From what I understand, If it is saline responsive it would suggest that the cause of the alkalosis is Volume depletion Volume depletion whether by GI losses or elsewhere would trigger RAAS and cause loss of potassium and that in turn would cause H+ loss via cell exchanges. As such by replenishing the volume with salt solutionsyou should see improvements as the RAAS system becomes deactivated. For Saline resistant. This would be a case of hyperaldosteronism where the despite you giving adequate salt and water the aldosterone or renin secreting tumour or pathology is still secreting aldosterone leadings to an eventual loss of potassium and hydrogen following suit as in the first example.
Thank you as always - you are great. This is something that also was in previous vidioes- about TZD, from what I understand by blocking the Na/CI symporter we are making the Na/K to work more and therefore we get the hypokalemia. Also the Na/K is on the basolateral membrane...Would appreciate very much your explanation!
Imo it should be like this: blocked Na-Cl-cotransport => more Na & Cl in tubule => compensatory: Na+ reabs. in exchange for K+ (secreted) => but too much K+ in tubule isn't good either => compensatory: K+ reabs. in exchange for H+ (secreted) => loss of H+ in urine => metabolic alkalosis
You didn't mention Saline sensitive vs Saline resistant metabolic alkalosis in detail. If you can talk about those that would be appreciated as well.
From what I understand,
If it is saline responsive it would suggest that the cause of the alkalosis is Volume depletion
Volume depletion whether by GI losses or elsewhere would trigger RAAS and cause loss of potassium and that in turn would cause H+ loss via cell exchanges.
As such by replenishing the volume with salt solutionsyou should see improvements as the RAAS system becomes deactivated.
For Saline resistant. This would be a case of hyperaldosteronism where the despite you giving adequate salt and water the aldosterone or renin secreting tumour or pathology is still secreting aldosterone leadings to an eventual loss of potassium and hydrogen following suit as in the first example.
Just to add that low UCI can also be caused by prior diuretics use; post hypercapnia; laxatives; CF.
Thank you!
Thank you as always - you are great. This is something that also was in previous vidioes- about TZD, from what I understand by blocking the Na/CI symporter we are making the Na/K to work more and therefore we get the hypokalemia. Also the Na/K is on the basolateral membrane...Would appreciate very much your explanation!
Imo it should be like this: blocked Na-Cl-cotransport => more Na & Cl in tubule => compensatory: Na+ reabs. in exchange for K+ (secreted) => but too much K+ in tubule isn't good either => compensatory: K+ reabs. in exchange for H+ (secreted) => loss of H+ in urine => metabolic alkalosis
thank you.
very nice one !
Thank you. really