I've been trying to get my head around why loss of HCO3 from diarrhoea or type 2 RTA leads to a non-anion gap acidosis, when the equation to calculate anion gap is:
[Na + K] - [Cl + HCO3]
I know that I've missed out a bit of physiology knowledge that would make it make sense but at the...
How alkalosis cuz hypokalemia?
if this is due to H and K pump then it means more H moves outside cell and K moves inside cell..So it should be Acidosis cuz more H in ECF is acidosis as like increase K in ECF is hYperkalemia.
I have seen that hypokalemia cuz metabolic alkalosis and hyperkalemia cuz metabolic acidocis. can anyone plz explain .
See addisons disease cuz metabolic acidosis and conns disease cuz metabolic alkalosis
What acid-base abnormalities occur with salicylate intoxication?
I read two different explanations,
- Salicylates at toxic doses suppress respiratory center (resp. acidosis).
- Increased anion gap metabolic acidosis develops due to accumulation of organic acids.
Patient develops hypoxemia 35 minutes after ingesting a lethal dose of barbituates. What is the patients abg look like?
PO2; PCO2; A-a
40; 50; 35
40; 60; 40
50; 25; 10
50; 80; 10
60; 35; 25
I got the question wrong. Was hoping somebody could help me work this problem out.
Why there's normal or decrease pco2 and respiratory alkalosis in emphysma??
I mean since it's an OBSTRUCTIVE disease i thought there should be CO2 retention and thus respiratory acidosis, not alkalosis.
Do we really have to know this for the exam? I mean, acid-base, especially mixed acid-base disorders, are hard enough by themselves. I don't think I can memorize these calculations. Really, did anyone had to do these calculations on the exam?
For some reason I always getting this concept wrong and rather than memorize I prefer to understand.
I just did a Uworld question which described a male approx 23 yrs old who had polydipsia and polyuria and whose breath had a fruity odor. Okay...so he had diabetes Type 1- diabetic ketoacidosis...
"Supplementary O2 must be cautious in patient with COPD because hypoxia drives their respiratory function (where in normal undivisual, the pCO2 medicates the resp. drive) UW"
Can anyone help me to understand this:
How does hypoxia drive their resp. function in patient with COPD ?