• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/67

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

67 Cards in this Set

  • Front
  • Back
What do organophosphorus esters inhibit?
Acetylcholinesterase
Are phosphates active or inactive toxicants?
active - that inhibit AchE
What are phosphorothioates?
protoxicants
What characteristic of OP make it able to be absorbed by inhalation and dermal contact?
it is lipophilic
Are OP long lasting in the environment? Why?
no - they are esters therefore hydrolyzed easily
What are OP used for?
-contact insecticides (malathion and chlorpyrfos)
-systemic insecticides
-chemical warfare
-industrial chemicals (plastics, lubricants)
OPs cause overstimulation of what?
muscarinic sites and the PNS
-nicotinic sites
CNS receptors
What is "aging" when referring to OPs?

-when does this occur?
when OPs bind to esteratic sites of AChE irreversibly (covalent bonds)

-expected in less than 60 minutes
What about RBCs is valuable for diagnosis?
true AChE is in mammalian RBCs therefore can be measured
What are the acute PSN, muscarinic clinical signs of OP poisoning?
-act on heart, GI and salivations
SLUD
S=increased salivation
L=increased lacrimation
U=increased urination
D=increased defecation (peristalsis)

-decreased HR
-decreased pupil size
-lack of response to pre-anesthetic dose of atropine
Do all animals show all the signs for OP poisoning?
no
What are the acute nicotinic receptor signs of OP poisoning?
tremors
What are the acute CNS signs of OP poisoning?
stimulation then block
-excitement then depression
What is the threshold for signs with OP poisoning?
<50% of AchE in RBCs
<30% of normal AchE in brain
-signs may last 1-5 days
What is the cause of death with OP poisoning?
resp. failure
What type of signs does atropine help with when treating OP poisoning?
muscarininc signs only
How do you administer atropine with OP poisoning?
1/4 IV
3/4 SC
What is used to regenerate AcHE at the muscarinic and nicotinic sites after OP poisoning?
-when is it given?
pralidoxime - 2-PAM
-given BEFORE aging
If you didn't give 2-PAM after OP poisoning, how long would it take to regenerate AChE?
1-5%/day
What is the treatment for intermediate syndrome OP poisoning?
wait and watch
Delayed effects of OPs occur with what type?
NTE inhibitors
-neurotoxic esterase
What can NTE inhibition predict?
if OPIDN will occur
(organophosphate delayed neuropathy)
Is NTE related to AchE inhibition?
no
Intermediate Syndrome of OP includes what?
a nicotinic effect at the NMJ that reverses with time
How long does it take for NTE inhibition to occur?
OPIDN?
-NTE inhibition - hours
-OPIDN - weeks
Activated protoxicants are inactivated by what?
-type A enzymes - not inhibited by OP (BIRDS lack these)
-type B enzymes (AChE, pChe, CbxE) --> ARE inhibited by OP
Are young more or less susceptible to inhibition of AChE or OPIDN?
-more susc. to inhibition of AChE
-less susc. to OPIDN
Are Carbamates more readily or less readily absorbed from the skin than OP?
less - less lipophilic
-more polar
Is the binding of carbamate to AChE reversible?
yes
Is there aging with Carbamate poisoning?
no
Is 2-PAM needed for Carbamate poisoning?
no - time is best

treatment is atropine + time
What action do neonicotinoids have?
agonist then antagonist at nicotinic sites (and autonomic ganglia)
-stimulate then block, esp at NMJs
What is the treatment for nicotine poisoning?
-artificial respiration
-possible use of a ganglionic blocker (macylamine)
What is the prognosis for nicotine poisoning?
poor
What is imidacloprid and what is it normally used for?
-neonicotinoid

-crop protection from sucking, but not chewing insects and a topical flea adulticide for dogs and cats
What occurs with neonicotinoid poisoning and what is the antidote?
-stimulates than blocks nicotinic receptors
-there is no antidote but recovery is usually in 12-24 hours without sequele
Ion channel insecticides target what?
Na channels - keep them open

Cl channels - GABA (inhibitory NT) has a Cl channel and can be blocked
What type of general symptoms does ion channel insecticides cause?

how are these treated?
stimulation of the NS (excitement)
-convulsions

-treated with time and removal from exposure, but general treatment is symptomatic (treat with GABA agonist anticonvulsants)
What mechanism does Fipronil inhibit?
GABA antagonist
Is fipronil readily absorbed from the skin and if it does get in the body, what happens to it?
-no
-if enters body, undergoes enterohepatic circulation
What is the action of pyrethrins and pyrethroids?
act on Na channels
Are pyrethrins/oids polar or non-polar?
polar
What animals are the most sensitive to pyrethrins/oids?
cats, birds, fish because metabolized by esterases and mixed function oxidases (also glucuronidation)
T syndrome from Type I pyrethroids show what type of signs?
tremors and excitation
CNS syndrome from Type II pyrethroids show what type of signs?
tonic/clonic seizures

- have a CN group (fenvalerate)
What is the treatment for pyrethrins/pyrethorid exposure?
wash
-treat symptoms (anticonvulsants)
-good prognosis
What type of compound is DDT?
organochlorine - chlorinated hydrocarbon
Do OC cause more acute or chronic signs and how do they work?
chronic
How do the multicyclic OC work?
they are GABA receptor antagonists
How do the aliphatic OC work?
prevent closing of Na channels
Are OC lipophilic?
yes therefore absorbed by all routes and distributed to all tissues

-stored in fat and gets into milk
What does it mean when OC biomagnify?
conc. in animal bodies increases as you get up the food chain
Are acute toxicities common with OCs?
no b/c may take <14 days after exposure to appear
What is the mechanism of action for chronic toxicities with OCs?
induction of microsomal enzymes that leads to reduction of steroid hormones (esp. androgens); this can occur with a single exposure because OCs stay in the body
What is amitraz normally used for?
mites, ticks, as a topical vet drug combined with semicarbazone, Na channel blocker for dogs and crops (catapillers)
What is the mechanism of action of amitraz?
alpha 2 agonist --> sedation
What is the treatment for amitraz toxicity?
alpha -2 antagonist
What is hydramethylnon used for?
stomach poison for fire ants
What are the symptoms of hydramethylnon poisoning and what is the treatment?
-increased salivation, tremors, GI
-treatment is symptomatic
What is boric acid used for?
to control ants and roaches
What are the symptoms of boric acid poisoning?
GI signs, kidney damage
Is activated charcol useful with boric acid?
no
How does DEET work?
decreases ability of insect to detect warmth and moisture
What is the mechanism of action of lufenuron?
interferes with chitin
-lipophilic and concentrates in milk
What is methoprene used for?
flies
What is rotenone used for and what is the most common adverse side effect?
topical for lice and mites, fish anesthetic
- dermal irritation
What are some negatives about using biological controls?
-introduce another species
-control agents often have limited spectrum