Exam 3: Pesticides Part I & II Flashcards
MOA, exposure, toxicity, and treatment options
organophosphaytes and carbamates
organophosphates and carbamates mechanism of action is inhibiting AChE. exposure can happen orally (contaminated feed or grooming behaviors), dermal, and inhalation. treatment options for both is gastric lavage, activated charcoal, and stropin. 2PAM can also work for OPs.
can be local (eyes and lungs) or systemic. acute, clinical signs ususally within the hour. SLUDGE. can be lethal. check level of inhibition og AChE activity
MOA, exposure, toxicity, and treatment options
organochlorines
DDT slows Na influx and K efflux. Aryl hydrocarbons and cyclodienes competitively inhibit GABA. absorbed readily topically or orally, bioaccumulates… toxcity is neurological
cats are most sensitive. no sntidote. supportive care. gastric lavage, activated charcoal, shampoo. can also use mineral oil
MOA, exposure, toxicity, and treatment options
pyrethroins and pyrethroids
flea and tick medicine. wrongly used on cats and toxicity happens, also with cat grooming or in contact with dog. binds to membrane lipid phase near Na channel. 1000x less sensitive in mammals than insects.
fish highly sensitive.
bathe, treat seizures. untreated cats can dies in 24 hours.
MOA, exposure, toxicity, and treatment options
rotenone
used in vet med to treat parasitic mites.inhibits oxidation of NADH to NAD. inhibtis transfer of electrons to complex I or mitochondria and leads to energy deficiency in cells. selective toxicity based on metabolism, more toxic in insects and fish than mammals.
poisoning is rare but treat symptoms and supportive care.
MOA, exposure, toxicity, and treatment options
Fipronil
it’s frontline, the flea and tick meds.
Noncompetitively inhibts GABA induced ion influx which bloack Cl influx and cuses hyperexcitability. can lead to tremors, convulsions, seizures and death. rabbits sensitive to it.
no treatment, symptomatic and supportive care.
MOA, exposure, toxicity, and treatment options
Imidacloprid
neonicotinoids act on post-synaptic nicotinic receptors. these receptros are located entirely in CNS in insects. A biphasic response is seen to neonicotinoid action — an initial increase in the frequency of spontaneous discharge followed by a complete block to nerve propagation.
large safety margin. no treatement. worry about the bees here.
MOA, exposure, toxicity, and treatment options
ivermectin and selamectin
in insects, increase permeability of cell membrane to Cl. in mammals, GABA agonist. toxicity with CNS. toxic to collie dogs becasue of mdr1 (PGP ABCB1) mutation.
no treatment, symptomatic and supportive.
MOA, exposure, toxicity, and treatment options
Amitraz
it’s a tick collar. a2 adrenergic agonist resulting in sedation. also inhibtor of monoamine oxidase. GI distrubance, nausea, vomiting. treat with yohimbine and atipamazole. atropine CONTRAINDICATED due to hypertension and ileus so maybe no activated charcoal.
MOA, exposure, toxicity, and treatment options
metaldehyde
molluscicide
MOA unknown butcan cross BBB
toxic to all, dogs most frquently poisoned.
no treatment, emetics, treat seizures and IV fluids.
MOA, exposure, toxicity, and treatment options
DEET
well absorbed from intact skin
toxicity and mechanisms largely unknown but DEET is pretty safe.
What are the most likely mechanisms for exposure to herbicides and fungicides and how do potential exposures relate to dose and toxicity?
phenoxy herbicides sprayed for application, lawns and such. toxin due t TCDD (dioxin) in some combinations with 2,4,5-T.mpotentioal MOA is uncoupling of oxidative phosphorylation as well as the direct irritant effect of these organic acids. energy is consumed and ATP is not generated. toxic doses came from pooled reas or undiluted cans.
ulcers, GI irritation…teratogenic in rodents, risk of canine malignant lymphoma and transitional cell carcinoma of the bladder
no specific treatment, diuresis can help
scottish terriers increased risk
What are the differences between paraquat and diquat with regards to mechanism of action and organ specific toxicities?
both NADPH (electron donor and H+ source in all cells), major protectant against ROS(reactive oxygen species)
Paraquat accumulates in lung tissue via the diamine-polyamine concentrator system that exists in alveolar epithelial cells
Diquat has poor oral bioavailability
Diquat is not preferentially concentrated in the lung
Diquat does show some preferential concentration in the GI, Liver and Kidneys
What is the toxic component of herbicide formulations?
toxin due ti TCDD (dioxin) in some combinations with 2,4,5-T. potentioal MOA is uncoupling of oxidative phosphorylation as well as the direct irritant effect of these organic acids.
What are the potential acute vs. chronic toxicoses associated with herbicide exposure for each of the agents discussed?
paraquat chronic toxin is cyanosis
