Neuro Flashcards
1
Q
Organophosphate Pesticides
A
- 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
2
Q
Organophosphate Pesticides Clinical signs
A
- 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
3
Q
OPIDN (organophosphate induced delayed neurotoxicity)
A
- sub-chronic to chronic stimulations
- OP compounds produce significant inhibition of neuropathy target esterase
- characterized by atonal degeneration of long motor neurons
- no treatment
4
Q
Ivermectin
A
- 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
5
Q
Ivermectin clinical signs and diagnosis
A
- 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
6
Q
Pyrethroid Pesticides
A
- 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
7
Q
Bromethalin
A
- 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
8
Q
Alprazolam (Xanax)
A
- 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)
9
Q
Zolpidem (ambien)
A
- 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
10
Q
What are Mycotoxins ?
A
- fungal metabolite that causes pathological, physiological, and/or biochemical alterations usually on several organ systems
- can effect all species
11
Q
What is peanut butter screened for ?
A
Aflatoxins
12
Q
Mycotoxin : slaframine
A
- 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
13
Q
Mycotoxin: fumonisin
A
- 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
14
Q
ELEM (equine leucoencephalomalacia)
A
- 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
15
Q
PPE (porcine pulmonary edema)
A
- 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
