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got it it is sec hyperparathyroidism.this thing occurs in conditions including osteomalacia and renal failure and pseudohypo parathyroidism[deficient responce to PTH at level of the receptor.there is hypocalcemia in both.but in severe cases of hyperparathyroidism there is heper calcemia becoz of increase in bone resorption.
again same ...ectopic calcification,bone pain[also in.o.]pruritis.
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How would v differentiate secondary hyperparathyroidism from primary lab wise?
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secondary hyperPTH----calsium and P decr
primary---calsium incr.P decr
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I think in [all?] sec hyperparathyroidism cases there is resistance to metabolic actions of pth.that leads to increase pth levels.with hypocalcemia.
given here in harrison is,clinical difference-pri and sec can be distinguished conceptually by the autonomous growth of the parathyroid glands in pri[presumably IRREVERSIBLE] AND the adaptive growth of the parathyroids in sec [presumably REVERSIBLE].
Infact reversal over weeks from an abnormal pattern of secretion, presumably accompanied by involution of parathyroid gland mass to normal, occurs in pts who hav been treated medically to reverse the resistance to PTH.
and also in primary -if acute look for malignancy
chronic look for sarcoidosis or other rare cause.
