Poisons affecting oxygen uptake to the tissue
Transcript of Poisons affecting oxygen uptake to the tissue
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Transition group metal with high
electrical and thermal conductivity.
Abbreviation Cu comes from the Latin
word cuprum which refers to the islandsof Cyprus.
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Whole grain cereals
Sprayed foliage
Salt licks Supplements
Ponds treated from copper
Poultry ( Manure)
Organ meats
Leafy green vegetables
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It is Caustic in nature.
Cu exists in the +2(cupric, divalent)
& +1(cuprous) oxidation states.
In sheep toxic dose is 20mg/kg
In cattle toxic dose is 200mg/kg
In chicks toxic dose is 325mg/kg
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Age
Species
Decrease in nutrition plane
Fasting
Physical Activity
Stress
Molybdenum Deficiency
Ingestion of hepatoxins
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Cu absorbed from intestine & enters a carrier statein blood (RBCs & Serum).
Liver removes from blood most of it but soft tissuesstore some also.
Cu bound to active site in nucleus, mitochondria &lysosomes.
Lysosomes increases in number, volume & density
to accumulate Cu.
This leads to peroxidative damage to lysosomalmembrane & leakage of hydrolytic enzymes.
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Cu also bound to other high affinity siteslike sulfhydryl groups of cytoplasmic(chelatin) & metal binding(metallothionein).
Cu can induce the synthesis of theseproteins.
Cu is not stored to same degree by liver
in all species, it excretes in bile butresorption from intestine also there.
Cu crosses the placenta also & stored infetal liver.
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In ruminants liver & other tissues cannot storean infinite amount.
So inhibition of vital enzymes & increase inhydrolytic enzymes from lysosomes lead tomalfunction & initiate liver necrosis.
Result in increased in serum glutamicoxaloacetic transaminase, plasma arginase &plasma bilirubin.
Ultrastructural changes in mitochondria, ER,Golgi apparatus & sinusoidal borders alsohistochemical distribution of acid phosphataseis disturbed.
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Vascular system is damaged resulting inloss of fluid & increased blood colloidalosmotic pressure.
Blood Cu enters in erythrocytes & cannotbe released leads to oncominghemolytic crisis.
Hemolysis occurs with a series ofreactions like conversion of ferrous
hemoglobin to methemoglobin,glutathione, peroxidation, protein &cell concentration.
Erythrocyte autoimmune mechanismalso involved.
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Kidney failure due to renal tubule &glomerular necrosis brought by excessiveCu.
Plasma creatinine phophokinaseconcentration indicate skeletal muscledamage thought to be due anoxia.
Brain lesions due to blood urea,
ammonia concentration & alteration inglial transport mechanism by inhibition ofATP caused by metabolic changes in theglia.
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Weakness, trembling, anorexia,hemoglobinurea, jaundice & bloody
nasal discharge. Signs of respiratory insufficiency
(dyspnea, panting) & shock (tachycardia, weak pulse, cold
extremities). Death occur in 1-4 days after onset of
clinical signs.
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Icterus, hemolysis, methemoglobinemia,&congestion of abomasum & intestine.
Liver enlarge, yellow or friable.
Gall bladder is distended & filled with thick greenish
bile.
Kidneys are large, hemorrhagic & friable.
Spleen is enlarged & dark brown to black.
Hemorrhagic heart & edematous lungs.
Excessive fluid in body cavities.
Muscular necrosis.
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Microscopically, lesions are consist
with gross findings.
Liver cell vacuolated & necrotic. Kidney manifest tubular & glomerular
necrosis & hemoglobin clogging in
tubules.
Brain manifest spongy degeneration &
astrocyte damage
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History Clinical examination Serum & whole blood copper
examination Urine examination for hemoblobinurea Blood Cu levels 10-20x normal(50-
200g/dl) K
idney Cu levels postmortem (>100ppm) Liver Cu levels postmortem (>350pp)
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Decreasing absorption
1) Water, Milk or Activated charcoal
Supportive measures Ammonium molybdate(50-500mg) + sodium
sulfite(0.3-1g) orally for 3weeks.
Chelating therapy
D-Penicillamine, Dimercaprol / BAL,Calcium disodium ethylenediaminetetraacetate.
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Nicholas H.Booth, Lieslie E. McDonald
(6th edition) Veterinary Pharmacologyand Therapeutics. 1023-1027.
Ramesh C.Gupta, Veterinary Toxicology.
427-429 www.google.com
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