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Ruminant Medicine Spring 2016 > L4: Ruminant Liver Disease (Reuss) > Flashcards

L4: Ruminant Liver Disease (Reuss) Flashcards

1
Q

What lab values are measured for liver function?

A 
GGT
SDH
ALP
AST
LDH
Bilirubin (can indicate cholestasis vs. hepatocellular dz; >0.5 = cholestasis)
Bile acids
Ammonia
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2
Q

Where is liver located on ultrasound? What does it look like?

A

Right ICS 6-12, sharp borders

GB right ICS 9-11, thin walled, round, anechoic

Portal vein round, CVC triangular.

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3
Q

Parallel channel sign

A

Distended bile ducts parallel to portal veins

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4
Q

CS of liver dysfunction

A

-portal hypertension, lymphatic leakage, hypoalbuminemia –> ascites

  • portal hypertension –> diarrhea
  • release of septic emboli from liver abscesses –> caudal vena cava syndrome/massive pulmonary hemorrhage
  • loss of factors 2,5,7,9,10 –> hemorrhage
  • photosensitization
  • hepatic encephalopathy
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5
Q

Hepatic encephalopathy

A
  • char. By behavior change, ataxia, circling, stupor, tenesmus, bellowing
  • can cause rectal prolapse
  • pathophys: caused by increasing ammonia, glutamine, serum auromatic amino acids, GABA tone
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6
Q

Fasciola hepatica

A
  • liver flukes from ingesting metacercariae on grass
  • snails IH
  • killed by drought, freeze, sustained heat
  • SR most susceptible
  • can be fatal/acute, subacute, or chronic depending on burden
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7
Q

Subclinical effects of Fasciola hepatica

A
  • reduced gain/efficiency
  • liver condemnation
  • increased with periods of nutritional stress/nematode burdens
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8
Q

CS of fasciola hepatica

A
  • weight loss, rough coat, ascites, edema, icterus
  • hypoproteinemia
  • biliary hyperplasia
  • proline-depression anemia
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9
Q

Pathology of fasciola hepatica

A

-tunnels of coagulative necrosis
-fibrosis (esp. Ventral)
+/- bile duct changes (cholangiohepatitis, calcification of bile ducts, discolored bile) if it’s been 6-8 wks since ingestion

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10
Q

Dx of fasciola hepatica

A
  • Fecal sedimentation (only detects eggs from adults)
  • ELISA 2 wks post infection
  • inc. GGT, eosinophilia, anemia, hypoalbuminemia
  • U/S, cholecystocentesis (look for fluke eggs in the bile)
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11
Q

Fascioloides magna

A

-liver fluke found in great lakes, NW, gulf coast
-cattle = dead end hosts
-SR = aberrant hosts
-deer, elk = DH
-

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12
Q

Pathology of Fasciola magna in CATTLE

A

Encapsulate in liver –> closed cysts –> carcass condemnation

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13
Q

Path. Of Fascioloides magna in SR

A

Continual migration –> extensive tissue damage

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14
Q

Liver fluke tx

A
  • Clorsulon for juveniles
  • Albendazole for adults and F. Magna
  • prevent snail infection by removing adults about 2 mos. after end of transmission season
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15
Q

Fat cow syndrome

A

Overconditioned periparturient dairy cows within 1-2 wks of calving at risk for hepatic lipidosis

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16
Q

Pathophys. Of hepatic lipidosis

A

1) Inc. FFA mobilization –> NEFAs
2) Liver extracts NEFAs and can only release once reesterified into triglycerides
3) TG production overwhelms ability to package into VLDLs, and TG is deposited in liver
4) insulin resistance perpetuates

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17
Q

Dx of hepatic lipidosis

A
  • NEFAs >1000 for lactating, >350 for peripartum
  • AST >100 (unreliable)
  • ketonuria
  • U/S
  • Liver biopsy (floats?)
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18
Q

Tx of hepatic lipidosis

A
  • positive energy balance
  • IV dextrose, insulin
  • propylene glycol
  • force feeding, transfaunation
  • steroids short-term
  • Vit. E, selenium, glucagon
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19
Q

Pyrrolidizine alkaloid toxicity due to what plants?

A

Senecio
Crotalaria
Heliotropium

Cattle 30x more sensitive than SR

20
Q

Pyrrolidizine alkaloid toxicity pathogenesis

A

Pyrroles (alkylating agents) –> cross link DNA, have anti-mitotic effect, megalocytes can’t divide, fibrosis, veno-occlusive disease, portal hypertension

-Chronic progressive intoxication

21
Q

CS of PA toxicity

A
  • d
  • wt. loss
  • tenesmus, rectal prolapse
  • ascites
  • photosensitization
  • hepatic encephalopathy
22
Q

Dx of PA toxicity

A
  • increased GGT, ALP, bile acids

- liver biopsy (see fibrosis, bile duct proliferation, megalocytosis)

23
Q

Tx of PA toxicity

A
  • no cure

- low protein high energy diet

24
Q

Aflatoxins

A
  • produced by fungi
  • inhibit protein synthesis
  • cause dec. feed efficiency –> hepatic failure –> hemorrhage, death as dose increases
  • carcinogenic to people
25
Q

GGT comes from what tissues

A

Liver
Mammary tissue
Pancreas

26
Q

Infectious Necrotic Hepatitis aka

A

“Black Disease”

  • caused by Clostridium novyi type B
  • ALPHA toxin
27
Q

Pathophys of Infectious Necrotic Hepatitis/Black Disease

A
  • requires pre-existing liver disease (ie. Liver flukes to create anaerobic env. For sporulation)
  • causes rapid putrefaction, hemorrhage of SC blood vessels, serosanguinous effusion, coagulative necrosis in the liever
28
Q

CS of Infectious Necrotic Hepatitis/Black Disease

A

-sudden death during fluke season
-fever, hypothermia, recumbency, death within hrs
(5-50% morbidity)
-affects well nourished adult sheep

29
Q

Dx of Infectious Necrotic Hepatitis/Black Water

A

Gram stain
Culture
Fluorescent Ab
Toxin ID

30
Q

Cause of Bacillary Hemoglobinuria/”Redwater”

A

Clostridium novyi type D

-BETA toxin

31
Q

Pathophys of Redwater

A
  • causes hepatic necrosis, hemolysis, hemorrhage, endothelial damage
  • requires anaerobic liver damage
  • can be carried in decomposing carcasses, carrier animals
  • follows flooding
  • affects well conditioned animals >1 yr in poorly drained pastures
  • 95% mortality!
32
Q

CS of Bacillary Hemoglobinuria/Redwater

A
  • sudden death
  • fever, arched back, separation from herd
  • tachycardia/pnea, agalactia, constipation, diarrhea
  • hemolysis –> icterus, hemoglobinuria
33
Q

Dx/necropsy of Bacillary Hemoglobinuria/Redwater

A
  • ischemic hepatic infarct
  • rapid putrefaction
  • SC and pulmonary edema
  • petechia/ecchymosis

Dx: Gram stain, culture, fluorescent Ab, toxin ID

34
Q

Tx/Prevention of Clostridium novyi

A

Tx rarely possible

  • penicillin, tetracycline
  • antitoxin

Prevent: multivalent vaccines, fluke control, remove carcasses

35
Q

Incidence of hepatic abscesses on feedlots

A

1-95% (2ary to high grain diets)

36
Q

Etiology of hepatic abscesses

A
  • polymicrobial anaerobes
  • Fusobacterium most common in cattle (normal in rumen)
  • Arcanobacterium (normal in rumen wall)
  • SR: Corynebacterium pseudotuberculosis most common
  • leading cause of liver condemnation*
37
Q

Pathophys of hepatic abscesses

A

1) Portal vein: Rumenitis-liver abscess complex:
- high grain diet –> rumenitis –> colonization of rumen wall –> portal circulation

2) Umbilical vein
3) hepatic a. (Requires primary source of bacteremia)
4) bile duct
5) direct extension (ie. Trauma to wall of liver)

38
Q

CS of hepatic abscesses

A
  • none, or wt. loss/poor production
  • CVC thrombosis syndrome: extension of abscess to CVC –> thrombus, septic emboli –> pulmonary embolus, pneumonia, endocarditis, hemoptysis, epistaxis
39
Q

Dx/Tx of hepatic abscesses

A
  • U/S
  • Necropsy

Tx: penicillin, macrolides; full recovery unlikely

40
Q

Prevention of hepatic abscesses

A
  • prophylactic abx (ie. Tylosin*)
  • vaccine
  • prevent ruminal acidosis
41
Q

Which ruminants most prone to Cu toxicosis?

A

Sheep&raquo_space; goats > cattle

42
Q

Etiology of Cu Toxicosis

A
  • eating horse/cattle feeds
  • drinking foot baths
  • fluke damage, PA toxicity predisposes
43
Q

CS of Cu Toxicosis

A
  • none in accumulation stage
  • stress –> large release –> hemolytic crisis
  • weakness, d, coli
44
Q

Dx of Cu Toxicosis

A
  • anemia, hyperbilirubinemia, azotemia
  • hemoglobinuria w/ isosthenuria
  • Inc. Cu lvls in serum, liver, kidneys
  • “Gunmetal kidney” on necropsy w/ centrilobular necrosis, fibrosis, bile duct hyperplasia
45
Q

Tx of Cu Toxicosis

A
  • fluids
  • blood transfusion
  • increase urinary Cu excretion with D-penicillamine or ammonium tetrathiomolybdate
  • tx flock with ammonium molybdate, Na thiosulfate
  • minimize stress

Ruminant Medicine Spring 2016 (18 decks)

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