Psychoneuroendocrinology and psychoimmunology — structured clinical viva · Psych Vivas

Prompt

You are examining a psychiatry registrar. A 34-year-old with treatment-resistant depression, early childhood trauma, mild CRP elevation during a respiratory infection, and a relative asking whether 'cortisol and inflammation tests can diagnose depression' is discussed. Separately, a patient on risperidone has amenorrhoea and galactorrhoea. Walk the panel through HPA biology and allostatic load, GR models, sickness behaviour and cytokine pathways, investigation limits (DST, CRP/IL-6), trauma programming, hyperprolactinaemia management, and how you formulate and treat without biomarker overclaim. Name landmark anchors.

Interpretation

Reveal interpretation

HPA and load. CRH–ACTH–cortisol with GR/MR feedback; chronic stress as allostatic load rather than a single fight-or-flight moment. [1][2]

Depression models. GR hypothesis (Holsboer); HPA abnormalities more prominent in severe/melancholic samples; childhood trauma programs stress systems. [3][5]

Immune. Sickness behaviour explains fatigue/anhedonia/withdrawal overlap; inflammation matters in a subset and in medical illness; not all MDD. [4][7]

Tests. DST is historical melancholia research, not modern MDD diagnosis. CRP/IL-6 do not diagnose depression. [8][2][7]

Prolactin. D2 blockade → hyperprolactinaemia; manage with confirmation, pregnancy exclusion if needed, dose/switch strategies, referral. [6]

Communication. Biology explains vulnerability and physical-health needs; diagnosis remains clinical; treat depression and medical issues; risk assessment clinical. [7]

Key points

References

[1]McEwen BS Protective and damaging effects of stress mediators N Engl J Med, 1998.PMID 9428819
[2]Pariante CM, Lightman SL The HPA axis in major depression: classical theories and new developments Trends Neurosci, 2008.PMID 18675469
[3]Holsboer F The corticosteroid receptor hypothesis of depression Neuropsychopharmacology, 2000.PMID 11027914
[4]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
[5]Heim C, Nemeroff CB The role of childhood trauma in the neurobiology of mood and anxiety disorders Biol Psychiatry, 2001.PMID 11430844
[6]Haddad PM, Wieck A Antipsychotic-induced hyperprolactinaemia: mechanisms, clinical features and management Drugs, 2004.PMID 15456328
[7]Miller AH, Raison CL The role of inflammation in depression: from evolutionary imperative to modern treatment target Nat Rev Immunol, 2016.PMID 26711676
[8]Carroll BJ, Feinberg M, Greden JF, et al. A specific laboratory test for the diagnosis of melancholia Arch Gen Psychiatry, 1981.PMID 7458567

Interpretation

Reveal interpretation

HPA and load. CRH–ACTH–cortisol with GR/MR feedback; chronic stress as allostatic load rather than a single fight-or-flight moment. [1][2]

Depression models. GR hypothesis (Holsboer); HPA abnormalities more prominent in severe/melancholic samples; childhood trauma programs stress systems. [3][5]

Immune. Sickness behaviour explains fatigue/anhedonia/withdrawal overlap; inflammation matters in a subset and in medical illness; not all MDD. [4][7]

Tests. DST is historical melancholia research, not modern MDD diagnosis. CRP/IL-6 do not diagnose depression. [8][2][7]

Prolactin. D2 blockade → hyperprolactinaemia; manage with confirmation, pregnancy exclusion if needed, dose/switch strategies, referral. [6]

Communication. Biology explains vulnerability and physical-health needs; diagnosis remains clinical; treat depression and medical issues; risk assessment clinical. [7]

Key points

References

[1]McEwen BS Protective and damaging effects of stress mediators N Engl J Med, 1998.PMID 9428819
[2]Pariante CM, Lightman SL The HPA axis in major depression: classical theories and new developments Trends Neurosci, 2008.PMID 18675469
[3]Holsboer F The corticosteroid receptor hypothesis of depression Neuropsychopharmacology, 2000.PMID 11027914
[4]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
[5]Heim C, Nemeroff CB The role of childhood trauma in the neurobiology of mood and anxiety disorders Biol Psychiatry, 2001.PMID 11430844
[6]Haddad PM, Wieck A Antipsychotic-induced hyperprolactinaemia: mechanisms, clinical features and management Drugs, 2004.PMID 15456328
[7]Miller AH, Raison CL The role of inflammation in depression: from evolutionary imperative to modern treatment target Nat Rev Immunol, 2016.PMID 26711676
[8]Carroll BJ, Feinberg M, Greden JF, et al. A specific laboratory test for the diagnosis of melancholia Arch Gen Psychiatry, 1981.PMID 7458567