Pesticides Flashcards
What are the sources of organochlorines?
- bacteria, fungi, plants, etc.
- volcanoes and other geothermal events
- oceans are main source, followed by soil
- also synthetic
What are the two main groups of organochlorines?
DDT-type compounds
Chlorinated alicyclics
What are the toxicokinetic features of organochlorines?
- dermal absorption most common
- GI absorption enhanced by fats or solvents
- inhalation also possible
- stored in body fat
- biliary, feces, milk, and urine excretion
What is the mechanism of action for DDT-type organochlorines?
- neuronal membrane permeability or transport of Na and K is altered
- axonal Na channels remain open and prevent repolarization
- hyper-excitability of nerve
What is the mechanism of action for chlorinated alicyclic type organochlorines?
- blocks Cl channels of GABAa receptors, inhibiting neurotransmission
- hyper-excitability of nerve
What are the clinical signs of organochlorine toxicosis?
CNS stimulation
- salivation, vomiting, weakness
- tremors, seizures, coma, death
How is organochlorine toxicosis treated?
- emesis, mineral oil, or activated charcoal
- wash with soap/water
- IV lipid or fat emulsion therapy
- symptomatic treatment
What are the toxicokinetic features of organophosphates?
- lipophilic: absorbed through skin, mucous membranes, GIT, and inhalation
- well distributed throughout body
- metabolized in liver, lethal synthesis
- storage activation
What is the mechanism of action of organophosphates?
- irreversible inhibition of cholinesterases
- muscarinic receptor over-stimulation, nicotinic receptor-overstimulation, and nicotinic blockade
What are the muscarinic effects of organophosphates?
- over-stimulation of PSNS
- diarrhea, urination, miosis, bronchspasm, emesis, lacrimation, salivation
What are the nicotinic effects of organophosphates?
- stimulation or fasciculations in muscle groups followed by depolarization and paralysis
- stimulation of SNS: sweating, hypertension, and tachycardia
What are the CNS effects of organophosphates?
- crosses BBB
- sensory and behavioral disturbances, incoordination, resp depression
- respiratory failure/paralysis
Describe organophosphate-induced delayed polyneuropathy
- develops 10-14 days post-exposure
- degeneration of motor and sensory axons of peripheral nerves and spinal cord
- muscle weakness, ataxia, rear limb paralysis
Describe organophosphate-induced intermediate syndrome
- 2-4 days after acute effects are no longer obvious
- no muscarinic signs or muscle fasciculations
- weakness or resp muscles and accessory muscles
How is organophosphate toxicosis diagnosed?
- detection of OP in stomach contents, hair and skin
- plasma Ach-esterase activity level
- Atropine response test (neg indicated poisoning)
How is organophosphate toxicosis treated?
- wash with soap/water, or emesis, activated charcoal
- supportive care
- Atropine
- cholinesterase reactivators
What are the toxicokinetic features of Carbamates?
- absorbed via inhalation and ingestion
- do not undergo storage activation
- do not penetrate CNS
- metabolized rapidly
What is the mechanism of action of Carbamates?
- reversible inhibition of Ach-esterase
What are the clinical signs of Carbamate toxicosis?
- salivation, lacrimation, urination, diarrhea
- death from resp failure and hypoxia
Properties of Naphthalene
- produced when things burn
- pure white balls, crystals, or flakes
- caustic
- noxious odor
What are the toxicokinetic features of Naphthalene?
- 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
What is the mechanism of action of Naphthalene?
oxidative metabolites in circulation cause methemoglobinemia and hemolysis
What are the clinical signs of Naphthalene toxicosis?
- vomiting
- mothball-scented breath
- pale or brown gums
- weakness, lethargy
- labored breathing
- tremors, seizures
How is Naphthalene toxicosis treated?
- emesis followed by activated charcoal
- sodium bicarbonate
- absorbic acid and methylene blue 1% to reduce methemoglobin to hemoglobin
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
What is the mechanism of action of Nicotine?
- stimulation of PSNS
- cholinergic receptor agonist
- stimulates CRTZ to trigger vomiting
What are the clinical signs of nicotine toxicosis?
- early: ataxia, lethargy, vomiting, bradycardia, tremors
- later: CNS depression, tachycardia, vasodilation, paralysis of resp muscles
How is nicotine toxicosis treated?
- emesis or gastric lavage
- activated charcoal
- IV fluids to enhance secretion
- atropine for PSNS effects
What are the properties and toxicokinetic features of Neonicotinoids?
- water soluble
- degraded by light
- poorly absorbed
- metabolized in liver
- excreted in bile and urine
What is the mechanism of action of Neonicotinoids?
- Ach agonist (nicotinic)
- irreversible binding
- over-stimulate and block the receptors
What are the toxicokinetic features of Rotenone?
- low GI and dermal absorption
- inhalation more toxic
- metabolized in liver
- excreted in urine/feces
What is the mechanism of action of Rotenone?
- blocks oxidative phosphorylation to citric acid cycle
- creates ROS
- oxidative stress results in neuronal apoptosis
What are the clinical signs of Rotenone toxicosis?
- local irritation
- depression and convulsions
- GI irritation, muscle tremors, lethargy, resp depression
- pulmonary irritation and asphyxia
