D-limonene/Metaldehyde Flashcards
what are the CS associated with EO overexposure?
- unsteadiness
- depression
- low body temp (in severe cases)
- vomiting
- diarrhea
what are the characteristics of D-Limonene?
- cyclic monoterpene hydrocarbon
- clear, colorless
- volatile
- lipophilic
what are the sources of exposure for D-Limonene?
- botanical insecticide
- 5% d-limonene - controls lice, fleas, ticks - botanical herbicide
- 70% d-limonene - broad spectrum weed killer - biodegradeable cleaning agents and solvents
- up to 100% d-limonene defatting and degreasing
what percentage of D-limonene is considered safe in a product?
1-5%
what are the toxicokinetics of D-limonene?
- lipid soluble
- readily absorbed through skin and GIT
- maximal blood concentrations 10 mins after dermal exposure
- metabolized by liver and excreted in urine
what is the MOA of D-limonene?
unknown
what CS do we see with d-limonene toxicity?
- ataxia
- weakness
- recumbency
- paralysis
- CNS depression
- hypothermia
- hypotension
- skin reaction
- smells like lemons
how do we treat D-limonene toxicity?
- decontaminate with shampoo and mild dish soap
- monitor temp
- other supportive care
what is the most common type of molluscicide used?
metaldehyde
- other types are ACh-esterase inhibitors (OPs), metal salts, and methiocarb (banned in 2014)
when using a molluscicide what is mollusk death due to?
- excessive mucus, dehydration, cell damage
what are the main properties of metaldehyde?
- restricted use
- polymer of acetylaldehyde
- highly flammable
- hydrophobic
- short soil half life
how are animals exposed to metaldehyde?
- ingestion of bait most common
- brightly colored and flavored –> dogs want to eat it
- sometimes malicious poisoning
- snail baits often mixed with tasty items that would attract other species by accident
what are the common routes of exposure for metaldehyde?
- inhalation = most toxic
- dermal = least toxic
- ingestion = most common and intermediate toxic
what are the toxicokinetics of metaldehyde?
- once ingested, undergoes GIT acid hydrolysis to acetaldehyde
- readily absorbed as wither metaldehyde or acetaldehyde
- both cross BBB (neurotox)
- rapidly metabolozed by liver by P450
- undergo enterohepatic recirculation (prolongs tox)
- enzyme inducers may decrease tox
- excreted in urine
what is the MOA of metaldehyde?
- decreased brain GABA -> neuro stimulation
- increased monoamine oxidase - decreased brain serotonin and NE –> reduced seizure threshold
- increased neuromuscular activity and production of metaldehyde metabolites –> metabolic acidosis, hyperthermia
- death from resp failure (acute) or liver failure (chronic)
what are the main CS with metaldehyde toxicity?
- acute neuro manifestations within 1-3hr after ingestion
- initial onset: severe muscle tremors, salivation, ataxia, tachycardia, hyperthermia
- progression into acidosis: V, D, depression, tonic convulsions that are unresponsive to ext stimuli
- seizures eventually lead to CNS depression, resp failure, and death within 4-24hrs
what are the lesions associated with metaldehyde poisoning?
- acute: nothing specific
- stomach contents will have a specific apple cider odor
- petechiae/ecchymoses in GIT
- congestion, edema, hemorrhage in lungs, liver, kidneys
- longer survival may result in degenerative changes in liver and brain (ganglion cells)
how do we treat metaldehyde poisoning?
- no specific antidote
- decontaminate
- emetics
- gastric lavage
- activated charcoal
- enemas
- fluids to address metabolic acidosis
- treat seizures
- muscle relaxants
what is the problem with some barbiturates when treating metaldehyde?
- some barbs (pento) can interfere with metabolism of acealdehyde and cause displacement from protein binding sites
- BUT phenobarb can help accelerate elimination of the toxin!
what is the LEAST accurate answer following acute exposure to metaldehyde?
- increase GABA
- increased monoamine oxidase
- decreased serotonin
- decreased NE
increased GABA