Toxicolocy

Question 1

Examples of situations where you might use intravenous lipid emulsion

Answer 1

Permethrin, THC/cannaboids, ivermectin, naproxen, bromethalin, vitamin D

Question 2

MofA apomorphine

Answer 2

Stimulates dopamine receptors in CRTZ

Question 3

An overdose of what drugs/types of drugs could cause seratonin syndrome

Answer 3

SSRI’s (block reuptake at presynaptic membranes), MAOIs (inhibit hepatic seratonin metabolism), 5HTP supplements, Mirtazapine

Question 4

Seratonin syndrome atidote

Answer 4

cypraheptadine - non selective 5HT2 antagonist

Question 5

Mechanism of toxicity of nicotine

Answer 5

Water soluble alkaloid, interacts with CNS, NM junction blockage, chemoreceptors (tachycardia/hypertension) and adrenal medulla

Question 6

ADHD drugs mechanism of toxicity

Answer 6

Release of catecholamines resulting in CNS stimulation, Monoamine oxidase inhibition (enzyme in catecholamine metabolism), alpha and beta stimulation

Question 7

Phenylpropanolamine mechanism of toxicity

Answer 7

sympathomimetic catacholamine
alpha stimulation and indirect alpha and beta stimulation via norepi
- CNS, CV, GI

Question 8

Pimobendan MofA
Overdose results:

Answer 8

Inodilator (calcium sensitizer and PDE3 inhibitor
- PDE3 inhibition - peripheral vasodilation with reflex tachycardia, SVT

Question 9

Inocybe mushroom mechanism of toxicity
Antidote

Answer 9

Targets muscarinic receptors causing SLUDDE signs, cannot cross BBB
Antidote - atropine

Question 10

Chocolate/methylxanthine mechanism of toxicity

Answer 10

Competitive inhibitor of phosphodiesterase (elevated cAMP) inhibits reuptake of Ca (increase free Ca concentration), compete with bezodiazepine receptors in CNS

Question 11

Clinical signs of chocolate toxicity

Treatment

Answer 11

ataxia, tremors, seizures, arrhythmias

Decomtamination (repeat activated charcoal b/c enterohepatic circulation)
Beta blocker for arrhythmias
Urinary catheter (methylxanthines reabsorbed through bladder wall)

Question 12

Cannabinoids/THC mechanism of toxicity, Clinical signs

Answer 12

Cannaboid receptor agonist in CNS
Clinical signs: CNS depression, hyperesthesia, mydriasis, urinary incontinence

Question 13

Bromethalin mechanism of toxicity

Clinical signs

Answer 13

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

Question 14

Bromethalin toxicity treatment

Answer 14

Decontamination (do not induce emesis if symptomatic); intralipid therapy. Treat cerebral edema with steroids or mannitol

Question 15

Pyrethrums and bromethalin - are cats or dogs more sensitive

Answer 15

Cats

• pyrethrums undergo hepatic metabolism and cats lack substantial glucuronide conjugation

Question 16

Pyrethrum mechanism of toxicity and clinical signs

Answer 16

Neurotoxin - prolongs sodium channel condution
Clinical signs similar to organophosphate toxicity (sludde) but less severe

Question 17

Treatment pyrethrum toxicity

Answer 17

Bathe, methocarbomol for tremors, seizure control, intralipid therapy

Question 18

Organophosphate/carbamates mechanism of toxicity

What is a naturally occuring organophosphate and what produces it?

Answer 18

Inhibition of acetylcholinsterase so ach accumulates and continues to bind post ganglionic receptors producing prolonged depolarization.

Anatoxin-a produced by blue green algae

Question 19

Clinical signs of organophosphate toxicity

Answer 19

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.

Question 20

Treatment for organophosphate toxicity

Answer 20

Decontaminate (bath, emesis, charcoal), Atropine (to control bradycardia and bronchiol secretions), 2-PAM to reactivate cholinesterase to control nicotinic signs.

Question 21

What is an example of a tremorgenic mycotoxin?

What is the mechanism of toxicity

Answer 21

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.

Question 22

What is afalotoxin produced by and what organ does it target

Answer 22

Produced by aspergillus and can cause liver failure

Question 23

Clinical signs of tremorogenic mycotoxins

Treatment

Answer 23

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

Question 24

Ivermectin mechanism of toxicity

Clinical signs

Answer 24

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