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Implications of human poisoning > Death by pesticides > Flashcards

Death by pesticides Flashcards

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1
Q

Insecticides

A

Cholinesterase Inhibitors; OP and Carbamates
Organochlorines; Chlorodecone, Lindane, DDT
Pyrethrins/Pyrethroids; Permethrin, Deltamethrin

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2
Q

Acetylcholine is located where?

A 
Sympathetic and Parasympathetic ganglia
Skeletal NMJ
Post ganglionic sympathetic nerves
Sympathetic sweat glands
CNS nerve endings
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3
Q

What is a muscarinic receptor?

A

G protein linked

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4
Q

What is a nicotinic receptor?

A

Ligand mediated ion channel

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5
Q

What is the Cholinergic Toxidrome acronym?

A 
DUMBBELS; Muscarinic
Diarrhea
Urination
Miosis
Bronchorrea
Bradycardia
Emesis
Lacrimation
Salivation
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6
Q

What are organic phosphorous compounds?

A

Increase ACh concentration in synapse muscarinic and nicotinic
Cholinergic toxidrome
X is the leaving group

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7
Q

Organic phosphorous compounds oxons vs. thions

A 
oxons = direct action on AChE
thions = prodrugs; must be converted to active compound by p450 enzymes
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8
Q

What is the mechanism of action for oxons and thions?

Ex of oxons: 2 PAM or praladoxime

A

binds to hydroxyl group of AChE active site
stable but reversible bond forms
speeds up rate of reactivation of AChE
aging occurs when oximes can’t reactivate AChE (bond becomes permanent)

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9
Q

What do OP’s and Carbamates inhibit?

A

carboxylic ester hydrolases in the body

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10
Q

Acute toxicity of cholinesterase inhibition presentation?

A

Awake and alert
anxiety, restlessness, myosis blurred vision, respiratory depression, tremor
altered mental status - confusion - coma
DUMBBELS

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11
Q

How to diagnose cholinesterase inhibition?

A

measure cholinesterase activity for organophosphate exposure by Red blood cell AChE or ButyrylChE
miosis, muscarinic signs, and SOB

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12
Q

What are carbamates?

A

Aging does not occur therefore, no permanent bond between carbamate and AChE

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13
Q

What is carbamate acute toxicity?

A

like OP toxicity
coma and respiratory failure
Shorter duration than OPs b/c reversible

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14
Q

What are delayed syndromes of AChE inhibitors?

A

NMJ dysfunction aka intermediate syndrome
delayed muscle weakness w/o cholinergic toxidrome
24-96 hours after exposure
muscle weakness leads to respiratory failure
1st sign is muscle weakness
OP cmpd induced delayed neuropathy
Drinking OH w/TOCP ginger jake developed delayed neuropathy

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15
Q

Acute/ Chronic OP exposure causes?

A

behavioral toxicity;
confusion, psychosis, anxiety, depression, and fatigue
EEG changes for weeks

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16
Q

What causes chronic toxicity of OPs?

A

occupational exposure
BuChE activity is the sensitive measure of exposure
RBC cholinesterase is like Neuronal cholinesterase
Neuronal Target Esterase Inhibition to look for delayed neuropathy

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17
Q

What is the primary cause of death for AChE inhibition?

What is the general management?

A

respiratory failure due to bronchorrea
adequate airway/drying up secretions with atropine
benzodiazepines for seizures

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18
Q

Pharmacotherapy for AChE inhibition?

A

Atropine sulfate for carbamates = competitive anatagonist at central and peripheral muscarinic receptors/crosses BBB
Pralidoxime (2-PAM) for OP’s = targets nicotinic receptors to reverse muscle weakness/reactivates cholinesterase/prevents aging of AChE

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19
Q

Antimuscarinic Therapy

A

does not reverse nicotinic effects

ex: atropine

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20
Q

What are oximes?

A

enhances phosphorylated AChE regeneration via hydrolysis

prevents aging and addresses nicotinic and muscarinic effects

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21
Q

Pralidoxime mechanism?

A

binds on anionic site of AChE by pulling off organophosphate there

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22
Q

What are Benzodiazapines?

A

given to prevent seizures from cholinergic syndrome
Ex: diazepam
can use for intubation induction
anticholinergic

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23
Q

What is decontamination?

A

remove all clothing
triple wash skin -water, soap, water and rinse with water
wear. neoprene/nitrile gloves
consider lavage for large acute ingestions
AC but protect airway to prevent vomiting

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24
Q

What are organochlorine compounds?

A

family of neuroexcitatory toxins; all neurotoxins
eggshell thinning so changed agriculture
Ex: DDT
Can bioaccumulate and potentially cause harm
Illegal in US
DDT eliminated malaria

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25
For organochlorine cmpd toxicity what do you give?
automatically give atropine and 2 PAM & it's safe in large doses
26
Hopewell Pesticide Spill?
``` made Kepone(chlordecone) dumped in James River neurotoxicity Kepone shakes Hepatic injury Testicular dysfunction ```
27
What are neurotoxins in Organic Chlorines?
interfere with repolarization and depolarization of neuronal membranes results in hyperexcitability Lindane is GABA antagonist
28
Acute Toxicity of Organic Chlorines?
CNS stimulation - seizure - respiratory failure - death
29
Chronic Toxicity of Organic Chlorines?
ex: hopewell epidemic body tremor AMS, Ataxia, weakness DDT linked to breast cancer
30
Treatment for organic chlorines?
supportive care lavage for recent ingestion AC cannot bind so not likely benzodiazepines for seizures and for greater strength can use barbiturates or propofol
31
Pyrethrins
extracts from Chysanthemum flower lipohilic sodium channel opening causing insect paralysis
32
Pyrethroids
synthetic derivative | limited human toxicity and no bioaccumulation so more common
33
Pyrethroid types?
Type I - simple ester bond, no cyano group ex: permethrin Type II - have a cyano group and more toxic
34
pyrethrins and pyrethroids mechanism?
prolong activation of voltage gated Na channel binds to open channel and keeps open paralyzes insect
35
Clinical effects of pyrethrin and pyrethroids?
most are allergic rxns
36
pyrethroid type 1 clinical effects?
type 1 - tremors and twitching human tox rare selective to insects
37
pyrethroid type 2 clinical effects?
more potent/toxic acute lung injury CS syndrome= choreoathetosis and salivation paresthesias, salivation, nausea, vomitng, AMS, seizures
38
pyrethrins and pyrethroids treatment?
``` supportive care skin decontamination by washing AC for ingestion BZD for seizures Vitamin E oil for cutaneous paresthesias ```
39
herbicides?
regulates plant growth mainly weed killer most widely sold pesticide in world
40
Bipyridyl compounds | paraquat and diquat
nonselective contact herbicides paraquat = most toxic pesticide (100% death for intentional poisoning) Diquat still fatal but less toxic
41
Paraquat and Diquat mechanism?
both highly irritating and corrosive - direct injury generate Reactive Oxygen Species - damages lipid membranes Redox Cycling =
42
clinical manifestation of paraquat and diquat?
``` GI symptoms nausea and vomiting oral and throat pain b/c corrosive necrosis of mucous membranes respiratory symptoms mainly w/ paraquat AKI MSOF and death ```
43
paraquat and diquat treatment?
``` supportive care resuscitate giving O2 makes injury worse b/c redox cycling decontamination fullers earth or AC ```
44
chlorphenoxy herbicides?
dioxin agent orange is nerve agent carcinogenic chloracne
45
agent orange
chlorphenoxy herbicide defoliant has dioxin plant growth hormone analogue cancer and birth defects
46
what are other herbicides?
``` glyphosate anilide derivatives: propanil, acetochlor cause methemoglobinemia treat with methylene blue ```
47
what is glyphosate?
kills weed which compete with crops used around world b/c no sever effect like paraquat doesn't inhibit ACh
48
glyphosate Toxicity?
``` inhibits 5-e-3-p synthase interferes with amino acids human toxicity mech not understood technically an OP but does not inhibit ACh surfactant coformulation = more toxic ```
49
clinical effects of glyphosate?
stomach pain, nausea, vomiting, diarrhea MSOF treatment: supportive care
50
fumigants
nonspecific pesticides so can kill rodents, nematodes, insects, weeds, fungi most common exposure = inhalation heavier than air so sinks down does not dissipate
51
list of fumigants?
phosphides/phosphine methyl bromide sulfuryl fluoride (vikane) - sucks up calcium in body
52
phosphides and phosphine fumigant?
metal phosphides cheap and effective seed viability unaffected mixed with grain/food storage mixed with moisture releases phosphine gas(PH3) smells like mown hay and no immediate effect
53
epidemiology of phosphides and phosphine?
increased incidence of poisoning high rate of mortality suicide attempts
54
physical properties of phosphides and phosphine
aluminum phosphide: greenish gray tablets, garlic odor zinc phosphide: dark gray powder, rotten fish odor gaseous PH3: colorless, decaying fish or garlic odor heavier than air
55
phosphides and phosphine mechanism of action?
non competive inhibition of cytochrome c oxidase (mitochondria electron transport chain) blocks oxidative phosphorylation
56
phosphide and phosphine clinical effects
tachycardia, SOB, tachypnea, | smell of garlic or rotting fish on breath
57
phosphides and phosphine treatment
``` remove from source give O2 use PPE remove clothes decontaminate with water AC in 1 hour supportive care ```
58
methyl bromide
``` fumigation poisoning colorless odorless gas heavier than air exposure by inhalation dermal and oral apsorption rapid distribution to tissue ```
59
methyl bromide fumigant mechanism?
cytotoxic - directly damages cells and dna alkylating inhibits microsomal metabolism and protein synthesis in animal models
60
methy bromide fumigant clinical effects
ARDS leads to respiratory failure and death skin and mucous membrane irritant CNS effects
61
methyl bromide fumigant treatment
``` ppe for provider protection remove from source remove clothing decontaminate with water or saline supportive care ```
62
fungicides
dithiocarbamates metabolized to carbon disulfide causes neuropathy disulfiram like rxns (asian flush from impairment of OH metabolism)
63
molluscicides
``` kills gastropod pests like snails and slugs includes: carbamates metal metaldehyde ```
64
Rodenticides
BRATS PANIC anticoagulant rodenticides most common in US clinical effects: bleeding, bruising Testing: elevation of coagulation parameters

Implications of human poisoning (10 decks)

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