Hyperparathyroidism

Question 1

D?

Answer 1

Elevated levels of parathyroid hormone in the blood due to overactivity of the parathyroid gland. Can be primary, secondary and tertiary depending on underlying cause

Question 2

RF?

Answer 2

• Female
• Age 50-60
• FH
• MEN 1, 2A,4
• Lithium
Jaw-tumour syndrome

Question 3

Ddx?

Answer 3

• Familial hypocalciuric hypercalcaemia-lower renal calcium and creatinine clearance
• Malignancy-low PTH but high PTHrP
• MM-signs
• Milk-alkali syndrome-high Ca, low PTH, antacid use
• Sarcoidosis-high Ca, low PTH
• Hyper VitaminD-high calcium and VitD, low PTH
• Thyrotoxicosis-low TSH
• Leukaemia-signs
• Immobilisation
• thiazides

Question 4

Epidemiology?

Answer 4

Age: 50-60
Sex: Female (3:1)
Ethnicity:

Question 5

Aetiology?

Answer 5

• Primary-abnormally active parathyroid glands
  
  • Adenoma
  • Hyperplasia and multiple adenomas
  • Carcinomas
  • MEN 1 or 2
• Secondary-hypocalcaemia causing reactive overproduction of PTH
  
  • CKD
  • Malnutrition
  • Vit D deficiency
  • Cholestasis
• Tertiary-Hypercalcaemia from untreated secondary, with constantly high PTH levels

Question 6

CP?

Answer 6

• Primary
• Most pts asymptomatic
• CVD
• Nephrolithiasis, nephrocalcinosis
• Polyuria and polydipsia
• Bone pain and pseudogout
• Osteitis fibrosa cystica-cyst-like brown tumours
• Granular decalcification/salt-and -pepper skull
• Weight loss
• Nausea and constipation
• Ulcers and pancreatitis
• Depression and anxiety, fatigue, sleep disorders
• Secondary
• Underlying cause
• Bone pain and increased fractures

Question 7

Pathophysiology?

Answer 7

• High level of PTH
• 4 parathyroid glands-chief cells make PTH in response to a low calcium conc
• Increases absorption intestines, reabsorption in PTH and increase osteoclasts and so more absorption of calcium
• Increases vitamin eD synthesis and so amplifies the above functions
• Primary-uncontrolled PTH secretion via tumour-increased absorption of Ca
• Secondary-less vitamin D or chronic renal fialure means less absorption of calcium from the above-PTH increases secretion to compensate and so cell hyperplasia occurs
• Tertiary-secondary continues for long period of time and hyperplasia of glands means baseline levels increases rapidly-when secondary treated to reduce levels-so more PTH is secreted so more calcium is released into the blood.

Question 8

Investigations?

Answer 8

See ON

Question 9

M?

Answer 9

See ON for primary
Secondary
• Increase calcium, vitamin D supplements and manage underlying disease
• Restrict phosphate and then add phosphate binders
• Ergocalciferol and sterols if low vitD

Question 10

P?

Answer 10

• Prognosis
• Primary has usually stable disease if not cured by surgery, and most common cause of mortality is CVD events.
Secondary follows progression of underlying cause

Question 11

C?

Answer 11

• Haematoma
• Recurrent and superior laryngeal nerve injury
• Hypocalcaemia
• Pneumothorax
• Osteoporosis
• Bone fractures
• nephrolithiasis
• Osteodystrophy
• Osteoporosis
• Ureamia
• Calciphylaxis