Pesticides Flashcards

(33 cards)

1
Q

What are the sources of organochlorines?

A
  • bacteria, fungi, plants, etc.
  • volcanoes and other geothermal events
  • oceans are main source, followed by soil
  • also synthetic
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2
Q

What are the two main groups of organochlorines?

A

DDT-type compounds

Chlorinated alicyclics

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3
Q

What are the toxicokinetic features of organochlorines?

A
  • dermal absorption most common
  • GI absorption enhanced by fats or solvents
  • inhalation also possible
  • stored in body fat
  • biliary, feces, milk, and urine excretion
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4
Q

What is the mechanism of action for DDT-type organochlorines?

A
  • neuronal membrane permeability or transport of Na and K is altered
  • axonal Na channels remain open and prevent repolarization
  • hyper-excitability of nerve
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5
Q

What is the mechanism of action for chlorinated alicyclic type organochlorines?

A
  • blocks Cl channels of GABAa receptors, inhibiting neurotransmission
  • hyper-excitability of nerve
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6
Q

What are the clinical signs of organochlorine toxicosis?

A

CNS stimulation

  • salivation, vomiting, weakness
  • tremors, seizures, coma, death
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7
Q

How is organochlorine toxicosis treated?

A
  • emesis, mineral oil, or activated charcoal
  • wash with soap/water
  • IV lipid or fat emulsion therapy
  • symptomatic treatment
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8
Q

What are the toxicokinetic features of organophosphates?

A
  • lipophilic: absorbed through skin, mucous membranes, GIT, and inhalation
  • well distributed throughout body
  • metabolized in liver, lethal synthesis
  • storage activation
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9
Q

What is the mechanism of action of organophosphates?

A
  • irreversible inhibition of cholinesterases

- muscarinic receptor over-stimulation, nicotinic receptor-overstimulation, and nicotinic blockade

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10
Q

What are the muscarinic effects of organophosphates?

A
  • over-stimulation of PSNS

- diarrhea, urination, miosis, bronchspasm, emesis, lacrimation, salivation

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11
Q

What are the nicotinic effects of organophosphates?

A
  • stimulation or fasciculations in muscle groups followed by depolarization and paralysis
  • stimulation of SNS: sweating, hypertension, and tachycardia
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12
Q

What are the CNS effects of organophosphates?

A
  • crosses BBB
  • sensory and behavioral disturbances, incoordination, resp depression
  • respiratory failure/paralysis
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13
Q

Describe organophosphate-induced delayed polyneuropathy

A
  • develops 10-14 days post-exposure
  • degeneration of motor and sensory axons of peripheral nerves and spinal cord
  • muscle weakness, ataxia, rear limb paralysis
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14
Q

Describe organophosphate-induced intermediate syndrome

A
  • 2-4 days after acute effects are no longer obvious
  • no muscarinic signs or muscle fasciculations
  • weakness or resp muscles and accessory muscles
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15
Q

How is organophosphate toxicosis diagnosed?

A
  • detection of OP in stomach contents, hair and skin
  • plasma Ach-esterase activity level
  • Atropine response test (neg indicated poisoning)
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16
Q

How is organophosphate toxicosis treated?

A
  • wash with soap/water, or emesis, activated charcoal
  • supportive care
  • Atropine
  • cholinesterase reactivators
17
Q

What are the toxicokinetic features of Carbamates?

A
  • absorbed via inhalation and ingestion
  • do not undergo storage activation
  • do not penetrate CNS
  • metabolized rapidly
18
Q

What is the mechanism of action of Carbamates?

A
  • reversible inhibition of Ach-esterase
19
Q

What are the clinical signs of Carbamate toxicosis?

A
  • salivation, lacrimation, urination, diarrhea

- death from resp failure and hypoxia

20
Q

Properties of Naphthalene

A
  • produced when things burn
  • pure white balls, crystals, or flakes
  • caustic
  • noxious odor
21
Q

What are the toxicokinetic features of Naphthalene?

A
  • absorbed orally, dermally, and by ingestion
  • lipid soluble
  • enters bloodstream
  • rapid distribution
  • high concentrations in adipose, kidneys, liver, lungs
  • excreted in milk
  • crosses placental barrier
  • metabolized in liver
22
Q

What is the mechanism of action of Naphthalene?

A

oxidative metabolites in circulation cause methemoglobinemia and hemolysis

23
Q

What are the clinical signs of Naphthalene toxicosis?

A
  • vomiting
  • mothball-scented breath
  • pale or brown gums
  • weakness, lethargy
  • labored breathing
  • tremors, seizures
24
Q

How is Naphthalene toxicosis treated?

A
  • emesis followed by activated charcoal
  • sodium bicarbonate
  • absorbic acid and methylene blue 1% to reduce methemoglobin to hemoglobin
25
What are the toxicokinetic features of nicotine?
- absorbed through skin, mucous membranes, resp tract, and GI (intestines) - distributed rapidly through bloodstream - liver extracts nicotine from blood - inactive metabolites extracted by kidney and excreted in urine
26
What is the mechanism of action of Nicotine?
- stimulation of PSNS - cholinergic receptor agonist - stimulates CRTZ to trigger vomiting
27
What are the clinical signs of nicotine toxicosis?
- early: ataxia, lethargy, vomiting, bradycardia, tremors | - later: CNS depression, tachycardia, vasodilation, paralysis of resp muscles
28
How is nicotine toxicosis treated?
- emesis or gastric lavage - activated charcoal - IV fluids to enhance secretion - atropine for PSNS effects
29
What are the properties and toxicokinetic features of Neonicotinoids?
- water soluble - degraded by light - poorly absorbed - metabolized in liver - excreted in bile and urine
30
What is the mechanism of action of Neonicotinoids?
- Ach agonist (nicotinic) - irreversible binding - over-stimulate and block the receptors
31
What are the toxicokinetic features of Rotenone?
- low GI and dermal absorption - inhalation more toxic - metabolized in liver - excreted in urine/feces
32
What is the mechanism of action of Rotenone?
- blocks oxidative phosphorylation to citric acid cycle - creates ROS - oxidative stress results in neuronal apoptosis
33
What are the clinical signs of Rotenone toxicosis?
- local irritation - depression and convulsions - GI irritation, muscle tremors, lethargy, resp depression - pulmonary irritation and asphyxia