metabolic bone disease Flashcards
two main physiological functions of bone
-structural -endocrine
structural functions of bone
-scaffold for the body -remodels in response to stress
endocrine functions of bone
- main storage site for calcium - perturbations in serum Ca or or calcium regulatory hormones lead to bone
bone turnover releases
calcium
mild decreases in serum calcium
increase bone resorption activity at the lining cell/osteocyte complexes (LCOCs)
lining cell/osteocyte couples LCOCs
compensate for small fluctuations in serum Ca
when the ability to compensate for low Ca is overcome, _____ acts to increase the number of active BMUs
PTH
BMU
bone multicellular units
PTH is released from ___ cells within the PT gland in response to _____ in serum Ca
-chief cells - decreases
Vitamin D and its affect on PTH
inhibits
what does PTH bind to?
PTH receptors on osteoblasts, then the osteoblasts secrete something in return
osteoblasts secrete
osteoclast activating factor OAF which includes RANK
RANK binds to
RANK receptor is on osteoclasts (which activates bone resorption)
do osteoclasts have PTH receptors?
no! only osteoblasts
steroid hormone synthesized in inactive form in the skin
cholecalciferol (vitamin D3)
Vit D3/cholecalciferol is converted to its active form by
hydroxylation in the liver and proximal renal tubule
function of cholecalciferol/vit D3
-increases available Ca2+/PO4 3- for mineralization -also enhances monocyte innate immune response
Vitamin D3 becomes ____ after hydroxylation in the liver
25 VitD3
UVB light is required to synthesize the inactive form of this
vit D3
bone disease primary pathway external to the skeletal system
extrinsic bone disease
serum calcium levels are often ____ in extrinsic bone disease
affected
etiology of primary hyperparathyroidism
adenoma (85%)
lab findings of primary hyperparathyroidism
increased Ca increased PTH increased normal alk phos
in both primary and secondary hyperparathyroidism, ____ become hormonally activated
osteoclasts
signs and symptoms of hypercalcemia
-stones (kidney stones) -groans ( PUD, pancreatitis, GI symptoms) -bones (high bone turnover, pain, arthralgia) -psychiatric overtones (fatigue, weakness, depressions)
osteitis fibrosa cystica
severe, generalized osteoclast activation, fibrous marrow replacement
histology of hyperparathyroidism
osteitis fibrosa cystica: - subperiosteal bone resorption -brown tumor/ cystic bone lesions
secondary hyperparathyroidism
- parathyroid hyperplasia in response to chronic increase in phosphate and/or decreased calcium
- (no bones,groans,tones, rhyme) -chronic renal disease, vit D deficiency, corticosteroids
lab findings for secondary hyperparathyroidism
low or normal calcium increased PTH (hyperphosphatemia) increased ALK phos
high turnover bone rate reflected by
elevated alk phos, creates pronounced bone symptoms
renal osteodystrophy
spectrum of bone pathology seen with CKD -decreased renal phosphate excretion, so increase it in serum, binds with serum ca and depletes serum ca, which ultimately inhibits renal hydroxylation of vitd3 and decreases Ca absorption, further decreasing serum Ca
most common cause of secondary hyperparathyroidism
renal osteodystrophy