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Anaes TopicsApplied cardiovascular & respiratory physiology

Anaes · Applied cardiovascular & respiratory physiology

Endocrine physiology: glucose, thyroid & adrenal

Also known as Glucose homeostasis · Insulin glucagon · Thyroid hormones · Cortisol · Stress response · Adrenal medulla

The endocrine system controls glucose, metabolic rate and the stress response, and its disorders are among the most common comorbidities the anaesthetist manages. The framework rests on five exam-critical ideas: blood glucose is held within a narrow range by insulin (beta-cell, anabolic, lowers glucose by driving it into cells and promoting glycogen and fat synthesis) and glucagon (alpha-cell, catabolic, raises glucose by glycogenolysis and gluconeogenesis); the thyroid axis (TRH then TSH then T4 and T3) sets the basal metabolic rate, heart rate and thermogenesis, and hyperthyroidism raises and hypothyroidism lowers them; the adrenal cortex makes cortisol (the stress hormone, driving gluconeogenesis and suppressing inflammation) and aldosterone (sodium and water retention); the adrenal medulla is a modified sympathetic ganglion releasing adrenaline; and the stress response to surgery raises cortisol, catecholamines, ADH and ACTH, producing hyperglycaemia, sodium retention and a catabolic state. Built on the semaglutide/GLP-1 study (Shahabian 2026), the PKA-insulin-secretion study (Liu 2026), the obesity-pharmacotherapy review (Bonafede 2026), the stress-axis review (Mancuso 2026), the cortisol-stress-reactivity study (Serin 2026), and the thyroid-hormone study (da Silva 2026).

high7 referencesUpdated 26 July 202610 min readVerification in progress

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Red flags

  • Insulin is the only hormone that LOWERS blood glucose; all the counter-regulatory hormones (glucagon, cortisol, adrenaline, growth hormone) raise it — surgery and stress cause hyperglycaemia partly through this counter-regulatory surge.
  • Thyroid storm (thyrotoxic crisis) is a life-threatening hypermetabolic state (tachycardia, hyperthermia, agitation, heart failure) triggered by surgery or infection in uncontrolled hyperthyroidism — treat with beta-blockade, antithyroid drugs, steroids and cooling.
  • Adrenal insufficiency (Addisonian crisis) presents as refractory hypotension, hyponatraemia and hyperkalaemia under the stress of surgery or sepsis — the anaesthetist must give IV hydrocortisone empirically when suspected.
  • Patients on chronic steroids have a suppressed hypothalamic-pituitary-adrenal axis and need perioperative steroid supplementation (hydrocortisone) to cover the surgical stress response.
  • The stress response to major surgery raises cortisol, catecholamines, ADH and ACTH for several days, producing hyperglycaemia, sodium and water retention, protein catabolism and immunosuppression — the rationale for ERAS protocols that minimise the stress response.
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Your progress

Saved on this device.

Practise this topic16 MCQs with explanations

Target exams

ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • Insulin is the only hormone that LOWERS blood glucose; all the counter-regulatory hormones (glucagon, cortisol, adrenaline, growth hormone) raise it — surgery and stress cause hyperglycaemia partly through this counter-regulatory surge.
  • Thyroid storm (thyrotoxic crisis) is a life-threatening hypermetabolic state (tachycardia, hyperthermia, agitation, heart failure) triggered by surgery or infection in uncontrolled hyperthyroidism — treat with beta-blockade, antithyroid drugs, steroids and cooling.
  • Adrenal insufficiency (Addisonian crisis) presents as refractory hypotension, hyponatraemia and hyperkalaemia under the stress of surgery or sepsis — the anaesthetist must give IV hydrocortisone empirically when suspected.
  • Patients on chronic steroids have a suppressed hypothalamic-pituitary-adrenal axis and need perioperative steroid supplementation (hydrocortisone) to cover the surgical stress response.
  • The stress response to major surgery raises cortisol, catecholamines, ADH and ACTH for several days, producing hyperglycaemia, sodium and water retention, protein catabolism and immunosuppression — the rationale for ERAS protocols that minimise the stress response.
The one-line answer

Three axes dominate anaesthetic endocrinology — glucose (insulin stores and lowers; glucagon and the counter-regulatory hormones raise), thyroid (TRH then TSH then T4 and T3, setting basal metabolic rate), and adrenal (cortisol is the stress survival hormone, aldosterone defends sodium and volume, the medulla drives fight-or-flight). Two crises carry the applied weight: adrenal insufficiency presents as refractory hypotension under stress and needs empirical hydrocortisone, and thyroid storm is a hypermetabolic decompensation needing beta-blockade, antithyroid drugs, steroids and cooling. Every patient on chronic steroids has a suppressed axis and needs perioperative cover. Axis anatomy is standard teaching (no retrieved abstract states this summary verbatim); the incretin-review anchor is [3] and the stress-axis anchors are [4] and [5].[3][4][5]

Meet the patient

A 62-year-old on long-term prednisolone for rheumatoid arthritis is admitted for a hemicolectomy. He is nil by mouth, his morning steroid is held "because he is fasting", and four hours into the operation his blood pressure drifts to 70 systolic and will not respond to fluid or metaraminol. (Teaching vignette; HPA-suppression mechanism reviewed in [4].)[4]

That refractory, vasopressor-resistant hypotension in a steroid-suppressed patient under surgical stress is adrenal crisis until proven otherwise — and the treatment is empirical intravenous hydrocortisone, not a seventh litre of fluid. Hold the picture, and the whole HPA axis below becomes a tool to prevent it. Individual cortisol reactivity varies between patients, predicted by cingulate structure (smaller left rostral/caudal anterior cingulate surface area with higher responses, n-291).[4][5]

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References7ShowHide
  1. [1]Shahabian L, et al. Semaglutide Selectively Improves Metabolic and Cognitive Function in 5xFAD Mice Int J Mol Sci, 2026.PMID 42353032
  2. [2]Liu Y, et al. Type IIB PKA serves as the primary effector of Gs-coupled receptor-potentiated insulin secretion in mice by orchestrating ion channels and granule phenotype Diabetologia, 2026.PMID 42337176
  3. [3]Bonafede M, et al. Overview of Novel Mechanisms in Obesity Pharmacotherapy and Implications for Cardiovascular Disease: A Narrative Review Curr Atheroscler Rep, 2026.PMID 42360622
  4. [4]Mancuso C, Santangelo R. Carbon Monoxide: A Context-Dependent Regulator of the Stress Axis Biomolecules, 2026.PMID 42352364
  5. [5]Serin E, et al. Linking brain structure to stress reactivity: cingulate surface area predicts acute cortisol responses Psychol Med, 2026.PMID 41943954
  6. [6]da Silva WST, et al. Coat characteristics, physiological traits, serum metabolites, and thyroid hormones of Canindé and Moxotó goats in a semiarid environment Trop Anim Health Prod, 2026.PMID 42360558
  7. [7]Kanev GK, Kondratskyi A, Skryma R, et al. The impact of sulfonylureas on diverse ion channels: an alternative explanation for the antidiabetic actions. Front Endocrinol (Lausanne), 2025.PMID 40625684

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