Insecticides

Insecticides

Learning objectives:

 Define major classes of insecticides.

 Identify sources and mode of exposure to insecticides.

 Recognize the pathophysiology of insecticides.

 Describe signs and symptoms of insecticides poisoning.

 Assess the severity of poisoning.

 Treat insecticides poisoning.

 Insecticides

Biological Synthetic
insecticides Insecticides Inorganic organic
from chemical insecticides
botanical insecticides
source e.g. Mercury
e.g. antimony
Pyrethrins, phosphorus
nicotine Arsenic
 Synthetic organic insecticides

Organochlorines Cholinestrase
e.g. D.D.T inhibitors
Toxaphene

Organophosphorus
compounds Carbamates
(Irreversible (reversible)
inhibitors) e.g Baygon,
e.g. parathion, Sevin Lannate
malathion
 Organophosphorus (OP) insecticides
Used for agricultural purpose to control crop-destroying insects.

Circumstances of poisoning

Suicidal
Accidental Homicidal

 Inhalational
or dermal
exposure

 Ingestion of
contaminated
food.
 Absorption

GIT Skin Conjuctiva Respiratory

Metabolism system

Hepatic
Activation Hydrolysis
Oxidation

For the conversion of O.P to an active form

Parathion  Paraoxon
6-24 hrs.
Excretion

Some stored in
Urine Faeces
fat stores.
 Pathophysiology
Inhibition of acetyl cholinesterase

Nervous Myoneural
system junction

Excess
acetylocholine

Initial Paralysis
stimulation
 Clinical picture
The signs and symptoms are related to the
effects on three separate areas of cholinergic
nervous system effects

Nicotinic
Muscarinic CNS
 Muscarinic effects
(wet finding)
Excessive secretion

Sweat gland Lacrimal

Salivary gland
 gland

sweating 
salivation
lacrimation

Urinary
Pupils
Respiratory bladder
GIT 
 system 
constricted
vomiting  urinary
diarrhea Bronchorrhea incontinence
cramps wheezes
C.V.S pulmonary edema

Bradycardia
hypotension
 Symbols for muscarinic effects

Diarrhea Salivation

DUMBELS
Urinary Lacrimation
incontinence
Emesis
Miosis

Bronchorrhea,
Bronchospasm,
Bradycardia
 Nicotinic effects

Neuromuscular Preganglionic
junction sympathetic stimulation

Muscle Dilated pupil

fasiculation tachycardia
cramping hypertension
weakness
paralysis
Central nervous system effects

Initial stimulation followed depression

by
Restlessness coma
death
anxiety ataxia
psychosis
convulsions
 Management

Investigation Treatment

Assay of cholinesterase (ChE)

enzyme activity

Erythrocyte Plasma
(true) (pseudo)
 More accurate  Inaccurate.
 Represent enzyme in  Disturbed by other diseases
nervous system

Mild toxicity  20-50%

Moderate toxicity  10-20%
Severe toxicity  less than 10%
 Treatment

1-Care of respiration 2- Care of circulation

 Clear patent airway. I.V. fluid to avoid dehydration
 Suction of secretion.
 Adequate ventilation.
 Oxygenation.

3-Decontamination:

Dermal GIT
 Removal of clothes Gastine lavage after endotracheal
 Wash skin with entubation
soap and water or
ethyle alcohol
 4-Antidotal therapy
A)Atropine
Mechanisms: Competitive antagonist of acetyle choline at the

muscarinic receptor sites

It cross B.B.B thus may have effect on CNS
toxicity
Dose: 2mg I.V and repeated every 10-15 minutes until
atropinization Drying of secretion Dilated pupil

N.B. Proper oxygenation and cardiac monitoring are essential

during atropine therapy
 B- Oximes
Pralidoxime Toxogonin
(2 PAM)

Used to antagonize the nicotinic effects of OP. But it can also

reverse the muscarinic and CNS effects.
Dose: Pralidoxime: 1gm I.V in saline
Toxogonine: ampoule (250 mg) I.V can be repeated after
1-2 h up to three ampoules

Mechanism of action of oximes

1. Break the bond.
2. Direct detoxification of O.P.
3. Have anticholinergic effects.
 Carbamate insecticides

(reversible cholinesterase inhibitors)

Clinical picture:
 Same clinical picture of O.P

Treatment:

 Similar to O.P but oximes are not indicated.