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IN MEDULLARY THYROID CARCINOMA
- INCREASE IN CALCITONIN BY THYROID PARAFOLLICULAR C CELLS
>> LEADS TO ACUTE DIARRHEA AND FACIAL FLUSHING
>> NEAR NORMAL CALCIUM LEVELS
** DOUBT**
- Although increased Calcitonin levels, Ca2+ levels are near normal values due to compensatory PTH Ca2+ reabsorption in PCT kidney and bone resorption?
- So pt can present w/ pathologic fractures then?
PLEASE ANSWER WITH AN EXPLANATION...
THANKS!
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Calcitonin (Like PTH) at LOW conc will ↑ Ca reabsorption path cAMP DCT + TAL.
Now, if you recall like PTH, calcitonin is G/protein engagement R & that would depend on where they hit can tickle either phospholipase C or adenylyl cyclase. In the heart of bone osteoclast orphan PTH R so it seems that they been the target with calcitonin (and that is the best way to id osteoblast if you want to) In osteoclast they boil cAMP then they attack one or few proteins kinase. Calcitonin block or slow down osteoclast/other word brings down the rate of bone turnover. You understand calcitonin lower serum Ca so not much effect Ca level. HOW ever as I just explain in top if malignancy of those parafollicular/C cell u gone see hypOCa bz they gone burn that system and they can’t catch with that much in system. However, in hypOCa action calcitonin is come to play that u see bone turnover goes up like pat with hyperparathyroidism good use.
So we can use that anitosteoclastic advantage in paget ? The problem with that few mins after exp of osteoclast that anti effect calcitonin begins to wane/so, the escape from hypOCa limit us in hypercalcemia. And who knows that maybe due fast downregualtion of that calcitonin R.
Now, if its bone metastases either sclerotic or lytic then yes pat risk to fracture from that. But not from what I just dissected for you.
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So, I think your confusion on LOW calcitonin not much or as u said close to Ca norm. But in malignancy of that C cell, remember you gone have hypOCa pat.
Hope that clear it for u.
