Liver Pathology and Patterns of Injury Flashcards
Chronic liver injuries lead to _____
fibrosis
How does a liver respond to acute injury?
death or regeneration
Key feature of cirrhosis
disruption of hepatocellular architecture by fibrosis w/ associated regions of regenerative hepatocytes
Stages of cirrhosis
normal –> expansion –> septae –> bridging of septae –> cirrhosis
Where does ALT live?
liver predominant (cytoplasm)
Where does GGT live?
bile canaliculus of hepatocyte –> indicator of biliary process
Where does AST live?
muscle, kidney, liver (cytoplasm and mitchondria)
Where does LDH live?
heart, kidney –> not a sign of liver involvement
Elevated serum enzymes result from ______ post cellular injury
cytoplasmic blebbing
In what cases is AST > ALT?
alcohol hepatitis and Wilson’s disease –> mitochondrial involvement
How does GGT increase after injury to the biliary tree?
increased synthesis (compensative) and secretion
What is different about the caudate lobe vs other lobes of liver?
has independent venous drainage into vena cava –> not dependent on hepatic vein –> safer during times of damage
Initial response to outflow blockage (e.g. right side heart failure).
hepatomegaly resulting in pain and leakage (ascites) –> congestion (zone 3) –> nutmeg liver
Chronic consequence of outflow blockage (e.g. right side heart failure).
cardiac type fibrosis (zone 3) in all lobes, atrophy of hepatocytes (low blood, pressure)
Consequence of outflow blockage (e.g. hepatic vein ala Budd-Chiari).
acute: caudate sparing, hepatomegaly, pain, ascites
chronic: caudate hepatomegaly, atrophy and fibrosis of rest of liver
What is a complication of caudate lobe enlargement?
compression of IVC
Consequence of inflow blockage (all vessels).
hepatic infarction w/ central necrosis + hyperemic rim –> unpredictable pattern b/c of areas of dual blood supply
Consequence of hypotension on liver?
diffuse ischemia (zone 3)
Consequence of inflow blockage (portal vein).
splenomegaly, initially no liver effect –> propagation of a thrombosus can lead to stenosis, obliteration of portal vein AKA portal tract venopathy –> portal hypertension (no pressure increase in sinusoids/cords so no ascites)
1 cause of portal hypertension w/o cirrhosis
schistosomiasis
Blood supply to bile duct
hepatic artery
Bile duct infarction
blockage of hepatic artery can result in infarction of bile duct –> biloma formation in liver b/c of blockage –> infection
Features of a hepatitic pattern of injury
lymphocytes in portal tracts, apoptotic hepatocytes in parenchyma due to FAS activation by lymphocytes, interface activity, ALT/AST elevation
What is hepatitis activity?
volume of lymphocytes in chronic hepatitis–> risk of fibrosis
Pathophysiology of Acetominophen acute hepatitis
metabolic product is toxic (NAPQ1) leads to acute zone 3 damage due to p450 metabolism in dose dependent manner
Complication of large dose acetominophen acute injury
fulminant hepatic necrosis
Steatohepatitis
fat in hepatocytes w/evidence of injury (inflammatory cells not necessary, can be due to ROS) –> elevated ALT, AST, GGT
Features of steatohepatitis
ballooning degeneration, mallory’s hyaline (nonspecific sign), glycogenated hepatocellular nuclei
Cholestasis
impediment of bile flow –> bile plugs, feathery degeneration due to bile salt buildup–> fibrosis and cirrhosis –> ALT, AST, GGT, ALK, bilirubin all high
What does a bile infarct suggest?
mechanical blockage
