Copper Flashcards
What are the 2 types of copper toxicosis?
Acute copper toxicosis
Chronic copper toxicosis (in sheep)
T/F: Acute copper toxicosis is not common
TRUE
What is the source of acute copper toxicosis?
Ingestion of high concentrations of copper (Cu sulfate in insecticides)
Clinical signs of acute copper toxicosis?
Rapid onset of severe GI signs including vomiting, colic, hemorrhagic diarrhea, dehydration and shock, due to the direct corrosive action of copper
What is the treatment for acute coper toxicosis?
Supportive and symptomatic therapy
What are the sources of chronic copper toxicosis in sheep?
- 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
What is the normal copper:molybdenum ratio?
6:1
What is the normal relationship between molybdenum and copper?
Molybdate (MoO42-) binds to copper in tissues at a ratio of 4:3, to form copper molybdate (CuMoO4) that is readily excreted in urine
What is the normal relationship between copper and sulfate in the body?
Rumen sulfates and sulfites are reduced to sulfides that bind to copper, reducing its absorption
What causes accumulation of copper in the liver?
Imbalances between copper, molybdenum, and sulfate
What are the normal feed and forage copper levels? When do these levels cause Cu accumulation?
Normal levels = 10-20 ppm
Cause accumulation when molybdenum is deficient (<1-2 ppm), or sulfate is unavailable
Accumulation requires about ______ exposure in sheep.
2-10 weeks
What might liver damage and stress cause?
- Liver damage might cause copper accumulation by hepatocytes (secondary copper toxicosis)
- Stress may cause sudden loss of copper from the liver to the blood
Where is copper absorbed from? What removes it?
Copper is absorbed from the intestine then carried by serum and erythrocytes to different tissues
The liver removes most of copper from the blood
What is copper bound to?
Hepatic lysosomes, mitochondria, and nucleus
How is copper mainly excreted?
Bile
What does copper accumulation in the liver cause?
Liver degeneration and necrosis
What will cause a hemolytic crisis?
Release of copper from the liver and excess copper in blood causes oxidation of erythrocyte membranes increasing their fragility–> hemolytic crisis
T/F: Copper also oxidizes hemoglobin to methemoglobin (cannot carry oxygen)
TRUE
What are the clinical signs of chronic copper toxicosis in sheep?
Sudden onset of weakness, anorexia, pale mm, icterus, hemoglobinuria, fever, dyspnea, and shock
Lesions of chronic copper toxicosis in sheep?
- 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)
What is found on chemical analysis following chronic Cu toxicosis in sheep?
- Elevated serum or whole blood Cu (> 1.5ppm)
- Elevated liver and kidney Cu (< 150ppm, and 15ppm respectively)
Are liver enzymes elevated following chronic Cu toxicosis in sheep?
Yes (AST, LDH), 3-6 weeks before a hemolytic crisis
Diagnosis for chronic Cu toxicosis in sheep?
History, sudden onset of hemoglobinuria, jaundice, and signs of shock and resp insufficiency, lesions of hemolysis, and lab diagnosis
DDx (chronic Cu toxicosis in sheep)?
- 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
Treatment of chronic Cu toxicosis (sheep)?
- 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)
Prevention of chronic Cu toxicosis in sheep?
- 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
T/F: Ammonium molybdate (50mg) and thiosulfate (0.3-1.0 g) orally per day prevents toxicosis in individual sheep
TRUE
T/F: Supplemental zinc (250ppm) reduces hepatic molybdenum accumulation
FALSE–it reduces hepatic copper accumulation
Chronic copper toxicosis in dogs?
- 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
T/F: Excess free copper causes chronic active hepatitis and liver necrosis due to lipid peroxidation of mitochondrial membranes
TRUE
T/F: Hemolytic crisis due to sudden release of copper is much more likely in dogs
FALSE–much less likely in dogs
