Calcium homeostasis, hypo- and hyper-calcaemia Flashcards
how does hypocalcaemia affect neurons?
destabilises neurons -> seizures.
check serum calcium if someone has a first fit.
what are the physical signs of hypocalcaemia and what is the cause of these symptoms?
carpopedal spasm (Trousseau’s sign) when using a cuff.
Chvostek’s sign.
low plasma calcium increases neuronal membrane’s permeability to sodium.
what are the consequences of hypercalcaemia?
acute: thirst and polyuria, abdominal pain.
chronic: constipation, musculoskeletal aches/weakness,
neurobehavioral symptoms, renal calculi, osteoporosis.
what should be measured if the albumin concentration is <20 g/l or in severe acute illness?
ionised calcium directly
which cells make parathyroid hormones?
chief cells in parathyroid glands.
what is PTH release determined by?
when serum calcium concentration falls below normal range
how does the parathyroid cell know when to make PTH?
calcium sensing receptor in parathyroid chief cells
how does magnesium levels affect PTH release?
low Mg prevents PTH release
where are the PTH1 receptors (biological effect)?
Bone and kidneys
what are the effects of PTH action?
Kidneys:
1. rapid calcium reabsorption: in loop of Henle, distal tubule, collecting ducts.
2. phosphate excretion in distal tubule.
3. renal synthesis of active vitamin D. calcium transporters and binding proteins increase absorption of calcium from gut.
Bone:
1. rapid action of PTH at osteocytic membrane pump.
2. calcium release from bone due to stimulation of osteoclasts.
how can primary hyperparathyroidism be diagnosed?
high serum calcium
low serum phosphate
PTH high / normal
what are the complications of hyperparathyroidism?
osteoporosis and bone cysts (if severe)
what are the indications of hypoparathyroidism?
low serum calcium
high serum phosphate
low / normal PTH
what are the causes of hypoparathyroidism?
iatrogenic: thyroidectomy, radical neck surgery.
autoimmune.
hypomagnesaemia.
genetic mutations.
how is blood Ca2+ concentration and bone mineral density maintained?
low concentration of calcium in blood > release of parathyroid hormone leading to: increase efflux of calcium from bone and decreased loss of calcium from urine > enhanced absorption of calcium from intestine.
What stimulates and inhibits 1,25(OH) vitamin D production from the kidney?
PTH stimulates 1,25(OH) vit D production from 25OH vit D. 1,25(OH) vit D then inhibits PTH secretion from parathyroid glands.
FGF23 inhibits 1,25(OH) vit D production which then stimulates FG23 production from bone.
How does the kidneys excrete phosphate?
osteocyte releases FGF23 causing renal phosphate excretion
What are the common causes of secondary hyperparathyroidism?
Low / normal serum calcium + high PTH:
low serum 25OH vitamin D: lack of sun exposure, GI problems - malabsorption, extensive surgery.
renal failure
Which conditions are caused by reduced vitamin D concentration?
Rickets
Looser’s zone associated with osteomalacia
