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
Why don't you want to give too much atropine?
There is no reversal
26
What treatment, alternative to atropine, only works for OP toxicosis?
2-PAM
27
What might 2-PAM not work for carbamates?
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
What can be used to treat OP/Carbamate toxicosis besides atropine and 2-PAM?
Glycopyrrolate
29
What should be done in addition to administering atropine (or the other 2 options) when treating OP/Carbamate toxicosis?
decontamination - activated charcoal or wash with soap/detergent (if dermal)
30
What is chlorpyrifos?
A common OP on the market
31
How does chlorpyrifos effect cats?
Intermediate syndrome Delayed signs (1-5 days) - tremors, ataxia, seizures, depression, and anorexia Persists for weeks
32
What cattle breeds does chlorpyrifos effect?
'exotic' breeds
33
What does chlorpyrifos do to cattle?
Delayed toxicosis - 10-14 days Classical signs Anorexia and weight loss
34
What environmental and food safety considerations need to be taken for OP/carbamate toxicosis?
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
What are the sources of nicotine toxicity?
Nicotiana tobacum - plant Tobacco products Nicotine patches and gum
36
___________ 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.
Black Leaf 40
37
What is the MOA of nicotine?
It mimics ACh and causes stimulation and excitement of neurons at low doses and paralysis and death at high doses
38
What initial clinical signs are associated with nicotine toxicosis?
Stimulation and excitement, hypersalivation, emesis, diarrhea, and tachypnea
39
What progressive clinical signs are associated with nicotine toxicosis?
Depression, muscle weakness, paralysis, dyspnea, respiratory paralysis, and death
40
What can nicotine toxicosis cause in livestock (specifically da babies)?
Structural abnormalities and birth defects
41
What samples can be used for diagnosis of nicotine toxicosis?
Urine, vomitus, serum, liver, and kidney
42
How do you treat nicotine toxicosis?
Stabilize the patient (artificial respiration), promote excretion, and do not give antacids (will increase absorption)
43
What are the sources of amitraz toxicosis?
Formamidine insecticide (mitiban, taktic/bovitraz, and preventic)
44
Is oral or dermal amitraz more toxic?
oral
45
What species should amitraz not be used in?
Cats or horses
46
What is the MOA of amitraz?
It is an alpha 2 adrenergic agonist that can cause GI stasis, hyperglycemia due to decreased insulin secretion, bradycardia, and sedation
47
When does the onset of clinical signs occur with amitraz toxicosis?
30 minutes to 3 hours
48
What clinical signs are associated with the therapeutic dose of amitraz?
Transient sedation, anorexia, vomiting, and diarrhea
49
What clinical signs are associated with a high dose of amitraz resulting in toxicosis?
CNS depression, ataxia and weakness, mydriasis, hyperglycemia (the hallmark), hypotension and hypertension, colic, respiratory failure, and death
50
How is amitraz toxicosis diagnosed?
History of exposure, compatible signs and lab work May see collar in GI tract GI impaction in equine
51
What will you see on serum chemistry in amitraz toxicosis cases?
hyperglycemia
52
Detection of amitraz can be found in _____, _______ ______, and ______. Detection confirms ______. High levels are suggestive of ______.
Plasma, stomach contents, and urine exposure poisoning
53
What is the antidote for amitraz?
Yohimbine | Atipamazole is also an option, but Yohimbine is preffered
54
How is amitraz toxicosis treated?
Stabilization (antidote) and decontamination
55
Why would atropine be a bad choice of drug in the treatment of amitraz toxicosis?
It causes GI stasis - we already have GI stasis due to the amitraz, we don't need more
56
Why would barbituates be a poor choice for treatment of amitraz toxicosis?
The patient is already sedated and bradycardic, no sense in making that worse
57
Why may activated charcoal be contraindicated in cases of amitraz toxicosis?
It increases the risk for aspiration pneumonia and is bad if going to surgery
58
What environmental and food safety considerations need to be taken for amitraz toxicosis?
There is little relay toxicosis | The food safety is unknown
59
What are the differentials for CNS depression?
Ivermectin, barbiturates, cannabinoids, opioids, and ethanol