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Mental Health

Notes, summaries and exam pearls for this rotation. Every note opens as a PDF in a new tab.

Use as a study guide only. These notes are part of a free open-access medical education (FOAMed) project and may contain errors or outdated information. Always verify against current guidelines (e.g. eTG, RACGP, local health district policies) and reputable sources before applying anything to patient care. See the full disclaimer.

From the wards

Clinical pearls & learnings

Tips and tricks collected over the years — a living list that grows with every rotation. Use as a study guide only and check current guidelines before acting on anything.

Mood disorders

Unipolar vs bipolar depression

Always screen for past mania or hypomania before starting an SSRI — in undiagnosed bipolar disorder an SSRI can flip the patient into a manic episode.

  • Ask about discrete periods of elevated mood, decreased need for sleep, racing thoughts, impulsive spending or risk-taking.
  • A family history of bipolar disorder raises the pre-test probability.
Dysthymia (persistent depressive disorder)

Chronic low-grade depressive symptoms (≥2 years) with relatively preserved function. It can precipitate or coexist with a major depressive episode (social and occupational dysfunction lasting at least 2 weeks) — so-called double depression.

  • Useful screening question for anhedonia: “The things that used to give you joy — do you still enjoy them the same as this time last year?”
  • Cover biological symptoms (change in appetite, weight, energy, sleep) and cognitive symptoms (preoccupation with death and dying, suicidal ideation).
  • Management: consider an SSRI for symptoms, plus personalised care — take a developmental history to gauge resilience and coping style.

Beware a low MoCA in a patient with previous strokes — refer to a memory clinic; they are at high risk of vascular dementia and “depression” may be early cognitive decline.

Melancholic depression
  • A severe, biological subtype of depression: diurnal mood variation (worse in the morning), early-morning waking, profound anhedonia and psychomotor change.
  • Responds well to TCAs and to ECT.
  • May be superimposed on chronic long-term mental illness and functional impairment, often unmasked by a crisis event.
  • Set an explicit timeline and goals of treatment with the patient.
Differentials for “depression”
  • Agoraphobia — restricted access to medications, check-ups and social contact can mimic or drive low mood.
  • Personality disorder (especially borderline).
  • Complex PTSD from early-life trauma.
  • Schizoaffective disorder and chronic psychotic depression.
  • Organic causes — early-onset dementia, learning disability, comorbid substance use.

Comorbidity is the rule, not the exception — patients rarely have just one mental health condition. Screen broadly.

Psychosis & named syndromes

Cotard syndrome (“walking corpse syndrome”)
  • Nihilistic delusions — a firm belief that one is dead, rotting or putrefying.
  • Denial of body parts — believing one's brain, heart, blood or soul no longer exists or functions.
  • Delusions of immortality — the contradictory but common belief that, being already dead, they can never truly die.
  • Self-neglect — refusing to eat or bathe, since a “dead” body needs no sustenance.

Classically seen in severe (psychotic) depression — ECT is often effective.

Delirium

Hypoactive delirium
  • The most common subtype — and the most missed, because the patient is quiet and “easy to manage”.
  • A major differential post-operatively.
  • A marker of increased morbidity and mortality — finding it should trigger a hunt for the cause.
Hunting the precipitant

The cause of delirium is often hard to identify — screen systematically:

Delirium precipitants — screen every column

DomainPrecipitantWhat to do
HaematologicalBlood loss / anaemiaFBC, look for an occult bleeding source
NeurologicalPrevious strokes — background cognitive vulnerabilityCollateral history of baseline cognition
DrugsBenzodiazepine or alcohol withdrawalTime since last dose/drink; chart a withdrawal scale
DrugsPolypharmacy — anticholinergics and sedativesMedication reconciliation and deprescribe
InfectionAny sepsis, especially urinary tract infectionSeptic screen; treat the source
EnvironmentSleep–wake cycle disruption, new environmentOrientation aids, daylight, familiar objects, glasses/hearing aids

Personality, therapy & defences

Borderline personality disorder & DBT
  • Dialectical behaviour therapy (DBT) is the best-evidenced treatment for BPD — low self-worth, impulsivity, emotional dysregulation, disrupted relationships, recurrent suicidal behaviour.
  • Self-harm (e.g. cutting) often functions as a way to distract from or regulate overwhelming emotional distress, rather than as a suicide attempt — ask about the function of the behaviour.
Defence mechanisms
MaturityExamplesPearl
ImmatureDenial, splitting, idealisation / devaluation, projectionPatients who struggle to voice criticism may hold an idealised view of others to cope
MatureHumour, sublimation, suppression, altruismPresence of mature defences is a positive prognostic sign

Transference and countertransference are phenomena of the therapeutic relationship (feelings redirected onto the therapist, and the therapist's response) — worth naming in a viva, but they are not defence mechanisms.

Trauma, PTSD & dissociation

PTSD pearls
  • Ask about family history — heritable vulnerability is real.
  • Patients sit at a lowered threshold for an adrenergic response — an intercurrent illness or infection can precipitate panic attacks via a positive biofeedback loop.
  • First-line: trauma-focused psychotherapy (trauma-focused CBT, EMDR); CBT also helps patients cope with concurrent medical treatment.
  • After sexual assault: refer to a specialised sexual assault service; therapy must be patient-lednever pressured.
  • Alcohol is a common (maladaptive) coping strategy — screen for it alongside anxiety symptoms.

Panic: attack vs disorder

Panic attackPanic disorder
TriggerClear, identifiable triggerRecurrent, unexpected attacks — no clear trigger
Between episodesWellAnticipatory anxiety about the next attack
Dissociation & memory loss
  • Types: derealisation, depersonalisation, dissociative amnesia.
  • A primitive defensive coping strategy to overwhelming stress — e.g. an abused child “switches off”, retreats to their room and retains only vague memories.
  • Triggers can be re-traumatising events (e.g. a violation, or even taking a medication associated with the trauma).
  • In consults, watch for the patient forgetting the question or spacing out — ask yourself: are they aware, present, or disconnected from their environment and body?
Clinician wellbeing: vicarious trauma & burnout
  • Vicarious trauma (from repeated exposure to others' trauma) → CBT plus deliberate self-care.
  • Burnout is dominated by emotional symptoms (exhaustion, depersonalisation, reduced accomplishment); chronic fatigue syndrome (ME/CFS) is dominated by physical symptoms — post-exertional malaise, muscle pain.
Adverse childhood experiences (ACEs) & chronic pain

ACEs are strongly associated with chronic pain syndromes — via dysregulation of the HPA axis and altered central pain processing. A trauma history is part of a chronic pain assessment.

MSE & risk assessment

MSE — appearance tells you more than you think
  • Comment on build, grooming and hygiene: e.g. “tall, thin; hair tidy; kempt”.
  • Good hygiene and grooming imply intact executive function — a positive prognostic sign.
  • Self-neglect points the other way, especially in someone who lives alone.
Risk assessment — cover every domain

Risk domains — name each one explicitly

DomainWhat to ask about
HarmSuicidal ideation, self-harm, harm to others — including being exploited by others
SubstancesType and volume; risk of overdose and of withdrawal
MisadventureFalls, subdural haemorrhage; physical sequelae — cirrhosis, encephalopathy, pancreatitis
SocialIsolation and lack of supportive relationships
FinancialFinancial risks that perpetuate the illness
CognitiveInsight and capacity for rational thinking
Smoking cessation ladder
  1. Varenicline (Champix) — most effective single agent
  2. Combination NRT (patch + short-acting)
  3. Single-agent NRT

Efficacy, highest first — combine any of these with behavioural support.

Alcohol use disorder & withdrawal

Assessment pearls
  • Withdrawal starts within 6–24 hours of the last drink, driven by CNS hyperexcitation and adrenergic overactivity; it peaks around day 2–3 — expect marked anxiety then.
  • Anxiety is often the precipitant of drinking, and drinking often started as a coping mechanism from an early age — leaving no opportunity to test out new coping strategies during adolescence.
  • Previous periods of abstinence are a good prognostic sign.
  • Chronic alcohol use damages the frontal lobes — impulsivity, disinhibition and executive dysfunction — and this cognitive impairment itself makes rehabilitation harder.
  • Alcohol is a depressant: aim for at least 2 weeks of abstinence before diagnosing depression — abstinence itself often treats the low mood better than an antidepressant.
  • Concurrent benzodiazepines potentiate alcohol — beware combined sedation.
Withdrawal management
  1. Chart an alcohol withdrawal scale (AWS) and treat to score
  2. Diazepam (e.g. 10mg QID initially, then taper)
  3. Substitute oxazepam if cirrhosis / advanced liver disease, elderly, or significant renal impairment (no active metabolites — but shorter-acting, so watch for breakthrough symptoms and delirium)
  4. Lower doses if respiratory compromise
  5. Thiamine (IV, before glucose) in everyone
  • Oxazepam ≈ 3× the diazepam dose for equivalence (diazepam 5mg ≈ oxazepam 15mg).
  • Check synthetic liver function — INR/PT and albumin — not just transaminases.
  • Examine for encephalopathy and cerebellar disease: nystagmus, ataxia, altered mental state.
  • Image the abdomen (USS ± CT abdomen/pelvis) if cirrhosis or complications are suspected.

Beware Wernicke's encephalopathy (thiamine deficiency — confusion, ataxia, ophthalmoplegia): highest risk in alcohol withdrawal and post gastric bypass. Give thiamine before any glucose load.

Relapse-prevention pharmacotherapy
AgentNotes
NaltrexoneFirst-line; reduces craving and heavy-drinking days
AcamprosateFirst-line; continue for at least 3 months and ideally ≥12 months for full effect
Topiramate (off-label)Useful alternative — favourable effect on drinking habit, weight and GGT, but twice-daily dosing
GLP-1 agonistsEmerging evidence of reduced alcohol intake — watch this space

Don't chase the GGT in isolation — quarterly LFTs are a reasonable monitoring rhythm, using biomarkers to track progress rather than police it.