Endocrinology & Metabolic

Autoimmune destruction of the adrenal cortex that removes cortisol and aldosterone together, so the clinical picture (fatigue and hypoglycaemia from cortisol loss, hyperpigmentation from unchecked ACTH, and salt-wasting hypotension from aldosterone loss) can be predicted from which hormone is missing.

A state of cortisol excess, most often from prescribed steroids, that drives protein catabolism, gluconeogenesis and fat redistribution in patterns predictable directly from cortisol's normal actions taken too far.

A medical emergency in which absolute or severe relative insulin deficiency unleashes unopposed lipolysis and ketogenesis alongside unrestrained hyperglycaemia, producing a life-threatening triad of hyperglycaemia, ketonaemia and acidosis that fluids, insulin and potassium replacement are designed to reverse in that order.

A state of thyroid hormone excess that accelerates metabolic rate across almost every tissue, so the clinical picture (weight loss despite hunger, heat intolerance, tachycardia and tremor) can be derived directly from asking what a sped-up metabolism looks like.

A state of thyroid hormone deficiency that slows metabolic rate in virtually every tissue, so the whole clinical picture (from bradycardia to cold intolerance to slowed cognition) can be predicted simply by asking what happens when metabolism runs too slowly.

A catecholamine-secreting tumour of the adrenal medulla that releases adrenaline and noradrenaline in unpredictable surges, producing the classic paroxysmal triad of headache, palpitations and sweating alongside episodic, sometimes crisis-level, hypertension.

Autonomous aldosterone secretion, independent of the renin-angiotensin system, that drives renal sodium retention and potassium/hydrogen loss, producing hypertension with a suppressed renin that is the biochemical signature the diagnostic test is built to detect.

An autoimmune disease that destroys pancreatic beta cells until insulin secretion fails almost completely, so glucose rises unchecked and unopposed lipolysis drives ketone production: the mechanism behind both the presentation and the risk of diabetic ketoacidosis.

A disease of insulin resistance plus progressive beta-cell failure that raises glucose enough to cause osmotic symptoms and long-term vascular damage; treatment lowers glucose while attacking the cardiovascular risk that actually kills patients.