This document discusses organophosphorus and organochlorine compounds. It begins by explaining that organophosphorus compounds are commonly used as pesticides and act by inhibiting cholinesterase. It then classifies organophosphates and describes their absorption, mechanism of action, signs and symptoms of poisoning, and management. The document also discusses organochlorines like DDT, describing their classification, mechanism of action as sodium channel activators, signs of CNS stimulation, fatal doses, and management of poisoning. Clinical features and post-mortem findings are provided for both types of compounds.

1. ORGANO PHOSPHOROUS
&
ORGANO CHLORINE

2. • Organophosphorus compounds are chemical agents used mainly as pesticides in
commercial agriculture, field sprays .
• Act by inhibiting choline-esterase .

3. CLASSIFICATION OF CHOLINE-ESTERASE
INHIBITOR
They can be classified as three categories:
1. Organic derivatives of phosphorous (OP )
2. Carbamic acid esters of alcohol having quarternary or tertiary ammonium groups
( carbamates )
3. Quarternary amines ( endrophonium )

4. USES
• Nerve agents
• Insecticides
• Glaucoma treatments
• Myasthenia gravis ( ENDROPHONIUM)
• Alziemers disease
• Lewy body dementia

5. CLASSIFICATION OF ORGANOPHOSPHATES
ALKYL PHOSPHATES ARYL PHOSPHATES
DEMETON DIZINON ( TIK 20 )
DIMEFOX CHLORTHION
HEXA ETHYL TETRA
PHOSPHATE
METHYL PARATHION
ISOPESTOX PARATHION
MALATHIONE PARAOXON
OCTAMETHYL PYROPHOSPHATE

6. ABSORPTION ROUTE
1. Cutaneous
2. Ingestion
3. Inhalation

7. MECHANISM OF
ACTION
Normally acetyl choline bind
cholinesterase at 2 site
• Nitrogen of choline attaches at
anionic site
• carboxyl group attaches to serine
residue at esteratic site

8. • Phosphate of OP attaches to the
hydroxyl group of a serine residue
at enzymes esteratic site .
• ACH increase at nerve endings thus
resulting in
 Ganglionic
 Parasymphathetic
 Neuromuscular synapse
overstimulation .

9. AGEING
• This involves breaking away of one
organic group ( R1) from the organo
phosphorous – choline esterase
conjugate ( dealkylation )
• This makes OP – CHE conjugate so
stable that oximes are not able to
reactivate choline esterase .
• This process is known as ageing .

12. CLINICAL FEATURES
It is useful to remember the toxidrome in terms of the 3 clinical effects on nerve
endings
1.Nicotinic effects at neuromuscular junctions and autonomic ganglia
2. Muscarinic effects
3. CNS effects,.

14. MUSCARINIC SYMPTOMS

15. “ DUMBBELSS “
• Diarrhea
• Urination
• Miosis
• Bradycardia
• Bronchospasm
• Emesis
• Lacrimation
• Limp
• Sweating

16. “SLUDGE”
Salivation
Lacrimation
Urination
Defecation
G.I upset
Emesis

17. NICOTINIC SYMPTOMS
• Muscle weakness
• Areflexia
• Tachycardia
• Cramps
• Hypertension

18. CNS SYMPTOMS
WASTE CHADDAR
• Weakness
• Ataxia
• Slurred speech
• Tremors
• Emotional lability
• Confusion , Convulsion, Coma
• Headache , hypothermia
• Drowsiness
• Depression of centers ( resp & CVS )
• Restlessness

20. HOW DO YOU GRADE THE SEVERITY-
DRIESBACH CLASSIFICATION

21. HOW LONG WILL IT TAKE TO PRESENT WITH
TOXIDROMES??
• Generally oral or respiratory exposures within three hours.
• While from dermal absorption may be delayed up to 12 hours.

22. LAB DIAGNOSIS
• Petroleum or garlic-like odor.
• A) blood – RBC cholinesterase activity
hyperglycemia ( hyperactivity of sympathetic ganglia release
catecholamine )
B ) p- nitrophenol test - it is a metabolite of several OP compound & is excreted in urine .
C ) thin layer chromatography .
Other 1. CXR - Evaluate pulmonary oedema 2. ECG - Cardiac arrhythmias 3. ABG &
Electrolytes 4. Urea

23. MANAGEMENT
PREVENTION OF FURTHER ABSORPTION
• Remove patient from site of exposure .
• Remove contaminated clothing .
• Wash exposed areas with soap & water f/b ethanol in water .
• Topical creams & lotions .
• In case of eye contamination irrigate eyes thoroughly in water for 15 min .

24. MAINTAIN AIRWAY
• Clean airway of secretions
• Endotracheal intubation
• Administration of oxygen
• Positive pressure ventilation
• Tracheostomy if necessary

25. REMOVAL OF UNABSORBED POISION
Stomach wash WITH 1:5000 KMNO4
ANTIDOTES
• Mechanical - Activated charcoal 1g/kg .
• Physiological - atropine sulphate 2-5 mg IV every 5-10 min until complete
atropinization .
• Atropine only reduces muscarinic & CNS actions . ( no affect on nicotinic action ).
• OXIMES

26. OXIMES
• Attach to phosphorous atom & form oxime
phosphate which then split away from
acetylcholinesterase
• Potentiate action of atropine thus decrease
the amount of atropine
• should be started as early as possible
otherwise ageing occur

27. PRALIDOXIME
• Most commonly used
• Available as 2- PAM ( pralidoxime chloride )
• Dose – 1-2 gm in 100 ml of 0.9 % NACL solution , given IV over 15-30 minutes

28. SIGN OF ATROPINISATION
1. Clear chest on auscultation with no wheeze
2. Heart rate >110 beats/min
3. Pupils no longer pinpoint
4. Dry axillae
5. Systolic blood pressure >90 mmHg

29. CAUSE OF DEATH
• Due to weakness of muscles of respiration
• Accumulation of excessive secreations in respiratory tract

30. POST MORTEM APPEARANCE
• Sign of asphyxia – congestion of face
cyanosis of lips , nose , fingers & extremities
blood stained froth at nose & mouth
• Constricted pupil
• Kerosene like odour
• Gastric mucosa – congested & haemorrhagic
• Respiratory passages – congested & contain frothy haemorrhagic exudate
• Heart – soft & flabby & show epicardial haemorrhages .
• Lungs – sub pleural petechiae

31. MEDICOLEGAL
IMPORTANCE
• Suicide – very common
• Accidental – common
• Homicide – rare

32. DHATURA ATROPA BELLADONNA

33. DHATURA & ATROPA BELLADONNA
• Active principles = scopolamine , atropine , hyoscyamine
• MOA - competitively inhibit “MUSCARINIC “ effect of acetyl choline .
• Signs -
1. pulse ( 120-150 / min )
2. BP ( 180 mmhg )
3. Respiratory rate increase
4. Temperature increase
5. Muscle tone increase
6. Hyperreflexia
7. Positive Babinski sign

34. ORGANOCHLORINES
• Organic compound carrying at least one chlorine atom .
• Used as insecticide
• CNS stimulants

35. CLASSIFICATION
• Based on their chemical nature –
a) Dichlorodiphenyltrichloroethane (DDT )
b) Benzene hexachloride or lindane
c) Cyclodienes ( aldrin , dieldrin, endrin , endosulfan , chlordane )
d) Toxophene

36. ABSORPTION
• Ingestion
• Inhalation
• Transdermal ( DDT & toxophene are poorly absorbed )

37. MECHANISM OF
ACTION
• Bind to activated sodium channel &
delay their inactivation
• Due to continuous entry of sodium
inside cell there is depolarisation &
repetative firing of nerve membrane
• This is clinically seen as prominent
tremors

38. SIGNS & SYMPTOMS
• Prodromal sign
• Agitation
• Confusion
• Dizziness
• Headache
• Nausea & vomiting

39. CNS STIMULATION
Myoclonous
Tremors
Seizures
Hyperthermia ( due to increased muscle activity )
Pupil dilated
Respiratory failure

40. FATAL DOSE
• DDT , lindane – 15-30 gm
• Aldrin , dieldrin , endrin = 2-6 gm

41. MANAGEMENT
• Rescue personnel should wear protective gear ( OC absorbed through skin )
• Immediate resuscitative measures
• Decontamination
contact – wash ( skin , hair , nail , eyes ) copiously with water .
ingestion (A) emetics (B) Gastric lavage
• Activated charcoal
• Fats , oils etc not to be given my mouth ( increase absorption )
• Specific antidote = none
• Atropine is contra indicated

42. POST MORTEM APPEARANCE
• Kerosene like smell
• Sign of asphyxia
• Centrilobular hepatic necrosis

43. MEDICOLEGAL IMPORTANCE
• Suicide & accidental poisoning = common
• Homicide= rare
• Endrin resist putrifection so detected in viscera for long time after death .