Yes, usually the albumin will drop due to the declining synthesis abilities of the liver and the globulin levels will tend to rise. The thing to watch is the A/G ratio (albumin/globulin) since it is a very sensitive marker to track this. Normal A/G levels will be greater than 1 (closer to 2 is ideal) and less than 1 is indicative of serious problems. Also, due to the declining synthesis abilities, the INR will trend higher as the liver disease progresses but this usually doesn't become pronounced until the liver function has deteriorated to roughly 20 to 30% or so. Platelets will drop primarily due to an enlarged spleen caused by portal hypertension but the liver disease can also reduce the platelet production as well. Unfortunately, all this can get quite messy and all the other parts of the portal flow system will be further stressed as the liver stops pulling it's load and they have to try "compensate" for as long as possible. Certainly those that keep doing things to insult the liver and other organs further will accelerate the process.
Decompensation can be present without clinically significant portal hypertension but is uncommon. From what I understand, this would be caused by the blood flow being "re-routed or short-circuited" past the active liver lobular portions (via the bridging scar tissue) as it makes it's way from the portal tracts to the central hepatic veins. That's if there is still positive/forward portal flow and viable hepatic veins still present of course.
Post Edited (bblbt) : 6/3/2014 12:34:45 AM (GMT-6)