--- module: 024-01 language: en chapter: 24 title: "Thyroid, Adrenal, Calcium, and Bone Physiology and Disease" module_title: "Foundations" source_sha256: 3acd1af15beac51ba8776a309f8d3a107904d9a757b3c62dd341dcfbfe3278a4 --- # Thyroid, adrenal, calcium, and bone foundations ## Thyroid hormone synthesis and action ### Sodium-iodide symporter concentrates iodide ### Thyroid peroxidase oxidises and attaches iodide #### Coupling forms thyroxine and triiodothyronine ### Colloid stores hormone until proteolysis ### Mostly thyroxine secreted #### Deiodinases make active or inactive forms ### Free hormone binds nuclear receptors ### Stimulating hormone and negative feedback ## Hypothyroidism ### Primary: autoimmunity, treatment, iodine, drugs ### Paired stimulating hormone and free thyroxine #### Primary: high stimulating hormone, low thyroxine #### Central: inappropriately low or normal ### Levothyroxine dose individualised #### Iron, calcium, food reduce absorption ### Myxoedema coma: severe decompensation #### Urgent hormone, glucocorticoid cover, triggers ## Thyrotoxicosis and structural thyroid disease ### Excess tissue exposure to thyroid hormone #### Graves disease stimulates the receptor #### Toxic nodules secrete autonomously #### Thyroiditis releases stored hormone #### Exogenous hormone bypasses synthesis ### Radionuclide uptake separates cause #### High uptake: active synthesis #### Low uptake: thyroiditis or exogenous hormone ### Thionamides inhibit synthesis #### Agranulocytosis: fever or sore throat is urgent ### Storm: block adrenergic effects to trigger ### Nodules: ultrasound risk and needle sampling ## Adrenal cortical organisation ### Glomerulosa: aldosterone via angiotensin, potassium ### Fasciculata: cortisol via adrenocorticotropic hormone ### Reticularis: adrenal androgens ### Cortisol supports vascular tone and gluconeogenesis ### Aldosterone acts on principal cells #### Sodium reabsorption, potassium secretion ### Renin: low perfusion, macula densa, sympathetic ## Adrenal insufficiency and crisis ### Primary: cortex destroyed #### Cortisol and aldosterone deficiency ### Central: aldosterone usually preserved ### Chronic glucocorticoids suppress the axis ### Pigmentation, salt craving, hyperkalaemia in primary ### Hyponatraemia in both forms ### Crisis: shock, vomiting, hypoglycaemia #### Do not delay treatment for testing #### Hydrocortisone, isotonic fluid, glucose ### Sick-day dosing, identification, rescue injection ## Cortisol excess ### Cushing syndrome most often iatrogenic ### Dependent: pituitary or ectopic secretion ### Independent: adrenal lesion ### Screening: suppression, free cortisol, nadir #### Confirm and exclude exogenous before localising ### Treat source; temporary replacement after cure ## Aldosterone disorders and adrenal masses ### Primary aldosteronism: hypertension, low renin #### Potassium may remain normal #### Aldosterone-renin screening, then localise #### Unilateral surgery, bilateral receptor blockade ### Catecholamine tumours: headache, sweating, palpitations #### Alpha blockade before beta blockade ## Calcium regulation ### Ionised calcium drives excitability and clotting #### Total calcium varies with albumin and pH ### Parathyroid hormone rises as calcium falls #### Renal calcium reabsorption, phosphate excretion ### Vitamin D: skin or diet, liver, kidney ### Magnesium needed for parathyroid function #### Severe deficiency: resistant hypocalcaemia ## Hypercalcaemia and hypocalcaemia ### Mostly hyperparathyroidism or malignancy ### Measure parathyroid hormone early #### High or normal: parathyroid dependent #### Suppressed: investigate other causes ### Severe: volume, antiresorptive, monitoring ### Hypocalcaemia: tingling, tetany, long QT #### Intravenous calcium with cardiac monitoring ## Bone remodelling and osteoporosis ### Osteoclasts resorb, osteoblasts form, osteocytes sense #### Excess resorption weakens architecture ### Silent vertebral, disabling hip fractures ### Exercise, falls prevention, calcium, vitamin D ### Antiresorptive versus anabolic drugs #### Some agents rebound: plan an exit