Lec 16 - Copper (part 1)

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Hepatoxicity

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28 Terms

1
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You hear copper, you say _____!

SHEEP

2
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Copper is an ____ trace element

essential

<p>essential</p>
3
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How do animals get exposed to copper?

commonly used a feed additive especially in PNW

4
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Why is copper used as a feed additive?

co-factor in lots of enzymes in lots of systems/wide variety of Cu-deficient disease in cattle, sheep, goats

5
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What are sources of copper toxicity in food animals?

dietary imbalances, feeding sensitive species feeds/mineral mixes dsigned for cattle, poultry, swine, mixing/math errors, liver dysfunction-biliary system

6
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Copper in feed: Cattle has up to ___ppm, Poultry up to ___ppm, Swine up to ___ppm

1500, 1000, 250

7
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Copper toxicity can also occur if ___ to ___ ratio is out of whack in diet

Copper, Molybdenum

8
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A copper sensitive species, ___, will have a total diet of copper ___ ppm

sheep, <50

9
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Give examples of primary vs secondary intoxication of copper

primary: mixing/math errors
secondary: liver dysfunction, biliary system

10
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What are sources of copper toxicity in small animals and exotics? (excluding copper storage disease)

coins - pre 1982 coins copper (post 1982 coins zinc) NOT like zinc, given time will dissolve in acidic environment, or pass

others: liver dysfunction of biliary system

too much copper in canine diets?

<p><strong>coins</strong> - pre 1982 coins copper (post 1982 coins zinc) <strong>NOT like zinc</strong>, given time will dissolve in acidic environment, or pass </p><p><strong>others</strong>: <strong>liver dysfunction of biliary system</strong></p><p>too much copper in canine diets? </p>
11
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Is copper toxicity commonly acute or chronic exposures?

commonly chronic exposures but with abrupt signs

12
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What species are susceptible? Which are most susceptible?

All susceptible, sheep most sensitive, then pre-ruminant calves, goats, llamas, alpacas

13
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Copper toxicity is not common in what animals?

young, small companion animals-exotics

14
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What elements will tie up copper?

Mo, S

15
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Mo and S will ___ excessive copper ____ and enhance excretion in ___.

slow down, absorption, bile

16
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Ratio of Cu:Mo that is greater than ___ could potentially be problematic chronically.

>6-10:1

17
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True or False? All forms of copper toxicity will results in the same presentation.

False. Not all forms of copper are created equal

18
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If a group of animals are presenting with toxicity think ____. If only a single animal is presenting with toxicity think ____.

primary, secondary

19
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NEED to determine ___ of copper.

source

20
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Describe the mechanism of action of copper. Storage? Metabolism? Excretion?

excess copper stored in liver, lysosomes and mitochondria, metabolizes if sufficient molybdenum and sulfate available and excreted mainly into bile as Cu-Mo-SO4 complex

21
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The liver has a high copper storage capacity, but if storage capcity is reached, a ___ event can cause what?

stressful,

Cu released → hepatocellular necrosis → serum Cu → hemolysis

22
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What is the end result of Cu release into serum?

acute hemolytic crisisW

23
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Why might you not see acute hemolytic crisis with copper toxicity?

with acute or peracute exposures and when dose is high, may just see hepatic and renal necrosis

24
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Describe the clinical signs of copper toxicity in LA

abrupt onset but sporadic occurrence in groups
weakness, abdominal pain, off feed, grinding teeth, lethargy, icterus, brown/red urine, nonspecific production losses prior to onset of severe signs

<p><strong>abrupt onset but sporadic occurrence</strong> in groups<br>weakness, abdominal pain, off feed, grinding teeth, lethargy, icterus, brown/red urine, nonspecific production losses prior to onset of severe signs </p>
25
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Describe the clinical signs of copper toxicity in SA

repeated bouts of hepatitis (chronic) - vomiting, abdominal pain, diarrhea, loss of appetite

acute NOT common and not common to see acute hepatic necrosis/hemolysis

26
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What lab abnormalities would you see with copper toxicity?

elevated liver enzymes: GGT, AST

anemia due to hemolysis

hemoglobinemia/uria, hyperbilirubinemia/uria

methemoglobinemia (brown blood)

UA changes hypoxia and hemoglobin related (casts, glucose, bilirubin, hemoglobin, azotemia etc)

<p>elevated liver enzymes: <strong>GGT, AST</strong></p><p><strong>anemia</strong> due to hemolysis</p><p><strong>hemoglobinemia/uria, hyperbilirubinemia/uria</strong></p><p><strong>methemoglobinemia</strong> (brown blood)</p><p>UA changes <strong>hypoxia</strong> and hemoglobin related (casts, glucose, bilirubin, hemoglobin, azotemia etc) </p>
27
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Describe the gross lesions of copper toxicity

icterus

enlarged, discolored kidneys

enlarged, friable, tan liver

enlarged, engorged spleen,

distended gallbladder

gastroenteritis if acute

<p>icterus</p><p>enlarged, discolored kidneys</p><p>enlarged, friable, tan liver</p><p>enlarged, engorged spleen, </p><p>distended gallbladder</p><p>gastroenteritis if acute</p>
28
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Describe the histopathologic lesions of copper toxicity

hepatic necrosis, varying patterns, granular gray-green pigement within Kupffer cells

acute renal tubule degeneration and necrosis with hemoglobin casts (due to hypoxia or hemoglobin)

gastroenteritis if acute

<p><strong>hepatic necrosis, varying patterns, </strong>granular gray-green pigement within Kupffer cells</p><p>acute renal tubule <strong>degeneration and necrosis with hemoglobin casts </strong>(due to hypoxia or hemoglobin)</p><p>gastroenteritis if acute </p>