First step is to make the presumptive diagnosis of osteoporosis from the clinical vignette . ( The supposed subtype in our patient is postmenopausal osteoporosis)
After this the next step is to make an association with the lab findings
The primary defect is a deficiency of estrogen .
Normally estrogen decreases osteoclast activity by
inducing apoptosis
increased formation of osteoprotegerin a decoy molecule which inhibits activation of RANK receptors
Net effect of losing estrogen is increased osteoclast activity ,and in this question
by extension RANK L concentration .
NOTE : ALP which is an indicator of osteoblast activity does not change/ increase in osteoporosis , as such avoid all options with an increase in osteoblast activity
briseBut wouldn't you need osteoblasts to have RANK L?+7
cassdawgYou still have osteoblasts, they just aren't doing their "build bone" job so their primary activity is decreased. Rather, they are stimulating osteoclasts by increasing RANKL. Similar to how parathyroid hormone stimulates osteoclasts through osteoblasts --> the osteoblasts are involved but not in doing their "build bone" job; however you would never say you increase osteoblast activity with PTH even though they are necessary for PTH function.+7
submitted by โandro(269)
First step is to make the presumptive diagnosis of osteoporosis from the clinical vignette . ( The supposed subtype in our patient is postmenopausal osteoporosis)
After this the next step is to make an association with the lab findings The primary defect is a deficiency of estrogen . Normally estrogen decreases osteoclast activity by
Net effect of losing estrogen is increased osteoclast activity ,and in this question by extension RANK L concentration .
NOTE : ALP which is an indicator of osteoblast activity does not change/ increase in osteoporosis , as such avoid all options with an increase in osteoblast activity