NBME 21 Increased parathyroid hormone (NBME Answers)

Retired NBME 21 Answers

nbme21/Block 2/Question#47 (reveal difficulty score)
A 55-year-old woman comes to the physician ...
Increased parathyroid hormone 🔍 / 📺 / 🌳 / 📖
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submitted by ∗hayayah(1212)

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Secondary hyperparathyroidism (usually d/t chronic renal failure).

Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).

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haliburton also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +4

cr why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +

nala_ula Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +2

privatejoker Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +1

fatboyslim @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption +3

suckitnbme @privatejoker ALP is included in the standard lab values +

makinallkindzofgainz @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +1

pg32 Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +

drzed @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases. +1

skonys FA 2019 341. What I am confused on is why the Ca is in the low-normal range? Why not hypercalcemia like in Primary HyperPTH +

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submitted by ∗lilmonkey(63)

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Remember PTH as Phosphate Trashing Hormone.

↑Phosphorus -> ↑PTH secretion -> ↑bone resorption -> ↑ALP and bone pain.

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submitted by cr(5)

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why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +

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usmle11a i believe increase 25OHcholecalciferol indicates the storage capacity of vit D, which wont be affected in case of CKD. it goes like this, kidneys wont respond to regular PTH, loses Ca and cant execrete PO4, PTH gets made and tries to burn bone to produce Ca, resulting in elevated levels of Ca and PO4, Ca will bind the calcium and go to kidneys, yet same story all over. add to that the fact that 1 oh hydroxylase wont be able to function in a dead kidney. +1

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submitted by ∗iwannabedonewiththis(1)

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just as a general question, would there be low levels of 1 25-(OH)2 ?

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sd22 Yes, kidney has 1-alpha hydroxylase which converts 25-HCC to 1,25-HCC. CKD -> low 1-a-OHase activity -> low 1,25-HCC +

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