SA Icterus and Hepatic Encepalopathy Flashcards
What are the 3 forms of icterus?
- Pre-hepatic (conjugation ad uptake of bilirubin -> liver overwhelmed)
- Hepatic (uptake, conjugation and excretion in hepatocytes overwhelmed)
- Post-hepatic (conjugation, excretion and uptake back into liver overwhelmed: CHOLESTASIS)
What IS icterus
Hyperbilirubinaemia
Where does the majority of bilirubin come from?
Senescent erythrocytes
What is newly formed bilirubin bound to? Why? When does it dissociate?
- Albumin
- Insoluble in water until conjugated in liver
- Dissociates before entering hepatocytes
What is bilirubin conjugated with in the liver?
Glucuronic acid
What is the rate limiting step of bile production?
Conjugation of bilirubin with glucuronic acid -> water soluble for excretion in urine
What are the Ddx for pre-hepatic anaemia?
> Haemolysis
- Babesia
- IMHA
- Toxins [Onions, lead, copper]
What history/PE findings indicate liver problems?
> GI - VD+ - Acholic feaces (white, indicates POST-HEPATIC) - Melaena (not sure why but commonly associated) - Ascites (portal hypertension) > Neuro (hepatic encepalopathy) - Personality change - Ptyalism in cats - Head pressing - Disorintation - Seizures - Stupor > Renal/uro - PUPD - Pollakuia (small, freq) - Stranguria (urgency) - Dysuria (difficulty) [ammonium urate crystals] - Billirubinuria > Heamatologic - Pale mms (anaemia due to GI haemorhage/chronic diseas [usually mild]/coagulation disorders/haemolysis)
Why are renal signs seen with liver problems
Build up of ammonium in blood -> formation of ammonium urate stones -> bloackage
What are he Ddx for hepatic icterus in the cat?
> Cat
- Suparative cholangiohepatitis
- Lymphocytic plasmacytic hepatitis
- Hepatic lipidosis (metabolic)
- Feline infectious peritonitis (viral, young cats, systemic disease)
- Toxins (Acetaminophen, aspirin)
- Neoplasiaggyg
What are the Ddx for hepatic icterus in the dog?
> dog
- Acute liver disease (toxins or drugs)
- Leptospirosis (also -> renal failure)
- Chronic hepatitis (may not -> icterus as generally long tem end stage liver failure)
- Neoplasia
What are the Ddx for post-hepatic icterus?
> Dogs and cats
- Pancreatitis -> leakage of enzymes, sever local peritonitis -> blockage of duodenal papilla
- Neoplasia (liver/duodenum/pancreas)
- Cholelithiasis (uncommon, usually 2* to cholangiohepatitis)
How would you differentiate between pre-hepatic and hepatic icterus?
> Bloods
- Pre: PCV low, TP normal
- Hepatic: PCV normal, TP low (if albumen low)
How would you differentiate hepatic and posthepatic icterus?
> Imaging
- Ultrasound/contrast radiographs to rule out post-hepatic
What diagnostics can be used to work up hepatic disease once pre- and post- have been ruled out?
- Heam/biochem/UA
- Liver FUNCTION
- Coagulation tests (esp important prior to biopsy)
- Abdo ultasound
- Aspirate effusion, cytology (ascites)
- Liver FNA
- FNA and culture of bile
- Liver biopsy: histo, culture
What can liver FNA diagnose? What may be needed following this?
- Lymphoma and hepatic lipidosis ONLY
- No other Dx can be made
- Require biopsy
What do raised liver enzymes indicate?
- Damage to liver cells
- Mostly reversible hepatocyte damage
Give 3 liver enzymes that may be used to evaluate liver health. How liver specific are these?
- ALT: liver specific
- AST: also present in muscle, intestine etc.
- AP: Specific to biliary duct cells throughout liver BUT isoenzymes may falsely raise levels (cortisol-induced in dogs, bone, intestine, placenta) -> look to see if AP ^ MORE than other liver enzymes, would indicate biliary duct cells affected.
What findings on routine biochem and heamatology indicate liver failure?
- low albumen
- low cholesterol
- low glucose
- low BUN (blood urea nitrogen)
Which test specifically links to liver function?
Bile acids
- produced in liver from cholesterol and recycled in enterohepatic circulation so SHOULD NOT enter systemic circulation.
- If not re-uptaken into liver hepatocytes, congestion in portal vein -> overflow -> ^ bile acids in systemic circulation
> First measurement fasted, then fed, measured post-prandial.
> indicates liver failure OR pss
Where should bile be present in the GIT?
Released from duodenal papilla
Reuptaken in ileum
What 2 substances are the main causes of hepatic encepalopathy?
- NH3
- Aromatic AAs
> released in digestion of proteins
> neurotoxic
> should be metabolised by liver
> instead shunted to systemic ciculation and able to cross BBB
What are the clinical signs associated with hepatic encepalopathy?
> CNS - Bizarre behaviour - Head pressing - Seizures - Intermitent blindness - Ptyalism in cats > Renal/uro - urate stones -> dysuria, pollakuria, stranguria (^ blood ammonium -> decreased ability to convert uric acid -> allantoin in liver -> more urate excreted in urine)
Give he 4 most common causes of hepatic encepalopthy in cats
- acute liver failure (toxic)
- Hepatic lipidosis
- Neoplasia
- PSS (rare in cats)
Give the 3 most common causes of hepatic encepalopathy in dogs
- PSS
- Liver failure (acute) - toxins, infections
- Liver failure (chronic) - cirrhosis
What is the pathogenesis of hepatic lipidosis in cats?
- Starvation -> release of FFAs and TGs
- Liver would normally B-oxidise or convert to VLDLs to transport in blood BUT starvation means no protein available to carry out either pathway.
- Lipid gets stuck in liver
What protein is required for B oxidation and why?
Carnitin requied to transport lipid into mitochondria
Why are proteins required to transport VLDLs in he circulation?
Otherwise not soluble in blood
How is hepatic lipidosis treated?
Feed protein -> otfen force feed!
Is hepatic lipidosis a 1* or 2* disease?
2*
- somethin else caused starvation initially
