Final Flashcards
The perfect pesticide:
Effect on to insect, causes no acute or chronic effects on non insect species, leaves no residue in tissue eggs or milk of non insect species
OP and carbamates
Not persistence in Indv, some persistence in environment, no translocation in plants, no bioacculuation
Toxokinetics of organophosphate and carbamates
Lipid soluble, rapidly and equally distrusted, rapidly cleared,
OP/Carb MOA
Binds and inhibit ache (acetylcholinesterase)
Ach acts as a neutrotramiter where?
Neuromuscular junction, parasympathetic, and sympathetic nervous system
Op/c symptoms
Mixed Nicotinic and muscarinic,
Tremors, muscle weakness, paralysis
Respiratory depression
OP/C diagnosis
Seen in tissue or body fluids,
Clinical signs,
Depressed cholinesterase activity
Measure ache in serum plasma or whole blood*best
Treatment of op/c poisoning
Decontaminate if asymp, wash w soap water NO EMESIS AS THEY CAN SIEZURE
Symptoms- seizure control, muscarinic receptor antgonists like atropine
OP- antidote oxicho reactivators
Neonicotinoid insecticides
Used in pest control, termite control, cat dog flea control , mimic ACh, bind to post synaptic nicotinic ACh receptors leading to build up of ACH
Neonic signs
Hyperexcitation, convolutions ,paralysis, death
Neonic have higher binding affinity at insect receptors meaning
Bind more tightly with insect receptors than mammalian
Neonicotinoids absorption
Rapidly and almost completed in GI tract
Oral treated w milk or water, if ingested then supportive therapy
Pyrethrins
Obtained from flowers of chrysanthemum
Pyrethroids
Synthetic compounds formulated to be more insecticidal and less toxic to mammals
Pyrethrin/oids
Found in shampoo, dips, floggers, spot on, sprays,
Do not bioacculate
1 no cyano group and 2 constrains alpha cyanogroup
Pyrethin/oids signs
Type 1 tremors and seizures
Type 2 weakness and paralysis
Pyrethrin/ion toxicokinetics
Moderate gi absorption, dermal minimal
Widely diatribes throughout body including Brain, metabolized rapidly
Pyrethin/oid dx tx
Symtom/supportive
Dermal- wash
No emesis
Activated charcoal
IV fluids
IV lipid therapy for severe tremors and seizures
Pyrethrin/pyrethoids species
Cats especiallly sens
Hydrocarbons
Compound of hydrogen and carbon, such as those that are the chief components of petroleum and natural gas
Petroleum distillate:
Hydrocarbon solvents derived from crude oil by distillation
Sources of hydrocarbons/petrol
Gas, kerosine, motor oil, paint thinners, diesel, tiki oil, baby or mineral oil
Low viscosity high volatility hydrocarbons
Gas and kerosine, can be aspirated easily
High viscosity hydrocarbons
Irritate gi or kill rumen micro
Hydrocarbons volatility general rule
Higher volatile higher toxicity
Lower weight higher tox
Lower viscosity higher Tox
Hydrocarbon toxicosis to various systems
Integumentary- hair loss irritation
Gi- oily dx, vt, near sea, bloat rumen Antony
Airway- aspiration pneumonia
Heart- arrhythmia
San- anesthetic effect on neutrotransmission ataxia, lethargy, depression, seizure, coma
Hydrocarbons treatment
No emesis or AC,
Anti vt drugs, fluids, monitor for aspiration pneumonia
Ruminants relieve bloat
Flush eye and wash skin if dermal
Acidic compounds mode of action
Rapid surface protein coag
Immediate pain
Immediate coag type necrosis
Alkaline mode of action
Penetrate deeply into tissues, saponified fat protein, delayed pain, small vessel thombosis, heat,
Acid/alkaline clinical signs
Gi- white grey to black wrinkled lesions, salivation ,vt, dysphagia, gi ulcers
Derma- hypermia, irrigated skin, damaged fur
Resp- strider cough tachypnea
Ocular- conjunct, viable ulcer, shock, peritonitis
What to note for alkaline acids
Product viscosity and concentration
Decontamination for corrosive agents is ___
BAD CONTRAINDICATED
Treatment for Corrosive acid -alkalosis
Establish airway, since oral eyes, scope for damage, analgesics, gi protectants, nutritional support like feeding tube
Rodenticide types
Anti coag,
No coag- bromethalin, strychnine, cholecalciferol’s (vit d), zinc phosphide, misc
Anti coag ADME
Slow but complete absorption; bound to plasma proteins like albumin, excreted via urine
Half life of 6d bro and 14hr warfarin
What is the earliest time to detect on coag test
30hrs, pt will be prolonged
Anti coag clinical signs
Lag period of 3-5d early as 24hrs,
Lethargy derpression, mouth bleeding bloody feces epistaxis, cough
Hematoma, irregular hr, weak pulse ,ataxia, convulsions
Anti coag diagnostics
History signs
Lab- bmbt, cbc chem, xray, pt 1 and then ptt 2nd
Gi contents if ingested
Anti coag lesions
Generalized hemorrhage, pulmonary hem, heart and gut hem, liver necrosis from anemia and hypoxia
Anti coag treatment if asymptomatic
Induce vt if in 1 hr, decontam w AC and cathartics, vit k therapy possibly
Anti coag treatment w clinical signs
Clotting factors, oxygen, vit k1, cage rest, icu
Why are anticoagulant present a risk to wildlife
Half life of 2nd gen anti coag is long, tissue levels in poisoned prey is source for wildlife
Consumer sized products
Less than 1 lb; only for chlorophacinone, bromadiolone, difenacoum
Block or past NO PELLETS
Must be in ready to use bait station
DCON active ingredient new
Vitamin d3
Bromethalin
Neurotoxic, cats more toxic, dx of metabolite in FAT brain liver or bait