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Toxicology > Unit 1 - Organophosphates and Carbamates > Flashcards

Unit 1 - Organophosphates and Carbamates Flashcards

1
Q

What are organophosphates derived from?

A

Phosphoric acid - they are esters of it

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2
Q

What are carbamates derived from?

A

carbamic acid

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3
Q

What are the sources of organophosphates and carbamates?

A

Corn rootworm products, external parasite control, premises, unintentional poisoning, and malicious poisoning

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4
Q

Organophosphates and carbamates are _______ absorbed, metabolized in the ______, distributed throughout ______ and _______, and excreted in _____ and ______.

A

Rapidly, liver, blood, CNS, urine, and feces

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5
Q

What is the MOA of organophosphates?

A

They irreversibly bind to acetyl cholinesterase thus inhibiting the breakdown of ACHe. This results in continued stimulation of nicotinic and muscarinic receptors

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6
Q

What is the MOA of carbamates?

A

They bind to acetylcholinesterase and spontaneously separate thus inhibiting the breakdown of ACHe. This results in continued stimulation of nicotinic and muscarinic receptors

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7
Q

T/F - Organophosphates and carbamates cause death within minutes because they are very toxic.

A

True - to put it in persepctive, a tablespoon is enough to kill an adult cow/bull

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8
Q

Are dogs or cats more susceptible to carbates and organophosphates? Brahman vs English Cattle? Males vs females?

A

Cats , Brahman, and males are more susceptible

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9
Q

When is the onset of clinical signs for organophosphates and carbamates?

A

Minutes to hours

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10
Q

What parasympathetic clinical signs are associated with organophosphate and carbamate toxicity?

A

Salivation, lacrimation, urination, and defecation (SLUD)

Miosis, bradycardia, bronchoconstriction, dyspnea, and vomiting

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11
Q

What neuromuscular clinical signs are associated with organophosphate and carbamate toxicity?

A

Tremors, stiffness, and paralysis

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12
Q

What CNS clinical signs are associated with organophosphate and carbamate toxicity?

A

Nervousness and seizures

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13
Q

What antemortem samples would be good for the diagnosis of organophosphates and carbamate toxicity?

A

Blood and vomitus

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14
Q

What will you find in an antemortem blood sample in a patient with organophosphate or carbamate toxicity?

A

Cholinesterase concentration

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15
Q

What will you find in an antemortem vomitus sample in a patient with organophosphate or carbamate toxicity?

A

The parent compound

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16
Q

What post mortem samples will have a high cholinesterase concentration in organophosphate or carbamate toxicity cases?

A

Brain and retina

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17
Q

What post mortem samples will have the parent compound in organophosphate or carbamate toxicity cases?

A

Rumen contents, stomach contents, and hair

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18
Q

Aside from patient samples, what else can you sample to help diagnose an organophosphate or carbamate toxicity? What will you find in these samples?

A

Bait/suspected material and feed

You would find the parent compound

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19
Q

The cholinesterase test is a screen meaning it will only increase if there is >__% inhibition. It is only suggestive of OP/carbamate toxicosis.

A

> 50% inhibition

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20
Q

What factors can affect cholinesterase levels?

A

Carbamates, autolysis, and freezing

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21
Q

What lesions are associated with OP/carbamate toxicosis?

A

There are no specific gross or microscopic lesions, but you may observe colorful/odd material in the GI tract

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22
Q

What is the antidote for OP/carbamate toxicosis? How does it work?

A

Atropine - it binds to muscarinic receptors and prevents ACh from binding

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23
Q

What do you need to be aware of when administering atropine?

A
  1. There are different concentrations in large and small animal bottles
  2. There is a decrease in efficacy after 2-3 doses
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24
Q

If you are unsure if it is an OP/carbamate toxicosis, what should you do?

A

Give 1/10 of the dose and monitor the response. If you are correct, the pupils will dilate

25
Q

Why don’t you want to give too much atropine?

A

There is no reversal

26
Q

What treatment, alternative to atropine, only works for OP toxicosis?

A

2-PAM

27
Q

What might 2-PAM not work for carbamates?

A

Since carbamates spontaneously separate, if we are trying to reactivate, the carbamate may have already separated so we are not doing a whole lot

28
Q

What can be used to treat OP/Carbamate toxicosis besides atropine and 2-PAM?

A

Glycopyrrolate

29
Q

What should be done in addition to administering atropine (or the other 2 options) when treating OP/Carbamate toxicosis?

A

decontamination - activated charcoal or wash with soap/detergent (if dermal)

30
Q

What is chlorpyrifos?

A

A common OP on the market

31
Q

How does chlorpyrifos effect cats?

A

Intermediate syndrome
Delayed signs (1-5 days) - tremors, ataxia, seizures, depression, and anorexia
Persists for weeks

32
Q

What cattle breeds does chlorpyrifos effect?

A

‘exotic’ breeds

33
Q

What does chlorpyrifos do to cattle?

A

Delayed toxicosis - 10-14 days
Classical signs
Anorexia and weight loss

34
Q

What environmental and food safety considerations need to be taken for OP/carbamate toxicosis?

A

It is an environmental contaminant and relay toxicosis is high because it is very stable in the environment
It should not be eaten or fed

35
Q

What are the sources of nicotine toxicity?

A

Nicotiana tobacum - plant
Tobacco products
Nicotine patches and gum

36
Q

___________ is an old insecticide that contains nicotine. It was canceled by the EPA in 2009 and the sale of its products ended December 31, 2013.

A

Black Leaf 40

37
Q

What is the MOA of nicotine?

A

It mimics ACh and causes stimulation and excitement of neurons at low doses and paralysis and death at high doses

38
Q

What initial clinical signs are associated with nicotine toxicosis?

A

Stimulation and excitement, hypersalivation, emesis, diarrhea, and tachypnea

39
Q

What progressive clinical signs are associated with nicotine toxicosis?

A

Depression, muscle weakness, paralysis, dyspnea, respiratory paralysis, and death

40
Q

What can nicotine toxicosis cause in livestock (specifically da babies)?

A

Structural abnormalities and birth defects

41
Q

What samples can be used for diagnosis of nicotine toxicosis?

A

Urine, vomitus, serum, liver, and kidney

42
Q

How do you treat nicotine toxicosis?

A

Stabilize the patient (artificial respiration), promote excretion, and do not give antacids (will increase absorption)

43
Q

What are the sources of amitraz toxicosis?

A

Formamidine insecticide (mitiban, taktic/bovitraz, and preventic)

44
Q

Is oral or dermal amitraz more toxic?

A

oral

45
Q

What species should amitraz not be used in?

A

Cats or horses

46
Q

What is the MOA of amitraz?

A

It is an alpha 2 adrenergic agonist that can cause GI stasis, hyperglycemia due to decreased insulin secretion, bradycardia, and sedation

47
Q

When does the onset of clinical signs occur with amitraz toxicosis?

A

30 minutes to 3 hours

48
Q

What clinical signs are associated with the therapeutic dose of amitraz?

A

Transient sedation, anorexia, vomiting, and diarrhea

49
Q

What clinical signs are associated with a high dose of amitraz resulting in toxicosis?

A

CNS depression, ataxia and weakness, mydriasis, hyperglycemia (the hallmark), hypotension and hypertension, colic, respiratory failure, and death

50
Q

How is amitraz toxicosis diagnosed?

A

History of exposure, compatible signs and lab work
May see collar in GI tract
GI impaction in equine

51
Q

What will you see on serum chemistry in amitraz toxicosis cases?

A

hyperglycemia

52
Q

Detection of amitraz can be found in _____, _______ ______, and ______. Detection confirms ______. High levels are suggestive of ______.

A

Plasma, stomach contents, and urine
exposure
poisoning

53
Q

What is the antidote for amitraz?

A

Yohimbine

Atipamazole is also an option, but Yohimbine is preffered

54
Q

How is amitraz toxicosis treated?

A

Stabilization (antidote) and decontamination

55
Q

Why would atropine be a bad choice of drug in the treatment of amitraz toxicosis?

A

It causes GI stasis - we already have GI stasis due to the amitraz, we don’t need more

56
Q

Why would barbituates be a poor choice for treatment of amitraz toxicosis?

A

The patient is already sedated and bradycardic, no sense in making that worse

57
Q

Why may activated charcoal be contraindicated in cases of amitraz toxicosis?

A

It increases the risk for aspiration pneumonia and is bad if going to surgery

58
Q

What environmental and food safety considerations need to be taken for amitraz toxicosis?

A

There is little relay toxicosis

The food safety is unknown

59
Q

What are the differentials for CNS depression?

A

Ivermectin, barbiturates, cannabinoids, opioids, and ethanol

Toxicology (32 decks)

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