Hormones and Bones Flashcards
how does most Ca travel in the blood?
bound to albumin
calcium oxalate
kidney stones
calcium phosphate
ectopic calcification in soft tissues
hypocalcemia symptoms
CATS GO NUMB
convulsions
arrythmias (long QT)
tetany
spasms, stridor
numbness
hypercalcemia symptoms
Stones (kidney stones) Bones (bone pain) Groans (abdominal pain, nausea) Thrones (constipation, polyuria) psychiatric overtones)
more common
treated w/ hydration and IV bisphosphate
is vitamin D3 active or inactive?
inactive`
how does the body sense calcium
Gq linked receptor (phospholipase C/IP3)- causes Ca release from ER
expressed in cheif cells of parathyroid (inhibits PTH)
principal cells and a-intercalated cells in kidney to promote Ca excretion
osteoblasts to promote bone remodeling
parathyroid hormone synthesis
starts as prepro, cleaved to a pro in ER, cleaved in golgi to mature PTH for secretion
parathyroid hormone receptor
Gs receptor- cyclic AMP
PTH effects in bone
transient levels increase bone formation d/t effect on osteoblasts
chronic levels increase bone resorbtion via RANK system- increases free Ca
PTH effects in kidney
increases Ca reabsorption, decreases PO4 reabsorption,
stimulates 25(OH)D3-hydroxylase
causes of hypercalcemia?
90% are cancers in parathyroid gland
vitamin D3 pathway
skin makes vitamin D3
liver converts it to 25(OH)D3
kidney converts to active 1,25(OH)D3
vitamin D3 receptor
binds vit D in cytoplasm and translocates to nucleus and binds response elements with RXR
vitamin D3 effects
90% of gut absorption of Ca
activates RANK system in bone osteoblasts/cytes
stimulates reabsorption of both Ca and PO4 in kidney
RANK system
vitamin D3, PTH stimulate osteoblasts
osteoblasts present RANK ligands to osteoclasts
has 2 effects via NF-kB:
stimulates differentiation into osteoclasts
activates quiescent osteoclasts
denosumab
competitive mAb for RANK ligand to prevent osteoporosis
FGF23
secreted in response to vit D and PO4
causes PO4 secretion from kdiney
decrease PO4 absorption from gut
net: decrease serum PO4
describe the bodies response to hypocalcemia
decreased activation of CaSR
causes:
increased PTH
increased Ca reabsorbtion via kidney
increased Ca/PO4 resorption in bone
PTH will then further increase Ca reabsorption (and PO4 secretion) and stimulate 1,25(OH)D3 hydroxylase
vit D will increase renal reabsorption via increase calbindin
PTH and vit D will activate RANK system at bone and cause resorbtion
vit D will also cause increased Ca absorption in gut
describe bodies response to hypercalcemia
increased CaSR
causes:
decreased PTH
decreased renal Ca reabsorption
increased bone mass
decreased PTH causes decreased Ca renal absorption, and decreased Vit D3
decreased PTH will suppress RANK system
osteoporosis
d/t increased reabsorption of bone
in postmenopausal women, d/t decreased estrogen
excess cortisol, thyroid hormone, hyperparathyroid or low Ca diet
treatment: exercise
rickets/osteomalacia
rickets- prior to epiphyseal closure, osteomalacia is after
caused by Vit D deficiencies
- genetic
- anticonvulsants
- aluminum toxicity
- excess flouride
treated w/ vitamin D3 and phosphate
what cells in the parathyroid hormone release PTH
chief cells