Step I Secondary Hyperparathyroidism

[wishingformore]

Hello,

I have a question about secondary hyperparathyroidism. In FA 2010 it states that it causes HYPOcalcemia and HYPERphosphatemia. However, in Kaplan Lecture Notes they have that it causes Hypocalcemia and HYPOphosphatemia. Can anyone explain what is the right answer?

Thanks in advance.

 

[DrTacoElf]

Here is my take on it. Secondary hyper PTH is caused by messed up kidneys. Calcium would be low stimulating lots of PTH to be made. Also Phosphate would be high since it can't be excreted.

PTH is elevated in secondary hyperPTH. PTH function is to put phosphate in the urine normally but it can't work in secondary hyper PTH due to damaged kidneys.

Thus you would have hypocalcemia and hyperphosphatemia in theory.

Also high phosphate levels will cause calcium to complex and be deposited into tissues (this will somewhat lower phosphate levels but probably to high/normal)

 

[greg1184]

Hello,

I have a question about secondary hyperparathyroidism. In FA 2010 it states that it causes HYPOcalcemia and HYPERphosphatemia. However, in Kaplan Lecture Notes they have that it causes Hypocalcemia and HYPOphosphatemia. Can anyone explain what is the right answer?

Thanks in advance.

Secondary hyperthyroidism is caused by low calcium and high phosphate.

High PTH doesn't cause hypocalcemia. It causes hypercalcemia, and low phosphate. Therefore, Kaplan is wrong assuming that it was worded like that.

 

[IMGUSMLEStep1]

DrTacoElf is right.

Secondary Parathyroidism is due to hypocalcemia.

Hypocalcemia can occur due to renal failure, in which case there would be hyperphosphatemia because the kidney wouldn't be able to excrete titratable acid.

Hypocalcemia can also occur due to other causes e.g. malabsorption of vitamin D. In this case the increased PTH would increase excretion of phosphate.

So basically it comes down to the specific cause of secondary hyperPTH.

 

[turkeyjerky]

DrTacoElf is right.

Secondary Parathyroidism is due to hypocalcemia.

Hypocalcemia can occur due to renal failure, in which case there would be hyperphosphatemia because the kidney wouldn't be able to excrete titratable acid.

Hypocalcemia can also occur due to other causes e.g. malabsorption of vitamin D. In this case the increased PTH would increase excretion of phosphate.

So basically it comes down to the specific cause of secondary hyperPTH.

definitely. The way FA is just assuming that secondary hyperparathyroidism is always due to Renal Failure. A better way to think of it is that renal failure causes hyperphosphatemia and hypovitaminosis D. This then leads to secondary hyperparathyrodism.

But if there was a different underlying cause (osteomalacia, loop diuretic causing hypocalcemia, etc) there'd be low phosphate lvls.

 

[wishingformore]

I think my confusion was that in Vit D deficiency it would lead to BOTH decreased levels of Ca2+ and Phosphate vs. in Chronic Renal Failure. So, the OP who stated that the levels would be depend on the underlying cause makes sense.

Thanks so much everyone for the clarification.

 

[BenCarson]

this is my understanding so far

If Renal problem: 1. Hypocalcemia b/c of no 1-alpha hydroxylase and thus no vitamin D synthesis and no Ca2+ reabsorption plus the excess Phosphate that builds up would drive Ca2+ into tissue offsetting the normal Ca2+ expected from the bone resorption action of PTH via Osteoblast then osteoclast.

2. Hyperphosphatemia simply due to the build up. PTH can't excrete phosphate b/c of bad kindey

The hypocalcemia and hypophosphatemia one is not clear to me how they end up getting hypocalcemia. This of course is non-renal problem like hypovitaminosis D due to malabsorption

here is my logic:
No vitamin D---> Low Ca2+---> PTH release--> 1. increase Ca2+ reabsorption in the kindey, 2. Vitamin D synthesis via 1alpha hydroxylase if the patient was getting enough sunlight 3. bone resorption via osteoblast then osteoclast--->eventual increase of calcemium level thus we should expect a normalized ca2+ eventually. I'm thinking they said hypocalemia as the initial reading but after a while it should become normal.

the hyposphatemia is simply due to the excess PTH trashing the phosphate since the kindey's are ok.

guys you can read my previous post where I talked about the relationship b/w PTH, Vitamin and hypocalcemia

 

[PokerDoc]

this is my understanding so far

If Renal problem: 1. Hypocalcemia b/c of no 1-alpha hydroxylase and thus no vitamin D synthesis and no Ca2+ reabsorption plus the excess Phosphate that builds up would drive Ca2+ into tissue offsetting the normal Ca2+ expected from the bone resorption action of PTH via Osteoblast then osteoclast.

2. Hyperphosphatemia simply due to the build up. PTH can't excrete phosphate b/c of bad kindey

The hypocalcemia and hypophosphatemia one is not clear to me how they end up getting hypocalcemia. This of course is non-renal problem like hypovitaminosis D due to malabsorption

here is my logic:
No vitamin D---> Low Ca2+---> PTH release--> 1. increase Ca2+ reabsorption in the kindey, 2. Vitamin D synthesis via 1alpha hydroxylase if the patient was getting enough sunlight 3. bone resorption via osteoblast then osteoclast--->eventual increase of calcemium level thus we should expect a normalized ca2+ eventually. I'm thinking they said hypocalemia as the initial reading but after a while it should become normal.

the hyposphatemia is simply due to the excess PTH trashing the phosphate since the kindey's are ok.

guys you can read my previous post where I talked about the relationship b/w PTH, Vitamin and hypocalcemia

In your first scenario you overlooked lack of renal Ca+ abs and PO4- excretion, but otherwise yeh, both things are happening at the same time