Liver Diseases Flashcards

1
Q

What breed of cattle is prone to hemochromatosis, and what is that disease?

a. Holstein - excessive iron uptake and storage in hepatocytes –> hepatic failure
b. Saler’s cattle - excessive iron uptake –> hemolysis – > iron accumulation in reticuloendothelial system
c. Holstein - excessive iron uptake –> hemolysis – > iron accumulation in reticuloendothelial system
d. Saler’s cattle - excessive iron uptake and storage in hepatocytes –> hepatic failure

A

d. Saler’s cattle - excessive iron uptake and storage in hepatocytes –> hepatic failure

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2
Q
  • What are the three histologic findings normally found in pyrrolizidine alkaloid toxicosis?
  • What are common toxic plants linked to PA toxicosis?
A
  • Fibrosis (portal to portal)
  • Bile duct proliferation
  • Megalocytosis
  • Crotalaria (SE) - rattlebox
  • Senecio (Western)
  • Fiddleneck
  • Heliotropium
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3
Q

The primary etiologic agent causing hepatic abscesses in feedlot and dairy cattle does not cause which of the following diseases?

  1. Calf diphtheria (laryngeal necrobacillosis
  2. Foot rot
  3. Foot abscesses
  4. Slurry Heel

What is the ethiologic agent? pathophysiology of hepatic abscess?

A

d. Slurry Heel

  • Fusobacterium necrophorum (G neg rod-pleo anaerobe) –> Leukotoxin (cannot cross intact mb)
  • Biotype A –> subs necrophorum –> more virulent (prod more leukotoxin) –> more common in liver abscess
  • Acidosis (chronic) –> rumenitis –> bacterial emboli to portal circulation –> liver –> eventually caudal vena cava thrombosis –> pneumonia
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4
Q

Dietary management of hepatic encephalopathy

A
  • Low protein with a high BCAA/AAA ratio (low protein/high starch)
    • Hepatic metabolism of aromatic aa is reduced → muscle and adipose tissue can metabolize branched-chain aa
    • AAA acts at false neurotransmisser → worsening signs of HE
  • Reduction of intestinal ammonia absorption
    • Neomycin → but nephrotoxic and increase risk for diarrhea, so not recommended > 2 days
    • Lactulose → acidifies intestinal contents → ammonia migrates from the blood to the colon → trapped as ammonium and expelled
    • Metronidazole → caution, it is metabolized in liver
    • Mineral oil
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5
Q

Most common cause of icterus in adult sheep and clinical effect

A

Copper toxicosis

  • Due to excessive Cu in diet : chicken litter, inap mineral mix, orchard pastures

high Cu:Mo/Sulfate ratio

  • Acute form due to injections

Intravasc hemolysis: Heinz body –> hemoglobinuria, ARF

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6
Q

Causative agent of black disease and main lesion in liver

A

Clostridium novyi type B

  • Preceeded by liver fluke migration

Coagulation necrosis of liver –> toxins to circulation –> neurons, vascular endothelium –> Sudden death

  • Black dz because venous congestion of skin
  • No bleeding
  • Gelatinous exudate in fascial planes
  • Pleural, pericardial and peritoneal serosanguineous fluid
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7
Q

Hepatic lipidosis can occur iin both cattle and horses (> ponies), however ruminants rarely develop hypertriglyceridemia and are more prompt to accumulate TG in liver. Why is this different between large animals?

A

Ruminants –> poor ability to export excess lipid from liver as VLDLs –> maybe due to shortage apolipoprotein A (> if low-prot diet regardless of energy balance)

–> TG accumulation in liver because it cannot be transported out

Ponies –> abnormal VLDL1 fraction –> reduce apolipoprotein B100 and increased apolipoprotein B48

–> leads to greater content of TG in VLDL (overproduction of VLDL)

–> Ponies tendency to be insulin-resistant –> LPL unable to bring TG inside adipocyte

Combined with high concentration of TG in blood in the VLDL –> TG accumulation in liver and circulation (and renal –> azotemia)

Ketone body formation pathway not well developed in horses –> FFA not used for E and accumulate as TG

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8
Q

Causative agent of Tyzzer’s disease? Diagnosis?

A

Clostridium piliforme, strains E and R1

Foals 7-40 days

  • Identification in histpath with Warthin-Starry method (silver stain)
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9
Q

What eggs can be misleading on fecal sedimentation testing for liver flukes, and why is is this important?

a. Haemonchus eggs look similar - tells you overall parasite burden
b. Paramphistomum eggs look similar - tells you how much fluke transmission is present, because it is spread by the same snail as F. hepatica
c. Paramphistomum eggs look similar - tells you about drug resistance to flukicides, because the drugs for F. hepatica should kill them too
d. Haemonchus eggs look similar - tells you about drug resistance to flukicides, because the drugs for F. hepatica should kill them too

A

b. Paramphistomum eggs look similar - tells you how much fluke transmission is present, because it is spread by the same snail as F. hepatica

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10
Q

Infectious necrotic hepatitis, Black Disease, is a peracute, highly fatal disease. Which of the following are true?

  1. Most commonly affects sheep in poor/lean condition
  2. Caused by C. novyi strains producing two potential exotoxins: alpha toxin and beta toxin
  3. Cutaneous necrosis caused by the exotoxins leads to its common name of black disease
  4. Diagnosis is only made by a simple gram stain of an impression smear of the margin of liver lesions
A

b. Caused by C. novyi strains producing two potential exotoxins: alpha toxin and beta toxin

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11
Q

Which of the folllowing describes the clinical course of theiler’s disease associated virus?

a. acute onset within 48 hours, fulminant hepatic necrosis, uniformly fatal
b. delayed onset of 4-8 weeks, fulminant hepatic necrosis, uniformly fatal
c. acute onset within 48 hours, majority have hepatitis but some subclinical, many die but some can survive and some are chronic carriers
d. delayed onset of 4-8 weeks, majority have hepatitis but some subclinical, many die but some can survive and some are chronic carriers

A

d. delayed onset of 4-8 weeks, majority have hepatitis but some subclinical, many die but some can survive and some are chronic carriers

  • “serum hepatitis” –> Hx of biologic product given 4-10 weeks prior
  • Centrilobullar-midzonal hepatocellular necrosis
  • “dishrag” aspect
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12
Q

What complication of neonatal isoerythrolysis leads to encephalopathy?

a. iron toxicity from intravascular hemolysis
b. uremia due to renal failure
c. kernicterus due to excessive bilirubin
d. infarctive necrosis due to coagulopathy

A

c. kernicterus due to excessive bilirubin

What is a risk factor for this?

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13
Q

What clinical sign of hepatic failure is mostly seen in ponies?

a. tenesmus
b. ascites
c. pharyngeal-laryngeal paralysis
d. yawning

A

c. pharyngeal-laryngeal paralysis

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14
Q

What is considered the “pathognomonic lesion” in bacillary hemoglobinuria?

A) fibrosis, bile duct proliferation, megalocytosis

B) megalocytosis

C) ischemic hepatic infarct

D) none of the above

A

C) ischemic hepatic infarct

ischemic hepatic infarct = zone of hyperemia at its interface with viable liver tissue due to progressive enlargement of the focus of coagulative necrosis because of bacterial toxins

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15
Q

Common cause of icterus in lambs

A

Yellow lamb disease by C. perfringens type A

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