Icterus and Hepatic Encephalopathy in the Dog and Cat Flashcards
describe the 3 types of icterus
- pre-hepatic: hemolysis
-conjugation and uptake of bilirubin into liver overwhelmed - hepatic: uptake, conjugation, and excretion of bilirubin in hepatocytes overwhelmed
- post-hepatic: cholestasis
-conjugation, excretion, and uptake back itno liver overwhelmed
describe history, clinical signs, and PE that can give clues to icterus and liver disease
- GI:
-vomiting
-diarrhea
-acholic feces
-melena
-abdominal effusion (ascites, cirrhoses) - neurologic (hepatic encephalopathy)
-personality change
-ptyalism (cats)
-head pressing
-disorientation
-seizures
-stupor - renal/urinary:
-PU/PD
-pollakuria, stranguria, dysuria
-bilirubinuria - hematologic:
-pale MM: anemia from GI hemorrhage, anemia of chronic disease, coagulation disorder, hemolysis
LOTS of things that can somehow relate back to the liver; ICTERUS is the most specific/quickest way to start pointing to liver
describe ddx for icterus
- pre-hepatic/hemolysis:
-immune hemolytic anemia (more common in dogs)
-babesia infection, mycoplasma felid, cytoxzoon
-toxins: onions, lead, copper - hepatic icterus:
-cats:
–suppurative cholangitis
–lymphocytic plasmacytic hepatitis
–hepatic lipidosis
–feline infectious peritonitis
–toxins (acetaminophen, aspirin)
–neoplasia
-dogs:
–acute liver disease (toxins)
–leptospirosis
–chronic hepatitis
–neoplasia
- post-hepatic
-pancreatitis
-neoplasia: liver, duodenum (bile duct empties into duodenum), pancreas
-cholelithiasis: usually secondary to some disease, commonly bacteria that a nidus forms around
-mucocele
how do you differentiate between prehepatic and hepatic icterus?
perform PCV/TS
prehepatic: PCV low (hemolysis), TS normal
hepatic: PCV usually normal, TS can be low if albumin low
how do you differentiate between hepatic and posthepatic icterus?
imaging
ultrasound will identify obstruction of gallbladder and masses or pancreatitis associated with it
describe the workup for hepatic diseases
- CBC, chem, UA
- abd US
- liver function tests
- coagulation tests
- aspirate effusions, cytology
- liver FNA
- FNA and culture of bile
- liver biopsy: histology, culture
describe liver enzymes in small animals
- elevations often seen in small animals, mostly due to reversible damage to hepatocytes
-liver has a huge capacity to regenerate! - ALT: most liver specific enzyme
-AST: also present in muscle and intestines - AP: biliary duct cells
-isoenzymes: cortisol induced (DOGS ONLY), bone, intestines, liver, placenta
describe indications for liver failure on chem profile
seen when the liver’s capacity to regenerate is overwhelmed
-fulminant acute liver failure (toxins), hepatic lipidosis in cats, endstage liver failure in dogs (cirrhosis)
- low albumin
- low cholesterol
- low glucose
- low BUN
describe bile acids, a liver function test
- bile acids are produced in the liver from cholesterol, then undergo enterohepatic circulation
-excreted into gallbladder and bile, enter small intestine, then in ileum are reabsorbed into the portal vein straight back to the liver (= always a circulating pool) - test:
-take a measurement, then give food which should cause gallbladder to contract and push bile acids into small intestine, then reabsorbed into liver
-rate-limiting step: re-uptake of bile acids from blood into hepatocytes
-elevated in liver failure/portosystemic shunt (not reabsorbed by liver)
describe ascites
classified according to protein and cell content
- transudate:
-low oncotic pressure: low albumin
-high hydrostatic pressure: portal hypertension (something blocking portal vein; liver fibrosis) - modified transudate:
-heart failure: right sided - exudate:
-neoplasia
-septic abdomen
-hemoabdomen
describe chronic hepatitis in dogs
- causes:
-copper accumulation
-familial predisposition: doberman, bedlington terrier, cocker spaniel, dalmation, sky terrier, poodle, labrador retriever, GSD, scottish terrier, beagle
-drugs
-infection - lab values:
-ALT and AP elevated
-if cirrhosis is already present: not much liver enzyme elvation!
-albumin and urea decreased
-bile acids and ammonium levels elevated
describe diagnosis and therapy for chronic hepatitis
diagnosis:
biopsies!
-laparotomy vs trucut
-lymphoplasmacellular inflammation and necrosis of the hepatocytes which lie adjacent to the portal tracts
therapy:
1. glucocorticoids: to decrease fibrosis
-taper as soon as clinical sign relief and liver enzymes return to normal
- UDCA
- antioxidants
- copper chelation: if Cu >2000ppm
-penicillamine
-zinc
describe hepatic encephalopathy
- digestion of proteins: NH3 and aromatic AA go directly into the blood without passing through liver first
- exposure of CNS to shunted gut-derived toxins
describe clinical signs of hepatic encephalopathy
- neuro:
-bizarre behavior
-head pressing
-seizures
-intermittent blindness
-cats: ptyalism - urate stone formation:
-dysuria, stranguria, hematuria
-pathogenesis: increased ammonium concentration in blood, decreased ability to convert uric acid to allantoin in liver = more urate excreted in urine
-can be first sign of hepatic insufficiency!! don’t miss!!
list the most important diseases causing hepatic encephalopathy in cats (4) and dogs (3)
cats:
1. acute liver failure (toxic)
2. hepatic lipidosis
3. neoplasia
4. portosystemic shunts
dogs:
1. portosystemic shunts
2. liver failure (acute): toxic, infectious
3. liver failure (chronic): cirrhosis
describe the pathogenesis of hepatic lipidosis
- starvation for any reason causes release of free fatty acids and triglycerides
- FFAs and TGs go to liver, which deals with it in 2 ways:
-make energy directly via oxidation of FFAs, so need to transport lipids into mitochondria, which requires carnithin (only comes from protein), so with no eating protein = decreased transport into mitochondria
-redirect FFAs and TGs to other organisms that need them by packaging into VLDLs that encircle the lipids for soluble transport in blood, but with no proteins coming in, liver cannot make VLDLs
-so FFAs and TGs stuck in liver!
- the only way to resolve this is by feeding the cat protein!!!!!!!!!!!!
describe treatment of portosystemic shunt with hepatic encephalopathy
- medical:
-diet change: low protein diet
-lactulose: metabolized by colonic
bacteria, which then produce acids and ionize ammonia to ammonium which cannot be absorbed so gets lost in feces
-enterally active antibiotics (amoxicillin): to decrease bacteria that produce ammonia
- surgical:
-ligation of shunt: over 1-2 surgeries depending on risk for portal hypertension
-difficult if intrahepatic in large breed dogs
