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Flashcards in Copper Deck (13):
1

Acute toxicosis

- not common
- comes from ingestion of lots of copper
- CS: severe GI signs due to corrosive nature
- supportive and symptomatic treatment

2

Source for Chronic copper toxicosis in sheep

- excess copper (feed additives, natural in soil, soil fertilized with pig or poultry litter)
- Molybdenum def.
- sulfate def.

3

what should the ratio of copper to molybdenum be

6:1

4

Properties

without molybdenum and sulfate, there is nothing to bind to copper to reduce absorption and help excretion

5

Toxicity

- Accumulation takes 2-10 weeks in sheep
- liver damage may hasten this
- stress can also release more copper

6

Toxicokinetics in sheep

- Absorbed from intestines
- liver removes most of it
- excreted in bile

7

MOA in sheep

- accumulation causes liver degeneration and necrosis
- excess copper in blood causes hemolytic crisis
- oxidizes hemoglobin to methemoglobin

8

Clinical signs in sheep

- sudden onset of weakness, anorexia, pale mm, icterus, blood in urine, fever , dyspnea, shock

9

Lesions in sheep

- Icterus
- hemolysis
- methemoglobinemia
- liver is enlarged, yellow and friable
- kidneys are enlarged, hemorrhagic, blue and friable- gunmetal
- spleen is enlarged and dark brown to black

10

Chem analysis of sheep

- Elevated blood or serum Cu
- Elevated liver and kidney Cu
- Elevated AST and LDH (3-6 weeks before crisis)

11

Treatment of sheep

- Ammonium tetrathiomolybate
- D- penicillamine
- Molybdenized copper phosphate sprayed on pastures
- fix food ratio
supplemental zinc

12

What breed is copper toxicosis seen in dogs

- Bedlington terrier
- autosomal recessive disorder
- 2-6 years of age
- also is westies, skye terriers and dobies

13

MOA in dogs

- Extra free copper= chronic active hepatitis and liver necrosis
- lipid peroxidation of mitochondrial membranes
- hemolytic crisis less likely