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NBME 23 Answers

nbme23/Block 4/Question#33

A 16-year-old girl with bulimia nervosa is brought ...

Potassium: decreased;
Chloride: increased;
Bicarbonate: decreased

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 +7  upvote downvote
submitted by nwinkelmann(187),

I literally just realized why this question confused me so much (and I've tried to figure it out a couple of times, lol). I let the colloquial definition of bulimia (i.e. vomiting) stick in my mind, that I forgot the actual medical definition = normal BMI (>18) + binge eating and purging (where purging could be induced vomiting or diuretic use or laxative use or/and excessive exercise). So really, what this question was asking is simply what is the electrolyte balance of excessive diarrhea? GEEZ! I made it so much harder in my head when trying to answer it originally.

Diarrhea causes non-anion gap (i.e. hyperchloremic) metabolic acidosis. Stool predominantly contains HCO3- and K+, so excessive diarrhea = excessive loss of HCO3- and K+. Chloride levels in the serum will be increased due to the normal HCO3-/Cl- equilibrium, so as negative charge dissipates due to loss of HCO3-, Cl- will increase correcting the anion-gap.

drdoom  Bulimia comes from Greek "ravenous hunger"; the term is a literal concatenation of the words for ox (bous) + hunger (limos). So, in Greek, bou-limia is literally "ox hunger", which is a nod to how the word is used in medicine = perpetual and insatiable appetite for food (the very "opposite" of vomiting). +1  
abhishek021196  I agree with your reasoning but the classic case description of Bulima lists electrolyte disturbance of HypOkalemia, HypOchloremia, and Metabolic Alkalosis, along with other things like parotid hypertrophy and dorsal hand calluses due to the induced vomiting. I tripped up there. :/ FA 20 Pg 567 +  
llamastep1  Take home lesson: reasoning > memorizing +  

Here’s a fun tangent! Bulimia comes from Greek “ravenous hunger”; the term is a literal concatenation of the words for ox (bous) + hunger (limos). So, in Greek, bou-limia is literally “ox hunger”, which is a nod to how the word is used in medicine = perpetual and insatiable appetite for food (which is precisely the “opposite” of vomiting!). So, remember, bulimia ≠ vomiting/purging (although people who are bulimic might also vomit/purge); rather, bulimia = ox hunger!

+5/- drdoom(369),

N.B., there are many ways to “purge”; the method of purge determines the observed electrolyte disturbance. A nice description of bulimia nervosa from MeSH:

BULIMIA NERVOSA. An eating disorder that is characterized by a cycle of binge eating (BULIMIA or bingeing) followed by inappropriate acts (purging) to avert weight gain. Purging methods often include self-induced VOMITING, use of LAXATIVES or DIURETICS, excessive exercise, and FASTING.

+/- drdoom(369),

 +0  upvote downvote
submitted by brookly_(0),

I thought bulimia give rise to metabolic alkalosis ...can someone elaborate ?

drdoom  Remember, bulimia itself does not mean “purging”; it means “ox-hunger”. It is purging (e.g., intentional vomiting, laxative abuse, diuretic abuse, excessive exercise, or extreme fasting) which creates metabolic disturbance. The type of disturbance depends on your preferred route of “exit”. +  

 +0  upvote downvote
submitted by rhsteps(1),

the question implies that it is a case of laxative abuse ( thus metabolic alkalosis) but the answer turns out to be the electrolyte disturbance of simply diarrhea (normal anion gap metablic acidosis) . question wrongly phrased and confusing

osgoodschlatter10  Not really. Diarrhoea and dehydration are A/Es of Laxative use (for Sketchy fans remeber the spoiling mud bath). +  

 -1  upvote downvote
submitted by dr.xx(93),

Abuse of laxatives => usually decreased serum potassium. As to chloride and bicarb, that depends. They could be increased or decreased.


Best comment i read was to treat this like it's a VIPoma. You would get all three electrolyte/metabolic disturbances.


Treat this like a VIPoma (Watery diarrhea, achlorhydria = reduced HCl in the lumen, & hypokalemia)

this will lead to metabolic acidosis d/t loss of bicarb in stool

btl_nyc  Chloride is increased though. +  
maxillarythirdmolar  This comment is gold. @btl_nyc, this is actually accute. you would expect hyperchloremia https://www.ncbi.nlm.nih.gov/books/NBK507698/ +  

 -2  upvote downvote
submitted by sheesher(0),

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. +4  
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). +5  
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-]** +2  
rainlad  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 +1