Toxicants Affecting the Circulatory & Hematopoietic Systems (11) Flashcards

1
Q

What are fumonisins?

A

mycotoxins produced by the fungus fusarium overticillioides

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2
Q

What does fumonisin induce in pigs?

A

porcine pulmonary edema

inhibits L type Ca2+ channel which decreases myocardial contractility = L-sided heart failure = pulmonary edema

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3
Q

What organ do fumonisins primarily target in pigs? Horses?

A

pigs: lungs

horses: brain

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4
Q

What are major factors in the content of ergot containing grain?

A

growing conditions
storage

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5
Q

What are the toxic principles in ergot toxicity?

A

ergonovine
ergotamine
lysergic acid amides
ergopeptines

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6
Q

What is the mechanism of toxicity of ergot?

A

acts agonistically at biogenic amine receptors in the animal’s body

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7
Q

Which molecules does ergot mimic in the body?

A

NE & epinephrine, dopamine, serotonin

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8
Q

What are clinical signs of ergot toxicity?

A

convulsions, hallucinations, abortion, paralysis, GI disturbance, gangrene of extremities

affects level of coronary band

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9
Q

What is fescue toxicity?

A

infected by the endophyte Neotyphodium coenophialum

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10
Q

How is fescue toxicity different than ergot toxicity?

A

fescue has an endophyte growing into the plant while ergot is on the outside

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11
Q

What is the most prevalent ergopeptine in fescue toxicity?

A

ergovaline - 90%

also have ergonovine and ergo line alkaloids

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12
Q

Why do cattle migrate to water with fescue toxicity?

A

ergovaline causes vasoconstriction (alpha-adrenergic) which makes them harder to regulate their body temperature

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13
Q

What is fescue foot?

A

having hoof lesions primarily at the coronary band because of blood supply

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14
Q

What is the toxin in black walnut?

A

juglone

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15
Q

What is the MOA for black walnut and which species does it affect? What does it cause?

A

wood shavings used for bedding for horses —> absorbed through then coronary band and skin

laminitis

horses

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16
Q

Blood and bone marrow toxicity may be a result of ____

A

off-target inhibition, leading to decreased bone marrow response or a result of peripheral effects

leads to destruction of blood cells

ROS - react with cells.ar proteins, lipids, other molecules = hemolysis

17
Q

What happens with Warfarin toxicity?

A

interferes with the clotting cascade

blocks vitamin K reductase

18
Q

What happens with warfarin blocking vitamin K reductase?

A

remains at oxidized form of vitamin K

19
Q

How do you treat rodenticide toxicity?

A

add reduced version of vitamin K

20
Q

What is the toxic agent in sweet clover?

A

coumarin —> dicoumarol which acts similar to warfarin and is an anticoagulant

21
Q

All anticoagulants have the basic ____ and ______ nucleus

A

coumarin
indanedione

22
Q

What do first generation anticoagulants require?

A

multiple feedings to result in toxicity

warfarin, pinion, coumafuryl, coumachlor

23
Q

What do “intermediate” anticoagulants require?

A

fewer feedings than “first generation” chemicals, and thus are more toxic to non target species

diphacinone

24
Q

What are characteristics of “second generation” anticoagulants?

A

highly toxic to non target species after a single feeding

ex. single feeding could kill rat

25
Q

What is the toxic principle in allium plants?

A

Trauma to the plant, like chewing, converts organosulfoxides to a sulfur-containing organic compounds

26
Q

What is the toxicologic mechanism for allium toxicity?

A

oxidative hemolysis, which occurs when the concentration of oxidants in the erythrocyte exceeds the capacity of the antioxidant metabolic pathways

causes oxidative hemolysis, red blood cells break up → Hb released → hemolytic anemia

27
Q

Why are allium spp. so toxic to dogs? Cats?

A

Dogs: catalase antioxidant activity in erythrocytes is low

Cats: 2-3x more susceptible to oxidative damage than the Hb in other species

28
Q

What does Allium form on red blood cells? Why?

A

Heinz bodies

sulfhemoglobin is less soluble than hemoglobin, so it precipitates, aggregates, and binds to the cell membrane

29
Q

How does one get zinc toxicity?

A
30
Q

What is the mechanism of toxicity of acetominophen in cats?

A

normally is metabolized by the UDP-glurcuronosyl transferase, but cats DO NOT have glucoronidase, so goes through the cytochrome P-450 pathway and is converted into N-acetyl-p-benzoquinoneimine which is toxic

31
Q

In acetaminophen toxicity, what regenerates glutathione (GSH)?

A

N-actyl cysteine