Copper Flashcards

1
Q

What is the importance of copper and why is there toxicity concern?

A

an essential element

range of toxicity is small

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2
Q

What other elements besides Mo does Cu interact with?

A

Zn, Fe, Se

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3
Q

What are sources of Cu poisoning?

A
excess supplmentation
improper Cu/Mo ratio in feed
sprays for parasites/fungi
foot dips
plants
algal treatments
mining operations
genetic predisposition
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4
Q

Which animals are more susceptible to Cu?

A

ruminants
sheep, llama and alpacas are 10x more than cattle (alpacas/llamas dont develop hemolytic crisis)

bedlington terriers (autosomal reccesive)

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5
Q

What is the unique feature to sheep and Cu levels?

A

more susceptible to toxicity but more resistant to deficiency than cattle

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6
Q

Why are pigs unique with Cu toxicity?

A

they metabolize completely different

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7
Q

What is the absorption/distribution?

A

well absorbed (depends on interaction with other metals)

Cu binds to albumin and cerulopaslmin, oxidase enzyme or metallothionein in plasma

storage in liver

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8
Q

What is the excretion?

A

in feces
biliary is limited but crucial for homeostasis

biliary excretion is absent in bedlington terriers (result in chronic Cu poisoning)

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9
Q

What is the pathogenicity of acute toxicity?

A

high levels Cu = protein coagulant
= severe gastroenteritis

Primary syndrome

levels slowly rise in liver (blood still normal until final stages)
Cu has oxidative properties so when it builds up = lipid peroxidation.

antioxidants are depleted

hemoglobin is oxidized to methemoglobin = hemolysis

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10
Q

what is the pathogenicity of chronic toxicity?

A

secondary

- from mineral imbalances in the liver

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11
Q

what are the two types of chronic Cu poisoning?

A

phytogenous chronic
- dietary Cu is normal but low Mo = excessive Cu accumulation in liver (no liver damage)

hepatogenous chronic
- ingestion of plants that cause liver damage (scenico)
= bile excertion impaired = Cu poisoning

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12
Q

What are the clinical signs of acute poisoning?

A

death in 24h
mostly GI
- abdominal pain, nausea, vomiting, salivation, shock, feces (green)

liver
- milk jaundice sometimes

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13
Q

What are the PM findings of acute poisoning?

A

gastroenteritis
erosion and ulceration of abumasum
congestion of other organs
possible centrilobular necrosis and enlargement of the liver

methemoglobin not usually present

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14
Q

What are the clinical signs of chronic poisoning?

A

many months for symptoms to develop (high mortality)
hemolysis = no treatment (rapid)

hemolysis
- hemoglobinuria, hemoglobinemia, methemoglobinemia

liver
- jaundice, elevated liver enzymes (24h prior)

GIT

  • generally normal
  • anorexia maybe before crisis

locomotor
- weakness, trembling

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15
Q

what are the PM changes of chronic poisoning?

A

liver***
- icterus, enlarged and friable, necrosis

kidney

  • hemorrhage, friable, degen, tubular necrosis
  • gun metal color

spleen

  • enlarged
  • black currant jam like

methemoglobin
- chocolate brown discoloration of tissues

GIT
- normal

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16
Q

what factors can precipitate crisis of chronic poisoning after accumulation has occurred?

A
declining plane of nutrition (weather change)
shipping (Stress)
lactation (stress)
exercise (stress)
stress
17
Q

what is the Dx of Cu poisoning?

A

prior to death Cu blood levels are normal
after crisis it rises dramatically

liver sample or Cu,Mo ratio

18
Q

what can Dx acute poisoniing?

A

acute gastroenteritis
GI contents blue-green
tissue levels normal

19
Q

What can Dx chronic poisoning?

A

analysis of feed and liver for Cu:Mo (should be 6-10:1
if poisoned > 15:1
elevated liver enzymes, hemoglobinuria are suggestive

20
Q

What is the Tx?

A

rarely succesful afte hemolysis

ammonium molybdate (oral)
sodium thiosufate (oral)
thiomolybdate
chelators
Add Mo and Zinc to diet