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Clinical implication of human poisoning > Lecture #8: Pesticides > Flashcards

Lecture #8: Pesticides Flashcards

1
Q

Insecticide classifications

A
  1. Cholinesterase Inhibitors
  2. Organochlorine
  3. Pyrethrins/ Pyrethoids
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2
Q

Insecticide classifications

A
  1. Cholinesterase Inhibitors
  2. Organochlorine
  3. Pyrethrins/ Pyrethroids
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3
Q

Insecticides: Cholinesterase Inhibitors 2 main types

A

Organophosphates and Carbamates

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4
Q

classifications of organophosphates

A

two types: Oxons and thions

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5
Q

Oxons

A

direct action on AchE

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6
Q

Thions

A

indirect, requires conversion into oxon first via desulfuration

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7
Q

mechanisms of oxons and thions

A

binds reversibly to AchE at the hydroxyl group

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8
Q

can irreversible binding occur with OP?

A

Yes

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9
Q

And what can irreversible OP binding cause?

A

Aging

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10
Q

Nerve agent vs organophosphates?

A

nerve agent causes aging, OP has the potential to cause againg

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11
Q

Nerve agent vs organophosphates?

A

nerve agent causes aging, OP has the potential to cause aging

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12
Q

Antidote for nerve agents/organophosphate?

A

Oxime

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13
Q

mechanism of oxime>

A

reactivation of Ache by attaching to the phosphorus and forming complex allowing to split away from AchE molecule

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14
Q

Does OP and carbamates inhibit other forms of enzymes aside from AchE?

A

yes

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15
Q

What are some treatment when aging occurs at RBC AchE?

A

get more RBC, but RBC takes 120 days to regenerate. this means patients will need to undergo ventilation for long period of time.

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16
Q

Toxicity of Organophosphates?

A

Respiratory complications- bronchorrea and spasm, muscle paralysis and skeletal muscle dysfunction (fasciculation)

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17
Q

What are other clinical presentations /independent effects other than respiratory complications?

A

independent effects such as hydrocarbon co-injury can occur from surfactants used to package the pesticide

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18
Q

is paralysis common in OP toxicity?

A

No, it is rare because it does not occur in isolation. only in patients who develop severe muscarinic toxicity and progression of nicotinic symptoms.

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19
Q

How to diagnostically test for OP toxicity?

A
  1. measure cholinesterase activities in RBC
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20
Q

RBC AchE vs plasma ButyrlCHE

A

RBC provides better estimation of neuronal ACHe levels, but regenerates much slower.
Butyyl is much faster

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21
Q

Why is carbamates less toxic than organophosphate?

A

It does not cause aging and not all inhibits cholinesterase and poisoning is less than 24 hours

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22
Q

What are some examples of carbamates?

A

Physostigmine used medicinally to treat anticholinergic poisoning

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23
Q

Acute toxicity of carbamates?

A

similar to OP, but shorter duration. However, can experience coma and respiratory failure with persistent aspiration

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24
Q

What are some other complications or delayed syndromes?

A

NMJD (neuromuscular junction dysfunction)

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25
Q

NMJD (neuromuscular junction dysfunction)

A

delayed muscle weakness that occurs 24-96 hours after exposure or resolution of chlolinergic crisis

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26
Q

NMJD (neuromuscular junction dysfunction)

A

delayed muscle weakness that occurs 24-96 hours after exposure or resolution of cholinergic crisis

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27
Q

OPIDN?

A

after chronic exposure for a few days to weeks and causes sensory problems due to inhibition of neuropathy target esterases

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28
Q

Ginger Jake Paralysis

A

substituted castor oil with TOCP.
caused OPIDN

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29
Q

Two main antidotes for OP and carbamates

A
  1. Atropine (antimuscurinic) to dry up the secretions. competitive anatagonist
  2. 2-PAM
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30
Q

what happens if patients devleop atropine toxicity?

A

can administer glycopyrolate instead and it does not cross the BBB but more potent than atropine

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31
Q

What does 2-PAM do?

A

acts on nicotinic receptors to reverse muscle weakness. it reactivates AcHE and prevents aging. however, timely administration is crucial.

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32
Q

decontamination for OP/cabamate toxicity?

A

removal of article of clothings
triple wash skin
lavage
AC - but requires secure airway.

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33
Q
  1. Organochlorines what are the 3 types
A

DDT, Chlorodecone(Kepone) and Lindane

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34
Q

What is DDT?

A

developed due to high response to worldwide Malaria

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35
Q

cons

A
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36
Q

consequences of DDT?

A

causes environmental persistence

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37
Q

Chlorodecone (kepone)

A

precursor for insecdicides
company industrial waste into James river

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38
Q

What are some treatment when aging occurs at RBC AchE?

A

get more RBC, but RBC takes 120 days to regenerate. this means patients will need to undergo ventilation for long period of time.

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38
Q

Does OP and carbamates inhibit other forms of enzymes aside from AchE?

A

yes

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39
Q

Organochlorines are

A

neutoexcitatory toxins

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40
Q

kepone shakes

A

outbreak due to kepone contamination resulting in tremors, stuttering speech, psuedotumor

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41
Q

lindane

A

GABA antagonist and is kinetically absorbed transdermally. used for things like scabies

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42
Q

lindaine is highly lipophilic

A

causes many seizures

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43
Q

Acute toxicity of organochlorines

A

overstimulation of CNS causing seizures- overhelemed body and eventually fatigues

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44
Q

treatment and care for organochlorine

A

supportive, lavage, AC is not beneficial because organochlorines are liquids. BENZO for seizures

45
Q
  1. Pyrethrins/Pyrethroids
A

Pyrethrins are derived from Chysanthymums

46
Q

Pyrethrins/Pyrethroids

A

lipophilic: specific to exoskeleton of insects (penetration) and are sodium channel opening- paralysis

46
Q

lipo

A
47
Q

Pyrethroids

A

synthetic deriviative and there are two groups

48
Q

2 types of pyrethroids

A

type 1: simple ester bind without cyano group
(ex. Permethrin)
type 2: binds with cyano group (deltamethrin)

49
Q

clincial effects on humans are usually

A

allergic reactions to the parent compound

50
Q

in large exposure, neurologic toxicity is greater in type ___ than type ____

A

2, 1

51
Q

what are clinical manifestations of type 1 and type 2 pyrethroids?

A

type 1: tremors, twitching
type 2: CS syndromes, paraesthesias, sallivation, seizures, AMS

52
Q

What are the types of Herbicides?

A
  1. Bipyridyl compounds
  2. Chlorophenoxy Agent orange/dioxin
  3. Glyphosate
53
Q

2 types of bipyridyl compound

A

paraquat, diquat

54
Q

paraquat

A

is the most toxic pesticide available!

55
Q

what are some causes from paraquat/diquat?

A

irritation/corrosive direct injuries

56
Q

what do they generate? and how?

A

free radicals that are directly toxic to tissues/ Redox cycling

57
Q

What does paraquats target directly?

A

pneumocytes in the lungs and can casue multi-organ failure

58
Q

clincia manifestation of paraquat?

A

GI, oral, throat abdominal pain, necrosis of mucous membranes. respiratory symptoms kicks in a day later

59
Q

management

A

supportive care, supplemental oxygen is not beneficial due to reactive oxygen generation.

60
Q

What is chlorophenoxy?

A

agent orange and dioxin. it is a plant growth hormone analog that causes uncontrolled growth that ultimately outstrips their water supply

61
Q

agent orange

A

contains dioxin

62
Q

g

A
63
Q

dioxin

A

carcinogenic, birth defects

64
Q

Glyphosate

A

most commonly used pesticide

65
Q

toxicity of glyphosate

A

inhibits enzyme in plants only knonwn as 5-E-3P synthase

66
Q

action of toxicity to plant enzymes

A

inhibits amino acid synthesis

67
Q

glyphosate is safe on its own except

A

the surfactant causes pnemonitis effects that causes direct cell membrane injury

68
Q

Fumigants type

A
  1. Phosphide/phosphine
  2. methyl bromide
69
Q

phosphine/phosphide

A

metal phospides aluminum and zinc are leading cause of pesticide poisoning

70
Q

when mixed with ambient moisture

A

becomes phosphine gas

71
Q

what is toxicity of phosphine gas?

A

mitochondrial shutdown

72
Q

physical characteristics

A

greenish grey, garlic, rotten fish

73
Q

mechanism of action?

A

noncompetitive inhibition of cytochrome c oxidase which blocks ETC

74
Q

clinical effects

A

abdominal pain, shock,

75
Q

secondary exposure to first responder

A

PPE required

76
Q

methyl bromide

A

used as sedative, colorless, odorless and is a nuerotoxin

77
Q

methyl bromide is ____

A

inhaled

78
Q

what are clinical effects

A

CNS effects

79
Q

fungicide

A

dithiocarbamates and metals

80
Q

dithiocarbamates

A

disulfiram like reactions - flushing neuropathy

81
Q

metals

A

potent mitochondrial toxin

82
Q

rodenticides

A

anticoagulants

83
Q

morphine

A

medical anticoagulant but short acting poison

84
Q

kepone shakes

A

outbreak due to kepone contamination

84
Q

lindane

A

GABA antagonist and is kinetically absorbed transdermally. used for things like scabies

84
Q

what are some causes from paraquat/diquat?

A

irritation/corrosive direct injuries

84
Q

Does OP and carbamates inhibit other forms of enzymes aside from AchE?

A

yes

84
Q

morphine

A

medical anticoagulant but short acting poison

84
Q

what do they generate?

A

free radicals that are directly toxic to tissues

84
Q

what are clinical manifestations of type 1 and type 2 pyrethroids?

A

type 1: tremors, twitching
type 2: CS syndromes, paraesthesias, sallivation, seizures, AMS

84
Q

only toxic to humans if massively ingested

A
84
Q

agent orange

A

contains dioxin

84
Q

What are some treatment when aging occurs at RBC AchE?

A

get more RBC, but RBC takes 120 days to regenerate. this means patients will need to undergo ventilation for long period of time.

84
Q

in large exposure, neurologic toxicity is greater in type ___ than type ____

A

2, 1

84
Q

What is chlorophenoxy?

A

agent orange and dioxin. it is a plant growth hormone analog that causes uncontrolled growth that ultimately outstrips their water supply

85
Q

Pyrethrins/Pyrethroids

A

lipophilic: specific to exoskeleton of insects (penetration) and are sodium channel opening- paralysis

85
Q

superwarfins

A

long acting anticoagulant to prevent bait avoidance from rodents.

86
Q

Does OP and carbamates inhibit other forms of enzymes aside from AchE?

A

yes

86
Q

Pyrethrins/Pyrethroids

A

lipophilic: specific to exoskeleton of insects (penetration) and are sodium channel opening- paralysis

86
Q

What are some treatment when aging occurs at RBC AchE?

A

get more RBC, but RBC takes 120 days to regenerate. this means patients will need to undergo ventilation for long period of time.

87
Q

lindane

A

GABA antagonist and is kinetically absorbed transdermally. used for things like scabies

87
Q

in large exposure, neurologic toxicity is greater in type ___ than type ____

A

2, 1

87
Q

only toxic to humans if massively ingested

A
87
Q

what do they generate?

A

free radicals that are directly toxic to tissues

87
Q

what are some causes from paraquat/diquat?

A

irritation/corrosive direct injuries

87
Q

what are clinical manifestations of type 1 and type 2 pyrethroids?

A

type 1: tremors, twitching
type 2: CS syndromes, paraesthesias, sallivation, seizures, AMS

87
Q

kepone shakes

A

outbreak due to kepone contamination

87
Q

agent orange

A

contains dioxin

88
Q

What is chlorophenoxy?

A

agent orange and dioxin. it is a plant growth hormone analog that causes uncontrolled growth that ultimately outstrips their water supply

Clinical implication of human poisoning (3 decks)

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