Clinical Pathology: Tests for Hepatic, Intestinal and Pancreatic Function Flashcards
Describe basically what markers show for:
1. Hepatocellular injury
2. Cholestasis
3. Hepatocellular function
4. Hepatic portal circulation
- Damage to hepatocytes leading to leakage of enzymes
- Reduced/blocked bile excretion- release of enzymes induced by retained bile
- Decreased production or catabolism of substances
- Decreased extraction of substances absorbed from the GI
What ‘leaky’ liver enzymes?
- ALT- alanine aminotransferase (largely liver-specific)
- AST- aspartate aminotransferase (liver and muscle)
- LDH- Lactic dehydrogenase (liver and muscle)
- ALP- alkaline phosphotase (horses and ruminants)
- GGT- gamma glutamyl transferase (horses and ruminants)
What is the significance of increased leakage enzymed?
Indicative of hepatocellular damage
* Myocyte can cause mild increase in AST, LDH or artefact
Magnitude of increase correlates with degree of hepatocellular damage but not with reversibility of injury
Increases may only be mild in chronic or reduction of hepatocellulas mass
Relatively how long are ‘leaky’ liver enzymes half-life
What is the significance?
Short half-life
* Days in dogs
* Hours in cats
Small increases significant in cats
What enzymes show cholestasis?
ALP- alkaline phosphate
GGT- gamma glutamyltransferase
What are the different forms of ALP?
Isoenzymes- intestinal and non-specific
Isoforms
Liver and Bone
(B-ALP, L-ALP)
What is C-ALP?
Unique to dogs
Induced by corticosteroids
(endogenous and exogenous)
Describe the mechanism for normal bilirubin breakdown
- Sensecent (old) RBC are a source of heme
- Breakdown of heme to bilirubin in macrophages
- Unconjugated bilirubin is transported through the blood to the liver
- Facilitated diffusion by the liver and conjugated with glucuronic acid
- Conjugated bilirubin is actively secreted into the bile and then the intestine
- Intestinal bacteria remove glucuronic acid producing urobillinogen
- Some reabsorbed into portal blood
- Some enterd urobillinogen cycle
- Remainder is transported to the kidney
- Converted to urobilin and excreted giving urine its charactersitic colour
What causes hyperbilirubinaemia?
What are the three types and causes?
Haemolysis
- Pre-hepatic- secondary to haemolysis- anaemia
- Hepatic- cirrhosis, viral hepatitis, drugs, tumours (decreased bilirubin uptake, conjugation and excretion)
- Post hepatic- carcinoma, gall stones
Obstruction of extrahepatic bile duct, often cholestatic enzymes much higher then leakage
How is bilirubin measured?
- Total and conjugated (direct)
- Unconjugated- total- direct
What are the clinical signs of hyperbilirubinaemia?
- Jaundice persists a long time after liver function has returned to normal
What shows low hepatocellular function?
- Decreased uptake and excretion of bilirubin and bile acids- increased unconjugated bilirubin
- Decreased conversion of ammonia to urea- increased ammonia, decreased urea
- Decreased synthesis of metabolites- albumin, cholestrol, glucose
- Decreased synthesis of coagulation proteins- fibrin, platelets
- Decreased immunologic function- increase immunoglobulina, decreased clearance of toxins
How can alterations of hepatic blood flow be identified?
- Decreased uptake and excretion of bile acids (increased)
- Decreased conversion of ammonia to urea (increased)
- Decreased immunologic function
Describe ammonia metabolism
- Produced in the GIT by protein digestion or bacteria metabolism
- Enters liver (portal vein)
- Uptaken by hepatocytes to synthesis urea, aminoacids
- Urea diffuses to sinusoidal blood or bile canaliculi
- Excreted through kidneys or intestine
When is ammonia significantly raised?
Hepatic encephalopathy
Elevated in congenital/acquired portosystemic shunts and liver failure
