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Toxicology > Op/Carbamates/pyrethrins > Flashcards

Op/Carbamates/pyrethrins Flashcards

1
Q

What are chlorinated hydrocarbons?

A
  • Highly lipid soluble
  • Persistent in environment
  • Bioaccumulate
  • Largely removed from market
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2
Q

What are the toxicokinetics of Chlorinated hydrocarbons

A
  • All animals susceptible
  • Lipid soluble - rapid absorption
  • Distribution to liver, kidney, brain, fat
  • Metabolism by mixed function oxidases to more toxic epoxides (for cyclodiene)
  • Excreted in bile and milk fat
  • Released to blood during weight loss
    • can cause bimodal progression of signs
    • Toxicosis after some other issue
  • Excretion half-life may have two compartments
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3
Q

What is the MOA of chlorinated hydrocarbons?

A
  • Lowers action potential thresholds
    • especially in CNS
    • Affects GABA receptors, similar to strychnine
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4
Q

What is the MOA of Diphenyl aliphatics (DDT)?

A
  • Interfere with Na+ flow in nerves
  • Lowers threshold for action potential
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5
Q

What is the MOA of Cyclodienes?

A
  • Inhibit prostynaptic binding of GABA
    • lowers threshold
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6
Q

What are the toxicity levels of chlorinated hydrocarbons?

A
  • Cats most sensitive - LD50 3-6 mg/kg
  • Dog LD50 50-65 mg/kg
  • Cattle min tox dose 10-25 mg/kg
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7
Q

What are the toxic levels for Lindane?

A
  • LD50:
    • Cats 25 mg/kg
    • Dog 40 mg/kg
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8
Q

What is the clinical picture associated with chlorinated hydrocarbon toxicosis?

A
  • Acute onset 12-24 hours
  • Behaior changes
    • hypersensitive, beligerent, walking backwards
  • Muscle tremors
    • especially head, face, neck
  • Tono-clonic convulsions
    • intermittent CNS depression
    • Almost appear normal between episodes
    • Death due to respiratory failure
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9
Q

How can chlorinated hydrocarbon toxicosis be diagnosed?

A
  • Clin path not helpful
  • Acute toxicosis
    • Measures residues in GI content, brain, liver
      • Body fat good sample as well
      • Milk, eggs
      • Long half-life
  • No specific lesions or no lesions at all
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10
Q

How is chlorinated hydrocarbon toxicosis treated?

A
  • Supportive care:
    • Control seizures -diazepam, phenobarb
    • Activated charcoal and cathartics
    • Wash with soup and water if dermal exposure
    • Prognosis variable
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11
Q

What chlorinated hydrocarbon is responsible for thin eggshells?

A

DDT (Deet)

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12
Q

What are Pyrethrins/Pyrethroids?

A
  • Pyrethrins:
    • Extracts of Chrysanthemum
    • Not very stable
  • Pyrethroids
    • Synthetic
    • Stable
    • Permethrin, cypermethrin, fenvalerate
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13
Q

What are the classes of Pyrethroids?

A
  • Type I (no a cyano)
    • allethrin
    • permethrin
    • phenothrin
    • resmethrin
    • sumithrin
    • telfluthrin
    • tetramethrin
  • Type II (has a cyano)
    • Cyfluthrin
    • Cyhalothrin
    • Cypermethrin
    • Deltamethrin
    • Fenvalerate
    • Flumethrin
    • Fluvalinate
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13
Q

What are the classes of Pyrethroids?

A
  • Type I (no a cyano)
    • allethrin
    • permethrin
    • phenothrin
    • resmethrin
    • sumithrin
    • telfluthrin
    • tetramethrin
  • Type II (has a cyano)
    • Cyfluthrin
    • Cyhalothrin
    • Cypermethrin
    • Deltamethrin
    • Fenvalerate
    • Flumethrin
    • Fluvalinate
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14
Q

What sit the MOA of Type I pyrethroids?

A
  • Slow the opening and closing of neural sodium and K+ and CL= channels
    • Lowers the threshold for firing of nerve and extends the action potential
  • CNS stimulation, muscle tremors, excitement
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15
Q

What sit the MOA of Type II pyrethroids?

A
  • Membrane depolarization predominates
  • Affects GABA (inhibitory) channels
  • Tendency to weakness, paralysis
16
Q

What is the clinical picture associated with pyrethroid toxicosis?

A
  • Onset often <1hr
  • Hyper excitable, tremors, seizures, ataxia, vomiting
  • Some products (type II) include more salivation, weakness, abnormal posture
  • Clinical poisoning usually goes to recovery (rarely death ) in 24-72 hrs
  • Topical allergic pruritus, hyperemia, urticaria, dermatitis not common
17
Q

What is the affect of Permethrin in Cats?

A
  • Toxicosis has occurred from contact with spot on treated dogs
  • Onset 2 min - 3 hrs
  • Hypersalivation, vomiting seizures, paw shaking, ear twitching, flicking of tail, twitching of dorsal skin
  • Agitation, seizures can occur 12-24 hrs post exposure
  • Seizures may be difficult to control
18
Q

How is pyrethroid toxicosis diagnosed?

A
  • History of exposure
  • General lab tests- Increased PMNs, glucose
  • Chemical analysis- brain, skin
    • Analysis shows presence not peak concentration
19
Q

What are differential diagnoses for pyrethroid toxicosis?

A
  • OPs
  • Clorinated hydrocarbons
  • metaldehyde
  • nicotine
  • strychnine
20
Q

What is the treatment for pyrethroid toxicosis?

A
  • Discontinue exposure, control tremors, general supportive care
    • Bathe with detergent (Dawn)
    • Methocarbamol (Robaxin) for tremors
    • Alternatively use valium or pentobarbital
    • Supportive care: fluids, thermoregulation
    • Check for hypoglycemia and treat as needed
  • Most recover in 24-72 hours
21
Q

What is the chemical structure of Organophosphates?

A
  • Aliphatic, cyclic, or heterocyclic esters of phosphoric acid
  • have P=O bond adjacent to the ester
    • more toxic
  • Organothiophosphates have a P=S group
    • More stable in environment
  • Phase I mixed function oxidases - Lethal synthesis
22
Q

What is the ADME of OPs?

A
  • Absorption rapid and complete
  • Distributed in plasma⇢ liver⇢ CNS
  • Metabolized by MFO system (oxidation)
    • deactivated by hydrolysis
  • Excretion of metabolites in urine and feces
23
Q

What is the toxic level of OPs?

A
  • LD50s less than 10 mg/kg
  • Cats> dogs
  • Brahman cattle > English
  • Bulls > cows
  • Poultry very susceptible to divhlorvos
24
Q

Wat is the MOA of OPs?

A
  • Inhibit acetylcholinesterase at cholinergic synapses
    • allows for continuous stimulation by accumulated acetylcholine
25
Q

What are the signs of OP toxicosis?

A
  • Signs reflect stimulation of parasympathetic nervous system and neuromuscular junctions
    • Muscarinic - SLUD syndrome
    • Nicotinic - tremors, ataxia, paralysis
26
Q

What is the clinical picture of OP toxicosis?

A
  • Acute onset - minutes to hours
  • Parasympathetic stimulation - muscarinic
    • SLUD, Emesis, bronchoconstriction, miosis, bradycardia
  • neuromuscular - nicotinic
    • Muscle tremors, stiffness, paralysis
  • CNS
    • apprehension, nervousness, seizures
  • death from respiratory failure
27
Q

How is OP toxicosis diagnosed?

A
  • Clinical signs
  • History of exposure
  • Cholinesterase activity
    • Blood, Brain, retina acceptable
    • Carbamate exposure regeneration to normal
  • Chemical analysis
    • detection of parent compound
28
Q

What are the differential diagnoses for OP toxicosis?

A
  • Chlorinated pesticides
  • Strychnine
  • Pyrethroids
  • Zinc phosphide
  • Nicotine
29
Q

What is the treatment for OP toxicosis?

A
  • Atropine sulfate ¼ IV rest SQ
    • SA - 0.2 mg/kg
    • LA - 0.5 mg/kg
    • Atropine loses efficacy after 2-3 doses
    • Do NOT OD
    • USE with extreme caution in horses (GI stasis)
  • Glycopyrrolate - alternate
    • doesn’t cross BBB
  • Oral activated charcoal
  • Reactivator oximes like 2-PAM
    • must give before aging
    • AChE irreversible binding
    • NOT for carbamates - spontaneously hydrolyze
  • Dermal - wash with soap and water

Toxicology (25 decks)

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