Liver Pathology Flashcards
general signs of liver disease
- change in size (inc or dec)
- change in color/texture/shape
- enhanced reticular pattern
liver cysts
epithelial lined, fluid filled spaces with sporadic distribution
multiple biliary cysts
biliary adenocarcinoma; occurs in biliary ducts
- incidental - does not always cause clinical signs
- common in cats
acquired cysts
often parasitic; larval stage forms a cyst
- not incidental
polycystic disease
cysts replace tissue parenchyma causing a loss of function
- certain breeds predisposed
causes of pale liver
- fibrosis
- fat
- inflammation
- mineral
- infiltration
- blood flow
- necrosis
liver fibrosis
deposition of collagen that occurs due to liver damage that leads to scarring
- results in loss of tissue
ex. milk spots in pigs (parasitic cause)
liver fat accumulation
causes diffuse pallor
- results in gain of tissue
liver inflammation
WBC infiltrates
- results in gain of tissue
ex. infection; causes multifocal pale regions due to hematogenous spread of bacteria
liver mineralization
mineral replaces tissue
- results in loss of tissue
liver infiltration
ex. tumors
- results in gain of tissue
liver decreased blood flow
acute –> pallor
chronic –> fibrosis
infarction is rare in the liver due to dual innervation
- if branches of portal vein become twisted, can cause collapse of portal vein
- leads to blood accumulation behind the torsion –> tissue death
liver necrosis
tissue death
- results in loss of tissue
normal liver size in small animals
3.5-4% BW
normal liver size in large animals
1.5% BW
causes of hepatomegaly
- metabolic abnormalities
- lack of venous return
- neoplasia
metabolic abnormalities –> hepatomegaly
- hepatic lipidosis
- diabetes mellitus
- hyperadrenocorticism
- iatrogenic (steroid therapy)
hepatic lipidosis
hepatomegaly with diffuse pallor
- negative energy balance causes mobilization of fat stores –> overwhelms with liver –> liver becomes fatty
ex. anorexic fat cat, postparturient cows
lack of venous return –> hepatomegaly
- passive venous congestion
- primary pulmonary hypertension
- endocardial fibroelastosis
passive venous congestion
right sided heart failure due to thickening in valve causes blockage of blood flow from liver to heart –> blood backs up to the liver –> hepatomegaly due to blood distention –> liver damage
causes hypertension –> ascites
common neoplasia in the liver
- hemangiosarcoma
- malignant histocytosis
- lymphoma
- bile duct carcinoma
- hepatic carcinoma
causes of microhepatica
- shunt
- cirrhosis
- massive necrosis
shunts
congenital or acquired vascular abnormalities that permit blood to bypass the liver and enter systemic circulation directly
congenital shunts
single vessel shunts
occurs in young (<1 yr) animals
can be intrahepatic (PDV) or extrahepatic
acquired shunts
multiple vessel shunts
occurs in older animals
cirrhosis/liver disease prevents blood from entering liver –> shunt must form to return blood to heart
causes portal hypertension and back flow causes splenic hypertension
bloodwork for shunts
increased bile acids and ammonia
- bile acids unable to return to liver via enterohepatic circulation
- decreased breakdown of ammonia into urea
clinical signs for shunts
- neurologic signs (encephalopathy)
- microhepatica
- ascites
- microcytosis
cirrhosis
end stage liver disease; liver becomes fibrotic/hard
causes of cirrhosis
- chronic toxic exposure
- chronic inflammation
- biliary obstruction
- cardiac cirrhosis
etc
liver responses to injury
- nodular regeneration
- fibrosis
- biliary hyperplasia
outcomes of cirrhosis
- ascites (from portal hypertension and hypoalbuminemia)
- acquired intrahepatic shunts
massive necrosis
must be necrosis in every lobule of every lobe to cause liver to shrink
- ex. hepatotoxic injury
hepatotoxic injury
ingestion of substances that are toxic to the liver
- causes cell death, lipid accumulation, neoplasia, etc
- often causes centrolobular necrosis (site of metabolism)
