Hepatobiliary Flashcards
Negative prognostic indicators for acute liver failure (4)
- PT> 100 s
- very old or very young animals
- marked ↑bilirubin
- Viral or idiosyncratic drug reaction as the cause
List 5 toxins that cause direct destructive hepatotoxicity:
- cycad palm
- blue green algae
- amanita
- aflatoxins
- xylitol
List 5 indirect hepatotoxins (disrupts function):
- acetominophen
- sulphonamides
- carprofen
- xylitol
- zonasamide
- benzodiazepine
Pathogenesis of portal hypertension:
- Increased resistance: damage to hepatocytes and non-parenchymal cells -> change in hepatic architecture
a. sinusoidal endothelial cells - overproduction of vasoconstrictors
b. hepatic stellate cells differentiate into contractile myofibroblasts - Increase in portal blood flow:
- splanchnic vasculature vasodilation -> decrease MAP and ECF
- RAAS activation: Na and water retention
- bacteria translocation stimulates hepatic kupffer cells + further HSC activation
How does acute liver failure affect coagulopathy?
Mostly hypocoagulable with hyperfibrinolysis, however small portion hypercoagulable:
- primary: theombocytopenia (reduced thrombopoietin production) + thrombocytopathia (increased platelet inhibitors, NO, prostacyclin)
- secondary: decreased coag factor synthesis
- increased factor utilisation
- Vit K deficiency due to decrease bile flow altering K absorption from GI
- dysfibrinogenemia
- increased production of anticoagulants
How to manage ascites?
- Na restirction (diet < 0.05g/110kcal of Na)
- Natriuresis with diuretics: spironolactone primary (takes time)
- Abdominal paracentesis: remove 20-50% of volume to improve renal blood flow, splanchnic venous return and respiration
Intrahepatic shunts are more common in?
Large dogs
Extrahepatic shunts are more common in?
Small dogs and cats (better outcomes)
List the 3 major post-op complications for PSS attenuation:
- Portal hypertension
- Coagulopathy
- Post attenuation neurologic signs (PANS)
The incompletely understood pathogenesis for primary hepatic lipidosis:
- obese cats with concurrent appetite disturbances
- excess peripheral lipid mobilisation to the liver
- difficiency of dietary proteins and other nutrients that would usually allow fat metabolism + transport out of the liver
- fat accumulates in hepatocytes, disrupting function
Important dietary proteins in cats:
- methionine: precursor to glutathione
- carnitine: important in FA transport through the mitochondrial membranes
- taurine: conjugation of bile acids to bile salts
- arginine deficiency: contribute to HE caused by decreased urea cycle activity
Ideal diet for hepatic lipidosis cats:
Protein 30-40% ME
Fat 50% ME
Low Carb 20% or lower (glucose intolerance & hyperglycemia common)