Difference between revisions of "Copper"

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==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 - Anatomy & Physiology|liver]]
 
**swollen
 
**soft
 
**orange in colour
 
*[[Urinary System - Anatomy & Physiology#Upper Urinary Tract|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====
+
*Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase).
*Bedlington and West Highland White Terriers
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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).
*copper toxicosis susceptibility
+
*Enterocyte regulation of absorption – metallothionein and a copper transport protein – ATPase7A.
*inherited as autosomal defect
+
*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.
*copper levels can be very high in the [[Liver - Anatomy & Physiology|livers]] of these animals
+
*ATPase7A – transmembrane copper transporter in a number of cell types.
*there is no haemolytic crisis
+
*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]].
=====Clinical=====
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*[[Copper Toxicity|Chronic diet excess of copper]] leads to accumulation in the [[Liver - Anatomy & Physiology|liver]] .
*ill thrift
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*Serum copper – in 2 pools
*progressive neurological signs due to [[Liver - Anatomy & Physiology|liver]] failure
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**Exchangeable pool – loosely bound to carrier molecules; 80% of it bound to transcuperin, the rest bound to albumin.
=====Gross=====
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**Other pool – tightly bound to carrier molecules.
*[[Liver - Anatomy & Physiology|liver]] is small and fibrosed
 
*jaundice is not a consistent feature
 
  
[[Category:Hepatotoxicity,_Chronic]][[Category:Sheep]]
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[[Category:Minerals]]

Latest revision as of 12:56, 15 February 2011


  • Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase).
  • Primarily absorbed through the small intestine and stomach (upper small intestine in the dog).
  • Enterocyte regulation of absorption – metallothionein and a copper transport protein – ATPase7A.
  • 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.
  • ATPase7A – transmembrane copper transporter in a number of cell types.
  • 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 and brain that have little of the transporter experience copper deficiency.
  • Chronic diet excess of copper leads to accumulation in the liver .
  • Serum copper – in 2 pools
    • Exchangeable pool – loosely bound to carrier molecules; 80% of it bound to transcuperin, the rest bound to albumin.
    • Other pool – tightly bound to carrier molecules.