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2. Smith and EIM > Smith 5 - Liver Dz > Flashcards

Smith 5 - Liver Dz Flashcards

1
Q

where does cell division take place

A

Rappaport’s zone 1; portal area

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2
Q

hemorrhage in liver disease

A

failure to synthesize factors:

II, V, VII, IX, X

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3
Q

icterus is seen in

A

acute dz, not chronic

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4
Q

ascites cause

A

portal hypertension

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5
Q

photosensitization

A

phylloerythrin - formed from chlorophyl degredation; should be excreted into bile, but in dz gets carried to skin

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6
Q

hemolytic crisis

A
  • horses only

- increased RBC fragility

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7
Q

SDH

A

elevated in acute disease only

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8
Q

GDH

A

not elevated in chronic dz

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9
Q

LDH

A

acute only

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10
Q

leakage enzymes

A 
AST
SDH
OCT
GDH
LDH
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11
Q

cholestasis enzymes

A

GGT
ALP
– chronic

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12
Q

albumin

A

reduced in chronic dz; half life 14-20 days

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13
Q

indicators of poor prognosis

A 
albumin <2.5g/dL
increased globulin
PT >30% normal
elevated GGT/ALP + SDH/LDH normal to low
fibrosis
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14
Q

most common cause of acute hepatitis in north america

A

theilers dz

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15
Q

equine parvovirus hepatitis

A
  • theilers

- acute necrotizing hepatitis

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16
Q

theilers

A
  • acute hepatic failure
  • blood product administration 1-3 months ago
  • fever absent or rare
  • dishrag liver
  • widespread necrosis, esp centrolibar and midzonal
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17
Q

black disease

A
  • sheep
  • c. novyi type B, alpha and beta toxins
  • fasciola hepatica
  • paracute death, fever, venous congestion under the skin
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18
Q

red water

A
  • bacillary hemoglobinuria
  • c. hemolyticum
  • beta toxin
  • hemoglobinuria
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19
Q

tyzzer’s dz

A
  • 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
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20
Q

EHV-1 dz in foals born

A
  • hepatic, resp, GI dz
  • commonly icteric
  • severe multifocal necrotizing hepatitis, inclusion bodies
  • do NOT have elevated liver enzymes
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21
Q

how can NI cause liver damage

A
  • chronic hepatic hypoxia
  • multiple blood transfusions (iron overload)
  • Tx: give deferoxamine to chelate iron before blood transfusion
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22
Q

iron toxicity in foals

A
  • if iron is given before colostrum
  • hepatic encephalopathy and icterus
  • high ammonia, bilirubin, GGT, ALP, PCV, SDH
  • prolonged PTT and PT
23
Q

PSS in foals

A
  • rare

- CS appear at 2-3 months old

24
Q

PSS in calves

A
  • encephalopathy signs and tenesmus
25
Q

Morgan Foal hepatic failure

A
  • CS appear after weaning; depression and weight loss
  • elevated liver enzymes and ammonia
  • fatal; terminal hemolytic crisis
26
Q

GBED

A

glycogen branching enzyme deficiency

  • fatal autosomal recessive disease of QH
  • cannot store and mobilize glycogen to maintain glucose homeostasis
27
Q

chronic active hepatitis

A
  • progressive, insidious onset
  • GGT and ALP elevated more than others
  • small fibrotic liver
  • diagnosed on biopsy
  • roids or abx, NSAIDs, VitE, pentoxy
28
Q

PA toxicity

A
  • 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
29
Q

Enzymes in PA

A
  • 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

30
Q

most common PA plants

A

senecio and crotalaria species

  • tansy ragwort
  • stinking willow
  • common groundsel
  • rattlebox
31
Q

lantana

A

necrosis and canalicular collapse

32
Q

cottonseed / gossypol

A

necrosis + cardiac lesions

33
Q

alsike clover

A

portal fibrosis + biliary hyperplasia

34
Q

moldy alfalfa

A

biliary hyperplasia, necrosis

35
Q

mycotoxins

A

centrilobar necrosis, biliary hyperplasia, megalocytosis

36
Q

hepatic abscess causes

A
  • fusobacterium necrophorum subs. necrophorum
  • leukotoxin is cytotoxic to PMNs, macrophages hepatocytes, and ruminal epithelial cells
  • 2nd most common is truperella pyogenes
37
Q

hepatic abscesses in cattle

A
  • bacteria enter from a primary site (TRP, rumen wall lesions caused by acidosis)
  • spread through portal vein
  • usually detected at slaughter
  • may embolize - CVCT
38
Q

hepatic abscesses in horses

A
  • Gi disease

- streps, e coli, bacteriodes fragiis, corynebacterium PT, f. necrophorum, peptostrep

39
Q

fat cow syndrome

A
  • 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
40
Q

preg tox

A
  • 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

41
Q

hyperlipemia in ponies

A
  • fatty liver and serum cloudy with lipids
  • triglycerides >500mg/dl
  • overproduction of VLDL
  • severe / life threatening
42
Q

hyperlipidemia in ponies

A
  • mildly elevated TG (100-500mg/dl)
  • clear plasma
  • no evidence of hepatic dysfunction
43
Q

Gilbert’s syndrome

A
  • congenital
  • unconjugated hyperbilirubinemia
  • normal erythrocyte life span
  • failure of unconj bilirubin to cross the liver cells and become conjugated
  • sheep
44
Q

Dubin-johnson syndrome

A
  • failure of conj bilirubin to enter bile canaliculi

- sheep

45
Q

Rift Valley fever

A

enzootic hepatitis

  • acute fever, anorexia, weakness, salivation, D+, and pain
  • hepatomegaly and hemorrhage
  • arthropod spread
46
Q

telangiectasia

A

sawdust livers

- re-brown foci in cattle livers

47
Q

flow-limited drugs

A
  • quickly and efficiently extracted by the liver
  • rate of elimination limited by hepatic blood flow
  • increase dose in patients w liver dz
48
Q

capacity-limited drugs

A
  • slowly extracted by the river
  • elimination is independent of blood flow
  • dependent on hepatocellular uptake and metabolism
49
Q

choledocholithiasis

A

stones in the common bile duct

50
Q

hepatolithiasis

A

stones in the intrahepatic bile ducts above the right and left hepatic ducts

51
Q

CS of choleliths

A
  • 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
52
Q

SAMe

A
  • augments glutathione synthase levels in the hepatocyte
  • stabilizes membrane function
  • modifies cytokine expression
  • inhibits apoptosis
53
Q

pentoxifylline

A

prevents micro thrombosis

2. Smith and EIM (22 decks)

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