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Forensic Toxicology

By Dr. Houssein Nofal (PhD) MD.
Ass. Professor of Forensic Medicine College of Medicine – KFU – Dammam – SA

Forensic Toxicology

It is a branch of Forensic Medicine dealing with Medical and Legal aspects of the harmful effects of chemicals on human beings. Forensic Toxicology is the study and practice of application of toxicology to the purposes of the law.

Incidence

The true incidence of poisoning in the United States is unknown. Approximately 2 million cases are voluntarily reported to poison control centers each year, and officially, a rather steady figure of about 700 deaths by poisoning is reported each year.

Incidence

Children under age 6 account for the majority of poisonings reported, but adults account for the majority of deaths by poisoning, most of which is intentional rather than accidental.

most frequently reported poisonings
1 - Household cleaning supplies 2 - Analgesics (aspirin, acetaminophen) 3 – Cosmetics 4 - Cough and cold remediesscrapes and 5 - Plant insect bites 6 – Pesticides 7 - Topical creams and lotions 8 - Hydrocarbons (gasoline, kerosene) 9 - Antimicrobacterial soaps 10 - Sedatives/hypnotics/ antipsychotics 11 - Food poisoning 12 – Alcohol

most frequent deaths by poisoning
1 - Antidepressant medications (aspirin, 2 - Analgesics acetaminophen) 3 - Street drugs 4 - Cardiovascular drugs 5 - Alcohol 6 - Gases and fumes 7 - Asthma therapies 8 - Industrial chemicals 9 - Pesticides 10 - Household cleaning supplies 11 - Anticonvulsant medications 12 - Food, plants, and

Paracelsus (1493-1541) once said "All substances are poisons; there is none which is not a poison. The right dose differentiates a poison and a remedy.“ It is not easy to distinguish toxic from non toxic substances. A key principle in toxicology is the Dose-Response Relationship.

There is a graded dose-response relationship in individuals, and a quantal dose-response relationship in the population. The quantal dose-response is the more important one, used to determine the median lethal dose (LDm) and judge what percentage of the population is affected by a dose increase. Quantal is a term meaning "all

Manner of Death by poisoning

Accidental poisoning cases are Most, but a large number are deliberate. Suicidal poisoning is probably the most common method of self-destruction. Corrosive agents (strong acids or alkalis) are used rarely because less painful substances are available. Homicide by poison is rare nowadays. Such weapons of the old fashioned poisoner as arsenic, strychnine or

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Poisoning
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Suicidal: (KCN, HCL, Opium, Barbiturates, organophosphorus, oxalic acid oleander etc), Homicidal (arsenic, aconite, thallium, organophosphorus, oleander, etc.).

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Poisoning

Older poisons like opium and arsenic are replaced by newer poisons. Common homicidal poisons are: Arsenic, Antimony, Oleander, NuxVomica, Madar, powdered glass and aconite. Cattle Poisoning is also common, the poison used are Arsenic, Yellow oleander, zinc phosphide, nitrates,

Important Definitions:
Toxicology  It is the science dealing with properties, action, toxicity, fatal dose, detection estimation of, interpretation of the result of toxicological analysis

Important Definitions:
Poison: A Poison is defined as any substance which when administered in living body through any route (Inhalation, Ingestion, surface absorption etc) will produce ill-health or death by its action which is due to its physical, chemical or physiological properties.

Important Definitions:
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Drug (WHO 1996): “Drug is any substance or product that is used or intended to be used to modify or explore physiological systems or pathological states for the benefit of the recipient.” e.g.: paracetamol, ciprofloxacin, salbutamol, oestrogen, insulin etc.

Important Definitions:
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Clinical Toxicology: Deals with human diseases caused by, or associated with abnormal exposure to chemical substances. Toxinology refers to toxins produced by living organism which are dangerous to man, e.g.: snake venom, fungal and bacterial

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Important Definitions:
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Chelating Agents: are the substances which act on absorbed metallic poisons. They have greater affinity for metals as compared to endogenous enzymes. The complex of agent and metal is more water soluble than metal itself, resulting in  higher renal excretion of the complex. E.g.: British anti-lewisite (B.A.L., dimercaprol), E.D.T.A. (ethylene diamine-acetic acid), Penicillamine (Cuprimine),

Important Definitions:
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Ecotoxicology: It is concerned with the toxic effects of chemical and physical agents on living organisms, especially in population and communities within defined population.

Important Definitions:
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Acute poisoning is caused by an excessive single dose, or several dose of a poison taken over a short interval of time. Chronic Poisoning is caused by smaller doses over a period of time, resulting in gradual worsening.

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Important Definitions:
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Subacute poisoning shows features of both acute and chronic poisoning. Fulminant poisoning is produced by a massive dose. In this death occur rapidly, sometimes without preceding symptoms.

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Important Definitions:
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Parasuicide (attempted suicide or pseudicide) is a conscious often impulsive, manipulative act, undertaken to get rid of an intolerable situation.

Culpable Homicide:  Causing death of a person by an act, with the intention of causing such bodily injury and is likely to cause death, or with the knowledge that he is likely, by such an act to cause death.

Important Definitions:
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Antidote: Antidotes are substances which counteract the effect of poison. They are divided into Mechanical, Chemical, Physiological and specific receptor antagonists.

Toxin & Poisons

A toxin is any material exerting a life threatening effect upon a living organism. Poisons are a subgroup of toxins

Toxin & Poisons

Poisons generally enter the body in a single massive dose, or accumulate to a massive dose over time. Toxins work in minute quantities or low levels, requiring sensitive analytical instruments for detection. Some toxins have medicinal value, but many produce irreparable damage.

Toxin & Poisons

Poisons can be combated by prompt treatment, and most organ damage (except for serious CNS injury) may be repairable.  Whereas poisons are somewhat easily identifiable by their symptoms, many toxins tend to disguise or mask themselves.

Sources of Poison
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Domestic or household sources. Agricultural and horticultural sources. Industrial sources Commercial sources. From uses as drugs and medicines Food and drink Miscellaneous sources - snakes bite poisoning,

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Domestic or household sources detergents, disinfectants, cleaning agents, antiseptics, insecticides, rodenticides etc. Agricultural and horticultural sourcesdifferent insecticides, pesticides, fungicides and weedicide. Industrial sources- In factories, where poisons are manufactured or poisons are produced as by products. Commercial sources- From store-houses, distribution centers and selling shops. From uses as drugs and medicines – Due to wrong medication, overmedication and abuse of drugs. Food and drink – contamination in way of use of preservatives of food grains or other

Classification of poisons
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According to the site and mode of action. Local Action Remote Action Combined local and remotes action According to motive or nature of use. Homicidal:. Suicidal: Accidental:. Abortifacient:. Stupefying agent: Agents used to cause bodily injury: Cattle Poison: Used for malingering

Classification of poisons
According to the site and mode of action b) Local Action  Corrosive  Irritant
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Remote Action Neurotics Cardiac Poisons

Classification of poisons
According to the site and mode of action Local Action Corrosive Strong Acid: mineral acid and organic acid Strong alkali Metallic: Mercuric Chloride Irritant Mechanical: Glass Powder Chemical Inorganic: weak acid, weak alkalies, Inorganic non-metals, Inorganic Metals.  Organic: Chemical preparations, Animal and vegetable origin.
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Remote Action Neurotics C.N.S. Poisons Somniferous: opium and its alkaloids, Barbiturates. Inebriant (Intoxicant): Alcohol, ether, Chloroform. Stimulant Deliriant: Dhatura, Belladona, Hyocyamus, cannabia indica. Stupefaciant Hallucinogens Convulsant:

Classification of poisons

 Spinal (Convulsant) XIII.Strychnos Nux Vomica  

Peripheral Nerves Local Anaesthetics: Cocaine, Procaine.

Classification of poisons
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Remote Action Cardiac Poisons KCN, NaCN, Digitalis, Aconite, Nicotine, Quinine, Oleander Asphyxiants: Carbon Dioxide(CO2), CO, hydrogen sulphide(H2S) Nephrotoxic: Oxalic Acid, Mercury, Cantherides Hepatotoxic: Phosphorus, Carbon tetrachloride, Chloroform. Miscellaneous: Food Poisons. Combined local and remotes action

Classification of poisons
 According to motive or nature of use:  Homicidal: Arsenic, Aconite, Digitalis, Abrus     

Precatorius, Strychnos nux-vomica. Suicidal: Opium, Barbiturate, Organophosphorus, carbolic acid, copper sulphate. Accidental: Aspirin, organophosphorus, copper sulphate, snakes bite, Ergot, CO, CO2, H2S. Abortifacient: Ergot, Quinine, Calotropis, Plumbago. Stupefying agent: Dhatura, cannabis, chloral hybrate. Agents used to cause bodily injury: Corrosive acids and alkalies.

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Ideal Suicidal poison: should be easily available, No bad taste, cause No pain, cheap, highly toxic, tasteless or pleasant taste, capable of being taken with food or drink..

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Ideal Homicidal poison: it should be cheap, easily available, colourless tasteless odourless, highly toxic, No residual product lest, S/S resembles natural diseases, No antidote, Shows no post-mortem changes capable of being administered with food or drink.

Route of Administration/absorption
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Oral (commonest) e.g.: alphos, acids, Inhalation: gas poison Parenteral (IM, IV, Sub-Cutaneous, Intra-Dermal) Natural Orifices other than mouth (Nasal, Rectal, Vaginal, Urethral), Ulcers, wounds and intact skin.

Fate of poison in body

A part of the poison taken orally gets eliminate unabsorbed by means of defecation and vomiting. Before absorption the poison may exert its effects in the G.I. Tract. When absorbed, the poison reaches different parts of the body and organs through circulation.

Fate of poison in body
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Cumulative poisons get accumulated in some organs or tissues. A part of poison is eliminated as such through different route of elimination. But major part is detoxified or metabolized in the body and than excreted after exerting its toxic effects on the body. Liver is the main organ to detoxify or metabolize most of the poisons. Certain poisons like Chloroform, Phosphorus, Nitrates and Acetic acid disappear by evaporation or oxidized or destroyed in the body and no trace of them can be detected

Excretion of poisons

Unabsorbed poisons are excreted through faeces and vomitus. Absorbed poisons are excreted mostly by urine. A part of volatile poison is exhaled out.

Factors influencing the actions of a poison in the body
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Quantity Physical form Chemical form Concentration Condition of the stomach Route of administration Age State of body health Presence of disease Intoxication arid poisoning states Sleep Exercise Cumulative action of poisons Tolerance Idiosyncracy

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1. Quantity: A high dose of poison acts quickly and often resulting in  fatal consequences. A moderate dose causes  acute poisoning. A low dose may have sub-clinical effects and causes  chronic poisoning on repeated exposure. Very large dose of Arsenic may produce  death by shock without dose irritant symptoms,

Factors influencing the actions of a poison in the body

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Factors influencing the actions of a poison in the body
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2. Physical form: Gaseous or volatile poisons are very quickly absorbed and are thus most rapidly effective. Liquid poisons are more rapid than solid poisons. Some poisonous vegetable seeds may pass through the intestinal canal

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3. Chemical form: Chemically pure arsenic and mercury are not poisonous because these are insoluble and are not absorbed. But white arsenic (arsenic oxide) and mercuric chloride are deadly poisonous. Barium sulphide is deadly toxic

Factors influencing the actions of a poison in the body

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4. Concentration (or dilution): concentrated form of poison are absorbed more rapidly and are also more fatal but there are some exceptions too.

Factors influencing the actions of a poison in the body

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5. Condition of the stomach: food content presence of food-stuff acts as diluent of the poison and hence protects the stomach wall. Dilution also delays absorption of poison. Empty stomach absorbs poison most rapidly. In cases of achlorohydria, KCN and

Factors influencing the actions of a poison in the body

6. Route of administration:

Factors influencing the actions of a poison in the body

absorption rate is different for different routes. 7. Age: some poisons are better tolerated in some age groups.
Opium and its alkaloids are tolerated better by elderly subjects but badly by children and infants.

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8. State of body health: A well built person with good health can tolerate the action of poison better than a weak person. 9. Presence of disease: In certain diseased conditions some drugs are tolerated exceptionally well

Factors influencing the actions of a poison in the body

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10. Intoxication arid poisoning states In certain poisoning cases some drugs are well tolerated, like, in case of strychnine poisoning, barbiturates and sedatives are better tolerated. Whereas in case of barbiturate poisoning any sedative or tranquilizer will accentuate the process of death.

Factors influencing the actions of a poison in the body

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11. Sleep Due to slow metabolic process and depression of other body functions during sleep, usually the absorption and action of the poison is also slow. But depressant drugs may cause, more harm during the state of sleep. 12. Exercise Action of alcohol on C.N.S. is slowed during exercise because more blood is drawn to

Factors influencing the actions of a poison in the body

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13. Cumulative action of poisons: Preparations of cumulative poisons

Factors influencing the actions of a poison in the body

(poisons which are not readily excreted from the body and are retained in different organs of the body for a long time) like lead may

not cause any toxic effect when enters the body in low dose.

But when such poisons enter over a long period of time, may cause harm when their concentration in different

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14. Tolerance may develop by individuals on long term exposure to a particular poison. 15. Idiosyncracy: some persons may react adversely to a particular drug though the general population tolerates the drug well.

Factors influencing the actions of a poison in the body

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Symptoms and Signs

The symptoms and signs may be different for different poisons and is responsible on the nature and action of the poison. They can be local, remote or combined and are will be taught in the individual poisons.

Poisons
Acids (nitric, hydrochloric, sulphuric) Aniline (hypnotics, nitrobenzene) Arsenic (metals, mercury, copper, etc.) Atropine (Belladonna), Scopolamine Bases (lye, potash, hydroxides) Carbon monoxide (CO) Carbolic acid (or other phenol) Cyanide

their Symptoms
Burns around mouth, lips, nose Skin of face and neck quite dark Severe, unexplained diarrhea Pupil of eye dilated Burns around mouth, lips, nose Skin is bright cherry red. Odor of disinfectant Quick death, red skin, odor of peach

Poisons Food poisoning Metallic compounds Nicotine Opiates Oxalic acid (phosphorous) Sodium fluoride Strychnine

their Symptoms Vomiting, abdominal pain Diarrhea, vomiting, abdominal pain Convulsion Pupil of eye contracted Odor of garlic Convulsion Convulsion, dark face and neck

Symptoms and Signs

Sometimes poisoning is difficult to recognise but there are signs and symptoms that may cause a doctor to think about poisoning. They are: Sudden vomiting and diarrhoea Unexplained coma in children and adults known to have depressive illness Rapid onset of a peripheral neuropathy Rapid onset of neurological or

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Diagnosis of poisoning
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In the Living In the Dead

Diagnosis of poisoning

In the Living
History of the case as stated by the patient himself and his/her relatives or friend. Full information about time of onset of the present illness, Initial symptoms, progress, relation with food, condition of other persons taking same food or drink, possible source, any previous history of poisoning, H/o depression, quarrel. Also note down the colour, smell, consistency, taste and quantity of the possible poisonous substance. Symptoms and Signs. Details of examination. Preservation and laboratory investigation of vomitus, excreta, stomach wash, scraps from any

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Diagnosis of poisoning
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In the Dead: History of the case as stated by police or relatives. H/o 2 or more vital points
(1 how long the victim survived after initial symptoms. 2. any treatment).

Post-mortem Examination (external and internal) Chemical Analysis: detection of poison in the body fluids. Preservation of viscera and other

Postmortem Findings in Case Of Death Due To Suspected Poisoning
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External Examination
Postmortem Staining: Deep blue - In case of asphyxiant poisons and aniline. Bright red or cherry red - In case of CO and HCN poisoning. Deep Cyanosis - With opium and cardiac poisons. Early Rigor mortis - With strychnine. Early appearance of the sign of

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Postmortem Findings: External Examination
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Haemorrhagic spots under the skin and mucus membrane: Phosphorus. . Ulceration on lips and near the angles of mouth - Corrosive poisons. Stain near mouth and on hands Nitric acid and copper sulphate. White froth from mouth and nose – Opium and its alkaloids. . Blood tinged froth from mouth and nose Organophosphorus compounds.

Postmortem Findings External Examination

Alopecia, hyper pigmentation and hyperkeratosis - Arsenic poisoning over a long period. Staining, erosion and ulceration near the female external genitalia - Use of abortifacient agents or torturing agents. Injection marks - Injection of poisons (snake bite or otherwise), sign of treatment.

Postmortem Findings in Case Of Death Due To Suspected Poisoning 
Internal findings:

The G.I.T. should be examined very carefully since signs of corrosive or irritant poisons are likely to be find therein. These signs are Hyperemia, Softening, Ulceration and Perforation.
Apart from this below given is a brief note of internal finding in cases of poisoning.

Postmortem Findings Internal findings:

Corrosion, ulceration and desquamation of inner aspects of lips, mucus membrane of mouth and tongue - Corrosive agents. Soft, swollen, sodden, translucent, bleached tongue and mucus membrane of mouth- Corrosive alkali Hardening of mucus membrane -

Postmortem Findings Internal findings:

Bluish discolouration - Copper sulphate Carbonization and charring- Conc. Sulphuric acid Chalky appearance and consistency of teeth - Sulphuric acid Blue lining in the gum - Chronic lead

Postmortem Findings Internal findings:

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Swollen gum, loose teeth, foetid smell Acute mercuric chloride poisoning; chronic phosphorus poisoning Corrosion, irritation, desquamation and haemorrhage in the inner wall of the esophagus - Corrosive and irritant poisons Hardening and whitish discolouration – Carbolic acid poisoning Discoloration and staining of inner aspects of mouth - With coloured poisons

Postmortem Findings Internal findings:
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Stomach Thickening and softening of the wall Corrosive and irritant poisons Hard wall- Carbolic acid Hard and leathery wall- Formaldehyde Hyperemia haemorrhage and desquamation of mucus membrane.Irritant poison Laceration and sloughing – Corrosive poison Perforation - H2SO4 and HN3 Yellowish discolouration of mucus membrane - HNO3; Bluish - CuSO4;

Postmortem Findings Internal findings:
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Stomach Stomach content – Blood - Corrosive and irritant; Yellowish – HNO3 Bluish - CuSO4 Luminous in dark - Phosphorus; Detectable tablet - soneryl; Powder oxalic acid, white arsenic; Detectable smell - kerosene, alcohol, chloroform, organophosphorus compounds, chlorinated hydrocarbons, opium, cyanogen, formaldehyde, phosphorus; Detectable liquid - kerosene.

Postmortem Findings Internal findings:

Small intestine – May show irruption, sometimes may show presence of poisonous remains. Large intestine - May show ulcerations, as in case of HgCI3 similar in appearance of ulcers of bacillary dysentery. It particularly involves the ascending and transverse colons.

Postmortem Findings Internal findings:

Liver – Different degenerative changes occur in cases of poisoning with poisons like phosphorus, carbon tetra-chloride, chloroform, tetrachlorethylene and many other poisons. The type and extent of the degenerative changes occur depending on the type of poison, dose, duration of the exposure and

Postmortem Findings Internal findings:
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Kidneys – Swollen, reddish, soft, sometime greasy in touch with haemorrhage in calyces and other degenerative changes - cases of poisoning with mercury, oxalic and carbolic acid, phosphorus, cantharides, viper snake venom and many others. In case oxalic acid poisoning, white powder of oxalate crystals are

Postmortem Findings Internal findings:

Urinary bladder – Haemorrhage in cases of abrus precatorius, viper snake bite, cantharide poisoning. Larynx and trachea – Hyperaemic, inflamed -In cases of inhalation of irritating gases leaking of corrosive agents while ingestion vomiting; froth in the lumen of trachea and larynx in case of opium and

Postmortem Findings Internal findings:

Chest cavity -Smell of volatile poisons cyanogen, opium etc. can be detected. Lungs - Voluminous, congested, presence of Tardieu's spots - In case of asphyxiants and inhaled poisons. Cut section gives blood stained frothyfluid in case of opium and other asphyxiants. Heart- Presence of subendocardial haemorrhagic spots in cases of arsenic,

Postmortem Findings Internal findings:

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Brain and spinal cord – Congestion and edema of brain and spinal cord in cases of cerebral and spinal poison (e.g. strychnine) Brain – may be congested. oedematous with occasional haemorrhagic points at places in cases of asphyxiant poisons. Uterus and vagina – Staining, congestion haemorrhage,


Preservation of viscera and other materials

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In all cases of poisoning Stomach with its full contents. Half of Liver or 500 gms whichever is more. A loop of Small Intestine. Half of Each kidney. Some portion of Spleen.

In some particular poisons
 Blood 100ml: in cases of absorbed poisons.  Urine 100ml in all cases where blood is        

preserved. Part of both lungs in cases of Volatile poisons. Heart in case of cardiac poisons. Brain in cerebral poisons. Spinal in spinal poisons. Bones in arsenic and lead. Hair in arsenic and copper. Nails in arsenic. Skin-scrap from areas stained with a suspected poison.

Preservative used

For Viscera: absolute alcohol or rectified spirit. Exception: alcohol, chloroform, chloral hydrate, formaldehyde, ether, phosphorus (alcohol prevents the luminosity of phosphorus in dark) etc. Blood should be preserved in fluoride, oxalate, E.D.T.A., gold chloride or citrate.

Management of a case of poisoning

Immediate resuscitative (Basic Management) measures in comatose patient should be adopted to stabilize respiration, circulation and the correct CNS depression.

 Airway: Opening Up and Cleaning the

Airways (oral cavity, Nostrils) of secretions, vomit or any foreign body. Pull Tongue forward  Breathing: Supplemental Oxygen Therapy

Specific Management
 Removal of patient from source     

of exposure. Removal of the unabsorbed poison. Diluting the poison Elimination of absorbed poison Use of specific antidote Symptomatic treatment.

 Removal of patient from source of exposure:

Specific Management

as quickly as possible.  Removal of the unabsorbed poison. In case of contact poison washing of affected area with soap water with gentle rubbing will be helpful. In cases of ingested poisons Gastric lavage is useful within 3 hours of ingestion and is done by stomach tube (Ewald or Boas tube) or by Ryle’s tube followed by emesis (physical or by drugs like Ipecacuanha 1-2 gm, mustard oil 1 Tsf in a glass of water, concentrated salt solution 6%, Zinc Sulfate 12gm in water, apomorphine hcl 1-2ml o 3 mg /ml). In case of injected poison ligature is

Specific Management
 Diluting the poison and delaying the

absorption by water or food.  Elimination of absorbed poison by increases urination (diuresis), increased perspiration (diaphoresis), Dialysis, use of chelating agents.  Use of specific antidote

Counterindications of gastric lavage with stomach tube:
 In corrosive poisons.  Convulsant poisons.  Unconscious or semi-conscious

patients  In infants and children: Ryle’s tube or infant feeding tube is used.

Antidote

Antidotes are substances which counteract the effect of poison. They are divided into Mechanical (physical), Chemical, Physiological and specific receptor antagonists.

Physical or Mechanical Antidote

It prevents the action of poison mechanically, without destroying or inactivating the damaging actions of the poisons. E.g.: Adsorbents like activated charcoal, Demulcents like egg albumin, starch or milk, Diluents like water or milk, bulky food like boiled rice

Chemical Antidotes

They are Substances which disintegrate and inactivate poisons by undergoing chemical reaction with them. E.g.: Weak acids and alkali,

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Physiological Antidote

They have their own action producing signs and symptoms opposite to that produced by the poison. E.g.: Naloxone for morphine, Neostigmine for datura or hyoscin group, Barbiturate for strychnine.

Serological Antidote

Anti-snake venom serum for snake bites poisoning.

Universal Antidote

It is a combination of physical and chemical antidotes. When the exact nature of poison is not known then universal antidote is used which acts against a wide range of poisons. Constituents Activated charcoal 2 parts Magnesium oxide 1 part Tannic acid 1 part Dose 1TSF (15gms) in a glass water (can be repeated)

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Household Antidotes
 Strong liquid tea (contains tannic

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acid) precipitate alkaloid and metallic poisons. Starch for iodine. Milk and raw egg for mercury, arsenic, heavy metal. Flour suspension and mashed potatoes can be used in place of activated charcoal. Milk of magnesia or soap solution for

Chelating Agents
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They are the substances which act on absorbed metallic poisons. They have greater affinity for metals as compared to endogenous enzymes. The complex of agent and metal is more water soluble than metal itself, resulting in  higher renal excretion of the complex.
E.g.: British anti-lewisite (B.A.L., dimercaprol), E.D.T.A. (ethylene diamine acetic acid), Penicillamine (Cuprimine), Desferroxamine etc.

B.A.L. (British AntiLewisite)

It is (2-3 dimercaptopropanol) has 2 unsaturated SH radicals which combines with metal in circulation , thus tissue enzymes are spared. It’s Useful in cases of Arsenic, mercury, copper, bismuth, gold etc
Dose: 3-4 mg/kg BW as a preparation of 10% with 20% Benzyl benzoate in arachis oil given deep intra-muscular (may cause embolism on

It combines with (Na+) sodium to form  sodium salt and then with (Ca++) calcium to form disodium calcium edentate which combines with free metal and  inactivates it biologically. It is best chelate for lead.

E.D.T.A. (Ethylene diamine tetra-acetic acid)

Penicillamine

It has stable SH radical which combines with free metal. Dose:
30mg/Kg BW/Day in 4 divide doses for 7 days.

Desferroxamine

It is specific antidote for iron. Dose: 8-12 gm orally. For absorbed iron 2gm I.V. with 50% laevulose solution.

 Try to save the life of the patient and give

Duties of a Registered Medical Practitioner in connection with poisoning cases
emergency necessary treatment.

 If necessary, the patient should be sent to a

better hospital, if possible a government hospital, if the condition of the patients demands and permits the shift. when and how the symptoms started, what is the progress; whether related to taking of any food or drink ; whether the number of sufferer is more

 Take a detailed history of the case as to

Duties of a Registered Medical Practitioner
 The doctor should himself record full

history of the case, the signs and symptoms and progress.

The doctor should collect and preserve the vomitus, stool, urine, clothes stained with poison or vomitus, doubtful container with remaining part of the poison, if any, and if necessary blood, for laboratory investigations.

Duties of a Registered Medical Practitioner

The doctor should inform the police station of the area about the case irrespective of whether the patient survives or dies and whether it appears to be a case of suicide or homicide or accident.. If death is apprehended then arrangement for recording dying declaration should be made.

COMMON POISONS AND DRUGS
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Corrosive poisons Irritant poisons Analgesic, Hypnotic, Tranquilliser, and Narcotic poisons. Stimulants, Excitants, and Convulsants poisons. Paralytic, Anticholinesterase and Antihistamine poisons. Gaseous and Volatile poisons. Industrial gaseous and Volatile poisons Poisons by Plants, flora, and fungi.

Corrosive Poisons

Inorganic Acids and alkalis. Organic Acids. Oxalic, Carbolic and Chromic Acids. Metallic Salt Corrosives.

Irritant Poisons

Metallic ( Arsenic, Antimony, Mercury, Lead, Copper, Zinc, etc.). Non-Metallic (phosphorus, etc.) Insecticides and Herbicides.

Analgesic (Aspirin, Antipyrin, Chloral, Paracetamol, etc.). Barbiturates. Glutethmides and Ureides, Tranquillisers. Opium, Morphine, Cannabis, and Synthetic

Analgesic, Hypnotic, Tranquilliser, and Narcotic Poisons.

Stimulants, Excitants, and Convulsants Poisons.
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Amphetamines. Atropine . Hyoscine . Camphor Cocaine Strychnine Aconite Veratrine, Picrotoxin, etc

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Coniine Curare Nicotine Anticholinesterases Antihistamines

Paralytic, Anticholinesterase and Antihistamine poisons

Gaseous and Volatile poisons
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Domestic. Ammonia fumes. Hydrocyanic acid. Carbon dioxide. Carbon monoxide. Alcohols. Glycols.

Industrial gaseous and Volatile poisons
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Sulphuric gases. Carbon bisulphide. Petroleum distillates. Aromatic compounds. Chlorinated hydrocarbons. ‘Glue-sniffing’

Poisons by Plants, flora, and fungi
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Waterside Country Town

Food Poisoning

The bacterial food poisoning should be clearly distinguished from toxic reaction due to: Contaminant Metals such as Arsenic, Lead, or Tin. Toxic Vegetable and Substances such as Muscarine or Amanitin from Fungi or Myelotoxin from Mussels. Allergic Reaction to food.

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Corrosive Poisons
  

Acids Acids-mineral, such as Hcl, HNO3, H2SO4 or HF and flourides; or organic, such as Oxalic, Acetic and Carbolic Acid (phenol), Cresols such as a Lysol. Alkalis-caustics such as NaOH (lye), KOH, CaOH (lime), Amonia, the alkaline or chlorinated household bleashes and detergents. Heavy metal salts-chlorides of Sb, Zn, or

Corrosive Poisons

Caustic substances (strong acids and alkalies), when swallowed,  can burn the tongue, mouth, esophagus, and stomach. These burns  may cause perforation (piercing) of the esophagus or stomach. Food and saliva leaking from a perforation  cause severe, sometimes deadly infection within the chest (mediastinitis or empyema) or abdomen (peritonitis). Burns that do not perforate can  result in scarring of the esophagus and stomach.

Corrosive Poisons

Industrial products are usually the most damaging because they are highly concentrated. However, some common household products, including drain and toilet bowl cleaners and some dishwasher detergents, contain damaging caustic substances, such as sodium hydroxide and sulfuric acid. Caustic substances are available as solids

Symptoms of Corrosive Poisons Pain in the mouth and throat develops rapidly,

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usually within minutes, and can be severe, particularly with swallowing. Coughing, drooling, an inability to swallow, and shortness of breath may occur. In severe cases involving strong caustic substances, a person may develop very low blood pressure (shock), difficulty breathing, or chest pain, possibly leading to death. Perforation of the esophagus or stomach may

Symptoms of Corrosive Poisons
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The esophagus may perforate into the area between the lungs (the mediastinum) or into the area surrounding the lungs (the pleural cavity).  Either circumstance causes chest pain, fever, rapid heart rate, very low blood pressure, and the development of an abscess that requires surgery. Peritonitis results in  severe abdominal pain. Scarring of the esophagus results in narrowing  (stricture), which causes difficulty in swallowing.

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an endoscope down the esophagus to look for burns, The extent of damage determines treatment. People with severe burns sometimes need immediate surgery . Corticosteroids and antibiotics are used to try to prevent strictures and infections. a person who has swallowed a caustic substance should not be made to vomit. If burns are mild, the person may be encouraged to begin drinking fluids fairly soon during recovery. Otherwise, fluids are given intravenously until drinking is possible. If strictures develop, a bypass tube may be placed in

Diagnosis and Treatment of Corrosive Poisons

the narrowed portion of the esophagus to prevent esophageal closure and

Irritant Poisons
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Metallic Irritant Arsenic
as the metal itself is not poisonous but its salts, called arsenites, are. Arsenic gas (AsH3) is poisonous also. White arsenic powder is highly soluble in hot liquids; it is almost tasteless, colourless and odourless in solution. Arsenic is still used in agriculture (sheepdips) and industry but weed-killers and

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Arsenical poisoning

The principal effects of poisoning are produced by combination of the poison with sulphhydryl (SH) enzymes. There are differences in acute and chronic arsenical poisoning.

Acute Arsenic poisoning

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Acute poisoning mimics cholera; there are signs of gastro-enteritis with abdominal pain, vomiting and diarrhoea, Dehydration and electrolyte imbalance lead to  cardiovascular failure and death.

chronic Arsenic poisoning poisoning The victim of chronic Arsenic

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may be suspected of suffering from some wasting systemic illness. The symptoms are the loss of appetite and weight, anaemia, mild nausea and skin changes, which are probably, more specific. Chronic arsenical poisoning causes a hyperkeratosis of the palms of hands, "raindrop" skin pigmentation,

Postmortem finding Arsenic poisoning
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At autopsy, in acute deaths only haemorrhagic gastritis can be found. The stomach mucosa is oedematous with bleeding along the top ridges of the folds ('red velvet' mucosa). In chronic poisoning there are degenerative changes in the liver, myocardium and the kidneys, stomach may show the signs of a chronic gastritis with excess mucus and patchy erosion.

Treatment of Arsenic poisoning
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In acute: gastric lavage Ferric hydroxide (precipitate any poison remaining in stomach) Antidote is BAL (greater affinity with sulphhydryl enzymes), as early as possible. In chronic ; Removed from the source BAL Hospital admitted.

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Mercury poisoning

is an industrial poison but previously it was used in the treatment of syphilis, as a protection from rheumatism (quicksilver was carried in the pocket) and as a diuretic. The symptoms and signs of acute poisoning are gastrointestinal, excess salivation and renal failure. Chronic poisoning leads to black gums, salivation, mandibular necrosis and encephalopathy. Antidote is Sodium Fomaldehyde Sulphoxylate.

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Iron poisoning

is best known for cases of acute poisoning in children who eat ferrous sulphate (attractivelooking tablets prescribed for anaemia). Gastrointestinal symptoms occur soon after ingestion, even 3-5 tablets may be sufficient for death to occur. This happens due to the liver damage and acidosis from release of free iron into the circulation, because the trasferrin system that binds iron to protein is overloaded. Antidote is desferrioxamine

Lead Poisoning
  

Although it is far less common since paint containing lead pigment was banned in 1977 and lead was eliminated from most gasoline, lead poisoning (plumbism) is still a major public health problem in U.S. cities on the East Coast. Workers in industries that handle lead are at risk of lead poisoning, as are children who live in older houses that contain peeling lead paint or lead pipes. Young children may eat enough paint chips to develop symptoms of lead poisoning. Lead affects many parts of the body, including the brain, nerves, kidneys, liver, blood, digestive tract, and sex organs.

Symptoms and Diagnosis of Lead Poisoning 
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Symptoms that do occur usually develop over several weeks or longer. Typical symptoms of lead poisoning include personality changes, headaches, loss of sensation, weakness, a metallic taste in the mouth, uncoordinated walking, poor appetite, vomiting, constipation, crampy abdominal pain, bone or joint pains, and anemia. Kidney damage often develops without symptoms.

Symptoms and Diagnosis of Lead Poisoning

Young children may become cranky and play less frequently . Encephalopathy can then begin suddenly and worsen over the next several days, resulting in persistent, forceful vomiting; confusion; sleepiness; and, finally, seizures and coma. Adults often develop loss of sex drive, infertility, and, in men, impotence. Encephalopathy rarely develops in adults. Lead poisoning is diagnosed with a blood test. In children, bone and abdominal x-rays often

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Treatment of Lead
Poisoning

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People with more serious lead poisoning are treated in the hospital with injections of chelating drugs, such as BAL, Penicillamine, and edetate calcium disodium. Because chelating drugs also can remove beneficial minerals, such as zinc, copper, and iron, from the body, the person often is given supplements of these minerals.

NON-METALLIC IRRITANTS Cyanides
 

Cyanides are extremely poisonous. Potassium and sodium cyanides need to be mixed with water or gastric acid before releasing free cyanide that acts as a cytochrome oxidase inhibitor. Cyanides are used as a wasp killer and in some laboratory techniques. Death is usually rapid but some victims have known to survive.  

NON-METALLIC IRRITANTS Cyanides
 

At autopsy, the smell of cyanide - bitter almonds may be obvious (but ~ 40% of people can not smell it); the organs will be dark red and congested. The oesophagus, in a case of swallowed cyanide, will be black due to erosion and haemorrhage. The skin in the areas of hypostasis will be of a purplish-pink colour due to

Alcohol
 

Alcohols: a group of organic liquids which have a particular chemical grouping (OH). Named according to the length of the carbon backbone

Methanol (methyl alcohol) Ethanol (ethyl alcohol) = "alcohol" ! Propanol (propyl alcohol) Butanol (butyl alcohol)

ABSORPTION OF ALCOHOL  Blood Alcohol Concentration (BAC);
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Urinary Alcohol Concentration (UAC); Vitreous Humour Alcohol Concentration (VHAC); Breath Alcohol Concentration (Br AC). 20% of ingested alcohol absorbed in the stomach 80% absorbed in the upper small intestine. Absorption is most rapid when the stomach is empty Absorption is generally complete in one to three hours.

ALCOHOL

The Widmark equation gives a rough estimate of peak BAC expected following ingestion of a known amount of alcohol. Peak BAC = Weight of alcohol ingested (g) x 100, divided by Body Weight (kg) x Widmark Factor

ELIMINATION OF ALCOHOL
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Alcohol is eliminated through all bodily routes of excretion. 5% is excreted in the breath; 5% in the urine 90% broken down in the body, mostly in the liver, by liver enzymes including hepatic alcohol dehydrogenase (Alc DH). Oxidation of the products (acetaldehyde and acetic acid) finally yields carbon dioxide (CO2) and water H2O.

Clinical Features of Alcohol Intake:
1. Acute alcohol intoxication 2. Pathological intoxication 3. Alcohol abuse 4. Alcohol dependence 5. Alcohol withdrawal: a) uncomplicated b) alcohol withdrawal fits c) alcohol withdrawal delerium d) Wernicke's encephalopathy e) Korsakoff syndrome f) alcoholic hallucinosis

1. Acute alcohol intoxication

Alcohol is a nervous system depressant. Stages of Intoxication 1. Excitement (<100) 2. Confusion (100-200) 3. Stupor (>200)

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Recovery

Recovery is in three phases

1) Drying out period of 1-10 days 2) Physical rehabilitation over 10 days to 2 months 3) Personality recovery takes months or years

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Physical, Psychological and Social complications are not confined to alcoholics, they can affect any individual who drinks heavily for a prolonged period

COMPLICATIONS OF EXCESSIVE ALCOHOL INTAKE

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a) Physical 1. Gastro-intestinal tract: oesophagitis, gastritis, duodenitis, peptic ulcer, small bowel malabsorption acute and chronic pancreatitis 2. Liver: fatty liver; alcoholic heptatitis; alcoholic cirrhosis. 3. Cardiovascular System: hypertension; cardiomyopathy and wet

COMPLICATIONS OF EXCESSIVE ALCOHOL INTAKE

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COMPLICATIONS OF EXCESSIVE ALCOHOL INTAKE a) Physical

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4. Central Nervous System: cerebral atrophy (alcoholic dementia); Wernicke-Korsakoff Syndrome due to thiamine (vitamin B deficiency); cerebellar degeneration, central pontine myelinosis, and peripheral neuropathy. 5. Metabolic Effects: imbalance of metabolism of many bodily compounds including glucose, uric acid, phosphate, magnesium, potassium, fats and proteins. 6. Endocrine Effects: male impotence; female infertility. 7. Others: Severe bruising of various ages due

b) Psychological Anxiety, depression, high suicide risk, dementia, pathological jealousy, alcoholic hallucinosis, sexual dysfunction. c) Social Marital & family problems, including domestic violence ,Work problems, unemploymentRoad accidents and crime.

COMPLICATIONS OF EXCESSIVE ALCOHOL INTAKE

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CAUSES OF DEATH IN CHRONIC ALCOHOLICS (Clark, 1988)
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1. Trauma. The largest group (26%). Fire deaths were the most common. Drunken falls were frequently followed by fatal head injury. Murder, Road traffic accidents (pedestrians), Drowning, Railway line accidents, Accidental poisonings, and Accidental hangings

CAUSES OF DEATH IN CHRONIC ALCOHOLICS
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Hypothermia 2. Incidental Natural Disease (25%). Ischaemic heart disease, cerebral haemorrhage, chronic obstructive airways disease and malignancy. 3. Alcohol Related Disease (22%). Bronchopneumonia and lobar pneumonia are the commonest. Cirrhosis of the liver due to ruptured varices or hepatic failure

CAUSES OF DEATH IN CHRONIC ALCOHOLICS

4. Acute Intoxication (24%). Simple intoxication causing respiratory depression 5.'Obscure' cause of Death

DRUG RELATED DEATHS & DRUG ABUSE
 

There is a spectrum of drug use, mis-use and abuse. The 6 main classes of misused drugs are : Opiates (morphine, heroin, methadone, dihydrocodeine) Depressants (barbiturates) Minor tranquilisers (benzodiazepines, e.g. Diazepam (Valium), Temazepam) Stimulants (cocaine, amphetamines, Ecstasy, ADAM, EVE, ICE) Hallucinogens (LSD, magic mushrooms,

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BENZODIAZEPINES
  3. 4. 5. 6. 7. 8. 9. 10. 11.

Acute intoxication Psychological: Relief of anxiety, Relaxation Impaired memory Paradoxical aggression Uncharacteristic criminal behaviour (shoplifting & indecent exposure) Uncontrollable emotions (giggling & weeping) 'Hangover' with drowsiness, inability to concentrate & impairment of skilled tasks Effects are potentiated by alcohol

BENZODIAZEPINES
  3. 4. 5. 6. 7. 8. 9.

Acute intoxication Physical: Dizziness, sedation, Incoordination Sexual dysfunction, weight gain Hypotension & coma with high dose

BENZODIAZEPINES
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Chronic effects: Tolerance Physical & psychological dependence A state of chronic intoxication with slurred speech, poor concentration, impaired comprehension, impaired memory, emotional liability, Irritability and depressed mood.

AMPHETAMINES

Amphetamines are synthetic stimulants. Their use is popular in rave culture. Amphetamines act by stimulating the release of catecholamines, particularly adrenaline within the body.

AMPHETAMINES
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Acute intoxication: Psychological Euphoria, self-confidence and self-esteem Feeling of calm, peace and friendliness towards strangers (the 'hug drug'), Heightened sense of awareness & concentration Increased energy, desire and ability to dance for long periods Irritability & restlessness Irrational behaviour, confusion Hallucinations Delusions, paranoia, psychosis Psychological dependence

AMPHETAMINES
Acute intoxication  Physical: 3. Tachycardia (fast pulse), 4. hypertension (high blood pressure), 5. Tachypnea (breathing) 6. Loss of appetite 7. Dilated pupils 8. Brisk reflexes 9. Dry mouth, sweating, 10. blurred vision, dizziness, flushing or pallor 11. Teeth grinding (bruxism), repetitive actions (stereotypy)

AMPHETAMINES
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Acute adverse affects Disturbances in the electrical rhythm of the heart (cardiac arrhythmias) Stroke due to elevated blood pressure bursting a blood vessel within the brain itself (intracerebral haemorrhage) on the surface of the brain (subarachnoid haemorrhage). Severe disturbance in the blood clotting mechanisms (DIC) Acute paranoid psychosis Hyperpyrexia): heat production by amphetamines

Chronic adverse effects 2. Chest pains 3. & muscle spasms 4. Anorexia, 5. malnutrition 6. & weight loss 7. Diarrhoea & vomiting 8. Damage to the heart muscle (cardiomyopathy) 9. Aggression, fatigue & insomnia 10. Depression 11. Chronic paranoid psychosis, schizophrenia
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AMPHETAMINES

Psychological dependence leads to anxiety, depression, disturbed sleep and irritability on cessation

COCAINE
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Acute intoxication: Short acting & dose dependent. It causes the body to secrete adrenaline in a similar fashion to amphetamines but the detrimental and pleasurable effects are more florid.

COCAINE
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Physical: Tachycardia, hypertension, Tachypnea Dilated pupils, Increased mental excitement Hyperpyrexia,

COCAINE
 2. 3. 4. 5. 6. 7.

Psychological: Euphoria & well-being Irritability & confusion Hallucinations, formication (sensation of insects crawling under the skin) Depression, paranoia as effects wear off

COCAINE
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Chronic effects & External signs of cocaine abuse: Intense psychological dependence Chest pains, muscle spasms Weight loss Male impotence & female orgasm problems Nasal septum may become ulcerated and perforated due to ischaemia and blood vessel spasm. Eyes may exhibit "crack keratitis" due to the local anaesthetic effect allows excessive rubbing of the eyes.

COCAINE

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Cocaine has serious detrimental effects both acutely and chronically on the coronary arteries, heart muscle and central nervous system

COCAINE

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The coronary arteries Proliferation and thickening of the inner lining reduces blood flow. Premature hardening and narrowing (atherosclerosis). (myocardial infarction) Increased incidence of coronary artery thrombosis & myocardial infarction).

COCAINE
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The heart muscle myocarditis. cardiomyopathy. As a result of this myocardial damage there is a risk of sudden death due to cardiac arrhythmia which is most likely to occur during acute intoxication

COCAINE
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Brain: Stroke, due to hypertensive blood vessel rupture within the brain (intracerebral haemorrhage) or on the surface of the brain (subarachnoid haemorrhage). In addition blood vessels may undergo spasm, causing ischaemic

Causes of Cocaine-Induced Death
 2. 3. 4. 5. 6. 

causes of cocaine-induced death are: convulsions, respiratory arrest, cardiac arrhythmia and coronary artery spasm and stroke. Although cocaine itself is quite short lived in the body it can be detected in the brain and blood within a short time of a hit and its metabolites are detectable for longer periods in nasal swabs, urine, hair and saliva.

OPIATE ABUSE
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Main drugs: Morphine Heroin (Diamorphine) Methadone Dipipanone (Diaconal ), Pethidine, Pentazocine (Foetal ), Buprenorphine (Temgesic) Medical uses are pain relief (analgesia), cough suppressants & antidiarrhoeal agents.

OPIATE ABUSE

Acute intoxication: Psychological: Rush of euphoria & contentment Relief of anxiety, inability to concentrate Physical: Constricted pupils Suppression of cough reflex Nausea & vomiting Decreased heart & breathing rate Unconsciousness, respiratory arrest and death Fatal reaction to impurities

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OPIATE ABUSE

Chronic effects: Tolerance Physical & psychological dependence Constipation Loss of libido Complications of intravenous injection

OPIATE ABUSE

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withdrawal syndrome
Symptoms (easily fabricated by the addict wanting more drugs): Craving for the drug, Anxiety, restlessness, irritability, insomnia Alternate sweating and shivering Generalised aches Pains and cramps in the back,

OPIATE ABUSE

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withdrawal syndrome

Physical signs: Dilated pupils Watering of the eyes (lacrimation), Yawning, Tachycardia, hypertension Cold clammy skin with goose flesh Loudly audible bowel sounds (borborygmy) Diarrhoea. Treatment with regular Diazepam & Lomotil (Diphenoxylate & Atropine) is often

OPIATE ABUSE

A similar withdrawal syndrome is seen on stopping benzodiazapines. Methadone treatment programs are aimed at reducing intravenous opiate abuse

OPIATE ABUSE
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Local complications of injecting Skin abscesses and ulceration Skin scarring and the needle track marks Fat necrosis due to injection beneath the skin Myositis (inflammation of the muscle) Thrombosis following repeated injection into veins Lymph channels become blocked and

OPIATE ABUSE

General complications of injecting Pulmonary granulomas (foreign body granulomas). Liver granulomas. Blood vessel and nerve cell damage in the brain. Infections Hepatitis B infection and HIV

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Thanks for attention