Pathophys of peripheral vasodilation in hepatorenal syndrome

[StevenRF]

Can anyone explain it to me?

So hepatic failure/cirrhosis/fibrosis -> portal hypertension -> blood diverted to splachnic circulation w/ vasodilation -> blood pools on venous side in spleen /GI

Low circulating volume -> RAAS, SNS, ADH activated -> lock down on kidneys

Magically the body vasodilates??? My thoughts... low pressures sensed by carotids, atria, aorta, and medulla all sense the low pressures / O2 delivery -> massive peripheral vasoconstriction to increase EDV and blood flow to brain, also SNS increase heart rate

So where does the vasodilation come in? Peripheral metabolites override and induce vasodilation (wouldn't that require severe hypoxia / acidosis) ? Liver / gut dumping NO (how do you make it when the liver is failing)? Inner soul recognizing the end is coming?

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[SocialistMD]

Can anyone explain it to me?

In short, no. The pathophysiology is not currently completely understood. All that is really known are specific observations that have been made (splanchnic vasodilation, renal vasoconstriction), but it is unknown what the mediators of each are.

 

[Tiger26]

maybe it's just me, but i secretly enjoy it when things like this aren't understood because that means i don't have to know the mechanism why, and so it's likely not going to be on the test