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Ok, so after reading Robbins for like over an hour trying to udnerstand one little concept, I have as a result, added a plethora of uselss knowlede and additional questions. So, help me understand this, if you will.
In osteomalacia and rickett's, the straw that breaks the camel's back is the HYPOPHOSPHATEMIA (which btw, I didn't know before--I always thought it was the hypocalcemia) that ensues as a result of almost complete calcium compensation by PTH, which ultimately leads to NEAR NORMAL calcium levels and hypophos-- resulting in an abnormal ca-phos solubility product-->ricketts or osteomalacia, correct??
1. Ok, so, my next question is that in chronic renal failure and secondary hyperpth, why is it that you get osteomalacia? In this case, is it because there is inadequate compensation of calcium release from bone and reabs from renal tubules? But, that doesn't make sense, because somehow in ricketts and OM, the calcium compensation is nearly complete despite vit d deficiency. In CRI, we have hypERphos, so I don't quite understand how you get OM? Unless, ofcourse, it's simply because of inadquate compensation of calcium by PTH. In Robbin's they do talk about some alluminum crap, which can increase in dialysis pts because of the dialysis solution, and that intereferes with calcium hydroxyappetite deposition, which can cause OM--but I think, there is a more accredited answer, as that seems like a "postulate". Maybe, i am thinking too much into this (damn robbins). Will appreciate some input.
2. Oh, and also, hyperphosphatemia DIRECTLY stimualtes PTH release?
In osteomalacia and rickett's, the straw that breaks the camel's back is the HYPOPHOSPHATEMIA (which btw, I didn't know before--I always thought it was the hypocalcemia) that ensues as a result of almost complete calcium compensation by PTH, which ultimately leads to NEAR NORMAL calcium levels and hypophos-- resulting in an abnormal ca-phos solubility product-->ricketts or osteomalacia, correct??
1. Ok, so, my next question is that in chronic renal failure and secondary hyperpth, why is it that you get osteomalacia? In this case, is it because there is inadequate compensation of calcium release from bone and reabs from renal tubules? But, that doesn't make sense, because somehow in ricketts and OM, the calcium compensation is nearly complete despite vit d deficiency. In CRI, we have hypERphos, so I don't quite understand how you get OM? Unless, ofcourse, it's simply because of inadquate compensation of calcium by PTH. In Robbin's they do talk about some alluminum crap, which can increase in dialysis pts because of the dialysis solution, and that intereferes with calcium hydroxyappetite deposition, which can cause OM--but I think, there is a more accredited answer, as that seems like a "postulate". Maybe, i am thinking too much into this (damn robbins). Will appreciate some input.
2. Oh, and also, hyperphosphatemia DIRECTLY stimualtes PTH release?