Lecture 3 Flashcards by Lauren Nykanen

What are the 6 neurotoxins we talked about

Pesticides
Pharmaceuticals
Mycotoxins
Ammoniated feed
Strychnine
Salt

How well did you know this?

Not at all

Perfectly

What are OPs used in

Pesticides (replaced organochlorine pesticides

Flea collars, dips, fly, ant, and roach bait

How well did you know this?

Not at all

Perfectly

What are examples of OPs

Parathion, malathion, chlorpyrifos

How well did you know this?

Not at all

Perfectly

What is the MOA of OPs

Reversible inhibition of AChE activity

How well did you know this?

Not at all

Perfectly

What are the clinical signs of OPs

Muscarinic- SLUDGE-M
Nicotinic- muscle fasciculations of face, generalized tremors, weakness, paralysis
CNS- resp depression, ataxia, nervousness, seizures

How well did you know this?

Not at all

Perfectly

What specific test can be used to diagnose OPs

Atropine challenge- if affects of atropine are observed, toxicosis is NOT from AChE inhibition

How well did you know this?

Not at all

Perfectly

How to treat OPs toxicosis

GI decontamination, bathing for dermal exposure
Atropine or glycopyrrolate for muscarinic signs
Oximes (protopam or 2-PAM) to reactivate AChE
Diazepam or other barbiturates for seizures

How well did you know this?

Not at all

Perfectly

What is OPIDN

Organophosphate induced delayed neurotoxicity; OP compounds that inhibit NTE

How well did you know this?

Not at all

Perfectly

What clinical signs will you see with OPIDN

Hindlimb weakness and paralysis from axonal degeneration of long motor neurons

How well did you know this?

Not at all

Perfectly

What is ivermectin used in? What are the most common toxicosis from?

Deworming medication, anthelminthic in livestock

Accidental overdoses from owners and veterinarians

How well did you know this?

Not at all

Perfectly

What dog breeds are sensitive to ivermectin

Border collies, australian shepherds, shelties

How well did you know this?

Not at all

Perfectly

Ivermectin MOA

GABA receptor agonist

**affects can be cumulative because of long half-life

How well did you know this?

Not at all

Perfectly

Clinical signs of ivermectin

Ataxia, lethargy, mydriasis, coma, blindness, bradycardia,
recumbency, disorientation, seizures in collies
resp distress before death,
anaphylactic shock if worms die off rapidly

How well did you know this?

Not at all

Perfectly

Ivermectin treatment

GI decontamination with activated charcoal and lipid emulsion
Supportive care- careful of benzodiazepines

How well did you know this?

Not at all

Perfectly

What is pyrethroid used in

Comes from flowers of chrysanthemum, and used as insectides

How well did you know this?

Not at all

Perfectly

Examples of pyrethroid pesticides

Pyrethrin, permethrin, allethrin, fenvalerate (pydrin, blockade)

How well did you know this?

Not at all

Perfectly

Who can pyrethroids not be used in

Cats because inefficient glucoronidation

How well did you know this?

Not at all

Perfectly

Pyrethroid MOA

Binds voltage gated sodium channels- causes hyperactivity

How well did you know this?

Not at all

Perfectly

Clinical signs of pyrthroids

Cats- drooling, paresthesia, muscle tremors and seizures, excessive muscle activity, hyperthermia

Dogs- paresthesia (shaking of legs, muscle fasciculations, rubbing of application site, agitation, nervousness)

How well did you know this?

Not at all

Perfectly

Treatment for pyrethroids

Stabilize tremors/seizures with methcarbamol

Bathe

Lipid infusion

IV fluids

How well did you know this?

Not at all

Perfectly

What is bromethalin

Rodenticide

How well did you know this?

Not at all

Perfectly

Bromethalin MOA

Oxidative phosphorylation in CNS leading to loss of ion gradients resulting in fluid accumulation in myelin sheaths

How well did you know this?

Not at all

Perfectly

Clinical signs of bromethalin

Ataxia, hindlimb paralysis, hyper excitability, severe muscle tremors, running fits, seizures

How well did you know this?

Not at all

Perfectly

How to diagnose bromethalin

Cerebral edema and cerebellar degeneration

Histological evidence of neuronal vacuolization and edema

How well did you know this?

Not at all

Perfectly

Bromethalin treatment

Emesis if recent exposure Activated charcoal Furosemide for cerebral and pulmonary edema Treat seizures Lipid infusion

Alprazolam MOA

Acts at the limbic, thalamic, and hypothalamic level of CNS

Clinical signs of alprazolam

Ataxia, depression, vomiting, tremors, tachycardia, diarrhea, hypothermia, liver failure

Treatment for alprazolam

Emesis, gastric lavage, and/or activated charcoal Flumazenil- benzodiazepine antagonist

Zolpidem MOA

Binds GABA receptors

Clinical signs of Zolpidem

Ataxia, vomiting, lethargy, disorientation, hyper salivation, hyperactivity and panting

Treatment of Zolpidem

Supportive and symptomatic

What is slaframine

Toxin produced by black patch fungus on red clover

MOA of slaframin

Muscarinic cholinergic agonist

Who is slaframine toxicity most common in

Horses and cattle

Clinical signs of slaframine

Copious salivation is main sign | May also see bloat, diarrhea, frequent urination, feed refusal

Treatment of slaframine

Remove source Atropine Rarely fatal

What is fumonisin

Very sinister toxin from moldy corn

MOA of fumonisin

Inhibits sphingosine-N-acetyltransferase causing increased levels of sphinganine which is toxic

What does fumonisin toxicity cause

Increase permeability of vascular enothelial cells leading to stroke, hepatic injury, and pulmonary edema

What species are susceptible to fumonisin

Horses/ponies, pigs, rabbites

What two diseases are associated with fumonisin

Equine leucoencephalomalacia and porcine pulmonary edema

Clinical signs of porcine pulmonary edema

Inactivity, increased resp rate, decreased heart reate, lethal pulmonary edema

Clinical signs of ELEM

Most common in late fall/early winter CNS- hysteria, profuse sweating, mania, excitability, post mortem liquefaction of brain Liver- jaundice, hepatic encephalopathy

Treatment of fumonisin

No treatment Remove contaminated feed Potentially ultrasorb S for pigs

Why is ammonia and other NPN added to feed

To fuel microbes in the rumen

What species does ammoniated feed toxicosis affect

Cows, sheep, goats

What does ammoniated feed toxicosis cause

Bovine bonkers- alternating between hyperexcitability and normal behavior

Treatment of ammoniated feed toxicosis (imidazole and NPN)

Just feed removal Possibly sedation to prevent self harm while bonkers

Strychnine MOA

Competitive antagonist of glycine receptors

Clinical signs of strychnine

Anxiety, restlessness, stiff gait and neck, stiff facial muscles, seizures, sawhorse stance, hyperthermia in dogs

Diagnosis of strychnine toxicity

Elevated CPK and LDH | Lactic acidosis, hyperkalemia, and leukocytosis

Treatment for strychnine

Decontamination Control seizures and prevent asphyxiation Methcarbamol/phenobarbital Ion trapping with ammonium chloride if animal is not acidotic

What causes salt toxicity and who is it most common in

Water deprivation of consumption of large amounts of salt in pigs and cattle

Salt MOA

Sodium diffuses into CSF, attracting water, and inhibiting glycolysis

Clinical signs of salt toxicity

Salivation, thirst, abdominal pain, circling, wobbling, aimless wandering, head pressing, blindness, seizures, partial paralysis Cattle may be belligerent and uncoordinated

Salt toxicity diagnosis

Na levels over 160 is diagnostic in pigs and cows

Salt treatment

Slow rehydration | Furosemide to prevent edema

What should you differentiate salt toxicosis from

Polio Lead Pesticides Encephalitis

What should you differentiate ammonia toxicosis from

OPs, grain overload, chlorinated hydrocarbon pesticides, meningitis, and encephalitis

What should you differentiate slaframine from

OPs and botulism

What is the primary cause of pharmaceutical toxicosis

Improper storage

Lecture 3 Flashcards

(61 cards)