oS teh btse i oculd dnfi saw in sFitr idA 2910 gp 634 dreun ciiabtDe ii.sdotcesaoK The gleharpyicemy nda rahkeyameipl ascue na mscotoi dsusirie so eht rentie bdyo setg epedtdle of .duislf eHcne wyh prat of teh taenrmtet rof DKA si VI il.usdf ouY htgim eevn rlye on thta epcie of niimaftonro elano ot arwsen stih qusetoin, atht DAK is eetartd wtih VI .sludfi
sasy htat ytyhprlrsoaimoe and iisodcsa taelr etalmn s.uatts
whihc etscearrlo with the tghri easnrw
.sp i otg ti ngwro too ):
Idk how you could say that it's from extracellular dehydration, but whatever I guess.
this is how I looked at it extra cellular osmoles> intracellular so it will pull the h20 out.... then the high osmotic pull of the sugar overwhelming the SGL2 transporter in the kidney will pull the h20 out of the body dehydrating the extracellular compartment
How will cerebral edema develope if there is increased ECF osmolality ie dehydration? Shouldn't it drag fluid out of the tissues?
a little messed up, but "Inability of neurons to perform glycolysis" seems like a tempting answer. But the reality is, the neurons are able to perform glycolysis, they ready to rock but just waiting on insulin. I still chose this as my answer tho.
I guess this is one of those choose the best answer questions. I think FA should add the reasoning behind cerebral edema, being that it's a major cause of death (but I couldn't find it in Robbins either). Having so much glucose in the blood vessels causes water to be drawn out (ICF --> ECF). So that's a intracellular dehydration.