Insecticides Flashcards
Organochlorine insecticides
-banned for use in Canada and USA… used in 1950s-1970s
-very persistent in environment (bioaccumulation, bioconcentration, biomagnification)
-modern poisonings uncommon but sometimes in old barns
Organochlorine insecticide options
-DDT
-methoxychlor
-lindane
-dieldrin
-chlordane
-aldrin
-endosulfan
-hepatochlor
-toxaphene
Mechanism of organochlorine insecticides
Interfere with action potentials and NTs in CNS
ex.
-DDT- interacts with Na and K influx/efflux
-GABA inhibition
-Enhanced acetylcholine release
-CNS excitation
Toxokinetics for organochlorine insecticides
-High lipophilicity (partition to fatty acids (brain and adipose), excreted in milk)
-very long elimination half life (months; enterohepatic recirculation)
Onset of organochlorine insecticides
Within hours
Clinical signs of organochlorine insecticides
- Behaviour changes (anxiety, agitation/aggression, jumping over invisible objects)
- GI (vomiting and saliva)
- CNS excitation (tremors, tonic clonic seizures, opisthotonus, paddling, jaw clamping, circling, stiff gait)
- progresses to coma and death
Management of organochlorine insecticides
-decontamination if not contraindicated= dermal wash
-anticonvulsants, methocarbamol, fluids, O2, mechanical ventilation, ILE, cholestyramine
Diagnosis for organochlorine insecticides
Some have pesticide screenings (for fat, liver, brain, gastric contents)
Public health implications for organochlorine insecticides
-long elimination half life
-human health concerns (endocrine disruption, carcinogenic)
-food animal residues
-persistent in environment; negative impact on wildlife populations
Organophosphate and carbamate
-most common group of pesticides/insecticides
*highly toxic but not environmentally persistent
-same mechanism of organochloride insecticides
What are organophosphate and carbamate insecticides used for?
-agriculture use
-flea and tick treatments
-shampoos
-dips
How do animals get exposed to organophosphate and carbamates?
-malicious poisoning
-accidental- access to chemicals, ingestion of cattle ear tags, spraying, treated crops, poisonied insects/animals
Mechanism of action of organophosphates and carbamates
Inhibition of acetylcholinesterase preventing acetylcholine breakdown and therefore the overstimulation of nicotinic and muscarinic receptors
*leads to CNS, neuromuscular junction, parasympathetic nervous system
Differences between organophosphates and carbamates
Clinical presentations of organophosphate and carbamate toxicity
- acute toxicosis
- intermediate syndrome
- OP-induced delayed polyneuropathy (OPIDPN)
Acute toxicosis route of exposure and onset of organophosphates and carbamates
-routes: ingestion, inhalation, dermal
-onset: as early as 15mins post exposure
3 categories of symptoms for acute toxicosis of organophosphates and carbamates
- symptoms from mAChR overstimulation
2.symptoms related to nAChR overstimulation - Symptoms related to CNS overstimulation
Symptoms from mAChR overstimulation
Symptoms from nAChR overstimulation
Symptoms from CNS overstimulation
How do organophosphates and carbamates cause acute toxicosis death?
-bronchoconstriction/bronchorrhea
-respiratory failure and hypoxia
Post mortem findings from acute toxicosis of organophosphate and carbamates
-No specific lesions (edema, congestion and hemorrhage present)
-can see insecticide granules or bait in stomach/rumen
Intermediate syndrome of organophosphate and carbamates toxicity
-dogs and cats
-Onset: 24-96hrs after surviving acute cholinergic crisis
Clinical signs of intermediate syndrome from organophosphate and carbamate toxicity
- Acute muscular weakness: abnormal posture, cervical ventroflexion, resp muscle weakness and depression
- Decreased acetylcholinesterase activity
Cause of OP-induced delayed polyneuropathy (OPIDPN) from organophosphates and carbamates
Due to degeneration of long motor nerves by the inhibition of neuropathy target esterase (NTE)
-axonopathy, myelinopathy
Onset and clinical signs of OP-induced delayed polyneuropathy (OPIDPN) organophosphate and carbamate toxicity
Onset: 1-4weeks after exposure to OP
Signs: ataxia, pelvic limb weakness, normal blood acetylcholinesterase
Management for acute toxicosis of organophosphate and carbamate toxicity
-Antidote= atropine to control bradycardia and bronchial secretions
*use a test dose first
-if known exposure (sometimes if unknown), may need to add in oximes (2-PAM) prior to enzyme aging
What to do if there is no history of organophosphate or carbamate exposure, but signs suggest cholinergic toxidrome?
Test dose atropine. If pupil dilation, increased HR, and salivation stops within 10-15mins then STOP, not toxicity. If not give more atropine
Basic supportive care for acute toxicosis
-O2, mechanical vent
-fluids
-seizure control
-anti-emetics
Management for intermediate syndrome
-no atropine because muscarinic signs not present
-2-PAM
-supportive care
-slow recovery
Management for OPIDPN
-no atropine because muscarinic signs not present
-supportive care
Diagnosis for organophosphate and carbamates
-history
-response to atropine
-antemortem: AChE activity of heparinized whole blood
*less than 50%=suspicious, less than 25%=diagnostic
-postmortem: brain AChE activity (freeze half of brain)
-analysis of stomach, urine, other tissues
Diagnosis of OPIDN
-history of exposure
-no specific gross lesions
-histo of nerves= Wallerian degeneration
-NTE test but not available in diagnostic lab
