About Alkaline Phosphatase elevations,Please Help!

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eduro25

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Dear Forum members, I usually browse the forum silently , but this is my first real post, I hope someone who is much more advanced in the Step 1 preparation can please help me.

My doubt is with the Alkaline Phosphatase elevations as seen on page 279 of FIRST AID 2008.

I really cant understand the pathophisiological processes underlying the elevations of AP in both vit. D deficiency and excess.

I do understand that AP is a marker of osteoblastic activity. I understand that in Hyperparathyroidism, it is elevated because PTH receptors are actually present on osteoblasts , and osteoclasts are indirectly activated. In Pagets , its elevated due to increased late osteoblastic activity (bone deposition). I do understand that vit D. increases resorption of old bone , but in fact increases deposition in new bone as well , so this might explain why in Vit. D intoxication AP might be elevated. But how come is it elevated in osteomalacia as well?. Can anyone explain please to me how can is this possible , or correct me if any of my previous sentences were wrong?

Thanks for your help in advance,
Regards,
Eduro
 
Dear Forum members, I usually browse the forum silently , but this is my first real post, I hope someone who is much more advanced in the Step 1 preparation can please help me.

My doubt is with the Alkaline Phosphatase elevations as seen on page 279 of FIRST AID 2008.

I really cant understand the pathophisiological processes underlying the elevations of AP in both vit. D deficiency and excess.

I do understand that AP is a marker of osteoblastic activity. I understand that in Hyperparathyroidism, it is elevated because PTH receptors are actually present on osteoblasts , and osteoclasts are indirectly activated. In Pagets , its elevated due to increased late osteoblastic activity (bone deposition). I do understand that vit D. increases resorption of old bone , but in fact increases deposition in new bone as well , so this might explain why in Vit. D intoxication AP might be elevated. But how come is it elevated in osteomalacia as well?. Can anyone explain please to me how can is this possible , or correct me if any of my previous sentences were wrong?

Thanks for your help in advance,
Regards,
Eduro


Everything you've stated sounds correct. Alkaline phosphatase is needed for normal mineral deposition, probably b/c the enzyme can hydrolyze inhibitors of mineralization such as inorganic pyrophosphate. So in the face of the decreased minerals present in osteomalacia, perhaps alkaline phosphatase is upregulated in order to make do with whatever mineral it can free up. Just a conjecture, not really sure about this.
 
Thanks for your kind reply Mortal_lessons.
I really didnt know the fact about AP hydrolizing an inhibitor of mineralization. Thanks.

I have come up with a cheap answer , based on a friend´s UPtoDate chart. It is similar to the FA one, although next to Vit D deficiency , it states w/ secondary Hyperparathyroidism. So asuming that add-on, I find it also very logical.

If anyone has a much better answer than mortals or mine , please share it with us.

Thanks in advance for everything,
 
Alk Phos breaks PPi down...PPi inhibits bone mineralization. Everything you need to know about Alk Phos can be derived from that fact.

I know I am just restating what Mortal_Lessons said, just simplifying it down to a one-liner.
 
PPi fact holds true for Prostate CA too...vertebral demineralization is a common part of the sequelae of Prost CA, therefore Alk Phos is released to help re-mineralize it.
 
Don't forget though that AP is normal in osteoporosis. Never really understood that one... just one for the memory banks for me.

😕
 
When Vitamin D is low (like in renal failure), you get secondary hyperparathyroidism. This high PTH is what is going to raise your Alk Phos by acting on the osteoblast PTH receptors.
 
Instatewaiter and everyone , thanks for your answers , yeah thats what I finally agreed to remember.

Once again , thanks.
Regards
Eduro
 
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