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Toxicology > Selenium toxicosis > Flashcards

Selenium toxicosis Flashcards

1
Q

T/F: Overdosing selenium deficiency treatment can lead to selenium toxicosis

A

TRUE

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2
Q

What levels are considered selenium deficient?

A

<0.05 ppm

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3
Q

Selenium deficiency diseases?

A
  • White muscle disease (WMD) or nutritional muscle dystrophy (NMD) in lambs, but also seen in calves and foals
  • Hepatosis dietetica in young pigs
  • Exudative diathesis in chicks
  • Nutritional pancreatic atrophy in chickens
  • Porcine stress syndrome in pigs
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4
Q

Where is selenium deficient soil common?

A
  • Northwest
  • Northeast
  • Southeast
  • Great lakes
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5
Q

What level of selenium qualifies soil as selenium-rich? Where is it located?

A
  • 2-10 ppm
  • South Dakota
  • North Dakota
  • Wyoming
  • Montana
  • Nebraska
  • Kansas
  • Utah
  • Colorado
  • New Mexico
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6
Q

What are the selenium requirements?

A

0.1 mg/kg (depends on vitamin E)

Remember: 0.1mg/kg = 0.1ppm

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7
Q

What are the various uses for selenium?

A
  • Feed supplements for cattle, sheep, swine, and poultry
  • Injectable selenium-vitamin E preparations
  • Antioxidant supplements (animal and human)
  • Used in medical shampoos for treatment of dermatitis
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8
Q

Sources of selenium?

A
  • Cattle, sheep, and horses may graze seleniferous plants
  • Swine and poultry may eat grains grown on selenium-rich soil
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9
Q

What are seleniferous plants? What are the various types?

A

Plants that accumulate Se in Se-rich soil

Obligate accumulators (Se-indicator plants), facultative accumulators, and passive accumulators

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10
Q

How much Se can obligate accumulators accumulate?

A

Up to 15,000 ppm Se

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11
Q

T/F: Obligate Se accumulators require Se for growth

A

TRUE

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12
Q

What plants are obligate accumulators of Se?

A
  • Astragalus (locoweed, milk vetch)
  • Stanleya (prince’s plume)
  • Oonopsis (golden wood)
  • Xylorrhiza (woody aster)
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13
Q

How much Se can facultative accumulators collect?

A

Accumulate up to 25-100 ppm

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14
Q

Do facultative accumulators require Se?

A

Nope, but they can accumulate it

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15
Q

Examples of facultative accumulators?

A
  • Aster
  • Atriplex (saltbush)
  • Castilleja (paint brush)
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16
Q

Passive accumulators: Se levels?

A

Accumulate up to 1-25 ppm Se

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17
Q

Where do passive accumulators build up Se?

A

Accumulate Se passively in Se-rich soil

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18
Q

Examples of passive Se accumulators?

A

Many plants including crop plants such as corn, wheat, oats, barley, grass, hay, and other plants

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19
Q

Causes of Se toxicosis?

A
  • Overdosage w/ Se preparations or supplements
  • Se-contaminate water causes teratogenic effects in waterfowl
  • Improper use of Se-medicated shampoos may cause toxicosis in small animals
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20
Q

What is this?

A

Astragalus (locoweed)

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21
Q

What is this?

A

Astragalus (milkvetch)

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22
Q

What is this?

A

Stanleya pinnata (prince’s plume)

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23
Q

T/F: Se is a non-essential trace element

A

FALSE–it is an essential trace element

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24
Q

What 3 states does Se have?

A

3 oxidation states: selenate (+6), selenite (+4), and selenide (+2)

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25
Q

What elements are Se’s physical and chemical properties similar to?

A

Sulfur and arsenic

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26
Q

T/F: Se combines with the -NH3 group of glutathione

A

FALSE–Se combines with the -SH group of glutathione

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27
Q

What is Se a component of?

A

Glutathione peroxidase (GSH-Px)

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28
Q

How does selenium act as an antioxidant?

A

By prevention of peroxide accumulation through reduction of glutathione

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29
Q

What is synergistic to GSH-Px?

A

Vitamin E

30
Q

What does Se-vitamin E prevent?

A

Cellular degeneration and cell membrane damage in animals and poultry

31
Q

T/F: Se is also found in 5-deiodinase (conversion of T4 to T3)

A

TRUE

32
Q

What is Se an irritant to?

A

Mucous membranes (like other metals)

33
Q

What is the toxicity of the various Se forms (greatest to least)?

A

Organic Se in plants > selenate = selenite > selenide > synthetic organoselenium compounds

34
Q

What are the acute toxic doses of oral selenium (selenite)?

A
  • 3.3 mg/kg in the horse
  • 10 mg/kg in cattle
  • 17 mg/kg in swine
35
Q

What is the oral Se subacute toxic level for swine?

A

20-50 ppm for 3 days or more

36
Q

What is the chronic toxic level of selenium?

A

5-10 ppm for several weeks or months in horses, cattle, and swine

37
Q

Which soil promotes formation of selenate?

A

Arid alkaline soil of the Great Plains

38
Q

T/F: Elemental Se is relatively nontoxic

A

TRUE

39
Q

What is toxicity reduced by?

A

High protein diet and ingestion of other elements that bind Se such as Cu

40
Q

T/F: Seleniferous plants are odorless and palatable

A

FALSE–Seleniferous plants have a bad odor and are unpalatable (only eaten when other forage is unavailable)

41
Q

Where is Se readily absorbed from?

A

Small intestine

42
Q

Which Se state is more readily absorbed?

A

The soluble organic Se in plants is more rapidly absorbed than selenite, selenate, and selenide

43
Q

Is elemental Se absorbed?

A

Nope–it’s not soluble in water

44
Q

Where is Se distributed in the body?

A

Distributed throughout the body particularly to the liver, kidney, and spleen

45
Q

Chronic exposure of Se leads to high concentrations where in the body?

A

Hair and hoof

46
Q

T/F: Se crosses the placenta (teratogenic) but is not excreted in milk

A

FALSE–it crosses the placenta and is excreted in milk

47
Q

Where is Se excreted? What increases its excretion?

A

Se is mainly excreted in urine, but also in bile

Arsenic increases biliary excretion

48
Q

T/F: Se causes irritation of GI mucosa (subacute and acute)

A

TRUE

49
Q

Se toxicosis causes dramatic depletion of what?

A

Tissue glutathione (GSH)

50
Q

What does Se replace following Se toxicosis?

A

Replaces sulfur in amino acids causing abnormal proteins

51
Q

What does Se toxicosis decrease?

A

Decreases ATP in chronic toxicosis

Decreased tissue absorbic acid

52
Q

What is death in acute and subacute Se toxicosis mainly due to?

A

Respiratory insufficiency resulting from pulmonary edema and hemorrhage

53
Q

What might death in chronic Se toxicosis be due to?

A

Starvation and thirst resulting from weakness, lameness, blindness

54
Q

Clinical signs of acute oral Se toxicosis?

A
  • Onset in a few hours to a few days
  • GI signs such as colic, bloat, and dark watery diarrhea
  • Resp signs such as labored resp w/ fluid sounds in the lungs, bloody froth from the nares, and cyanosis
  • Other signs include fever, polyuria, mydriasis, and uncertain gait
  • Death in hours
55
Q

Clinical signs of acute parenteral Se toxicosis?

A

Neuro signs including mydriasis and incoordination

56
Q

What do ranchers call subacute Se toxicosis in cattle?

A

“Blind staggers”

57
Q

Clinical signs during stage 1 of subacute Se toxicosis in cattle?

A
  • Poor appetite
  • Aimless wandering
  • Circling
  • Walking through objects
  • Normal respiration and temperature
58
Q

Clinical signs during stage 2 of subacute Se toxicosis in cattle?

A
  • Stage 1 signs +:
  • Depression
  • Incoordination
  • Foreleg weakness and walking on the knees
  • Complete anorexia
59
Q

Clinical signs during stage 3 of subacute Se toxicosis in cattle?

A
  • Colic
  • Hypothermia
  • Emaciation
  • Clouded corneas near blindness
  • Paresis
  • Coma
  • Death in a few hours
60
Q

Clinical signs of subacute Se toxicosis in sheep?

A

Signs are similar to cattle but the stages are not well defined

61
Q

Clinical signs of subacute Se toxicosis in swine?

A
  • A neuroparalytic condition called “porcine focal symmetrical poliomyelomalacia”
  • Neuro signs include coordination, lameness, and paralysis
  • Other signs including alopecia, hoof abnormalities and separation of the hoof
62
Q

Clinical signs of chronic toxicosis (alkali disease)?

A
  • Rough hair coat, loss of hair from mane and tail
  • Hoof deformities and sloughing, stiffness of joints, and lameness
  • Partial blindness, anemia, lethargy, emaciation, infertility, and birth defects
63
Q

What are the lesions of acute Se toxicosis?

A
  • Hemorrhagic gastroenteritis
  • Congestion of organs
  • Hemorrhages
  • Pulmonary edema
  • Hydrothorax
  • Gut contents may smell like rotten garlic or rotten horseradish (hydrogen selenide)
64
Q

What are the lesions of subacute Se toxicosis in swine?

A

Focal symmetrical poliomyelomalacia

65
Q

What are the lesions of chronic Se toxicosis?

A
  • Abnormal hooves
  • Cardiac damage
  • Hepatic necrosis
66
Q

Lab analysis of Se toxicosis (acute vs. chronic)?

A
  • Elevated Se (> 2ppm in acute and >5ppm in chronic)
    • Acute: blood, kidney, liver
    • Chronic: hair and hoof (must be washed before analysis)
  • Blood or plasma glutathione peroxidase activity correlates well w/ blood Se concentration in cattle, sheep, and swine (but NOT in horses)
67
Q

DDx for acute or subacute Se toxicosis?

A
  • Pneumonia
  • Infectious hepatitis
  • Enterotoxemia
  • Pasteurellosis
68
Q

DDx for chronic Se toxicosis?

A
  • Molybdenum toxicosis
  • Flouride toxicosis
  • Freezing
  • Ergotism
  • Laminitis
69
Q

What is the treatment for acute Se toxicosis?

A
  • Saline cathartics
  • Symptomatic therapy (oxygen, treatment for pulmonary edema, circulatory shock, and gastroenteritis)
  • Acetylcysteine (140mg/kg IV, followed by 70mg/kg daily in 4 divided doses)
70
Q

What are some preventions for subacute and chronic Se toxicosis?

A
  • Soil and forage should be tested regularly for Se levels
  • Remove the animals from seleniferous areas
  • Addition of Cu to the diet, high protein diet, increasing Su-containing proteins may reduce toxicosis
  • Addition of organic arsenicals to the diet increases biliary excretion of Se
71
Q

Prognosis of acute Se toxicosis?

A

Poor–animals die quickly

Toxicology (22 decks)

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