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Copper (view source)

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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 Overview - 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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~~====Genetic inheritance====~~

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*Bedlington and West Highland White Terriers

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*copper toxicosis susceptibility

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*inherited as autosomal defect

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*copper levels can be very high in the [[Liver - Anatomy & Physiology|livers]] of these animals

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*there is no haemolytic crisis

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~~=====Clinical=====~~

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*ill thrift

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*progressive neurological signs due to [[Liver - Anatomy & Physiology|liver]] failure

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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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~~== Copper and liver disease ==~~

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*Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase).

*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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*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 - Anatomy & Physiology|Liver]] and brain that have little of the transporter experience copper deficiency.

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*Chronic diet XS of copper leads to accumulation in the [[Liver - Anatomy & Physiology|liver]] .

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*[[Copper Toxicity|Chronic diet excess of copper]] leads to accumulation in the [[Liver - Anatomy & Physiology|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.

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[[Category:Minerals]]

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[[Category:~~Hepatotoxicity,_Chronic]][[Category:Liver Diseases - Sheep]]~~

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~~[[Category:To_Do_-_Clinical~~]]

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