Difference between revisions of "Copper"
Jump to navigation
Jump to search
| (5 intermediate revisions by the same user not shown) | |||
| Line 1: | Line 1: | ||
| + | ==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==== | ||
| + | *Bedlington and West Highland White Terriers | ||
| + | *copper toxicosis susceptibility | ||
| + | *inherited as autosomal defect | ||
| + | *copper levels can be very high in the [[Liver - Anatomy & Physiology|livers]] of these animals | ||
| + | *there is no haemolytic crisis | ||
| + | =====Clinical===== | ||
| + | *ill thrift | ||
| + | *progressive neurological signs due to [[Liver - Anatomy & Physiology|liver]] failure | ||
| + | =====Gross===== | ||
| + | *[[Liver - Anatomy & Physiology|liver]] is small and fibrosed | ||
| + | *jaundice is not a consistent feature | ||
| + | |||
| + | == Copper and liver disease == | ||
*Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase). | *Copper – cofactor for enzymes (lysyl oxidase), electron transport proteins (cytochrome c oxidase) and antioxidant molecules (superoxide dismutase). | ||
| − | *Primarily absorbed through the [[Small Intestine | + | *Primarily absorbed through the [[Small Intestine - Anatomy & Physiology|small intestine]] and [[Forestomach - Anatomy & Physiology|stomach]] (upper small intestine in the dog). |
*Enterocyte regulation of absorption – metallothionein and a copper transport protein – ATPase7A. | *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. | *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. | *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 | + | *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. |
| − | * | + | *Chronic diet XS of copper leads to accumulation in the [[Liver - Anatomy & Physiology|liver]] . |
*Serum copper – in 2 pools | *Serum copper – in 2 pools | ||
**Exchangeable pool – loosely bound to carrier molecules; 80% of it bound to transcuperin, the rest bound to albumin. | **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. | **Other pool – tightly bound to carrier molecules. | ||
| − | [[Category: | + | |
| + | [[Category:Hepatotoxicity,_Chronic]][[Category:Sheep]] | ||
| + | [[Category:To_Do_-_Clinical]] | ||
Revision as of 22:23, 28 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
Copper and liver disease
- 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 XS 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.