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ToxFall17 COPY for AeJ > Selenium > Flashcards

Selenium Flashcards

1
Q

What is the most common source of selenium toxicosis?

A

selenium accumulating plants

**seleniferous plants

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2
Q

T/F: All selenium deficiency diseases are necrotizing

A

true

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3
Q

What are the geographic locations of selenium deficient soil?

A

Northwest
Northeast
Southeast
Great lakes

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4
Q

What are the geographic locations of selenium rich soil (2-10ppm) ?

A 
South Dakota
North Dakota
Wyoming
Montana
Nebraska
Kansas
Utah 
Colorado
New Mexico
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5
Q

What is the basic selenium requirements for animals?

A

0.1 mg/kg (depends on vitamin E)

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6
Q

What animals have selenium in their feed supplements?

A

Used in supps for cattle, sheep, swine, and poultry

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7
Q

What animals are most susceptible to grazing upon seleniferous plants?

A

cattle, sheep, and horses

*swine and poultry may eat grain grown in selenium rich soil

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8
Q

Up to how many ppm Se do obligate accumulators hold?

A

15,000 ppm Se

these plants require Se for growth

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9
Q

What plants are Se obligate accumulators?

A

Astragalus - locoweed/ milk vetch
Stanleya - prince’s plum
Oonopsis- golden wood
Xylorrhiza - woody aster

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10
Q

T/F: Obligate Se accumulating plants are very palatable to herbivores

A

FALSE

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11
Q

Up to how many ppm do faculatative Se accumulating plants hold?

A

25-100 ppm Se

These plants DO NOT require Se for growth, they just accumulate it

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12
Q

What are some examples of facultative Se accumulating plants?

A

Aster
Atriplex - saltbush
Castilleja - paintbrush

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13
Q

Up to how many ppm do passive Se accumulating plants hold?

A

1-25 ppm Se

accumulate Se passively when in Se rich soil

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14
Q

What are some examples of passive Se accumulating plants?

A 
crop plants such as:
Corn
wheat
oats
barley
grass
hay
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15
Q

What category of Se accumulating plants are the most common to cause toxicosis?

A

Passive accumulators

these are the most edible plants

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16
Q

When may you see selenium toxicosis in small animals?

A

Improper use of selenium medicated shampoos

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17
Q

T/F: Waterfowl are resistant to selenium contaminated water

A

FALSE

Causes teratogenic effects

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18
Q

What are the three oxidative states of selenium?

A

selenate (+6)
selenite (+4)
Selenide (-2)

**selenate and selenite can be toxic

Selenide is not absorbed and will go straight through and out the GI tract

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19
Q

T/F: Selenium is an irritant to mucus membranes

A

TRUE

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20
Q

In therapeutic doses Selenium and vitamin E do what?

A

Prevent cellular degeneration and cell membrane damage

Se also:

  • Plays a role in conversion of T4 - T3
  • is a component of glutathione peroxidaes - acts as an antioxidant
  • binds with the -SH group of glutathione
21
Q

What is the acute toxic oral dose of selenium (selenite) in horses, cattle, and swine?

A

Horse - 3.3 mg/kg
cattle - 10 mg/kg
swine - 17 mg/kg

Highly toxic

Toxicity:
organic selenium > selenate/selenite > selenide > synthetic organoselenium compounds

22
Q

The selenium oral subacute toxic level for swine is ____ ppm for 3 days or more

A

20 - 50 ppm

23
Q

The chronic toxic level for horses, cattle, and swine is ____ ppm for several weeks or months

A

5-10 ppm

24
Q

What kind of soil will promote formation of selenate?

A

Arid alkaline soil of the great plains

25
Q

T/F: Elemental Se is highly toxic

A

False

relatively non toxic

26
Q

What kind of diet can reduce Se toxicity?

A

high protein diet and ingestion of other elements that bind Se (such as copper)

27
Q

T/F: The soluble organic selenium in plants is more rapidly absorbed than selenite, selenate, and selenide

A

TRUE

  • readily absorbed in the small intestine
  • elemental Se is NOT absorbed - insoluble in water
28
Q

Where is Se distributed in the body?

A

throughout - more so to the liver, kidney, and spleen

In chronic toxicity - high levels will be in the hair and hooves

29
Q

How is Se excreted?

A

Mostly in the urine but it also crosses the placental (teratogenic) and can be excreted in the milk

30
Q

What heavy metal will increase biliary excretion of selenium?

A

Organic arsenic

31
Q

What is the MOA of selenium toxicosis?

A
  • Irritation of the GI mucosa (acute and subacute)
  • Dramatic depletion of tissue glutathione (GSH)
  • Selenium replaced sulfur in amino acids causing abnormal proteins (hoof/hair damage)
  • decrease ATP
  • decrease tissue ascorbic acid
32
Q

What is the main cause of death in acute and subacute Se toxicosis?

A

Respiratory insufficiency from pulmonary edema and hemorrhage

due to decreased energy –> capillary damage

33
Q

What is death in chronic Se toxicosis most commonly associated with?

A

Starvation and thirst resulting from weakness, lameness, blindness

34
Q

What is the time frame and clinical signs associated with acute Se toxicosis?

A

Onset in a few hours to a few days

GI signs: colic, bloat, watery dhr
Resp. signs: labored respiration with fluid sounds in the lung, bloody froth from the nares, cyanosis
Fever, polyuria, mydriasis, uncertain gait

death in hours

35
Q

What is the layman’s term for Subacute Se toxicosis in cattle?

A

Blind staggers

*dude to locomotor signs (patients are not blind)

36
Q

What are the clinical signs associated with subacute Se toxicosis?

A

Stage 1: poor appetite, aimless walking, circling, normal resp/temp

Stage 2: added - depression, incoordination, foreleg weakness/walking on the knees, anorexia

Stage 3: colic, hypothermia, emaciation, clouded corneas - near blindness, paresis, coma, death in hours

*sheep are similar but stages are less well defined

37
Q

What clinical signs are associated with Se toxicosis in swine?

A

“porcine focal symmetrical poliomyelomalacia”

Neuro signs - incoordination, lameness, paralysis

alopecia, hoof abnormalities, separation of the hoof

38
Q

What clinical signs are associated with chronic Se toxicosis?

A

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

aka Alkali dz

39
Q

What lesions are associated with Acute Se toxicosis?

A

HGE, congestion of organs, hemorrhages, pulmonary edema, hydrothorax, - gut contents have foul rotten garlic smell

40
Q

What lesions are associated with subacute Se toxicosis in swine?

A

Focal symmetrical poliomyelomalacia

41
Q

Abnormal hooves, cardiac damage, and hepatic necrosis are all lesions associated with which stage of Se toxicosis?

A

Chronic

42
Q

T/F: When sending the hoof for chemical analysis (Se) you should wash it first

A

TRUE

this is an exception to the rule - but you want to make sure selenium from the soil on the exterior of the hoof is not contaminating the actual tissue

43
Q

What specimens should be collected for chemical analysis in acute Se toxicosis?

A

blood, kidney, liver

specimens in chronic toxicosis = hair and hoof

44
Q

Blood or plasma glutathione peroxidase activity correlates well with blood Se concentration in which species?

A

Cattle, sheep, and swine

NOT horses

45
Q

What are DDX for acute Se toxicosis?

A

Pneumonia, infectious hepatitis, enterotoxemia, and pasteurellosis

46
Q

What are DDX for acute Se toxicosis?

A

Molybdenum tox, fluoride tox, freezing, ergotism, laminitis

47
Q

What treatments are available for Se. toxicosis?

A

No specific antidote

Saline cathartics
Symptomatic therapy - O2, IVF, tx for HGE

Acetylcysteine

48
Q

What should be done to prevent Se toxicosis?

A
  • Test soil/forage regularly, *remove animals from seleniferous areas, *addition of copper to the diet, *high protein diet, *increasing sulfur containing proteins may prevent toxicosis
  • addition of organic arsenicals to the diet to increase biliary excretion of Se
49
Q

What is the prognosis of acute Se toxicosis?

A

POOR - animals die quickly

ToxFall17 COPY for AeJ (38 decks)

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