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someone off of an actual incident of child abuse when it has happened it absolutely has to be clear andsomething that we need to revisit we'll move on next to 3.6.2 deficiency and osteomalacia in adultsVideo 3-6-2section 3.6.2 deficiency in osteomalacia having gone through rickets with quite a bit of depth I'm goingto go through these next two sections relatively quickly Okay so osteomalacia we've already talked aboutthis um as a component of rickets it is the softening of Bones rickets occurs only in growing children butosteomalacia can be a component of the um pathology that we see in rickets where the bones becomesofter part of that pathology is due to decreased mineralization at the at the growth plate but part ofthat pathology is due to the fact that in order to provide calcium to the blood there can be increasedresorption of that bone mineral Mass from the bones whatever happens to be laid down during timeswhen there is adequate calcium that resorption can lead to a softening so we typically think ofosteomalacia as occurring in older adults we mostly talk about it as occurring in older adults but it canoccur in people of any age and it can be a component of rickets in osteomalacia bone mineral resorptionis excessive but the Matrix is well preserved and so it is considered a subset of osteoporosis but is alsoconsidered different from it has a different Hallmark characteristic compared to overt osteoporosisbecause in osteoporosis there is a loss of both the bone mineral content and the Matrix on which it isstored and in osteomalacia The Matrix is often relatively well preserved but it has been demineralized sothe bone mineral content relative to the proportion of of collagen is decreased it's most often seen dueto severe vitamin D deficiency and with osteoporosis where we lose both the Matrix and we lose themineral content we see typically Calcium deficiency and vitamin D deficiency and that is often linked toolder age in osteomalacia as we said which can occur at any age it is most often seen due to severevitamin D deficiency and is treated primarily with vitamin D Administration and as I said already it'sconsidered a component of osteoporosis not a separate disease poor vitamin D status will lead to as wealready know impaired calcium absorption because the proteins that mediate calcium absorption in thesmall and large intestine are regulated genomically by active vitamin D when there are reductions inblood calcium this can cause elevated secretion of parathyroid hormone parathyroid hormone wouldnormally activate one alpha hydroxylase resulting in increased conversion of 25 hydroxide see vitamin Dto 125 dihydroxy vitamin D which should start to augment the absorption of calcium from the smallintestine which would remedy the situation but in the event that 25 hydroxy vitamin D as a substrate forone alpha hydroxylase is is deficient is low in the blood then we will have an inability to generate enoughactive hormone pth in that case parathyroid hormone in that case will act alone and as you recall the pthreceptor is not present in the gastrointestinal tract which means that it will primarily act to increase theresorption that the reabsorption of calcium from the urinary tract from the renal filtrate byphosphorylating but uh resulting in the phosphorylation of trpv5 and by inducing renal Cal binding d28k

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