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Agricultural Animals > Liver disease > Flashcards

Liver disease Flashcards

1
Q

What is the reserve capacity of the liver?

A

Large. 80% damaged before u start to see clinical signs.

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2
Q

TPR values with liver disease are decreased/normal/elevated?

A

Often normal

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3
Q

Clinical signs seen with liver disease?

A 
Depression
Anorexia
Weight loss (chronic)
Abdominal pain
Diarrhea (chronic)
Ascites (portal hypertension)
Photosensitivity
Clotting defects (terminal dz)
Hepatic encephalopathy
Icterus
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4
Q

What is hepatic encephalopathy?

A

Liver disease leading to blindness, head pressing, circling, ataxia, wandering, coma.

Mechanism is unclear
Possibly due to ammonia in brain

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5
Q

Are liver biopsies helpful?

A

Not with focal disease

contraindicated if abscess is suspected and in terminal dz (clotting defects)

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6
Q

Tests for liver function?

A 
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 elevation
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7
Q

what do elevations in AST, SDH, LDH, ALP, and GGT mean?

A

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

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8
Q

What are PA containing plants? Spell PA.

A

Pyrrolizidine Alkaloid

Senecio (tanzy ragwort, common groundsel)

Crotalaria

Fiddleneck

They’re not palatable
toxicity uncommon

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9
Q

Species sensitivities to PA’s?

A

Horses most sensitive
Cattle less sensitive
sheep/goats not sensitive

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10
Q

PA pathogenesis?

A

Pyrrolizidine alkaloid bioactivated to toxic pyrroles in liver. Impacts cell division resulting in megalocytes in chronic liver disease.

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11
Q

PA hallmark lesions?

A

Megalocytosis, hepatic fibrosis, bile duct proliferation

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12
Q

Common way PA occurs?

A

Accidentally mixed into hay

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13
Q

PA toxicity prognosis?

A

Poor, fibrotic areas of liver don’t regenerate

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14
Q

Where is PA toxicity common?

A

common cause of chronic liver dz in PNW

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15
Q

What are mycotoxins?

A

Toxic metabolites produced by a fungus

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16
Q

Give example of a mycotoxin and what it’s produced by

A

Aflatoxin produced by toxigenic Aspergillus

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17
Q

Aflatoxin
contaminates what feed?
pathogenesis/physiology?

A

corn, cottonseed, soybeans

bioactivated in liver to compound that causes hepatocellular necrosis. Also teratogenic and carcinogen.

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18
Q

Drugs that cause hepatotoxicity?

A 
Sulfonamides
Corticosteroids!!!
Aspirin
Macrolide antibiotics
(SCAM drugs) xp
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19
Q

Neonatal liver abscess

A

infection travels up umbilical vein to liver, causes sepsis.

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20
Q

Neonatal liver abscess signs?

A

swollen umbilicus, abdominal pain, +/- fever, anorexia

21
Q

Neonatal liver abscess Dx?

A

ultrasound!!!

+/- inflammatory leukogram and high liver enzymes

22
Q

Neonatal liver abscess Tx?

A

Antimicrobials

drain umbilical abscess

23
Q

Neonatal liver abscess Px?

A

naval dipping

24
Q

Common reason for liver abscess in cattle? What kind of cattle?

A

liver abscess secondary to rumenitis or rumen acidosis, in feedlot and dairy cattle.

25
Q

Cause of rumen acidosis?

A

Sudden feed change to high grain diet, feeding little roughage.

26
Q

Pathogen that commonly causes liver abscesses? and how?

A

Fusobacterium necrophorum.
Normal inhabitant of rumen. Rumenitis leads to compromised rumen wall, bacteria enters blood, travels to liver via portal vein.

27
Q

Liver abscess signs? (common signs)

A

Most subclinical, found at necropsy.

pain, +/- fever, anorexia

28
Q

Liver abscess Dx?

A

U/S

+/- inflam. leukogram, high liver enzymes

29
Q

Liver abscess Tx?

A

difficult

30
Q

Liver abscess sequelae?

A 
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 occasionally
31
Q

CVCT syndrome?

A 
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 fatal
32
Q

Liver Flukes. PF? Intermediate host? Signs?

A

Grazing near water. Snails.

Often subclinical, signs occur with heavy loads

33
Q

Two important liver flukes?

A 
Fasciola hepatica
    sheep: not resistant, acute dz
    cattle: resistant, chronic dz, subclinical
               liver condemnation
Fasciola magna
    sheep: no encapsulation, death
    cattle: fibrotic capsule
               liver condemnation
34
Q

Liver fluke pathogenesis/physiology?

A

migration in liver> coagulative necrosis tracts> fibrosis

Fluke produced proline enzyme to suck blood > anemia

35
Q

Liver fluke signs in cattle and sheep?

A 
cattle: usually subclinical 
in chronic clinical cattle:
      depression reduced rate of gain, 
      weight loss, emaciation, anemia, 
      hypoproteinemia, ascites, death
sheep: acute dz, death
36
Q

Liver flukes, clinical pathology?

A 
anemia
eosinophilia
\+/- high liver enzymes
hypoproteinemia
increased globulins
37
Q

Liver fluke Dx?

A

fecal sedimentation most commonly

38
Q

Liver fluke Px?

A

control snails and environment

39
Q

Liver fluke Tx?

A

Albendazole

40
Q

Important clostridial pathogen?

A

Clostridium novyi type B

aka Black Disease

41
Q

C. novyi type B PF and pathophysiology?

A

parasite migration cause liver damage > create anaerobic condition > C. novyi spores germinate > toxin release > coagulative necrosis and toxemia > endothelial damage > damage

42
Q

C. novyi clinical signs?

A

fever, depression, anorexia, lethargy, recumbency

dark skin from venous congestion

43
Q

How to differentiate C. novyi type B and D?

A

Type D causes hemoglobinuria

44
Q

C. novyi Dx?

A

difficult b/c of sudden death
liver impression smear to see bacteria
gross and histologic lesions

45
Q

C. novyi Tx?

A

Difficult b/c sudden death
grave prognosis

penicillin

46
Q

C. novyi Px?

A

Control snails (albendazole) and environment

8-way Clostridial vaccine

remove carcasses

47
Q

What is photosensitization?

A

When liver failure leads to photodynamic agent accumulation in non-pigmented skin, activated by UV light > skin ulceration

48
Q

What causes type 1 photosensitization?

A

Primary photosensitization
Overload of ingesting photodynamic agents.

ingesting St. John’s Wort, buckwheat, some sulfonamides

49
Q

What’s type III photosensitization?

A

Secondary photosensitization
Diseased liver can’t eliminate phylloerythrin (formed from chlorophyll by bacteria in GI tract) in bile > accumulates > UV activated

Agricultural Animals (3 decks)

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