GI2- Liver 1

  1. Major categories of liver function. (4)
    metabolic, circulatory, secretion/excretion, storage/filtration
  2. Metabolic functions of the liver. (3)
    carb/fat/protein metabolism, vitamin and mineral metabolism, detoxification and clearance
  3. How does the liver support glucose homeostasis? (3)
    glycogen storage after eating and breakdown during fasting, gluconeogenesis; insulin and glucagon are also affected by liver function
  4. Why do animals get hypoglycemic in liver failure? (2)
    • functional failure: synthetic failure (70% of functional tissue obliterated)--> decreased gluconeogenesis, decreased insulin degradation
    • Paraneoplastic to hepatic neoplasia: tumors secrete insulin-like growth factor, driving glucose down
  5. Liver functions associated with fat metabolism. (6)
    cholesterol synthesis, bile acid synthesis, ketogenesis, FA and TG metabolism, lipoprotein synthesis, phospholipid metabolism
  6. Altered fat metabolism in the liver can lead to... (4)
    decreased serum cholesterol (decreased synthetic function) OR increased serum cholesterol (secondary to cholestasis); target cells, hepatic lipidosis
  7. Protein metabolism functions of the liver. (6)
    albumin synthesis, globulin synthesis (ish), coagulation factor synthesis, amino acid regulation, ammonia detoxification, urea synthesis
  8. Albumin is synthesized in the ___________; it is responsible for...
    liver ONLY; maintaining plasma oncotic pressure
  9. Decreased synthetic function of the liver indicates _____(2)_____.
    severity and chronicity
  10. Is decreased albumin specific for the liver?
    No- GI or renal protein-losing -opathies
  11. What are the 3 mechanisms of bleeding disorders in liver disease?
    decreased synthesis of clotting factors, DIC (hypercoagulable: source of AT, plasminogen, and factor clearance), Vit K deficiency
  12. What are liver functions associated with vitamins/minerals? (3)
    fat soluable vitamin storage, water soluble vitamins, storage or iron/copper/zinc/etc
  13. The liver is responsible for detoxification and clearance of... (5)
    pathogens (Kupffer cells), drugs, toxins, hormones, metabolites.
  14. What are the 2 phases of drug metabolism in the liver?
    • Phase I: Oxidation
    • Phase II: Conjugation
  15. How should you handle administration of drugs metabolized by the liver to patients with liver disease?
    lower the dose- monitor more closely
  16. Photosensitivity due to liver disease occurs in ___________.
  17. Biochem markers of decreased synthetic function. (7)
    increased ammonia, increase coag factors, decreased glucose, decreased cholesterol, decreased BUN, decreased albumin, increased serum bile acids
  18. Biochem markers of liver cell necrosis. (2)
    increased ALT and AST
  19. Biochem markers of cholestasis. (6)
    increased coag factors, increased bilirubin, bilirubinuria, increase cholesterol, increased serum bile acids, increased ALP and GGT
  20. Biochem markers of portosystemic shunting. (2)
    increased post-prandial bile acids and blood ammonia
  21. Hepatic blood flow is contributed to by... (2)
    hepatic artery, portal blood flow
  22. The liver is drained by the ____________.
    caudal vena cava
  23. Portal blood drains from... (4)
    intestines, stomach, pancreas, spleen
  24. What is a portosystemic shunt?
    vascular communication b/w portal and systemic venous systems, bypassing the liver
  25. What are potential causes of a single portosystemic shunt?
    congenital malformation (no portal hypertension, no abdominal effusion, no hyperbili)
  26. What are potential causes of multiple portosystemic shunts?
    portal hypertension, congenital or acquired (often associated with ascites, other evidence of liver dz)
  27. What are consequences of portosystemic shunts? (3)
    hepatic encephalopathy, urate urolithiasis, hepatic atophy (small liver, evidence of synthetic dysfunction)
  28. What are causes of hepatic encephalopathy? (3)
    portosystemic shunt, loss of critical hepatic mass (massive necrosis, cirrhosis), urea cycle enzyme deficiency
  29. Describe the pathophysiology of hepatic encephalopathy.
    brain is affected by substances (ammonia, synergistic toxins, altered neurotransmitters, oxidative stress, inflammatory mediators) normally metabolized by the liver
  30. What are clinical signs of portosystemic shunts? (14)
    anorexia, lethargy, disorientation, head-pressing, circling/pacing, ataxia, weakness, dull, difficulty training, behavioral changes, blindness, hypersalivation, seizures, coma
  31. What brain cells are the target of toxins in hepatic encephalopathy?
  32. Describe ammonia metabolism in the body.
    NH3 produced in colon by bacterial action on dietary protein--> absorbed from colon--> portal blood--> NH3 carried to liver--> converted to urea (BUN) in hepatocytes--> NH3 low in peripheral blood
  33. What are supporting points for the hypothesis that ammonia toxicity causes hepatic encephalopathy? (4)What is the argument against it?
    • For: NH3 is neurotoxic and increased NH3 causes CNS signs, PSS dogs are usually worse after a meal, NH3 causes type II astrocytosis, NH3 modulates neurotransmitters
    • Against: poor correlation b/w blood NH3 levels and signs
  34. What are the general principals of treating hepatic encephalopathy? (4)
    correct precipitating events, restrict dietary protein, decrease colon NH3 absorption, alter intestinal bacteria
  35. What are potential precipitating events of hepatic encephalopathy? (8)
    high protein meal, GI bleeding, blood transfusion, constipation, dehydration, azotemia, infection, alkalosis/ hypokalemia
  36. What drugs are usually used to treat the precipitating events of hepatic encephalopathy? (6)
    corticosteroids, NSAIDs, tranquilizers, anticonvulsants, anesthetics, diruretics
  37. What dietary changes are usually recommended for patients with hepatic encephalopathy/PSS?
    lower protein- avoid red meat or organ meat-based diets; soy based diets are best, chicken or egg based diets are second best
  38. How can you alter intestinal bacterial to reduce NH3 absorption from the colon in hepatic encephalopathy?
  39. What are the mechanisms of increased resistance and portal hypertension? (3 groups)
    • Post-hepatic: CVC and heart, mass/CHF, pericardial effusion
    • Intrahepatic: cirrhosis, hypoplastic portal system
    • Pre-hepatic: portal vein obstruction (thrombus, mass)
  40. What are consequences of portal hypertension? (4)
    ascites, hepatomegaly, acquired PSS, gastric ulcers
  41. You tap the abdomen of an animal with abdominal effusion; what conclusion can you draw if the fluid has high protein content? Low protein content?
    • High protein: ascites- intrahepatic obstruction and portal hypertension
    • Low protein: pre-hepatic obstruction and portal hypertension
  42. What mechanisms of liver disease can lead to GI ulceration? (3)
    decreased mucosal blood flow, decreased gastric epithelial turnover (d/t negative nitrogen balance, hypoalbuminemia), +/- increased gastric acid secretion
  43. What are the components of bile? (5)
    bile salts, bilirubin, cholesterol, electrolytes, water, others
  44. What is cholestasis?
    increased amounts of substances (bile acids,bilirubin, cholesterol) in the blood that are normally excreted in bile
  45. What substances are increased in the blood with cholestasis? (3)
    bile acids, bilirubin, cholesterol
  46. What are the different mechanisms of cholestasis? (2)
    extrahepatic (mechanical- gallbladder, common bile duct, main bile duct), intrahepatic (functional)
  47. Briefly describe normal bilirubin metabolism.
    senescent RBCs are sent to the liver through the portal vasculature (unconjugated bili)--> hepatocytes conjugate it (conjugated bili)--> delivered to gallbladder and dumped to intestines through bile duct--> excreted in feces/urine
  48. What is unique about bilirubinemia in horses?
    they get fasting hyperbili- icterus of anorexia
  49. What are the functions of Vit K?
    activation of clotting factors in hepatocytes
  50. Fats and fat-soluble vitamins require _____________ for absorption.
    micelle formation
  51. How does liver disease lead to Vit K deficiency?
    intestinal malabsorption of Vit K because of lack of bile acids for proper micelle formation [cholestatic disorders- mechanical biliary obstruction, severe intrahepatic cholestasis]
  52. What route of administration is essential to treat Vit K deficiency due to biliary obstruction?
    parenteral b/c dietary deficiency is not the problem....the animal can't absorb it from the intestines
  53. If an animal has hyperbilirubinemia, should you test their bile acids?
    No- you already know that bile acid flow is going to be blocked- waste of time and money
Card Set
GI2- Liver 1
vetmed GI2