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haha I picked this too bc she's 44.... isn't celiac something that would present much younger?? but I don't think IBS would cause an iron deficiency anemia is the hint they were trying to give us.
If it was IBS, they would have mentioned something about them having abdominal pain, different stool frequency, and then relief after defecation, me thinks.
I was between celiac sprue and IBS but what pushed me towards celiac's was a few things:
1. The Iron deficency anemia (I think that would be unlikely in IBS)
2. Steatorrhea (which would also be unlikley in IBS)
3. Osteopenia- I was think vitamin D deficency
4. Lack of a psychiatric history
IBS is a diagnosis of exclusion. If you haven't excluded Celiac (and this can't be excluded based on epidemiology alone), you can't diagnose IBS.
I think you may have confused it with IBD, IBS would not present like this.
I don't think so. I know that K+ levels decrease with laxative use, due to dehydration, which activates the RAAS, which increased aldosterone, which cause Na+ re-absorption and K+ wasting. Aldosterone also causes the alpha intercalated cells to secrete more H+ into the urine, which causes a serum alkalosis. Therefore, in order to correct that, bicarb re-absorption decreases in the kidneys, which brings the pH closer to normal. As far as Chloride, I guess that must be re-absorbed with Na+ due to it being negatively charged (?). That's the one thing I'm not sure about.
I think what they are getting at is that it is Diarrhea--> Non-anion gap metabolic acidosis (HARDASS). This would mean that HCO3- would be low and chloride would be high (in non-anion gap acidosis the chloride increases and that's why you don't have a gap).
Normally, stool's electrolyte content primarily consists of bicarb, potassium, and sodium. Since the colon reclaims sodium in exchange for potassium, the potassium content of stool is usually double that of sodium. Most of our bicarb loss in stool actually occurs through the loss of organic acid anions, i.e. bicarb that's been titrated by the organic acids formed by bacterial fermentation in the colon (e.g. lactic acid).
*Bottom line: our stool is alkaline, with mostly bicarb and potassium.*
Diarrhea is a cause of *NON-anion gap metabolic acidosis* due to bicarb loss in the stool. We aren't adding any acids to the mix -- we're simply losing anions -- which is why our anion gap remains normal. Potassium goes along for the ride and we end up with *hypokalemic* metabolic acidosis. And because we're losing anions, we want to compensate by *increasing retention of Cl-*.
**Anion gap = Na+ - [Cl- + HCO3-]**
another observation to support this: The patient's RR is 30/min, which demonstrates a compensatory respiratory alkalosis, in response to the non-anion gap metabolic acidosis