Psych MEQs / SAQs · Consultation-liaison psychiatry
Endocrine psychiatry: thyroid, Cushing, Addison, and steroids (MEQ)
FRANZCP-style MEQ on endocrine psychiatry covering syndrome map, Cushing depression, steroid psychosis, AI crisis, lithium–thyroid, and residual prognosis.
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(i) Syndrome map. Thyrotoxicosis: anxiety, irritability, insomnia, panic-like spells, rare mania/psychosis, with suppressed TSH and adrenergic physical signs — sister’s Graves was mislabelled panic until labs.[6] Hypothyroidism: depression, slowing, cognitive fog; rare myxoedema psychosis in severe untreated disease.[6] Cushing: major depression common (Sonino series), irritability/anxiety, cognitive change, less often mania/psychosis — index patient’s progressive depression with cushingoid somatic change.[3][4] Adrenal insufficiency: chronic apathy/low mood; crisis with delirium, shock, hyponatraemia — medical emergency.[5] Exogenous steroids: dose/time-linked insomnia, hypomania/mania, depression, psychosis/delirium — overnight dexamethasone case.[1][2] Discriminators: temporal hormone/drug link, physical signs, labs, and improvement when the driver is corrected versus primary psychiatric longitudinal course.
(ii) Management. Cushing depression: joint care — definitive treatment of hypercortisolism (e.g. transsphenoidal pathway for Cushing disease) is central; assess suicide risk, safety planning, and supportive psychotropics only as adjuncts (e.g. sertraline 25–50 mg oral daily titrated if residual MDD after medical stabilisation allows). Antidepressants alone do not replace cortisol control.[3][4][8] Steroid psychosis: confirm temporal link; liaise to reduce/taper dexamethasone if neurologically safe; environmental safety; short-term low-dose antipsychotic for danger (e.g. olanzapine 2.5–5 mg oral with monitoring, or haloperidol 0.5–2 mg); do not diagnose lifelong bipolar I from a single steroid episode.[1][2]
(iii) Investigations and crises. TSH/free T4 (± free T3) for thyroid phenotypes; hypercortisolism screens with endocrinology if not already confirmed; electrolytes/glucose; short Synacthen pathway when AI suspected.[5][6] Adrenal crisis: parenteral hydrocortisone and fluids immediately per Endocrine Society primary AI guidance — do not delay for MSE completion.[5] Thyroid storm/severe thyrotoxic agitation: medical emergency pathway plus psychiatric safety.[6]
(iv) Lithium–thyroid and prognosis. Baseline and periodic TSH (free T4 if abnormal); lithium associates with hypothyroidism classically and hyperthyroidism in systematic review — both matter.[7] After Cushing control, psychiatric and cognitive features often improve but residual burden is common; arrange follow-up rather than assuming automatic full recovery.[4][8]
References
- [1]Warrington TP, Bostwick JM Psychiatric adverse effects of corticosteroids Mayo Clin Proc, 2006.PMID 17036562
- [2]Dubovsky AN, Arvikar S, Stern TA, et al. The neuropsychiatric complications of glucocorticoid use: steroid psychosis revisited Psychosomatics, 2012.PMID 22424158
- [3]Sonino N, Fava GA, Raffi AR, et al. Clinical correlates of major depression in Cushing's disease Psychopathology, 1998.PMID 9780396
- [4]Pivonello R, Simeoli C, De Martino MC, et al. Neuropsychiatric disorders in Cushing's syndrome Front Neurosci, 2015.PMID 25941467
- [5]Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline J Clin Endocrinol Metab, 2016.PMID 26760044
- [6]Feldman AZ, Shrestha RT, Hennessey JV Neuropsychiatric manifestations of thyroid disease Endocrinol Metab Clin North Am, 2013.PMID 24011880
- [7]Fairbrother F, Petzl N, Scott JG, et al. Lithium can cause hyperthyroidism as well as hypothyroidism: A systematic review of an under-recognised association Aust N Z J Psychiatry, 2019.PMID 30841715
- [8]Piasecka M, Papakokkinou E, Valassi E, et al. Psychiatric and neurocognitive consequences of endogenous hypercortisolism J Intern Med, 2020.PMID 32181937