Phosphate levels in secondary hyperparathyrodism

[phd89]

---

Members don't see this ad.

In FA it say that secondary hyperPTH has hyperphosphatemia, but Kaplan physio states that there is a dec in phosphate levels: "Even though the elevated PTH increases phosphate resorption from bone PTH also inhibits phosphate reabsorption by the kidneys thereby promoting phosphate excretion and a drop in plasma phosphate

Online it say that it can differ what based on cause ie Vit D def or Chronic renal Failure, If they ask about it in the up/down arrow questions then what would the phosphate levels be increased or decreased. Can someone please elaborate


thanks

 

[Ronin786]

Hypocalcemia in Renal Failure is due to more than one cause. First, PTH is unable to stimulate 1-a-Hydroxylase, so Vitamin D won't be activated in the intestines and you'll get hypocalcemia and hypophosphatemia.

However, the kidney is also unable to excrete Phosphate which will bind the free calcium in the blood leading to an even greater decrease in Calcium with high phosphate levels and higher PTH levels to make up for the hypocalcemia.

As far as what Uworld has to say, the net effect of all these processes is a low calcium level, a low calcitriol level, hyperphosphatemia and hyperparathyroidism.

 

[Phloston]

I've seen this in multiple practice questions.

On the USMLE, for secondary hyperparathyroidism, you're going to have increased serum phosphate because your kidneys are failing.

 

[Phloston]

I also don't trust Kaplan btw. They strike me oddly, in such a way that I feel they don't really prep people for the USMLE, but instead just teach a broader medicine course, focusing erratically on any number of insignificant variables. At least that's my impression now that I've finished their QBook, QBank and have flipped through various parts of the notes. They supply a lot of info, but it's just off the mark.

 

[ashik33]

Consider it this way. In secondary hyperparathyroidism, the rise in PTH is the effect rather than the cause. From the feedback loop for PTH hormone, we can know that hyperphosphatemia INDUCES PTH secretion ( and that's why it is secondary). So when we analyse this patient's serum, it gives us high phosphate levels (the cause) and high PTH level (the effect)

Had it been primary hyperPTH, the rise in PTH would have been the CAUSE for further changes thus leading to phosphate leaking and henced hypophosphatemia.

It's basically the same thing as previously mentioned, just in a different way.

 

[OveractiveBrain]

In FA it say that secondary hyperPTH has hyperphosphatemia, but Kaplan physio states that there is a dec in phosphate levels: “Even though the elevated PTH increases phosphate resorption from bone PTH also inhibits phosphate reabsorption by the kidneys thereby promoting phosphate excretion and a drop in plasma phosphate

Online it say that it can differ what based on cause ie Vit D def or Chronic renal Failure, If they ask about it in the up/down arrow questions then what would the phosphate levels be increased or decreased. Can someone please elaborate


thanks

Calcium sensing receptors modulate the function of PTH. PTH goes to the bone to reabsorb Ca and Phos (both Ca and Phos go up). It goes to the kidneys and does two things: (1) makes vitamin D to increase absorption of Calcium and Phos (both Ca and Phos go up). The only way phos goes down is if the renal tubules are doing their job. Thats (2), PTH tells the kidney to hold onto ca and get rid of phos.

The kidney wins. Remember that, so long as the kidney is working, the kidney wins. Period.

Ok, so you've got secondary hyperparathyroidism. Where does that come from? It comes from EARLY renal failure. The failure is in Vit D. You still make urine, you still have GFR, your tubules are still functioning (you aren't on dialysis, after all), but what breaks first is Vit D. So, if Vit D down, Calicum reabsorption from the gut down, calcium down, PTH will be released. PTH takes Ca and Phos from the Bones, TRIES to make Vit D and fails, and, because the kidney is working, kidneys win... so they hold on to Ca and lose Phos.

In early renal failure secondary hyperparathyroidism causes decreased phos, elevated PTH because the calcium is trying to be maintained at normal.

Ok, you've got a patient on dialysis. They too have hyperparathyroidism. But why. Because now the kidney is GONE. In LATE renal failure, that is, end stage, the kidneys DON'T work. Not Vit D, not the tubules, nothing. So you can PTH the shit of them, nothing is going to happen. In end stage renal failure PTH up, Calcium normal, Phos ELEVATED.

Early renal failure with maintained tubule function: Phos low
Latre renal failure with End Stage renal disease: Phos high (give the drug Phos-lo)

 

[Ronin786]

I also don't trust Kaplan btw. They strike me oddly, in such a way that I feel they don't really prep people for the USMLE, but instead just teach a broader medicine course, focusing erratically on any number of insignificant variables. At least that's my impression now that I've finished their QBook, QBank and have flipped through various parts of the notes. They supply a lot of info, but it's just off the mark.

What ticks me off the most about Kaplan is the fear mongering they do. They appear to be aimed more at IMGs and they'll stir up a bunch of baloney just to get people to take their courses.