Unit 1 - Organophosphates and Carbamates Flashcards
What are organophosphates derived from?
Phosphoric acid - they are esters of it
What are carbamates derived from?
carbamic acid
What are the sources of organophosphates and carbamates?
Corn rootworm products, external parasite control, premises, unintentional poisoning, and malicious poisoning
Organophosphates and carbamates are _______ absorbed, metabolized in the ______, distributed throughout ______ and _______, and excreted in _____ and ______.
Rapidly, liver, blood, CNS, urine, and feces
What is the MOA of organophosphates?
They irreversibly bind to acetyl cholinesterase thus inhibiting the breakdown of ACHe. This results in continued stimulation of nicotinic and muscarinic receptors
What is the MOA of carbamates?
They bind to acetylcholinesterase and spontaneously separate thus inhibiting the breakdown of ACHe. This results in continued stimulation of nicotinic and muscarinic receptors
T/F - Organophosphates and carbamates cause death within minutes because they are very toxic.
True - to put it in persepctive, a tablespoon is enough to kill an adult cow/bull
Are dogs or cats more susceptible to carbates and organophosphates? Brahman vs English Cattle? Males vs females?
Cats , Brahman, and males are more susceptible
When is the onset of clinical signs for organophosphates and carbamates?
Minutes to hours
What parasympathetic clinical signs are associated with organophosphate and carbamate toxicity?
Salivation, lacrimation, urination, and defecation (SLUD)
Miosis, bradycardia, bronchoconstriction, dyspnea, and vomiting
What neuromuscular clinical signs are associated with organophosphate and carbamate toxicity?
Tremors, stiffness, and paralysis
What CNS clinical signs are associated with organophosphate and carbamate toxicity?
Nervousness and seizures
What antemortem samples would be good for the diagnosis of organophosphates and carbamate toxicity?
Blood and vomitus
What will you find in an antemortem blood sample in a patient with organophosphate or carbamate toxicity?
Cholinesterase concentration
What will you find in an antemortem vomitus sample in a patient with organophosphate or carbamate toxicity?
The parent compound
What post mortem samples will have a high cholinesterase concentration in organophosphate or carbamate toxicity cases?
Brain and retina
What post mortem samples will have the parent compound in organophosphate or carbamate toxicity cases?
Rumen contents, stomach contents, and hair
Aside from patient samples, what else can you sample to help diagnose an organophosphate or carbamate toxicity? What will you find in these samples?
Bait/suspected material and feed
You would find the parent compound
The cholinesterase test is a screen meaning it will only increase if there is >__% inhibition. It is only suggestive of OP/carbamate toxicosis.
> 50% inhibition
What factors can affect cholinesterase levels?
Carbamates, autolysis, and freezing
What lesions are associated with OP/carbamate toxicosis?
There are no specific gross or microscopic lesions, but you may observe colorful/odd material in the GI tract
What is the antidote for OP/carbamate toxicosis? How does it work?
Atropine - it binds to muscarinic receptors and prevents ACh from binding
What do you need to be aware of when administering atropine?
- There are different concentrations in large and small animal bottles
- There is a decrease in efficacy after 2-3 doses
If you are unsure if it is an OP/carbamate toxicosis, what should you do?
Give 1/10 of the dose and monitor the response. If you are correct, the pupils will dilate
Why don’t you want to give too much atropine?
There is no reversal
What treatment, alternative to atropine, only works for OP toxicosis?
2-PAM
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
What can be used to treat OP/Carbamate toxicosis besides atropine and 2-PAM?
Glycopyrrolate
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)
What is chlorpyrifos?
A common OP on the market
How does chlorpyrifos effect cats?
Intermediate syndrome
Delayed signs (1-5 days) - tremors, ataxia, seizures, depression, and anorexia
Persists for weeks
What cattle breeds does chlorpyrifos effect?
‘exotic’ breeds
What does chlorpyrifos do to cattle?
Delayed toxicosis - 10-14 days
Classical signs
Anorexia and weight loss
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
What are the sources of nicotine toxicity?
Nicotiana tobacum - plant
Tobacco products
Nicotine patches and gum
___________ 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
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
What initial clinical signs are associated with nicotine toxicosis?
Stimulation and excitement, hypersalivation, emesis, diarrhea, and tachypnea
What progressive clinical signs are associated with nicotine toxicosis?
Depression, muscle weakness, paralysis, dyspnea, respiratory paralysis, and death
What can nicotine toxicosis cause in livestock (specifically da babies)?
Structural abnormalities and birth defects
What samples can be used for diagnosis of nicotine toxicosis?
Urine, vomitus, serum, liver, and kidney
How do you treat nicotine toxicosis?
Stabilize the patient (artificial respiration), promote excretion, and do not give antacids (will increase absorption)
What are the sources of amitraz toxicosis?
Formamidine insecticide (mitiban, taktic/bovitraz, and preventic)
Is oral or dermal amitraz more toxic?
oral
What species should amitraz not be used in?
Cats or horses
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
When does the onset of clinical signs occur with amitraz toxicosis?
30 minutes to 3 hours
What clinical signs are associated with the therapeutic dose of amitraz?
Transient sedation, anorexia, vomiting, and diarrhea
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
How is amitraz toxicosis diagnosed?
History of exposure, compatible signs and lab work
May see collar in GI tract
GI impaction in equine
What will you see on serum chemistry in amitraz toxicosis cases?
hyperglycemia
Detection of amitraz can be found in _____, _______ ______, and ______. Detection confirms ______. High levels are suggestive of ______.
Plasma, stomach contents, and urine
exposure
poisoning
What is the antidote for amitraz?
Yohimbine
Atipamazole is also an option, but Yohimbine is preffered
How is amitraz toxicosis treated?
Stabilization (antidote) and decontamination
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
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
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
What environmental and food safety considerations need to be taken for amitraz toxicosis?
There is little relay toxicosis
The food safety is unknown
What are the differentials for CNS depression?
Ivermectin, barbiturates, cannabinoids, opioids, and ethanol
