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Welcome to stepwarriorโ€™s page.
Contributor score: 29


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 +1  visit this page (nbme20#10)
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Wouldn't chronic alcoholism also reduce available NAD and thus inhibit pyruvate decarboxylation by PDH?

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andro  It may also potentially do that , But that has no connection with our patients current symptoms - perifollicular hyperkeratosis and hemorrhages . Inhbition of PDH would be more relevant if they were talking about Alcoholic Lactic Acidosis or decreased energy in alcoholics +1
failingnbme  I thought the same :( +1

 +15  visit this page (nbme20#34)
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You're just going to diss the son like that right in front of him?

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splanchnic  made an account to upvote this +8
snoodle  I agree - I was stuck between this and "Was he under any unusual stress at home/school or did he have any problems with a gf when all of this started?" and I chose the latter. I didn't want to choose this because why would you want to call the son frightening in front of the son?! I didn't want to choose the answer I chose, either, because you aren't supposed to imply he's straight :/ annoying af +1
makingstrides  I don't think that's what frightening meant. It's meant to describe the mother who is worried about the son. +1

 +1  visit this page (nbme20#16)
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all fine and dandy except bicarbonate isn't constant with flow rate

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 +2  visit this page (nbme20#41)
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They love picking these cases right on the border. Just barely outside of that sexually active age range

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 +1  visit this page (nbme20#24)
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this is clearly another one of those trap questions for overthinkers

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 +5  visit this page (nbme20#39)
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This is where the hernia begins but ultimately where it bulges out varies depending on how far down the inguinal canal the hernia goes. It could pop out well below the inguinal ligament. The wording is crap, they should have just shown a picture of the patient.

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 +2  visit this page (nbme20#35)
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The incorrect labeling of the gross pecimen makes this question a bona fide piece of garbage.

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 -2  visit this page (nbme20#1)
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You should find out whether or not she wants her parents to know first

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misterdoctor69  She's a minor though. +2

 +2  visit this page (nbme20#8)
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I ruled out most of them because of no evidence of person-to-person transmission and only people with pre-existing conditions were affected. The rest would probably also affect children or other attendees or spread to others in the nursing home.

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 +0  visit this page (nbme20#30)
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Looked this up. Starvation causes GH resistance. Never heard of this, unfortunately fell into the trap of thinking increased GH would increase IGF-1. Punished for overthinking.

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bgreen27  Ok, from what I understand, starvation may induce GH resistance, but starvation STILL stimulates its production. The question asked which hormone would be increased in concentration, so this doesn't really explain why IGF1 is wrong. One possible explanation I found is that AGING inhibits GH secretion, which is not the case for cortisol. +1
drdoom  It makes evolutionary sense that if your body is in starvation mode it is not going to be releasing an ANABOLIC signal (Growth Hormone). If you're starving, you'll need to stop โ€œputting on massโ€ and continue to catabolize fatty acids, glycogen and whatever other stores your body has left. (It will have to way away at itself simply to generate enough ATP for vital functions [fuel for heart, brain, kidney].) +1
drdoom  eat* away +1
bgreen27  I totally get where youre coming from, but the fact is that starvation DOES increase release of GH (but apparently also increases GH resistance). So my qualm was with the question stem asking about which one increases in concentration, and GH and cortisol both increase during starvation. Have you found something different? +1

 -1  visit this page (nbme20#10)
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I don't think you're going to find any evidence for this one. It's just the test-writers' opinion

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 +0  visit this page (nbme20#41)
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this question was utter BS, but the way I justified "same epitopes" was that it said "in the context of anti-serum X," i.e., which epitopes would have been developed in the context of the antibodies present. It's unlikely that anti-X antibodies would bind to epitopes on Y that aren't on X. But you could argue there are theoretical epitopes on Y that could be bound by another antibody that doesn't exist in this scenario.

Very drawn out and took me 5 minutes to actually figure out on the test, honestly a waste of time in my opinion, but there you go.

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Subcomments ...

submitted by monoloco(155), visit this page
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As a rule of thumb, if you give someone an ACE inhibitor and they get a problem, they had renal artery stenosis (usually bilaterally, or so we were taught at our med school). Probably has to do with decreased GFR thanks to decreased Angiotensin IIโ€“selective vasoconstriction of the efferent arteriole => decreased sodium delivery to macula densa => increased renin release.

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lilyo  Vasoconstriction of the EFFERENT arteriole actually leads to increased GFR. It selective VASODILATION of the efferent arteriole effect of ACE inhibitors since they undo Angiotensin II actions. This patient already has rescued renal blood flow due to bilateral renal artery stenosis, the addition of an ACE inhibitor further decrease GFR prompting an increase in renin due to loss of negative feedback. +4
drpee  We should always expect GFR to drop a little after adding an ACE-inhibitor due to efferent arterial vasodilation. For this reason we should also expect Renin levels to rise via tubuloglomerular feedback. So it's not really the reaction to the ACE inhibitor that gives this away as RAS (which is why I got it wrong). I think what we are expected to be looking at it are lab values: Hypokalemia, and secondary hyperaldosteronism. https://www.aafp.org/afp/2017/1001/hi-res/afp20171001p453-t5.gif +
stepwarrior  ACE inhibitors would actually have the opposite effect of AT-II, and result in efferent dilation. But the actual mechanism of increased renin activity per UWorld is lack of systemic vasoconstriction by AT-II leading to blood shunting away from the kidney. +1


submitted by hayayah(1212), visit this page
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Add on to the other comment: SICKFACES.COM (when I Am drinking Grapefruit juice) is the mnemonic for remembering the CYP450 Inhibitors:

  • S odium valproate
  • I soniazid
  • C imetidine
  • K etoconazole
  • F luconazole
  • A cute alcohol abuse
  • C hloramphenicol
  • E rythromycin/clarithromycin
  • S ulfonamides
  • C iprofloxacin
  • O meprazole
  • M etronidazole

  • A miodarone

  • Grapefruit juice
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charcot_bouchard  Its not a cytochrome question. IK because i go t it wrong +1
waterloo  both azoles and PPI inhibit cytochrome P450. So one isn't causing the other's lack of effect. +9
stepwarrior  Nope. Inhibiting CYP450 would enhance the effect of itraconazole, so that can't be the mechanism. +2


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