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Liver disease Flashcards

(49 cards)

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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?

Study These Flashcards
A

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

21
Q

Neonatal liver abscess Dx?

Study These Flashcards
A

ultrasound!!!

+/- inflammatory leukogram and high liver enzymes

22
Q

Neonatal liver abscess Tx?

Study These Flashcards
A

Antimicrobials

drain umbilical abscess

23
Q

Neonatal liver abscess Px?

Study These Flashcards
A

naval dipping

24
Q

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

Study These Flashcards
A

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

25
Cause of rumen acidosis?
Sudden feed change to high grain diet, feeding little roughage.
26
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.
27
Liver abscess signs? (common signs)
Most subclinical, found at necropsy. | pain, +/- fever, anorexia
28
Liver abscess Dx?
U/S | +/- inflam. leukogram, high liver enzymes
29
Liver abscess Tx?
difficult
30
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 occasionally ```
31
CVCT 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 fatal ```
32
Liver Flukes. PF? Intermediate host? Signs?
Grazing near water. Snails. | Often subclinical, signs occur with heavy loads
33
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 condemnation ```
34
Liver fluke pathogenesis/physiology?
migration in liver> coagulative necrosis tracts> fibrosis Fluke produced proline enzyme to suck blood > anemia
35
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, death ```
36
Liver flukes, clinical pathology?
``` anemia eosinophilia +/- high liver enzymes hypoproteinemia increased globulins ```
37
Liver fluke Dx?
fecal sedimentation most commonly
38
Liver fluke Px?
control snails and environment
39
Liver fluke Tx?
Albendazole
40
Important clostridial pathogen?
Clostridium novyi type B | aka Black Disease
41
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
42
C. novyi clinical signs?
fever, depression, anorexia, lethargy, recumbency | dark skin from venous congestion
43
How to differentiate C. novyi type B and D?
Type D causes hemoglobinuria
44
C. novyi Dx?
difficult b/c of sudden death liver impression smear to see bacteria gross and histologic lesions
45
C. novyi Tx?
Difficult b/c sudden death grave prognosis penicillin
46
C. novyi Px?
Control snails (albendazole) and environment 8-way Clostridial vaccine remove carcasses
47
What is photosensitization?
When liver failure leads to photodynamic agent accumulation in non-pigmented skin, activated by UV light > skin ulceration
48
What causes type 1 photosensitization?
Primary photosensitization Overload of ingesting photodynamic agents. ingesting St. John's Wort, buckwheat, some sulfonamides
49
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

Agricultural Animals (3 decks)

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