Toxicolocy Flashcards
Examples of situations where you might use intravenous lipid emulsion
Permethrin, THC/cannaboids, ivermectin, naproxen, bromethalin, vitamin D
MofA apomorphine
Stimulates dopamine receptors in CRTZ
An overdose of what drugs/types of drugs could cause seratonin syndrome
SSRI’s (block reuptake at presynaptic membranes), MAOIs (inhibit hepatic seratonin metabolism), 5HTP supplements, Mirtazapine
Seratonin syndrome atidote
cypraheptadine - non selective 5HT2 antagonist
Mechanism of toxicity of nicotine
Water soluble alkaloid, interacts with CNS, NM junction blockage, chemoreceptors (tachycardia/hypertension) and adrenal medulla
ADHD drugs mechanism of toxicity
Release of catecholamines resulting in CNS stimulation, Monoamine oxidase inhibition (enzyme in catecholamine metabolism), alpha and beta stimulation
Phenylpropanolamine mechanism of toxicity
sympathomimetic catacholamine
alpha stimulation and indirect alpha and beta stimulation via norepi
- CNS, CV, GI
Pimobendan MofA
Overdose results:
Inodilator (calcium sensitizer and PDE3 inhibitor
- PDE3 inhibition - peripheral vasodilation with reflex tachycardia, SVT
Inocybe mushroom mechanism of toxicity
Antidote
Targets muscarinic receptors causing SLUDDE signs, cannot cross BBB
Antidote - atropine
Chocolate/methylxanthine mechanism of toxicity
Competitive inhibitor of phosphodiesterase (elevated cAMP) inhibits reuptake of Ca (increase free Ca concentration), compete with bezodiazepine receptors in CNS
Clinical signs of chocolate toxicity
Treatment
ataxia, tremors, seizures, arrhythmias
Decomtamination (repeat activated charcoal b/c enterohepatic circulation)
Beta blocker for arrhythmias
Urinary catheter (methylxanthines reabsorbed through bladder wall)
Cannabinoids/THC mechanism of toxicity, Clinical signs
Cannaboid receptor agonist in CNS
Clinical signs: CNS depression, hyperesthesia, mydriasis, urinary incontinence
Bromethalin mechanism of toxicity
Clinical signs
Uncouples osidative phosphorylation decreasing cellular ATP and NA/K ATPase failure. Osmotic control within cell is lost d/t water diffusion and Na retension in cell.
Clinical signs: results in CSF fluid accumulation and increased CNS pressure - seizures, ataxia, coma, respiratory muscle paralysis, death
Bromethalin toxicity treatment
Decontamination (do not induce emesis if symptomatic); intralipid therapy. Treat cerebral edema with steroids or mannitol
Pyrethrums and bromethalin - are cats or dogs more sensitive
Cats
- pyrethrums undergo hepatic metabolism and cats lack substantial glucuronide conjugation
Pyrethrum mechanism of toxicity and clinical signs
Neurotoxin - prolongs sodium channel condution
Clinical signs similar to organophosphate toxicity (sludde) but less severe
Treatment pyrethrum toxicity
Bathe, methocarbomol for tremors, seizure control, intralipid therapy
Organophosphate/carbamates mechanism of toxicity
What is a naturally occuring organophosphate and what produces it?
Inhibition of acetylcholinsterase so ach accumulates and continues to bind post ganglionic receptors producing prolonged depolarization.
Anatoxin-a produced by blue green algae
Clinical signs of organophosphate toxicity
SLUDDE effects, neuromuscular effects - muscle tremors, paralysis, CNS, tachypnea/dyspnia, respiratory failure, cardiac arrest, death.
Can have delayed neurological complication - weakness of forelimbs or neck, can have a neuropathy 2-4 weeks post exposure leading to hindlimb ataxia.
Treatment for organophosphate toxicity
Decontaminate (bath, emesis, charcoal), Atropine (to control bradycardia and bronchiol secretions), 2-PAM to reactivate cholinesterase to control nicotinic signs.
What is an example of a tremorgenic mycotoxin?
What is the mechanism of toxicity
Toxins produced by mold on food with high carbohydrate content. Ex. penicillum
Indole alkaloids - facilitation of nerve transmission at end plates, inhibition of glycine (inhibitory neurotransmitter), increased resting nerve potentials.
What is afalotoxin produced by and what organ does it target
Produced by aspergillus and can cause liver failure
Clinical signs of tremorogenic mycotoxins
Treatment
Appear normal at rest with occasional fine tremors but stimulation results in altered movements (spasticity, hypersalivation, whole body tremors, seizures, opsthotonus). Can lead to hyperthermia, metabolic acidosis, rhadomyolysis
Treatment is supportive care (diazepam) and decontamination
Ivermectin mechanism of toxicity
Clinical signs
P glycoprotein substrate, increased CNS concentration due to absence of a functional protein to efflux it out in some breeds. GABA agonist, enhancing inhibition.
Lethargy, depression, hypersalivation, mydriasis, blindness, ataxia, seizures, respiratory depression, death
