7. Organophosphates and carbamates

Which of the following is not true about organophosphates? A. Lethal synthesis is more toxic to young patients and if enzyme inducers are present B. Irreversible inhibition of cholinesterases C. Increase ACH at all cholinergic sites D. All of the above are correct E. None of the above are correct

A. Lethal synthesis is more toxic to young patients and if enzyme inducers are present *Lethal synthesis is LESS toxic to young patients and is MORE if enzyme inducers are present

What do Organophosphates often contain in their name? (4) (slide 9)

'phos', 'phosphate', 'phoro', or 'thione'

What carbamate is contraindicated when trying to treat with 2-PAM?

*Carbaryl*

What are the chemical properties of Organophosphates? (3)

- Degrade relatively quickly in the environment (Most persist 2-4 weeks (though some last longer). Can penetrate intact skin, waxy coatings of leaves and fruits.) - Subject to 'storage activation' (Parathion, malathion, diazinon, coumaphos. If sealed and stored 1-2 years, more toxic.) - Technical grades more toxic (Heat isomeration, impurities).

Look at slide 18-19

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Look at slide 24 for specific atropine information

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Look at slide 33 - 34

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How many years of being stored does it take for an organophosphate to become more toxic?

1 - 2 years

How quickly can clinical signs show from organophosphate toxicity?

15 minutes to one hour

Some Organophosphates have ____ activity. Others have none and must be _________ before they become active.

AChe desulfurated

What are some acute signs of CNS stimulation with organophosphate toxicity? What happens in ruminants?

Anxiety, restlessness, hyperactivity, may proceed to tonic- clonic seizures *Seizures are less likely CNS depression in ruminants

Put the steps of the mechanism of action for organophosphates in order from first to last.(slide 16) A. Nicotinic blockage (ganglionic and NM blockade, CNS depression) B. Muscarinic receptor stimulation C. Nicotinic receptor stimulation (ganglionic and neuromuscular stimulation, CNS stimulation)

B, C, A

What are two major differences between carbamates and organophosphates?

Carbamates do not require hepatic bioactivation, have a faster onset and shorter duration, and cause reversible inhibition of acetylcholinesterase.

Continued exposure to organophosphate can lead to tolerance due to: A. Enzyme induction B. Functional adaptation to decreased esterases C. Adaptation of ACH receptors to excessive amounts of ACH (receptor down regulation) D. All of the above are correct E. None of the above are correct

D. All of the above are correct *Muscarinic receptors regulate more readily

Which the following is not true about acetylcholinesterase activity level? (slide 21) A. Can be run on tissue as well (postmortem) B. Correlates well to brain cholinesterase activity, but not necessarily to clinical signs C. Usually <50% activity is 'suspicious' and <25% activity is diagnostic D. All of the above is correct E. None of the above is correct

D. All of the above is correct

Which the following is not true about the direct detection of organophosphates (laboratory diagnosis)? (slide 20) A. Usually do not test liver/kidney b/c metabolism is rapid B. Stomach or rumen contents, hair/skin with dermal exposure C. With chlorpyrifos may find residues in fat/liver D. All of the above is correct

D. All of the above is correct

Which of the following are not initial signs of muscarinic stimulation? A. Diarrhea, urination B. Emesis and salivation C. Bronchoconstriction and bradychardia D. Tremors and a stiff gait E. Lacrimation and myosis

D. Tremors and a stiff gait DUMBBELS *Associated with nicotinic stimulation

How to treat organophosphate toxicity? (General categories not specifics) (4)

Decontamination, Supportive care, Avoid(certain drugs), Atropine, 2-PAM (Pralidoxime, Protopam)

Which of the following isn't considered an insecticide? A. Organophosphates and Carbamates B. Pyrethrins and Pyrethroids C. D-Limonene, Nicotine, and DEET D. Amitraz, Naphthalene, and Ivermectin E. All of the above are insecticides

E. All of the above are insecticides

True or false: organophosphates are lipophobic.

False. Organophosphates are lipophilic.

True or false: organophosphates cause specific lesions in acute death.

False. There is no specific lesions in acute death

What is the prognosis of an animal with organophosphate toxicity?

If the live the prognosis is better.

Organophosphates are well distributed throughout the body (not including, including) the CNS. They show no significant tissue accumulation.

Including

What is the atropine response test? (Slide 22)

Is a test run to see if there is an organophosphate toxicity. You administer atropine 0.02 mg/kg. If strong response to low dose atropine (full mydriasis, significant increase in HR or dry mouth within 15 minutes) then less likely OP toxicity.

How is 2PAM given? What is it used for?(Slide 25)

Is given by IV. It is used to treat organophosphate toxicity.

What does the prognosis of an animal with organophosphate toxicity depend on?

It depends on dose and how long it's been since exposure. Clinical signs are already present may depend on finances. Mild to moderate signs generally treatable. Acute cases that respond to treatment can recover within 24 hours.

What is a positive about carbamates having a faster onset and shorter duration than organophosphates?(Slide 31)

Low exposure may recover without treatment. *Being metabolized very rapidly could also lead to the animal being dead before you're able to treat then.

_________ _______ due to organophosphate toxicity causes these acute clinical signs: paralysis, CNS depression, coma, dyspnea and death (resp. failure).

Nicotinic blockade

What drugs/drug groups should be avoided when treating organophosphate toxicity?(3)(slide 23)

Phenothiazines,aminoglycosides,muscle relaxants, drugs that depress respiration (opioids)

What is the cause of death in high exposure to organophosphate's?

Respiratory failure (paralysis)

Where are organic phosphates metabolized?

The liver (causes toxic effect)(a.k.a. lethal synthesis)

What is a similarity for most carbamates?

The names contain "carb"

What is the mechanism of action for carbamates?(Slide 32)

They cause a reversible inhibition of acetylcholinesterase

True or false: Muscle fasciculation, tremors, twitching, spasm, hypertonicity, stiff gait are all associated with nicotinic stimulation.

True

True or false: Pancreatitis has been reportedly found in some dogs with the more lipophilic compounds.

True