Who wants to explain this phys concept (from BRB phys)

[Re3iRtH]

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On page 171 from BRB phys (4th ed.) under D. Magnesium (Mg2+)
"In the thick ascending limb, Mg2+ and Ca2+ compete for reabsorption;
therefore, hypercalcemia causes an increase in Mg2+ excretion.."

Now, I think it would have sense if that stated "hypercalciuria", since more
Ca2+ would be in the urine, hence pushing Mg2+ out of the way.
But before you say, hypercalcemia MEANS hypercalciuria, I am not
convinced that this is the case. If it is so, how come loop diuretics are
used to treat hypercalcemia? If hypercalcemia automatically meant
hypercalciuria, wouldnt this even further exsacerbate the hypercalicuria
predisposting the pt to stones even more. Same goes for thiazides treating
"idiopathic hypercalciuria". If hypercalciuria automatically means hyper-
calcemia, the these patients would have an exsacerbating of their
hypercalcemia, which doesnt seem like a good idea?

So my buddies from class who are superstars couldn't exactly explain
this, how about you guys.

While we are on the subject, how does AII stimulate release of ADH
from posterior pituitary? (pg. 425 of 08 FA,) "Actions of AII"

 

[Slide]

It's like this:

In the thick ascending limb, Mg+2/Ca+2 reabsorption is passively due to Na/2K/Cl absorption. This is mainly due to a positive electrochemical gradient caused by potassium seeping out. Now, the reason why loop diuretics are good for hypercalcemia in this case is that the Ca+2 does not get absorbed due to abolishment of this potassium gradient that would've been present if Na/2K/Cl were being absorbed. The late distal tubule has nothing to do with what's happening here.

For thiazides, the treatment for hypercalciuria it's a little different. Now, there is also a Na/K ATP-ase pump on the blood side of the cell, which basically pumps sodium out of the cell in order to keep the Na/Cl pump on the luminal side working. Inhibiting the Na/Cl pump decreases the conc of sodium inside the cell. The decrease then strengthens the Na/Ca+2 gradient on the interstitial side, which pumps sodium inside and pumps calcium outside into the interstitium. The result is a decrease in Ca+2 inside the cell, which makes the Ca+2 port bring in more sodium. This is why thiazides are used for hypercalciuria; the increase in Ca+2 reabsorption decreases the chance of calcium precipitating in the form of ions. Loop diuretics decrease reabsorption of Ca+2 in the loop and does not affect the physiology of the late tubule. A person with hypercalciuria does not necessarily have hypercalcemia because there could be a defect in earlier calcium reabsorption, or increased secretion somehow. Likewise, hypercalcemia does not necessarily mean hypercalciuria because of increased calcium reabsorption.

Hope thi shelps.

On page 171 from BRB phys (4th ed.) under D. Magnesium (Mg2+)
"In the thick ascending limb, Mg2+ and Ca2+ compete for reabsorption;
therefore, hypercalcemia causes an increase in Mg2+ excretion.."

Now, I think it would have sense if that stated "hypercalciuria", since more
Ca2+ would be in the urine, hence pushing Mg2+ out of the way.
But before you say, hypercalcemia MEANS hypercalciuria, I am not
convinced that this is the case. If it is so, how come loop diuretics are
used to treat hypercalcemia? If hypercalcemia automatically meant
hypercalciuria, wouldnt this even further exsacerbate the hypercalicuria
predisposting the pt to stones even more. Same goes for thiazides treating
"idiopathic hypercalciuria". If hypercalciuria automatically means hyper-
calcemia, the these patients would have an exsacerbating of their
hypercalcemia, which doesnt seem like a good idea?

So my buddies from class who are superstars couldn't exactly explain
this, how about you guys.

While we are on the subject, how does AII stimulate release of ADH
from posterior pituitary? (pg. 425 of 08 FA,) "Actions of AII"

 

[Re3iRtH]

Well done. Should be good for a 250+ 😉
I wish I studied half as hard as I do now first year.
For the record I <3 UW. I never started thinking about
mechanisms when I was doing kaplan qbank 👎

 

[psychforme]

So my buddies from class who are superstars couldn't exactly explain
this, how about you guys.

They are definitely not superstars.