question about tertiary hyperparathyroidism

[mhtwus]

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can someone please explain the pathogenesis of tertiary hyperparathyroidism? i understand that it is oversecretion of PTH accompanied by increase in Ca2+, but i don't understand how it progresses from renal failure, or why it's called tertiary in the first place.

also, is the reason there's hyponatremia in SIADH due to compensation by other parts of the nephron trying to reduce volume by putting Na+ in the lumen?

 

[cetona]

can someone please explain the pathogenesis of tertiary hyperparathyroidism? i understand that it is oversecretion of PTH accompanied by increase in Ca2+, but i don't understand how it progresses from renal failure, or why it's called tertiary in the first place.

also, is the reason there's hyponatremia in SIADH due to compensation by other parts of the nephron trying to reduce volume by putting Na+ in the lumen?

Not sure about your first question, but the hyponatremia in SIADH is just because your body is reabsorbing so much water that it is diluting the serum sodium - it's only a result of excess water, not a deficiency in sodium.

 

[mhtwus]

Not sure about your first question, but the hyponatremia in SIADH is just because your body is reabsorbing so much water that it is diluting the serum sodium - it's only a result of excess water, not a deficiency in sodium.

you roxors my soxors (and boxors... if you are into that kinda thing)

 

[Step1Hash]

can someone please explain the pathogenesis of tertiary hyperparathyroidism? i understand that it is oversecretion of PTH accompanied by increase in Ca2+, but i don't understand how it progresses from renal failure, or why it's called tertiary in the first place.

So in Secondary hyperPTH its bc of the decrease in Vit D and the lack of calcium that the body increases PTH. You still have a low calcium bc the increase in PTH isnt enough. Tertiary is basically secondary that has been going on for such a long time that the increase in PTH has become autonomous and not dependent on the kidney as a stimulus and thus you get high calcium now. They call it tertiary bc the stimulus now is not the renal disease (secondary) and its not a parathyroid adenoma (primary).

 

[Celestine]

If I understand correctly, tertiary hyperparathyroidism occurs when the parathyroid glands become autonomous (following prolonged secondary hyperparathyroidism from chronic renal failure) and start secreting PTH without respect to current calcium concentrations. As a result, you get very high PTH, and high calcium.

So even if you've been treating chronic renal failure with calcium supplements, the parathyroids are no longer sensitive to this increase in serum concentration and will keep on secreting PTH. Treatment is removal of the glands.

Please correct me if I'm wrong, I had a hard time wrapping my head around this concept.

 

[bbydoc]

you roxors my soxors (and boxors... if you are into that kinda thing)

wtf?

 

[turkeyjerky]

If I understand correctly, tertiary hyperparathyroidism occurs when the parathyroid glands become autonomous (following prolonged secondary hyperparathyroidism from chronic renal failure) and start secreting PTH without respect to current calcium concentrations. As a result, you get very high PTH, and high calcium.

So even if you've been treating chronic renal failure with calcium supplements, the parathyroids are no longer sensitive to this increase in serum concentration and will keep on secreting PTH. Treatment is removal of the glands.

Please correct me if I'm wrong, I had a hard time wrapping my head around this concept.

yes, exactly--the parathyroids, after years of being stimulated by low ionized calcium and low 1,25 hydroxy-vitamin D, eventually undergo nodular hypertrophy and become independent--this leads to high or high-normal calcium levels and astoundingly high pth levels (like >1000). Treatment is w/ a sub-total (3.5 gland) parathyroidectomy; alternatively calcimimetics could be used (ie poor surgical candidiate).