Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Distinguish unipolar depression from bipolar, psychiatric, neurological, endocrine, sleep, substance and medicine-related causes through chronology, examination and targeted tests while avoiding both diagnostic overshadowing and indiscriminate screening.
Unipolar depression is a longitudinal diagnosis. Ask about every previous episode and recovery, not only the current low mood. A period of elevated or irritable mood with reduced need for sleep, increased activity, talkativeness, grandiosity or risky behaviour raises bipolarity. Clarify duration, impairment, substance relationship and whether antidepressants preceded activation. Family history supports probability but cannot decide the diagnosis. Refer when bipolar disorder remains plausible rather than escalating antidepressant monotherapy automatically.
Psychiatric differentials overlap. Grief may bring waves tied to reminders and preserved positive emotion, although depression can coexist. Adjustment disorder remains related to an identifiable stressor without the full depressive pattern. Generalised anxiety, panic and PTSD can produce insomnia, fatigue and concentration difficulty but have distinct worry, panic, intrusion, avoidance or hyperarousal mechanisms. Negative symptoms, early psychosis, eating disorders, ADHD, autism and personality-related crises require developmental and longitudinal evidence rather than labels based on one presentation.
Distinct activation with reduced sleep need and increased energy, activity or risk-taking separates possible bipolar illness from ordinary mood reactivity.
Distress may fluctuate around reminders and retain connection or positive emotion, while pervasive anhedonia and worthlessness suggest coexisting depression.
Systemic symptoms, physical signs, medicine exposure or atypical onset support targeted thyroid, calcium, glucose, organ-function or nutritional testing.
Snoring, witnessed apnoeas, morning headache, restless legs or profound daytime sleepiness may explain fatigue and cognitive symptoms beyond depression.
Focal signs, seizure, parkinsonism, altered arousal or rapid cognitive change requires neurological assessment rather than a purely affective formulation.
Identifying previous activation changes antidepressant decisions and can prevent treatment-emergent mood destabilisation or delayed mood-stabilising care.
Sleep apnoea, pain, anaemia, inactivity, poverty and depression can coexist, making treatment of one factor an incomplete diagnostic experiment.
Routine bloods do not test grief, bipolarity, PTSD, sleep apnoea, epilepsy or structural disease without the appropriate clinical method.
Symptoms beginning after initiation, dose escalation or withdrawal increase suspicion but still require assessment of alternative and interacting causes.
Confusion, insomnia, activation or psychosis after childbirth can progress rapidly and demands specialist assessment beyond routine depression follow-up.
Starting antidepressant treatment without asking about previous mania or hypomania.
Ordering a universal blood panel and calling depression excluded when results are normal.
Attributing fatigue to mood without assessing sleep, pain, medicines and physical disease.
Diagnosing substance-induced symptoms from a urine result without timing or clinical correlation.
Pathologising ordinary grief while missing a coexisting pervasive depressive syndrome.
Ignoring postpartum timing, safeguarding and risk to the baby.
Leaving incidental or abnormal results without a named reviewer and communication plan.
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A patient with recurrent depression reports prior episodes of four days with markedly reduced sleep need, increased goal-directed activity and uncharacteristic risky investments. Which differential needs priority?
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Medicines and substances matter. Corticosteroids can alter mood; sedating, anticholinergic or dopamine-active medicines can affect energy and cognition. Alcohol may temporarily reduce distress while worsening sleep, mood and suicide risk; stimulant withdrawal can cause marked dysphoria. Ask dose, pattern, last use and withdrawal rather than recording recreational drugs yes or no. Do not infer causation from one positive urine screen, and avoid abrupt cessation of dependence-forming medicines without a safe plan.
Investigations should answer questions. FBC, U&E, eGFR, liver tests, calcium, glucose or HbA1c, TSH, B12 and folate are common choices when history supports them or before particular treatment. Add pregnancy testing, infection tests, inflammatory markers, ECG, sleep study or neuroimaging for relevant clues. A universal panel can generate incidental findings without excluding major differentials. Document the question, limitation and who will review each result.