organophosphates

What is the order of clinical signs

1. Muscarinic stimulation 2. Ganglionic stimulation, neuromuscular stimulation and CNS stimulation 3. Ganglionic blockade, Neuromuscular blockade and CNS depression

When do OP toxicosis symptoms appear

10 minutes and often under 24 hrs (Acute)

Why is succinylcholine not recommended for treatment with OPT

As a muscle relaxant it can increase toxicity

Treatment for OP toxicosis includes

Atropine sulfate and 2 PAM chloride (parlidoxime) O2 and supportive therapy

Who is most sensitive to organophosphates

Cats

What is a differential diagnosis to consider with suspected OP toxicosis

Chlorinated hydrocarbon insecticide toxicosis, but especially Carbamate and Nicotine toxicosis

After absorption and distribution, OP pesticides have the highest concentration where

Distributed throughout the body with NO accumulation in a particular tissue

Chlorinated hydrocarbons leave a residue in animal tissue (bioaccumulation) where is it mainly stored and what is a good sample

Fat is the main storage When animal is dead a good sample is the brain when alive, whole blood

What type of toxicity are organophospates

High toxicity

What is the MOA for OP

Irreversible inhibition of cholinesterases, increase ACh at all cholinergic sites

Are organophosphates persistent in the environment

Most are not (2-4 weeks)

What are 2 systemic OPs and 2 Non systemic

Non Systemic = Malathion and Parathion (Parathion has a quick OOA) Systemic = Dichlorvos and Coumaphos (Coumaphos has a slower OOA)

Which OP is more/less toxic in young animals

Parathion is LESS TOXIC b/c it requires enzyme activation Dichlorvos is MORE TOXIC b/c do not require enzyme activation

What are clinical signs of chlorinated hydrocarbon toxicosis

Produce more severe excitement and convulsions accompanied by elevation of body temp Do not cause parasympathetic signs

The cause of death in high OP exposure is

Respiratory failure

To help confirm your diagnosis of organophosphate poisoning in DEAD angus steer, you should look for the parent compound in what specimen

Rumen contents (tests are tedious and expensive)

What are the clinical signs of OP toxicosis

Salivation, Lacrimation, Urination, Defecation tremmors, stiff gait paralysis CNS depression

What would you do first for an animal with respiratory failure due to organophosphate toxicosis

Ventilate (give 2-PAM later)

What is the best sample to submit to a toxicology laboratory to help confirm a diagnosis of organophosphate in a live cow

Whole blood (look at acetylcholinesterase levels) levels should be "low activity"

Which animals are more sensitive to chlorinated hydrocarbons

cats

The first clinical signs in organophosphate poisoning are MAINLY due to

muscarinic stimulation

Clinical signs of delayed organophosphate toxicosis are MAINLY due to

peripheral neurotoxicity (muscle weakness, ataxia especially in rear legs that may progress to paralysis -can be reversible or irreversible)

2-PAM antagonizes the toxic effects of organophosphates by

reactivating acetycholinesterase

What can cause toxicity to increase with OP

storage activation muscle relaxants and NM blockers Enzyme inducers Interactions w chlorinated hydrocarbon-pesticides Vehicles (organic solvents, oils or sticking agents)