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Toxicology > Unit 1 - Cu, Mo, Se > Flashcards

Unit 1 - Cu, Mo, Se Flashcards

1
Q

What are the sources of copper for toxicity?

A

Feed/premixes, mineral blocks, injectable products, forage, water, and footbaths

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2
Q

In regards to dietary sources of copper for toxicosis, when do we typically get into problems?

A

Mis-mixes, off-label use, combination rations, and ration sharing

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3
Q

What species is extremely sensitive to elevated feed Cu levels?

A

Sheep

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4
Q

What elements are antagonists to Cu?

A

Mo, Fe, S, Zn, P, and Cd

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5
Q

What does thiomolybdate (Mo + S) do to copper? Where is it located?

A

It chelates it and decreases absorption

Located in the rumen

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6
Q

What are the different forms of copper?

A

Organic vs inorganic

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7
Q

Why is the absorption of Cu so low in rumininants and high in pre-ruminant individuals?

A

Ruminants have thiomolybdate in the rumen which ties up Cu and thus it is not absorbed. Non-ruminants do not have that

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8
Q

Where is copper excreted?

A

in the bile and feces

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9
Q

What is the MOA of copper?

A

There is Cu accumulation over time - when there is excess copper, the liver is completely saturated and there are high levels
Then there is a stress event and there is a massive release of that copper into the system
Initially the liver is able to compensate and store the Cu but then there is necrosis and Cu is no longer stored
Cu enters the blood stream and there is a hemolytic crisis and lysis of RBCs

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10
Q

What does Cu do once it hits the kidney? (this is a terrible question)

A

Changes its color - gun metal kidney

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11
Q

What stressful events can cause the massive release of copper from the liver?

A

Transport, handling, disease processes, extreme weather, attacked or chased, hepatotoxins, and consumption of garbage

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12
Q

What acute clinical signs are associated with copper toxicosis?

A

diarrhea, liver damage, and shock

Mimics As, Fe, and Se

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13
Q

When, during the copper toxicosis process, are there no clinical signs?

A

During the accumulation phase

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14
Q

What clinical signs are associated with post copper release?

A

Anorexia, weakness, depression, icterus, and hemoglobinuria (red wine urine)

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15
Q

What is the optimal sample for Cu status?

A

The liver

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16
Q

Why would we want the kidney if we have the liver in Cu toxicosis cases?

A

If there was a massive release of Cu then the liver concentration should be normal, however it will go to the kidneys once it leaves the liver so you may have high levels of Cu in the kidney

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17
Q

What samples are used for histopath exam in Cu toxicosis cases?

A

Fixed liver and kidney

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18
Q

Aside from liver and kidney, what samples are collected in Cu toxicosis cases?

A

Feed and feed labels

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19
Q

When will kidney values be elevated in cases of copper toxicosis?

A

Following a hemolytic crisis

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20
Q

Should you be concerned if there is a newborn ruminant with high liver Cu?

A

Do not be alarmed, during the last period of gestation, the mom is mobilizing her Cu to her calf

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21
Q

What will your clin path results be in a patient with copper toxicosis?

A

Elevated liver enzymes, red colored urine, and hemoglobin casts

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22
Q

What gross lesions do you see in a patient with copper toxicosis?

A 
Icterus in the mucus membranes, visceral tissue, and fat
Gun metal to black kidney
Friable +/- yellow liver
Hemolyzed serum (dark red to brown)
Hemoglobinuria
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23
Q

What microscopic lesions do you see in a patient with copper toxicosis?

A

Necrosis, fibrosis, and infiltration of the liver

Renal tubular necrosis and hemoglobin casts

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24
Q

How is copper toxicosis treated on the herd level?

A

Decrease or eliminate Cu with Na molybdate (SLOWLY) and increase Zn to 100-200 ppm

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25
Q

How is copper toxicosis treated on an individual level?

A

Chelators - D-penicillamine or Ammonium tetrathiomolybdate

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26
Q

How is copper toxicosis prevented?

A

Evaluate the feed and water sources

Know the geology of the region and the Cu levels in the soil

27
Q

What breeds have canine copper storage disease?

A

Bedlington, Skye, West Highland, and Doberman

28
Q

What is canine copper storage disease?

A

Chronic accumulation of Cu associated with decreased liver function

29
Q

How does canine copper storage disease clinically manifest?

A

Chronic hepatopathy/icterus, anorexia, vomiting, weakness, lethargy, dehydration, and coagulopathy

30
Q

Molybdenum is prominent in soils that are what?

A

Wet, poorly drained, and acidic

31
Q

What environments do you need to worry about molybdenum in the air?

A

Around aluminum and steel mills

32
Q

What is the MOA of molybdenum?

A

It is a copper antagonist so it results in copper deficiency

It promotes Cu excretion and decreases Cu absorption

33
Q

What are the clinical effects of molybdenum toxicity?

A

Greenish/bubbly diarrhea, decreased immune system function, decreased melanin synthesis, anemia, and decreased collagen strength

34
Q

What samples are important for detection of molybdenum toxicity?

A

Liver, serum, feed, forage, and water soil

35
Q

What lesions are associated with molybdenum toxicity?

A

Gross - swollen and friable liver and pale and swollen kidneys
Microscopic - rental tubular necrosis

36
Q

How is molybdenum toxicity treated?

A

Dietary change - decrease exposure to Mo or increase Cu

37
Q

What injectable products can be used to treat molybdenum toxicity?

A

Copper glycinate and multimin 90

38
Q

What are the sources of Se in cases of toxicosis?

A

Plants, injectables, and feed supplementation

39
Q

What are the antagonists of Se?

A

sulfur and arsenic

40
Q

What do selenium and sulfur fight for?

A

Intestinal transporters because they use the same ones

41
Q

Selenium is ____ absorbed, and is excreted in the ______ and ______.

A

readily, urine, feces

42
Q

What are the theorized MOA of selenium?

A

Production of free radicals, displacement of S from proteins, inhibition of RNA synthesis, and decreased ATP synthesis

43
Q

What are the three classical syndromes of selenium toxicity?

A

Acute, subacute, and chronic

44
Q

What is subacute selenium toxicity associated with and when does it occur?

A

There is onset within 1-4 weeks

They are typically associated with elevated feed

45
Q

What is chronic selenium toxicity associated with and when does it occur?

A

Onset - weeks to months

Source - plant sources; dietary contamination over time

46
Q

What obscure syndrome does seleneium toxicity cause?

A

White muscle disease

47
Q

What clinical signs are associated with acute selenium toxicity?

A

Labored breathing and respiratory distress
+/- gastroenteritis
Convulsive spasms
Death

Typically presents as shock

48
Q

What are the most common causes of acute selenium toxicity?

A

Misuse of injectables

Rations/supplementation misformulation

49
Q

What clinical signs are associated with subacute selenium intoxication?

A

Swine - hind limb ataxia that results in progressive posterior paresis, decreased intake and growth, lameness
Avian - decreased reproduction, decreased hatchability, and malformations

50
Q

What are the two different diseases that chronic selenium intoxication causes?

A

Alkali disease and blind staggers

51
Q

What clinical signs are associated with alkali disease?

A

Weakness/depression, lameness due to hoof over growth, hair loss, and hair discoloration

52
Q

What clinical signs are associated with blind staggers?

A

Blindness, wandering around, inability to eat or drink, and death

53
Q

What samples can/should be collected for Se analysis?

A

Serum, whole blood, liver, kidney, feed/forage/plants, hair, and hoof wall

54
Q

What conditions may hair and hoof wall be useful for?

A

Chronic selenium toxicity

55
Q

What samples can be used for histopathology in cases of selenium toxicosis?

A

Heart, lung, spinal cord, liver, kidney, and skeletal muscle

56
Q

T/F - A high liver value of selenium is indicative of toxicity.

A

False, it does not always indicate toxicity. You should be aware of what was given and when it was given

57
Q

What gross lesions are associated with acute selenium toxicity?

A

Pulmonary - edema, congestion, and hemorrhage

58
Q

What gross lesions are associated with subactue selenium toxicity?

A

Hood separation

59
Q

What gross lesions are associated with chronic selenium toxicity?

A

Hoof malformations and loss of hair

60
Q

What microscopic lesions are associated with chronic selenium toxicity?

A

Bilateral poliomyelomalacia in the spinal cord
Edema, congestion, and hemorrhage in the lungs
Cortical necrosis in the kidneys

61
Q

How is acute selenium toxicity treated?

A

There is no effective treatment - just treat for shock

62
Q

How is subacute selenium toxicity treated?

A

Just wait for Se depletion

63
Q

How is chronic selenium toxicity treated?

A

There is no good treatment

Focus on prevention

64
Q

How can selenium toxicity be prevented?

A

Eliminate and decrease exposure

Have high sulfur and low Se diets

Toxicology (32 decks)

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