secondary hyperPTH question.

[RussianJoo]

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So I ran into this a couple of times and thought i'd post and see what the mass public thinks of this. Kaplan notes say that in secondary hyperPTH you'll have low Ca+2 and low phosphorus levels, and I agree, but USMLE World twice now have said that in secondary hyperPTH you'll have low Ca+2 and High Phosphorus..

here's my reasoning for the low Ca and low phosphorus.. lets say it's due to renal failure.. so Vit D can't be activated and thus there's low blood Ca, PTH is then secreted to increase Ca levels, but it can't because the kidneys can't activated vit D, also pth causes a decrease in phosphorus (PTH= Phosphorus Trashing Hormone) so you end up with both low Ca and Low phosphorus.. but USMLE World says you'd have high Phosphorus..

I think my reasoning is correct and this is just another one of those mistakes in USMLE World... What do you guys think?

 

[docmd2010]

secondary hyperpthism is primarily the case in renal failiure. The Kidneys don't function properly hence vitamin d has a problem getting activated by the 1 beta hydroxylase enzyme. Further, PTH now has hindrance upon reabsorbing Calcium and excreting phosphate. Remember normally (as in primary hyperparathrydoism) pTH breaks down bone which releases equal amounts of phosphate and calcium however the difference exists in handling once it gets to the kidney. calcium is reabsorbed a lot and phosphate is excreted alot. hence in primary, high calcium, low phosphate.

in 2ndary, as in renal failiure, phosphate levels go up and calcium goes down. There are two primary reasons for this

1) PTH is trying to work, but the kidneys are compromised, so phosphate can't be excreted and calcium has a tough time coming back in to the body.

2) Phosphate levels get so high in the blood in this situation, that it starts complexing with calcium to form calcium phosphate. Thus, Free calcium levels deplete, but the phosphate levels are so high that a little bit of phosphate binding to calcium has a modest effect on the plasma phosphate concentration.

Thus, you can see why in 2ndary you get high phosphate and low calcium and why in primary you get the exact opposite.

I hope this helps!!!

 

[RussianJoo]

secondary hyperpthism is primarily the case in renal failiure. The Kidneys don't function properly hence vitamin d has a problem getting activated by the 1 beta hydroxylase enzyme. Further, PTH now has hindrance upon reabsorbing Calcium and excreting phosphate. Remember normally (as in primary hyperparathrydoism) pTH breaks down bone which releases equal amounts of phosphate and calcium however the difference exists in handling once it gets to the kidney. calcium is reabsorbed a lot and phosphate is excreted alot. hence in primary, high calcium, low phosphate.

in 2ndary, as in renal failiure, phosphate levels go up and calcium goes down. There are two primary reasons for this

1) PTH is trying to work, but the kidneys are compromised, so phosphate can't be excreted and calcium has a tough time coming back in to the body.

2) Phosphate levels get so high in the blood in this situation, that it starts complexing with calcium to form calcium phosphate. Thus, Free calcium levels deplete, but the phosphate levels are so high that a little bit of phosphate binding to calcium has a modest effect on the plasma phosphate concentration.

Thus, you can see why in 2ndary you get high phosphate and low calcium and why in primary you get the exact opposite.

I hope this helps!!!

what prevents phosphate excretion? doesn't PTH prevent phosphate reabsorption in the kidney thus increasing it's excretion??

 

[wmc24]

i think it may have to do with the increased absorption of phosphate in the intestines due to the increased pth and the renal failure would produce a decreased filtration which would lead to phosphate build up.

 

[alpha06]

what prevents phosphate excretion? doesn't PTH prevent phosphate reabsorption in the kidney thus increasing it's excretion??

Yes, it does. But in chronic renal failure, your kidneys are not functioning properly so they are NOT excreting phosphate ====> thus increased serum phosphate.

 

[RussianJoo]

ok thanks guys.. fcking kaplan what a waste of money...

 

[alpha06]

ok thanks guys.. fcking kaplan what a waste of money...

😕

I thought this was from UW....

 

[It'sElectric]

😕

I thought this was from UW....

Re-read his original post. UW had it right, Kaplan had it wrong.

 

[Blesbok]

So I ran into this a couple of times and thought i'd post and see what the mass public thinks of this. Kaplan notes say that in secondary hyperPTH you'll have low Ca+2 and low phosphorus levels, and I agree, but USMLE World twice now have said that in secondary hyperPTH you'll have low Ca+2 and High Phosphorus..

here's my reasoning for the low Ca and low phosphorus.. lets say it's due to renal failure.. so Vit D can't be activated and thus there's low blood Ca, PTH is then secreted to increase Ca levels, but it can't because the kidneys can't activated vit D, also pth causes a decrease in phosphorus (PTH= Phosphorus Trashing Hormone) so you end up with both low Ca and Low phosphorus.. but USMLE World says you'd have high Phosphorus..

I think my reasoning is correct and this is just another one of those mistakes in USMLE World... What do you guys think?

In renal failure, the tubular cells fail to secrete phosphate in response to PTH and they fail to reabsorb calcium in the distal convoluted tubule. The kidney also fails to form 1,25-OH-VitD. These together are the reason they have hyperphosphatemia, hypocalcemia, and increased PTH. This hyperphosphatemia leads to renal osteodystrophy, vascular calcification, and distal extremity ulcers.

 

[RussianJoo]

In renal failure, the tubular cells fail to secrete phosphate in response to PTH and they fail to reabsorb calcium in the distal convoluted tubule. The kidney also fails to form 1,25-OH-VitD. These together are the reason they have hyperphosphatemia, hypocalcemia, and increased PTH. This hyperphosphatemia leads to renal osteodystrophy, vascular calcification, and distal extremity ulcers.

thank you. now i'll get the question correct....

 

[RussianJoo]

😕

I thought this was from UW....

yeah kaplan fcked up.. that's why i didn't waste time with their qbank because if their notes are such garbage then their qbank must be as well. Man not only is it miss typed in the kaplan notes but also the lecturer spent like 20min on their dvd explaining the process.. What a bunch of scum bags, and I complained to them about their mistakes they told me they don't edit their books but just change the mistakes that students submit and that I should submit any mistakes I find, I asked for some sort of compensation for my troubles and they practically laughed at me, so I said with that attitude you can go screw yourselves... even First Aid pays students if they publish the correction they submit..

Now that Falcon Review has online videos I highly recommend them over money hungry Kaplan..

 

[TonyDaTigrUprct]

yeah kaplan fcked up.. that's why i didn't waste time with their qbank because if their notes are such garbage then their qbank must be as well. Man not only is it miss typed in the kaplan notes but also the lecturer spent like 20min on their dvd explaining the process.. What a bunch of scum bags, and I complained to them about their mistakes they told me they don't edit their books but just change the mistakes that students submit and that I should submit any mistakes I find, I asked for some sort of compensation for my troubles and they practically laughed at me, so I said with that attitude you can go screw yourselves... even First Aid pays students if they publish the correction they submit..

Now that Falcon Review has online videos I highly recommend them over money hungry Kaplan..

yeah I was just doing a question about this in Kaplan Qbank, and in the explanations they have it correct.. but if you switch over to the Re-Kap tab.. they have it incorrect.. so those of you out there using Kaplan Qbank.. if something doesn't make sense to you, make sure to look at other sources to verify.. a little frustrating at times, but most of the stuff so far is good.