Trace element : Copper

  • Serum copper is critical for the functioning of several enzymes
  • Lysyl oxidase: It is important for the cross linking of collagen and elastin such that deficiencies lead to problems in connective tissues such as bones
  • Cytochrome oxidase : Involved in temperature maintenance
  • Tyrosinase :Necessary for pigmentation
  • Superoxide dismutase
  • Normally, 40% to 60% of daily ingested copper (2 to 5 mg) is absorbed in the stomach & duodenum.
  • It is transported to the liver loosely complexed with albumin.
  • Free copper dissociates and is taken up into hepatocytes, where it is incorporated into an Alpha-globulin synthesized in the endoplasmic reticulum to form ceruloplasmin (a copper-containing metallothionein) and resecreted into plasma.
  • Ceruloplasmin accounts for 90% to 95% of plasma copper.
  • Circulating ceruloplasmin is desialylated as part of normal plasma protein aging
  • Desialylated ceruloplasmin is endocytosed by the liver, degraded within lysosomes, and its copper is excreted into bile.
  • Copper is excreted in the bile into GI tract from which it is not reabsorbed. So normally urine contains only traces of copper. Since copper homeostasis is maintained almost exclusively by biliary excretion, any disease which hampers its biliary excretion will lead to accumulation of Cu in liver → increased blood levels & increased urinary 
  • cexcrition. So cholestatic hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis show increased copper excretion in urine
  • Estimated total body copper is only 50 to 150 mg.
  • Normocytic hypochromic anemia
  • Neutropenia
  • Growth retardation
  • Defective keratinization and pigmentation of hair
  • Hypothermia
  • Degenerative changes in aortic elastin
  • Osteopenia, subperiosteal hematoma
  • The average fatal period of copper poisoning is 1-3 days.
  • Acute copper sulphate poisoning can manifest with acute hemolysis.
  • The pathogenesis of this effect is not known but it may be related to copper induced oxidation of intracellular glutathione, hemoglobin and NADPH as well as inhibition of Glucose 6 phosphate dehydrogenase by copper.
  • Patients with acute copper poisoning also presents with severe nausea, vomiting, thirst, metallic taste in mouth, burning pain and salivation. Oliguria, hematuria, uremia and albuminuria is also seen. 
  • Death in copper sulphate poisoning occurs due to Renal failure.
Treatment of copper poisoning:

  1. Stomach wash with 1 percent solution of potassium ferrocyanide which acts as an antidote by forming an insoluble cupric ferrocyanide
  2. Emetics are contraindicated.
  3. Copper sulfate poison is not dialyzable.
  4. Demulcent drinks form insoluble albuminate of copper
  5. Castor oil
  6. Chelation with penicillamine/ EDTA/ BAL
  • Blue green (or purple-green) pigmentation of hair, skin, mucosa and perspiration, purple (blue) green line on gums and bluish green frothy discharge from mouth and nostrils is seen in chronic poisoning of copper salt.
  • Wilson's disease :has defect in copper binding P type ATPase (ATP 7B protein) which cause defective excretion of copper into bile & reduction in incorporation of copper into apoceruloplasmin leading to accumulation of Cu in liver, brain, kidney & RBC.
  • Menkes kinky hair syndrome caused due to defect in the copper transport.
  • Indian childhood cirrhosis : increased hepatic, urinary and serum copper concentration are characteristic of ICC.
  • Chalcosis is a term used to describe the deposition of the copper (Cu) in the tissues .
  • Chalocosis in occular tissues generally occurs from the presence of a copper foreign body within the eye.
  • The most toxic intraocular foreign body is a particle of Copper.
Exam Question
  • Copper sulphate poisoning manifests with Acute hemolysis.
  • Copper containing enzymes are Superoxide dismutase , Cytochrome oxidase ,Tyrosinase.
  • Increased copper excretion in urine is seen in Primary sclerosing cholangitis , Wilson's disease , Primary biliary cirrhosis.
  • Copper is mainly transported by Ceruloplasmin.
  • Purple lining over gums is seen in chronic poisoning of Copper.
  • The average fatal period of copper poisoning is 1-3 days.
  • The probable diagnosis in a person found dead with bluish green frothy discharge at the angle of mouth and nostrils is Copper poisoning.
  • Copper sulfate poison is not dialyzable. Diseases related to copper metabolism :- Wilson's disease , Menkes kinky hair syndrome ,Indian childhood cirrhosis.
  • Copper deficiency leads to normocytic hypochromic anemia.
  • The most toxic intraocular foreign body is a particle of Copper.
  • Chalcosis is deposition of Copper.
  • Death in copper sulphate poisoning occurs due to Renal failure.
  • Antidote for copper poisoning is Potassium ferrocyanide.
  • Chelating agent for copper, mercury, lead which is given by oral route is Penicillamine.
  • Copper sulfate acts both as poison and antidote.
  • Copper binding protein is Ceruloplasmin.
  • Menke's disease" is a disease of Impaired copper transport.

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