4.7 Endocrine mineral homeostasis Flashcards
what are the 3 hormones that control mineral homeostasis aka regulate calcium?
1) vitamin D
2) parathyroid hormone (PTH)
3) calcitonin (follicular cells)
main places we regulate Ca?
1) gut = absorb in1st palce
2) kidney = reabsorb
3) bone = take Ca+ out of storage
what does calcitonin do?
lowers blood Ca levels and inhibits bone resorption
1) Vitamin D is synthesized where?
2) what type of hormone?
3) main role is located in?
1) synthesized in skin via UV light (or can ingest
2) steroid hormone (from cholesterol)
3) main role is in gut
what is active form of Vitamin D?
cholesterol + UV light + OH + OH
exaplin vit D synthesis?
- *7-dehyrocholesterol + UV light = Vit D3 aka cholecalciferol)
1) 1st hydroxylation occurs in liver - *Vit D3 + OH= 25-hydroxyvitamin D3
2) 2nd hydroxylation occurs in kidney - *25-hydroxyvitamin D3 + OH = 1,25-dihydroxyvitamin D3
what is active form of Vit D?
1,25-dihydroxyvitamin D3
vit D synthesis must have TWO _______ events (one in liver, one inkidney)
hydroxylation events
enzymes used in 2nd hydroxilation are stimulated by?
PTH (parathyroid hormone)
primary effect of vit D?
directly increase intestinal absorption of Ca
secondary effect on Vit D?
indirect effects on bone resoprtion (and possibly kidney reabsorption) of Ca via PTH
how does low Ca affect Vit D regulation?
- decrease plasma Ca++ =
- increase PTH =
- stimulation of kidney enzyme =
- final hydroxylation of Vit D
Calcium in intestine?
1) increase Ca binding protein to keep free Ca low
2) increase active transport of Ca out of mucosal cell via vit D-dependent Ca pump
* *increase intestinal absorption of Ca
Calcium in bone?
increase action of PTH = increase bone resorption
*may also directly cause bone resorption by itself
Calcium in kidney?
increase action of PTH = increase Ca reabsorption and decrease in P reabsorption
*may have direct actions on kidney that cause Ca++ reabsorption
PTH and Vit D relationship???
PTH helps activatre Vit D
*so Vit D helps PTH by increasing the action of PTH on bone for resorption
what all does Vit D help reabsrop?
Ca and phosphate
what type of hormone in PTH?
located?
parathyroid hormone is a protein
*CHEIF cells of parathyroids are imbedded intyroid
why can’t the parathyroid be removed?
need at least ONE to regulate blood Ca! otherwise you die
what is the MOST important hormone for raising blood Ca levels?
PTH
PTH directly and indirectl raises blood ca how?
- directly thru bone and kidney action
* indirect action on intestine via Vit D synthesis
PTH regulates cell activites of?
osteoclasts, osteocytes, kidney tubule cells
PTH stimulates enzyme in kidney that performs?
final hydroxylation of Vit D (intestinal absorption of Ca)
how is PTH regulated?
feedback inhibition of Ca++ on parathyroids =negative feedback
calcitonin is what type of hormone? secreted from what cell?
peptide hormone from parafollicular cells (aka C cells) of thyroid
why is calcitonin NOT considered a thyroid hormone like T3 or T4?
it is coming from C cells that is found BETWEEN the functional follicles of thyroid; but still coming from thyroid
primary effects of calcitonin?
***
Keep blood Ca levels low
- inhibition of osteoclastic and osteocytic bone resorption
- stimulationf of osteoblastic and osteocytic bone formation
secondary effects of calcitonin?
decrease Ca and PO$ reabsorptionin kidney
what INHIBITS secretion of calcitonin?
low levels of Ca+
remember peptide hormones?
have cell membrane receptors
*acts via cAMP
describe hypervitaminosis D
too much vit D
*increases action of PTH which increased resorption of bone
vit D deficiency aka hypovitaminosis D names fro child and adutls?
rickets= child osteomalacia= adult
describe rickets and osteomalacia?
vit D deficiency aka hypovitaminosis D
*decreases bone mineratlzation
BOTH hypo and hypervitaminosis D causes soft, flexable bones why?
1) a lot of Vit D helps PTH take stuff out of bones = soft
2) not enough Vit D means we never had enought to mineralize bone to start with = soft bones
secondary effects of rickets and osteomalacia? only occurs during?
dentinal and enamel HYPOPLASIA (only IF deficiency occurs DURING tooth development)
PTH hyperparathyroidism primary effect?
secreting excess PTH (which main role is to resorb bone)
***osteitis fibrosa cystica= replacementof bone with fibrous tissue
osteitis fibrosa cystica
= replacementof bone with fibrous tissue
**means one has bone demineralized by excess PTH and replaced with fibrous tissue
PTH hyperparathyroidism secondary effect?
1) neuromuscular depression
- –due to excess plasma Ca+
2) cardiac spasm
- –due to excess plasma Ca+
3) metastatic calcification
- –due to excess Ca pyrophosphate, can;t keep ahead of it!
metastatic calcification
due to excess Ca pyrophosphate, can;t keep ahead of it! because of PTH hyperparathyroidism secondary effect
**START to see mineralization of tissue that we don’t want!
hypoparathyroidism primary effect?
decrease osteoclastic and osteocytic bone resorption
*due to tumor or removal of thyroif with malfunctioning parathyroid
hypoparathyroidism secondary effect?
1) dentinal and enamel hypoplasia (if during tooth development)
2) hypocalcemia -low Ca in blood (and hyperphosphatemia)
3) hypocalcemis tetany = spasms starting in extremities
what all causes hypocalcemic tetany??
1) hypoparathyroidism
2) low plasma Ca
renal failure is associated iwth high or low Ca levels?
high
what are otherfactors essentual for growth and maintenance?
1) thyroxine (growth)
2) growth hormone (growth)
3) estrogen (keeps Ca+ and PO4 in bone)
4) Vat A (for normal osteoclasts to remodel)
5) Vit C (for normal collagen)
why do menopausal women have trouble with osteoporosis?
they have low levels of estrogen
What all causes bone resorption when in EXCESS and HOW?
1) vit D, thyroxine, and Vit A all increase osteoclast activity
2) cortisol decreases osteoBlast activity
3) prostaglandins sometimes cause formation and sometimes resorption BUT if too high, cause more resorption
what does fluoride do?
stabilizes bone minerals (make hydroxyapetie more stable)
*&may stimulate ostoblastic activity
