Heavy metals: Copper Dr. Shokry

Question 1

What types of copper toxicosis are seen?

Which one most common

Answer 1

Acute & Chronic

Chronic most common

Question 2

Acute copper toxicosis when it does happens has what CS

Tx?

Answer 2

severe GI signs:

vomiting, colic, hemorrhagic diarrhea, dehydration, shock

• less common now that US coins (penny) are made mostly of zinc!*
• Supportive & symptomatic tx*

Question 3

sources of chronic copper toxicosis

Answer 3

Excess copper:

feed additives

natural copper in soils & plants

contaminated soils (mines)

soil fertilized w/ poultry litter or swine manure - these 2 spp are resistant to copper toxicosis so may have incr Cu levels in manures

Molybdenum deficiency:

normal Cu/Mo 6:1

Unavailability of sulfates

Question 4

what 3 things have a metabolic relationship in Ruminants only

Answer 4

Copper (Cu)

Molybdenum (Mo)

inorganic sulfate

Question 5

which spp is most sensitive to copper toxicosis

Answer 5

sheep

Question 6

Normal Cu/Mo ratio

Answer 6

6:1

Question 7

Properties of Cu

Answer 7

normally molybdate binds to copper in tissues at a ratio of 4:3 forming copper molybdate that is readily excreted in urine

In rumen sulfates & sulfites are reduced to sulfides binding copper which decr absorption

Question 8

what is the sink organ for copper

Answer 8

liver

Question 9

How does chronic copper toxicosis in sheep happen?

Answer 9

excess Cu accumulatesin liver (damaging hepatocytes ⇒ 2° Cu toxicosis)

Stress causes sudden release of copper from liver to blood → Cu damages RBC membranes ⇒ acute hemorrhagic crisis (hemolytic crisis)

Question 10

toxicokinetics fo Cu toxicosis

Answer 10

Cu absorbed from intestine → removed from blood by liver, bound to hepatic lysosomes, mitochondria & nucleus

Mainly excreted in bile

Question 11

MoA of Cu toxicosis

Answer 11

Cu accumulation in liver ⇒ hepatic degeneration & necrosis

release of Cu from liver ⇒ oxidation of RBC membranes → hemolytic crisis

Cu oxidizes hemoglobin to methemoglobin

Question 12

CS of Cu toxicosis

Lesions seen

Answer 12

sudden onset weakness, anorexia, pale mm, icterus, hemoglobinuria, fever, dyspnea & shock

Icterus, hemolysis & methemoglobinemia

• liver*: enlarged, yellow & friable
• kidney*; enlarges, hemorrhagic, bluish & friable (gunmetal kidneys)
• spleen*: enlarged & dark brown to black (blackberry jam spleen)

Question 13

Ddx of Cu toxicosis

Answer 13

hemolytic agents:

Zinc, naphthalene, phenolics, DMSO, guaifenesin

plants:

Onion, gossypol, red maple, mustard

Snake venoms

Infectious dz:

Lepto, babesiosis, anaplasmosis, bacillary hemoglobinuria

Question 14

Tx of Cu toxicosis

Px

Answer 14

addition of molybdenum:

ammonium tetrathiomolybate (parental)

molybdenized copper phosphate on pasture

addition of molybdenum to rations

D-penicillamine = chelating agent

Zinc supplementation also decr hepatic Cu accumulation

Poor

Question 15

Chronic Cu toxicosis in dogs

Answer 15

mainly Bedlington terrier - genetic, 2-6 years of age

can see in Westies, Skyes & Dobes also

excess free Cu causes chronic active hepatitis & liver necrosis in dogs, hemolytic crisis much less likely