Hepatobiliary 1 Flashcards
when loss of 60-80% functional hepatic tissue occurs, ___________ results
hepatic failure
(occurs late in disease)
what are at least 5 signs of hepatic failure
decreased appetite, vomiting, lethargy, weight loss, icterus, hepatic encelopathy, abdominal effusion and/or pain, micro hepatica or hepatomegaly, fever (if infectious or bile peritonitis)
name bloodwork findings for: pre-hepatic disease
pale and icteric
anemia
name bloodwork and US findings for: hepatic disease
normal PCVC, elevated liver enzymes (ALT due to hepatocellular injury), no evidence of post-hepatic obstruction on US
name bloodwork and US findings for: post-hepatic disease
normal PCV, elevated liver enzymes (ALP, bili, GGT (cholestatic indicators)
post-hepatic obstruction on US
what is hepatic encelopathy?
NEUROLOGICAL signs arising from liver dysfunction due to accumulation of toxic byproducts (proposed toxins include AMMONIA , aromatic AAs, false NTs); the toxins accumulate due to altered hepatic clearance and metabolism
hepatic enceloppathy common therapies target decreasing _____ concentrations
ammonia
cat presents with intermittent signs of confusion, dull behaviour, head pressing, seizures and hypersalivation; these seem to be associated around mealtimes. what is your suspicion based on these C/S?
hepatic encelopathy
(mild presentation; acute severe presentation would be coma, recumbency, death)
note cats hyper salivate, not dogs
what are 3 most common HE-associated conditions in cats?
diversion of portal blood flow (congenital shunting), fulminant acute hepatic necrosis, and hepatic lipidosis
what are 3 most common HE-associated conditions in dogs?
diversion of portal blood flow (congenital shunting), fulminant acute hepatic necrosis, and reduction in hepatic mass with diversion of portal flow (acquired shunting)
how is HE treated
- Abx: neomycin, metronidazole, amoxicillin
- lactulose to trap ammonia, PO or PR
- reduced protein diet, as much protein as tolerated
- if severely affected patients: hospitalize, decrease colonic bacteria with cleansing enemas
HE treatment: what 2 things are not synthesized as much with HE
serum proteins (albumin, tpt proteins) and glycogen storage/glucose synthesis are decreased in advanced hepatic disease
ethologies of ascites
main: portal hypertension -> collagen deposition -> disorganization of parenchyma and interruption of vasculature -> increased hydrostatic pressure and acquired shunts
minor: hypoalbiminemia
note, not commonly seen in liver disease cats
fat cat was left several days without food and now is vomiting, inappetent, lethargic, dehydrated, icteric, and has palpable liver margins. what is wrong
likely hepatic lipidosis
what bloodwork and urine findings would you expect with hepatic lipidosis
bili, ALP increased, ALT moderate increase, but GGT NORMAL (or mild increase)
bilurubinuria
high albumin (dehydrated)
no inflammatory leukogram, no elevated globulins, and no fever
cat AUS shows hyper echoic parenchyma and hepatomegaly. cytologyy shows >80% of hepatocytes infiltrated with lipid. what is going on? do you need a biopsy to confirm
supportive dx for hepatic lipidosis. often is a presumptive dx based on lab findings, +/- cytology, and response to tx
don’‘t biopsy. liver is fragile and can bleed
tx for hepatic lipidosis
food!!!!: high calorie high protein, not protein restricted
start at 25 RER then increase daily to full RER
NE then esophageal or gastric tube (coat testing prior, via K)
fluid therapy with normosol, .9% saline, or plasmalyte A; monitor for hypophos and hypokalemia
antiemetics (Cerenia, metoclopramide which is also pro kinetic)
secondary therapies for tx of hepatic lipidosis
Sam-e, ursodiol, carnitine, taurine; most important is tx of primary dz if identified
liver disease in cats: what are 3 components of triaditis
cholangitis, pancreatitis, inflammatory bowel dz
what is neutrophilic cholangitis
neutrophils in bile duct lumen and epithelium; can extend into parenchyma; due to ascending infection from GIT? ; can be classified as acute or chronic
compare and contrast neutrophilic and lymphocytic cholangitis: signalment and history
neutrophilic: middle aged to older cats, typically acute presentation
lymphocytic: young cats mostly, Persian breed
compare and contrast neutrophilic and lymphocytic cholangitis: C/S and clin path findings
neutrophilic: febrile, anorexia, lethargy, pyrexia, icteric, vomiting
neutrophilic leukocytosis, elevated hepatic enzymes
lymphocytic: icterus, afebrile, hyperglobulinemia, elevated liver enzymes and bilirubin, +/- ascites and enlarged mesenteric LNs, abdominal distension possible, abdominal fluid is often yellow tinged with high protein content
what is required for definitive diagnosis of neutrophilic or lymphocytic cholangitis
liver biopsy cuture and histopath
also you should do HI and pancreas histopath plus bile cytology and culture bc liver sample will take awhile to process
how to treat neutrophilic cholangitis
Abx based on C&S; Clavamox good initially, 6-8 weeks
fluids and antiemetics
hepatic support: ursodiol, same-E
enteral nutrition if anorexic
what is etiology of lymphocytic cholangitis
unknown, immune mechanism suspected
how to treat lymphocytic cholangitis
corticosteroids: prednisolone 1-2 mg/kg q12h PO; taper to LED
supportive care: ursodiol, sam-e, enteral nutrition if anorexic
you perform PE, CBC chem, urinalysis due to suspicion of hepatic lipidosis. findings are supportive. are you considering any other additional tests?
PT/PTT - need to perform clotting tests prior to a biopsy
FeLk/FIV in case of contact w other cats
AUS for comorbidities and to assess liver
what is the most common hepatobiliary congenital anomaly
portosystemic shunt (this is direct venous communication between portal vein and systemic circulation, ie. bypassing liver)
describe typical signalment of PSS
1-2 years, any breed dog: small breed yorkies, Maltese, cairn terrier, pug, extrahepatic most common; large breed intrahepatic most common; cats less common, get extrahepatic
young dog growing poorly, poor recovery under anesthesia, PUPD, HE, and (30% have) urinary tract signs. blood: microcytosis, hypoalbuminemia, low BUN, ALT and ALP (may have) mildly elevated. what might be going on?
PSS
what are UA findings with PSS
low. USG: over 50% hyposthenuric or isisthenuric
ammonium bitrate crystals: 50% dogs, 15% cats
besides bloodwork, UA, what are other diagnostic findings with PSS
increased ammonia levels: Se but not done in clinical practice
increase bile acids: Se
abdominal rads: micro hepatica common, bilateral renomegaly,ammonium bitrate calculi but these don’t show on rads
how is definitive dx of PSS made
US, direct visualization, CT are preferred
what are some concurrent defects that occur w PSS
cryptorchid
heart our jr
Cu colorez irises cats
prior to definitive sx therapy, what do you need to do for PSS patients
stabilize them
treat HE
pre-op anti-epileptic meds may be recommended
what is portal vein hypoplasia
microscopic anomaly of portal veins; abnormal connections between portal veins and systemic circulation at microscopic level; con occur concurrently with PSS
what breeds are predisposed to macroscopic shunts
same as with PSS (Maltese, Pug, small breed Yorkies, Cairn Terrier); latter 2 overrepresented
what are the 2 clin pres of PVH
asymptomatic
symptomatic: C/S develop later in life than PSS; mild GI signs or signs of HE possible; will be milder than with PSS
what is tx for PVH
supportive: treat HE if present; consider hepatic supportive therapies (Same-e)
rule out other vascular abnormalities; may have concurrent PSS
no sx therapy
