Difference between revisions of "Copper"

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==Hepatotoxicity==
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*sheep are very susceptible
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**they have poor ability to excrete copper in the bile
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*copper accumulates in hepatocytes until it reaches a critical level
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**the hepatocytes die and release the copper into the blood
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**causes haemolysis of the red blood cells
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*this haemolysis further damages the hepatocytes
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**releases even more copper
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====Predisposing factors====
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*contamination of foodstuffs and pasture with copper
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*any damage to the biliary system as in ragwort poisoning
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*pastures low in molybdenum
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**increases the availability of dietary copper
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**molybdenum combines with copper to form insoluble complexes in the gut
  
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====Gross====
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*carcass
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**jaundiced
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**reddish
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*[[Liver - Anatomy & Physiology|liver]]
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**swollen
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**soft
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**orange in colour
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*[[Urinary System - Anatomy & Physiology#Upper Urinary Tract|kidneys]]
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**deep red
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**red urine due to haemoglobinuria
  
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====Microscopically====
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*periacinar hepatic necrosis and profuse bile due to haemolysis and cholestasis
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*copper can be demonstrated with special stain - rhodanine
  
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*Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase).
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====Genetic inheritance====
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*Primarily absorbed through the [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and [[Monogastric Stomach - Anatomy & Physiology|stomach]] (upper small intestine in the dog).
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*Bedlington and West Highland White Terriers
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*Enterocyte regulation of absorption – metallothionein and a copper transport protein – ATPase7A.
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*copper toxicosis susceptibility
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*Metallothionein is a low molecular wt cytoplasmic protein, in all tissues; expression in response to heavy metals, various hormones and stress. metallothionein in cytoplasm of enterocytes leads to absorption of copper.
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*inherited as autosomal defect
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*ATPase7A – transmembrane copper transporter in a number of cell types.
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*copper levels can be very high in the [[Liver - Anatomy & Physiology|livers]] of these animals
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*Defective in people with Menke’s disease – the animal model is the mottled mouse – results in faulty transport of copper out of the cell –leads to copper accumulation in enterocytes. [[Liver - Anatomy & Physiology|Liver]] and brain that have little of the transporter experience [[Copper Deficiency|copper deficiency]].
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*there is no haemolytic crisis
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*[[Copper Toxicity|Chronic diet excess of copper]] leads to accumulation in the [[Liver - Anatomy & Physiology|liver]] .
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=====Clinical=====
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*Serum copper – in 2 pools
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*ill thrift
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**Exchangeable pool – loosely bound to carrier molecules; 80% of it bound to transcuperin, the rest bound to albumin.
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*progressive neurological signs due to [[Liver - Anatomy & Physiology|liver]] failure
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**Other pool – tightly bound to carrier molecules.
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=====Gross=====
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*[[Liver - Anatomy & Physiology|liver]] is small and fibrosed
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*jaundice is not a consistent feature
  
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[[Category:Minerals]]
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[[Category:Hepatotoxicity,_Chronic]][[Category:Sheep]]

Revision as of 22:28, 7 June 2010

Hepatotoxicity

  • sheep are very susceptible
    • they have poor ability to excrete copper in the bile
  • copper accumulates in hepatocytes until it reaches a critical level
    • the hepatocytes die and release the copper into the blood
    • causes haemolysis of the red blood cells
  • this haemolysis further damages the hepatocytes
    • releases even more copper

Predisposing factors

  • contamination of foodstuffs and pasture with copper
  • any damage to the biliary system as in ragwort poisoning
  • pastures low in molybdenum
    • increases the availability of dietary copper
    • molybdenum combines with copper to form insoluble complexes in the gut

Gross

  • carcass
    • jaundiced
    • reddish
  • liver
    • swollen
    • soft
    • orange in colour
  • kidneys
    • deep red
    • red urine due to haemoglobinuria

Microscopically

  • periacinar hepatic necrosis and profuse bile due to haemolysis and cholestasis
  • copper can be demonstrated with special stain - rhodanine

Genetic inheritance

  • Bedlington and West Highland White Terriers
  • copper toxicosis susceptibility
  • inherited as autosomal defect
  • copper levels can be very high in the livers of these animals
  • there is no haemolytic crisis
Clinical
  • ill thrift
  • progressive neurological signs due to liver failure
Gross
  • liver is small and fibrosed
  • jaundice is not a consistent feature
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