What cells secrete parathyroid hormone?
Cheif cell
When the parathyroid hormone is produced by parathyroid glands?
In response to low calcium (hypocalcaemia)
How does PTH act to increase calcium levels in the blood?
Parathyroid hormone acts to raise blood calcium level by:
- Increasing osteoclast activity in bones (reabsorbing calcium from bones)
- Increasing calcium absorption from the gut
- Increasing calcium absorption from the kidneys
- Increasing vitamin D activity
Relation of PTH and vitamin D
- Vitamin D acts to increase calcium absorption from the intestines
- Parathyroid hormone acts on vitamin D to convert it into active forms
(So vitamin D and parathyroid hormone act together to raise blood calcium levels)
Primary hyperparathyroidism:
- cause
- what happens to Ca++ levels
Cause: a tumour in parathyroid gland -> secretion of excess of PTH
Result: hypercalcaemia (high Ca++ in the blood)
Treatment for primary hyperparathyroidism
Surgical resection of the tumour
Secondary parathyroidism
- cause
- what happens to parathyroid gland
Cause: insufficient vitamin D or renal function -> low Ca++ absorption from intestines, kidney and bones
PTH gland responds: production of excess PTH -> hyperplasia of PTH gland -> serum calcium low/normal and PTH high
PTH and Ca++ serum levels in secondary hyperparathyroidism
- PTH - high
- Ca++ either low or normal (normal if compensated by PTH excess production in response to serum hypocalcaemia that is due to kidney or vit D failure)
Treatment of secondary hyperparathyroidism
- vitamin D replacement
- renal transplant (if renal failure is a cause)
What’s the cause of tertiary hyperparathyroidism?
What happens to Ca++ levels?
- It is on the background to secondary hyperparathyroidism (when the hyperplasia of PTH gland occurs)
- In tertiary: even is a cause of secondary hyperparathyroidism is treated -> we will have excess of PTH due to PTH gland hyperplasia
- Result: high absorption of Ca++ in kidney, intestine and bone -> hypercalcaemia
Treatment for tertiary hyperparathyroidism
resection of part of the parathyroid gland
(so less PTH will be produced -> to normalise Ca++ levels)
Primary hyperparathyroidism
- cause
- levels: PTH and Ca++
Secondary hyperparathyroidism
- cause
- levels of PTH and Ca++
Tertiary hyperparathyroidism
- cause
- levels of PTH and Ca++
Primary hypoparathyroidism
- cause
Low PTH secretion
Cause: due to thyroid surgery
Serum levels abnormalities in primary hypoparathyroidism
low PTH -> low Ca++ and high phosphate
Treatment of primary hypoparathyroidism
Alfacalcidol
(vitamin D3)
Symptoms of hypoparathyroidism (5)
Symptoms are secondary to hypocalcaemia
- tetany (muscles twitching, camping and spasm)
- Trousseau sign
- Chvostek sign
- chronic: depression, cataracts
- ECG: prolonged QT interval
What are Torsseau and Chvostek signs?
Signs of hypocalcaemia
- Trousseau sign: carpal spasm when brachial a. occluded by inflated BP cuff with pressure above systolic
- Chvostek sign: tapping over parotid -> facial muscles twitch
Pathophysiology of pseudohypoparathyroidism
- abnormality in protein G -> target cells are insensitive to PTH
- Result: high PTH, low calcium, high phosphate
Associations of pseudohypoparathyroidism (symptomatic features)
- low IQ
- short stature
- short 4th and 5th metacarpals
Diagnosis of pseudohypoparathyroidism
- investigations
- result for: a) hypoparathyroidism b) pseudohypoparathyroidism
infusion of PTH -> then measuring urinary levels of cAMP and phosphate
a) hypoparathyroidism: infusion of PTH will cause an increase in both cAMP and phosphate
b) pseudohypoparathyroidism: infusion of PTH will not cause an increase in cAMP and phosphate (as target cells not responsive to PTH)
What’s pseudopseudohypoparathyroidism?
It’s similar phenotype to pseudohypoparathyroidism (abnormalities in G protein and insensitivity to PTH), but normal biochemistry
