diagnostic criteria, aetiology (biological + psychosocial), clinical assessment, differential diagnosis, to the full spectrum of management (pharmacological, psychosocial, physical, dietary). This is a core psychiatry lecture that is directly tested in Fourth Summative exams via MCQs, SAQs, and minicases. [1]
Big Idea: Depression is common, disabling and associated with suicide, but effective psychological, pharmacological and physical treatments exist. The clinical challenge is recognising varied presentations (especially in younger and older people), assessing immediate safety, excluding bipolarity and other causes, and choosing treatment collaboratively. The slide deck's epidemiological estimates date from 2023 and earlier; current WHO figures are distinguished below.
The two-week criterion is diagnostic, not a waiting period for care. Severe suicidality, psychosis, catatonia, dehydration or rapidly worsening function requires action immediately [11].
Is depression always pathological? Mood fluctuations in response to disappointment, frustration and losses in everyday life are usually short-lived. Natural despondency can have an important survival function, resulting in reorientation and maturation. [1]
This is a critical conceptual distinction. Everyone feels sad sometimes. Normal sadness:
- Has an identifiable trigger (loss, frustration)
- Is proportionate to the trigger
- Is self-limiting (days to a few weeks)
- Does not significantly impair function
- Can serve adaptive purposes (introspection, recalibration)
Major depressive disorder is different because:
- Symptoms are severe (DSM-5 uses words like "marked," "significant")
- They impair adaptation and are often disabling
- When enduring, depression impairs function at work, school, and in the family [1]
Why This Matters
Examiners love asking you to differentiate grief/adjustment from MDD. Use the whole syndrome—severity, duration, symptom count, functional impairment and context. Suicidal thoughts, psychomotor change or psychosis demand assessment, but no single symptom should be interpreted without the clinical picture.
The 2023 lecture quotes WHO estimates of 5% of adults and approximately 280 million people worldwide. [1]
Current context: WHO's 2025 fact sheet estimates 5.7% of adults and approximately 332 million people worldwide; women are affected about 1.5 times as often as men. These updates do not invalidate the lecture's core point that depression is common, but the older numbers should be labelled by date [10].
| Statistic | Value | Source |
|---|---|---|
| Global lifetime prevalence (high-income) | 14.6% | Bromet et al. 2011 [1] |
| Global 12-month prevalence (high-income) | 5.5% | Bromet et al. 2011 [1] |
| Female:male ratio | ~2:1 | [1] |
| HK 1-week prevalence mixed anxiety & depression | 6.9% (~1 in 14) | Lam et al. 2015 (HKMMS) [1] |
| HK 1-week prevalence depressive episode | 2.9% | Lam et al. 2015 [1] |
Why is depression more common in women? Postulated reasons include: (1) greater readiness to report symptoms; (2) misdiagnosis as alcohol-related disorder in men; (3) social disadvantages; (4) female hormones may sensitize the brain to stress effects. [3]
Depression is a leading contributor to health loss. In the slide's GBD chart, depressive disorders move upward from outside the top 20 causes of total DALYs in 1990 into the top 20 by 2016. The graphic ranks total DALYs, not disability alone, and is historical rather than a current league table [1].
High Yield for Exams
The durable exam point is that depression is a major cause of disability. The lecture's HK survey found mixed anxiety-depressive disorder in approximately 1 in 14 adults and a depressive episode in 2.9%; retain these as study-specific estimates, not today's universal prevalence [1].
3. Impact of Depression
Depression increases non-suicidal mortality. 72% of 61 reports demonstrated positive association. RR = 1.2–4.0. [1]
Possible mediators (important for understanding why depression kills even without suicide):
- Behavioural risk factors: poor treatment adherence, inactivity, ↑ alcohol consumption
- Biological associations: inflammatory, autonomic and thrombosis-related pathways have been proposed
- Subclinical/prevalent disease: especially cardiovascular disease [1]
The lecture's evidence set quotes over 700,000 deaths per year, a 20-fold association and a 6% long-term proportion in older affective-disorder cohorts. [1]
Current WHO reporting estimates 727,000 deaths by suicide in 2021. The other percentages in this section come from historical cohorts and psychological-autopsy studies; they demonstrate a strong association but are not precise predictions for an individual patient [10].
| Key Finding | Detail |
|---|---|
| Suicide risk attributable to depression | 20-fold increase |
| Long-term suicide risk in depression (Sweden, 54–64y follow-up) | 6.0% |
| HK adults 15–59: Population-attributable risk of suicide from MDD | 27% (even with non-disease social risk factors) |
| HK elderly ≥60: % suicide subjects with psychiatric problems | 86%, commonest = MDD |
Among the psychiatric problems, major depression was the commonest diagnosis in elderly suicide in Hong Kong. [1]
Suicide Assessment Is an Immediate Clinical Task
Ask directly about thoughts of death and suicide, intent, plans, preparatory acts, access to means, past attempts, recent escalation, intoxication/impulsivity, psychosis, agitation, supports and reasons for living. If there is considerable immediate danger, arrange urgent specialist/emergency care; do not leave the person alone while organising safe transfer. A checklist or a “low/medium/high” label must not be used to predict suicide, decide discharge or replace a collaborative formulation and safety plan [11][12].
Exam Trap
Students underestimate the mortality of depression. It is not just about suicide — depression independently increases all-cause mortality through cardiovascular and other mechanisms. When asked about "complications of depression," always include both suicide AND increased medical mortality/morbidity.
In some younger people, the first obvious sign may be loss of interest in friends, decline in school performance, self-injury or bulimia or drug use. In some older people, symptoms may mimic dementia — deterioration of cognitive functioning and self-care. In some tragic cases, symptoms may be masked until the person is found dead by suicide. [1]
This is critical because depression does NOT always present as someone saying "I'm depressed":
| Age Group | Atypical Presentation |
|---|---|
| Children/Adolescents | Irritable mood (DSM-5 allows this), school decline, social withdrawal, self-harm, eating disorders, substance use |
| Older adults | Cognitive decline, psychomotor slowing, sleep/appetite change, pain or loss of self-care. “Depressive pseudodementia” is a descriptive pattern, not a reliable binary test: depression and neurocognitive disorder can coexist, so investigate cognitive symptoms and reassess after treatment [2] |
| General medical | Somatic complaints (fatigue, pain, GI symptoms) masking underlying depression, especially in Chinese populations (somatization) [4] |
5. DSM-5 Diagnostic Criteria for Major Depressive Disorder
Major Depressive Disorder requires at least 2 weeks' duration, with 5 or more of the following symptoms present, at least 1 of which must be either (1) depressed mood or (2) markedly diminished interest/pleasure. [1]
| # | Symptom | Detail from Lecture | Why It Matters |
|---|---|---|---|
| (1) | Depressed mood | Most of the day, nearly every day. Subjective (feels sad, empty, hopeless) or observed (appears tearful). In children/adolescents: can be irritable mood. | Core symptom — at least one of (1) or (2) must be present |
| (2) | Markedly diminished interest or pleasure (anhedonia) | In all or almost all activities, most of the day, nearly every day | Core symptom — this is the PHQ-2 screening question |
| (3) | Significant weight change | > 5% body weight in a month, or ↓/↑ appetite nearly every day. In children: failure to make expected weight gain | Captures both weight loss AND weight gain (atypical depression) |
| (4) | Insomnia or hypersomnia | Nearly every day | Insomnia = typical; hypersomnia = atypical |
| (5) | Psychomotor agitation or retardation | Observable by others (not just subjective) | Must be objectively observable — important exam point |
| (6) | Fatigue or loss of energy | Nearly every day | Most common somatic complaint |
| (7) | Feelings of worthlessness or excessive/inappropriate guilt | May be delusional. Not merely self-reproach about being sick | When guilt becomes delusional → severe depression with psychotic features |
| (8) | Diminished ability to think/concentrate, or indecisiveness | Nearly every day | Contributes to pseudodementia picture in elderly |
| (9) | Recurrent thoughts of death/suicidal ideation | Not just fear of dying. Includes recurrent suicidal ideation ± plan ± attempt | Always assess — critical for risk stratification |
Symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. The episode is not attributable to substance or another medical condition. Not better explained by schizoaffective disorder, schizophrenia, etc. Absence of previous manic or hypomanic episode. [1]
Critical Exam Point
The ABSENCE of previous manic or hypomanic episode is part of the diagnostic criteria for MDD. If there has EVER been a manic/hypomanic episode, the diagnosis is bipolar affective disorder — current depressive episode, NOT MDD. This is one of the most commonly tested discriminators. [1]
Bipolar screen before prescribing: Ask specifically about past periods of elevated or markedly irritable mood with increased energy/activity, decreased need for sleep, pressured speech, racing thoughts, increased confidence, impulsive spending/sexual or other risk-taking, and functional change; seek collateral history where possible. Early onset, recurrent episodes, family history, mixed symptoms, psychosis or previous antidepressant activation increase suspicion but are not diagnostic. Refer for specialist assessment when bipolar disorder is possible; routine antidepressant monotherapy is not the treatment pathway for bipolar depression [11][13].
Specifiers include: course (single vs. recurrent), severity (mild/moderate/severe/with psychotic features/remission), and other specifiers: anxious distress, mixed features, melancholic features, atypical features, mood-congruent vs. mood-incongruent psychotic features, catatonia, peripartum onset, seasonal pattern. [1]
| Specifier | Key Features | Clinical Significance |
|---|---|---|
| Melancholic | Pervasive anhedonia, worse in morning (diurnal variation), early morning awakening, psychomotor changes, excessive guilt, significant anorexia/weight loss | Historical teaching links it to biological treatment response; do not use the specifier alone to choose a TCA or ECT |
| Atypical | Mood reactivity preserved, overeating, oversleeping, leaden paralysis, rejection sensitivity | Historical teaching links it with MAOI response, but current treatment is individualised |
| Psychotic | Delusions and/or hallucinations. Mood-congruent themes include guilt, worthlessness, disease, death or punishment | Mood congruence should be recorded but does not diagnose schizoaffective disorder; establish whether psychosis ever persists outside mood episodes |
| Peripartum onset | Onset during pregnancy or within 4 weeks postpartum | Critical for O&G exam questions — see 2024 MCQ Q14 [7] |
| Seasonal pattern | Onset autumn/winter, recovery spring/summer (recurrent episodes only) | Postulated to relate to daylight duration → bright light therapy |
| Catatonia | Psychomotor retardation → mutism, immobility, waxy flexibility | May need ECT urgently |
The DSM-5 “peripartum onset” specifier uses pregnancy or onset within 4 weeks after birth, but clinical postnatal depression services use a broader postpartum window. Do not dismiss a clinically significant episode simply because it begins after week 4 [14].
Removal of the "bereavement exclusion" — depressive symptoms may be understandable/appropriate to significant loss but clinical judgment is needed. [1]
This is important: previously, DSM-IV said you couldn't diagnose MDD within 2 months of bereavement. DSM-5 removed this because:
- Grief can trigger a true MDD
- Withholding treatment because the depression is "understandable" can be harmful
- Clinical judgment should determine whether grief has evolved into a depressive episode
Dysthymia → persistent depressive disorder (includes both chronic MDD and previous dysthymic disorder). [1]
Two new disorders: Disruptive mood dysregulation disorder (children, persistent irritability + explosive outbursts) and Premenstrual dysphoric disorder (mood symptoms in final week before menses). [1]
ICD-11 cardinal symptoms: depressed mood or diminished interest occurring most of the day, nearly every day, for at least two weeks. Additional symptoms: difficulty concentrating, feelings of worthlessness/guilt, hopelessness, suicidal thoughts, appetite/sleep changes, psychomotor agitation/retardation, reduced energy/fatigue. [1]
The ICD-10 system (still used clinically in HK) uses 3 core symptoms: (1) depressed mood, (2) loss of interest/anhedonia, (3) reduced energy/fatigability — and requires ≥2 core + ≥2 additional for a depressive episode. [3]
| Feature | DSM-5 MDD | ICD-10 Depressive Episode |
|---|---|---|
| Core symptoms | 2 (depressed mood, anhedonia) | 3 (depressed mood, anhedonia, anergia) |
| Total required | ≥5 of 9 (including ≥1 core) | ≥2 core + ≥2 additional |
| Duration | ≥2 weeks | ≥2 weeks |
| Severity grading | Mild/moderate/severe/with psychotic features | Mild (4 total), moderate (6 total), severe (7+ total) |
7. Aetiology
Depressive disorder is caused by a combination of biological, social and psychological factors, which disturb the brain's capacity for stress management. [1]
7a. Biological Hypotheses
Classical "serotonin hypothesis": diminished activity of serotonin pathways plays a causal role. Reserpine (depleted monoamines) produced a depressive state. Diminished monoaminergic activity detected in brains of suicide decedents and bodily fluids of depressed people. [1]
Why this matters: Monoamine signalling is one pharmacological target, but treatment response does not prove that depression is simply a deficiency state. The lecture itself cautions:
Evidence suggests that the cause of depression is far more complicated than a reduced level of serotonin. [1]
| Monoamine | Role | Evidence in Depression |
|---|---|---|
| Serotonin (5-HT) | Body temperature, sleep/wake, mood, impulse control | Low metabolites in suicide decedents' brains and depressed patients' CSF; reduced serotonin functioning [1] |
| Norepinephrine (NE) | Mood and anxiety levels | Mood symptoms in patients taking propranolol [1] |
| Dopamine (DA) | Motor/mental activity, attention, motivation, pleasure (mesolimbic reward pathway) | Diminished dopaminergic neurons in suicidal decedents with depression [1] |
Besides monoamines, abnormalities in glutamate, GABA, and substance P have been detected in patients with depression. [1]
Volume reduction and decreased glial cells in subgenual cortex, reduced hippocampal size. [1]
These are group-level research associations, not diagnostic scans; structural imaging is ordered for a clinical neurological indication, not to “confirm depression.”
HPA axis dysregulation, lower estradiol (women) and testosterone (men), decreased T3 and TSH, diminished BDNF level. [1]
BDNF Connection
Brain-derived neurotrophic factor (BDNF) supports neuronal survival and plasticity. Altered BDNF signalling is one proposed component of depression biology, and exercise may influence neuroplasticity alongside sleep, social, behavioural and physiological pathways. Avoid presenting “low BDNF → depression” as a proven single causal chain [1].
7b. Psychosocial Hypotheses
Early environment: parental separation, physical/sexual abuse, non-caring or overprotective parenting. Lack of supportive networks. Stress and trauma: long-term difficulties, recent life events (especially entrapment and humiliation). Personality: sociotropy, neuroticism. [1]
Cognitive distortions include: [1]
| Distortion | Chinese | Explanation |
|---|---|---|
| Selective abstraction | 斷章取義 | Focusing on a detail, ignoring the bigger picture |
| Overgeneralisation | 以偏概全 | Drawing general conclusions from a single incident |
| Personalisation | 過度自責 | Relating external events to oneself without justification |
| Arbitrary inference | 妄下判斷 | Drawing conclusions without evidence, or even against evidence |
These cognitive distortions are the targets of Cognitive Behavioural Therapy (CBT).
Loss of an 'object', insecure attachments. [1]
8. Assessment
History (including medical and medication history), mental state examination, use of standardised instruments, physical examination and investigation to rule out medical conditions. [1]
Basic: CBP, R/LFT, thyroid function test. Others if indicated: blood alcohol level, blood/urine toxicology screen, HIV test, cosyntropin (ACTH) stimulation test (for Addison disease), EEG (for epilepsy), CT/MRI (for organic brain syndrome or hypopituitarism). [1]
This is the lecture's broad assessment list, not a mandatory panel for every patient. Investigation should follow history, examination, age, medication/substance exposure and atypical features; there is no laboratory or imaging test that diagnoses MDD [11].
| Investigation | Purpose |
|---|---|
| CBP | Anaemia (fatigue), infection |
| RFT | Renal failure (uraemic encephalopathy) |
| LFT | Hepatic encephalopathy |
| TFT | Hypothyroidism is a classic medical mimic of depression |
| Blood alcohol, toxicology | Substance-induced depression |
| HIV | HIV-related depression |
| ACTH stimulation | Addison's disease |
| CT/MRI brain | Organic cause (tumour, NPH, stroke) |
| EEG | Epilepsy (especially temporal lobe epilepsy) |
HAM-D, MADRS, PHQ-9, BDI, CES-D. Special groups: Geriatric Depression Scale, Cornell Scale for Depression in Dementia, Edinburgh Postnatal Depression Scale. Useful but NOT diagnostic — should not substitute for clinical diagnosis. [1]
Two-Question Screening
The two core questions ask about little interest/pleasure and feeling down, depressed or hopeless. The scored PHQ-2 uses the past 2 weeks; the older Whooley case-finding questions and the cited past paper use the past month.
These are validated brief screens, not diagnoses. Any positive response requires a comprehensive assessment of symptoms, function, bipolarity, physical/substance causes and suicide risk [6][11].
9. Differential Diagnosis
Adjustment disorder with depressed mood, manic episode with irritable mood or mixed episodes, persistent depressive disorder, anxiety disorder, substance/medication-induced depressive disorder, mood disorder due to another medical condition. [1]
| Condition | Key Differentiator from MDD |
|---|---|
| Adjustment disorder | Onset ≤3 months of stressor; does NOT meet full MDD criteria; resolves within 6 months of stressor cessation [3] |
| Persistent depressive disorder (dysthymia) | Chronic depressed mood with associated symptoms for ≥2 years in adults; persistent major depressive episodes can occur within this category |
| Bipolar disorder — depressive episode | History of ≥1 manic/hypomanic episode |
| Mixed anxiety-depressive disorder | Very common in primary care (6.9% HK); neither depression nor anxiety criteria fully met |
| Substance-induced | Temporal relationship with substance use/withdrawal |
| Schizoaffective disorder | Requires a period of ≥2 weeks of delusions/hallucinations without a major mood episode, with mood episodes present for most of the illness duration [3] |
Depression can be associated with medical conditions: [1]
| Category | Examples |
|---|---|
| Neurological | Epilepsy, Parkinson's, dementia, MS, Huntington's, CVD, migraine |
| Endocrine | Hypothyroidism, hyperthyroidism, Cushing's, Addison's, prolactinoma, hyperparathyroidism |
| Drug-related | Reserpine, methyldopa, steroids, sex hormones, H2 blockers, sedatives, chemotherapy, alcohol/cocaine/cannabis abuse |
| Infectious | Mononucleosis, HIV, Hepatitis C, Lyme disease, syphilis |
| Neoplastic | Pancreatic cancer (classic association with depression) |
| Chronic diseases | CAD, type 2 DM |
| Others | Chronic pain, psychosomatic conditions, OSA |
Classic Exam Trap
Reserpine, methyldopa, pancreatic cancer and hypothyroidism are classic lecture associations. Clinically, avoid attributing depression to one medicine or disease without establishing temporality and the full syndrome; order tests according to the presentation rather than treating this list as a universal screen [1][11].
10. Management
Though changes in monoamines constitute only part of the aetiological picture, the monoamine systems provide the most accessible treatment avenue. [1]
| Class | Examples | Mechanism |
|---|---|---|
| TCAs (non-selective monoamine reuptake inhibitors) | Amitriptyline, imipramine, nortriptyline, clomipramine, dothiepin | Block reuptake of 5-HT + NE (+ anticholinergic, antihistaminic, α-blocking effects → side effects) |
| Tetracyclic | Mianserin | Similar to TCA |
| SSRIs | Fluoxetine, paroxetine, sertraline, citalopram, escitalopram | Selectively inhibit serotonin reuptake |
| SNRIs | Duloxetine, venlafaxine, desvenlafaxine | Block serotonin + norepinephrine reuptake |
| NDRIs | Bupropion | Block norepinephrine + dopamine reuptake |
| MAOIs/RIMAs | Tranylcypromine, phenelzine, isocarboxazid, selegiline, moclobemide | Inhibit monoamine oxidase (irreversible or reversible) |
| Melatonergic | Agomelatine | MT1/MT2 agonist + 5-HT2C antagonist |
| Others | Trazodone, mirtazapine, vortioxetine | Mirtazapine: noradrenergic/specific serotonergic effects with antihistaminic sedation/weight gain; vortioxetine is multimodal serotonergic, not a conventional SSRI |
Key Evidence (Cipriani et al. 2018 Network Meta-Analysis)
The 2018 network meta-analysis reported higher average efficacy for agomelatine, amitriptyline, escitalopram, mirtazapine, paroxetine, venlafaxine and vortioxetine, and higher average acceptability for agomelatine, citalopram, escitalopram, fluoxetine, sertraline and vortioxetine. [1]
Older antidepressants (TCAs, MAOIs) are associated with significant adverse events and drug-drug interactions. There is marked inter-individual variation in tolerability. Choice determined by clinical circumstances, particularly physical comorbidity and concomitant medications. [1]
First-Line Antidepressant Choice
If medication is chosen for an adult with unipolar depression, an SSRI is often a reasonable first option, but there is no universal “best” drug. Match choice to prior response, preference, symptoms, physical illness, interactions, sexual/weight/sedative effects, pregnancy, overdose toxicity and withdrawal burden. The product photographs on slides 16-17 illustrate classes; they are not brand endorsements [1][11].
Antidepressant Safety Before and After the Prescription
- Screen for bipolarity first. Antidepressant monotherapy is not routine treatment for bipolar depression; new hypomania/mania requires urgent review [11][13].
- Ask about suicide risk and consider overdose toxicity and quantity supplied; TCAs have the greatest overdose risk and should not routinely be started when suicide risk is significant [11].
- Explain possible early agitation/anxiety and emergent suicidal thoughts. Review at about 1 week after starting or increasing a dose in people aged 18-25 or when suicide risk is a concern [11].
- Do not stop abruptly. Withdrawal can be severe or prolonged; taper collaboratively in stages, especially with shorter half-life drugs such as paroxetine and venlafaxine [11].
- Avoid dangerous serotonergic combinations, particularly an SSRI/SNRI/TCA with an MAOI, and check interactions and required washout periods [11].
The lecture describes CBT and interpersonal therapy as effective in mild and moderate depression and quotes remission as high as 85% in selected combined-treatment studies. [1]
The 85% is not a general expected remission rate. Current care is stepped and preference-sensitive: for less severe depression, guided self-help and psychological treatments are usually considered before medication; do not routinely offer an antidepressant first-line unless it is the person's informed preference. More severe depression may be treated with psychological therapy, medication or their combination depending on need and preference [11].
| Therapy | Core Approach |
|---|---|
| Interpersonal Therapy (IPT) | Problems understood in interpersonal context: facilitate grieving, encourage role transition, explore interpersonal disputes, improve interpersonal skills [1] |
| Cognitive Behavioural Therapy (CBT) | Monitor/evaluate/modify negative dysfunctional thoughts and distorted perceptions. Use cognitive techniques (list pros & cons, examine evidence). Increase activity scheduling [1] |
| Problem-Solving Therapy | Improve ability to deal with everyday problems: identify problems → brainstorm solutions → evaluate effectiveness → best solution [1] |
| Supportive Therapy | Facilitate affect expression, highlight positives, offer empathy, therapeutic optimism, empathic listening [1] |
Systematic review: pooled SMD = -0.40 for exercise vs. control. Inverse association between duration of intervention and magnitude of effect. Mechanisms: normalise BDNF, change neurotransmitter functioning (serotonin, endorphin), improve psychological/social wellbeing. [1]
These are proposed mediators and an older pooled estimate, not proof that BDNF or a single transmitter explains exercise benefit. Adapt activity to preference, physical health and safety, and do not use exercise alone for severe/high-risk depression.
Tai Chi RCT in HK: 12-step sitting Tai Chi for caregivers with depressive symptoms was well tolerated. [1]
Read the graph (slide 40): HAM-D scores fall more sharply in the sitting-Tai-Chi group by week 6, but the two plotted groups converge by week 24. The image supports feasibility and a possible early symptom effect; it does not by itself establish durable superiority or replace depression treatment in a high-risk patient [1].
10d. Physical Treatments
Where prompt action is needed e.g. strongly suicidal. Side effects: headache, confusion, memory impairment. Also consider need for anaesthesia, costs, inconvenience, stigma. [1]
Read the photograph (slide 41): This is modified ECT, delivered by a multidisciplinary team under general anaesthesia with physiological monitoring and a muscle relaxant—not an unmodified convulsion. The image is a useful antidote to the common media stereotype.
Current indications and safeguards: Consider ECT for severe depression when the person prefers it based on prior response, a rapid response is needed (for example, life-threatening refusal of food/fluids), or other treatments have failed. High suicide risk prompts urgent safety care and may make rapid treatment important, but does not automatically make ECT the sole “first-line” action. Discuss anaesthetic/medical risk, cognitive effects and the risk of no treatment; obtain valid, non-coerced consent when the person has capacity and follow local legal safeguards otherwise. Stop if harms outweigh benefits, and provide relapse-prevention treatment after response [11].
Common acute effects include headache, nausea, myalgia and confusion. Memory effects may include anterograde and retrograde impairment; autobiographical gaps can be distressing and occasionally persistent, so cognition and the person's experience should be monitored [11].
Non-invasive. Creates a potent (~1.5T) but brief (µs) magnetic field stimulating nerve tissue. Patient awake and alert. [1]
The lecture quotes older trials in which remission was 4× sham and an adjunct cohort had 58% response and 37% remission. [1]
These are study-specific figures, not guaranteed outcomes. rTMS uses a treatment coil positioned at the scalp to stimulate a defined cortical target over repeated sessions. NICE found no major safety concerns and adequate short-term efficacy, while emphasising variable response and informed discussion of alternatives [16]. It is not a substitute for emergency containment or ECT when an immediate life-saving response is required.
Non-invasive. Anode increases cortical activity; cathode decreases it. Modulates spontaneous neuronal network activity. Limited side effects. [1]
Pilot study in older adults with late-life depression: significant HAM-D reduction, sustained at 1- and 3-month follow-up. [1]
Read the images (slides 45-46): The 9-volt battery is a visual analogy for low direct current, while the coloured brain maps and electrode-cap photograph show that current distribution depends on electrode placement; clinical tDCS is not a consumer-battery DIY procedure. The late-life study was an open-label pilot of only 15 participants, so it cannot establish efficacy. NICE recommends tDCS only with special governance, consent and audit/research arrangements because administration and durability remain uncertain [17].
The slide proposes antioxidants, complex carbohydrates, protein-rich foods and a Mediterranean pattern, while acknowledging that no specific diet has been proven to relieve depression. [1]
Support a balanced diet as part of general health and wellbeing, but avoid promising that individual foods will “calm” or “boost alertness.” The slide's 2011 claim that omega-3 can be used as antidepressant monotherapy exceeds current evidence; NICE found low/very-low-certainty evidence for augmentation and does not position omega-3 as a replacement for established treatment [11].
| Population | Recognition and treatment safeguards |
|---|---|
| Children/adolescents | Irritability, school decline, social withdrawal, self-harm, eating symptoms and substance use may be presenting signs. Ask the young person privately and directly about bullying/abuse, substances, self-harm and suicide. Psychological therapy is central; antidepressant treatment requires child/adolescent specialist assessment, usually concurrent therapy, and close monitoring for emergent suicidal behaviour, self-harm or hostility. NICE identifies fluoxetine as the antidepressant whose benefits most clearly outweigh risks for moderate-severe depression in this group [15]. |
| Older adults | Depression and neurocognitive disorder may coexist. Review pain, bereavement, isolation, sensory loss, medicines and medical illness. With antidepressants, check interactions and monitor falls/fractures and hyponatraemia, especially with diuretics. ECT risk-benefit and cognition require individual review; age alone is not an absolute contraindication [11]. |
| Pregnancy/postpartum | Balance risks of untreated illness against medication and fetal/neonatal risks; avoid abrupt discontinuation and involve perinatal mental-health/obstetric expertise. NICE supports psychological therapy and, when indicated after informed discussion, a TCA/SSRI/SNRI. Consider ECT in pregnancy for severe depression, mixed states, mania or catatonia when maternal or fetal physical health is at serious risk [14]. |
| Possible bipolar depression | Clarify lifetime mania/hypomania and mixed symptoms before an antidepressant. Seek collateral history, refer when suspected, and do not default to unipolar antidepressant monotherapy [11][13]. |
| Clinical situation | Current approach |
|---|---|
| Less severe | Shared decision; guided self-help or psychological treatment is often least intrusive. Active monitoring is appropriate only when the person prefers no treatment or is improving, with planned follow-up—not passive “watchful waiting” [11] |
| More severe | Shared choice among high-intensity psychological therapy, antidepressant medication or combined treatment, matched to clinical need, preference and prior response [11] |
| Psychotic depression | Specialist care; consider antidepressant plus antipsychotic or ECT, with physical monitoring and a relapse plan [11] |
| Limited response | Recheck diagnosis, bipolarity, adherence, dose/duration, comorbidity and psychosocial drivers; then collaboratively switch/augment or use ECT/rTMS with specialist input [11][16] |
| Immediate danger/catatonia/life-threatening self-neglect | Urgent specialist/emergency care. Consider ECT for severe depression when a rapid response is needed, but safety measures begin immediately and are not replaced by the procedure [11] |
The PHQ-2 (first two items of PHQ-9) is a validated brief screen. In its standard scored form, ask how often each symptom occurred over the last 2 weeks:
- Little interest or pleasure in doing things (anhedonia)
- Feeling down, depressed, or hopeless (depressed mood)
These map directly onto the two core DSM-5 symptoms. The past-paper wording uses “in the past month,” which resembles the older Whooley case-finding questions. Either way, a positive screen requires full clinical assessment; a negative screen does not overrule strong clinical concern.
This was directly tested in 2023 Fourth Summative MCQ Q80 — the answer was option B ("little interest in doing things"), as it targets the core symptom of anhedonia. [6]
86% of elderly suicide subjects in HK suffered from psychiatric problems, most commonly major depression. [1]
Always assess suicide risk in any depressed patient. Key domains include:
- Suicidal ideation (passive → active)
- Plan (method, access to means)
- Intent (desire to die, hopelessness)
- Protective factors (reasons for living, social support, dependents)
- Dynamic/contextual factors: previous attempts, recent escalation, access to means, substance use, agitation/insomnia, psychosis, pain/illness, loss/humiliation, isolation, unemployment and debt [1][11]
Risk factors inform a formulation, not a numerical prediction. Document the person's current needs, foreseeable changes, supports, agreed means-safety steps, crisis contacts and follow-up. Do not rely on “no-suicide contracts” or a global low/medium/high label [12].
In the presence of non-disease-related social risk factors (unemployment and unmanageable debt), current MDD independently accounted for 27% of the population-attributable risk of suicide. [1]
Exam Intelligence
| Trap | Correct Understanding |
|---|---|
| "Depression is just low mood" | Must have ≥5/9 symptoms including ≥1 core, for ≥2 weeks, with functional impairment |
| Starting an antidepressant without a lifetime mood history | Ask about mood elevation with increased energy/overactivity, reduced need for sleep and disinhibition; possible bipolar depression needs a different pathway |
| Missing medical causes | Review medicines/substances and examine for medical mimics; order TFT and other tests when clinically indicated rather than using one universal panel |
| PHQ-9 = diagnostic | Rating scales are useful but NOT diagnostic — should not substitute for clinical diagnosis [1] |
| Psychomotor agitation/retardation is subjective | DSM-5 requires it to be observable by others |
| Bereavement exclusion still applies | Removed in DSM-5. You CAN diagnose MDD during bereavement if criteria are met |
| “Suicide risk = low” after a scale | Scales and low/medium/high labels do not predict suicide or determine discharge; formulate needs and safety collaboratively [12] |
| ECT is either punishment or an automatic first-line response to suicidal thoughts | Modern ECT is an anaesthetised, monitored treatment considered for severe depression when rapid response is needed, preferred or other treatments failed [11] |
| All antidepressants are interchangeable | Average efficacy differs modestly; individual choice is driven by prior response, preferences, comorbidity, interactions, overdose toxicity and withdrawal burden |
| Dysthymia = mild episodic depression | Persistent depressive disorder is chronic (≥2 years in adults) and may include persistent major depressive episodes |
A man with low mood, lack of motivation, early morning wakening and hopelessness was assigned Delusion of Guilt in the 2020 MCQ because it was the only mood-congruent depressive option. Strictly, the stem does not describe a fixed false belief or guilt, so it does not independently establish a delusion. In practice, clarify content, conviction, cultural plausibility and resistance before labelling psychosis [5].
High Yield Summary
Core takeaways
- DSM-5 MDD requires ≥5 of 9 symptoms (including depressed mood or anhedonia) for ≥2 weeks with distress/impairment and exclusion of substance/medical causes.
- The two-week rule is not a reason to delay urgent care for suicide risk, psychosis, catatonia, dehydration or severe deterioration.
- Ask about lifetime mania/hypomania before diagnosing unipolar depression or prescribing; increased energy/overactivity is crucial.
- Brief scales such as PHQ-2/PHQ-9 support recognition and monitoring but are not diagnostic and do not replace direct suicide assessment.
- Formulate suicide risk dynamically; do not use a score or low/medium/high label to predict suicide or determine discharge.
- Aetiology is biopsychosocial; neither “low serotonin” nor a brain scan is a diagnostic explanation.
- Treatment is shared and stepped: guided self-help/psychological approaches are often first for less severe depression; more severe illness may need medication, therapy or both.
- When prescribing, consider early activation/suicidality, bipolarity, overdose toxicity, interactions and withdrawal; taper rather than stop abruptly.
- Modern ECT is anaesthetised and monitored. Consider it for severe depression when rapid response is needed, it is preferred based on past response, or other treatments failed.
- The visual treatment evidence has limits: the Tai Chi groups converge by week 24; TMS responses vary; the 15-person open-label tDCS study is hypothesis-generating.
- Children/adolescents, older adults and perinatal patients require population-specific assessment, monitoring and specialist input.
Active Recall - Mood Disorders: Depression
[1] Lecture slides: GC 164. I am depressed Mood disorders.pdf [2] Senior notes: Maksim Medicine Notes.pdf (Geriatrics - Dementia section) [3] Senior notes: Ryan Ho Psychiatry.pdf (Ch 7 Mood Disorders) [4] Lecture slides: Seminar 2 - Psychopathology - Dr Simon SY Lui_1_9_2025.pdf [5] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q93) [6] Past papers: 2023 Fourth Summative MCQ.pdf (Q80) [7] Past papers: 2024 Fourth Summative MCQ.pdf (Q14) [10] World Health Organization. Depressive disorder (depression). Updated 29 August 2025. https://www.who.int/news-room/fact-sheets/detail/depression [11] NICE. Depression in adults: treatment and management (NG222). Published 2022; current recommendations. https://www.nice.org.uk/guidance/ng222/chapter/Recommendations [12] NICE. Self-harm: assessment, management and preventing recurrence (NG225). Published 2022. https://www.nice.org.uk/guidance/ng225/chapter/recommendations [13] NICE. Bipolar disorder: assessment and management (CG185). Updated 2025. https://www.nice.org.uk/guidance/cg185/chapter/recommendations [14] NICE. Antenatal and postnatal mental health: clinical management and service guidance (CG192). https://www.nice.org.uk/guidance/cg192/chapter/recommendations [15] NICE. Depression in children and young people: identification and management (NG134). Reviewed 2024. https://www.nice.org.uk/guidance/ng134/chapter/Recommendations [16] NICE. Repetitive transcranial magnetic stimulation for depression (HTG396). https://www.nice.org.uk/guidance/htg396 [17] NICE. Transcranial direct current stimulation (tDCS) for depression (HTG382). https://www.nice.org.uk/guidance/htg382/chapter/1-recommendations
GC163 I Am A Superman Bipolar Disorder
Bipolar disorder is a chronic mood disorder characterized by episodic fluctuations between mania (or hypomania)—during which grandiose delusions such as believing oneself to be a superhero may occur—and depression, with intervening periods of euthymia.
GC165 I Can’t Fall Asleep Sleep Physiology And Sleep Disorders
Sleep physiology encompasses the neurobiological mechanisms regulating the sleep-wake cycle, including circadian and homeostatic processes, while sleep disorders such as insomnia, narcolepsy, and obstructive sleep apnea represent disruptions in these processes leading to impaired sleep initiation, maintenance, or quality.