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 -2  (nbme23#33)

I'm assuming that because bicarbonate is decreased, this has to be metabolic acidosis caused by acetazolamide? Missed this question because I was looking for metabolic acidosis (increased bicarbonate) caused by a loop diruetic...

sympathetikey  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.
aknemu  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).
2zanzibar  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-]**




Subcomments ...

submitted by colonelred_(46),

The diagnosis is strawberry hemangioma, commonly happens in kids, often resolves on its own as they get older.

shaeking  A strawberry hemangioma is normally pink or red (which is why it is named strawberry). The description has a flat purplish lesion which makes me think of a port wine stain on the face. How do you know to think of strawberry hemangioma over port wine based on this question stem? +1  
sheesher  This sounds more like a nevus simplex, which is very similar to a port wine stain, though it regresses over time. +2  
seagull  the age is key here. Newborns have strawberry hemangiomas typically on their face. Sturge-Weber could also be the case but none of the answer choices matched to that description. +1  
vshummy  I would agree with Sturg Webber nevus flammeus but I also noticed First Aid says it's a non-neoplastic birth mark so I should have known not to pick malignant degeneration or local invasion. Also because capillary hemangiomas don't have to be flat but the nevus flammeus is consistently flat. But I'm also reading on Wiki that the nevus flammeus doesn't regress so they must be trying to describe strawberry hemangioma even though I don't agree with their color choice... +  
nala_ula  Maybe (and I can only hope I'm right and the test makers are not -that much of- sadists) they would have made sure to write "in a cranial nerve 5 (either ophthalmic or maxillary) distribution" if it were Sturge-Weber. +1