Liver disease Flashcards
What is the reserve capacity of the liver?
Large. 80% damaged before u start to see clinical signs.
TPR values with liver disease are decreased/normal/elevated?
Often normal
Clinical signs seen with liver disease?
Depression Anorexia Weight loss (chronic) Abdominal pain Diarrhea (chronic) Ascites (portal hypertension) Photosensitivity Clotting defects (terminal dz) Hepatic encephalopathy Icterus
What is hepatic encephalopathy?
Liver disease leading to blindness, head pressing, circling, ataxia, wandering, coma.
Mechanism is unclear
Possibly due to ammonia in brain
Are liver biopsies helpful?
Not with focal disease
contraindicated if abscess is suspected and in terminal dz (clotting defects)
Tests for liver function?
Total bilirubin (direct and indirect)
* elevated with liver failure
Bile Acids
* elevated with liver damage
* large range of normal in cattle so look
for marked elevationwhat do elevations in AST, SDH, LDH, ALP, and GGT mean?
hepatocellular (leakage):
AST: liver & muscle so check CK
SDH: liver specific
LDH: not liver specific
cholestatic (bile ducts)
ALP - also elevated in growing animals
GGT - also present in colostrum
What are PA containing plants? Spell PA.
Pyrrolizidine Alkaloid
Senecio (tanzy ragwort, common groundsel)
Crotalaria
Fiddleneck
They’re not palatable
toxicity uncommon
Species sensitivities to PA’s?
Horses most sensitive
Cattle less sensitive
sheep/goats not sensitive
PA pathogenesis?
Pyrrolizidine alkaloid bioactivated to toxic pyrroles in liver. Impacts cell division resulting in megalocytes in chronic liver disease.
PA hallmark lesions?
Megalocytosis, hepatic fibrosis, bile duct proliferation
Common way PA occurs?
Accidentally mixed into hay
PA toxicity prognosis?
Poor, fibrotic areas of liver don’t regenerate
Where is PA toxicity common?
common cause of chronic liver dz in PNW
What are mycotoxins?
Toxic metabolites produced by a fungus
Give example of a mycotoxin and what it’s produced by
Aflatoxin produced by toxigenic Aspergillus
Aflatoxin
contaminates what feed?
pathogenesis/physiology?
corn, cottonseed, soybeans
bioactivated in liver to compound that causes hepatocellular necrosis. Also teratogenic and carcinogen.
Drugs that cause hepatotoxicity?
Sulfonamides Corticosteroids!!! Aspirin Macrolide antibiotics (SCAM drugs) xp
Neonatal liver abscess
infection travels up umbilical vein to liver, causes sepsis.
Neonatal liver abscess signs?
swollen umbilicus, abdominal pain, +/- fever, anorexia
Neonatal liver abscess Dx?
ultrasound!!!
+/- inflammatory leukogram and high liver enzymes
Neonatal liver abscess Tx?
Antimicrobials
drain umbilical abscess
Neonatal liver abscess Px?
naval dipping
Common reason for liver abscess in cattle? What kind of cattle?
liver abscess secondary to rumenitis or rumen acidosis, in feedlot and dairy cattle.
Cause of rumen acidosis?
Sudden feed change to high grain diet, feeding little roughage.
Pathogen that commonly causes liver abscesses? and how?
Fusobacterium necrophorum.
Normal inhabitant of rumen. Rumenitis leads to compromised rumen wall, bacteria enters blood, travels to liver via portal vein.
Liver abscess signs? (common signs)
Most subclinical, found at necropsy.
pain, +/- fever, anorexia
Liver abscess Dx?
U/S
+/- inflam. leukogram, high liver enzymes
Liver abscess Tx?
difficult
Liver abscess sequelae?
A. subclinical
B. gradual weight loss/ill-thrift
elevated globulins***
\+/- high enzymes b/c liver good at
walling off abscesses
C. CVCT syndrome
caudal vena cava thrombosis synd.
happens occasionallyCVCT syndrome?
Caudal vena cava thrombosis synd.
occasionally occurs with liver abscess.
1. acute anaphylaxis
abscess rupture into CVC or hepatic
vein>acute shock>rapidly fatal
2. thrombosis of CVC
septic thrombus into CVC
CVC obstruction>liver enlargement>
ascites
3. epistaxis
septic thrombus travels to lung>
erosion into airway>epistaxis, often fatalLiver Flukes. PF? Intermediate host? Signs?
Grazing near water. Snails.
Often subclinical, signs occur with heavy loads
Two important liver flukes?
Fasciola hepatica
sheep: not resistant, acute dz
cattle: resistant, chronic dz, subclinical
liver condemnation
Fasciola magna
sheep: no encapsulation, death
cattle: fibrotic capsule
liver condemnationLiver fluke pathogenesis/physiology?
migration in liver> coagulative necrosis tracts> fibrosis
Fluke produced proline enzyme to suck blood > anemia
Liver fluke signs in cattle and sheep?
cattle: usually subclinical
in chronic clinical cattle:
depression reduced rate of gain,
weight loss, emaciation, anemia,
hypoproteinemia, ascites, death
sheep: acute dz, deathLiver flukes, clinical pathology?
anemia eosinophilia \+/- high liver enzymes hypoproteinemia increased globulins
Liver fluke Dx?
fecal sedimentation most commonly
Liver fluke Px?
control snails and environment
Liver fluke Tx?
Albendazole
Important clostridial pathogen?
Clostridium novyi type B
aka Black Disease
C. novyi type B PF and pathophysiology?
parasite migration cause liver damage > create anaerobic condition > C. novyi spores germinate > toxin release > coagulative necrosis and toxemia > endothelial damage > damage
C. novyi clinical signs?
fever, depression, anorexia, lethargy, recumbency
dark skin from venous congestion
How to differentiate C. novyi type B and D?
Type D causes hemoglobinuria
C. novyi Dx?
difficult b/c of sudden death
liver impression smear to see bacteria
gross and histologic lesions
C. novyi Tx?
Difficult b/c sudden death
grave prognosis
penicillin
C. novyi Px?
Control snails (albendazole) and environment
8-way Clostridial vaccine
remove carcasses
What is photosensitization?
When liver failure leads to photodynamic agent accumulation in non-pigmented skin, activated by UV light > skin ulceration
What causes type 1 photosensitization?
Primary photosensitization
Overload of ingesting photodynamic agents.
ingesting St. John’s Wort, buckwheat, some sulfonamides
What’s type III photosensitization?
Secondary photosensitization
Diseased liver can’t eliminate phylloerythrin (formed from chlorophyll by bacteria in GI tract) in bile > accumulates > UV activated
