Final Exam - FA Hepatobiliary Disease Flashcards
what animals don’t have gallbladders?
horses & camelids
if you have an increase in unconjugated bilirubin, what does that indicate?
decreased hepatic function
T/F: increased liver enzymes don’t equate to liver failure
true - liver failure can exist with normal enzyme levels especially if you only have cellular enzymes on chemistry
T/F: early liver disease is easy to detect & diagnose in food animals
false - often inapparent to owner & vet
what are some clinical signs of liver disease in production animals?
lethargy, anorexia, weight loss, ‘poor doer’
jaundice, photosensitivity, hepatic encephalopathy (abnormal mentation, vocalization, circling, head pressing), coagulopathies, & hemolysis
what is your biggest diagnostic test for liver disease in production animals?
chemistry panel
what are the benefits of using an ultrasound for suspected liver disease in production animals?
structural disease especially on the right - tumors or abscesses & it is non-invasive
not great for toxic/metabolic/infectious causes
what are the benefits of a liver biopsy for liver disease in production animals?
definitive diagnosis & prognostic capabilities, sample of choice for most assessments, & ruminants are relatively easy/safe to biopsy
what vaccine should you give prior to a liver biopsy in a ruminant?
clostridial +/- penicillin
what are the most common agents involved in liver abscesses?
fusobacterium necrophorum & truepurella pyogenes
other than the most common agents, what can be another cause of liver abscess?
traumatic reticuloperitonitis - especially in dairy cows
liver abscesses are most common in what animals?
cattle on a high grain diet - dairy cattle, feedlot cattle, & show cattle
what is the pathogenesis of liver abscesses in production animals on a high grain diet?
chronic rumen acidosis damages the rumen mucosa - bacterial translocation into portal circulation - infiltration into the liver
what is the best antemortem diagnostic for liver abscesses?
ultrasound
what is the treatment for liver abscesses in food animals?
prolonged antimicrobials (macrolide or penicillin) for valuable animals or cull
how can we prevent liver abscesses?
gradual adaptation to diet to prevent acidosis, feed additives (tylosin), increase roughage
what are the clinical signs of liver abscesses in production animals?
generally subclinical with normal lab values - may have elevated globulins from long standing inflammation
what is a major complication associated with liver abscesses? what is the pathogenesis of it?
vena cava thrombosis syndrome
liver abscess erodes into vena cava & it seeds the lungs (embolic/metastatic pneumonia) - animal may present as respiratory disease
foci in pulmonary vasculature can erode through vessel walls causing hemorrhage into lumen of alveoli/smaller air passages - death
what animals are more susceptible to flukes than cattle?
sheep, goats, camelids
where do flukes thrive?
warm, wet conditions
what is the intermediate host of flukes?
snails
what is the most common liver fluke in this region?
fasciola hepatica - flukes mature & become encapsulated in the liver
what are the clinical signs of flukes dependent on?
worm burden
what are some effects of flukes on production?
negligible at < 10 flukes per animal
possible at 10-40 flukes per animal
probable at > 40 flukes per animal
clinical disease at > 200 flukes
what are some clinical signs associated with fascioliasis?
decreased productivity, weight loss, ill-thrift, anemia, bottle jaw/edema, hypoproteinemia
exacerbated by periods of nutritional stress
what is the clinical pathology associated with liver flukes?
increased GGT, ALP due to biliary obstruction or changes
hypoproteinemia, anemia, +/- mild eosinophilia
how are liver flukes diagnosed?
fecal sediment, clinical signs, necropsy
selecting 10-15 random animals from a herd is a decent diagnostic
what is the treatment for liver flukes?
albendazole for adults & clorsulon for immature flukes
how can liver flukes be prevented?
deworm in the fall after the infection period & optional spring deworming for heavily affected herds
what agent causes redwater disease?
clostridium haemolyticum - clostridium novyi type D
what is the pathogenesis of redwater disease?
liver damage (caused by fluke migration) creates anaerobic environment for clostridial spores - spores produce beta toxin causing hepatocyte necrosis, intravascular hemolysis, & damage to the endothelium systemically - hemolytic anemia leads to hemoglobinuria
when are redwater outbreaks seen?
occur after flooding or otherwise seasonal following fluke migration
what is another name for redwater?
bacillary hemoglobinuria
what are the clinical signs associated with redwater?
sudden death most common - hemoglobinuria, icterus, weakness, ataxia, anemia
how is redwater diagnosed?
necropsy - liver infarct with hyperemic zone bordering normal liver, gram stain, fluorescent antibody test, & pcr for organism
what is the treatment & prevention of redwater?
treatment is unrewarding - maybe high doses of penicillin
fluke prevention & vaccination for clostridium novyi type D
what is another name for black disease?
infectious necrotic hepatitis
what is the agent that causes black disease?
clostridium novyi type B
what animals are most commonly affected by black disease?
sheep - other ruminants & horses
what exotoxins are produced in black disease?
alpha & beta toxin
what is the pathogenesis of black disease?
same as red water - flukes cause damage & allow for proliferation
what are the clinical signs of black disease?
sudden death - may see fever, lethargy
how is black disease diagnosed?
clinical signs & necropsy - skin blackened from venous congestion/capillary rupture, pale areas of coagulative hepatic necrosis
need combo of history, clinical signs, necropsy findings, & pathogen isolation from liver
what is the treatment & prevent for black disease?
treatment is unrewarding - vaccinate for clostridials & have good fluke control
what plant is this? what does it cause?
fiddleneck (pyrrolizidine alkaloid) - photosensitization
what are the clinical signs associated with pyrrolizidine alkaloid toxicosis?
delayed signs - usually in liver failure at time of presentation
how is pyrrolizidine alkaloid toxicosis diagnosed?
liver biopsy & necropsy
what 3 major changes are seen on necropsy of an animal with pyrrolizidine alkaloid toxicosis?
megalocytosis, bridging fibrosis, & biliary hyperplasia
what is the toxin produced from blue-green algae?
cyanobacteria that produces hepatotoxic microcystins
when is blue-green algae usually a problem?
warm months when water temperatures are higher & the water is stagnant
what clinical signs are associated with blue-green algae toxicosis?
acute mortality event in herds - severe hepatocellular damage leading to hypovolemia & shock due to blood loss
nervousness, reluctance to move, recumbency, diarrhea, & pale mucus membranes
what may be seen on diagnostics for an animal with suspected blue green algae toxicosis?
increased GGT, AST, bile acids, & ALP with hypoglycemia & hyperkalemia
what is the treatment for blue green algae toxicosis?
unrewarding
what is hepatic lipidosis?
fat animal that abruptly experiences a negative energy balance - body mobilizes fat stores which go to the liver & overwhelm its capacity to the point of compromising function
lactation - fat dairy cows
gestation - fat beef heifer
fat goats with pregnancy toxemia
what are some clinical signs of hepatic lipidosis?
anorexia, lethargy, decreased milk production
how is hepatic lipidosis diagnosed in production animals?
ultrasound, biopsy, FNA
how do you treat hepatic lipidosis in production animals?
get them out of a negative energy balance - palatable foods, IV dextrose
how is hepatic lipidosis prevented?
don’t let animals become overconditioned prior to calving
identify & treat/prevent comorbidities
what disease causes this appearance?
red water disease
