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

L3: Neurotoxicants (Martyniuk) Flashcards

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
Q

mycotoxin

A

fungal metabolite which causes pathological, physiological and/or biochemical alteration usually on several organ systems simultaneously
-esp. concern for LA

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26
Q

aflatoxins are carcinogenic

A

:)

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27
Q

slaframine source and action

A
  • produced by “black patch” fungus on red clover
  • ACh mimic; muscarinic cholinergic agonist, esp. in exocrine glands
  • most common in LA
  • rarely fatal
28
Q

symptoms of slaframine toxicity

A

copious salivation**
bloat, d, frequent urination
+/- feed refusal

29
Q

dx and tx of slaframine toxicity

A

Dx: ID of clover w/ black patch
Tx: remove source, maintain hydration, electrolytes, atropine

30
Q

fumonisin source

A
  • metabolite of Fusarium spp. found in corn

- occurs in years of drought followed by wet weather

31
Q

fumonisin MOA

A
  • inhibition of sphingosine-N-acetyltransferase cuasing inc. levels of cytotoxic sphinganine
  • affects vascular endothelial cells –> stroke, hepatic injury, pulmonary edema
32
Q

susceptible species to fumonisin toxicity

A

equids
swine
rabbits

33
Q

2 diseases linked to fumonsins

A 
Equine leucoencephalomalacia (ELEM)
Porcine pulmonary edema (PPE)
34
Q

Porcine Pulmonary Edema (PPE) CS

A
  • inactivity, inc. RR, dec. HR –> pulmonary edema –> resp. distress
  • hepatic lesions
35
Q

Dx of PPE

A
  • 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
Q

Equine Leukoencephalomalacia (ELEM) CS

A
  • targets brain and liver
  • anorexia, ataxia, circling, drowsiness, blindness, hysteria
  • hyperexcitability, mania, profuse sweating
  • hepatotoxicity
  • brain liquefication
  • nearly 100% mortality rate
37
Q

Dx of ELEM

A
  • CS + analysis of feed for fumonisin
  • severe liver injury and lesions (elevated liver enzymes)
  • post-mortem CNS necrosis and liquefaction
38
Q

Tx of fumonisin toxicity

A
  • No tx
  • isolate affected animals to prevent injury to self and others
  • change feed
39
Q

tremorgenic mycotoxins source and MOA

A
  • produced from fungi of genera Penicillium, Aspergillus, Claviceps, Acremonium
  • MOA: release of NTs from synaptosomes in the CNS
40
Q

tremorgenic mycotoxin CS

A

tremors, stiff gait, ataxia

2ary photosensitization, jaundice, pulm. edema

41
Q

Ammoniated feed toxicosis

A

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
Q

symptoms of ammonia toxicity/imidazoles

A 
rapid onset of:
intermittent hyperexcitability w/ imidazoles
SLUD
convulsions
inc. RR
43
Q

Dx of ammonia toxicosis

A

Hx, CS
analysis of feed or blood/rumen fluid for ammonia lvls
inc. ammonia, glucose, BUN
dec. blood pH

44
Q

Tx of ammonia toxicosis

A

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
Q

prognosis for imidazole vs. NPN toxicosis

A

imidazole: good if feed removed

NPN toxicosis: poor if recumbent

46
Q

strychnine source

A
  • seeds of Indian tree
  • used to control pocket gophers
  • restricted use; often used as malicious poison**
47
Q

which species is resistant to strychnine?

A

birds

48
Q

strychnine MOA

A

-competitive antagonist at postsynaptic spinal cord and medulla glycine receptors –> disinhibition (stimulation) of all muscles

49
Q

CS of strychnine toxicity

A
  • rapid onset
  • anxiety, stiff neck/gait, “grinning”, ear twitch, sawhorse stance –> tetanic seizures –> respiratory distress/failure –> death
50
Q

Dx of strychnine toxicity

A
  • 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
Q

Tx of strychnine toxicity

A
  • 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
Q

salt toxicity mech.

A

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
Q

symptoms of salt toxicity

A

primarily CNS (salivation, inc. thirst, abd. pain and d –> more severe CNS signs, uncoordination)

54
Q

Dx of salt toxicity

A

high brain Na conc.
cerebral edema
rule-out polio, Pb, pesticides, encephalitis

55
Q

Tx of salt toxicity

A

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
Q

1ary cause of pharmaceutical toxicity

A

careless storage

57
Q

top prescribed pharmaceuticals

A

vicodin (pain)
synthyroid (hypothyroid)
Zocor and Lipitor (high chol.)
Lisinopril (high blood pressure)

58
Q

Alprazolam (Xanax) MOA

A
  • GABA agonist

- acts at limbic, thalamic, and hypothalamic lvl of CNS

59
Q

CS of alprazolam toxicity

A

acute ataxia, depression, vomiting, tremors, tachycardia, diarrhea, excess salivation, hypothermia

60
Q

Dx of alprazolam/Zolpidem toxicity

A

based on suspected ingestion and CS

61
Q

Tx of alprazolam toxicity

A
  • emesis if recent and no signs
  • gastric lavage, act. charc. if ingested a LOT
  • flumazenil specific antagonist
  • fluids, meds to support respiration
62
Q

Zolpidem (Ambien)

A

sleep aid; acts similar to benzos

-rapid absorption!

63
Q

Zolpidem MOA

A

inhibits neuronal excitation by binding to the benzo omega-1 receptors

64
Q

CS of Zolpidem

A 
ataxia
vomiting
lethargy
disorientation
hypersalivation
\+/- hyperactivity/panting
65
Q

Tx of Zolpidem toxicity

A

mild: keep pet quiet and warm

- if excitement devleops, symptomatic tx

Toxicology 5172 (Fall 2014) (8 decks)

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