Tox Exam 2 Pesticides Flashcards
Strychine is used to control what animals?
gophers, deer mice, moles, prairie dogs, rats, porcupines, chipmunks, rabbits, pigeons
What pesticide is linked to the 2008 rabies outbreak in Bali where 130,000 dogs were killed using it?
strychnine
Chemical properties of strychnine?
Alkaloid from strychnos nun vomica seeds. Bitter taste, white powder, moderately water soluble. In bait form–poorly water soluble & adheres to soil particles.
How long does strychnine persist in soil?
up to 40 days
What animals are susceptible to strychnine?
ALL! dogs most frequently poisoned but cats are most sensitive
Where is strychnine metabolized & excreted?
metabolized in the liver, excreted in urine as both metabolites & unchanged toxin
Most of strychnine dose is eliminated within ____ hrs.
24 hrs
Distribution of strychnine?
does not accumulate in any particular tissue, DOES cross the BBB, not highly protein bound
Absorption of strychnine?
in GIT readily, vomiting decreases toxicity, food may increase/decrease absorption
MOA of strychnine?
Blocks the post-synaptic effect of glycine in the spinal cord–glycine important inhibitory NT to motor neurons & interneurons in spinal cord, brainstem, thalamus. Leads to exaggerated reflex arcs, muscle spasms, severe muscle rigidity, tonic seizures.
Clinical signs of strychnine?
early signs–>apprehension, panting, nausea/V+, mydriasis, stiffness, muscle twitching, hyperthermia
progresses to–>tonic seizures & opisthotonos
May exhibit sardonic grin and rapid death d/t resp failure.
Onset of action of strychnine?
RAPID–10 min to 2 hrs
T/F Seizures caused by strychnine are not elicited by external stimuli such as light, sound, touch.
FALSE! seizures are elicited by external stimuli
Preferred postmortem specimens for strychnine diagnosis.
stomach contents and liver
Lesions seen postmortem in strychnine poisoning.
few or no lesions–hemorrhage, congestion, cyanosis
rapid rigor mortis
stomach contents may still contain bait
Preferred antemortem specimens for strychnine poisoning.
stomach contents, bait, serum, urine
Available test for strychnine toxicity?
IDEXX TC1030–takes 5-7 working days, around $140
What can you use for decontamination for strychnine poisoning?
Emesis if not contraindicated, gastric lavage (NO bicarb or antacids in lavage fluid), activated charcoal w/ cathartic, enhance renal excretion w/ ammonium chloride or methionine–if patient not acidotic.
What drugs should be avoided in animals with strychnine poisoning?
opioids, phenothiazines, neuromuscular blockers, dissociative anesthetics
Prognosis for strynchine poisoning?
early, aggressive therapy within 24-72 hrs good outcome
Treatment options for the muscle tremors/rigidity caused by strychnine poisoning?
methocarbamol, diazepam
T/F Stychnine poisoning may require sedation for 24-72 hours.
TRUE!
Treatment options for the seizures caused by strychnine poisoning?
diazepam CRI, propofol, barbiturates, avoid stimuli–keep in a quiet, dark place
Zinc phosphide are used to control what species?
rats, mice, squirrels, gophers, voles, moles
What other phosphide formulations have similar toxic effects to zinc phosphide?
aluminum and magnesium phosphide
T/F Relay (secondary) zinc phosphide toxicosis has not been reported or seen in the field.
FALSE. It has not been reported but it has been seen in the field.
How are caged birds commonly exposed to zinc phosphide?
rodents tracking it onto their food
Odor and appearance of zinc phosphide?
acetylene, garlic, dead fish smell—grey-black powder
How long until zinc phosphide decomposes in the environment?
within 2 weeks
What happens with zinc phosphide is exposed to acid?
pH less than 4 liberates phosphine gas (PH3)–phosphine gas release is slower when zinc phosphide is exposed to water
Is acute toxicity due to phosphine gas or zinc phosphide?
phosphine gas
Is chronic toxicity due to phosphine gas or zinc phosphide?
may be due to BOTH!
Lethal dose of zinc phosphide is lowest in what species?
caged birds
T/F Stomach acid increases toxicity of zinc phosphide.
TRUE! dogs on an empty stomach can handle higher than the lethal dose of zinc phosphide & survive
Properties of phosphine gas?
irritant, flammable & toxic
MOA of zinc phosphide toxicity?
Direct irritation of GI mucosa from zinc phosphide. Toxicity primarily due to phosphine gas—inhibits oxidative phosphorylation & cellular energy production resulting in cell death & causes increased oxygen radicals.
Zinc phosphide toxicity has the greatest effects on what tissues?
Tissues with high oxygen demands (heart, brain), kidneys, liver, tissues with high phosphine (lungs).
ADME of zinc phosphide toxicity?
A=zinc phosphide & phosphine gas via GIT & phosphine gas via inhalation
D=serum/tissue zinc levels may be elevated
M=oxidized to less toxic compounds
E=in urine
Onset of clinical signs of zinc phosphide toxicity?
within minutes to hours–death can result in 3-48 hrs
Clinical signs of zinc phosphide toxicity?
anorexia, V+ sometimes with blood, increased rate/depth of respiration, wheezing, dyspnea
Specific clinical signs of zinc phosphide toxicity associated with cattle?
abdominal pain & bloat
Specific clinical signs of zinc phosphide toxicity associated with dogs?
CNS excitation–>compulsive hypermotility, ‘mad dog run’, yelping, convulsions (like strychnine)
Pathology of zinc phosphide toxicity?
acetylene, garlic, fishy odor to stomach contents, vomit or bait–gastroenteritis, V+ (+/- blood), congested liver, kidneys, lungs
Lab Dx of zinc phosphide toxicity?
metabolic acidosis, dehydration, hypocalcemia, elevated serum zinc
What tests are available to diagnose zinc phosphide toxicity?
Drager detector tubes, silver nitrate impregnated paper. paper turns black held above diluted & heated stomach contents for 15-20 minutes.
Prognosis of zinc phosphide toxicity?
no signs by 8-12 hrs post ingestion or 12-24 hrs after vomiting–good prognosis
severe signs of tissue damage–guarded to poor
T/F Zinc phosphide toxicity can cause rare delayed injury. Explains why you should monitor kidney/liver values after 3-5 days in all symptomatic survival patients.
TRUE!
Is there is specific antidote for zinc phosphide?
NO!
What can you use to decontaminate an animal with zinc phosphide toxicity?
emetics, gastric lavage w/ dilute K permanganate, antacids, mineral oil, activated charcoal
Another name for fluoroacetate?
compound 1080, “sodium monofluoracetate”
What kind of pesticide is fluoroacetate?
rodenticide
Currently the only use of compound fluoroacetate?
livestock protection collar for controlling coyotes preying on sheep & goats
only used as a pesticide in NZ & Australia
The plants that contain fluoroacetate are found in what continents of the world?
Africa & South America
Chemical properties of fluoroacetate?
irritant, odorless, water soluble, relatively insoluble in organic solvents, yellow in color
T/F Fluoroacetate remains undegraded in the environment.
FALSE–degraded by soil microorganisms & plant enzymes
What animals are most sensitive to fluoroacetate?
dogs
ADME of fluoroacetate?
A=readily from GIT, lungs or open wounds–NOT through intact skin
D=throughout body
M=to monofluoracetic acid (toxic) by hydrolysis
E=parent & metabolite are excreted in urine
Onset of clinical signs of fluoroacetate?
rapid in onset, as early as 30 mins or up to 2-4 hrs post ingestion
Clinical signs in dogs w/ fluoroacetate toxicity?
CNS–>running in straight line, barking, yelping, intermittent tonic-clonic seizures, opisthotonos
GI–>V+, D+, urination, hyperirritability, hypermotility, tenesmus
death w/in 2-12 hrs d/t to resp failure/anoxia
Clinical signs in horses/cattle/sheep/goats w/ fluoroacetate toxicity?
CV–>heart failure signs, arrhythmias
CNS–>staggering, terminal convulsions (d/t cerebral anoxia)
horses=mostly cardiac signs, colic
death d/t arrhythmias or resp failure/anoxia
Clinical signs in cats/pigs w/ fluoroacetate toxicity?
CNS–>depression or excitement, vocalization, hyperesthesia, hypothermia
CV–>bradycardia, arrhythmias
T/F CNS signs in dogs d/t fluoroacetate toxicity are NOT as easy to elicit with stimuli as with strychnine.
TRUE
T/F Fluoroacetate causes a delayed onset of rigor mortis.
FALSE–rapid onset of rigor mortis
Diagnosis of fluoroacetate toxicity?
chem analysis of GI contents, elevated citrate levels in kidney, brain, blood are supportive, hyperglycemia, metabolic acidosis, low ionized calcium (total Ca normal though)
Treatment of fluoroacetate toxicity?
onset so rapid–may not get to treat
decontamination–>emesis, activated charcoal
supportive/symptomatic–>O2, fluids, IV calcium, Na bicarb for metabolic acidosis
antidote
Emesis is sometimes contraindicated in fluoroacetate toxicity in dogs due to?
b/c risk of seizures is high in dogs
Sodium bicarb is used to treat metabolic acidosis in fluoroacetate toxicity but it can exacerbate this?
low levels of ionized calcium
List the antidotes that are used in fluoroacetate toxicity.
All are acetate donors which compete w/ the toxin to reduce conversion to monofluoroacetic acid.
Glyceryl monoacetate, acetic acid/ethanol, acetamide/dextrose.
T/F A higher dose of acetamide/dextrose is necessary for treatment of cats with fluoroacetate toxicity.
FALSE–lower dose required
Prognosis in fluoroacetate toxicity?
guarded to grave
MOA of fluoroacetate?
Condenses w/ oxaloacetate to fluorocitate–>competes w/ regular citrate as a substrate for aconitase in the TCA cycle–causes slowing of the TCA cycle & decreasing cellular respiration & energy–>high E demand organs hit hardest. Buildup of citrate that is not being used–>citrate to (binding of Ca), inhibition of some enzymes (glutamate, PFK, etc). Inhibition of aconite has variable effects in different species.
What type of pesticide is metaldehyde?
molluscicides
Is metaldehyde a RUP or a GUP?
RUP–restricted use pesticide
Metaldehyde can be used alone or in combo with these?
carbamates
Chemical properties of metaldehyde?
polymer of acetaldehyde, irritant, flammable, poorly soluble in water
What animals are susceptible to metaldehyde toxicity?
dogs, cats, livestock, horses
T/F Cats are more sensitive to metaldehyde toxicity than dogs.
TRUE–but dogs are more likely to ingest it
What animals are considered endangered species in the UK due to them feeding on slugs/snails treated with metaldehyde?
hedgehogs
Which route is more toxic—inhalation or ingestion of metaldehyde?
inhalation is more toxic–yet ingestion is the more common route
ADME of metaldehyde?
A=gastro environment, some MET undergoes acid hydrolysis to ACE–MET abs readily from GIT & also some ACE absorbed
D=both metaldehyde & acetaldehyde cross the BBB
M=MET in liver by microsomal enzymes (p450) & ACE metabolized by hepatic aldehyde dehydrogenase– converted to CO2 & exhaled
E=enterohepatic recycling
T/F Enzyme inducers such as phenobarbital may increase toxicity of metaldehyde.
FALSE–decrease toxicity!
Clinical signs of metaldehyde poisoning?
acute neurotoxicosis & hyperthermia–“shake & bake”
GI–>salivation, V+, D+
CNS–>incoordination, muscle tremors, hyperesthesia, convulsive seizures, opisthotonis–seizures eventually lead to CNS depression, resp failure & death w/in 4-24 hrs
Onset of signs d/t metaldehyde poisoning?
3 hrs–may recover w/in 2-3 weeks
T/F Seizures elicited by metaldehyde poisoning may be caused by stimuli in cats & sometimes in dogs.
TRUE
Specific clinical signs seen in cats d/t metaldehyde poisoning?
nystagmus & mydriasis
Specific clinical sign seen in dogs d/t metaldehyde poisoning?`
reversible blindness
MOA of metaldehyde poisoning?
in mice–decreases brain GABA, norepinephrine & serotonin. decreased GABA (main inhibitory NT in CNS)–lead to seizures & CNS excitation. decreased NE & serotonin lead to decreased MAO.
also causes direct GI irritation, metabolic acidosis, CNS excitation.
What is the cause of death in metaldehyde poisoning?
respiratory failure. also dogs that survive acute dz may develop liver failure.
Pathology of metaldehyde poisoning?
petechiae/ecchymoses in GI mucosa; congestion, edema, hemorrhage in liver, lungs, kidneys
longer survival–degenerative changes in liver & brain
Lab diagnosis of metaldehyde poisoning?
detection of MET or ACE–stomach contents, bait, serum, urine, liver tissue
Differential diagnosis for metaldehyde poisoning?
CNS toxicants or dz–severity of hyperthermia & elicitable nature of seizures helps to narrow Ddx
Treatment of metaldehyde poisoning?
no specific antidote.
decon–>emetics, gastric lavage, charcoal, enema w/ tepid water
fluid therapy to address metabolic acidosis, monitor & manage hyperthermia
tx seizures–>diazepam or pentobarbital
tx muscle relaxers–>methocarbamol or GG
phenobarbital–>enzyme inducer–accelerate elimination of toxin
xylazine & acepromazine in horses
Prognosis of metaldehyde poisoning?
good if they survive 24 hrs–full recovery may take 2-3 wks
