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 +1  (nbme23#12)

my approach to this question was to eliminate all the answer choices that mentioned specificity or sensitivity, since the data here did not provide information about any sort of screening test.

that left me with two possible answer choices: I eliminated the one about consistency of other studies, since no other studies were mentioned in the question stem.

not sure if I oversimplified things, but it led me to the right answer!


 +0  (nbme21#12)

How do we explain the bruit in this case? Also why isn't it left artery aneurysm? That seems like it would better explain the bruit

gdupgrant  The bruit is basically just turbulent flow, which is most commonly caused by artery narrowing. I was just reading https://emedicine.medscape.com/article/463015-clinical on renal artery aneurysm and it looks like most of the hypertension is actually related to a pre aneurysm stenosis, so i think stenosis is the "better" answer, esp. since the pt has like every risk factor for stenosis. To be honest I had not ever really thought about RAA for this case because bruit over RA has been drilled into my head as renal artery stenosis, but i apprecaite seeing how this is a super reasonable answer - just the stenosis is "more likely"

 +0  (nbme21#38)

would we be worried about using G-CSF given that he has acute leukemia? would it stimulate growth of his cancer cells?

suckitnbme  I think we're assuming that we eradicated the leukemia with the chemo. However at the same time a lot of normal stem cells were also killed off so we give GCSF to help recovery especially since they have an infection.

 +0  (nbme20#37)

Hypochloremic, hypokalemic metabolic alkalosis is the classic electrolyte and acid-base imbalance of pyloric stenosis.

Persistent vomiting results in loss of HCl. The chloride loss results in a low blood chloride level which impairs the kidney's ability to excrete bicarbonate. This is the factor that prevents correction of the alkalosis leading to metabolic alkalosis.

A secondary hyperaldosteronism develops due to the decreased blood volume. The high aldosterone levels causes the kidneys to retain Na+ (to correct the intravascular volume depletion), and excrete increased amounts of K+ into the urine (resulting in a low blood level of potassium).





Subcomments ...

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). +4  
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 +  


submitted by hello(107),

why is plasma oncotic pressure wrong?

rainlad  I think it's because we would expect to see some more proteinuria/albuminuria if the plasma oncotic pressure had increased to compensate +  


submitted by seagull(535),

This is a panic attack. Hyperventilation drops pCO2 leading to a respiratory alkalosis. po2 is relatively unaffected (don't ask me how?)

sympathetikey  Yeah haha I had the same conundrum. +  
sajaqua1  If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected. +4  
imnotarobotbut  lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol +  
soph  Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances). +  
charcot_bouchard  PErioral tingling- due to transient hypocalcemia induced by resp alkalosis. +  
rainlad  I believe CO2 diffuses ~20x faster than O2, so increases in her respiratory rate have more effect on her PCO2 than her PO2 +