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Toxicology > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

What are the 6 neurotoxins we talked about

A 
Pesticides
Pharmaceuticals
Mycotoxins
Ammoniated feed
Strychnine
Salt
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2
Q

What are OPs used in

A

Pesticides (replaced organochlorine pesticides

Flea collars, dips, fly, ant, and roach bait

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3
Q

What are examples of OPs

A

Parathion, malathion, chlorpyrifos

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4
Q

What is the MOA of OPs

A

Reversible inhibition of AChE activity

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5
Q

What are the clinical signs of OPs

A

Muscarinic- SLUDGE-M
Nicotinic- muscle fasciculations of face, generalized tremors, weakness, paralysis
CNS- resp depression, ataxia, nervousness, seizures

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6
Q

What specific test can be used to diagnose OPs

A

Atropine challenge- if affects of atropine are observed, toxicosis is NOT from AChE inhibition

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7
Q

How to treat OPs toxicosis

A

GI decontamination, bathing for dermal exposure
Atropine or glycopyrrolate for muscarinic signs
Oximes (protopam or 2-PAM) to reactivate AChE
Diazepam or other barbiturates for seizures

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8
Q

What is OPIDN

A

Organophosphate induced delayed neurotoxicity; OP compounds that inhibit NTE

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9
Q

What clinical signs will you see with OPIDN

A

Hindlimb weakness and paralysis from axonal degeneration of long motor neurons

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10
Q

What is ivermectin used in? What are the most common toxicosis from?

A

Deworming medication, anthelminthic in livestock

Accidental overdoses from owners and veterinarians

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11
Q

What dog breeds are sensitive to ivermectin

A

Border collies, australian shepherds, shelties

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12
Q

Ivermectin MOA

A

GABA receptor agonist

**affects can be cumulative because of long half-life

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13
Q

Clinical signs of ivermectin

A

Ataxia, lethargy, mydriasis, coma, blindness, bradycardia,
recumbency, disorientation, seizures in collies
resp distress before death,
anaphylactic shock if worms die off rapidly

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14
Q

Ivermectin treatment

A

GI decontamination with activated charcoal and lipid emulsion
Supportive care- careful of benzodiazepines

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15
Q

What is pyrethroid used in

A

Comes from flowers of chrysanthemum, and used as insectides

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16
Q

Examples of pyrethroid pesticides

A

Pyrethrin, permethrin, allethrin, fenvalerate (pydrin, blockade)

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17
Q

Who can pyrethroids not be used in

A

Cats because inefficient glucoronidation

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18
Q

Pyrethroid MOA

A

Binds voltage gated sodium channels- causes hyperactivity

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19
Q

Clinical signs of pyrthroids

A

Cats- drooling, paresthesia, muscle tremors and seizures, excessive muscle activity, hyperthermia

Dogs- paresthesia (shaking of legs, muscle fasciculations, rubbing of application site, agitation, nervousness)

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20
Q

Treatment for pyrethroids

A

Stabilize tremors/seizures with methcarbamol

Bathe

Lipid infusion

IV fluids

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21
Q

What is bromethalin

A

Rodenticide

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22
Q

Bromethalin MOA

A

Oxidative phosphorylation in CNS leading to loss of ion gradients resulting in fluid accumulation in myelin sheaths

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23
Q

Clinical signs of bromethalin

A

Ataxia, hindlimb paralysis, hyper excitability, severe muscle tremors, running fits, seizures

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24
Q

How to diagnose bromethalin

A

Cerebral edema and cerebellar degeneration

Histological evidence of neuronal vacuolization and edema

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25
Q

Bromethalin treatment

A

Emesis if recent exposure

Activated charcoal

Furosemide for cerebral and pulmonary edema

Treat seizures

Lipid infusion

26
Q

Alprazolam MOA

A

Acts at the limbic, thalamic, and hypothalamic level of CNS

27
Q

Clinical signs of alprazolam

A

Ataxia, depression, vomiting, tremors, tachycardia, diarrhea, hypothermia, liver failure

28
Q

Treatment for alprazolam

A

Emesis, gastric lavage, and/or activated charcoal

Flumazenil- benzodiazepine antagonist

29
Q

Zolpidem MOA

A

Binds GABA receptors

30
Q

Clinical signs of Zolpidem

A

Ataxia, vomiting, lethargy, disorientation, hyper salivation, hyperactivity and panting

31
Q

Treatment of Zolpidem

A

Supportive and symptomatic

32
Q

What is slaframine

A

Toxin produced by black patch fungus on red clover

33
Q

MOA of slaframin

A

Muscarinic cholinergic agonist

34
Q

Who is slaframine toxicity most common in

A

Horses and cattle

35
Q

Clinical signs of slaframine

A

Copious salivation is main sign

May also see bloat, diarrhea, frequent urination, feed refusal

36
Q

Treatment of slaframine

A

Remove source
Atropine
Rarely fatal

37
Q

What is fumonisin

A

Very sinister toxin from moldy corn

38
Q

MOA of fumonisin

A

Inhibits sphingosine-N-acetyltransferase causing increased levels of sphinganine which is toxic

39
Q

What does fumonisin toxicity cause

A

Increase permeability of vascular enothelial cells leading to stroke, hepatic injury, and pulmonary edema

40
Q

What species are susceptible to fumonisin

A

Horses/ponies, pigs, rabbites

41
Q

What two diseases are associated with fumonisin

A

Equine leucoencephalomalacia and porcine pulmonary edema

42
Q

Clinical signs of porcine pulmonary edema

A

Inactivity, increased resp rate, decreased heart reate, lethal pulmonary edema

43
Q

Clinical signs of ELEM

A

Most common in late fall/early winter

CNS- hysteria, profuse sweating, mania, excitability, post mortem liquefaction of brain

Liver- jaundice, hepatic encephalopathy

44
Q

Treatment of fumonisin

A

No treatment

Remove contaminated feed

Potentially ultrasorb S for pigs

45
Q

Why is ammonia and other NPN added to feed

A

To fuel microbes in the rumen

46
Q

What species does ammoniated feed toxicosis affect

A

Cows, sheep, goats

47
Q

What does ammoniated feed toxicosis cause

A

Bovine bonkers- alternating between hyperexcitability and normal behavior

48
Q

Treatment of ammoniated feed toxicosis (imidazole and NPN)

A

Just feed removal

Possibly sedation to prevent self harm while bonkers

49
Q

Strychnine MOA

A

Competitive antagonist of glycine receptors

50
Q

Clinical signs of strychnine

A

Anxiety, restlessness, stiff gait and neck, stiff facial muscles, seizures, sawhorse stance, hyperthermia in dogs

51
Q

Diagnosis of strychnine toxicity

A

Elevated CPK and LDH

Lactic acidosis, hyperkalemia, and leukocytosis

52
Q

Treatment for strychnine

A

Decontamination
Control seizures and prevent asphyxiation
Methcarbamol/phenobarbital
Ion trapping with ammonium chloride if animal is not acidotic

53
Q

What causes salt toxicity and who is it most common in

A

Water deprivation of consumption of large amounts of salt in pigs and cattle

54
Q

Salt MOA

A

Sodium diffuses into CSF, attracting water, and inhibiting glycolysis

55
Q

Clinical signs of salt toxicity

A

Salivation, thirst, abdominal pain, circling, wobbling, aimless wandering, head pressing, blindness, seizures, partial paralysis

Cattle may be belligerent and uncoordinated

56
Q

Salt toxicity diagnosis

A

Na levels over 160 is diagnostic in pigs and cows

57
Q

Salt treatment

A

Slow rehydration

Furosemide to prevent edema

58
Q

What should you differentiate salt toxicosis from

A

Polio
Lead
Pesticides
Encephalitis

59
Q

What should you differentiate ammonia toxicosis from

A

OPs, grain overload, chlorinated hydrocarbon pesticides, meningitis, and encephalitis

60
Q

What should you differentiate slaframine from

A

OPs and botulism

61
Q

What is the primary cause of pharmaceutical toxicosis

A

Improper storage

Toxicology (8 decks)

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