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PED3011 Toxicology > Organophosphates > Flashcards

Organophosphates Flashcards

1
Q

Describe the difference between herbicides, fungicides and pesticides

A

Herbicides: kill plants e.g glyphosate
Fungicides: stop fungal disease e.g triazole
Pesticides: harmful to pests

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2
Q

What are the benefits of pesticides

A

Improve/protect our health
Allow production of abundant, inexpensive and agricultural products

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3
Q

What are the risks of pesticides

A

Toxicity to non-target species
Pervasive in environment

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4
Q

How can we decrease the risks of pesticides

A

Use pesticides that have selective targets
Introduce regulations to reduce exposure

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5
Q

Describe insecticides

A

Neurotoxicants i.e act by targeting the insects nervous system
Cause hyperexcitabilty of NS = paralysis and death
Variety mechanisms of action
Generally non-selective so affect mammalian NS targets too

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6
Q

What is the target and effect of organophosphates as an insecticide

A

Acetylcholinesterases
Inhibition

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7
Q

Describe an organophosphate

A

Organic derivative of phosphates, phosphonates or phosphinates
Can be used as insecticides, lubricants, flame retardants and nerve agents

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8
Q

What does acute toxicity of organophosphates look like

A

0.5-6hrs after exposure
Tears
Salivation
Sweating
Bronchospasm
Bradycardia
Miosis

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9
Q

What part of the NS do organophosphates affect

A

Parasympathetic innervation
ACh and muscarinic receptors

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10
Q

What is the main cause of death after acute organophosphate poisoning

A

Respiratory failure
Parasympathetic bronchoconstriction and NMJ twitching
Paralysis of diaphragmatic muscles

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11
Q

What is an oxon

A

Insecticides have a phosphate-sulphur bond
When absorbed bioactivated to oxons during Phase I
P=S -> P=O
Inhibits AChEs

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12
Q

Why do nerve agents act quicker than other similar toxins

A

Already have P=O bond instead of P=S so don’t have to be bioactivated to cause effects

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13
Q

Describe how oxons cause acute toxicity

A

Normally ACh bind to AChE = weak bond that’s broken easily
Oxons target AChEs and phosphorylate them = strong bond between the 2
Can take hours/days to break bound therefore AChE is not free to hydrolyse ACh = build up

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14
Q

Describe detoxication of organophosphates

A

A-esterases such as PON1 can hydrolyse the Oxon = reactivated AChE
Hydrolysis produces excreted

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15
Q

How do polymorphisms affect detoxification of OPs

A

PON1 polymorphisms = different catalytic efficiencies towards OPs
-> some ethnicities are more affected by OPs

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16
Q

Describe ageing of OPs

A

Oxon binds to AChE and if one alkyl group is hydrolysed
= irreversible inhibited -> no detoxication

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17
Q

Can you overcome ageing of OPs

A

Yes only if the AChE function is restored by replenishing AChEs stores which can take days

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18
Q

What is a treatment for OP acute toxicity

A

Oximes
Atropine
Benzodiazepines

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19
Q

What is the mechanism of action of oxmines

A

Attaches to AChE and breaks the bond between P on oxon and AChE
= reactivated AChE

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20
Q

What is the main limiting factor to oxime treatment

A

Must be given within a relatively short amount of time after exposure to OPs
Before ageing occurs

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21
Q

Why is atropine useful in acute toxicity OP treatment

A

Muscarinic receptor antagonist = blocks the effect of excess ACh at the receptors
Relieves parasympathetic nervous system activation

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22
Q

How are benzo’s useful in acute OP toxicity

A

Allosteric modulators of GABAaR
= reduce the overstimulation of the neurones in the brain and act as anti-convulsants

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23
Q

What happens if treatment for acute OP toxicty is not administered

A

If the person hasn’t died from the toxicity intermediate syndrome can develop
Approx 24-96hrs post cholinergic crisis

24
Q

Describe intermediate syndrome

A

Weakness/ paralysis of muscles innervate by cranial nerves
Respiratory paralysis so need ventilation
May lead to death

25
Why does recovery take up to 30 days after intermediate syndrome
Excess ACh is being removed from the synaptic clefts
26
What is the proposed toxicological mechanism for intermediate syndrome
Nicotinic receptors overstimulated and become deactivated Muscles are damage due to localised hyper contractions at the NMJ
27
What is OP-induced delayed neuropathy
Loss of sensory or motor activation in the distal ends that is not related to nerve agents or insecticides Develops 2-3 weeks after exposure
28
What is axonopathy
Axon is affected and not related to the AChE inhibition
29
Describe delayed neuropathy due to OPs
OPs target another esterase called neuropathy targeted esterase (NTE) NTE found in neurones and important in membrane phospholipid homeostasis = affected axons
30
What can low level repeated exposure to OPs lead to
Memory and attentional deficits Increased risk of anxiety disorders and depression
31
What is the effect on OPs on neuronal activity
Increases activity Mediated by muscarinic and glutamate receptors
32
Describe how oxons increase 5-HT
Increase neurotransmission via ACh = increase glutamate release = activates glutamate receptors on 5-HT neurones
33
What is the suggested mechanism for why people exposed to OPs are at an increased risk of anxiety and depression
Decrease in inhibitory 5-HT1a receptor sensitivity Decrease in 5-HT transporter Increase in firing rate
34
What are the 3 consequences to high level of OP toxicity
Acute/hypercholinergic toxicity Intermediate syndrome Delayed neuropathy
35
What are carbamates
Derivatives of carbamic acid AChE inhibitors
36
Why are the effects of carbamates short lasting compared to OPs
Carbamylation of AChE is short lasting compared to phosphorylation by OPs = rapid regeneration of AChE compared to inhibition by OPs
37
What is the carbamate Physostigmine used for
Improve muscle tone in GI tract Treat poor gut motility
38
What is the carbamate Rivastigmine used for
Treatment in Alzheimer’s Disease Improve cholinergic transmission in CNS = compensates for neurodegeneration
39
What are organochlorines
Organic compounds that contain at least one covalently bonded chlorine atom
40
Why are organochlorines not easily metabolised
Very lipophilic and bioaccumulate in humans and animals and environment = persistent organic pollutant
41
Name 3 example of an organochlorine
Chlorinated ethane derivatives Hexachlorocyclohexanes Cyclodienes
42
Describe acute toxicity after DDT exposure
Quite rare Hypersensitivity of the mouth followed by ‘pins and needles’ Headaches, fatigue, tremor, muscle weakness and convulsion CNS effects and often reversible
43
Describe chronic low level exposure of DDT
Associated with psychological illness, peripheral neuropathy and Parkinsonism
44
Describe the mechanism of action for chronic low level exposure from DDT
Increased excitability of CNS = slow closures of Na+ channels so depolarising phase of AP is prolonged = increased probably of repetitive firing
45
Describe acute toxicity after exposure to hexachlorocyclohexanes and cyclodienes
Convulsions casued by increased excitability Blocking of inhibitory GABAa receptor channel opening by binding to picrotoxin site
46
How is acute toxicity after HCHs and cyclodienes treated
Diazepam
47
What are pytherins and pyrethroids
Insecticides with higher insecticidal potency compared to mammalian potency = safer Used in people’s homes Pytherin: natural but decompose rapidly in the light Pyrethoids: synthetic analogue of pytherins
48
Describe acute toxicity after pyrethin or pyrethroid exposure
Tremor, seizures and death Occupation exposures Short lived
49
How can pyrethroids be divided
Based upon toxic signs Type 1 and Type 2
50
Describe type 1 pyrethroids
Arousal, aggression and fine tremors
51
Describe type 2 pyrethroids
Profuse salivation coarse tremors and convulsions
52
What is the mechanism of action for type 1 pyrethroids
Stop the Na+ channels from causing causing respective firing
53
What is the mechanism of action for type 2 pyrethroids
Keep the channels open longer = depolarisation dependent block
54
How can pyrethroids affect development
Exposure increases the risk of ADHD Children with 3-PBA metabolite levels above limits of detection more likely to be diagnosed with ADHD
55
What was the evidence in animal studies that supported epidemiological findings that pyrethroids have an affect of ADHD
Detrimental exposure to deltamethrin = increased transporter levels -> decrease in extracellular DA levels -> compensatory increase in D1 receptors = increased activity and impulsive behaviour

PED3011 Toxicology (11 decks)

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