Neuro

Question 1

Organophosphate Pesticides

Answer 1

• used in flea collars, dips, fly/ant/roach baits
• other names: parathion, malathion, chlorpyrifos
• H2O soluble and acute toxicity
• mechanism= irreversible inhibition of AchE (does not let esterase degrade Ach, causes way too much Ach activation and cholinergic stimulation within minutes or hrs)
• clinical signs: other card
• diagnosing: atropine challenge, history, RBC AchE by over 50%
• treatment: GI decontamination, atropine sulfate for muscarinic signs, oximes, diazepam, time

Question 2

Organophosphate Pesticides Clinical signs

Answer 2

• muscarinic : SLUDGE-M
• nicotinic : muscle fasciculations beginning with the face, eyelid, and tongue; generalized tremors, weakness, paralysis
• CNS : respiratory depression, ataxia, nervousness, clinic- tonic seizures
• – may last 1-5days

Question 3

OPIDN (organophosphate induced delayed neurotoxicity)

Answer 3

• sub-chronic to chronic stimulations
• OP compounds produce significant inhibition of neuropathy target esterase
• characterized by atonal degeneration of long motor neurons
• no treatment

Question 4

Ivermectin

Answer 4

• worm medication
• border collies, aust. Shepherds, Shellies are susceptible
• crosses BBB
• mechanism: GABA receptor agonist (increases inhibitory input and decreases ability to respond to stimuli)
• can cave commutative toxicosis
• clinical signs: other card
• diagnosis: other card
• treatment: GI decontamination with activated charcoal, supportive care with Epi and short acting barbiturates, good prognosis if dose was <5mg/kg

Question 5

Ivermectin clinical signs and diagnosis

Answer 5

• signs: ataxia, lethargy, mydriasis, coma, blindness, bradycardia, respiratory distress precedes death, recumbency, disorientation, can see anaphylactic reactions
• diagnosis: history, brain ivermectin concentration, measure GI content, no visible lesions, no diagnostic bloodwork

Question 6

Pyrethroid Pesticides

Answer 6

• mechanism: binds voltage-gated Na channels causing them to stay open and have repetitive nerve discharge
• more common in cats due to their glucuronide conjugation
• lipophilic
• clinical signs: paresthesia in cats and dogs; cats: drooling, hyperthermia
• diagnosis is difficult, needs to do chemical analysis
• treatment: methocarbamol, bath, IV fluids to protect kidney
• good prognosis

Question 7

Bromethalin

Answer 7

• mechanism: damages mitochondrial function inhibiting oxidative respiration
• clinical signs: ataxia, hindlimb paralysis, hyper–excitability, severe muscle tremors
• diagnosis: cerebral edema and cerebellar degeneration with histological evidence of neuronal vacuolization
• treatment: emesis is recent enough exposure, activated charcoal, furosemide
• poor prognosis if high dose

Question 8

Alprazolam (Xanax)

Answer 8

• mechanism: acts on lambic, thalamic, and hypothalamic levels
• clinical signs: ataxia, depression, vomiting, tremors, tachycardia, diarrhea, ptylism, low body temp
• clinical signs start after about 30min
• can show CNS excitation first at very high doses
• diagnosis: history
• treatment : decontamination, flumazenil (only GABA antagonist available)

Question 9

Zolpidem (ambien)

Answer 9

• sleep aid
• mechanism: binds to GABA site of receptor
• fast absorption
• clinical signs: ataxia, vomiting, lethargy, hypersalivation
• diagnosis: history
• treatment: just keep an eye on them and supportive care

Question 10

What are Mycotoxins ?

Answer 10

• fungal metabolite that causes pathological, physiological, and/or biochemical alterations usually on several organ systems
• can effect all species

Question 11

What is peanut butter screened for ?

Answer 11

Aflatoxins

Question 12

Mycotoxin : slaframine

Answer 12

• produced by black patch fungus on red clover
• it is an ACh mimic acting on mostly muscarinic cholonergic agonists, especially in exocrine glands
• most common in horses and cattle
• sings: copious salivation “slobbers”, bloat, diarrhea, frequent urination, may see feed refusal
• diagnose by history of consumption
• make sure to differentiate from OPs and botulism
• treat by removing source and maintaining hydration, can give atropine if clinical signs are bad
• rarely fatal, signs better within 48hrs of contaminated feed removal

Question 13

Mycotoxin: fumonisin

Answer 13

• found almost exclusively on corn after years of drought followed by wet weather
• inhibits sphingosine-N-acetyltransferase causing increased levels of sphinganine (which is cytotoxic)
• diagnostic is finding lots of sphinganine in the blood
• also effects endothelial cells leading to stroke, hepatic injury, and pulmonary edema
• susceptible species: horses, ponies, swine, rabbits
• ELEM and PPE
• no treatment, change feed, isolate infected animals, pigs recover after about 48hrs

Question 14

ELEM (equine leucoencephalomalacia)

Answer 14

• caused by fumonisin
• most common in late fall early winter
• almost 100% mortality rate
• main targets :
• ->CNC: anorexia, ataxia, mania, sweating
• ->liver toxicity
• postmortem CNS necrosis and liquefaction

Question 15

PPE (porcine pulmonary edema)

Answer 15

• due to fumonisin
• clinical signs : inactivity, increased RR and decreased HR
• signs happen about 12hrs after consumption, with leather pulmonary edema within 4-7days of consumption
• postmortem : pulmonary pathology and edema, hepatic lesions, tissue necrosis

Question 16

Ammoniated feed toxicosis

Answer 16

• non protein nitrogen sources are added to cattle feed, found in mineral licks
• species effected: bovine, caprine, ovine
• ruminants are way more susceptible
• calves can be effected through milk
• leads to bovine bonkers : hyperexciability
• animal can alternate between hyperexcitability and normal behavior if caused by imidazoles
• death within 24hrs
• diagnose by exposure history and blood/ feed/ rumen levels of ammonia
• no specific treatment

Question 17

Strychnine

Answer 17

• animal will most likely die
• often used as malicious poison
• mechanism: competitive antagonist at postsynaptic spinal cord and medulla glycine receptors
• clinical signs : anxiety, Sawhorse stance, grinning facial muscles, ear twitch, violent tetanic seizures initiated by external stimuli (diagnosis)
• death from respiratory failure
• causes hyperthermia in dogs, elevated CPK and LDH in serum, lactic acidosis, hyperkalemia and leukocytosis
• treat with aggressive decontamination, control seizures, ion trapping with ammonium chloride

Question 18

Salt toxicity

Answer 18

• can be water deprivation or large consumption of salt
• common in pigs but also seen in cattle
• diffuses Na into CNS when plasma levels are high, which leads to inhibition of glycolysis and ATP, attraction was water
• signs : salivation, abdominal pain, thirst, circling, wondering, partial paralysis, may be uncoordinated
• diagnose by measuring Na levels
• treatment: SLOW re-hydration, furosemide to prevent pulmonary edema