Copper Flashcards

1
Q

How do livestock vs companion animals get access to copper?

A

Livestock:
-forages
-trace mineral supplements

Companion animals:
- food

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

Where is copper stored?

A

liver

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

Ways copper poisoning occurs in ruminants?

A
  1. Excess dietary intake- rations or supplements for cattle and horses OR mixing errors
  2. Over supplementation
    -copper boluses for parasite control
  3. deficient biliary excretion
  4. Metabolic defect in copper metabolism
  5. previous liver damage
  6. Chewing on treated lumber
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the mechanism of copper toxicity?

A

Oxidative damage

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

Species sensitivity of copper toxicity

A

Sheep> goats> cattle> monogastrics

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

Why are sheep so sensitive to copper toxicity?

A

-high affinity for Cu in liver
-limited ability to upregulate metal binding proteins
-limited ability to store Cu binding protein complexes
-impaired ability to excrete copper in bile

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

What two presentations of copper toxicity occur in ruminants?

A
  1. acute copper toxicosis
  2. chronic copper toxicosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute copper toxicosis in ruminants

A

-rare
-from ingestion of high Cu or massive overdose

See severe gastroenteritis and mucosal erosions, diarrhea +blood, colic signs, green/blue coloured feces

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

How do you manage acute copper toxicosis in ruminants?

A

fluids and gastroprotectants

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

Chronic copper toxicosis ruminants

A

-most common for of copper poisoning
-hemolytic crisis triggered by a stressful event = release of Cu from lysosomes in liver
-depression, anorexia
-rumen stasis
-brow/yellow MM, jaundice, hemoglobinuria, port wine urine
-weak, lethargy, recumbency

Death in 1-2 days

**stressful events= transport, lactation/pregnanacy, exercise, disease, starvation, shearing

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

Mechanism of chronic copper toxicosis in ruminants

A

1.Cu stored in lysosomes in liver
2. Excessive Cu= apoptosis of hepatocytes preventing livers ability to clear debris. Also damages kidneys
3. Release of high Cu into blood = oxidative damage hemolytic anemia
4. intravascular hemolysis= splenomegaly

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

Clinical pathology of chronic Cu toxicity in ruminants

A

-decreased PCV
-regenerative anemia
-heinz bodies
-methemoglobin
-hyperbilirubinemia
-high liver enzymes
-azotemia
-isosthenuria

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

Management of clinically affected or at risk ruminants?

A

-Ammonium tetrathiomolybdate- antagonizes copper absorption

-MetHb= methylene blue
-sodium thiosulfate
-Vit C
-D-penicillamine
**many of theses are off label uses and need to contact FARAD for withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Management of herd Cu tox?

A

Individual treatment or put on concentrate feed

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

General management of copper toxicity in ruminants

A

-ID source of high Cu
*test feed, supplements, treatments
-supportive care
-poor prognosis for clinically affected animals
-ID other at risk animals= blood chem for liver enzymes, liver biopsy for Cu

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

Postmortem findings for Cu toxicity in ruminants

A

-generalized jaundice
-splenomegaly (dark)
-hepatomegaly (deep orange)
-dark kidneys
-dark red/brown urine

17
Q

Postmortem histology for Cu toxicity in ruminants

A

-acute hepatic necrosis

-tubular degeneration and necrosis

18
Q

Diagnosis of live ruminants for Cu toxicity

A

-cannot use blood Cu levels before or after hemolysis because lysosomes must have burst first and then short window where Cu is present in the blood after the liver and before it goes to kidneys
**do not rely on this test!

-high liver enzymes, hemolysis, hematuria

-liver biopsies

-clinical signs

19
Q

Diagnosis of dead ruminants for Cu toxicity

A

-use combination of classic PM lesions and elevated tissue copper

-submit both liver and kidney for Cu testing

20
Q

How do you test feed for Cu toxicity?

A

Check ratio of Cu: Mo

6:1 to 10:1 is normal

21
Q

DDx for Cu toxicity

22
Q

Common companion animal breeds susceptible to Cu toxicity

A

-copper storage disease in bedlington terriers= COMMD1 gene=impaired Cu excretion

-Other breeds, likely gene mutation but unknown

23
Q

Clinical signs of companion animal Cu toxicity

A

1.period of no symptoms when Cu accumulates over yrs

2.Period of chronic active hepatitis = weight loss, anorexia, lethargy, vomiting

  1. Liver failure (ascites, hepatic encephalopathy)
24
Q

Diagnosis of Cu toxicity in companion animals

A
  1. Liver biopsy
    -ex lap or laparoscopy
    -Check histology and for copper concentrations
  2. Abdominal US/radiographs
    -not very sensitive or specific
25
Q

Management of Cu toxicity

A

-decreased Cu absorption and increase Cu excretion

-low Cu diet

-oral chelation therapy (D-penicillamine

-Zn supplements

-hepatoprotectants

-monitor liver enzymes every 6mths

**no cure, just management

26
Q

Prognosis of companion animal toxicity? What decreases prognosis?

27
Q

What is copper hepatopathy a differential for in dogs?

A

Chronic hepatitis