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88 Cards in this Set
- Front
- Back
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Pesticide
-defintion |
-any substance/mixture used intentionally to kill pests
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Pest
-definition |
-depends on the person being effected
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Pesticides that are extremely common in causing unintentional animal poisoning
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-Anticholinesterases (organophosphates, carbamates)
-Pyrethrins/pyrethroids -Anticoagulants |
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What is one of the most common types of pesticides used today?
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-anticoagulants
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Pesticides that are occasionally common in causing unintentional animal poisoning?
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-cholecalciferol
-strychnine -zinc phosphide -bromethalin -metaldehyde -sodium fluoroacetate -chlorinated hydrocarbons |
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Organophosphate
-type of pesticide |
-anticholinesterase
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Organophosphate
-active site |
-phosphate:oxygen (-oxon)
-manufactured with phosphate:sulfur bond (-thion) |
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Organophosphate
-how is the active site activated |
-by oxidase enzyme in the liver
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Organophosphates
-which acitive site bond is more stable |
-Phosphate:oxygen bond with acetylcholinesterase
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Carbamate
-type of pesticide |
-organophosphate
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Carbamate
-active site bond |
-carbon:oxygen
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Carbamates
-is the carbamate-enzyme bond stable |
-No
-metabolized and excreted |
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Organophosphates
-sources |
-agriculture
-pesticides for houses and gardens -direct application of carbamate to animals -accidental feed/water contamination -malicious feed contamination |
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Anticholinesterase with a very tight bond?
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-Organophosphate
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Organophosphate products that are not in high enough concentration to cause poisoning
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-insect bait traps
-pet shampoos/powders |
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Organophosphate
-mechanism of action |
-organophosphates bind to Acetylcholinesterares, inhibiting them and allowing for continual stimulation by acetylcholinesterase
-paralysis can occur with continual overstimulation |
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Organophosphate
-effects |
-parasympathomimetic effects (smooth muscle and glands effected)
-neuromuscular effects (nicotinic receptors) -cumulative effect |
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Delayed Neuropathy
-associated with |
-organophosphates (chlorpyriphos)
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Delayed neuropathy
-due to |
-inhibition of NTE which is essential for neuronal phospholipid homeostasis and ER functions
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Organophosphate
-clinical signs |
-salivation, vomiting, diarrhea, respiratory rales
-muscle tremors, paresis, seizures, respiratory muscle failure -CNS effects -long duration in ruminants due to slow absorption |
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Organophosphate
-diagnosis |
Live animals
-ChE inhibition in serum/whole blood Dead animals -ChE inhibition in brain Chemical detection in liver, kidney, brain, fat |
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Organophosphate
-treatment |
-needs to be early!
-remove source -bathe with soap for skin contamination -Activated charcoal -Atropine to counter cholinergic effects -2-PAM to release OP from ChE -Supportive treatment (respiratory, hydration) |
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Organophosphate
-management |
-control access to agricultural and household chemicals
-avoid repeated use -don't use near milk producers -consider ecological impacts |
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Pyrethrins/Pyrethroids
-general effect |
-excitatory neurotoxic effects
-high toxicity in aquatic animals |
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Pesticide poisoning that will be seen most often in veterinary practice
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-Pyrethrins
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Pyrethrin vs. Pyrethroid
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-Pyrethrin: naturally occuring from Chrysanthemum
-Pyrethroid: synthetic derivative |
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Pyrethroid
-synergist most often used -why |
-Piperonyl butoxide
-inhibits p450 allowing for a longer half-life in insect |
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Pyrethrin/Pyrethroid
-risk factors |
-animal contact following environmental application
-off-label use in animals -dose errors -ingestion |
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Pyrethrin/Pyrethroid
-kinetics |
-dissolves in lipids
-metabolized by p450 -reservoir in skin and fat ---> flip flop kinetics |
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Pyrethrin/Pyrethroid
-mechanism of toxicity |
-Slows the opening and closing of voltage sensative ion channels (Na, Ca, Cl)
-results in nerve depolarization -uncontrolled nerve impulses -local irritant on skin and membranes |
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Pyrethrin/Pyrethroid
-clinical effects |
-salivation (from lack of swallowing)
-hyperaesthesia -ear twitching, tail flicking -muscle tremors -abnormal behavior |
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Pyrethrin/Pyrethroid
-treatment |
-no antidote
-decontamination (clean with dishwashing detergent; activated charcoal) -control neuro effects (diazepam, methocabamol, pentobarbital) -supportive treatment (IV with dextrose; monitor temp) |
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Pyrethin/Pyrethroid
-reason for long recovery |
-flip-flop kinetics
-can take 24-48 hrs |
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Pyrethrin/Pyrethroid
-prognosis |
-good
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Anticoagulants
-found where |
-rodenticides
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Anticoagulant
-types |
1st generation
-less potent, short acting 2nd generation -more common -more potent, long acting -coumarins? |
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Anticoagulant
-mechanism of toxicity |
-interference with Vit K recycling
-can't be used by clotting factors II, VII, IX, X |
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Anticoagulant
-half-lives(generations) |
-1st generation = hours
-2nd generation = days |
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Anticoagulant
-kinetics |
-duration increased by liver suppressing drugs
-cimetidine -sulfonamides -fluconazole -phenylbutazone |
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Anticoagulant
-clinical signs |
-delayed signs
-varied bleeding signs (anemia, melena, bleeding mucous membranes, epistaxis, bleeding into joints/feet, bleeding from venipuncture sites) |
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Anticoagulant
-clin path results |
-regenerative/nonregenerative normocytic, normochromic anemia
-leukocytosis -thrombocytopenia -abnormal clotting profile |
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Anticoagulant
-post mortem signs |
-bleeding signs
-liver tissue for anticoagulant screening |
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Anticoagulant
-treatment |
-decontamination
-Vitamin K -Blood transfusions -Prognosis (good if treated early) |
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Cholecalciferol
-aka |
-Vit D3
-rodenticide |
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Cholecalciferol
-mechanism of toxicity |
-active metabolites formed in the liver
-increases Ca and PO4 absorption in the GIT -inc. Ca reabsorption by the renal tubules -inc. osteoclast bone resorption -hypercalcemia and hyperphosphatemia |
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Cholecalciferol
-clinical signs |
-lag time of 36-48 hrs
Signs from hypercalcemia -ataxia -vomiting -constipation -melena -PU/PD -bradycardia -tissue mineralization |
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Cholecalciferol
-diagnostic confirmation |
Clin Path
-low PTH -hypercalcemia and calciuria Post mortem -tissue mineralization |
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Cholecalciferol
-treatment |
-decontaminate (emesis, activated charcoal)
-restrict dietary Ca & P -monitor Ca in blood every 24 hrs -Prednisolone, Furosemide, IV fluid -Pamidronate disodium -Metoclopramide, antacids, GI protectants |
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Cholecalciferol
-prognosis |
-good w/o hypercalcemia
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Strychnine
-normal use |
-formulated into baits to control pest animals
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Strychnine
-mechanism of toxicity |
-blocks glycine on inhibitory GABA receptors
-suppresses Chloride conductance --> depolarization --> uncontrolled nerve depolarization -pronounced in motorneurons and interneurons of the spinal cord, brainstem, thalamus -muscle spasms, convulsions |
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Strychnine
-clinical signs |
-rapid onset
-apprehension, anxiety, salivation -muscle spasms, extensor rigidity, tonic convulsions |
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Strychnine
-diagnosis |
-history
-test stomach content (also may be in serum, urine, liver, kidney) |
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Strychnine
-treatment |
-decontamination (emesis, activated charcoal, cathartics)
-control muscle spasms (pentobarbital, diazepam) -supportive (IV fluid, control hyperthermia, acidosis, hypoxia) |
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Strychnine
-prognosis |
-guarded
-depends on early intervention |
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Most important toxicity to use activated charcoal for decontamination
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-Strychnine
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Zinc Phosphide
-what is it commonly used for |
-rodenticide against moles and gophers
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Zinc Phosphide
-mechanism of toxicity |
-Highly corrosive (gastric enteritis)
-Reacts with stomach acid releasing phosphine gas (rapidly absorbed, cytotoxic, herat, brain, liver, kidneys vulnerable) |
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Zinc Phosphide
-clinical signs |
-rapid onset
-GIT upset and hemorrhage (vomiting, salivation) -Tremors, respiratory distress, convulsions, shock -death in hrs -garlicky breath (phosphine gas) |
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Zinc Phosphide
-diagnostic confirmation |
-gas dissipates rapidly (collect in airtight containers from stomach contents)
-elevated Zn in stomach, liver, kidney |
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Zinc Phosphide
-treatment |
-avoid human exposure to gas
-decontamination (antacids, gastric lavage) -control muscle contractions (propofol, pentobarbital, methocarbamol) |
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Bromethalin
-normal found as |
-rodenticide
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Bromethalin
-mechanism of toxicity |
-Blocks mitochondrial energy production
(especially in the CNS) |
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Bromethalin
-major toxic effect |
-cerebral edema
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Bromethalin
-clinical signs |
High doses
-signs @ 4-24 hrs -muscle tremors, hyperthermia, hyperaesthesia, seizures Low doses -signs @ 2-7 days -CNS depression, ataxia, paresis, hind limb paralysis, coma |
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Bromethalin
-Diagnostic Confirmation |
-white matter vacuolization
-CNS edema -identification in fat, brain, liver, kidney |
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Bromethalin
-treatment |
-decontaminate (emesis, activated charcoal)
-Control CNS edema and seizures (mannitol diuresis, corticosteroids, barbituates) |
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Bromethalin
-prognosis |
-grave if comatose or paralyzed
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Metaldehyde
-normally used as |
-moluscicide
-attractive to dogs |
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Metaldehyde
-mechanism of toxicity |
-suppress GABA production --> lack of inhibition of CNS neuronal activity
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Metaldehyde
-clinical signs |
-w/n 3 hrs
-depression, salivation, diarrhea -hyperaesthesia, muscle tremors, ataxia, convulsions -respiratory paralysis --> death -liver failure in 2-3 days |
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Metaldehyde
-complicated by |
-methiocarb
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Metaldehyde
-diagnostic confirmation |
-hyperthermia
-bait material in stomach with formaldehyde-like smell -chemical analysis of GIT content |
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Metaldehyde
-treatment |
-decontamination (emesis, gastric lavage, enema, activated charcoal)
-control convulsions (diazepam, barbituates) -control hyperthermia -supportive treatment (IV fluid, acidosis) |
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Metaldehyde
-prognosis |
-fair
-guarded with liver failure |
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Sodium monofluoroacetate
-normal use |
-predator control
-poison collars on sheep and goats |
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Sodium monofluoroacetate
-mechanism of toxicity |
-aconitase inhibitor
-blocks the krebs cycle -most severe in the CNS and heart (most dependent on oxidative pathway) |
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Sodium monofluoroacetate
-animals where heart is mainly affected -animals where CNS is mainly affected |
-heart = livestock
-CNS = carnivores |
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Sodium monofluoroacetate
-clinical signs |
Carnivores
-vomiting, salivation, urination, tenesmus, hyperaesthesia, hyperthermia, convulsions, coma, respiratory failure -death in 12 hrs Livestock -acute heart failure especially after exercise/stress |
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Sodium monofluoroacetate
-diagnostic confirmation |
-history of exposure and clinical signs
-chemical analysis of stomach contents -rapid, firm rigor mortis |
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Sodium monofluoroacetate
-treatment |
-decontamination (emesis, activated charcoal)
-convulsion control (barbituates) -supportive care (IV fluids, acidosis) |
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Sodium monofluoroacetate
-prognosis |
-poor prognosis once clinical signs seen
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Chlorinated hydrocarbons
-normal use |
-insecticides
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Chlorinated hydrocarbons
-kinetics |
-high lipid solubility
-resistant to environmental breakdown -bioaccumulate |
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Chlorinated hydrocarbons
-mechanism of toxicity |
-lowers CNS action potential threshold by affecting GABA receptors
similar to Strychnine |
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Chlorinated hydrocarbons
-clinical signs |
-agitation, hyperexcitability, ataxia
-intermittent seizures -respiratory failure --> death |
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Chlorinated hydrocarbons
-treatment |
-wash with soap if topical
-decontaminate if oral (emesis, activated charcoal) -control seizures (diazepam, barbiturates) -control hyperthermia, acidosis |
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Chlorinated hydrocarbons
-prognosis |
-varies depending on dose and time before treatment
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