Copper

Question 1

What are the 2 types of copper toxicosis?

Answer 1

Acute copper toxicosis

Chronic copper toxicosis (in sheep)

Question 2

T/F: Acute copper toxicosis is not common

Answer 2

TRUE

Question 3

What is the source of acute copper toxicosis?

Answer 3

Ingestion of high concentrations of copper (Cu sulfate in insecticides)

Question 4

Clinical signs of acute copper toxicosis?

Answer 4

Rapid onset of severe GI signs including vomiting, colic, hemorrhagic diarrhea, dehydration and shock, due to the direct corrosive action of copper

Question 5

What is the treatment for acute coper toxicosis?

Answer 5

Supportive and symptomatic therapy

Question 6

What are the sources of chronic copper toxicosis in sheep?

Answer 6

• Excess copper
  
  • Feed additives
  • Natural copper in soil and plants (mostly clovers)
  • Soils contaminated by mining
  • Soils fertilized w/ poultry litter or swine manure
• Molybdenum deficiency
• Unavailability of sulfate

Question 7

What is the normal copper:molybdenum ratio?

Answer 7

6:1

Question 8

What is the normal relationship between molybdenum and copper?

Answer 8

Molybdate (MoO₄^2-) binds to copper in tissues at a ratio of 4:3, to form copper molybdate (CuMoO₄) that is readily excreted in urine

Question 9

What is the normal relationship between copper and sulfate in the body?

Answer 9

Rumen sulfates and sulfites are reduced to sulfides that bind to copper, reducing its absorption

Question 10

What causes accumulation of copper in the liver?

Answer 10

Imbalances between copper, molybdenum, and sulfate

Question 11

What are the normal feed and forage copper levels? When do these levels cause Cu accumulation?

Answer 11

Normal levels = 10-20 ppm

Cause accumulation when molybdenum is deficient (<1-2 ppm), or sulfate is unavailable

Question 12

Accumulation requires about ______ exposure in sheep.

Answer 12

2-10 weeks

Question 13

What might liver damage and stress cause?

Answer 13

• Liver damage might cause copper accumulation by hepatocytes (secondary copper toxicosis)
• Stress may cause sudden loss of copper from the liver to the blood

Question 14

Where is copper absorbed from? What removes it?

Answer 14

Copper is absorbed from the intestine then carried by serum and erythrocytes to different tissues

The liver removes most of copper from the blood

Question 15

What is copper bound to?

Answer 15

Hepatic lysosomes, mitochondria, and nucleus

Question 16

How is copper mainly excreted?

Answer 16

Bile

Question 17

What does copper accumulation in the liver cause?

Answer 17

Liver degeneration and necrosis

Question 18

What will cause a hemolytic crisis?

Answer 18

Release of copper from the liver and excess copper in blood causes oxidation of erythrocyte membranes increasing their fragility–> hemolytic crisis

Question 19

T/F: Copper also oxidizes hemoglobin to methemoglobin (cannot carry oxygen)

Answer 19

TRUE

Question 20

What are the clinical signs of chronic copper toxicosis in sheep?

Answer 20

Sudden onset of weakness, anorexia, pale mm, icterus, hemoglobinuria, fever, dyspnea, and shock

Question 21

Lesions of chronic copper toxicosis in sheep?

Answer 21

• Icterus, hemolysis, and methemoglobinemia
• Liver is enlarged, yellow, and friable
• Kidneys are enlarged, hemorrhagic, bluish-dark, and firable (gunmetal kidneys)
• Spleen is enlarged and dark brown to black (blackberry jam spleen)

Question 22

What is found on chemical analysis following chronic Cu toxicosis in sheep?

Answer 22

• Elevated serum or whole blood Cu (> 1.5ppm)
• Elevated liver and kidney Cu (< 150ppm, and 15ppm respectively)

Question 23

Are liver enzymes elevated following chronic Cu toxicosis in sheep?

Answer 23

Yes (AST, LDH), 3-6 weeks before a hemolytic crisis

Question 24

Diagnosis for chronic Cu toxicosis in sheep?

Answer 24

History, sudden onset of hemoglobinuria, jaundice, and signs of shock and resp insufficiency, lesions of hemolysis, and lab diagnosis

Question 25

DDx (chronic Cu toxicosis in sheep)?

Answer 25

* Hemolytic agents * Zinc, naphthalene, phenolics, DMSO, guaifenesin * Poisonous plants * Onion, gossypol (cottonseed), rad maple (*Acer rubrum*), mustard * Certain snake venoms * Infectious diseases * Lepto, babesiosis, anaplasmosis, bacillary hemoglobinuria

Question 26

Treatment of chronic Cu toxicosis (sheep)?

Answer 26

* Ammonium tetrathiomolybate (1.7-3.4 mg/day IV or SC for 3 treatments on alternate days) * D-penicillamine (50mg/kg orally for up to 6 days)

Question 27

Prevention of chronic Cu toxicosis in sheep?

Answer 27

* Molybdenized Cu phosphate sprayed on pastures at the rate of 4 ounces/acre * Sheep rations should contain Cu:Mo at 6:1 ratio * Addition of molybdate to sheep rations at 2-4ppm for prevention

Question 28

T/F: Ammonium molybdate (50mg) and thiosulfate (0.3-1.0 g) orally per day prevents toxicosis in individual sheep

Answer 28

TRUE

Question 29

T/F: Supplemental zinc (250ppm) reduces hepatic molybdenum accumulation

Answer 29

FALSE--it reduces hepatic **copper** accumulation

Question 30

Chronic copper toxicosis in dogs?

Answer 30

* Mainly seen in Bellington terriers due to an autosomal recessive disorder at 2-6 years of age * Other breeds including West highland white terriers, Skye terriers, and Doberman pinschers are also susceptible

Question 31

T/F: Excess free copper causes chronic active hepatitis and liver necrosis due to lipid peroxidation of mitochondrial membranes

Answer 31

TRUE

Question 32

T/F: Hemolytic crisis due to sudden release of copper is much more likely in dogs

Answer 32

FALSE--much **les****s** likely in dogs