ECC2- Insecticides

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  1. Parathion and Malathion are examples of...
    Organophosphates
  2. What is the mechanism of action of organophosphates?
    Inhibit cholinesterase, which is responsible for inactivating Ach at the NMJ; reversible binding before bonds "age"; within 24 hours, irreversible covalent bond forms ("aged").
  3. Describe the selective toxicity of malathion.
    • In insects, it is rapidly converted to toxic metabolite (maloxon); then it sticks around because it is slowly converted to inactive metabolites
    • In mammals, it is slowly converted to active metabolite and is rapidly converted to inactive metabolite
  4. Describe the selective toxicity of parathion.
    • In insects, it is rapidly converted to active metabolite (paraoxon) and slowly converted to inactive metabolites
    • In mammals, it is rapidly converted to active metabolite and rapidly converted to inactive metabolites
  5. What are symptoms of toxicity of organophosphates?
    SLUDE, vomiting, dyspnea, miosis, bradycardia, muscle tremors, fasciculation, paralysis, CNS depression/ seizures, death d/t respiratory paralysis
  6. How is organophosphate toxicity diagnosed?
    History, analysis of stomach contents, blood analysis for depression of RBC enzyme activity (true cholinesterase) and plasma cholinesterase (pseudo-cholinesterase)
  7. What are the treatments/ antidotes for organophosphate toxicity? (5)
    • Block muscarinic effects by giving atropine
    • Emetics if very recent exposure
    • Activate charcoal
    • 2-PAM (pralidoxime- protopam) is given during the first 24 hours before bonds age and become covalent bonds
    • Respiratory support/ oxygen
  8. What is the mechanism of toxicity of carbamates?
    Inhibit cholinesterase, which is responsible for inactivating Ach; reversible binding
  9. What are signs of carbamate toxicity?
    SLUDE, vomiting, dyspnea, miosis, bradycardia, muscle tremors, fasciculation, paralysis, CNS depression/ seizures, death d/t respiratory paralysis
  10. How do you diagnose carbamate toxicity?
    History, analysis of stomach contents, blood analysis for depression of RBC enzyme activity (true cholinesterase) and plasma cholinesterase (pseudo-cholinesterase)
  11. What are the treatments/antidotes for carbamate toxicity? (4)
    • Block muscarinic effects with atropine
    • Emetics if recent exposure
    • Activated charcoal
    • Respiratory support/ oxygen
  12. What is the mechanism of toxicity of pyrethrins and pyrethroids?
    Type I and II decrease sodium conductance in axonal membranes; decreased action potential amplitude and increased repetitive nerve impulse--> muscle tremors and excitement; type II only blocks GABA channel at higher concs
  13. Pyrethrins/ pyrethroids are usually formulated with __________, which...
    Piperonyl butoxide (cytochrome P450 inhibitor); causes a synergistic reaction by delaying metabolic inactivation.
  14. Describe the selective toxicity of pyrethrins and pyrethroids.
    Insects are more sensitive because their Na+ channels are 1000x more sensitive and because mammalian channels recover much faster
  15. What are symptoms of pyrethrins/ pyrethroid toxicity?
    • Hypersalivation, muscle twitching, hyperesthia, [higher doses] vomiting, diarrhea, muscle tremors, ataxia, [very high doses] seizures and death
    • Maybe dermal signs urticaria, hyperemia, pruritus
  16. What are the treatments/ antidotes for pyrethrin/ pyrethroid toxicity?
    • If dermally exposed, wash with mild soap
    • Monitor hypothermia
    • Methocarbamol to reduce muscle twitching
    • Diazepam or phenobarbital for seizures and severe tremors
    • Activated charcoal to reduce enterohepatic cycling
  17. How does fipronil work/ it's metabolism?
    • Applied topically and it absorbed and accumulates in the sebaceous glands for prolonged action
    • If orally ingested, it distributes to fatty tissues and is metabolized by the liver and excreted
  18. What is the mechanism of toxicity of phenylpyrazoles (fipronil)?
    Blocks GABA Cl- channels, thus preventing influx of Cl- --> hyperpolarization and loss of inhibitory control; this results in excessive neuronal stimulation and death of targeted insect
  19. Describe the selective toxicity of phenylpyrazoles (fipronil).
    Fipronil exhibits higher binding affinity for invertebrate GABA receptors than for mammalian receptors d/t configuration differences
  20. What are symptoms of phenylpyrazole toxicity?
    • If ingested, gastritis
    • Dermal hypersensitivity, erythema, pruritus, alopecia, [toxic dose] gait changes, tremors, convulsion, seizures
  21. What are the treatments/ antidotes for phenylpyrazole toxicity?
    • Skin hypersensitivity- bathe, antihistamines, steroids, maybe antibiotics for secondary infections
    • If oral ingestion- activated charcoal, fluids to produce diuresis, treat seizures with diazepam
  22. What is the mechanism of toxicity of imidacloprid and spinosad?
    • Bind nicotinic cholinergic receptors, causing persistent depolarization of motor neurons and hyperexcitability
    • Imidacloprid: binds nicotinic cholinergic receptors within the CNS of insects; not degraded by cholinesterase and causes persistent depolarization, producing initial stimulation followed by transmission failure
    • Spinosad: acts at nicotinic receptor site that is distinct from neo-nictinoids; insects show involuntary muscle contractions and tremors resulting from activation of motor neurons
  23. Describe the selective toxicity of imidacloprid and spinosad.
    Due to structural differences in nicotinic Ach receptors, these drugs show low affinity for mammalian nicotinic Ach receptors, while exhibiting high affinity for these receptors in insects
  24. What are treatments of imidacloprid and spinosad toxicity?
    • Skin hypersensitivity- bathing with follicular flushing shampoo, antihistamines, steroids
    • Emetics if ingestion
  25. What are symptoms of imidacloprid and spinosad toxicity?
    Vomiting, increased salivation, [high dose] lethargy, diarrhea, muscle weakness, ataxia
  26. What is the mechanism of toxicity of avermectins/ milbemycin?
    Bind glutamate-gated Cl- channels that are specific to invertebrates--> increased influx of Cl- ions, resulting in hyperpolarization, paralysis, and death
  27. Describe the selective toxicity of avermectins/ milbemycin.
    • Mammals lack glutamate-gated Cl- channels
    • In mammals, these same compounds interact with type A-gated GABA channels, which are only within the CNS; the drug does not cross the BBB so it is safe [except in collies and sheepdogs, which have a gene mutation that allows this drug to accumulate in the CNS]
  28. What are symptoms of avermectin/ milbemycin toxicity?
    Lethargy, ataxia, hypersalivation, tremors, mydriasis, blindness, bradycardia, [high dose] coma, seizures, death
  29. How is avermectin/ milbemycin toxicity diagnosed?
    Response to physostigmine is suggestive
  30. What is the treatment for avermectin/ milbemycin toxicity?
    • No specific antidote for macrocyclic-induced toxicosis [symptomatic txt, supportive]
    • Induce emesis
    • Physostigmine in severe cases to increase Ach at synapses in periphery and CNS

Card Set Information

Author:
Mawad
ID:
326040
Filename:
ECC2- Insecticides
Updated:
2016-11-26 01:43:50
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vetmed ECC2
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vetmed ECC2
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