MCAT Question – Endocrine

[premed_2021]

A young woman presents to the ER with a broken hip. She denies any recent medical history of trauma to the joint. Blood tests reveal a calcium concentration of 11.5mg/dL (normal 8.4-10.2). Which tissue is likely responsible for these findings?

(Kaplan MCAT Biology, 3rd Edition, page 396)


The correct answer is parathyroid, and the explanation alludes to the possibility of overactivity and increased osteoclast activity, which makes sense. Why can't it be the thyroid gland/ reduced osteoblast activity, though? Parathyroid and thyroid are both options in the question.

In other words, why can't low calcitonin cause the same pathophysiology as increased PTH?

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[Cornfed101]

I may be off, but why would your body downregulate calcitonin in this situation? The body is much more likely to upregulate osteoclast activity because it needs to break down the sharp edges of the broken bone. I think this is a good example of a correct answer vs the best answer.

 

[ploidy]

PTH and calcitrol act in conjunction to increase serum levels of calcium. If I recall correctly PTH stimulates calcitrol release from the kidneys. Calcitrol also acts in the intestines to increase calcium absorption. End effect is that calcitonin is less effective at decreasing serum calcium then PTH is at increasing serum calcium, mainly because PTH acts in 3 locations (bonds, kidneys to increase calcium reabsorption, and indirectly in the intestines by promoting calcitrol release).

 

[premed_2021]

I may be off, but why would your body downregulate calcitonin in this situation? The body is much more likely to upregulate osteoclast activity because it needs to break down the sharp edges of the broken bone. I think this is a good example of a correct answer vs the best answer.

Hey, there's an angle I didn't think of! I was thinking more along the lines of "the bone must be brittle, so osteoclasts might be acting more extensively than osteoblasts". It makes sense that after the injury osteoclast activity might have to be upregulated. Thank you.

PTH and calcitrol act in conjunction to increase serum levels of calcium. If I recall correctly PTH stimulates calcitrol release from the kidneys. Calcitrol also acts in the intestines to increase calcium absorption. End effect is that calcitonin is less effective at decreasing serum calcium then PTH is at increasing serum calcium, mainly because PTH acts in 3 locations (bonds, kidneys to increase calcium reabsorption, and indirectly in the intestines by promoting calcitrol release).

This makes perfect sense. Thank you so much for your help.

 

[Blueprint Med School]

A young woman presents to the ER with a broken hip. She denies any recent medical history of trauma to the joint. Blood tests reveal a calcium concentration of 11.5mg/dL (normal 8.4-10.2). Which tissue is likely responsible for these findings?

(Kaplan MCAT Biology, 3rd Edition, page 396)


The correct answer is parathyroid, and the explanation alludes to the possibility of overactivity and increased osteoclast activity, which makes sense. Why can't it be the thyroid gland/ reduced osteoblast activity, though? Parathyroid and thyroid are both options in the question.

In other words, why can't low calcitonin cause the same pathophysiology as increased PTH?

Couple of really good answers up there, just wanted to add that some of it has to do with the relative weakness of calcitonin as a hormone. Most patients with low or high calcitonin levels really don't see many changes in their lab values or clinical condition. Only high doses of calcitonin use for certain diseases really seems to move the needle. Calcitonin is for all intents and purposes on the way out evolutionarily, where is parathyroid hormone is much stronger and so mild arrangements cause clinically important effects.

Hope this helps!

David D, MD - USMLE and MCAT Tutor
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