Endocrine disorders
Diabetes, thyroid, parathyroid and adrenal disorders: pathology and imaging clues
Diabetes, thyroid, parathyroid and adrenal disorders for FCPS Part 1: hormone patterns, thyroid tests, cancers, Cushing, Conn and phaeochromocytoma. Each pattern is linked to its pathology and imaging clue.
Diabetes mellitus: how damage happens
- Type 1: autoimmune β-cell loss. Type 2: insulin resistance.
- Complications arise from non-enzymatic glycation, the sorbitol pathway (lens, nerves) and capillary basement membrane thickening.
- Retinopathy: pericyte loss gives microaneurysms. Nephropathy: microalbuminuria is the earliest sign; nodular (Kimmelstiel–Wilson) glomerulosclerosis.
- Foot: neuropathy plus ischaemia; ulcers under pressure points. Osteomyelitis on MRI is confluent low T1 marrow next to an ulcer. Charcot foot is hot, swollen and painless. Gangrene of toes and fingers from small and large vessel disease.
| Diabetic finding | Imaging clue and mechanism |
|---|---|
| Vas deferens calcification | Bilateral, symmetrical, smooth tubular calcification converging behind the bladder on the prostate (mural, from diabetic medial calcification); irregular intraluminal calcification suggests TB or gonorrhoea |
| Glycogen hepatopathy | Poorly controlled type 1 diabetes with repeated extra insulin plus sugar: insulin drives glucose into hepatocytes as glycogen; liver large and bright on ultrasound but denser than spleen on CT (fat would be darker); reversible with control |
| Mucormycosis (ketoacidosis) | Black, non-enhancing nasal mucosa |
| Malignant otitis externa | Skull base erosion, facial palsy |
| FDG-PET | High glucose competes with FDG |
- Diabetic gastroparesis (autonomic neuropathy) causes vomiting and bloating; visible peristalsis with succussion suggests gastric outlet obstruction instead.
Diabetes in pregnancy
- High glucose at conception causes anomalies: cardiac defects commonest; caudal regression most characteristic.
- Fetal hyperinsulinism gives macrosomia (shoulder dystocia), polycythaemia, jaundice and neonatal hypoglycaemia. Gestational diabetes predicts later type 2 diabetes.
Thyroid function and tests
- The thyroid releases mostly T4 (about 90%); T3, the active hormone, is made mainly in peripheral tissues by 5'-deiodinase. Hormones are inactivated by deiodination (inner-ring deiodination gives inactive reverse T3) and by hepatic conjugation (glucuronide and sulfate) with biliary excretion.
- Serum TSH is the best single first-line test of primary thyroid dysfunction: high TSH with low free T4 is primary hypothyroidism; low TSH with high T4 is hyperthyroidism. Low TSH with low T4 suggests pituitary failure, which TSH screening misses.
- Hyperthyroidism: tachycardia, tremor and sweating because thyroid hormone increases the number and sensitivity of β-adrenergic receptors (beta-blockers relieve them).
- Hypothyroidism: raised TSH, cholesterol (fewer LDL receptors), CK and prolactin (TRH excess); menorrhagia, weight gain, constipation. Treat with levothyroxine (T4).
Thyroid: overactivity and inflammation
- Graves disease: TSH receptor-stimulating IgG (type II hypersensitivity). Antibodies cross the placenta (neonatal thyrotoxicosis).
- Graves orbitopathy: enlarged muscle bellies with tendon sparing (inferior and medial recti first); apical crowding compresses the optic nerve.
- Hashimoto thyroiditis: anti-TPO; T-cell (type IV) destruction; Hürthle cells; risk of thyroid lymphoma.
- Subacute and postpartum thyroiditis: hormone leaks from damaged follicles; isotope uptake low.
- Toxic multinodular goitre: several hot nodules. Endemic goitre from iodine deficiency.
- Thyroid hemiagenesis: one lobe (usually the left) never formed; ultrasound shows no tissue on that side and the scan a hockey-stick shape. Scintigraphy alone cannot separate agenesis from a suppressed lobe.
- Tracheomalacia: a huge goitre pressing on the trachea for decades softens the cartilage rings; after thyroidectomy the trachea collapses on expiration, causing stridor with normally moving cords. Exclude haematoma and recurrent laryngeal nerve palsy first.
Thyroid: underactivity and its effects
- Congenital hypothyroidism: commonest cause dysgenesis (including lingual thyroid); absent distal femoral epiphysis at term.
- Pericardial effusion in hypothyroidism accumulates slowly, so the pericardium stretches and tamponade rarely develops; a large globular heart may be fluid, not cardiomegaly.
- Slipped capital femoral epiphysis in a short, overweight hypothyroid child: lack of thyroid hormone weakens and widens the growth plate (delayed maturation of the hypertrophic zone); often bilateral, so image both hips. Growth hormone therapy and renal osteodystrophy do the same.
Thyroid nodules and cancer
- Most nodules are cold and benign; ultrasound with FNAC is the next step.
| Tumour | Cell and features | Spread |
|---|---|---|
| Papillary (commonest) | Ground-glass nuclei, grooves, psammoma bodies | Lymphatic |
| Follicular | Needs capsular or vascular invasion on histology | Blood (bone, lung) |
| Medullary | C cells, calcitonin, amyloid; RET (MEN 2) | Nodes and blood |
| Anaplastic | Elderly, rapid growth | Survival months |
Parathyroid and calcium
- PTH comes from chief cells.
- Primary hyperparathyroidism (adenoma, the commonest cause; localised by sestamibi): subperiosteal resorption, brown tumours, nephrocalcinosis, stones, band keratopathy, peptic ulcer.
- Pancreatitis in hypercalcaemia: high calcium in acinar cells triggers premature intra-acinar activation of trypsinogen and calcium deposits block ducts. In established pancreatitis, fat necrosis lowers calcium, so a normal calcium can hide hyperparathyroidism.
- Tetany on day 1–2 after thyroidectomy: hypocalcaemia from parathyroid ischaemia or removal (usually temporary); positive Chvostek and Trousseau signs.
- Secondary (renal failure) and tertiary hyperparathyroidism; pseudohypoparathyroidism (GNAS, short 4th and 5th metacarpals).
Adrenal glands
| Disorder | Key point |
|---|---|
| Addison disease | Low sodium, high potassium, pigmentation |
| Secondary failure | No hyperkalaemia, no pigmentation |
| Cushing syndrome | Central obesity, moon face, buffalo hump, purple striae, thin skin, proximal myopathy, hyperglycaemia, osteoporosis, hypertension, hypokalaemia; screen with overnight dexamethasone test or 24-hour urinary cortisol |
| Conn syndrome | High aldosterone, low renin, hypokalaemia |
| Phaeochromocytoma | Plasma or urine metanephrines; MEN 2, VHL, NF1 |
| 21-hydroxylase deficiency | Virilised 46,XX with normal uterus and ovaries; salt wasting |
- Adrenal vein sampling: the left adrenal vein drains into the left renal vein and is easy to enter; the right adrenal vein is short and enters the IVC directly (posterior wall), so right-sided sampling often fails. Confirm each sample by its cortisol level (an accessory hepatic vein can mimic it).
- Negative MIBG scan with strongly positive metanephrines: MIBG enters chromaffin cells by the noradrenaline transporter (uptake-1), which tricyclic antidepressants (amitriptyline), cocaine and labetalol block. Stop them before scanning; a negative scan does not exclude the tumour.
- Neuroblastoma is the commonest adrenal medullary tumour of children under 4. Waterhouse–Friderichsen syndrome: bilateral adrenal haemorrhage in meningococcal sepsis.
- Adrenal adenoma: lipid-rich, below 10 HU, rapid washout.
Remember Tendons spared means thyroid eye disease; tendons involved means inflammation such as pseudotumour.
Exam trap Follicular carcinoma cannot be diagnosed on FNAC; it needs histology showing capsular or vascular invasion.
Exam trap A negative MIBG scan in a patient on a tricyclic does not exclude phaeochromocytoma.
How FCPS asks about this
- Best first-line thyroid test: serum TSH.
- Main hormone released by the thyroid: T4; converted to T3 peripherally; inactivated by deiodination and hepatic conjugation.
- Bright liver on ultrasound but dense on CT in a type 1 diabetic: glycogen accumulation.
- Slow pericardial effusion without tamponade in hypothyroidism: the pericardium stretches.
- Hypercalcaemia causing pancreatitis: premature trypsinogen activation.
- Why the right adrenal vein is hard to sample: it is short and enters the IVC directly.
- MIBG negative on amitriptyline: uptake-1 blocked.
Test yourself on this topic
5 of the 93 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 60-year-old woman with untreated hypothyroidism (TSH 85 mU/L) has a large pericardial effusion, yet her blood pressure is normal, her jugular venous pressure is not raised and there is no pulsus paradoxus. Why does tamponade rarely develop in this setting?
Answer: It accumulates slowly, letting the pericardium stretch
In hypothyroidism, increased capillary permeability and reduced lymphatic drainage, along with glycosaminoglycan accumulation, cause fluid to collect in the pericardium. The effusion builds up over months, and the fibrous pericardium gradually stretches, so a large volume can be held without a big rise in intrapericardial pressure. Tamponade depends on the speed of accumulation more than the volume; a small but rapid effusion, as after trauma, can cause tamponade. The effusion usually resolves with thyroxine replacement.
Myxoedema effusion
- Leaky capillaries, slow lymph drainage
- Accumulates slowly
- Pericardium stretches
- Tamponade rare; resolves with thyroxine
Remember Speed, not size, decides tamponade.
Exam trap An enlarged heart shadow in a hypothyroid patient may be fluid rather than cardiomegaly; do not diagnose heart failure without checking.
Why the other options are wrong
- The fluid is too thick to compress the heart Fluid thickness does not prevent pressure rising in the pericardial sac.
- Hypothyroid hearts beat too strongly to be compressed Contractility is reduced, not increased, in hypothyroidism.
- The pericardium becomes rigid and calcified Constrictive calcification would worsen, not prevent, haemodynamic compromise.
- The effusion lies only behind the left atrium A large effusion surrounds the heart and is not limited to one site.
A 72-year-old diabetic man has severe pain in the right ear, discharge and granulation tissue in the floor of the ear canal. Pseudomonas is grown, and the infection has eroded the canal floor and spread into the soft tissue below the skull base. Which cranial nerve is usually affected first?
Answer: Facial nerve at the stylomastoid foramen
Malignant (necrotising) otitis externa is an invasive Pseudomonas aeruginosa infection, usually in elderly diabetics, whose small-vessel disease and impaired immunity let it spread. From the floor of the canal it passes through the fissures of Santorini and the bony–cartilaginous junction into the soft tissue below the temporal bone, causing skull base osteomyelitis. The facial nerve, emerging from the stylomastoid foramen just below the canal, is the first nerve involved. Further spread reaches the jugular foramen (IX, X, XI) and hypoglossal canal (XII).
Malignant otitis externa
- Pseudomonas in elderly diabetics
- Granulation in the canal floor
- Spread through fissures of Santorini
- First nerve: facial (stylomastoid foramen)
Remember Diabetic with ear pain and facial palsy: skull base osteomyelitis.
Exam trap Severe pain out of proportion to the otoscopic findings in a diabetic suggests skull base spread, not simple otitis externa.
Why the other options are wrong
- Vagus nerve at the jugular foramen Can be affected later as infection spreads medially to the jugular foramen.
- Hypoglossal nerve in its canal Affected late, after medial spread along the skull base.
- Abducens nerve at the petrous apex Involved only if infection reaches the petrous apex, which is uncommon.
- Trigeminal nerve at foramen ovale Lies far forward at the skull base and is rarely affected early.
A 45-year-old woman with primary hyperparathyroidism has renal ultrasound because of polyuria. The renal pyramids are diffusely echogenic in both kidneys, brighter than the cortex, with faint acoustic shadowing; the cortex and collecting systems are normal. What is the most likely explanation?
Answer: Medullary nephrocalcinosis from hypercalciuria
In primary hyperparathyroidism, high filtered calcium exceeds what the tubules can reabsorb, causing hypercalciuria. Calcium phosphate and oxalate precipitate in the renal medulla, where urine is most concentrated, producing medullary nephrocalcinosis: echogenic pyramids, sometimes with shadowing, on ultrasound. Other causes include distal renal tubular acidosis and medullary sponge kidney. Cortical nephrocalcinosis follows cortical necrosis or chronic glomerulonephritis and affects the cortex, not the pyramids.
Bright pyramids
- Medullary nephrocalcinosis
- Causes: hyperparathyroidism, distal RTA
- Also medullary sponge kidney
- Cortex spared
Remember Echogenic pyramids with high calcium: medullary nephrocalcinosis.
Exam trap Nephrocalcinosis can be present before stones appear and is a reason to treat even mild hyperparathyroidism surgically.
Why the other options are wrong
- Cortical nephrocalcinosis from cortical necrosis Affects the cortex, as a rim or tramline, not the pyramids.
- Renal papillary necrosis Shows sloughed or cavitated papillae, often with ring shadows on urography, not diffusely bright pyramids.
- Normal neonatal pattern of the pyramids Neonatal pyramids are dark, not bright; transient bright pyramids are seen only in neonates.
- Obstructive hydronephrosis Shows a dilated collecting system, which is normal here.
A 55-year-old man with long-standing primary hyperparathyroidism has a grey-white horizontal band across both corneas in the area exposed between the eyelids, with clear zones at the edges near the limbus. In which corneal layer is the calcium deposited?
Answer: Bowman layer
Band keratopathy is deposition of calcium phosphate salts in the superficial cornea, mainly in Bowman layer and the subepithelial region. It forms in the interpalpebral zone, where evaporation of tears and loss of carbon dioxide raise local pH and concentration and favour precipitation. A clear zone is often left near the limbus. Systemic causes include hyperparathyroidism, vitamin D excess, sarcoidosis and renal failure; local causes include chronic uveitis.
Band keratopathy
- Calcium in Bowman layer
- Interpalpebral band
- Clear zone near the limbus
- Causes: hypercalcaemia, renal failure, uveitis
Remember High calcium leaves a band across the exposed cornea.
Exam trap Do not confuse it with a Kayser–Fleischer ring, which is peripheral, golden-brown and in Descemet membrane.
Why the other options are wrong
- Corneal endothelium The innermost layer, which pumps fluid out of the stroma; it is not the site.
- Descemet membrane Copper deposits in Wilson disease (Kayser–Fleischer ring) occur in Descemet membrane, not calcium in this pattern.
- Deep stroma near the endothelium Calcium deposits are superficial, not deep.
- Tear film Deposits are within the cornea, not in the tear film.
A 9-year-old girl who is short, overweight and constipated has bilateral hip pain from slipped capital femoral epiphyses. Her TSH is markedly raised. How does her endocrine disorder predispose to this?
Answer: It weakens and widens the growth plate
Thyroid hormone is needed for normal maturation of the growth plate: it drives chondrocytes through hypertrophy and mineralisation. In hypothyroidism the hypertrophic zone is disorganised and the physis remains wide and weak, and skeletal maturation is delayed, so the physis stays open longer. Obesity adds shear stress across the weakened plate, and the epiphysis slips. SUFE outside the usual age range (under 10 or over 16), or bilateral at presentation, should prompt a search for hypothyroidism, growth hormone treatment or renal osteodystrophy.
Atypical SUFE
- Age under 10 or over 16
- Think hypothyroidism, GH, renal disease
- Wide, weak hypertrophic zone
- Often bilateral
Remember A young child with SUFE needs thyroid tests.
Exam trap SUFE in an atypical age group is often bilateral, so the other hip must be imaged and watched.
Why the other options are wrong
- It increases the speed of bone growth Hypothyroidism slows growth rather than speeding it.
- It causes early fusion of the growth plates Fusion is delayed, not early, in hypothyroidism.
- It causes avascular necrosis before the slip AVN may follow a slip, but it is not how hypothyroidism causes it.
- It strengthens the femoral neck periosteum There is no such strengthening; the physis is the weak point.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Musculoskeletal and endocrine disorders, Diabetes, thyroid, parathyroid and adrenal disorders
Read next
Drug dose pages
Doses, cautions and practical tips for drugs in this chapter.