Pathophysiology of AST/ALT in PSS

[bluevet]

I am trying to explain the pathogenesis of certain bloodwork abnormalities of a portosystemic shunt. I am stuck on AST/ALT. I know the a PSS would cause decreased bloodflow from portal blood so there would be decreased nutrients but would this actually cause hepatocellular damage and leakage of ALT/AST? All I can find is that it would cause atrophy and hepatic insufficiency but since these are leakage enzymes I don't understand.

Also, prolonged PT but normal PTT?

Please help!

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[No Imagination]

I can't help you much now, because I don't have my notes in front of me, but iirc, AST/ALT would not be elevated specifically from a congenital PSS. However, an acquired PSS (from liver cirrhosis) would show an increase in liver enz. like AST/ALT as well as bile acids. Obviously congenital PSS would also show increased bile acids. As for the coagulation, I no longer remember the entire extrinsic vs. intrinsic pathway, but with early liver failure I believe you will see a decrease in whatever factor has the shortest half life (perhaps due to Vit. K def.). Basically, whatever pathway PT measures should contain a cofactor that has a short(er) halve life. With what you told us, and what I remember, I am guessing that the PSS is acquired from LD; which would explain the increased liver enz. Not sure if that works with your pathogensis; but it was fun trying to put it together.

 

[david594]

Just kind of thinking outloud here...
PT increase is seen with factor VII dysfunction. And increases in PT are seen before PTT changes due to factor VII having the shortest half-life of all the vitamin-K dependent coagulation factors. (which is why PT is more sensitive than PTT in suspected rodenticide cases)

The mechanism for the lack of factor VII could come from two different things. One would be a primary lack of production of the factors them self. Or the other would be secondary dietary insufficiency due to malabsorption of vitamin-K which can occur with liver disease.