good students answer this question

[krishna reddy]

clinical condition in which there is intracellular acidosis ,extracellular alkalosis and high acidity in urine?

[Dr. X]

wow.. this q. did throw me off in the beginning. i havent done renal system yet, and this is mostly from studying/listening to goljan rr - fluid hemodynamics. its a good thing i came across this (intracell/extracell variation) before step1 cause i wouldnt have had the time to think thorougly during the test.

key here is extracellular alkalosis. since we measure this, we know this person is suffering from "alkalosis". so we could have two situations where: meta or resp. (i = increase, d = decrease)

i = ph -- i Pco2 i i HCO3- (metabolic alkalosis) compensated w/ resp. acidosis.

i = ph -- dd Pco2 d HCO3- (respiratory alkalosis) compensated w/ meta. acidosis.

just know where there is H+, it will be acidic. In the above case, more likely that there is a kidney abnormalities because urine is acidic. we know aldosterone retains Na+ and kicks out K+ and H+ in the distal tubule and does lil bit of retaining of K+ in the collecting tubule. so for some reason, aldosterone is doing its job too well. Mineralocorticoid excess diseases come into play. Hyperreninism for example would do this. so we know losing out K+ would result in Hypokalmia and losing out H+ would result in acidic urine. There is also a gain in HCO3- in these diseases, which causes the extracellular to be more alkalosis. Increasing the (negative HCO3 in the extracellualar would push/keep the positive proton H+ into the intracellular causing it to be more acidic. so we have..

intracellular acidosis, extracelluar alkalosis, acidic urine, hypokalemia.

For the greater minds: we are so caught up with thinking that hyperreninism causes hyperaldosteronism. Remeber, renin-angiotensin-aldosterone pathway? It is possible to have hyperreninism and hypoaldosterinim. anyone wish to crack this? if nething, i'll post it in few days on the same thread.

[Dr. X]

i dont know if i mentioned it or you got it.. it is metabolic alkalosis (out of the 2 i wrote above)

[krishna reddy]

thk u 4 replying to my question correctly

[navpreet]

wow.. this q. did throw me off in the beginning. i havent done renal system yet, and this is mostly from studying/listening to goljan rr - fluid hemodynamics. its a good thing i came across this (intracell/extracell variation) before step1 cause i wouldnt have had the time to think thorougly during the test.

key here is extracellular alkalosis. since we measure this, we know this person is suffering from "alkalosis". so we could have two situations where: meta or resp. (i = increase, d = decrease)

i = ph -- i Pco2 i i HCO3- (metabolic alkalosis) compensated w/ resp. acidosis.

i = ph -- dd Pco2 d HCO3- (respiratory alkalosis) compensated w/ meta. acidosis.

just know where there is H+, it will be acidic. In the above case, more likely that there is a kidney abnormalities because urine is acidic. we know aldosterone retains Na+ and kicks out K+ and H+ in the distal tubule and does lil bit of retaining of K+ in the collecting tubule. so for some reason, aldosterone is doing its job too well. Mineralocorticoid excess diseases come into play. Hyperreninism for example would do this. so we know losing out K+ would result in Hypokalmia and losing out H+ would result in acidic urine. There is also a gain in HCO3- in these diseases, which causes the extracellular to be more alkalosis. Increasing the (negative HCO3 in the extracellualar would push/keep the positive proton H+ into the intracellular causing it to be more acidic. so we have..

intracellular acidosis, extracelluar alkalosis, acidic urine, hypokalemia.

For the greater minds: we are so caught up with thinking that hyperreninism causes hyperaldosteronism. Remeber, renin-angiotensin-aldosterone pathway? It is possible to have hyperreninism and hypoaldosterinim. anyone wish to crack this? if nething, i'll post it in few days on the same thread.
hyperreninism.....but hypoaldosteronism in primary hypoaldosteronism,renin high but no inc in aldosterone.
like in 21-hydroxylase deficiency.
neither 11-deoxycorticosterone nor corticosterone production..bp falls--renin increases.
in case of ,17-oh & 11-oh def,11-deoxycorticosterone is being produced,bp rises....renein falls.

let me know if there is an addition to above facts,.....please.
thanks.

[krishna reddy]

the absolute answer is increased mineralocorticoid i.e;hyperaldosteronism