Copper Flashcards
1
Q
Acute toxicosis
A
- not common
- comes from ingestion of lots of copper
- CS: severe GI signs due to corrosive nature
- supportive and symptomatic treatment
2
Q
Source for Chronic copper toxicosis in sheep
A
- excess copper (feed additives, natural in soil, soil fertilized with pig or poultry litter)
- Molybdenum def.
- sulfate def.
3
Q
what should the ratio of copper to molybdenum be
A
6:1
4
Q
Properties
A
without molybdenum and sulfate, there is nothing to bind to copper to reduce absorption and help excretion
5
Q
Toxicity
A
- Accumulation takes 2-10 weeks in sheep
- liver damage may hasten this
- stress can also release more copper
6
Q
Toxicokinetics in sheep
A
- Absorbed from intestines
- liver removes most of it
- excreted in bile
7
Q
MOA in sheep
A
- accumulation causes liver degeneration and necrosis
- excess copper in blood causes hemolytic crisis
- oxidizes hemoglobin to methemoglobin
8
Q
Clinical signs in sheep
A
- sudden onset of weakness, anorexia, pale mm, icterus, blood in urine, fever , dyspnea, shock
9
Q
Lesions in sheep
A
- 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
Q
Chem analysis of sheep
A
- Elevated blood or serum Cu
- Elevated liver and kidney Cu
- Elevated AST and LDH (3-6 weeks before crisis)
11
Q
Treatment of sheep
A
- Ammonium tetrathiomolybate
- D- penicillamine
- Molybdenized copper phosphate sprayed on pastures
- fix food ratio
supplemental zinc
12
Q
What breed is copper toxicosis seen in dogs
A
- Bedlington terrier
- autosomal recessive disorder
- 2-6 years of age
- also is westies, skye terriers and dobies
13
Q
MOA in dogs
A
- Extra free copper= chronic active hepatitis and liver necrosis
- lipid peroxidation of mitochondrial membranes
- hemolytic crisis less likely
