Endocrinology Revision Guide ✅

🧬 Endocrinology is physiology made clinical. Most conditions are best understood by asking: which gland?, too much or too little hormone?, primary gland problem or pituitary/hypothalamic problem?, and acute emergency or chronic disease? For exams, always link symptoms to hormone action: thyroxine changes metabolic rate, insulin controls glucose entry/storage, cortisol supports stress response and blood pressure, aldosterone controls salt/potassium, and ADH controls water balance.

✅ 1. Core Endocrine Principles

🔁 1.1 Feedback Loops

• Most endocrine axes use negative feedback: end-organ hormone feeds back to suppress pituitary and hypothalamus.
• Primary endocrine disease means the target gland is abnormal: pituitary hormones usually move in the opposite direction.
• Secondary disease means pituitary or hypothalamic drive is abnormal: target gland hormone is low or high because the signal is wrong.
• Dynamic testing is often needed when baseline hormone levels are hard to interpret.
• Always interpret endocrine tests with timing, acute illness, pregnancy, medication and assay interference in mind.

🧠 Exam pearl: “Normal” pituitary hormone levels can be abnormal if they are inappropriate for the end-organ hormone level. For example, a normal TSH with a low free T4 may suggest central hypothyroidism.

🧪 1.2 Endocrine Testing Pitfalls

• Acute illness can alter cortisol, thyroid tests, glucose and sodium handling.
• Biotin supplements can interfere with some thyroid and hormone immunoassays.
• Steroids suppress the hypothalamo-pituitary-adrenal axis and can mask adrenal insufficiency.
• Oestrogen therapy increases thyroid-binding globulin and cortisol-binding globulin, affecting total hormone levels.
• Always check medication history: amiodarone, lithium, antipsychotics, opioids, steroids, diuretics and SGLT2 inhibitors are common endocrine disruptors.

🍬 2. Diabetes Mellitus

🍭 2.1 Classification

• Type 1 diabetes: autoimmune beta-cell destruction causing absolute insulin deficiency; high risk of DKA.
• Type 2 diabetes: insulin resistance with progressive beta-cell dysfunction; strongly linked with adiposity, age, ethnicity and family history.
• LADA: latent autoimmune diabetes in adults; slower autoimmune beta-cell failure, often initially resembles type 2 diabetes.
• MODY: monogenic diabetes; young onset, strong family history, often non-obese.
• Type 3c diabetes: pancreatogenic diabetes from pancreatic damage, such as chronic pancreatitis, pancreatic cancer or pancreatic surgery.
• Gestational diabetes: glucose intolerance first recognised in pregnancy.

🧪 2.2 Diagnosis

• Diabetes can be diagnosed using HbA1c, fasting plasma glucose, random glucose with symptoms, or oral glucose tolerance testing depending on context.
• HbA1c is unreliable in haemoglobinopathy, recent transfusion, haemolysis, pregnancy and some anaemias.
• Symptoms of hyperglycaemia: thirst, polyuria, nocturia, weight loss, fatigue, blurred vision, recurrent infections.
• Ketones should be checked in unwell patients, suspected type 1 diabetes, rapid weight loss or severe hyperglycaemia.
• Consider type 1 diabetes in adults with rapid onset, weight loss, ketosis, personal/family autoimmune disease or low BMI.

💉 2.3 Type 1 Diabetes

• Pathology: autoimmune beta-cell destruction causes absolute insulin deficiency.
• Treatment requires insulin replacement: basal-bolus injections or insulin pump therapy.
• Education includes carbohydrate counting, sick-day rules, ketone testing, hypoglycaemia management and driving safety.
• Continuous glucose monitoring can improve safety and time-in-range for many patients.
• Complications: DKA, severe hypoglycaemia, retinopathy, nephropathy, neuropathy and cardiovascular disease.

💊 2.4 Type 2 Diabetes

• Pathology: insulin resistance, impaired insulin secretion, increased hepatic glucose output and abnormal incretin physiology.
• Initial management includes personalised nutrition, physical activity, weight management, smoking cessation and cardiovascular risk reduction.
• Metformin remains a common first-line glucose-lowering drug if tolerated and not contraindicated.
• SGLT2 inhibitors are especially important when heart failure, chronic kidney disease or high cardiovascular risk is present, according to current pathways.
• GLP-1 receptor agonists can support weight loss and glycaemic control in selected patients.
• Individualise HbA1c targets for frailty, hypoglycaemia risk, comorbidities and patient priorities.

📌 Clinical reasoning: Modern type 2 diabetes management is not just “lower HbA1c”. It also asks whether the patient has heart failure, chronic kidney disease, atherosclerotic cardiovascular disease, obesity, frailty or hypoglycaemia risk.

🚨 3. Diabetic Emergencies

🚨 3.1 Diabetic Ketoacidosis

• DKA is caused by insulin deficiency plus counter-regulatory hormone excess, leading to lipolysis, ketone production, acidosis and dehydration.
• Typical features: polyuria, thirst, vomiting, abdominal pain, Kussmaul breathing, ketotic breath, dehydration and reduced consciousness.
• Triggers: infection, missed insulin, new type 1 diabetes, myocardial infarction, stroke, steroids, SGLT2 inhibitors.
• Diagnosis: hyperglycaemia or known diabetes, ketonaemia/ketonuria and metabolic acidosis.
• Management principles: IV fluids, fixed-rate IV insulin, potassium monitoring/replacement, identify trigger and monitor ketone clearance.
• Do not stop basal insulin during DKA treatment unless specifically advised; it helps prevent rebound ketosis.

🧊 3.2 Hyperosmolar Hyperglycaemic State

• HHS is severe hyperglycaemia and hyperosmolality without significant ketoacidosis, usually in type 2 diabetes.
• Onset is slower than DKA, often days to weeks.
• Features: profound dehydration, confusion, seizures, focal neurology, infection or vascular trigger.
• Mortality is higher than DKA because patients are often older with comorbidity.
• Management focuses on cautious fluid replacement, osmolality reduction, potassium monitoring and delayed/low-dose insulin when appropriate.

🍯 3.3 Hypoglycaemia

• Symptoms: sweating, tremor, hunger, palpitations, anxiety, confusion, drowsiness, seizures or coma.
• Common causes: insulin, sulfonylureas, missed meals, alcohol, renal impairment, exercise, weight loss, medication errors.
• If conscious and safe swallow: rapid-acting carbohydrate followed by longer-acting carbohydrate if needed.
• If unconscious or unsafe swallow: IM glucagon or IV glucose according to local protocol.
• Sulfonylurea-induced hypoglycaemia can recur and may need prolonged observation and specialist treatment.

🚨 Exam pearl: SGLT2 inhibitors can cause euglycaemic DKA - the glucose may not be dramatically high, so check ketones in an unwell patient with diabetes even if glucose looks “not too bad”.

🦋 4. Thyroid Disease

🧊 4.1 Hypothyroidism

• Common causes: autoimmune Hashimoto’s thyroiditis, thyroidectomy, radioiodine, iodine deficiency, drugs such as amiodarone or lithium.
• Symptoms: fatigue, weight gain, cold intolerance, constipation, low mood, dry skin, hair loss, menorrhagia.
• Signs: bradycardia, delayed relaxation of reflexes, periorbital puffiness, hoarse voice, goitre.
• Primary hypothyroidism: high TSH with low free T4.
• Treatment: levothyroxine, adjusted to symptoms and TSH in primary disease.
• Start cautiously in older patients or those with ischaemic heart disease because thyroxine increases myocardial oxygen demand.

🔥 4.2 Hyperthyroidism / Thyrotoxicosis

• Causes: Graves’ disease, toxic multinodular goitre, toxic adenoma, thyroiditis, excess thyroid hormone, amiodarone.
• Symptoms: weight loss, heat intolerance, tremor, palpitations, anxiety, diarrhoea, oligomenorrhoea.
• Signs: tachycardia, AF, tremor, warm sweaty skin, lid lag, goitre, proximal myopathy.
• Graves’ clues: eye disease, diffuse goitre, thyroid bruit, pretibial myxoedema.
• Bloods: low TSH with high free T4/T3 in primary hyperthyroidism.
• Treatment options: antithyroid drugs, radioiodine or surgery depending on cause, severity, pregnancy status and patient preference.
• Beta-blockers help adrenergic symptoms while definitive treatment takes effect.

👁️ 4.3 Graves’ Orbitopathy

• Features: gritty eyes, watering, photophobia, lid retraction, proptosis, diplopia.
• Smoking worsens Graves’ orbitopathy and reduces treatment response.
• Red flags: reduced visual acuity, colour desaturation, corneal exposure, severe pain or ophthalmoplegia.
• Urgent ophthalmology is needed if sight-threatening disease is suspected.

🧱 4.4 Thyroid Nodules and Goitre

• Most thyroid nodules are benign, but malignancy must be considered.
• Red flags: rapid growth, hoarseness, dysphagia, cervical lymphadenopathy, childhood neck radiation, family history of thyroid cancer.
• Assessment includes TSH, ultrasound risk stratification and fine-needle aspiration when indicated.
• A suppressed TSH suggests an autonomously functioning “hot” nodule, which is less likely malignant.

🚨 5. Thyroid Emergencies

🔥 5.1 Thyroid Storm

• Life-threatening extreme thyrotoxicosis with systemic decompensation.
• Triggers: infection, surgery, trauma, radioiodine, childbirth, untreated Graves’ disease.
• Features: fever, severe tachycardia/AF, agitation, delirium, vomiting, diarrhoea, heart failure, shock.
• Management: urgent senior/ICU input, beta-blocker, antithyroid drug, iodine after antithyroid drug, steroids, cooling, fluids and trigger treatment.

🧊 5.2 Myxoedema Coma

• Rare life-threatening severe hypothyroidism, usually in older patients.
• Features: hypothermia, bradycardia, hypotension, hypoventilation, hyponatraemia, hypoglycaemia, reduced consciousness.
• Triggers: infection, cold exposure, sedatives, trauma, stroke, MI.
• Management: ICU care, thyroid hormone replacement, stress-dose hydrocortisone until adrenal insufficiency excluded, cautious warming and supportive care.

🧂 6. Adrenal Disease

🧂 6.1 Adrenal Insufficiency / Addison’s Disease

• Primary adrenal insufficiency means the adrenal cortex fails to produce cortisol ± aldosterone.
• Causes: autoimmune adrenalitis, TB, metastatic disease, adrenal haemorrhage, congenital adrenal hyperplasia, drugs.
• Symptoms: fatigue, weight loss, nausea, abdominal pain, dizziness, salt craving.
• Signs/labs: postural hypotension, hyperpigmentation, hyponatraemia, hyperkalaemia, hypoglycaemia, eosinophilia.
• Primary disease: low cortisol with high ACTH; secondary disease has low/inappropriately normal ACTH and usually no hyperpigmentation.
• Treatment: glucocorticoid replacement, mineralocorticoid replacement if primary, sick-day rules and steroid emergency card.

🚨 6.2 Adrenal Crisis

• Adrenal crisis is acute cortisol deficiency causing shock and can be fatal.
• Features: hypotension, vomiting, abdominal pain, fever, confusion, hypoglycaemia, hyponatraemia, hyperkalaemia.
• Triggers: infection, surgery, trauma, vomiting/diarrhoea, missed steroids, abrupt steroid withdrawal.
• Treat immediately if suspected: do not wait for cortisol result.
• Emergency treatment: hydrocortisone 100 mg IV/IM, IV 0.9% saline, glucose if hypoglycaemic, then ongoing hydrocortisone and fluids per protocol.

🌕 6.3 Cushing’s Syndrome

• Chronic glucocorticoid excess; exogenous steroid use is the commonest cause overall.
• Features: central weight gain, facial rounding, proximal myopathy, thin skin, easy bruising, purple striae, hypertension, diabetes, osteoporosis, mood change.
• Causes: exogenous steroids, pituitary ACTH adenoma, adrenal tumour, ectopic ACTH.
• Screening tests: overnight dexamethasone suppression test, late-night salivary cortisol or 24-hour urinary free cortisol.
• Complications: infection, VTE, cardiovascular disease, fractures and psychiatric disease.

🍌 6.4 Primary Hyperaldosteronism

• Autonomous aldosterone production causing sodium retention, hypertension and potassium wasting.
• Think of Conn’s syndrome in resistant hypertension, hypertension with hypokalaemia, adrenal incidentaloma or young-onset hypertension.
• Screen with aldosterone:renin ratio under appropriate medication/posture/salt conditions.
• Causes: bilateral adrenal hyperplasia or aldosterone-producing adenoma.
• Treatment: adrenalectomy for unilateral adenoma; mineralocorticoid receptor antagonist for bilateral disease.

⚡ 6.5 Phaeochromocytoma

• Catecholamine-secreting tumour causing episodic sympathetic surges.
• Classic triad: headache, sweating and palpitations.
• Other features: paroxysmal hypertension, tremor, pallor, anxiety, weight loss, hyperglycaemia.
• Test: plasma free metanephrines or urinary fractionated metanephrines.
• Treatment: alpha-blockade before beta-blockade, then surgery; beta-blockade first can cause unopposed alpha vasoconstriction.

🚨 Exam pearl: In suspected adrenal crisis, give hydrocortisone immediately. A cortisol sample can be taken first if it does not delay treatment, but treatment must not wait.

🧠 7. Pituitary Disease

🧠 7.1 Pituitary Adenomas

• Microadenoma: less than 10 mm; macroadenoma: 10 mm or larger.
• Mass effects: headache, bitemporal hemianopia from optic chiasm compression, cranial nerve palsies if cavernous sinus involved.
• Functional tumours secrete hormone; non-functioning tumours may cause hypopituitarism by compression.
• Assessment: pituitary profile, visual fields, MRI pituitary and endocrine referral.

🍼 7.2 Hyperprolactinaemia

• Causes: prolactinoma, pregnancy, breastfeeding, antipsychotics, metoclopramide, hypothyroidism, renal failure, stalk effect.
• Symptoms in women: galactorrhoea, oligomenorrhoea/amenorrhoea, infertility, low libido.
• Symptoms in men: low libido, erectile dysfunction, infertility, galactorrhoea less common.
• Very high prolactin suggests prolactinoma, but always consider drug causes and macroprolactin.
• Treatment of prolactinoma: dopamine agonists such as cabergoline under specialist care.

🦶 7.3 Acromegaly

• Usually caused by growth hormone-secreting pituitary adenoma.
• Features: enlarged hands/feet, coarse facial features, prognathism, sweating, headaches, carpal tunnel, arthropathy.
• Metabolic complications: diabetes, hypertension, sleep apnoea, cardiomyopathy.
• Screen with IGF-1; confirm with failure of GH suppression during oral glucose tolerance test.
• Treatment: transsphenoidal surgery, somatostatin analogues, GH receptor antagonist or radiotherapy depending on case.

🚨 7.4 Pituitary Apoplexy

• Acute haemorrhage or infarction of the pituitary, often into an adenoma.
• Features: sudden severe headache, visual loss, ophthalmoplegia, vomiting, collapse, reduced consciousness.
• Can cause acute ACTH deficiency and adrenal crisis.
• Management: urgent hydrocortisone, MRI/CT, neurosurgical and endocrine input.

💧 8. Water Balance: SIADH and Diabetes Insipidus

💧 8.1 SIADH

• Excess ADH causes water retention, dilutional hyponatraemia and concentrated urine.
• Causes: pneumonia, CNS disease, malignancy especially small cell lung cancer, SSRIs, carbamazepine, opioids, surgery.
• Features: nausea, headache, confusion, seizures if severe/rapid.
• Bloods: low serum osmolality, inappropriately high urine osmolality, high urine sodium, clinically euvolaemic.
• Management: treat cause, fluid restriction, careful sodium correction; severe symptomatic hyponatraemia may need hypertonic saline under senior guidance.

🚰 8.2 Diabetes Insipidus

• DI causes inability to concentrate urine, leading to polyuria and polydipsia.
• Cranial DI: deficient ADH secretion; causes include pituitary surgery, trauma, tumours and infiltrative disease.
• Nephrogenic DI: renal resistance to ADH; causes include lithium, hypercalcaemia, hypokalaemia and kidney disease.
• Features: large-volume dilute urine, thirst, nocturia, hypernatraemia if unable to drink.
• Diagnosis: paired serum/urine osmolality, water deprivation testing or copeptin-based pathways under specialist care.
• Treatment: desmopressin for cranial DI; treat cause and use specialist strategies for nephrogenic DI.

🦴 9. Calcium, Parathyroid and Bone Endocrinology

⬆️ 9.1 Hypercalcaemia

• Common causes: primary hyperparathyroidism and malignancy.
• Symptoms: “bones, stones, groans and psychiatric overtones” - bone pain, renal stones, constipation, abdominal pain, confusion, depression.
• ECG: shortened QT interval.
• Initial assessment: corrected calcium, phosphate, PTH, vitamin D, renal function, myeloma screen if indicated.
• If PTH high/inappropriately normal: primary/tertiary hyperparathyroidism.
• If PTH suppressed: malignancy, vitamin D excess, granulomatous disease, thyrotoxicosis or drugs.
• Severe hypercalcaemia: IV fluids first; bisphosphonate/calcitonin depending on cause and severity.

⬇️ 9.2 Hypocalcaemia

• Causes: hypoparathyroidism after thyroid surgery, vitamin D deficiency, CKD, pancreatitis, hypomagnesaemia, massive transfusion.
• Symptoms: perioral tingling, paraesthesia, cramps, tetany, seizures.
• Signs: Chvostek sign, Trousseau sign, prolonged QT.
• Severe/symptomatic hypocalcaemia requires IV calcium with ECG monitoring.
• Check magnesium because hypomagnesaemia can cause refractory hypocalcaemia.

🧱 9.3 Primary Hyperparathyroidism

• Usually due to parathyroid adenoma.
• Blood pattern: high calcium with high or inappropriately normal PTH.
• Can present with renal stones, osteoporosis, constipation, fatigue or incidental hypercalcaemia.
• Management: parathyroidectomy if criteria met; monitoring and bone/renal protection if not surgical.

☀️ 9.4 Vitamin D Deficiency and Osteomalacia

• Risk factors: low sunlight exposure, darker skin, covering clothing, malabsorption, CKD/liver disease, anticonvulsants.
• Symptoms: bone pain, proximal muscle weakness, falls, fragility fractures.
• Bloods may show low vitamin D, low/normal calcium, low phosphate, high ALP and secondary hyperparathyroidism.
• Treatment: vitamin D replacement and calcium if dietary intake is inadequate.

🌸 10. Reproductive Endocrinology

🌸 10.1 Polycystic Ovary Syndrome

• PCOS involves hyperandrogenism, ovulatory dysfunction and polycystic ovarian morphology.
• Features: irregular periods, subfertility, hirsutism, acne, androgenic alopecia, weight gain.
• Associated with insulin resistance, type 2 diabetes risk, dyslipidaemia and endometrial hyperplasia risk if prolonged amenorrhoea.
• Exclude mimics: pregnancy, thyroid disease, hyperprolactinaemia, congenital adrenal hyperplasia, Cushing’s, androgen-secreting tumour.
• Management: lifestyle/weight support, combined hormonal contraception for cycle control/hyperandrogenism, metformin in selected cases, fertility treatment if trying to conceive.

🍂 10.2 Menopause

• Menopause is diagnosed clinically after 12 months of amenorrhoea in the appropriate age group.
• Symptoms: hot flushes, night sweats, sleep disturbance, mood change, brain fog, vaginal dryness, urinary symptoms, reduced libido.
• Long-term effects: bone loss and cardiometabolic changes.
• HRT can be very effective; choice depends on uterus status, risk factors, age, time since menopause and patient preference.
• Offer vaginal oestrogen for genitourinary syndrome of menopause when appropriate, including many patients who cannot or do not want systemic HRT.

♂️ 10.3 Hypogonadism

• Male hypogonadism: low libido, erectile dysfunction, infertility, reduced shaving, low mood, fatigue, low muscle mass, osteoporosis.
• Primary hypogonadism: low testosterone with high LH/FSH.
• Secondary hypogonadism: low testosterone with low/normal LH/FSH; consider pituitary disease, obesity, opioids, systemic illness.
• Female hypogonadism: amenorrhoea/oligomenorrhoea, infertility, low oestrogen symptoms and low bone density.

🚨 11. Endocrine Emergencies

🚨 Safety pearl: Endocrine emergencies often look like sepsis, delirium or dehydration. Check glucose, ketones, sodium, calcium and medication history early - these simple tests can reveal a reversible endocrine crisis.

📚 12. OSCE / Exam Pearls

• Primary hypothyroidism: high TSH, low T4.
• Central hypothyroidism: low T4 with low or inappropriately normal TSH.
• Graves’ disease: hyperthyroidism plus eye signs, diffuse goitre or positive TSH receptor antibodies.
• DKA can occur with only modest glucose elevation in patients taking SGLT2 inhibitors.
• Never delay hydrocortisone in suspected adrenal crisis.
• Phaeochromocytoma: alpha-block before beta-block.
• Hypercalcaemia with high PTH suggests primary hyperparathyroidism; hypercalcaemia with low PTH suggests malignancy or non-PTH cause.
• Polyuria with high sodium suggests diabetes insipidus; hyponatraemia with concentrated urine suggests SIADH.
• Prolactin can rise from antipsychotics, pregnancy, hypothyroidism and stalk compression - not just prolactinoma.
• Acromegaly causes diabetes, hypertension, sleep apnoea, carpal tunnel and enlarged hands/feet.

📌 13. Quick Differentials Table

📚 References

• NICE. Type 2 diabetes in adults: management. NG28.
• NICE. Type 1 diabetes in adults: diagnosis and management. NG17.
• NICE. Thyroid disease: assessment and management. NG145.
• Society for Endocrinology. Emergency management of acute adrenal insufficiency / adrenal crisis in adults.
• Joint British Diabetes Societies guidance should be checked for local DKA, HHS, perioperative diabetes and inpatient insulin pathways.

⚠️ Disclaimer

This article is for medical education and exam revision. Clinical decisions should follow current local guidelines, endocrine emergency protocols, diabetes sick-day rules, insulin safety policies, pregnancy guidance, formularies, senior advice and national guidance. Endocrine emergencies such as DKA, HHS, adrenal crisis, thyroid storm, myxoedema coma, pituitary apoplexy and severe calcium disturbance require urgent senior input.