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)