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Retired NBME 21 Answers

nbme21/Block 1/Question#24 (reveal difficulty score)
A 23-year-old man drinks alcohol heavily on a ...
Fatty change ๐Ÿ” / ๐Ÿ“บ / ๐ŸŒณ / ๐Ÿ“–
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 +12  upvote downvote
submitted by โˆ—vonhippelindau(21)
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Itโ€™s acute alcohol consumption so fatty change more likely. Cellular swelling indicates alcoholic hepatitis which requires chronic alcohol consumption (See FA 2019 pg 385). At least thatโ€™s the logic I used to pick fatty change.

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seagull  Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset. +51
nc1992  I think it's just a bad question. It should be "on weekends" +17
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +27
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +1
sympathetikey  @seagull I agree! +
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +1
linwanrun1357  Do NOT think the answer of this question is right. Cell swelling make more sense! +1
fkstpashls  some asshole in suspenders and a bowtie definitely wrote this q, as I've seen both acute swelling and fatty change be used to describe one episode of drinking. +15
msw  short term ingestion of as much as 80gm of alcohol (six beers) over one to several days generally produces mild , reversible hepatic steatosis . from big robin 8th edition page 858. Basically to develop alcoholic hepatitis with cellular swelling etc you have to have sustained long term ingestion of alcohol while steatosis can develop with a single six cap . hope that helps . ps i got it wrong too . +3
msw  six pack8 +
mariame  After even moderate intake of alcohol, lipid droplets accumulate in hepatocytes increasing with amount and chronicity of alcohol intake. (...) Fatty change is completely reversible if there is abstention from further intake of alcohol. The swelling is caused by accumulation of fat, water and proteins. Therefore this will occur later. From big Robins 9th pg842. +
l0ud_minority  Just thinking about this Alcohol is a Mitochondrial poison which would lead to stress uncoupling of oxidative phosphorylation and cellular swelling. I got it wrong with that logic though which is frustrating. +



 +9  upvote downvote
submitted by โˆ—usmleuser007(464)
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As per FA 1) fatty infiltration 2) cellular ballooning 3) eventual necrosis

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hyperfukus  thanks u saved me time in looking that up :) +
violethall11  Those are for non-alcoholic fatty liver disease. Definitely missing some info in the question stem, however, I believe that the whole point is that the individual is NOT an usual alchoholic . +
mumenrider4ever  FA2020 pg. 391 +



 +6  upvote downvote
submitted by โˆ—azibird(279)
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FA2020 p72

Ethanol metabolism increases NADH/ NAD+ ratio in liver, causing:

Hepatosteatosisโ€” Increased conversion of DHAP to glycerol-3-P; acetyl-CoA diverges into fatty acid synthesis, which combines with glycerol-3-P to synthesize triglycerides

Increased NADH/NAD+ ratio inhibits TCA cycle -> acetyl-CoA used in lipogenesis (-> hepatosteatosis).

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 +2  upvote downvote
submitted by โˆ—sweetmed(157)
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Fatty Change in Liver [2/2 High NADH made by ADH and AldDH -> inhibits FA oxidation, impaired lipoprotein assembly and secretion-> FA accumulates.]

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 +1  upvote downvote
submitted by โˆ—youssefa(162)
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Wouldn't acute alcohol consumption even in moderate amount cause reversible hepatic cellular injury characterized by cellular ballooning? It should be the right answer unless the question stem means "Weekends"

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hello  No. The order of liver damage due to alcohol is: fatty changes --> cellular swelling (cellular balooning) --> necrosis. This Q stem states to the patient consumed large amount of alcohol on a weekend -- he has acutely drank a large amount of alcohol on one weekend --> this corresponds with fatty changes +3
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +
krisgsxr600  Its kind of in pathoma Chapter 1, "free radical Injury", Section 2 "examples of free radical injury" goes over how free radicals (caused by drinking) lead to fat accumulation +
sallz  You can't get the steatohepatitis before getting the steatosis (fatty change). All the FAs caused by the alcohol consumption eventually lead to cytokine release, inflammation and finally the hepatitis seen in balloon swelling. +



 +0  upvote downvote
submitted by krisgsxr600(1)
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Was just going over Pathoma again and he explanes this concept really well in CH 1, "Free Radical Injury", Section II "Examples of Free Radical Injury"

ultimately cell swelling (the hallmark of acute/reversible injury) = ribosomes off RER = decreased protein synth = decreased Apolipoprotein synth = fat accumulation in cells

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drschmoctor  Yes, he does explain very well how both cellular swelling & fat accumulation occur. ... which is exactly why this question is some chicken vs egg BS. +3



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