As per FA 1) fatty infiltration 2) cellular ballooning 3) eventual necrosis
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).
Fatty Change in Liver [2/2 High NADH made by ADH and AldDH -> inhibits FA oxidation, impaired lipoprotein assembly and secretion-> FA accumulates.]
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"
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
submitted by โvonhippelindau(21)
Itโs 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 thatโs the logic I used to pick fatty change.