Hyperparathyroidism

Question 1

Types of hyperparathyroidism

Answer 1

Primary: Autonomous overproduction of PTH which results in derangement of calcium metabolism

Secondary: Elevation of PTH levels as a response to hypocalcaemia

Tertiary: Autonomous PTH secretion following chronic secondary hyperparathyroidism

Question 2

Aetiology of primary hyperparathyroidism

Answer 2

Inappropriate secretion of PTH → Hypercalcaemia

Parathyroid adenoma (85%)
Multiple adenoma and hypertrophy of all 4 glands (less common)
Inherited forms (10-20%): MEN 1, MEN 2, MEN 4 and HPT-jaw tumour syndrome
<1% are due to parathyroid malignancies
External neck irradiation, lithium therapy

Question 3

Aetiology of secondary hyperparathyroidism

Answer 3

Hypocalcaemia → appropriate elevation of PTH

CKD: Loss of 1-𝛼-hydroxylase, unable to make 1,25-vitD
Malabsorption syndromes e.g. Crohn’s, Coeliac, C. Pancreatitis, gastric bypass surgery
Inadequate exposure to sunlight: Vit D deficiency
Increased calcium loss/metabolic requirement e.g. bone growth, after pregnancy, bisphosphonates, loop diuretics, rhabdomyolysis, sepsis

Question 4

Aetiology of tertiary hyperparathyroidism

Answer 4

Secondary hyperparathyroidism that has been untreated → autonomous secretion

Question 5

Symptoms of hyperparathyroidism

Answer 5

80% with primary hyperparathyroidism are asymptomatic in developed countries, but >80% of patients are symptomatic in resource-poor nations

Bones: bone pain (aching), fractures
Stones: renal stones
Abdominal groans: peptic ulceration, constipation, pancreatitis
Psychic moans: depression, fatigue, anxiety, memory loss
Polydipsia, polyuria
Myalgia
HTN
Corneal calcification
Short QT

Question 6

How do you differentiate primary vs secondary hyperparathyroidism on examination

Answer 6

Secondary → Hypocalcaemia:
- Chvostek’s sign
- Trousseau’s sign
- Peri-oral tingling/paraesthesia

Question 7

Investigations for hyperaparathyroidism

Answer 7

ECG: Short QT
24h urinary calcium: High/normal in primary hyperPTH (low in FHH)
BM: exclude DM

Bone profile:
- Primary: Calcium raised, Phosphate reduced, PTH raised
- Secondary: Calcium reduced/normal, phosphate reduced, PTH raised (Phosphorus raised indicates CKD)
- Tertiary: Calcium raised, phosphate raised, PTH raised
25-hydroxyvitamin D: ?secondary hyperPTH
Serum ALP: raised (high turnover bone disease)
Renal function
VBG: hyperchloraemic acidosis with nomal anion gap

DEXA: ?osteoporosis
Sestamibi scanning: solitary adenom/ multi-gland involvement/ parathyroidsm gland hyperplasia
US neck: parathyroid gland hyperplasia
X-ray: ‘multiple well-defined lucencies in the calvaria consistent with a pepper pot skull appearanc

Question 8

Management for hyperparathyroidism

Answer 8

Acute hypercalcaemia: give IV fluids, 4-6L/24h

Conservative management (calcium <2.85 + >50yo + no end-organ damage):
1. Avoid exacerbating factors e.g. thiazide diuretics
2. Maintain adequate hydration (at least 6-8 glasses of water a day)
3. Moderate calcium and vit D intake
Bisphosphonates
4. Treat underlying cause

Primary → total parathyroidectomy

Question 9

Describe the total parathyroidectomy procedure

Answer 9

Risks of failure to cure, haematoma, voice change (recurrent laryngeal nerve damage)
Recovery - will be home day 1, 1-2 weeks off of work
Follow-up - Ca/PTH at 2 weeks and 6 months

Question 10

Complications of hyperparathyroidosim

Answer 10

Primary: Bone resorption, renal tubular calcium reabsorption, hypercalcaemia
Secondary: bone resorption and turnover - osteitis fibrosa cystica

Osteopenia/porosis
Renal calculi/nephrocalcinosis/failure
Cardiovascular -HTN, LVH, arrhythmia
Abdominal - pancreatitis, constipation
Neuropsychiatric - concentration, mood, tiredness, brain fog

Question 11

Prognosis for hyperparathyroidism

Answer 11

Secondary or tertiary: same prognosis as CKD