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RUSVM Toxicology > Pesticides > Flashcards

Pesticides Flashcards

1
Q

Common Organochlorines

A

DDT & Chlorinated alicyclics

Lindane & Endosulfan - still available in US

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2
Q

Organochlorine Exposure

A

miscalculation of concentrations for sprays/drips; contaminated feed/water, lack of PPE, dermal -most common, inhaled

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3
Q

Mechanism of action: DDT

A

permeability of neuronal membranes or Na/K altered

Na channels remain open - hyperexcitability

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4
Q

Mechanism of action of chlorinated alicyclics

A

GABA antagonist at chloride ionophore complex - hyperexcitability

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5
Q

clinical signs with organochlorines

A

Mainly CNS stimulation - salivation, V+, weakness, incoordination, disorientation, tremors, muscle fasciculations, spastic gait, hyperthermia, tonic-clonic seizures, opisthotonos, coma, death

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6
Q

DDx organochlorines

A

swine- dehydration/Na, pseudorabies;

dogs and cats- strychnine, fluoroacetate, lead, OP, metaldehyde, rabies, tetanus;

cattle- OP, lead, urea, polioencephalomalacia, infectious thromboembolic meningoencephalitis, ketosis, nervous forms of coccidiosis

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7
Q

treatment of Organochlorines

A

no specific antidote;

decontamination- emesis, wash with soap/water, activated charcoal, IV lipid therapy

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8
Q

organochlorines are excreted through..

A

bile- enterohepatic recycling

milk, feces, and urine

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9
Q

mechanism of action of prganophosphates

A

Irreversibly inactivate acetylcholinesterase

Phosphate- direct effect on AChE activity;

Thiophosphates- desulfurized by liver enzymes;

Muscarinic overstimulation→ nicotinic overstimulation → nicotinic blockade

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10
Q

clinical signs of organophosphates

A

muscarinic effects- DUMBELLS: D+, urination, miosis, bronchospasm, emesis, lachrymation, salivation; nicotinic effects - initial stimulation/fasciculation in muscle followed by depolarization and paralysis, sweating, hypertension, tachycardia

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11
Q

what are some of teh delayed effects seen with organophosphate toxicity

A

organophosphate-induced delayed polyneuropathy (10-14 days post exposure)- muscle weakness, ataxia, rear limb paralysis

organophosphate-induced intermediate syndrome (2-4 days post exposure) - NO muscarinic signs/muscle fasciculations, weakness of resp. muscles and accessory muscles (neck, proximal limb)

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12
Q

Dx organophosphates

A

history, clinical signs +/- lab tests; atropine response test - neg. High likelihood of OP

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13
Q

treatment of organophosphate

A

decontaminate - emesis (NOT if respiration is depressed or seizures), activated charcoal, wash gently, atropine, cholinesterase reactivators (oximes), supportive care

AVOID: phenothiazines, aminoglycosides, muscle relaxants, drugs that depress respiration (opioids)

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14
Q

which pesticide undergoes “storage activation”

A

organophosphates

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15
Q

what is storage activation

A

seal and stored for 1-2 years

more toxic

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16
Q

which type of OP undergo lethal synthesis

A

thiophosphate OPs

17
Q

T/F carbamtes are derived from carbamic acid and work in similar fashion to OPs

A

True

18
Q

mechanism of action of carbamates

A

reversible inhibition of acetylcholinesterase

19
Q

clinical signs of carbamates

A

similar to OP

SLUD - salivation, lacrimation, urination, D+

death from resp. failure and hypoxia due to bronchoconstriction→ tracheobronchial secretion and pulmonary edema

20
Q

treatment of carbamate

A

atropine

21
Q

T/F carbamtes require bioactivation like OPs

A

False

Don’t require bioactivation - faster onset & shorter duration than OP

22
Q

lab tests for carbamates

A

cholinesterase levels

23
Q

carbamates do/don’t undergo storage activation

A

Don’t

24
Q

mechanism of action of nicotine

A

potent stimulant of parasympathetic nervous system, cholinergic receptor agonist

25
Q

clinical signs of nicotine

A

early stimulation-ataxia, lethargy, hypersalivation, V+, bradycardia, tremors, convulsions

Later (or with higher dose) - CNS depression, tachycardia, vasodilation, ultimately paralysis or resp. muscles causes death

26
Q

DDx of nicotine

A

strychnine, methylxanthines, tremorgenic mycotoxins, organophosphates, carbamates, and depressants

27
Q

treatment of nicotine

A

decontamination- emesis, gastric lavage, activated charcoal;

enhance excretion-IV fluids, lower pH or urine;

atropine, diazepam

28
Q

mechanism of action of neonicothoids

A

binds to nicotinic acetylcholine receptors - irreversible

29
Q

clinical signs of neonicothoids

A

high levels overstimulate and block receptors → paralysis and death

Signs similar to nicotine toxicity

30
Q

Mechanism of action of Naphthalene

A

oxidative metabolites cause methemoglobinemia and hemolysis;

dissolve slowly (stomach acid) and toxicity can be delayed by several days

31
Q

clinical signs of Naphthalene

A

V+, mothball-scented breath, pale or brown gums, weakness or lethargy, labored breathing, tremors, seizures;

severe cases- damage to liver or kidneys

32
Q

Dx of naphthalene

A

hematologic changes-hemolysis, heinz bodies, methemoglobinemia, hemoglobinuria

33
Q

DDx of Naphthalene

A

heinz bodies - acetaminophen, onions, and nitrates

34
Q

treatment if Naphthalene

A

decontamination - emesis, activated charcoal +/- cathartics, sodium bicarb;

ascorbic acid & methylene blue 1% (methemoglobinemia);

diazepam (seizures)

35
Q

mechanism of action od rotenone

A

block oxidative phosphorylation in citric acid, TCA, or Krebs cycle,

interferes with mitochondrial ETC & NADH during ATP production

36
Q

Clinical signs of rotenone

A

local irritation (conjunctivitis, congestion, dermatitis)

depression and convulsions (predominant CS), muscle tremors, lethargy, incontinence, resp. stimulation followed by depression, chronic/acute liver changes reported

37
Q

treatment of rotenone

A

no specific treatment, detoxification, supportive treatment

38
Q

lab results with rotenone

A

hypoglycemia, liver enzymes, hypoxemia/hypercapnia

RUSVM Toxicology (9 decks)

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