Psych CASC / OSCE · Foundations — psychoneuroendocrinology and psychoimmunology
Explain stress hormones, inflammation, and prolactin side-effects to a patient and partner — CASC communication station
MRCPsych/FRANZCP-style CASC: plain-language HPA/immune biology, biomarker humility, trauma framing, and antipsychotic prolactin counselling.
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Target exams
Station brief
Format. Communication station, approximately 7–10 minutes after reading. You are the psychiatry registrar in an outpatient clinic. [2]
Candidate instructions. Build rapport. Explain how stress systems (HPA) and inflammation can influence energy, motivation, and mood without claiming cortisol or CRP diagnose depression. Place interferon as a known risk context for mood change. Address childhood trauma as a vulnerability factor, not irreversible doom. Explain risperidone-related prolactin effects in plain language and what monitoring/management means. Invite questions; safety-net severe medical symptoms. Avoid jargon dumps and invented certainty. [1][3][4][5]
Candidate scenario
Patient may say: 'Can we just measure cortisol and prove the diagnosis?' Partner may say: 'Trauma ruined the hormone system permanently.' Respond: diagnosis is clinical (history and mental state); labs help physical health and sometimes medical differentials; stress systems can change with recovery and treatment; hope and agency matter. [2][5]
Marking domains
- Empathy, plain language, collaborative stance
- Accurate HPA/immune overview without chemical cartoons [1][2]
- Honest limits of DST/cortisol/CRP for psychiatric diagnosis [2][3]
- Trauma framed as vulnerability, not hopeless determinism [5]
- Prolactin mechanism and practical next steps at lay depth [4]
- Organic red-flag safety netting without unnecessary alarm
- Hope, shared plan, risk/safety check
- No invented legal section numbers
Reveal assessor key
Open. Role, agenda-setting, check understanding and fears. [2]
Core biology. Stress and immune signals can change brain systems for energy and motivation; medical treatments such as interferon can contribute to low mood in some people; this helps explain symptoms, it does not mean depression is 'only infection.' [1][3]
Tests. We do not diagnose depression with cortisol or inflammation blood tests. We use blood tests for physical health and when we worry about a medical cause. [2][3]
Trauma. Early adversity can sensitise stress systems; brains and people can still recover with treatment and support. Avoid fatalism. [5]
Prolactin. Some antipsychotics raise the hormone prolactin by blocking dopamine pathways that normally keep it in check; that can cause milk leakage and missed periods; we can check a blood test and adjust medicine if needed. [4]
Close. Summarise depression treatment plan; coordinate medical care; safety-net suicidal thoughts and severe physical symptoms; invite questions. [2][3]
References
- [1]Dantzer R, O'Connor JC, Freund GG, et al. From inflammation to sickness and depression: when the immune system subjugates the brain Nat Rev Neurosci, 2008.PMID 18073775
- [2]Pariante CM, Lightman SL The HPA axis in major depression: classical theories and new developments Trends Neurosci, 2008.PMID 18675469
- [3]Miller AH, Raison CL The role of inflammation in depression: from evolutionary imperative to modern treatment target Nat Rev Immunol, 2016.PMID 26711676
- [4]Haddad PM, Wieck A Antipsychotic-induced hyperprolactinaemia: mechanisms, clinical features and management Drugs, 2004.PMID 15456328
- [5]Heim C, Nemeroff CB The role of childhood trauma in the neurobiology of mood and anxiety disorders Biol Psychiatry, 2001.PMID 11430844