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End stage liver failure
30%
45/152
Insufficient Ca intake
28%
42/152
Parathyroid adenoma
10%
15/152
Decreased functioning of the calcium-sensing receptor (CASR)
22%
33/152
Sarcoidosis
8%
12/152
Select Answer to see Preferred Response
The patient, suffering from chronic renal failure, has hyperparathyroidism secondary to decreased production of active vitamin D (loss of renal 1-alpha-hydroxylase activity). 1-alpha hydroxylase activity as well as 25-hydroxylase are required to make the active form of vitamin D, 1,25 dihydrocholecalciferol. 25-hydroxylase is produced in the liver and in end stage liver disease you would be unable to produce active 1,25 vitamin D. Secondary hyperparathyroidism is the increase in parathyroid hormone (PTH) as a result of decreased calcium. This may occur due to decreased calcium intake, hyperphosphatemia, as well as decreased serum levels of vitamin D (i.e., renal failure, liver failure). When vitamin D levels are decreased, there is decreased Ca absorption from the GI tract, leading to decreased serum Ca levels -- resulting in increased PTH release. Incorrect Answers: Answer 2: Though insufficient Ca intake can lead to hyperparathyroidism, the mechanism is not driven by decreased levels of vitamin D. Answer 3: Parathyroid adenomas cause hyperparathyroidism due to increased secretion of PTH from the mass -- primary hyperparathyroidism. Answer 4: Decreased functioning of the CASR can cause increased release of PTH from chief cells, however this is not driven by low vitamin D levels. Answer 5: Sarcoidosis granulomas contain 1-alpha-hydroxylase, and would be associated with an increase in vitamin D and no hyperparathyroidism.
2.2
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