GI Final--Cattley & Boothe Flashcards
(51 cards)
3 components of the portal triad
portal venule
bile duct
hepatic artery
What is the idea of metabolic zonation of hepatocytes?
hepatocytes will vary in their functions and enzymes depending on their location along the gradient
4 functions of Kupffer cells
plasma protein turnover
clearance of endotoxin
erythrophagocytosis
phagocytosis of particulates (bacteria)
What are the 3 mechanisms by which jaundice can occur?
1) Overproduction (increased extravascular hemolysis)
2) decreased uptake, conjugation, and secretion (impaired liver function)
3) reduced outflow of bile (obstructed bile ducts)
Two major mechanisms of liver-associated ascites formation
portal hypertension (increased hydrostatic pressure)
decreased albumin production (decreased plasma oncotic pressure)
What are the 4 factors that contribute to CNS signs with hepatic encephalopathy
Ammonia elevation (increases glutamate and GABA)
endogenous benzodiazepine ligands from gut microbes can interact with GABA
astrocyte injury (ammonia related)
manganese–neurotoxic
Give the cause for each type of photosensitizaiton
1) Type 1
2) Type 2
3) Type 3
1) ingestion and deposition of preformed photoreactive pigments
2) congenital
3) liver failure
Which photodynamic pigment is involved in liver failure-associated photosensitization (type 3)
Phylloerythrin (PE)–produced from chlorophyll by GI bacteria and usually excreted in bile
Why are central lobular cells most susceptible to toxic drugs and chemicals?
they have the highest amount of CYP450 which activates toxins
What patterns of hepatocellular injury do we expect with infectious agents?
Random
4 patterns of hepatic fibrosis and what they are secondary to
diffuse (secondary to chronic parenchymal process)
biliary (portal inflammation)
postnecrotic (focally extensive necrosis)
centrilobular (congestive heart failure)
Prolonged/sustained increases in glucocorticoids are associated with?
glycogen accumulation
Concerning hepatic lipidosis, what are the 2 main categories of how it’s caused
1) physiological (dietary or adipose mobilization)
2) pathological (injury impairs utilization)
What type of shunt primarily impacts small breed dogs? what veins are usually anatomosed?
Extrahepatic congenital shunt;
portal vein and caudal vena cava OR azygous vein
Which type of shunt is seen in large breed dogs? what’s the cause?
Intrahepatic congenital shunt;
persistence of fetal ductus venosus
Thought they present similarly, how will congenital shunts and portal vein hypoplasia differ on clinical presentation?
Hepatic microvascular dysplasia WILL have portal hypertension and therefore, ascites
What type of hepatic necrosis presents with infectious canine hepatits
Centrilobular
different than most infectious agent which cause a random pattern
How does CAV-1 (infectious hepatitis) lead to DIC?
it likes to replicate in endothelial cells, and that damage leads to consumption of coag factors
Mutation of what gene in Bedlington Terriers predisposes them to copper storage hepatitis
Mutated COMMD1 gene
What is the function of the COMMD1 gene?
helps diret the ATP7B-Cu complex to the lysosome
The toxin associated with aflatoxicosis
Aflatoxin B1 (binds proteins, DNA, and RNA leading to cell injury and necrosis)
4 histopathic changes seen in horses with pyrrolizidine alkaloid (PA) toxicity
hepatocyte loss
fibrosis
bile duct proliferation
megalocytosis
These flukes reside in the bile ducts of sheep and cattle and lead to chronic cholangitis, liver atrophy, and poor body condition
Fasciola hepatica
These flukes of sheep and cattle migrate through the parenchyma and cause extensive damage; they occasionally become encased in fibrotic cysts
Fascioloides magna
