Copper Flashcards

1
Q

What are the 2 types of copper toxicosis?

A

Acute copper toxicosis

Chronic copper toxicosis (in sheep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T/F: Acute copper toxicosis is not common

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the source of acute copper toxicosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical signs of acute copper toxicosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment for acute coper toxicosis?

A

Supportive and symptomatic therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the sources of chronic copper toxicosis in sheep?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the normal copper:molybdenum ratio?

A

6:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the normal relationship between molybdenum and copper?

A

Molybdate (MoO42-) binds to copper in tissues at a ratio of 4:3, to form copper molybdate (CuMoO4) that is readily excreted in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes accumulation of copper in the liver?

A

Imbalances between copper, molybdenum, and sulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Normal levels = 10-20 ppm

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Accumulation requires about ______ exposure in sheep.

A

2-10 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What might liver damage and stress cause?

A
  • Liver damage might cause copper accumulation by hepatocytes (secondary copper toxicosis)
  • Stress may cause sudden loss of copper from the liver to the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is copper absorbed from? What removes it?

A

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

The liver removes most of copper from the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is copper bound to?

A

Hepatic lysosomes, mitochondria, and nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is copper mainly excreted?

A

Bile

17
Q

What does copper accumulation in the liver cause?

A

Liver degeneration and necrosis

18
Q

What will cause a hemolytic crisis?

A

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

19
Q

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

A

TRUE

20
Q

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

A

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

21
Q

Lesions of chronic copper toxicosis in sheep?

A
  • 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)
22
Q

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

A
  • Elevated serum or whole blood Cu (> 1.5ppm)
  • Elevated liver and kidney Cu (< 150ppm, and 15ppm respectively)
23
Q

Are liver enzymes elevated following chronic Cu toxicosis in sheep?

A

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

24
Q

Diagnosis for chronic Cu toxicosis in sheep?

A

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

25
Q

DDx (chronic Cu toxicosis in sheep)?

A
  • 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
26
Q

Treatment of chronic Cu toxicosis (sheep)?

A
  • 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)
27
Q

Prevention of chronic Cu toxicosis in sheep?

A
  • 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
28
Q

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

A

TRUE

29
Q

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

A

FALSE–it reduces hepatic copper accumulation

30
Q

Chronic copper toxicosis in dogs?

A
  • 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
31
Q

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

A

TRUE

32
Q

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

A

FALSE–much less likely in dogs