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Toxicology 5172 (Fall 2014) > L3: Neurotoxicants (Martyniuk) > Flashcards

L3: Neurotoxicants (Martyniuk) Flashcards

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1
Q

most toxic natural substance on the planet

A

botulinum toxin

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2
Q

groupings of neurotoxin symptoms

A

peripheral, centrl

excitatory, depressive

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3
Q

strychnine

A

rodenticide isolated from plant
very toxic
now a restricted compound
often involved in intentional poisonings

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4
Q

first use of pesticides

A

arsenic AD 70. Has been transition from natural to synthetic pesticides

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5
Q

era of synthetic organic pesticides

A

beginning in 1940s w/ use of organochlorines (DDT), organophosphates (parathion), carbamates, dithiocarbamtes, synthetic pyrethrins.

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6
Q

how many pesticides in use in US?

A

300

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7
Q

what percentage of pesticide usage is non-commercial?

A

> 50%

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8
Q

Organophosphate (OP) pesticides and chars.

A
  • parathion, malathion, chlorpyrifos
  • have replaced banned organochlorine pesticides
  • high water solubility and acute toxicity
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9
Q

OP MOA

A

irreversible inhibition of AChE activity –> acute ACh overstimulation

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10
Q

symptoms of anti-esterase toxicity

A

Resp. distress –> resp. m. paralysis –> death

  • Muscarinic stimultion: salivation, lacrimtion, urination, defecation, GI upset, emesis, miosis (SLUDGE-M)
  • Nicotinic stim: muscle fascicultions w/ face, tremors, weakness, paralysis
  • CNS: resp. depression, ataxia, nervousness, clonic-tonic seizures
  • last 1-5d
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11
Q

Horse specific symptoms of anti-esterase toxicity

A

colic, dehydration

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12
Q

Cattle specific symptoms of anti-esterase toxicity

A

rumen stasis. No miosis. Severe depression

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13
Q

Sheep specific symptoms of anti-esterase toxicity

A

severe depression

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14
Q

dogs and cats specific symptoms of anti-esterase toxicity

A

CNS stimulation –> convulsions

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15
Q

cat specific symptoms of anti-esterase toxicity with chlorpyrifos

A

more severe nicotinic signs. (Cats are more tolerant to muscarinic stimultion*)

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16
Q

dx of anticholinesterase toxicity

A
  • Hx, CS
  • Atropine Challenge: if normal signs of atropine administration (dry mouth, mydriasis, inc. HR are present, toxicity NOT due to cholinesterase inhibitor because OPs overwhelm any effect would have atropine)
  • Dec. RBC AChE
  • Non-specific pathology such as pulmonary edema, petechial hemorrhage in GI mucosa
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17
Q

tx of anti-esterase toxicity

A
  • GI decon
  • bathe for dermal exposure
  • atropine sulfate for muscarinic-only signs
  • oximes (protopam, 2-PAM) to reactivate AChE
  • diazepam or barbiturates for seizures
  • time
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18
Q

2-PAM is most effective for:

A

tx of ACUTE anti-esterase toxicity

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19
Q

Organophosphate-induced delayed neurotoxicity (OPIDN)

A
  • when OP compounds produce significant inhibition of neuropathy target esterase (NTE) –> delayed neuropathy
  • AChE overstimulated and neurons (esp. motor neurons) start to degenerate
  • hindlimb weakness, paralysis
  • NO tx
  • sensory neurons more resistant
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20
Q

Ivermectin source and use

A
  • produced by soil fungus Streptomyces abermitilis
  • worm med
  • can cross BBB in Collies, Aust. Sheps, Shelties (contraindicated!)
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21
Q

Ivermectin MOA in CNS

A
  • GABA agonist
  • neurotoxicant in CNS
  • increased inhibitory input decreases ability to respond to other stimuli
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22
Q

symptoms of ivermectin toxicity

A

CS: mydriasis, respiratory depression, ataxia, coma, blindness, bradycardia
-anaphylactic rxns in dogs due to worm die-off

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23
Q

dx of ivermectin toxicity

A

Hx
high ivermectin conc. in brain, GI content, liver, fat, feces
no visible lesions

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24
Q

tx of ivermectin toxicity

A

GI decon if recent (act. charc, saline cathartics)
short acting barbiturate for convulsions
supportive care
EP, fluids for anphylaxis

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25
mycotoxin
fungal metabolite which causes pathological, physiological and/or biochemical alteration usually on several organ systems simultaneously -esp. concern for LA
26
aflatoxins are carcinogenic
:)
27
slaframine source and action
- produced by "black patch" fungus on red clover - ACh mimic; muscarinic cholinergic agonist, esp. in exocrine glands - most common in LA - rarely fatal
28
symptoms of slaframine toxicity
copious salivation** bloat, d, frequent urination +/- feed refusal
29
dx and tx of slaframine toxicity
Dx: ID of clover w/ black patch Tx: remove source, maintain hydration, electrolytes, atropine
30
fumonisin source
- metabolite of Fusarium spp. found in corn | - occurs in years of drought followed by wet weather
31
fumonisin MOA
- inhibition of sphingosine-N-acetyltransferase cuasing inc. levels of cytotoxic sphinganine - affects vascular endothelial cells --> stroke, hepatic injury, pulmonary edema
32
susceptible species to fumonisin toxicity
equids swine rabbits
33
2 diseases linked to fumonsins
``` Equine leucoencephalomalacia (ELEM) Porcine pulmonary edema (PPE) ```
34
Porcine Pulmonary Edema (PPE) CS
- inactivity, inc. RR, dec. HR --> pulmonary edema --> resp. distress - hepatic lesions
35
Dx of PPE
- CS + analysis of feed for fumonisin - inc. in serum and tissue sphingoid bases - inc. ALT, ALP, GGT, bilirubin, bile acids, cholesterol (indicators of hepatic damage) - post-mortem pulm. path.
36
Equine Leukoencephalomalacia (ELEM) CS
- targets brain and liver - anorexia, ataxia, circling, drowsiness, blindness, hysteria - hyperexcitability, mania, profuse sweating - hepatotoxicity - brain liquefication - nearly 100% mortality rate
37
Dx of ELEM
- CS + analysis of feed for fumonisin - severe liver injury and lesions (elevated liver enzymes) - post-mortem CNS necrosis and liquefaction
38
Tx of fumonisin toxicity
- No tx - isolate affected animals to prevent injury to self and others - change feed
39
tremorgenic mycotoxins source and MOA
- produced from fungi of genera Penicillium, Aspergillus, Claviceps, Acremonium - MOA: release of NTs from synaptosomes in the CNS
40
tremorgenic mycotoxin CS
tremors, stiff gait, ataxia | 2ary photosensitization, jaundice, pulm. edema
41
Ammoniated feed toxicosis
due to addition of non-protein nitrogens (NPN) (i.e. urea, biuret, ammonium salts) added to cattle feed such as hay - ruminants most susceptible - leads to "bovine bonkers"
42
symptoms of ammonia toxicity/imidazoles
``` rapid onset of: intermittent hyperexcitability w/ imidazoles SLUD convulsions inc. RR ```
43
Dx of ammonia toxicosis
Hx, CS analysis of feed or blood/rumen fluid for ammonia lvls inc. ammonia, glucose, BUN dec. blood pH
44
Tx of ammonia toxicosis
imidazole toxicosis: No tx, remove feed (sedation, milking out cows may help) NPN toxicosis: no specific tx (can try cold water, vinegar by stomach tube)
45
prognosis for imidazole vs. NPN toxicosis
imidazole: good if feed removed | NPN toxicosis: poor if recumbent
46
strychnine source
- seeds of Indian tree - used to control pocket gophers - restricted use; often used as malicious poison**
47
which species is resistant to strychnine?
birds
48
strychnine MOA
-competitive antagonist at postsynaptic spinal cord and medulla glycine receptors --> disinhibition (stimulation) of all muscles
49
CS of strychnine toxicity
- rapid onset - anxiety, stiff neck/gait, "grinning", ear twitch, sawhorse stance --> tetanic seizures --> respiratory distress/failure --> death
50
Dx of strychnine toxicity
- CS, lack of clonic/tonic seizures - chemical analysis of bait, stomach contents, liver - elevated GOT, CPK, LDH - lactic acidosis, hyperkalemia, leukocytosis - rule out of other seizure-causing compounds
51
Tx of strychnine toxicity
- control seizures and prevent asphyxiation - emesis if no CS present yet - gastric lavage, act. charc. forced diuresis once anesthetized - ion trapping with ammonium chloride if not acidotic - bicarb if acidosis develops
52
salt toxicity mech.
diffusion of sodium into CSF when plasma Na lvls are high. When plasma Na lvls drop, Na slowly leaves CSF which attracts water to maintain osmotic balance --> increase in CSF volume and pressure
53
symptoms of salt toxicity
primarily CNS (salivation, inc. thirst, abd. pain and d --> more severe CNS signs, uncoordination)
54
Dx of salt toxicity
high brain Na conc. cerebral edema rule-out polio, Pb, pesticides, encephalitis
55
Tx of salt toxicity
SLOW rehydration over 2-3d IV hyperosmotic fluids low in Na Furosemide to prevent pulmonary edema (blocks Na/K transporters so Na reabsorbed instead of excreted)**
56
1ary cause of pharmaceutical toxicity
careless storage
57
top prescribed pharmaceuticals
vicodin (pain) synthyroid (hypothyroid) Zocor and Lipitor (high chol.) Lisinopril (high blood pressure)
58
Alprazolam (Xanax) MOA
- GABA agonist | - acts at limbic, thalamic, and hypothalamic lvl of CNS
59
CS of alprazolam toxicity
acute ataxia, depression, vomiting, tremors, tachycardia, diarrhea, excess salivation, hypothermia
60
Dx of alprazolam/Zolpidem toxicity
based on suspected ingestion and CS
61
Tx of alprazolam toxicity
- emesis if recent and no signs - gastric lavage, act. charc. if ingested a LOT - flumazenil specific antagonist - fluids, meds to support respiration
62
Zolpidem (Ambien)
sleep aid; acts similar to benzos | -rapid absorption!
63
Zolpidem MOA
inhibits neuronal excitation by binding to the benzo omega-1 receptors
64
CS of Zolpidem
``` ataxia vomiting lethargy disorientation hypersalivation +/- hyperactivity/panting ```
65
Tx of Zolpidem toxicity
mild: keep pet quiet and warm | - if excitement devleops, symptomatic tx

Toxicology 5172 (Fall 2014) (8 decks)

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