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PMCOL 303 > Final exam select topics-pesticides > Flashcards

Final exam select topics-pesticides Flashcards

1
Q

Organophosphates target/ mechanism

A

phosphorylates acetylcholinesterase

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2
Q

what os oxon

A

formed when parent compound is metabolized by oxidative desulfuration (compound derived from another chemical in which a P=S bond has been replaced by a P=O bond)

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3
Q

what is aging

A

non enzymative hydrolysis of one of the 2 alkyl groups on Organophosphates

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4
Q

what is structure of Organophosphates

A

R1 R2 X and =O (or S, needs to be removed) on P

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5
Q

what is the mechanism of pramlidoxone + when can it be used

A

dephosphorylation of serine active site with Organophosphates poisoning, ONLY if it has not been aged

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6
Q

which pesticide causes induced delayed polyneuropathy + mechanism

A

Organophosphates, neuropathy target esterase (NTE) must be aged for it to occur

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7
Q

what pesticide causes intermediate syndrome + mechanism

A

Organophosphates, unknown (not AChE)

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8
Q

what is the mechanism of DDT

A

targets Na+ and slows down their opening and closing

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9
Q

what is an example of organochlorine compounds

A

DDT

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10
Q

what kind of thing is DDT

A

organochlorine

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11
Q

what is the less and more toxic form of DDT

A

more is p,p less is o,p

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12
Q

what is the mechanism of pyrethroids (type 2)

A

targets Na+ and slows down their opening and closing + also inhibits GABA

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13
Q

what is the mechanism of pyrethroids (type 1)

A

targets Na+ and slows down their opening and closing

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14
Q

what does DDT not effect in the cell

A

resting potential, rising phase or peak amplitudes

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15
Q

what is name of type 1 pyrethroids disease

A

type 1 syndrome (T) t for tremor

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16
Q

what is name of type 2 pyrethroids disease

A

type 2 syndrome (CS) sc for choreoathetosis salivation

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17
Q

what is the structure difference between type 1 and 2 pyrethroids

A

type one is R-C=O- R

type two is R-C-CN-R

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18
Q

what do pyrethroids do exactly to sodium channels (what type)

A

bind to VGSC subunit, slows rate of activating/opening and closing/inactivaion - hyperexitable state

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19
Q

what type of thing is nithiazine

A

neonicitinoid pesticide

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20
Q

what is the binding site diff with insects and mammals for neonicitinoids

A

insects its positively charged, mammals its negative

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21
Q

how do neonicotinoids affect insects

A

it must be absorbed by plants then the bug eats the plant

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22
Q

what does a high logP value mean for neonicotinoids

A

that it is very lipophilic so more toxic

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23
Q

what does a low logP value mean for neonicotinoids

A

that it is not very lipophilic so less toxic

24
Q

how do first gen neonicotinoids work

A

nAChR overstimulation, desensitization, death

25
Q

how do second gen neonicotinoids work

A

poor nAChR agonist, full AChR agonist in periphery and maybe mAChR agonist

26
Q

what is the metabolite of first gen neonicotinoids

A

6-chloronicotinic acid

27
Q

what is the metabolite of second gen neonicotinoids

A

clothianidin

28
Q

what is clothianidin

A

metabolite of second gen neonicotinoids

29
Q

what is 6-chloronicotinic acid

A

metabolite of first gen neonicotinoids

30
Q

what causes bee colony collapse disorder

A

imidacloprid

31
Q

what is imidacloprid

A

first gen neonicotinoids

32
Q

what is an example of first gen neonicotinoids

A

imidacloprid

33
Q

what is the mechanism of phosphine

A

inhibits cyt c and ETC

34
Q

what results from phosphine

A

lipid peroxidation, protein denaturation, alveolar capillary damage

35
Q

how do biopesticides work

A

contain Cry and VIP genes

36
Q

what is the structure of Cry

A

1 domain forms a pore

2 domains affinity for gut carbs in insects

37
Q

how does cry work (5 steps)

A 
1-attaches to cadherin in gut
2-binds to aminopeptidase receptor
3-proteolytic cleavage of cry toxin
4-pore into membrane
5-flux of K+ and sucrose, so water rushes in
38
Q

what are 3 treatments for OP

A

atropine, diazepam, pralidoxime

39
Q

what is the lipophilicity of OPs

A

high lipophilic

40
Q

where does DDT accumulate in our body

A

adipose

41
Q

what is acute DDT poisoning like + what causes death

A

unrest, tremors, seizors then maybe death resp failure

42
Q

what happens in type 1 pyrethroid syndrome (4)

A

aggressive, still tonic seizure, tremors, sensitive

43
Q

what happens in type 2 pyrethroid syndrome (4)

A

clonic seizures, choreostasis, salivation, burrowing

44
Q

what does chronic DDT do to you

A

increase liver weight (hepatic cell hypertrophy)

45
Q

what happens with dermal exposure of pyrethroid

A

some paresthesia but reverses

46
Q

what happens with chronic pyrethroid exposure + Does it cause cancer

A

mild liver enlargement, probably not teratogen or mutagen (so probably no cancer)

47
Q

what is a pyrethroid treatment

A

vitamin E

48
Q

is nicotine more toxic to mammals or insects

A

mammals

49
Q

what is the half life of nicotine in enviro

A

short

50
Q

what is the lipophilicity of nicotine + why

A

short bc protonated at neutral and low Ph

51
Q

what happens at the nithiazine binding site common to both insects and mammals

A

H bonding site

52
Q

what may cause 2nd gen pyrethroid toxicity

A

clothianidin

53
Q

what are the 2 phases of phosphine symptoms (Cardiac)

A

1-sinus tachycardia

2-ST segment changes, dysrhythmia

54
Q

what are the general symptoms for phosphine

A

nausea, vomit, breathless, paresthesia, cardiac collapse

55
Q

what is the main type of biopesticies

A

bacillus thuringienis

56
Q

how do bugs die when they eat biopestidies

A

they die of stavation

57
Q

what is the alternative Cry mechanism (4)

A
  • toxin binds cadherin
  • stimulates apoptosis
  • insertion/activation of ion channels
  • Mg++ floods in and death

PMCOL 303 (25 decks)

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