OP poisoning
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Transcript of OP poisoning
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ORGANOPHOSPHORUS COMPOUNDS & CLINICAL
FEATURESPresenter :Dr.Milan Bhusal
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HISTORY First synthesized in early 1800 by Lassaigne
Lange and Schrader investigated the use as insecticides
German Military prevented the use; developed arsenal for chemical warfare
In 1941, re-introduced worldwide for pesticide use
Used in various terrorist attacks and regional wars
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OP COMPOUNDS
Dichlorvos Fenthion Malathion Ethion
Diazinon Parathion Chlorpyrifos
DIMETHYL COMPOUNDS DIETHYL COMPOUNDS
NERVE AGENTS G agents- Sarin, Tabun, Soman V agents- VX, VE
INSECTICIDES
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Inhibit esterase enzymes
Acetylcholinesterase in synapses and on red cell membranes & Butyrylcholinesterase in plasma
Accumulation of ACh and overstimulation of ACh receptors in synapses of ANS, CNS and NMJ
Recovery Aging
MECHANISM OF ACTION
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Common OP compounds available in Nepal
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National poison information centre:
9851038490
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Clinical features:
IV/IM within 30 min.
Oral or respiratory exposures - signs or symptoms within three hours.
Symptoms of toxicity from dermal absorption - delayed 12 hours.
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INHALATION Cough Difficulty in breathing Bronchitis Pneumonia
EYE CONTACT Irritation Pain Lacrimation Miosis Blurring vision Photophobia
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SIGNS AND SYMPTOMS
MUSCARINIC EFFECTS
NICOTINIC EFFECTS
CNS EFFECTS
NEUROPSYCHIATRIC EFFECTS
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MUSCARINIC:
Cardiovascular : Bradycardia, hypotension
Respiratory : Rhinorrhea, bronchorrhea, bronchospasm, cough, severe respiratory distress
Gastrointestinal : Hypersalivation, nausea and vomiting, abdominal pain, diarrhea, fecal incontinence
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Genitourinary: Incontinence
Ocular: Blurred vision, miosis
Glands : Increased lacrimation, diaphoresis
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CLINICAL PRESENTATIONMUSCARINIC: SLUDGE
S-SalivationL-LacrimationU-UrinationD-DiarrhoeaG-GI upsetE-Emesis
NICOTINIC: MATCHM-Muscle weakness and fasciculationA-Adrenal medulla activity ↑T-TachycardiaC-Cramping of skeletal muscleH-Hypertension
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CNS EFFECTS @C.E.A.S.T.A.R. Anxiety
Emotional liability
Restlessness
Confusion
Ataxia
Tremors
Seizures and coma
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Neuropsychiatric effects
Chronic
Headache, blurred vision, muscle weakness, depression, memory and concentration problem
The mechanism is not proven
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NEUROLOGICAL MANIFESTATIONS:
Type I paralysis or Acute paralysis.
Type II paralysis or Intermediate syndrome.
Type III paralysis or Organophosphate- induced delayed polyneuropathy(OPIDP)
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Type 1 paralysis or Acute paralysis
Muscles fasculations ,
Muscles cramps.
Twitching and weakness
Respiratory muscles weakness and paralysis.
CNS depression.
Respiratory arrest.
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TYPE II (INTERMEDIATE SYNDROME):
Develops after 24-96 hours ; persists 4-18 days
Respiratory distress, weakness of proximal muscles, neck and trunk, with relative sparing of distal muscles
Doesn’t respond to oximes or atropine, needs assisted ventilation
Recovery in 5-18 days
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IMS AND OPIDPIMS Time of onset 1-4 days Proximal limb muscle
weakness Neck muscle + Respiratory muscles + Recovery time 4-18 days Agents: Fenthion, Dimethoate,
Monocrotophos
OPIDP Time of onset 2-3 weeks Distal limb muscle weakness Neck muscle - Respiratory muscles - Recovery incomplete Agents: Methamedophos,
Trichlorfon, Leptophos
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TYPE III PARALYSIS: Delayed polyneuropathy
Occurs 2-3 weeks after exposure to large doses of certain organophosphates, last up to 12 months
Damage to the afferent fibres and associated inhibition of neuropathy target esterase
Distal muscle weakness/paralysis/paresthesia with sparing of the neck muscles, cranial nerves and proximal muscles Recovery incomplete
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