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28 Cards in this Set
- Front
- Back
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What are some degenerative changes/accumulations in the liver?
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Hepatocellular swelling Fatty change Steroid-induced hepatopathy Amyloidosis |
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What is hepatocellular swelling?
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Energy production decreases, membrane pumps fail due to lack of ATP, intracellular water accumulates, reversible
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What is fatty change?
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Lipid accumulates in cytoplasm of injured hepatocytes - unable to metabolise/function, reversible but may progress to lipidosis/steatosis. Liver is pale yellow, friable and greasy. Hepatocytes distended by discrete circular lipid vacuoles which displace the nucleus to the periphery of the cell. |
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What is steroid-induced hepatopathy
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Dogs: hepatocytes distended by "feathery" cytoplasmic vacuoles, which do not displace the nucleus, excessive glycogen accumulation in the presence of high levels of corticosteroids - ballooning degeneration may be present. |
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What is amyloidosis?
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Primary: familial - shar peis, siamese Secondary - usually follows chronic inflammation - liver is enlarged, pale and firm but friable, with rounded borders. Amyloid protein is deposited extracellularly along sinusoids in spaces of Disse and around portal areas. |
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Patterns of hepatocellular necrosis?
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Single cell necrosis Focal to multifocal necrosis Zonal necrosis - centrilobular, periportal, midzonal Massive necrosis |
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What is centrilobular necrosis?
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Hepatocytes are vulnerable to hypoxic damage (anaemia, chronic venous congestion). Also susceptible to toxic insult by toxins requiring hepatic biotransformation.
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What is massive necrosis?
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Necrosis of whole lobules, including cells and connective tissue scaffold - more serious and/or longer duration insult - followed by "post-necrotic lobular collapse" and fibrosis
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What is the hepatocyte response to inflammation?
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Hypertrophy Regenerative hyperplasia/nodular regeneration of existing mature hepatocytes |
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What is nodular hyperplasia of the liver?
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Common incidental finding in older dogs - discrete, unencapsulated nodules of hepatocytes which retain some lobular architechture
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What is hepatic progenitor cell proliferation?
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Regeneration of new hepatocytes and bile ducts - proliferation of biopential stem cells located in the terminal bile ductules Often just proliferation of bile duct type cells "biliary hyperplasia" |
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How can hepatic atrophy occur?
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Pressure on the liver parenchyma - external/internal space occupying lesions Anoxia/hypoxia Impairment of bile flow - chronic biliary dx |
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Discuss healing by fibrosis in response to inflammation?
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Centrilobular fibrosis Portal fibrosis Post-necrotic scarring Diffuse hepatic fibrosis |
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What is cirrhosis?
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Diffuse, irreversible, end-stage hepatic disease: combination of hepatocyte destruction, nodular regeneration, biliary hyperplasia, bridging fibrosis and portal-centrilobular vascular anastomoses.
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Describe some mechanical/traumatic conditions?
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Displacement - acquired diaphragmatic hernia, eg trauma due to RTA Rupture - trauma eg RTA |
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Developmental conditions?
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Congenital cysts Vascular anomalies Displacement Biliary atresia and absence of gall bladder (normal in horses) |
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Describe congenital vascular anomalies
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Porto systemic shunts - anomalous development of portal vein either prior to the liver (extrahepatic) or within the liver (intrahepatic). Liver and portal vein hypoplasia. Primary portal vein hypoplasia Intra-hepatic arteriovenous fistulae |
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Acquired disturbances of hepatic circulation?
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Telangiectasis - dilataion of groups of sinusoids filled with blood (incidental finding) Vascular obstruction - portal vein, hepatic vein Acquired portosystemic vascular shunts - usually secondary to portal hypertension. |
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What is hepatitis?
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Inflammation of the liver parenchyma
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Acute hepatitis?
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Usually associated with hepatocellular necrosis Bacterial, viral, protozoal, fungal, trematodiasis, toxic |
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Chronic hepatitis?
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Mixture of tissue damage, nodular regeneration and fibrosis, together with cellular reaction (copper-associated hepatopathy, chronic Cu toxicity sheep)
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What is cholangiohepatitis?
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Inflammation of the biliary tree and hepatocellular parenchyma Inflammation starts in the bile ducts and extends into parenchyma |
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Give some examples of biliary disease |
Cholangitis - chronic lyphocytic cholangitis Cholecystitis Cystic mucinous hyperplasia - hyperplasia of gall bladder wall and lining with mucin production Parasitic obstruction Stenosis Cholelithiasis (gall stones) |
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Examples of hepatic neoplasia?
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Hepatocellular tumours - carcinomas more common than adenomas Cholangiocellular tumours (bile duct) Vascular tumours - primary haemangiosarcoma Metastatic neoplasia to liver Multicentric neoplasia |
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Give a developmental condition of the exocrine pancreas?
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Pancreatic acinar atrophy (hypoplasia) Autosomal recessive inheritance - exocrine pancreatic insufficiency |
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Give some pancreatic acquired conditions?
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Interstitial pancreatitis Acute pancreatic necrosis Nodular hyperplasia Neoplasia Calculi |
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Describe interstitial pancreatitis
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Acute: systemic toxoplasmosis Chronic: commences in ducts, concurrently with cholangitis and enteritis in cats (triaditis) - can lead to exocrine pancreatic insufficiency/diabetes mellitus |
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Describe acute pancreatic necrosis
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Important in small breed dogs: activation of trypsinogen to trypsin within the pancreas, autodigestion - necrosis of the pancreas, adjacent connective tissue and abdominal fat.Sequelae: Resolution - fibrosis and nodular regenerationChronic relapsing pancreatitisDiabetes mellitus
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