Endocrinology & Metabolic

Primary adrenal insufficiency: the cortex fails, so cortisol and usually aldosterone are lost together, and any physiological stress can tip a stable patient into adrenal crisis.

Chronic glucocorticoid excess, usually caused by prescribed steroids, produces a recognisable catabolic and metabolic phenotype; endogenous disease needs specialist biochemical confirmation and source localisation.

Diabetes insipidus is the passage of excessive dilute urine because arginine vasopressin is deficient (AVP-D, formerly cranial DI) or the kidney is resistant to it (AVP-R, formerly nephrogenic DI); the immediate danger is hypernatraemic dehydration when thirst, water access or desmopressin fails.

Insulin deficiency lets the liver overproduce glucose and acidic ketone bodies at once, giving hyperglycaemia, ketonaemia and a high-anion-gap metabolic acidosis on top of profound osmotic dehydration.

Hereditary haemochromatosis is inherited dysregulation of iron absorption, usually from HFE C282Y homozygosity, causing progressive parenchymal iron overload; early recognition and specialist venesection can prevent irreversible liver, endocrine, cardiac and joint damage.

Hypercalcaemia is a raised albumin-adjusted serum calcium, most often caused by primary hyperparathyroidism or malignancy; PTH is the pivotal fork, while severe or rapidly symptomatic hypercalcaemia is an emergency requiring careful rehydration and specialist treatment.

In hyperosmolar hyperglycaemic state (HHS), residual insulin suppresses ketone production but not hyperglycaemia, so days of osmotic diuresis produce extreme dehydration and hyperosmolality rather than acidosis.

Hyperparathyroidism is excessive parathyroid hormone secretion: primary disease causes hypercalcaemia through autonomous gland activity, while secondary disease is an appropriate response to chronic kidney disease or vitamin-D deficiency and tertiary disease becomes autonomous after prolonged stimulation.

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.

Hypocalcaemia is low biologically available serum calcium, usually from hypoparathyroidism, vitamin-D deficiency, chronic kidney disease or hypomagnesaemia; rapid or symptomatic hypocalcaemia causes tetany, seizures, laryngospasm and QT prolongation and requires urgent treatment.

The brain can neither make nor store glucose, so when circulating insulin outlasts the available carbohydrate the counter-regulatory response cannot keep up and neuroglycopenia follows within minutes.

Hypoparathyroidism is deficient parathyroid hormone secretion or action, most often after neck surgery, causing hypocalcaemia with hyperphosphataemia; acute symptoms need emergency calcium treatment, while chronic care balances active vitamin D and calcium against hypercalciuria and renal injury.

Hypopituitarism is deficiency of one or more pituitary hormones, producing secondary adrenal, thyroid, gonadal or growth-hormone failure; glucocorticoid deficiency is the immediate life threat, so cortisol replacement and stress cover come before thyroid replacement.

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.

Metabolic syndrome is a high-risk clustering of central adiposity, dysglycaemia, raised blood pressure and atherogenic lipids; it is a risk marker rather than a separate disease, so management is formal cardiovascular-risk assessment plus targeted treatment of weight, glucose, lipids and blood pressure.

Obesity is chronic excess adiposity that impairs health, shaped by biological, environmental, social and genetic factors; assess risk beyond BMI, treat complications and offer sustained behavioural support, escalating to NICE-approved medicines or bariatric services when eligible.

A catecholamine-secreting tumour of adrenal chromaffin tissue causing episodic or sustained catecholamine excess, with headache, palpitations, sweating and potentially life-threatening cardiovascular instability.

Non-diabetic hyperglycaemia, often called prediabetes, is glucose above the usual range but below the diagnostic threshold for diabetes; it identifies increased type 2 diabetes and cardiovascular risk and is an opportunity for intensive prevention.

Autonomous aldosterone secretion with suppressed renin, causing sodium retention, hypertension and sometimes hypokalaemia; it is a treatable cause of secondary hypertension that may be unilateral or bilateral.

Refeeding syndrome is a potentially fatal metabolic and fluid complication of restarting nutrition in a severely malnourished or starved person; insulin shifts phosphate, potassium and magnesium into cells, while carbohydrate use can expose thiamine deficiency and sodium-water retention can cause fluid overload.

SIADH is inappropriate antidiuresis causing water retention and euvolaemic hypotonic hyponatraemia with inappropriately concentrated urine; it is a diagnosis of exclusion and management depends first on symptoms, then on the cause and risk of over-correction.

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.

Progressive hyperglycaemia caused by insulin resistance with relative beta-cell failure; safe care treats acute metabolic decompensation, cardiorenal risk and complications as well as glucose.