Liver disease (SA) Flashcards
presentation of hyperbilirubemia
jaundice/icterus
categories of causing of hyperbilirubinameia
Pre-hepatic – Haemoglobin
Hepatic – Liver and intrahepatic Biliary tract
Post-hepatic – Biliary excretion (extrahepatic)
pre-hepatic differentials
haemolytic anaemia:
- acquired: Hypophosphataemia (part of lipid bilayer) or oxidative damage
- genetic defects in Somali, Abyssian. Beagles and Spaniels.
- immune-mediated: IMHA, drugs/toxins
- mechanical injury: DIC, haemangiosarcoma
pre-hepatic diagnostics
Look for evident of haemolytic, then find cause
- anemia (classically macrocyclic, hypo chromic, regenerative)
- blood smear shows spherocytes, auto-agglutination
- serum may look red
- Further tests for specific disease (IMHA)
hepatic differentials or hyperbilrubin
hepatic disease meaning liver cannot process and excrete bilirubin, or compressing the surrounding billiary tree
- infectious (Hepatitis): leptospirosis top ddx, also CAV, FIV, FIP, FeLV
- inflammatory: cholangiohepatitis
- neoplasia - lymphoma, MCT
- toxins - NSAIDs, paracetamol
- degenerative - lipidosis in cats, amyloidosis, cirrhosis
or PROXIMAL biliary disease (still within liver before they travel to duodenum)
- Cholangitis, Cholangiohepatitis
diagnostics for abnormal hepatic function
hepato-cellular damage
- ALT: quite specific to liver. Low cell numbers (Ie chirossis) or focal disease (neoplasia) can present with low ALT though
- AST: Found in liver and muscle. Not very specific
cholestasis
- ALP: concentrated in the biliary tree (but also bone, steroid induced). quite specific. short half life in cats so small elevations more significant. rises slower than ALP
- GGT: less specific and not used much in small animals
In hepatic disease – ALT and ALP likely to rise to a similar degree (Or ALT more)
general diagnostics for liver function
Liver has to lose ~ 70% of function first
- Bilirubin: high as liver not excreting/processing
- Urea: Low values suggest liver isn’t processing protein and ammonia to create urea. Non-specific
- Ammonia: High value suggests liver isn’t removing nitrogenous compound
- Albumin: Produced by liver so low amounts support liver disease
- Clotting factors: ALL produced by liver, so prolonged APTT and OSPT
- Bile acid stimulation test: for liver function and biliary flow. Bile acids should never reach the jugular vein, they should just go from liver, to duodenum, jejunum and then back to the liver via portal circualtion. Could be hepatic or post-hepatic issue.
Markers of hepatoceluar damage
ALT: most specific (small increases significant in cats)
AST: Also increased with muscle inflammation
markers of cholestasis
ALP:: most specific, rises slower gan ALT. Also increased by steroids and bone lesions
GGT: less specific (GI, renal cortex, pancreas)
What is needed to definitive diagnosis for hepatic causes
Biopsy
Risk of bleeding especially if concurrent coagulpathy
post hepatic differentials for hyperbilirubinaemia
Bile duct is no longer transporting bilirubin to be excreted, causing back pressure.
Most likely an obstruction
Intraluminal: Cholelithiasis (stone) Gall Bladder Mucocoele (Border Terriers), Inspissated Bile (dry bile), Gall bladder polyps, Cysts (Cats)
Mural: Cholangitis, cholecystitis, neoplasia
Extra-mural: Consider path of whole tract
- Pancreatic disease, duodenal disease,
post-hepatic diagnostics
- ALP is cholestatic marker so will be released into serum
- Cholesterol excreted in bile so elevated
- Urea, Albumin and Clotting times are usually normal.
Image; Biliary tree, pancreas, duodenum
signs of liver disease
depression
anorexia
weight loss
V/D
Pu/PD
Jaundice
Hepatic encepathlopahty
Ascites
Drug intolerance
Coagulopathy
what cases gi signs
Portal hypertension = adverse effect on GIT
what causes ascites
portal hypertension
and hypoalbuminaea (albumin synthesised in liver)
