Hepatobiliary System, Pt. 3 Flashcards
(31 cards)
What 6 insults commonly cause hepatocyte death?
- hypoxia
- toxins (centrilobular zone)
- microorganisms (miliary)
- immunological events and inflammation
- severe metabolic disturbances
- trauma
What are the main patterns of necrosis an their cause?
- massive (panlobular) - toxic and nutritional
- zonal (zone 3) - toxic or hypoxia
- multifocal random (miliary) - infectious agents, like viruses, bacteria, and protozoa
What is a common cause of massive (panlobular) necrosis of pig liver?
hepatosis dietetica from a deficiency in vitamin E and/or selenium
- bright/dark red marbled necrosis affecting all lobes
- ACUTE massive mecrosis
What is the most common form of zonal necrosis of the liver? What is it caused by? How does it look grossly?
centrilobular area (zone 3)
hypoxia or toxins
linear trabecular pattern of pallor necrosis affecting one zone
What is the most common cause of multifocal random necrosis of the liver? How does it look grossly?
infectious agents, including viruses, bacteria, and certain protozoa
multifocal, small, miliary, pallor spots of necrosis randomly distributed throughout the liver
(equine herpesvirus infection, foal)
What is the most common sequelae to massive chronic hepatic injury? What does it look like grossly?
cirrhosis, end-stage liver
multifocal nodules of regeneration after parenchymal death with fibrosis between nodules —> liver will not completely regenerate and will be smaller
How much can the liver regenerate after damage/surgical removal?
70% of normal liver can be regenerated without clinical insufficiency
What are the 3 steps to hepatic regeneration?
- hepatocellular loss is replaced by proliferation of bipotential progenitor cells with the ability to mature into hepatocytes or biliary epithelium, resulting in ductular reactions and biliary hyperplasia
- endothelial buds establish sinusoidal channels
- hepatic stellate (Ito) cells replicate and synthesize extracellular matric rich in collagen, leading to fibrosis
Hepatic injury and development of fibrosis:
damage to reticulin framework = no regeneration
What 4 things happen during cirrhosis (end-stage liver)?
- loss of hepatic parenchyma
- nodular regeneration
- bridging fibrosis
- biliary hyperplasia
What is the consequence of cirrhosis in dogs? How does this happen?
acquired portosystemic shunts
- hepatic fibrosis causes portal hypertension
- blood vessels unable to make it to the liver redirect to the caudal vena cava, bypassing liver sinusoids
- decrease in liver function due to decreased nutrition causes ascites
How can nodular regeneration and nodular hyperplasia be differentiated?
REGENERATION = response to a loss of hepatocytes and contains fibrosis
HYPERPLASIA = common incidental finding in older dogs lacking fibrosis
What are 6 causes of cirrhosis?
- chronic toxicity
- chronic cholangitis and/or obstruction
- chronic congestion (right-sided heart failure)
- inherited disorders of metal metabolism
- chronic hepatitis
- idiopathic
Cirrhosis, histology:
n = regenerative nodules surrounded by fibrosis + loss of hepatic structure
What is happening in the histology of this cirrhotic liver?
- ductular reaction of disassociated hepatocytes
- blue cells = hyperplastic biliary epithelium (usually only seen in portal triad bile duct)
+ cytokeratin 7 stain, an epithelial marker for biliary epithelium
What are the 2 most common causes of circulatory disturbances of the liver? What are 3 other causes?
- congestion
- portosystemic shunts/vascular anomalies
- portal vein hypoplasia
- portal thrombi
- infarction
Acute passive liver congestion:
- due to right-sided heart failure causing fluid back up into the liver
- dark red
What is the most common gross presentation of chronic passive congestion of the liver?
nutmeg liver - central vein surrounded by a reticular pattern of pale necrosis and congestion
What is a common cause of passive congestion in cattle? What is the pathogenesis?
high-altitude disease, brisket disease
- high altitude causes hypoxia and pulmonary arterial vasoconstriction
- this causes right-sided heart failure and hepatic congestion (nutmeg liver!)
- this further causes increased intravascular hydrostatic pressure, leading to ascites and peripheral edema in the brisket area
What does the development of a portosystemic shunt cause? What are the 2 types of congenital portosystemic shunts?
portal blood bypasses the liver and its sinusoids
- INTRAHEPATIC: large breed dogs; patent ductus venosus
- EXTRAHEPATIC: cats and small breed dogs; portocaval, portoazygos
What is a common sign of extrahepatic congenital portosystemic shunt?
hepatic encephalopathy due to an accumulation of ammonium —> ammonium biurate crystals in urine
(portal vein takes GI nutrients/toxins to liver, if it bypasses it, the contents of the blood directly reach systemic circulation)
How do congenital and acquired portosystemic shunts compare?
CONGENITAL
- usually affects a single large caliber vessel
- NO portal hypertension or ascites (just bypassing liver, no resistance)
- early onset in young animals
ACQUIRED
- involves multiple small vessels
- associated with portal hypertension and ascites
Congenital portosystemic shunts:
portal vein connects to vena cava and bypasses liver sinusoids
How does congenital portosystemic shunts appear grossly?
small liver and abnormal singular vascular anastomosis
v = single anomalous vessel connecting portal circulation with systemic circulation
