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Gitelman syndrome...and thiazide diuretic too, I guess

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thawunandonly

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Can anyone explain how these cause hypocalciuria (and assuming this means hypercalcemia) and also why how hypomagnesemia comes into play [at least for Gitelman syndrome]?
 

jjuva

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Can anyone explain how these cause hypocalciuria (and assuming this means hypercalcemia) and also why how hypomagnesemia comes into play [at least for Gitelman syndrome]?

Thiazides diuretics increase calcium reabsorption in the dct. Calcium and magnesium compete for reabsorption there too, so if there's greater calcium reabsorption, there will be less magnesium reabsorption, leading to hypercalcemia and hypomagnesemia.
 

thawunandonly

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I've never even heard of Gitelman syndrome and I take the test on Monday :(

Lol sorry i can't help though.

Don't fret! It's probably beyond the scope of the test, but Gitelman syndrome is pretty much the same as a thiazide diuretic. Whereas the diuretic blocks the channel, Gitelman is a defect in the channel itself. So same effects.

Thiazides diuretics increase calcium reabsorption in the dct. Calcium and magnesium compete for reabsorption there too, so if there's greater calcium reabsorption, there will be less magnesium reabsorption, leading to hypercalcemia and hypomagnesemia.

Really sorry. Could you clarify the actual nephron physiology? Like maybe flow chart of channels or something. I'm looking at it and something is probably escaping my mind. The way I understood it via Kaplan videos and the explanation of thiazide diuretics is that if the Na+/Cl- channel is open, sodium is being reabsorbed which will, along with the Na+/K+ ATPase pump on the basolateral side, create a gradient for the Na+/Ca2+ exchanger and increase levels of Ca2+ in the blood. But blocking it is actually what increases calcium? :confused:
 

preDoGuy24

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Don't fret! It's probably beyond the scope of the test, but Gitelman syndrome is pretty much the same as a thiazide diuretic. Whereas the diuretic blocks the channel, Gitelman is a defect in the channel itself. So same effects.



Really sorry. Could you clarify the actual nephron physiology? Like maybe flow chart of channels or something. I'm looking at it and something is probably escaping my mind. The way I understood it via Kaplan videos and the explanation of thiazide diuretics is that if the Na+/Cl- channel is open, sodium is being reabsorbed which will, along with the Na+/K+ ATPase pump on the basolateral side, create a gradient for the Na+/Ca2+ exchanger and increase levels of Ca2+ in the blood. But blocking it is actually what increases calcium? :confused:


My understanding of thiazides was blocking the luminal Na pump creates a preferential gradient for the absorption of Ca in the basolateral Ca/Na pump, i.e. less intracellular Na so the gradient is increased even more leading to a favored electrochemical gradient for the pump-->increasing Ca+ reabsorption.
 

voicesinmyhead

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Yeah, i was wondering what the cause of Hypomagnesemia would be in Gitelman, considering its in the DCT and not at the TAL!

and why is there normal Mg in Barrter's, when it affects the TAL?
 
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Psai

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Probably because paracellular transport is nonspecific so if you have hypercalcemia then you have more calcium being filtered into the tubular lumen and if you have more calcium, more of the calcium will go through the the paracellular transporter rather than magnesium.
 
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