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It is a science which deals with the properties, mechanism of action, clinical features, lethal dose
and treatment of a poison.
Difference between drug and poison
Effective dose: Dose of a substance which is therapeutically effective in 50% of individuals
receiving it.
Lethal dose (Totally depends on intention): use of substance which is sufficient to produce
death in 50 % of laboratory animals.
Drug: Any substance in effective dose is a drug.
Toxin: Any substance in lethal dose is a toxin.
Classification of poisons
1) Corrosive: These include inorganic acids, organic acids and alkalis.
Inorganic acids include HCl, H2SO4, HNO3
Organic acids include oxalic acid, carbolic acid, salicylic acid, hydrogen cyanide
(vegetable source)
Alkalis include NaOH, KOH, NH4OH
2) Irritants: These are organic and non-organic
Non organic are metallic and non-metallic
Nonmetallic which include phosphorus, chlorine, iodine, bromine
Metallic: mercury, lead, copper, lithium
Organic can be of animal source which include snakes , insect, spiders
Vegetables include castor oil croton oil
Mechanical which include powdered glass, Diamond dust, needles and hair
3) Neurotropic
Acting on Brain: Opium, alcohol, benzodiazepine, barbiturates
Acting on spinal cord: strychnine
Acting on nerve: Curare, conium maculatum
Somniferous: causing sleep
Inebriants: which cause excitement, narcosis
Deliriants: which cause delirium
4) Asphyxiants: irrespirable gases
CO, CO2, Coal gases, H2S
5) Cardiac toxins
Digitals, aconite, hydro cyanic acid
6) Miscellaneous
Paracetamol
Tricyclic Anti-depressants
Antipsychotics
Food poisoning
Antidote
Substances which are used to minimize effect of toxins.
1) Chemical antidote: Substances which bind a toxin and convert them into nontoxic
substances.
Oxalic acid + Ca will convert into calcium oxalate which is nontoxic
2) Physical antidote
Demulcents: make protective layer on mucosa e.g. egg albumin, barley water
Delucents: milk or water
Bulky food: boiled rice or vegetables
3) Receptor antidote: which compete with toxins for receptors
Atropine for organ phosphorus.
Morphine poisoning receptor antagonist
4) Dispositional antidote: substance which produce alteration in metabolism and excretion
of toxin in body.
Paracetamol N-Acetyl cysteine (increase glutathione in hepatocytes)
5) Functional antidote: substance which produce exactly opposite effect by acting on
different system.
Asphyxiants:
Carbon monoxide poisoning
Carbon monoxide is colorless, tasteless, order less, non-irritating gas which is a silent killer.
Carbon monoxide is a product of incomplete combustion of carbon matter.
It is present in air about 0.001%.
Domestic gas: 6-7 % → burning will increase its level in air.
Mechanism of action
Carbon monoxide has great affinity for hemoglobin leading to formation of
carboxyhemoglobin hemoglobin
Hb cannot bind with oxygen
So hypoxia to body tissue occurs
02-10% → asymptomatic
10-20 % → headache with flushing and Dizziness
20-30 % → throbbing headache with dizziness
30-40% → dizziness with confusion, nausea and vomiting
40-50% → syncope, tachypnea and tachycardia
50-60% → will cause coma
60-70 % → fits, decreased pulse decreased respiratory rate and eventually death
70-80% → feeble pulse and death within an hour
80-90% → cause death within one hour
Fatal dose:
1% concentration in air → will cause unconsciousness in 15 to 20 minutes
Coal gas 5-7 % in air → takes 3-5 minutes
Key to diagnosis:
PaO2: normal
O2 Saturation: decreased
Medico legal:
Accidental → in most cases
Suicidal → which is rare
Homicidal → which is also rare
Treatment:
Medical duties and legal duties
Medical duties:
Resuscitation
decontamination which is removed patient from source that is carbon monoxide
bring patient fresh air
Antidote: hyperbaric oxygen O2
Add 5 % CO2 → disassociate carboxy Hb additional
Can be given steroids and mannitol to treat cerebral edema
Postpartum appearance:
External Internal
Congested conjunctiva Blood will be Cherry red
Fine froth at mouth Brain, stomach, lungs, Kidneys are congested
Cyanosis
Hypostatis / Cherry red post mortem lividity (PML)
Hypostasis: which is pooling of blood in tone less vessels after death in dependent part of body
color will be blue.
Hydrocyanic acid (HCN) or Cyanide poisoning
Known as Vegetable acid, colored gas or bitter almond smell
Source:
Cherry
Plum
Jet berry brush
Apple seeds
Apricot
bitter almond oil
Uses:
lab workers
metal cleaning
Steel hardening
Rubber Industry
Refining/extracting of gold
photography
Mechanism of action:
Fetal dose:
60 milligrams → pure acid
60 drops → bitter almond oil
200 milligram → KCN
Medico legal:
suicidal → mostly because cheap and easy availability
accidental →
homicidal → never due to bitter taste
Clinical Features:
increase cyanide level of blood
signs and symptoms include headache, flushing, confusion, increased pulse, increased
respiratory rate, fits, feeble pulse, death
Clinical features also include skin flushing, breathing difficulty and palpitations.
Diagnostic:
bitter almond smell
General measures:
removal of patients from source
removal of clothes
wash with plenty of water
Antidote: cyanide antidote kit
amyl nitrate inhalant
sodium nitrate
sodium thiosulphate
Mechanism of action:
Nitrates convert hemoglobin into met hemoglobin and met hemoglobin has great affinity for
cyanide. Cyanide leaves cytochrome oxidase and bind with met hemoglobin to form cyano met
hemoglobin which is non-toxic.
Corrosive:
They have ability to damage any surface they become in contact with.
Mineral acids include H2SO4, HCL and HNO3
Most of them have local actions except shock.
Mechanism of action is local corrosive action → binds with hemoglobin to form acid hematin +
extraction of water from body tissue.
H2SO4
Heavy, oily, colorless Odorless, no fuming
Fatal dose is 10-15 ml
It turns all the body tissues brown due to increase in production of acid haematin.
HNO3
colorless , fuming, pungent smell
HNO3 + protein → nitric oxide + trinitro phenol (picric acid)
Xanthoproteic reaction → turns body tissues yellow.
HCL
Colorless, fuming, stain white sour taste
Produce Lethal erosion
Vitriolage:
Throwing of acid on somebody for jealousy, disfigurement and Visual impairment.
In 1820 → Glasgow → industrial riots
Clinical features:
intense burning pain from mouth to stomach
intense vomiting
clothes → will be perforated/stained
lips → will be excoriated
persistent vomiting
Teeth → white and brittle
oral cavity → damaged mucosa filled with froth and stain
tongue → will be swollen and stain
angle of mouth → will have streak of acid
Dyspnea → due to damage of epiglottis and larynx
Shock → dehydration and vomiting
Medico legal:
Suicidal (rare accidental)
Accidental (mostly)
Homicidal (not very common)
Cause of death:
Shock
respiratory obstruction
perforation of stomach → peritonitis
Treatment
Medical treatment includes
resuscitation
no gastric lavage → contraindicated
No Emetics
Antidote:
buffer solutions
sodium hydrogen phosphate
potassium hydrogen phosphate
Organic acids
Oxalic acid
Hypokalemic and nephropathy
White crystalline substance dissolved in water
Uses:
cleaning brass
removal stains
metal cleaning
Rubber Industry
Fatal dose: is 15 to 20 grams
Fatal period: One hour which is very important
Mechanism of Action:
is local corrosive action
hypokalemic/will cause tetany (formation of Ca oxalate)
Renal damage → crystal nephropathy → oxaluria
Shock → due to Intense vomiting leads to death
Christison’s saying
If a patient after eating a crystalline substance whose taste is strongly acidic presents with violet
vomiting, pain in stomach, feeble pulse, cold sweats, shock and dies within one hour → there is
hardly any doubt regarding oxalic acid poisoning.
Postmortem appearance
External Internal
Steak → angle of mouth whitish Mucosa of esophagus, stomach is damaged having
Lips, tongue, oral cavity is excoriated gelatinous acidic fluid
And whitish stain
Diagnosis
Oxalic acid crystals → that is present in stomach and renal tubes (Kidneys)
Medico legal:
Always suicidal