Pesticides

Question 1

Common Organochlorines

Answer 1

DDT & Chlorinated alicyclics

Lindane & Endosulfan - still available in US

Question 2

Organochlorine Exposure

Answer 2

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

Question 3

Mechanism of action: DDT

Answer 3

permeability of neuronal membranes or Na/K altered

Na channels remain open - hyperexcitability

Question 4

Mechanism of action of chlorinated alicyclics

Answer 4

GABA antagonist at chloride ionophore complex - hyperexcitability

Question 5

clinical signs with organochlorines

Answer 5

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

Question 6

DDx organochlorines

Answer 6

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

Question 7

treatment of Organochlorines

Answer 7

no specific antidote;

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

Question 8

organochlorines are excreted through..

Answer 8

bile- enterohepatic recycling

milk, feces, and urine

Question 9

mechanism of action of prganophosphates

Answer 9

Irreversibly inactivate acetylcholinesterase

Phosphate- direct effect on AChE activity;

Thiophosphates- desulfurized by liver enzymes;

Muscarinic overstimulation→ nicotinic overstimulation → nicotinic blockade

Question 10

clinical signs of organophosphates

Answer 10

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

Question 11

what are some of teh delayed effects seen with organophosphate toxicity

Answer 11

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)

Question 12

Dx organophosphates

Answer 12

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

Question 13

treatment of organophosphate

Answer 13

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)

Question 14

which pesticide undergoes “storage activation”

Answer 14

organophosphates

Question 15

what is storage activation

Answer 15

seal and stored for 1-2 years

more toxic

Question 16

which type of OP undergo lethal synthesis

Answer 16

thiophosphate OPs

Question 17

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

Answer 17

True

Question 18

mechanism of action of carbamates

Answer 18

reversible inhibition of acetylcholinesterase

Question 19

clinical signs of carbamates

Answer 19

similar to OP

SLUD - salivation, lacrimation, urination, D+

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

Question 20

treatment of carbamate

Answer 20

atropine

Question 21

T/F carbamtes require bioactivation like OPs

Answer 21

False

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

Question 22

lab tests for carbamates

Answer 22

cholinesterase levels

Question 23

carbamates do/don’t undergo storage activation

Answer 23

Don’t

Question 24

mechanism of action of nicotine

Answer 24

potent stimulant of parasympathetic nervous system, cholinergic receptor agonist

Question 25

clinical signs of nicotine

Answer 25

**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

Question 26

DDx of nicotine

Answer 26

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

Question 27

treatment of nicotine

Answer 27

decontamination- emesis, gastric lavage, activated charcoal; enhance excretion-IV fluids, lower pH or urine; atropine, diazepam

Question 28

mechanism of action of neonicothoids

Answer 28

binds to nicotinic acetylcholine receptors - **irreversible**

Question 29

clinical signs of neonicothoids

Answer 29

high levels overstimulate and block receptors → paralysis and death Signs similar to nicotine toxicity

Question 30

Mechanism of action of Naphthalene

Answer 30

oxidative metabolites cause methemoglobinemia and hemolysis; dissolve slowly (stomach acid) and toxicity can be delayed by several days

Question 31

clinical signs of Naphthalene

Answer 31

V+, mothball-scented breath, pale or brown gums, weakness or lethargy, labored breathing, tremors, seizures; severe cases- damage to liver or kidneys

Question 32

Dx of naphthalene

Answer 32

hematologic changes-hemolysis, heinz bodies, methemoglobinemia, hemoglobinuria

Question 33

DDx of Naphthalene

Answer 33

heinz bodies - acetaminophen, onions, and nitrates

Question 34

treatment if Naphthalene

Answer 34

decontamination - emesis, activated charcoal +/- cathartics, sodium bicarb; ascorbic acid & methylene blue 1% (methemoglobinemia); diazepam (seizures)

Question 35

mechanism of action od rotenone

Answer 35

block oxidative phosphorylation in citric acid, TCA, or Krebs cycle, interferes with mitochondrial ETC & NADH during ATP production

Question 36

Clinical signs of rotenone

Answer 36

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

Question 37

treatment of rotenone

Answer 37

no specific treatment, detoxification, supportive treatment

Question 38

lab results with rotenone

Answer 38

hypoglycemia, liver enzymes, hypoxemia/hypercapnia