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Toxicology > Organophospates - Carbamates > Flashcards

Organophospates - Carbamates Flashcards

1
Q

what is the MOA of organophosphates?

A

irreversibly inactivate acetylcholinesterase = persistent acetylcholine activity

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2
Q

what are the common exposure routes for organophosphates?

A
  • contaminated feed or drinking water
  • use of empty pesticide containers for feeding/watering animals
  • dusting, spraying of animals or animal grounds or housing
  • sheep dip
  • flea treatment, meds
  • overdose
  • intentional poisoning
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3
Q

Why are organophosphates more toxic after 1-2 years in storage?

A

subject to storage activation

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4
Q

are organophosphates lipo or hydrophilic?

A

lipophilic - readily absorbed through the skin and mucus membranes, GIT, and inhalation

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5
Q

how are organophosphates normally metabolized?

A

in liver - excretion/bioactivation

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6
Q

Which organophosphate requires lethal synthesis?

A

thiophosphate

  • liver enzymes (CYP450) metabolize or bioactivate
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7
Q

what can happen with continued low dose/chronic exposure of OPs?

A
  • can lead to adaptation to decreased acetylcholinesterase - homeostatic response
  • enzyme induction or increased acetylcholinesterase production
  • receptor down regulation or decrease in acetylcholine receptor
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8
Q

thiophosphates are biologically inactive until transformed by?

A

the liver to -oxon metabolites

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9
Q

what is the major route of elimination for thiophosphates?

A

paraoxonase - a serum bound enzyme –> hydrolysis of paraoxon

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10
Q

what is the MOA of OPs? (plus primary - tertiary)

A

Irreversible inhibition of cholinesterases! (end result = increase in acetylcholine!)

  • OP binds to cholinesterase
  • aging = conformational change in OP-AChesterase complex that results in increased or irreversible binding of complex over time

primary: muscarinic receptor over stimulation
seconary: nicotinic receptor over stimulation (neuromuscular and CNS stim)
tertiary: nicotinic blockage (neuromuscular blockade, CNS depression)

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11
Q

what is the result of high exposure with OPs?

A

paralysis of diaphragm leading to pulmonary edema, asphyxia, and death due to respiratory failure

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12
Q

delayed neurotoxicity is possible with what OP?

A

thiophosphates

“OP induced delayed polyneuropathy”

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13
Q

what are the muscarinic effects of OP toxicity?

A

DUMBELLS

  • diarrhea
  • urination
  • miosis
  • bronchospasm
  • emesis
  • lacrimation
  • salivation
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14
Q

what are the CNS effects of OP toxicity?

A
  • cross the BBB
  • increase sensory and behavioral distrubances, incoordination, depressed motor function, and resp depression
  • resp paralysis
  • increased pulmonary secretions coupled with resp failure = USUAL CAUSE OF DEATH
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15
Q

what is the normal cause of death in a patient with OP toxicity?

A
  • increased pulmonary secretions coupled with respiratory failure
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16
Q

what is OP-induced delayed polyneuropathy?

A
  • develops 10-14 days after exposure
  • distal degeneration of long/large diameter motor and sensory axons of peripheral nerves and spinal cord
  • clinical signs = muscle weakness, ataxia, rear limb paralysis
  • chickens most sensitive
17
Q

what is OP-induced intermediate syndrome?

A
  • occurs 2-4 days after acute cholinergic effect and signs of the acute effects are no longer obvious
  • symptoms and signs occur after apparent recovery from acute effects
  • NO muscarinic signs or muscle fasciculations
  • weakness of resp muscles and accessory muscles
18
Q

what is the pathology of OP toxicity?

A
  • acute death, no specific lesions

non specific lesions

  • pulm edema
  • congestion
  • cyanosis
  • hemorrhages
  • edema of various organs
  • necrosis of skeletal muscle

delayed effects: degeneration and demyelination of peripheral and spinal motor neurons

19
Q

what lab diagnosis can we use for OPs?

A
  • plasma achetylcholinesterase activity level

- <50% is suspicious, <25% is diagnostic!

20
Q

what test can we run to see if an animal has been exposed to OPs?

A

atropine response test

  • if the test is POS (dry MM, increased HR, dilated pupils) = LOW LIKELY OP poisoning!
  • if the test is NEG (no signs seen) = LIKELY OP POISONING
21
Q

what DRUG do we use to treat OP poisoning?

A

Atropine
- specific ACh
antagonist
- repeat with decreasing doses 3-6 hours based on clinical response

22
Q

what is the main goal for atropine therapy with OP poisoning?

A

to suppress or dry pulmonary secretions

main concern with OP tox is resp failure from excessive airway secretions

23
Q

How can we treat OP poisoning with 2-PAM?

A
  • it is a cholinesterase reactivator - “oximes”

- binds to OP-inactivated acetylcholinesterase and reverses the binding

24
Q

Carbamate pesticides are derived from?

A

carbamic acid

25
Q

What was the first successful carbamate insecticide?

A

Carbaryl

  • broad spectrum of insect control
  • very low mammalian, oral, and dermal toxicity
  • outdoors - used as a lawn and garden insecticide
  • indoors - used in sprays or baits in the control of pests
26
Q

what is the MOA of Aldicarb?

A
  • mimics the structure of acetylcholine

- MOST TOXIC Carbamate

27
Q

do carbamates undergo storage activation?

A

NO

28
Q

what are the toxicokinetics of carbamates?

A
  • do not penetrate the CNS - effects are mostly resp
  • do NOT require hepatic bioactivation (most toxic than some OPs in very young patients)
  • faster onset and shorter duration than OPs
29
Q

what is the MOA of carbamates?

A
  • REVERSIBLE inhibition of acetylcholinesterase (competitive inhibition)
30
Q

what are the clinical signs associated with Carbamate poisoning?

A
  • similar to OP toxicity
  • SLUD (salivation, lacrimation, urination, diarrhea)
  • death results from resp failure and hypoxia due to bronchoconstriction leading to tracheobronchial secretion and pulmonary edema
31
Q

what is the main drug treatment for carbamate poisoning?

A

atropine!

32
Q

are oximes or 2PAM effective against carbamates?

A

no - reversible binding reduces benefit

Toxicology (12 decks)

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