Pesticides Flashcards
Common Organochlorines
DDT & Chlorinated alicyclics
Lindane & Endosulfan - still available in US
Organochlorine Exposure
miscalculation of concentrations for sprays/drips; contaminated feed/water, lack of PPE, dermal -most common, inhaled
Mechanism of action: DDT
permeability of neuronal membranes or Na/K altered
Na channels remain open - hyperexcitability
Mechanism of action of chlorinated alicyclics
GABA antagonist at chloride ionophore complex - hyperexcitability
clinical signs with organochlorines
Mainly CNS stimulation - salivation, V+, weakness, incoordination, disorientation, tremors, muscle fasciculations, spastic gait, hyperthermia, tonic-clonic seizures, opisthotonos, coma, death
DDx organochlorines
swine- dehydration/Na, pseudorabies;
dogs and cats- strychnine, fluoroacetate, lead, OP, metaldehyde, rabies, tetanus;
cattle- OP, lead, urea, polioencephalomalacia, infectious thromboembolic meningoencephalitis, ketosis, nervous forms of coccidiosis
treatment of Organochlorines
no specific antidote;
decontamination- emesis, wash with soap/water, activated charcoal, IV lipid therapy
organochlorines are excreted through..
bile- enterohepatic recycling
milk, feces, and urine
mechanism of action of prganophosphates
Irreversibly inactivate acetylcholinesterase
Phosphate- direct effect on AChE activity;
Thiophosphates- desulfurized by liver enzymes;
Muscarinic overstimulation→ nicotinic overstimulation → nicotinic blockade
clinical signs of organophosphates
muscarinic effects- DUMBELLS: D+, urination, miosis, bronchospasm, emesis, lachrymation, salivation; nicotinic effects - initial stimulation/fasciculation in muscle followed by depolarization and paralysis, sweating, hypertension, tachycardia
what are some of teh delayed effects seen with organophosphate toxicity
organophosphate-induced delayed polyneuropathy (10-14 days post exposure)- muscle weakness, ataxia, rear limb paralysis
organophosphate-induced intermediate syndrome (2-4 days post exposure) - NO muscarinic signs/muscle fasciculations, weakness of resp. muscles and accessory muscles (neck, proximal limb)
Dx organophosphates
history, clinical signs +/- lab tests; atropine response test - neg. High likelihood of OP
treatment of organophosphate
decontaminate - emesis (NOT if respiration is depressed or seizures), activated charcoal, wash gently, atropine, cholinesterase reactivators (oximes), supportive care
AVOID: phenothiazines, aminoglycosides, muscle relaxants, drugs that depress respiration (opioids)
which pesticide undergoes “storage activation”
organophosphates
what is storage activation
seal and stored for 1-2 years
more toxic
which type of OP undergo lethal synthesis
thiophosphate OPs
T/F carbamtes are derived from carbamic acid and work in similar fashion to OPs
True
mechanism of action of carbamates
reversible inhibition of acetylcholinesterase
clinical signs of carbamates
similar to OP
SLUD - salivation, lacrimation, urination, D+
death from resp. failure and hypoxia due to bronchoconstriction→ tracheobronchial secretion and pulmonary edema
treatment of carbamate
atropine
T/F carbamtes require bioactivation like OPs
False
Don’t require bioactivation - faster onset & shorter duration than OP
lab tests for carbamates
cholinesterase levels
carbamates do/don’t undergo storage activation
Don’t
mechanism of action of nicotine
potent stimulant of parasympathetic nervous system, cholinergic receptor agonist
clinical signs of nicotine
early stimulation-ataxia, lethargy, hypersalivation, V+, bradycardia, tremors, convulsions
Later (or with higher dose) - CNS depression, tachycardia, vasodilation, ultimately paralysis or resp. muscles causes death
DDx of nicotine
strychnine, methylxanthines, tremorgenic mycotoxins, organophosphates, carbamates, and depressants
treatment of nicotine
decontamination- emesis, gastric lavage, activated charcoal;
enhance excretion-IV fluids, lower pH or urine;
atropine, diazepam
mechanism of action of neonicothoids
binds to nicotinic acetylcholine receptors - irreversible
clinical signs of neonicothoids
high levels overstimulate and block receptors → paralysis and death
Signs similar to nicotine toxicity
Mechanism of action of Naphthalene
oxidative metabolites cause methemoglobinemia and hemolysis;
dissolve slowly (stomach acid) and toxicity can be delayed by several days
clinical signs of Naphthalene
V+, mothball-scented breath, pale or brown gums, weakness or lethargy, labored breathing, tremors, seizures;
severe cases- damage to liver or kidneys
Dx of naphthalene
hematologic changes-hemolysis, heinz bodies, methemoglobinemia, hemoglobinuria
DDx of Naphthalene
heinz bodies - acetaminophen, onions, and nitrates
treatment if Naphthalene
decontamination - emesis, activated charcoal +/- cathartics, sodium bicarb;
ascorbic acid & methylene blue 1% (methemoglobinemia);
diazepam (seizures)
mechanism of action od rotenone
block oxidative phosphorylation in citric acid, TCA, or Krebs cycle,
interferes with mitochondrial ETC & NADH during ATP production
Clinical signs of rotenone
local irritation (conjunctivitis, congestion, dermatitis)
depression and convulsions (predominant CS), muscle tremors, lethargy, incontinence, resp. stimulation followed by depression, chronic/acute liver changes reported
treatment of rotenone
no specific treatment, detoxification, supportive treatment
lab results with rotenone
hypoglycemia, liver enzymes, hypoxemia/hypercapnia
