Hyperparathyroidism

Question 1

Hyperparathyroidism Types

Answer 1

• Causes serum calcium to rise, phosphate to fall
• Primary: one gland produces excess PTH, may be asymptomatic
• Secondary: increased PTH in response to low calcium because of kidney, liver or bowel disease
• Tertiary: autonomous secretion of PTH because of chronic kidney disease (glands grow large after prolonged hypocalcaemia from CKD)

Question 2

Hyperparathyroidism Role of PTH

Answer 2

• Increases release of calcium from bone matrix
• Increase calcium reabsorption in the kidneys
• Increase intestinal absorption of calcium
• Increase phosphate excretion

Question 3

Primary Hyperparathyroidism Epidemiology and Aetiology

Answer 3

• Third most common endocrine disorder
• Most common in postmenopausal women
• Excess PTH produced by one or more gland
• Single parathyroid adenoma in 85%
• Double adenomas and carcinomas rare
• Aetiology of adenomas is largely unknown

Question 4

Primary Hyperparathyroidism Presentation

Answer 4

• 70-80% asymptomatic and diagnosis made after incidental hypercalcaemia is found
• Bones, stones, groans, moans
• Features due to
• Excessive calcium resorption from bone
• Osteopenia and osteoporosis, presenting as bone pain and pathological fractures
• Renal calculi (most common presentation) from renal calcium excretion
• Hypercalcaemia causes muscle weakness, anorexia, nausea, committing, peptic ulcer disease, polyuria, polydipsia,…
• Depression, dementia

Question 5

Primary Hyperparathyroidism Differentials

Answer 5

• Familial benign hypercalcaemia
• Lithium induced
• Tertiary HPT
• Malignancy

Question 6

Primary Hyperparathyroidism Ix

Answer 6

• In someone presenting with hypercalcaemia; look for drug causes (lithium, thiazides), repeat plasma albumin-adjusted calcium, ensure renal function is normal, measure PTH
• Raised PTH, hypercalcaemia, hypophosphataemia

Question 7

Primary Hyperparathyroidism Management

Answer 7

• Surveillance if middle elevated calcium and normal renal and bone status
• Vitamin D
• Surgery is only potential for cure
• Can cause hypocalcaemia (hungry bone syndrome) until normal glands regain sensitivity , recurrent laryngeal nerve injury, haematoma
• If no surgery, cinacalcet may work

Question 8

Secondary Hyperparathyroidism Aetiology

Answer 8

• Most commonly seen in CKD
• PT glands hyper plastic after long term stimulation due to hypocalcaemia
• Can occur in any condition

Question 9

Secondary Hyperparathyroidism Presentation

Answer 9

• Almost all patients with CKD have SHPT so clinical presentation is often that of CKD
• Skeletal and cardiovascular problems in CKD
• Low calcium, raised PTH
• Treat underlying cause
• Calcium and vitamin D supplementation

Question 10

Tertiary Hyperparathyroidis Aetiology

Answer 10

• Usually after prolonged SHPT
• Glands become autonomous producing excessive PTH even after hypocalcaemia corrected
• Results in hypercalcaemia
• Ix with PTH and calcium bloods
• Manage with cinacalcet
• Total or subtotal parathyoidectomy is recommended