Endocrinology - Calcium and Phosphate Regulation
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- เผยแพร่เมื่อ 13 ก.ค. 2024
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I think its worth mentioning phosphate doesn't need Vitamin D for uptake from the diet. This is part of the reason why in chronic kidney disease, you have low serum calcium but high serum phosphate. The kidney can't make Vitamin D if its diseased, so calcium uptake is not enough, but phosphate can still get across from the intestines into the blood. Cheers Armando you rock by the way : )
CKD - Decreased GFR, Kidney cannot excrete enough phosphate, phosphate increases FGF-23 which blocks 1-alpha-hydoxylase. Decrease Calcitriol, decrease intestinal absorption of ca and phosphate, yet kidney cannot excrete enough phosphate so phosphate remains high and binds free calcium. Decreased calcium stimulates increase in PTH, PTH increases bone turnover, leads to metabolic bone disease, pt over time has bone pain, fractures. PTH normally stimulates kidney to lose phosphate, but decreased GFR and kidney injury causes phosphate to not be excreted.
I was looking for this. Thank you so much.
Anything apart from kidney disease that causes low serum calcium and high serum phosphate?
ahh thank you!
@@samuelbenson1 saved my life thank you!
This video just taught me more in 11 minutes than my lecturer has in like 235 powerpoint slides :))))))) ur the best
Exactly 👌🏻
Asweer chale 😂
U dey UG?
@@kingbobbie5196 ye
Oh nice... which year?
If you're looking for a few extra steps and more in-dept:
The precursers of vit D comes from foods (like oily fish; D3), plants (D2) and the sun D3. In the skin the suns UV-rays converts 7-dehydrocholesterol into cholecalciferol D3 (done non-enzymatically by heat). Cholecalciferol then moves into the liver (transported from the skin by vitamin D-binding-protein (DBP), and by cholemicrons from the diet) for the first part of its activation. Here it is converted by the enzyme (cytochrome P-450-based enzyme) into 25-hydroxy vit D3 (25-OH-D) (calcidiol) the step is called 25-hydroxylation, it then moves to the kidney for its second and last activation. Here the 25-OH-D/DBP complex is taken up at the surface by renal proximal cells by a specific mechanism involving cell surface receptors; megalin and cubulin. In the kidney 25-OH-D is converted to 1,25 dihydroxy vit D (1,25-(OH)2D) (calcitriol) by renal-1α-hydroxylase - this activation is called 1α-hydroxylation (patients with renal failure therefore cannot perform this step). The 1α-hydroxylase comprises 3 proteins: Cyt P-450, a ferredoxin and a ferredoxin reductase for activity. 1α-hydroxylase is strongly downregulated by 1,25-(OH)2D (calcitriol) and strongly upregulated by PTH as a calcium homeostatic loop.
You forgot to mention that PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney, which means more phosphate is excreted through the urine!
Adnan Bashi I think he included that in one of his older videos which is the "bonehomeostasis (calcium phosphate) hormones" video :D
exactly what i was confused about okay so i did understand the concept
Thanks adnan
Adnan Bashi that's the fosfaturic action of PTH, exactly!! On the other hand, calcitriol does not do that treating equally calcium and phosphate (reabsobring both of them, PTH only reabsorbed calcium) and so, if there's an excess of calcitriol (vit D), they can precipitate.
not true i have both high phosphate and pth with low low t4 wich i take meds for but nothing i can do for my pth issues so im fct, this condition was missed for years now i have perment bone and liver problems now and heart racing issues.
what would i do in med school without your videos
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trueee
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you are such a lifesaver. this was so clear. cleared a lot of confusion I had on the main hormone that controls bone growth and remodeling. keep up the great work! looking forward to more of your work.
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i had an eyegasm while watching this, also your accent is so good!! tysm for this, i search everywhere for a good video about calcium homeostasis and here i am. tysm for explaining it this way. also, the drawings, i loved them!! thank you thank you
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Possible Correction: I may be wrong about this but after some researching, I found that C-FMS you mentioned on osteoclast is actually the gene that encodes CSFR-1 which is the receptor on osteoclast. If someone else could also research and confirm or deny this, that would be great! Thanks! Your videos are awesome!
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This video is a great way to recap physiology of Ca2+. Pictures help alot. Thanks!
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Thank You! Finally a good explanation of the calcium system. I wonder why it is often claimed that one cannot feel when bone is decreasing or osteoporosis sets in. The acid that "eats" the bone due to the osteoclast activity must be painful. Acid/nerves=pain.
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Came here for Rank Ligand actvt and did a quick review of The 3 hormones!! Thanks a lot! ✊
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Great! :) Please explain rapid and slow action of calcium homeostasis as well
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