Rapid review: endocrinology and diabetes

• This is a revision page. It distils the endocrine section into classic presenting pictures: what the patient looks like, the single most likely diagnosis, the best first test, the best first treatment, and the commonest trap.
• Every block links to the full MedGrasp topic, which carries the full clinical detail, doses, reference ranges, special groups and low-resource notes.
• It is written in original words. The facts and the clinical approach are taken from the full MedGrasp topics on the same conditions and from the open-access guidelines they cite: the 2024 American Diabetes Association (ADA) hyperglycaemic crisis consensus, the 2026 ADA Standards of Care (hypoglycaemia chapter), the 2018 European Thyroid Association (ETA) Graves guideline, the 2016 Endocrine Society primary adrenal insufficiency guideline, and the 2017 Turner review of hypercalcaemia. StatPearls, NICE, WHO and the society guidelines cited by the full topics are flagged in the blocks rather than re-cited as if they were new sources.
• Presentation links are given as plain discipline/slug text, for example endocrinology/dka-and-hhs. The full topics are free to read with no sign-in.
• Read the block, answer the linked check-yourself question in your head, then open the full page for the details.

By the end of this page you should be able to:

1. Recognise the classic presenting picture of each endocrine emergency and chronic presentation listed below.
2. State the single most likely diagnosis, the best first test and the best first treatment for each.
3. Name the commonest trap students and doctors fall into for each.
4. Decide which full MedGrasp topic to open next from the link given.
5. Use the flowchart to sort a newly presenting patient into the right block in under a minute.

Read the presenting pictures aloud in clinical words you would use at the bedside. Do not memorise every first test: what you are trying to build is the habit of asking, for any sick endocrine patient, what is the diagnosis, what test would prove it in the least steps, and what would I do while waiting for that test. The answers below are intentionally short. Each one ends with the full topic link; open it when the patient, or the exam, asks for depth.

Presenting picture in plain clinical words. Either crisis begins with days of polyuria, polydipsia and weight loss, with dehydration and a large osmotic gap. In DKA the patient is younger, in type 1 diabetes, with vomiting, abdominal pain, Kussmaul breathing and ketotic breath, developing over hours to a day or two. In HHS the patient is older, in type 2 diabetes, dehydrated, confused and polyuric over days to weeks, with little or no ketosis on the bedside strip; infection, stroke, myocardial infarction and dehydration are common triggers, and the mixed picture is frequent. Euglycaemic DKA, often around an SGLT2 inhibitor, is the commonest recent pitfall. ^[1]

Most likely diagnosis. DKA and HHS are diagnoses of degree, not separate diseases: the same insulin deficiency plus stress-hormone surge, separated by how much residual insulin is left to suppress ketogenesis. ^[1]

Best first test. Do not wait for a laboratory before starting treatment in a sick patient. Draw glucose, ketones (preferably blood beta-hydroxybutyrate), venous blood gas, electrolytes and renal function, an ECG and a screen for infection or ischaemia, then treat. Osmolality is added when HHS or mixed disease is suspected. The anion gap is not a resolution criterion. ^[1]

Best first treatment. Volume before insulin, and potassium before insulin. Give 0.9% saline or a balanced crystalloid at 500 to 1000 mL per hour for the first 2 to 4 hours in adults without renal or cardiac compromise, then correct deficits over 24 to 48 hours. Start a fixed-rate intravenous insulin infusion at 0.1 units per kilogram per hour once potassium has been assessed. Potassium replacement takes priority whenever the level is low, because insulin and fluid resuscitation drive potassium into cells, and hypokalaemia below 3.5 mmol per litre occurs in about 55% of DKA and 51% of HHS during treatment. Add 5 to 10% dextrose once glucose falls below roughly 250 mg per dL, halving the insulin rate. In HHS use a lower insulin rate (0.05 units per kilogram per hour, or 0.1 if mixed) and slow the fall of glucose, sodium and osmolality. Find and treat the trigger throughout. Transition to subcutaneous insulin requires a 1 to 2 hour overlap, with the basal dose given 1 to 2 hours before the infusion stops. ^{[1] [2][4]}

Commonest wrong answer. "Give a large insulin bolus and wait for the glucose to drop" is the classic wrong approach: insulin drives potassium into cells, fixed-rate infusion with potassium-guided replacement and judicious fluids is safer; the second commonest trap is treating mixed DKA-HHS as ordinary DKA and failing to anticoagulate or to correct slowly enough. ^[1]

Full topic: endocrinology/dka-and-hhs

Presenting picture in plain clinical words. A person with diabetes who becomes sweaty, tremulous and hungry or confused after insulin or a sulfonylurea, with a measured low plasma glucose. Whipple triad, not a number on its own, defines hypoglycaemia; nocturnal sweating, nightmares and morning confusion are the nocturnal equivalent. In people without diabetes, fasting symptoms dominate with insulinoma, while postprandial symptoms suggest nesidioblastosis, post-bariatric or autoimmune disease. ^[2]

Most likely diagnosis. In type 1 or type 2 diabetes treated with insulin or a secretagogue, hypoglycaemia is usually iatrogenic. In a non-diabetic adult with fasting or overnight symptoms, insulinoma is the commonest cause of endogenous hyperinsulinaemic hypoglycaemia; it is small, usually benign, and secretes insulin regardless of glucose. ^[2]

Best first test. Confirm the glucose in the laboratory at the time of symptoms, then insulin, C-peptide, proinsulin and a drug screen while the patient is low; on a ward a supervised fast, with monitoring every few hours, catches most cases within 24 to 48 hours. Insulin inappropriately present below 3 mmol per litre of glucose, with C-peptide preserved, points to endogenous insulin (insulinoma or a secretagogue); suppressed C-peptide points to factitious insulin. ^[2]

Best first treatment. For a conscious patient with glucose below 3.9 mmol per litre, give glucose by mouth (glucose itself is preferred to other carbohydrate, without fat or protein), reassess at 15 minutes and repeat. For an unconscious or fitting patient, give intravenous glucose or glucagon and call for help. An insulinoma in the interval before resection is managed with small frequent complex-carbohydrate meals while it is localised; surgery is curative once the tumour is found, and medical control of hypoglycaemia (diazoxide, somatostatin analogues, everolimus and other systemic options) is reserved for inoperable or metastatic disease. ^[2]

Commonest wrong answer. Treating the number on a continuous glucose monitor without Whipple triad or a laboratory glucose is the commonest trap; the second is missing the diagnosis of insulinoma (or non-insulin-mediated causes such as cortisol or growth hormone deficiency) because a low glucose in a non-diabetic adult was assumed to be irrelevant. ^[2]

Full topic: endocrinology/hypoglycaemia

Presenting picture in plain clinical words. Thyrotoxicosis makes itself felt as heat intolerance, sweating, weight loss despite increased appetite, tremor, palpitations, anxiety and loose stools, with a fine tremor, warm moist skin, palmar erythema, lid retraction and a goitre; older adults may have apathetic thyrotoxicosis with weight loss, confusion or atrial fibrillation and few adrenergic signs. Thyroid storm is diagnosed clinically: fever, marked tachycardia, atrial fibrillation, heart failure, delirium, vomiting or jaundice in a thyrotoxic patient. A scoring system such as Burch-Wartofsky can support the clinical diagnosis but is not a substitute for it. Myxoedema is the opposite picture: cold intolerance, weight gain, constipation, apathy, dry skin and hair, menorrhagia, a slow relaxed tendon reflex and, when severe, confusion, hypothermia and coma. ^[3]

Most likely diagnosis. In iodine-adequate areas, Graves disease is the commonest cause of thyrotoxicosis (driven by TSH receptor antibodies); hypothyroidism is most often autoimmune Hashimoto thyroiditis. Myxoedema coma is rare but kills if untreated. ^[3]

Best first test. For thyrotoxicosis, TSH and free T4 with free T3, then TRAb and thyroid uptake or ultrasound to identify the cause; beware T3 thyrotoxicosis when only free T3 is raised and a TSH-secreting pituitary adenoma when TSH is inappropriately normal. For suspected myxoedema, TSH and free T4, with a higher threshold of suspicion when a very sick patient has hyponatraemia, hypoglycaemia or an unexplained high TSH from another cause. ^[3]

Best first treatment. For uncomplicated Graves disease in most non-pregnant adults, a thionamide (methimazole or carbimazole) with a beta blocker, titrated to free T4 and free T3 over 12 to 18 months, with radioactive iodine or surgery as definitive options; in pregnancy, propylthiouracil is preferred in the first trimester with low-dose titration; thyroid storm is treated in order, supportive care then beta blockade, high-dose antithyroid drug, corticosteroid and iodine given at least one hour later. For hypothyroidism, levothyroxine replacement titrated to TSH, with a stress-dose steroid plan already in place if adrenal insufficiency cannot be excluded. ^[3]

Commonest wrong answer. Attributing an older patient's thyrotoxicosis to anxiety, depression or ageing instead of checking thyroid function; or giving thyroxine to hypothyroidism without first excluding adrenal insufficiency, which can precipitate an adrenal crisis. A second trap is assuming that a normal TSH rules out thyroid disease in the first weeks of treatment. ^[3]

Full topic: endocrinology/hyperthyroidism and endocrinology/hypothyroidism

Presenting picture in plain clinical words. Chronic primary adrenal insufficiency looks like persistent fatigue, weight loss, nausea, salt craving, abdominal discomfort, postural dizziness and, in primary disease only, increasing pigmentation on exposed skin, creases and scars; women lose axillary and pubic hair. Add autoimmune disease (thyroid disease, type 1 diabetes, vitiligo) and the picture sharpens. The adrenal crisis is an emergency: severe weakness, vomiting, abdominal pain that mimics an acute abdomen, confusion and hypotension, usually on a background of missed or withdrawn glucocorticoids, infection, trauma, surgery or myocardial infarction. Secondary and tertiary disease lack pigmentation and hyperkalaemia because aldosterone is preserved. ^[4]

Most likely diagnosis. Autoimmune destruction of the cortex is the commonest cause of primary (Addison) disease in adults; chronic glucocorticoid therapy and its withdrawal is the commonest cause of secondary and tertiary disease overall. Phaeochromocytoma presents with headache, sweating and palpitations from catecholamine surges; Cushing syndrome with central weight gain, easy bruising, proximal weakness, hypertension and dysglycaemia; primary hyperaldosteronism with resistant hypertension and hypokalaemia. ^[4]

Best first test. In a stable patient, a paired morning cortisol and ACTH (with renin, aldosterone and DHEAS), proceeding to a short Synacthen (250 microgram) test if the result is uncertain; in an acutely unwell patient, treatment comes first. In suspected phaeochromocytoma, plasma free or urinary fractionated metanephrines before any imaging. In Cushing syndrome, confirmation rests on proper biochemical screening; the common simple clinical tests remain the first step at the bedside. ^[4]

Best first treatment. For an adrenal crisis, a parenteral hydrocortisone 100 mg immediately (50 mg per square metre in children), followed by 200 mg over 24 hours (or 50 to 100 mg per square metre in children), together with rapid saline resuscitation, glucose if hypoglycaemic, and energetic treatment of the trigger; delay is what kills. For chronic primary disease, hydrocortisone 15 to 25 mg (or cortisone acetate 20 to 35 mg) in divided oral doses, fludrocortisone 50 to 100 micrograms daily, plus written sick-day rules, a steroid emergency card and a pre-filled hydrocortisone injection kit. Maintain the distinction between primary and central disease: fludrocortisone is not needed in glucocorticoid-induced or pituitary disease, and hyperkalaemia in central disease is absent. ^[4]

Commonest wrong answer. Calling the presentation depression, gastroenteritis or functional illness because the symptoms are non-specific; failing to cover and retest after glucocorticoid withdrawal; and giving thyroxine to a hypothyroid patient without excluding adrenal insufficiency. Secondary pitfall: stopping hydrocortisone in a sick patient because the laboratory has not confirmed the diagnosis. ^[4]

Full topics: endocrinology/adrenal-insufficiency, endocrinology/cushing-syndrome, endocrinology/phaeochromocytoma, endocrinology/primary-hyperaldosteronism, endocrinology/congenital-adrenal-hyperplasia

Presenting picture in plain clinical words. Pituitary tumours are a diagnostic chameleon. A prolactinoma in a woman presents with oligomenorrhoea or amenorrhoea, galactorrhoea and infertility; in a man, impotence and low libido. Acromegaly presents with changing ring and shoe sizes, coarsened facial features, enlarged hands and feet, hyperhidrosis and carpal tunnel. An ACTH-secreting tumour (Cushing disease) adds central obesity, facial plethora, striae and proximal weakness. A non-functioning macroadenoma declares itself with headache, loss of the outer halves of the visual fields (bitemporal hemianopia) and hypopituitarism; a pregnant woman or postpartum woman with headache, visual change or polyuria may have apoplexy or Sheehan syndrome. In children, growth failure or delayed puberty is the clue. ^[4]

Most likely diagnosis. Prolactinoma is the commonest secretory pituitary tumour; non-functioning adenoma is the commonest macroadenoma found in adults. Acromegaly and Cushing disease are less common but more clinically consequential. Hypopituitarism, from any cause, is often missed behind these. ^[4]

Best first test. For suspected prolactinoma, a single serum prolactin (with a concurrent pregnancy test in women of reproductive age). For suspected acromegaly, IGF-1 then an oral glucose tolerance test if needed. For pituitary mass effect or suspected Cushing disease, MRI of the pituitary with appropriate dynamic testing under endocrine guidance. For any child or adult with red flags, MRI and a full baseline endocrine panel including thyroid, cortisol and gonadotrophins. ^[4]

Best first treatment. Prolactinomas respond dramatically to a dopamine agonist, with shrinkage over weeks; non-functioning macroadenomas with chiasmal compression are treated surgically (transsphenoidal), followed by hormone replacement as needed; acromegaly and Cushing disease are managed by transsphenoidal adenomectomy, with medical therapy (somatostatin analogues, dopamine agonist, growth hormone receptor antagonist) or radiosurgery for residual disease; an incidental microadenoma usually needs observation rather than treatment. Every patient on glucocorticoids for pituitary disease has the same sick-day and stress-dose plan as adrenal insufficiency. ^[4]

Commonest wrong answer. Treating a small incidental pituitary microadenoma, or operating on a non-functioning tumour without mass effect, when observation would be correct; missing a prolactinoma behind infertility or impotence; and forgetting that a very high prolactin can be from stalk compression rather than a true prolactinoma, which changes treatment from dopamine agonist to surgery. ^[4]

Full topics: endocrinology/pituitary-tumours-nonfunctioning-and-craniopharyngioma, endocrinology/hyperprolactinaemia, endocrinology/acromegaly, endocrinology/hypopituitarism, endocrinology/pituitary-incidentaloma-and-apoplexy

Presenting picture in plain clinical words. Hypercalcaemia is usually found by accident, then explains tiredness, constipation, polyuria and polydipsia, bone pain and low mood. Primary hyperparathyroidism is chronic, mild and asymptomatic in most cases; malignancy-associated hypercalcaemia is rapid, severe and occurs in an unwell patient. Hypocalcaemia presents with perioral paraesthesia, carpopedal spasm, tetany, seizures, QT prolongation and, when severe, laryngospasm or bronchospasm; late presentation as cataract or basal ganglia calcification is possible in untreated hypoparathyroidism. A very high or rapidly rising calcium, or one with confusion, vomiting, renal impairment or arrhythmias, is a medical emergency. Corrected or ionised calcium is the rule, because low albumin hides high ionised calcium. ^[5]

Most likely diagnosis. In outpatients, primary hyperparathyroidism, most often from a single benign adenoma; in inpatients, malignancy acting through parathyroid hormone-related peptide or through bone. For hypocalcaemia, hypoparathyroidism after neck surgery, vitamin D deficiency and chronic kidney disease lead. Hyperparathyroidism-jaw tumour and MEN2A are the inherited traps. ^[5]

Best first test. A paired corrected calcium and PTH at the same time (or ionised calcium if paraprotein is present), 25-hydroxyvitamin D, kidney function and, when hypocalcaemia is chronic, magnesium. An inappropriately normal or high PTH in the face of high calcium is the fork in the road: high points to the parathyroid, suppressed points to malignancy, granuloma, drugs or thyrotoxicosis. A urine calcium to creatinine clearance ratio below 0.01 in a mild case separates familial hypocalciuric hypercalcaemia from primary hyperparathyroidism. ^[5]

Best first treatment. For almost every hypercalcaemic patient, the first step is the same: restore euvolaemia with isotonic saline, often over 24 to 48 hours, with a loop diuretic reserved for volume overload. In severe or crisis cases, add cause-specific therapy: an intravenous bisphosphonate for early effect, calcitonin for speed, glucocorticoid for granulomatous or vitamin D-mediated disease, or denosumab or dialysis when bisphosphonates are unsafe or renal function is poor. Parathyroidectomy is the only cure for primary hyperparathyroidism. For hypocalcaemia, give intravenous calcium gluconate (or calcium chloride by central line) for tetany or symptoms, then correct vitamin D, magnesium and kidney function; chronic hypoparathyroidism requires active vitamin D analogues and calcium supplements with regular monitoring. See the full topics for adult doses and renal limits. ^[5]

Commonest wrong answer. Treating the calcium without asking why it is high; giving bisphosphonates or loop diuretics before, or instead of, adequate hydration; forgetting to correct for albumin or to repeat the test; and operating on neck glands without genetic testing in a young patient or family with endocrine tumours. ^[5]

Full topics: renal-genitourinary/hypercalcaemia, renal-genitourinary/hypocalcaemia, endocrinology/hyperparathyroidism, endocrinology/hypoparathyroidism, endocrinology/osteoporosis

Presenting picture in plain clinical words. A postmenopausal woman or an older adult with a low-trauma fracture (wrist, vertebra or hip), loss of height or kyphosis, or back pain after a trivial bend or lift. It is silent until the fracture. A vertebral fracture multiplies the risk of another vertebral fracture about five-fold, and a hip fracture in older age carries a large excess mortality in the following year. ^[5]

Most likely diagnosis. Osteoporosis by the WHO DXA criterion, or any adult fragility fracture; osteopenia with a high enough 10-year fracture probability also warrants drug treatment. See the full topic for the thresholds and how FRAX is used. ^[5]

Best first test. DXA of the hip and lumbar spine, vertebral imaging when compression is suspected, and a screen for secondary causes (blood count, albumin-adjusted calcium, phosphate, liver and renal function, 25-hydroxyvitamin D, PTH, with sex hormone and protein studies added selectively). The exact FRAX thresholds and screening ages are in the full topic. ^[5]

Best first treatment. Calcium and vitamin D repletion, weight-bearing and resistance exercise, balance and falls reduction, smoking and alcohol advice, and usually an antiresorptive drug: a bisphosphonate (alendronate or zoledronic acid) is the routine first-line class, with denosumab, teriparatide, abaloparatide or romosozumab reserved for higher-risk, intolerant or anabolic-requiring patients. Each class has its own cautions (rebound vertebral fractures after stopping denosumab, osteonecrosis of the jaw and atypical femoral fracture after bisphosphonates, and the cardiovascular boxed warning with romosozumab). A bisphosphonate drug holiday may be considered after several years in low-risk patients, but denosumab must not simply be stopped without a follow-on antiresorptive. See the full topic for exact adult doses, renal limits and monitoring. ^[5]

Commonest wrong answer. Treating the BMD number without assessing falls; giving zoledronic acid intravenously without checking renal function; and stopping denosumab without sequencing another antiresorptive, which can produce multiple rebound vertebral fractures within 7 to 19 months. ^[5]

Full topic: endocrinology/osteoporosis

Presenting picture in plain clinical words. A short child (more than two standard deviations below the mean, roughly the third percentile or below), or a child whose growth velocity is falling through the percentiles, with or without delayed or absent puberty. Red flags include severe shortness, disproportion, dysmorphism, midline defects, neurological or systemic symptoms, and a height far below the family range. In a clinical words version: a child who looks younger than their age, with delayed bone age and a family history of late bloomers, usually has constitutional delay; a proportionate small child with short parents and on-time development usually has familial short stature. ^{[4] [2][6]}

Most likely diagnosis. The commonest explanations are familial short stature and constitutional delay of growth and puberty, both benign. Pathological causes include growth hormone deficiency, hypothyroidism, chronic systemic disease (often coeliac or bowel or kidney disease), skeletal dysplasia and, in girls with unexplained short stature, Turner syndrome. ^{[4] [6]}

Best first test. Accurate auxology on a suitable growth chart, recorded on more than one visit to derive growth velocity; bone age from a left hand and wrist X-ray; a cheap screening panel (full blood count, kidney and liver function, coeliac screen, thyroid function, IGF-1); and a karyotype for all girls with unexplained short stature. Bone age is delayed in constitutional delay, growth hormone deficiency, hypothyroidism and Turner syndrome, but close to chronological age in familial short stature; precocious or hyperthyroid states accelerate it. ^[4]

Best first treatment. Treat the cause, not the height. Reassure and monitor the normal variants; levothyroxine for hypothyroidism; control of chronic disease; and recombinant growth hormone given daily subcutaneously for confirmed growth hormone deficiency (with regular monitoring, safety and stopping rules detailed in the full topic) or Turner syndrome (started early and continued while growth potential remains), plus planned pubertal induction with low-dose sex steroids at the appropriate bone age. See the full topic for adult dosing, stopping rules and monitoring. ^{[4] [6]}

Commonest wrong answer. Reassuring the family that the child "takes after a short parent" without measuring growth velocity or bone age; treating familial short stature with growth hormone when the gain is modest; and forgetting that poor growth is a sensitive marker of chronic disease (often coeliac, inflammatory bowel or kidney disease) that responds more to treating the disease than to hormone therapy. ^[4]

Full topics: pediatrics/short-stature-and-growth-hormone-disorders, pediatrics/puberty-and-sexual-development, pediatrics/hypogonadism-and-delayed-puberty, pediatrics/turner-syndrome-and-gonadal-dysgenesis, pediatrics/congenital-hypothyroidism-and-newborn-screening

Presenting picture in plain clinical words. A young patient, or one with a family history, with early parathyroid or pituitary disease or pancreatic neuroendocrine tumour in the same family: think MEN1, an autosomal dominant tumour-suppressor syndrome on chromosome 11. A family with medullary thyroid cancer, with or without phaeochromocytoma, points to MEN2 on RET. Distinctive facies, mucosal neuromas, a marfanoid habitus, gut ganglioneuromatosis and inability to produce tears in infancy point to MEN2B. A milder, later picture with parathyroid and pituitary tumours but fewer pancreatic tumours points to MEN4. ^[7]

Most likely diagnosis. MEN1 is inherited on MEN1; MEN2, with medullary thyroid cancer and usually phaeochromocytoma, is inherited on RET; MEN4 resembles MEN1 but is rarer and milder. All are autosomal dominant, so about half of first-degree relatives are at risk. ^[7]

Best first test. Germline genetic testing, with the clinical criteria of the syndrome guiding the order: MEN1 mutational analysis (with multiplex ligation if sequencing is negative) and, for MEN2, RET testing (hotspots first, then the whole coding region); plus syndrome-directed biochemistry (age-based MEN1 surveillance of parathyroid, pituitary, pancreatic and thymic disease, and metanephrines before any surgery in MEN2). ^[7]

Best first treatment. Syndrome-directed management led by genetics, not the most pressing single tumour: in MEN1, subtotal parathyroidectomy with thymectomy for the parathyroid disease, proton pump inhibitors for the gastrinoma, timed surgery for pancreatic tumours above 1 to 2 cm, dopamine agonists or transsphenoidal surgery for the pituitary; in MEN2, prophylactic thyroidectomy by RET risk level (highest-risk M918T in infancy, high-risk C634 or A883F at or before five years, moderate-risk in childhood or young adulthood guided by calcitonin), and always screen and treat a phaeochromocytoma before any neck surgery. ^[4]

Commonest wrong answer. Treating a single tumour without considering the syndrome, or operating on a MEN2 neck without biochemically excluding a phaeochromocytoma first; a second trap is missing MEN2B early, when thyroidectomy is still curative, because the mucosal and skeletal stigmata were not recognised. ^[4]

Full topic: endocrinology/multiple-endocrine-neoplasia

• For any sick endocrine patient, state the most likely diagnosis, arrange the least-step test and start the treatment in the same minute.
• Hyperglycaemic crises: fluids and potassium before insulin; mixed DKA-HHS is common and dangerous; in HHS the correction must be slow. ^[1]
• Hypoglycaemia: Whipple triad before action; oral glucose if conscious; glucagon or intravenous glucose if not. Insulinoma is the classic fasting tumour and surgery is curative. ^[2]
• Thyrotoxicosis: heat intolerance, weight loss and tremor in younger patients, apathetic disease and atrial fibrillation in older ones; myxoedema favors lower thyroid hormone, not excess. ^[3]
• Adrenal crisis is treated before the test comes back: 100 mg of intravenous hydrocortisone and saline immediately, then a clear sick-day, card and injection plan for life. ^[4]
• Hypercalcaemia: correct for albumin or use ionised calcium, measure PTH, hydrate first, then cause-directed therapy. ^[5]
• Osteoporosis: a fragility fracture in an adult is itself the diagnosis; falls and fracture risk, not BMD alone, drive treatment. ^[5]
• Short stature: measure accurately, derive velocity, and look at bone age; the commonest explanations are benign variants, but treat chronic disease or hypothyroidism or Turner syndrome when clues point to them. ^[4]
• MEN: let genetics drive surveillance; operate on MEN2 early enough to be curative, and never operate on an unscreened phaeochromocytoma. ^[4]

• endocrinology/dka-and-hhs and endocrinology/hypoglycaemia
• endocrinology/hyperthyroidism and endocrinology/hypothyroidism
• endocrinology/hypothyroidism in children and congenital hypothyroidism and newborn screening
• endocrinology/adrenal-insufficiency, endocrinology/cushing-syndrome, endocrinology/phaeochromocytoma, endocrinology/primary-hyperaldosteronism
• endocrinology/pituitary-tumours-nonfunctioning-and-craniopharyngioma, endocrinology/hyperprolactinaemia, endocrinology/acromegaly, endocrinology/hypopituitarism
• renal-genitourinary/hypercalcaemia and renal-genitourinary/hypocalcaemia
• endocrinology/hyperparathyroidism, endocrinology/hypoparathyroidism
• endocrinology/osteoporosis
• pediatrics/short-stature-and-growth-hormone-disorders, pediatrics/puberty-and-sexual-development, pediatrics/hypogonadism-and-delayed-puberty, pediatrics/turner-syndrome-and-gonadal-dysgenesis
• endocrinology/multiple-endocrine-neoplasia