Selenium Flashcards by holly prychka

What is the most common source of selenium toxicosis?

selenium accumulating plants

**seleniferous plants

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T/F: All selenium deficiency diseases are necrotizing

true

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What are the geographic locations of selenium deficient soil?

Northwest
Northeast
Southeast
Great lakes

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

South Dakota
North Dakota
Wyoming
Montana
Nebraska
Kansas
Utah 
Colorado
New Mexico

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What is the basic selenium requirements for animals?

0.1 mg/kg (depends on vitamin E)

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What animals have selenium in their feed supplements?

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

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What animals are most susceptible to grazing upon seleniferous plants?

cattle, sheep, and horses

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

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Up to how many ppm Se do obligate accumulators hold?

15,000 ppm Se

these plants require Se for growth

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What plants are Se obligate accumulators?

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

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

FALSE

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

25-100 ppm Se

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

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What are some examples of facultative Se accumulating plants?

Aster
Atriplex - saltbush
Castilleja - paintbrush

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

1-25 ppm Se

accumulate Se passively when in Se rich soil

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What are some examples of passive Se accumulating plants?

crop plants such as:
Corn
wheat
oats
barley
grass
hay

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

Passive accumulators

these are the most edible plants

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When may you see selenium toxicosis in small animals?

Improper use of selenium medicated shampoos

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T/F: Waterfowl are resistant to selenium contaminated water

FALSE

Causes teratogenic effects

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What are the three oxidative states of selenium?

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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T/F: Selenium is an irritant to mucus membranes

TRUE

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In therapeutic doses Selenium and vitamin E do what?

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

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

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

Highly toxic

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

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

20 - 50 ppm

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

5-10 ppm

What kind of soil will promote formation of selenate?

Arid alkaline soil of the great plains

T/F: Elemental Se is highly toxic

False relatively non toxic

What kind of diet can reduce Se toxicity?

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

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

TRUE * readily absorbed in the small intestine * elemental Se is NOT absorbed - insoluble in water

Where is Se distributed in the body?

throughout - more so to the liver, kidney, and spleen In chronic toxicity - high levels will be in the hair and hooves

How is Se excreted?

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

What heavy metal will increase biliary excretion of selenium?

Organic arsenic

What is the MOA of selenium toxicosis?

* 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

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

Respiratory insufficiency from pulmonary edema and hemorrhage due to decreased energy --> capillary damage

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

Starvation and thirst resulting from weakness, lameness, blindness

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

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

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

Blind staggers *dude to locomotor signs (patients are not blind)

What are the clinical signs associated with subacute Se toxicosis?

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

What clinical signs are associated with Se toxicosis in swine?

"porcine focal symmetrical poliomyelomalacia" Neuro signs - incoordination, lameness, paralysis alopecia, hoof abnormalities, separation of the hoof

What clinical signs are associated with chronic Se toxicosis?

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

What lesions are associated with Acute Se toxicosis?

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

What lesions are associated with subacute Se toxicosis in swine?

Focal symmetrical poliomyelomalacia

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

Chronic

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

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

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

blood, kidney, liver | specimens in chronic toxicosis = hair and hoof

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

Cattle, sheep, and swine NOT horses

What are DDX for acute Se toxicosis?

Pneumonia, infectious hepatitis, enterotoxemia, and pasteurellosis

What are DDX for acute Se toxicosis?

Molybdenum tox, fluoride tox, freezing, ergotism, laminitis

What treatments are available for Se. toxicosis?

No specific antidote Saline cathartics Symptomatic therapy - O2, IVF, tx for HGE Acetylcysteine

What should be done to prevent Se toxicosis?

* 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

What is the prognosis of acute Se toxicosis?

POOR - animals die quickly