Search Results for ‘acid-base-’

Hey, 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...

patient with aspirin overdose will have which of the following as abg.. PH pco2 hco3- a) 7.45 30 20 b) 7.36 22 12

how does chlorine toxicity cause metabolic acidosis...mechanism?? thanks

hey does anyone know the reason of normal anion gap for the following circumstances Hyperalimentation Addision Disease Renal tubular acidosis Diarrhea Acetazolamide Sprionolactone...

1) why it causes hypOKalemia, hypOnatremia and hypOchloremia. it should not cause hypOnatremia but Uworld mentioned hypOnatremia also. 2) which diuretic cause contraction alkalosis.

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.

Can someone explain the mechanism of hypocalcaemia in Alkalosis and whether it causes tetany or not and what happens to level of calcium in acidosis?

ARDS and RDS both have clinical symptom of TACHYPNEA so it means both of them cuz respiratory Alkalosis???

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

Why not acidosis? Simple ques for u...pls tell me why. :o

can anyone please explain abg values for pulmonary embolism? everytime i think i have the got the concept n try a question..its wrong..:o:o thanks!!

What acid-base abnormalities occur with salicylate intoxication? I read two different explanations, Kaplan pharma: - Salicylates at toxic doses suppress respiratory center (resp. acidosis). - Increased anion gap metabolic acidosis develops due to accumulation of organic acids. Uworld: -...

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. Please help!

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?

Is there defect in renal ammoniogenesis in renal tubular acidosis? As i know normally ammonia is made from glutamine in kidneys. what is the source of ammonia in renal tubular acidosis?

Among the following video sources which is the best for Renal physiology and Acid/Base: Kaplan 2010 (Dunn), Kaplan 2007 (Kudrath), Falcon (Udani), or PASS (Wolf)? Thanks.

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...

Patients labs shows Hypocalcemia with Metabolic acidosis. His oral mucosa is moist. Next step in management? a. Calcium gluconate b. Sodium bicarboate c. Normal saline d. 5% dextrose e. ETOH

Hello.. "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 ? Thanks,