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RUSVM Toxicology > Iron, Copper, and Molybdenum Toxicosis > Flashcards

Iron, Copper, and Molybdenum Toxicosis Flashcards

1
Q

What are the usual sources of iron toxiciosis?

A

Accidental ingestion of human oral supplements

Overdosage in pet or piglets

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2
Q

What are the three forms that iron is present in?

Which is the most irritating and astringent?

A

Elemental
Divalent (ferrous)
Trivalent (ferric) —> most irritating and astringent

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3
Q

T/F: toxicity of oral iron preparations is more toxic than parenteral preparations

A

False

Parenteral is more toxic than oral

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4
Q

Greater than 5000ppm iron in diet can lead to ________ in piglets because it interferes with phosphate absorption

A

Rickets

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5
Q

How is iron absorbed ??

A

Ferrous iron absorbed in small intestine using energy-dependent carrier

Ferrous iron is oxidized to ferric iron once absorbed

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6
Q

Ferric iron binds to ___________ in plasma and is distributed throughout the body

A

Transferrin

70% to hemoglobin
10% to myoglobin
Rest to enzymes or stored in liver/spleen/bones

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7
Q

What is the MOA of iron toxicosis ?

A

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

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8
Q

Injectable iron can cause what type of reaction causing an acute rapid death?

A

Anaphylactic reaction -histamine release

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9
Q

What are the 4 stages of acute iron toxicosis?

A
  1. Nausea, vomiting, diarrhea, GI hemorrhage
  2. Apparent recovery
  3. Vomiting, diarrhea, GI hemorrhage, metabolic acidosis, coagulation disorders, hepatic failure, CV collapse
  4. GI obstruction
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10
Q

What lesion is associated with parenteral preparations of iron?

A

Yellowish-brown discoloration at injection site and near lymph node

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11
Q

What lesions are seen with oral preparations of iron?

A

GI ulcer and hemorrhagic enteritis

Congestion of liver, kidney, liver necrosis, icterus, and hemoglobinuria

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12
Q

How do you treat iron toxicosis?

A

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

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13
Q

What is more common, acute or chronic copper toxicosis?

A

Chronic

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14
Q

Vomiting, colic, hemorrhagic diarrhea, dehydration, and shock are signs of acute/chronic copper toxiciosis?

A

Acute

—> direct corrosive action of copper on GI

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15
Q

What are the sources of chronic copper toxiciosis?

A

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

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16
Q

What normally binds copper in tissues and forms a compound that is readily excreted in the urine?

A

Molybdenum

Binds to copper at 4:3 ratio —> copper molybdate (CuMoO4)

17
Q

What is reduced in the rumen that binds copper to reduce its absorption?

A

Sulfites are reduced to sulfides

18
Q

T/F: Normal feed and forage copper levels can cause toxicity when molybdenum or sulfate is unavailable

A

True

19
Q

How long does it take for copper accumulation to occur in sheep?

A

2-10weeks exposure

20
Q

What is the MOA of copper toxicosis?

A

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

21
Q

What are the clinical signs of chronic copper toxicity?

A

Sudden onset of weakness, anorexia, pale mucous membranes, icterus, hemoglobinuria, fever, dyspnea, and shock

22
Q

What lesions do you see in chronic copper toxicosis?

A

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)

23
Q

What is the DDX for copper toxicity?

A

Hemolytic agents- zinc, naphthalene, DMSO, Guaifenesin

Poisonous plants- onion, gossypol, red maple

Snake venoms

Infectious diseases - lepto, babesisosis, anaplasmosis, bacillary hemoglobinuria

24
Q

What is the treatment of copper toxicosis?

A

Ammonium tetrathiomolybate

D-penicillamine

25
Q

How can copper toxicosis be prevented?

A

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

26
Q

What are sources of molybdenum toxicosis?

A 
Excess molybdenum 
-soil rich in molybdenum
-plant accumulation 
-industrial contamination 
-fertilizers 
Copper deficiency
27
Q

What is the normal function of molybdenum ?

A

Component of xanthine oxidase, which converts the purine xanthine to uric acid

Elevated molybdenum interferes with copper absorption
Excess molybdenum causes copper deficiency

28
Q

What animals are the most susceptible animals to molybdenum toxicosis?

A

Cattle

29
Q

What species are resistant to molybdenum toxicosis?

A

Horses and pigs

30
Q

High dietary levels of __________ increases molybdenum toxicosis, while high dietary levels of ________ will decrease toxicosis?

A

Sulfate; copper

31
Q

Where is molybdenum excreted?

A

Milk

32
Q

What is the MOA of molybdenum toxicosis?

A

Copper deficiency
—> lack of hematopoeisis, CT metabolism, myelin formation, pigmentation, and bone formation
—> lack of cytochrome oxidase and aromatic amino acid-metabolizing enzymes

33
Q

What are clinical signs associated with molybdenum toxicosis?

A

Severe diarrhea
Rough hair coat and depigmentation

Loss of weight, anemia, osteoporosis, exostosis, lameness, pica
Decreased libido in bulls and infertility in cows

34
Q

How do you treat molybdenum toxicosis?

A

Copper glycinate SC

Copper sulfate added to diet

RUSVM Toxicology (23 decks)

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