oS het tsbe i lduoc fnid swa in tFisr dAi 0129 pg 364 reund tDiaecib Kicdsa.etisoo Teh icegharyeplym dan almherykpiea ueasc an coomist riieusds so het nretei ydbo gest pdeedlte fo d.slifu eHecn yhw rtap of teh etettamnr fro DKA si IV lfidu.s Yuo gthim evne reyl on thta ceipe fo otmaoifnrni alone to senraw sthi qosein,ut htta KDA si etrdeat whit VI slu.ifd
yssa hatt ylaprysohtrioem dna sisaicdo atrel anlmet sastut.
hiwch oslractree whti eth hgtir awresn
ps. i gto ti nowgr oto :)
Idk how you could say that it's from extracellular dehydration, but whatever I guess.
How will cerebral edema develope if there is increased ECF osmolality ie dehydration? Shouldn't it drag fluid out of the tissues?
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
What i think it is that, ECF osmolarity is increased, draws water and K out of cell --> intracellular dehydration Osmotic diuresis in the kidneys, loss of glucose and water in kidneys --> Extracellular dehydration
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.