Iron, Copper, and Molybdenum Toxicosis Flashcards
What are the usual sources of iron toxiciosis?
Accidental ingestion of human oral supplements
Overdosage in pet or piglets
What are the three forms that iron is present in?
Which is the most irritating and astringent?
Elemental
Divalent (ferrous)
Trivalent (ferric) —> most irritating and astringent
T/F: toxicity of oral iron preparations is more toxic than parenteral preparations
False
Parenteral is more toxic than oral
Greater than 5000ppm iron in diet can lead to ________ in piglets because it interferes with phosphate absorption
Rickets
How is iron absorbed ??
Ferrous iron absorbed in small intestine using energy-dependent carrier
Ferrous iron is oxidized to ferric iron once absorbed
Ferric iron binds to ___________ in plasma and is distributed throughout the body
Transferrin
70% to hemoglobin
10% to myoglobin
Rest to enzymes or stored in liver/spleen/bones
What is the MOA of iron toxicosis ?
Primary on GI tract: GI tract, liver, and CV leading to shock and death
GI: direct corrosion of the GI mucosa, vomiting, diarrhea, and shock
Liver: accumulation causing mitochondrial damage, acidosis and shock
CV: free radical lipid peroxidation and damage to membranes, increased vascular permeability, hemorrhage, vasodilation, CV collapse, and shock
Injectable iron can cause what type of reaction causing an acute rapid death?
Anaphylactic reaction -histamine release
What are the 4 stages of acute iron toxicosis?
- Nausea, vomiting, diarrhea, GI hemorrhage
- Apparent recovery
- Vomiting, diarrhea, GI hemorrhage, metabolic acidosis, coagulation disorders, hepatic failure, CV collapse
- GI obstruction
What lesion is associated with parenteral preparations of iron?
Yellowish-brown discoloration at injection site and near lymph node
What lesions are seen with oral preparations of iron?
GI ulcer and hemorrhagic enteritis
Congestion of liver, kidney, liver necrosis, icterus, and hemoglobinuria
How do you treat iron toxicosis?
GI decontamination:
- emesis, or gastric lavage before onset of clinical signs
- activated charcoal is NOT effective
- milk of magnesia to precipitate iron
Supportive therapy
- IV fluids, dehydration, acidosis, and hypovolemic shock
- GI protectants like sucralfate
Chelation therapy
-only indicated in severe toxicosis with deferoxamine
What is more common, acute or chronic copper toxicosis?
Chronic
Vomiting, colic, hemorrhagic diarrhea, dehydration, and shock are signs of acute/chronic copper toxiciosis?
Acute
—> direct corrosive action of copper on GI
What are the sources of chronic copper toxiciosis?
Excess copper
- feed additives
- natural in soil/plants
- contaminated by mining
- fertilized with poultry litter/swine manure
Molybdenum deficiency
-normal ratio is 6:1 copper/molybdenum
Unavailability of sulfate
What normally binds copper in tissues and forms a compound that is readily excreted in the urine?
Molybdenum
Binds to copper at 4:3 ratio —> copper molybdate (CuMoO4)
What is reduced in the rumen that binds copper to reduce its absorption?
Sulfites are reduced to sulfides
T/F: Normal feed and forage copper levels can cause toxicity when molybdenum or sulfate is unavailable
True
How long does it take for copper accumulation to occur in sheep?
2-10weeks exposure
What is the MOA of copper toxicosis?
Copper accumulates in liver causing liver degeneration and necrosis
Release of copper from the liver and excess in blood —> oxidation of erythrocytes membranes —> hemolytic crisis
Oxidation of hemoglobin to methemoglobinemia
What are the clinical signs of chronic copper toxicity?
Sudden onset of weakness, anorexia, pale mucous membranes, icterus, hemoglobinuria, fever, dyspnea, and shock
What lesions do you see in chronic copper toxicosis?
Icterus, hemolysis, and methemoglobinemia
Liver is enlarged, yellow, and friable
Kidney is enlarged, hemorrhagic, bluish-dark, and friable (gunmetal )
Spleen is enlarged, dark brown to black (blackberry jam)
What is the DDX for copper toxicity?
Hemolytic agents- zinc, naphthalene, DMSO, Guaifenesin
Poisonous plants- onion, gossypol, red maple
Snake venoms
Infectious diseases - lepto, babesisosis, anaplasmosis, bacillary hemoglobinuria
What is the treatment of copper toxicosis?
Ammonium tetrathiomolybate
D-penicillamine
How can copper toxicosis be prevented?
Molybdenized copper phosphate sprayed on pastures
Sheep rations should contain Cu/Mo at 6:1 ratio
Addition of molybdate to sheep ratios at 2-4ppm for prevention
Ammonium molybdate and thiosulfate orally per day prevents copper toxicosis in individual sheep
Supplemental since reduces hepatic copper accumulation
What are sources of molybdenum toxicosis?
Excess molybdenum -soil rich in molybdenum -plant accumulation -industrial contamination -fertilizers Copper deficiency
What is the normal function of molybdenum ?
Component of xanthine oxidase, which converts the purine xanthine to uric acid
Elevated molybdenum interferes with copper absorption
Excess molybdenum causes copper deficiency
What animals are the most susceptible animals to molybdenum toxicosis?
Cattle
What species are resistant to molybdenum toxicosis?
Horses and pigs
High dietary levels of __________ increases molybdenum toxicosis, while high dietary levels of ________ will decrease toxicosis?
Sulfate; copper
Where is molybdenum excreted?
Milk
What is the MOA of molybdenum toxicosis?
Copper deficiency
—> lack of hematopoeisis, CT metabolism, myelin formation, pigmentation, and bone formation
—> lack of cytochrome oxidase and aromatic amino acid-metabolizing enzymes
What are clinical signs associated with molybdenum toxicosis?
Severe diarrhea
Rough hair coat and depigmentation
Loss of weight, anemia, osteoporosis, exostosis, lameness, pica
Decreased libido in bulls and infertility in cows
How do you treat molybdenum toxicosis?
Copper glycinate SC
Copper sulfate added to diet
