Smith 5 - Liver Dz Flashcards
where does cell division take place
Rappaport’s zone 1; portal area
hemorrhage in liver disease
failure to synthesize factors:
II, V, VII, IX, X
icterus is seen in
acute dz, not chronic
ascites cause
portal hypertension
photosensitization
phylloerythrin - formed from chlorophyl degredation; should be excreted into bile, but in dz gets carried to skin
hemolytic crisis
- horses only
- increased RBC fragility
SDH
elevated in acute disease only
GDH
not elevated in chronic dz
LDH
acute only
leakage enzymes
AST SDH OCT GDH LDH
cholestasis enzymes
GGT
ALP
– chronic
albumin
reduced in chronic dz; half life 14-20 days
indicators of poor prognosis
albumin <2.5g/dL increased globulin PT >30% normal elevated GGT/ALP + SDH/LDH normal to low fibrosis
most common cause of acute hepatitis in north america
theilers dz
equine parvovirus hepatitis
- theilers
- acute necrotizing hepatitis
theilers
- acute hepatic failure
- blood product administration 1-3 months ago
- fever absent or rare
- dishrag liver
- widespread necrosis, esp centrolibar and midzonal
black disease
- sheep
- c. novyi type B, alpha and beta toxins
- fasciola hepatica
- paracute death, fever, venous congestion under the skin
red water
- bacillary hemoglobinuria
- c. hemolyticum
- beta toxin
- hemoglobinuria
tyzzer’s dz
- clostridium piliforme (E and R1)
- acute hepatitis in foals
- age 7-42 d
- acute to peracute; depression, fever, colic, D+, -> blind, coma, death
- +/- icterus!
- overwhelming sepsis
- hypoglycemia, acidosis
- increased bilirubin, BAs, SHD, GGT, AST, ALP, LDH-5
EHV-1 dz in foals born
- hepatic, resp, GI dz
- commonly icteric
- severe multifocal necrotizing hepatitis, inclusion bodies
- do NOT have elevated liver enzymes
how can NI cause liver damage
- chronic hepatic hypoxia
- multiple blood transfusions (iron overload)
- Tx: give deferoxamine to chelate iron before blood transfusion
iron toxicity in foals
- if iron is given before colostrum
- hepatic encephalopathy and icterus
- high ammonia, bilirubin, GGT, ALP, PCV, SDH
- prolonged PTT and PT
PSS in foals
- rare
- CS appear at 2-3 months old
PSS in calves
- encephalopathy signs and tenesmus
Morgan Foal hepatic failure
- CS appear after weaning; depression and weight loss
- elevated liver enzymes and ammonia
- fatal; terminal hemolytic crisis
GBED
glycogen branching enzyme deficiency
- fatal autosomal recessive disease of QH
- cannot store and mobilize glycogen to maintain glucose homeostasis
chronic active hepatitis
- progressive, insidious onset
- GGT and ALP elevated more than others
- small fibrotic liver
- diagnosed on biopsy
- roids or abx, NSAIDs, VitE, pentoxy
PA toxicity
- liver failure
- PAs are activated to toxic alkaloids (pyrrole) in the liver
- cross link DNA = anti-mitotic effect
- cells die and are replaced with fibrosis
- venous occlusion = portal hypertension = D+ and ascites in ruminants but not horses
Enzymes in PA
- SDH/GDH/LDH may elevate initially but be normal by the time CS develop
- GGT and ALP, BAs very elevated
- proteins usually normal
Fibrosis + bile duct proliferation + megalocytosis
most common PA plants
senecio and crotalaria species
- tansy ragwort
- stinking willow
- common groundsel
- rattlebox
lantana
necrosis and canalicular collapse
cottonseed / gossypol
necrosis + cardiac lesions
alsike clover
portal fibrosis + biliary hyperplasia
moldy alfalfa
biliary hyperplasia, necrosis
mycotoxins
centrilobar necrosis, biliary hyperplasia, megalocytosis
hepatic abscess causes
- fusobacterium necrophorum subs. necrophorum
- leukotoxin is cytotoxic to PMNs, macrophages hepatocytes, and ruminal epithelial cells
- 2nd most common is truperella pyogenes
hepatic abscesses in cattle
- bacteria enter from a primary site (TRP, rumen wall lesions caused by acidosis)
- spread through portal vein
- usually detected at slaughter
- may embolize - CVCT
hepatic abscesses in horses
- Gi disease
- streps, e coli, bacteriodes fragiis, corynebacterium PT, f. necrophorum, peptostrep
fat cow syndrome
- dairy cows post partum
- NEB induced fat mobilization
- depressed / weak / off feed
- elevated OCT, bilirubin, AST, trigly, cholesterol, NEFAs
- fat liver is more hyperechogenic on US
- gold standard is biopsy: classify liposis
preg tox
- ewes and does late gestation (last 2-4wks)
- anorexia, depression, recumbency, neuro signs
- ketonuria
- acidosis, low Ca and K levels
- BHB elevate
Tx: administer glucose and remove the fetuses
hyperlipemia in ponies
- fatty liver and serum cloudy with lipids
- triglycerides >500mg/dl
- overproduction of VLDL
- severe / life threatening
hyperlipidemia in ponies
- mildly elevated TG (100-500mg/dl)
- clear plasma
- no evidence of hepatic dysfunction
Gilbert’s syndrome
- congenital
- unconjugated hyperbilirubinemia
- normal erythrocyte life span
- failure of unconj bilirubin to cross the liver cells and become conjugated
- sheep
Dubin-johnson syndrome
- failure of conj bilirubin to enter bile canaliculi
- sheep
Rift Valley fever
enzootic hepatitis
- acute fever, anorexia, weakness, salivation, D+, and pain
- hepatomegaly and hemorrhage
- arthropod spread
telangiectasia
sawdust livers
- re-brown foci in cattle livers
flow-limited drugs
- quickly and efficiently extracted by the liver
- rate of elimination limited by hepatic blood flow
- increase dose in patients w liver dz
capacity-limited drugs
- slowly extracted by the river
- elimination is independent of blood flow
- dependent on hepatocellular uptake and metabolism
choledocholithiasis
stones in the common bile duct
hepatolithiasis
stones in the intrahepatic bile ducts above the right and left hepatic ducts
CS of choleliths
- recurrent abdominal pain, intermittent pyrexia, and icterus
- increased liver enzymes, BAs, bilirubin, glob and fibrinogen
- parallel channel sign (dilated inter hepatic biliary radicals adjacent to portal vein) on US
SAMe
- augments glutathione synthase levels in the hepatocyte
- stabilizes membrane function
- modifies cytokine expression
- inhibits apoptosis
pentoxifylline
prevents micro thrombosis
