LIVER LIVER LIVER Flashcards
What are the three categories of liver disease?
hepatcellular dmg, cholestasis, dec liver fx
(hepatocellular damage)
- see what in SA?
- in LA?
- increased AST, ALT
- increased AST, SDH +/- GGT
(does not indicated cause or reversibility)
(pre-hepatic cholestasis)
- caused by what?
- lab abnormalities?
- increased RBC destruction
- regen anemia, hyperbilirubinemia(uria), possible hemoglobinemia (uria)
usually ALP, GGT WRI if untreated
ALT, AST, SDH may increase secondary to hepatocellular hypoxia
(so no increased prod, but can get dmg if hypoxia)
(intra) hepatic cholestasis
1. caused by what?
in what two forms?
- failure of clearance by liver
liver failure (not enough hepatocyte fx) or functional intrahepatic cholestasis (interference of receptor uptake of bilirubin
(Post-hepatic cholestasis)
- hyperbilirubinemia from what?
- caused by what?
- Lab Changes?
- blocked bile flow
in bile ducts in liver or distal (gall bladder, common bile ducts)
- pressure from tumor/inflammation
blockage in gall bladder (stones, sludging, mucocele)
blockage after bile ducts exit liver (tumors, pancreatitis)
- ^ALP & GGT (less common w/ other cholestasis)
^cholesterol w/ increased time/severity
hyperbilirubinemia/icterus if renal elimination doesn’t keep pace
(Decreased Liver FX)
- will start seeing abnormalities when what percent of liver fx remains?
- Will see decreases in what?
- will see increases in what?
- 30% (has large fx reserve)
- albumin, cholesterol, urea, glucose, USG (impaired urea/water regulation)
- bilirubinemia/uria, PT, PTT, FDPs
- Are liver enzymes helpful in confirming liver failure?
- are low enzymes diagnostically significant?
- NO! (unpredictable)
can elevate with hepatocellular dmg, but sometimes too few to cause increase
- NO!
- Specific diagnosis of decreased liver fx often requires what?
- biopsy
(cytology ok in some - lipidosis, malignancy id)
(histopath often required - inflam liver dz, some cancer)
(common tests of liver function)
- what aren’t used and why?
- What is used?
- albumin, BUN, glucose, cholesterol, USG, PT/PTT
affected by too much
- serum bile acids and blood ammonia
(these are also affected but not as much)
(Bilirubin)
- low levels excreted in normal urine of dog or cat?
- What comes first - uria or emia?
- will you get an increase with renal failure?
- decrease means?
- increase = ?
- in what animal do you see an increase with fasting?
- dog (never normal in cat!)
- uria (always do UA!)
(when renal capacity overcome get emia)
- DOES NOT INCREASE WITH RENAL FAILURE
- not significant
- hemolysis (poss high), cholestasis (high - mild if assoc w/ sepsis/anorexia in horses), dec liver fx (mild)
- horses (12 hrs, may ^5-8X in 2-4 days)
(Bile Acids - Physiology)
- produced in liver from what?
- conjugated/secreted into bile to do what?
- reabsorbed into what?
- extracted by what?
- cholesterol
- ^ fat digestion
- portal circulation
- hepatocytes
(almost complete recycling in health)
- Serum bile acid conc ^ w/ what?
- decreased liver fx and (post)hepatic cholestasis
1-5. See increased serum bile acids due to
6-7. What decreases?
- post-prandial (mild and normal)
- dec liver fx (too few hepatocyte for recovery)
- cholestasis (bile retention –> reflux into circ)
- shunt (from intestine to circ)
- spontaneous gall bladder contraction
- intestine malabsoprtion
- insufficienct liver prod (not seen clinically - would be dead at this point)
(Blood Ammonia)
- produced in intestines how?
- portal to liver -> converted to what?
- Is this test less/more sens that serum bile acids? why?
- by microbial digestion of AA and urea
- urea
- **LESS **(liver has large capacity for detoxifying ammonia)
1-4. What cause hyperammonemia?
- hypoammonemia?
- decreased liver fx (most common)
- ammonia overload from diet (ruminants)
- excessive gut flora prod/compromised gut wall (colic in horses)
- urea cycle enzyme deficiency (rare)
- insignificant
