Icterus and Hepatobiliary Specific Diseases: SA Flashcards
describe congenital portosystemic shunts
- congenital vascular anomaly
-abnormal blood vessel between portal system and systemic circulation - blood returning from GI tract shunted away from the liver
-toxins are not cleared, resulting in hepatic encephalopathy
-growth factors do not reach liver = microhepatica - can be within the liver parenchyma (intrahepatic) or outside the liver parenchyma (extrahepatic)
-macro shunts: can see with naked eye
describe signalment and clinical signs of congenital portosystemic shunts
signalment:
-extrahepatic: small and toy breed dogs <1 year of age (yorkie, pug, chi, etc.)
-intrahepatic: large breed dogs, >1 year old (irish wolfhound, goldens, labs)
clin signs:
1. neurologic: hepatic encephalopathy
2. GI: vomiting anorexia, failure to thrive, ptyalism in cats
3. urinary: stranguria, hematuria (some cats present only with this)
4. random clin sign: copper irises in cats (NAVLE loves this fact)
some animals present with no clinical signs
describe diagnosis of congenital PSS
- bloodwork:
-CBC: microcytic, normochromic, non-regenerative anemia, neutrophilia
-chem panel:
–low BUN, hypocolesterolemia, hypoalbuminemia, hypoglycemia
-serum bile acids: elevated
-ammonia: elevated
- definitive diagnosis:
-via diagnostic imaging or visualization in surgery: US, CT angiogram
describe treatment of congenital PSS
- medical:
-treat signs of hep encephalopathy and decrease toxin levels
-lactulose, hepatic support diet (low protein), antibiotics - surgical attenuation:
-definitive tx: results in longer lifespan than med mgmt alone
-ligation vs gradual occlusion device
-for intrahepatic: endovascular coiling is also an option
-outcome: 3-7% have post-ligation seizures, if not 80% are good to excellent outcome
-complications: portal hypertension, bleeding, seizures, development of multiple acquired shunts
describe microvascular dysplasia- portal vein hypoplasia
- small intrahepatic portal vessels and portal endothelial hyperplasia that allows abnormal flow of blood between the portal and systemic circulation
-microshunt = cannot see on imaging or visualize!!! - signalment, clin signs, and bloodwork abnormalities similar to extrahepatic PSS
-may be diagnosed at an older age - diagnosis: liver histopathology
-no shunt visible on diagnostic imaging
-can obtain liver biopsy via open or laparoscopic techniques - treatment: medical management only
- animals may have EHPSS and MVD-PVH at the same time!
-bile acids still high after sx fix PSS
describe acquired PSS
- typically called multiple acquired shunts
- can occur secondary to liver cirrhosis, portal hypertension, or from too rapid closure of a PSS
- clin signs:
-ascites!!!!!
-hepatic encephalopathy - diagnosis:
-abdominal ultrasound
-CT angiogram
-visualization in surgery; typically near left kidney - treatment: medical management only
describe hepatic lipidosis
- excessive lipid mobilization due to anorexia or stress
-leads to deficiencies in dietary methionine, carnitine, and taurine
-can develop low hepatic and RBC glutathione concentrations, vitamin K insufficiency, severe electrolyte imbalances, and thiamine and cobalamin deficiencies - signalment:
-overconditioned cats most common - clinical signs:
-icterus!!
-GI signs: vomiting, ptyalism, ileus
-weakness and/or head/neck ventroflexion due to marked hypokalemia or hypophosphatemia
describe diagnosis of hepatic lipidosis
- blood work abnomalities:
-hyperbilirubinemia
-ALP > ALT
-normal GGT - abdominal ultrasound:
-hyperechoic hepatic parenchyma (due to fatty infiltrates)
-hepatomegaly - liver aspirate cytology:
-fatty infiltrates involving >80% of aspirated hepatocytes - definitive diagnosis based on all 3 tests above
describe treatment of hepatic lipidosis
- FEED
-feeding tube (e-tube) usually required
-but AVOID refeeding syndrome - supportive care:
-vitamin K
-antioxidants
-fluids, K+ supplementation
-treat GI signs: anti-emetic if nauseous/vomiting
-may need to treat for hepatic encephalopathy
describe feline supperative cholangitis/cholagiohepatitis
- most common acquired inflammatory liver disease in cats!!
- cholangitis: inflammation of portal region of liver with infiltration into bile duct epithelium or within the duct lumen
- cholangiohepatitis: inflammation that has extended into periportal areas and surrounding hepatocytes beyond limiting plate
- typically acute onset but can also be chronic
- signalment: young to middle aged adult cats
describe clinical signs of feline supperative cholangitis/cholangiohepatitis
- fever, weight loss, icterus
- may also note hepatomegaly and cranial abdominal pain on pE
- may also have pancreatic and/or SI inflammation resulting in extrahepatic biliary obstruction
-often referred to as triaditis (pancreas, liver, and SI all inflamed)
describe diagnostics for feline supperative cholangitis/cholangiohepatitis
- CBC: leukocytosis with a left shift, anemia
- chem panel: elevations in AST most common followed by elevation in ALT and total bilirubin
-ALP also elevated in some cases - abdominal ultrasonography:
-hepatomegaly
-hyperechoic parenchyma
-may see extrahepatic biliary obstruction - FNA of liver and bile for cytology and culture +/- liver biopsy
describe treatment of feline supperative cholangitis/cholangiohepatitis
- broad spectrum abx: downgrade based on culture results if possible
- supportive care:
-IV fluids
-feeding tube or appetite stimulants
-anti-emetics
-treat coagulopathy if present
describe copper storage hepatopathy
- abnormal copper excretion leads to hepatic copper accumulation
-leads to secondary inflammation and eventually fibrosis and liver dysfunction - signalment:
-bedlington terrier
-labrador retriever
-doberman
-dalmation
-skye terrier
-westies
describe clinical signs and diagnosis of copper storage hepatopathy?
clinical signs:
1. occur late in disease
2. vomiting, diarrhea, anorexia, weight loss
3. may also have hepatic dysfunction: icterus, hepatic encephalopathy, ascites, PU/PD
diagnosis:
1. elevated ALT is susceptible breed
2. copper quantification from liver biopsy: 1 gram needed for testing (NOT histopath, something special)
describe treatment for copper storage hepatopathy
most effective with early diagnosis (before clin signs)
- chelation:
-D-penicillamine - restricted copper diet
- antioxidants/hepatic protectants
- glucocorticoids if inflammation present
- zinc supplementation: only AFTER chelation
describe gallbladder mucocele
- progressive accumulation of yellow to green, thick mucin-laden bile
- accumulates in gallbladder; can extend to cystic duct, common bile duct, and hepatic ducts
- can result in extrahepatic biliary obstruction
- worst case: gallbladder ischemia and necrosis resulting in bile peritonitis/septic bile peritonitis
describe signalment of gallbladder mucocele
- middle to older age dogs
-esp shelties, mini schnauzers, and cocker spaniels
-genetic mutation in the ABCB4 (MDR3) phospholipase flippase transporter - increased risk with endocrinopathies: cushing’s, hypothryoidism, DM
-Addison’s has NOT been linked to this!!
-WILL BE ON EXAM - increased risk with hyperlipidemia or hypercholesteremia
- can occur in cats but more rare than in dogs
describe clinical signs and diagnosis of gallbladder mucocele
clinical signs:
1. range from non (incidental finding) to vomiting, anorexia, and cranial abdominal pain
- if obstructed or ruptured may see icterus
diagnosis: abdominal ultrasound
1. classic kiwi appearance
2. non-gravity dependent sludge within gallbladder
3. evaluate cystic duct and common bile duct for enlargement/obstruction
4. differentiate from gallbladder sludge, which is an incidental finding
describe treatment for gallbladder mucocele
- early surgical intervention (even before clinical signs) may result in decreased mortality and better outcomes
-cholecystectomy = treatment of choice
-flush common bile duct to relieve obstruction (if needed)
-cultures of gallbladder wall and liver taken and abx considered post-op (start abx before even get culture back)
-ursodiol: thin biles to prevent more obstructions elsewhere - if no clinical signs:
-can monitor for signs, risk of developing obstruction/bile peritonitis
-consider starting ursodiol and SAMe
-but if mucocele still rec sx for better outcome! - treat any underlying endocrinopathies
outcomes:
1. mortality rate: up to 20% but lower if no clinical signs prior to cholecystectomy
2. complications: bile leakage/bile peritonitis, persistent obstruction of common bile duct
describe cholelithiasis
- less common in dogs and cats
- most contain calcium carbonate and calcium bilirubinate crystals
- signalment:
-middle to older age dogs and cats
-possible predilection for small breed dogs - clinical signs:
-range from none (incidental finding) to vomiting, anorexia, icterus, and cranial abdominal pain (secondary to biliary obstruction) - diagnosis: abd ultrasound or rads
-can look severe but not need to come out!
describe treatment of cholelithiasis
if not obstructed:
1. broad spectrum abx
2. ursodiol
3. antioxidants/hepatic protectants
if obstructed:
1. cholecystectomy: if stone can be moved back to gallbladder or into duodenum: most common
2. choledochotomy or cholecystoenterostomy more rarely
describe acute liver injury/failure
- often secondary to toxin/drug exposure or infectious agent
-history very important!! - signalment: dogs > cats
- clin signs:
-vague, nonspecific
-GI
-neuro
-urinary
-weakness
-bleeding
-icterus
describe diagnostics and treatment of acute liver injury/liver failure
based on what you think is going on!
diagnostics:
1. bloodwork: elevate liver enzymes
+/- hyperbilirubinemia, elevated PT/PTT, hypoglycemia
2. is suspect leptospirosis: PCR or MAT
treatment: supportive care!
1. IV fluids, dextrose if needed
2. anti-emetics
3. antibiotics is suspect bacteria
4. vitamin K if coagulopathic
5. hepatoprotectants
6. manage hepatic encephalopathy if present
7. gastric absorbant (activated charcoal) if recent toxin exposure suspected/known
describe common toxins and infectious agents of acute liver injury/liver failure
toxins:
1. drugs: acetaminophen, phenobarbitol, azothiaprine, carprofen (dogs), potentiated sulfas (dogs), oral diazepam (cats), methimazole (cats)
2. alfatoxins
3. amanita mushrooms
4. blue-green algae
5. sago palms
6. zylitol
infectious agents:
1. leptospirosis: also causes AKI, tx with doxy or penicillin, core vx available
2. canine adenovirus-1: infectious canine hepatitis, core vaccine, supportive care only
3. many others
