Hyperparathyroidism

Question 1

Definition

Answer 1

Where parathyroid glands create high amounts of PTH in the bloodstream, resulting in weakening of the bones through loss of calcium

PTH helps maintain the right balance of calcium for proper functioning.

Can be primary or secondary.

Question 2

Clinical Presentation

Answer 2

Symptoms can be mild, so mild that they dont seem related to parathyroid function

weak bones

kidney stones

excessive urination

stomach pain

tiring easily or weakness

depression or forgetfulness

bone and joint pain

frequent complaints of illness with no clear cause

nausea, vomiting or loss of appetite

Question 3

Aetiology

Answer 3

Caused by factors that increase the production of parathyroid hormone.

Primary hyperparathyroidism:
- occurs when there is a problem with one or more of the 4 parathyroid glands
– adenoma (non cancerous growth) on a gland (most common)
– enlargement (hyperplasia) of 2 or more parathyroid gland
– cancerous tumour (very rare)

Secondary hyperparathyroidism:
– severe calcium deficiency
– severe vitamin D deficiency
– chronic kidney failure

Question 4

Risk factors

Answer 4

Menopause

lithium (usually taken for bipolar)

had radiation treatment for cancer that has exposed your neck to radiation

Question 5

Complications

Answer 5

Osteoporosis- loss of calcium from bones

Kidney Stones- too much calcium in blood may lead to too much in urine. This can cause small, hard deposits of calcium and other substances to form in kidneys (kidney stones)

cardiovascular disease- exact reason unknown, but high levels of calcium are associated with cardiovascular disease

neonatal hypoparathyroidism- severe, untreated hyperparathyroidism in pregnant women may cause dangerously low levels of calcium in new-borns

Question 6

Investigations

Answer 6

In most cases, elevated calcium is found by blood tests ordered for other reasons.

Blood tests- many conditions can raise calcium levels. But can diagnose if levels of PTH are high as well

Additional tests can be done:
– bone mineral density test- see if osteoporosis has been developed (uses x-ray)
– urine test- see how much calcium passed in urine
– imagining tests of kidney- kidney stones or other kidney problems (uses x-ray)

Question 7

Treatment

Answer 7

Waiting watchfully:
– monitoring
– calcium levels
– kidney function
– bone density

Surgery (most common):
– removal of glands affected
– if all 4 affected, then 3 and maybe a portion of 4th removed at most

Drugs:
Calcimimetics:
– drug that mimics calcium circulating in the blood. May trick parathyroid gland into releasing less PTH.
– side effects: joint and muscle pain, diarrhoea, nausea, and respiratory infection

Hormone replacement therapy:
– for women, who have gone through the menopause and have signs of osteoporosis, may help bones keep calcium.
– prolonged use, can increase the risk of blood clots and breast cancer.
– side effects: breast pain and tenderness, dizziness, headaches

Bisphosphonates:
– prevent the loss of calcium from bones and may lessen osteoporosis caused by hyperparathyroidism.
– side effects: low blood pressure, fever and vomiting

Question 8

Pathophysiology

Answer 8

Primary hyperparathyroidism pathophys- Increase in PTH will act on the bone and draw calcium and phosphate from the bone into the blood (increasing calcium blood levels). PTH will also act on the kidney releasing the active form of vitamin D (1,25 hyroxycholecalciferol). Increased vitamin D will act on gastrointestinal tract increasing the calcium absorption across GIT into the blood, leading to hypercalcaemia from both kidney and bone.

Secondar hyperparathyroidism pathophys:

3 things that can cause hyperparathyroidism from chronic kidney disease:
– a reduction in glomerular filtration rate- means there is less phosphate filtration, meaning high levels of phosphate in the blood.
—- phosphate in the blood can bind to calcium, meaning there’s less free calcium within the blood (hypocalcaemia).

– impaired kidney tubules (DCT and PCT)- when PTH is released, it doesn’t have an affect on tubules, meaning phosphate can still be absorbed from the blood leading to same affects as last time.
—- also an impaired DCT decreases calcium resorption into the blood leading to hypocalcaemia

– vitamin D deficiency- impaired kidney will release less vitamin D, so less vitamin D will act on the GIT, which usually increases the calcium resorption into the blood, however this isn’t happening.
—- leading to hypocalcaemia

– all of these can lead to chronic hypocalcaemia