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Toxicology > Pesticides > Flashcards

Pesticides Flashcards

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
Q

What are the toxicokinetic features of nicotine?

A
  • 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
Q

What is the mechanism of action of Nicotine?

A
  • stimulation of PSNS
  • cholinergic receptor agonist
  • stimulates CRTZ to trigger vomiting
27
Q

What are the clinical signs of nicotine toxicosis?

A
  • early: ataxia, lethargy, vomiting, bradycardia, tremors

- later: CNS depression, tachycardia, vasodilation, paralysis of resp muscles

28
Q

How is nicotine toxicosis treated?

A
  • emesis or gastric lavage
  • activated charcoal
  • IV fluids to enhance secretion
  • atropine for PSNS effects
29
Q

What are the properties and toxicokinetic features of Neonicotinoids?

A
  • water soluble
  • degraded by light
  • poorly absorbed
  • metabolized in liver
  • excreted in bile and urine
30
Q

What is the mechanism of action of Neonicotinoids?

A
  • Ach agonist (nicotinic)
  • irreversible binding
  • over-stimulate and block the receptors
31
Q

What are the toxicokinetic features of Rotenone?

A
  • low GI and dermal absorption
  • inhalation more toxic
  • metabolized in liver
  • excreted in urine/feces
32
Q

What is the mechanism of action of Rotenone?

A
  • blocks oxidative phosphorylation to citric acid cycle
  • creates ROS
  • oxidative stress results in neuronal apoptosis
33
Q

What are the clinical signs of Rotenone toxicosis?

A
  • local irritation
  • depression and convulsions
  • GI irritation, muscle tremors, lethargy, resp depression
  • pulmonary irritation and asphyxia

Toxicology (9 decks)

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