Philippus Aureolus Theophrastus Bombastus von Hohenheim

Also known as Paracelsus which means equal or greater than Celsus

Paracelsus wrote

"All things are poison, and nothing is without poison; only the dose permits something not to be poisonous."

PARACELSUS
The Father of Toxicology He is the one who started the field of toxicology in the sixteenth century.

DEFINITION OF TERMS

DEFINITON OF TERMS
TOXICOLOGY
Science of poison science of poison that deals with origin, properties, physiologic action and symptoms. lethal doses, proper antidotes, specific identification and quantitative determination, evaluation and interpretation of these analytical results

DEFINITON OF TERMS
Toxicology is divided now to three subfields which includes: INDUSTRIAL TOXICOLOGY
a science that deals with potential harmful effects of materials, products and wastes on health and environments.

CLINICAL TOXICOLOGY
Deals with human diseases caused by, or associated with abnormal exposure to chemical substances.

FORENSIC TOXICOLOGY
The science of detecting and identifying the presence of drugs and poisons in body fluids, tissues, and organs.

DEFINITON OF TERMS
POISON
any substances applied to the body, ingested, inhaled or developed within the body that causes or may cause damage or disturbance of function

TREATMENT
management and care of patient's condition, overcoming or combating a disorder

SYMPTOMS
An evidence of disease or of patients' condition a change in patient's condition indicative of some bodily or mental state

DEFINITON OF TERMS
THERAPEUTIC
Science or act of healing or scientific account of the treatment of disease

TOXICITY
ability of a chemical to cause injury or interfere with the normal processes of an organisms

POISONING
morbid condition produced by a poison

DEFINITON OF TERMS
POSOLOGY
the form and quantity of medicine to be administered at one time or within a certain period

DOSE
quantity of medicine to be administered at one time or within a certain period.

MINIMUM DOSE
smallest dose that produces therapeutic effects or beneficial action upon a sick person.

DEFINITON OF TERMS
AVERAGE DOSE OR CUSTOMARY DOSE
dose that may be expected ordinarily to produce the therapeutic effects for which the preparation is employed

MAXlMUM DOSE
largest amount which can be safely used in ordinary cases

TOXIC DOSE or POISONOUS DOSE

dose that is harmful to both the healthy and sick but is not fatal

DEFINITON OF TERMS
LETHAL DOSE or FATAL DOSE
dose which kills or dose which is just sufficient to cause death

MEDIAN LETHAL DOSE (LD50)

dose which kills 50% of a group of test animals or tested on 50 animals

DEFINITON OF TERMS
RIGOR MORTIS or CADAVERC RIGIDITY
Stiffening of the muscles of the body throughout its entire extent and probably due to he coagulation of myosin in the muscles which usually takes place within 6 hours or less after death. Its duration is from 16 to 24 hours until putrefaction sets in. Heat shortens and cold prolongs rigor mortis It begins in the muscles of the eyes then affects the muscles of the lower jaw and neck, chest and upper extremities and lastly the muscles of the abdomen and the lower extremities.

DEFINITON OF TERMS
COMA
state of profound insensibility

SYNCOPE
suspended animation due to failure in the heart action

ASPHYXIA
Condition of more or less complete suspension of respiration

ORIGIN OF POISON

ORIGIN OF POISON
1. Plants
morphine, atropine, nicotine, aconitine

2. Animal
snake venom, epinephrine, insulin

3. Minerals
arsenic, mercury, lead, bismuth

4. Synthetic
barbiturates. Antihistamines

ORIGIN OF POISON - PLANTS

PLANTS BETEL NUT CALABAR BEAN SANTONICA BELLADONNA POISONS ARECOLINE PHYSOSTIGMINE SANTONINE ATROPINE

ORIGIN OF POISON - PLANTS

PLANTS BITTER BARK TOBACCO NUX VOMICA AMANITA POISONS QUININE NICOTINE BRUCINE, STRYCHNINE MUSCARINE

ORIGIN OF POISON - PLANTS

PLANTS ACONITE DEATH ANGEL FOX GLOVE CASSAVA POISONS CONIINE PHALLOIDINE DIGITOXIN MANIHOTOXIN

ORIGIN OF POISON - PLANTS

PLANTS FISH BERRIES MARIJUANA JEQUIRITY SEEDS CASTOR CARAMBOLA/STAR FRUIT POISONS PICROTOXIN CANNABINOL (THC) ABRIN RICIN OXALIC ACID

ORIGIN OF POISON - ANIMALS

ANIMALS SNAKES RED ANTS RUSSIAN OR SPANISH FLY OYSTERS FROGS POISONS HYALURONIDASE FORMIC ACID CANTHARADIN

CLUPEOTOXIN BUFOTOXIN

ORIGIN OF POISON - ANIMALS

ANIMALS
MACKEREL SARDINES TUNA INEDIBLE ORGANS OF FISH PUFFER FISH SCORPION

POISONS
GEMBLID VENERUPIN SAURINE CIGUATOXIN TETRODOTOXIN 5-HYDROXY-TRYPTAMINE

GOLDEN POISON FROG BATRACHOTOXIN

PUFFER FISH TETRODOTOXIN

ORIGIN OF POISON MICROBIAL

MICROBIAL SOURCE POISON OR DISEASE REMARKS

MOSTLY GRAM (-)

ENDOTOXINS

Salmonella typhosa Proteus species

Typhoid Proteus

Lipoidal, low toxicity at high dose become lethal Causes typhoid fever Typhoid

ORIGIN OF POISON MICROBIAL

MICROBIAL SOURCE POISON OR DISEASE REMARKS

MOSTLY GRAM (+)

EXOTOXINS

Clostridium botulinum Clostridium tetani Clostridium perfringens

Botulinum toxin

tetanospasmin Cytotoxin

Proteinaceous, at some doses it has the ability to cause disease and sometimes lethal Neuromuscular poison, from spoiled canned food Caused tetany Causes gas gangrene

Gas gangrene

Muscular tetany

ORIGIN OF POISON MICROBIAL

MICROBIAL SOURCE POISON OR DISEASE REMARKS

Staphylococcus aureus

Staphylococcus aureus

Corynebacterium diptheriae

Vibrio cholerae

Most common cause of food poisoning. Heat stable and can lead TOXIC SHOCK SYDROME Diphtheria cytotoxin Protein synthesis inhibitors esp. in nerves, heart and kidney cells. Cholera enterotoxin Rice watery stool

ORIGIN OF POISON MICROBIAL

MICROBIAL SOURCE
Escherichia coli

POISON OR DISEASE
Escherichia enterotoxin

REMARKS
Travelers diarrhea

Dinoflagellates

Saxitoxin

Aspergillus Flavus

Aflatoxin

RED TIDE poisoning, paralytic shellfish poisoning Found in STALE PEANUTS, carcinogenic

ORIGIN OF POISON MICROBIAL

MICROBIAL SOURCE
Aspergillus flavus

POISON OR DISEASE
Aflatoxin

REMARKS
Found in stale peanuts, carcinogenic Spoiled food Stale milk and dairy products Ergotism

Bacterial putrefaction Bacterial putrefaction Claviceps purpurea

Ptomaine Tyrotoxicon Ergot

ORIGIN OF POISON - MINERALS

SOURCE SYNONYMS REMARKS

Phenol

Carbolic acid

Nitric acid Acetic acid

Aqua fortis, Engravers acid Glacial acetic acid, vinegar

WHITISH BLEACHING burns, denatures and precipitates proteins Nitration, causes yellow stain Mouth scalded appearance, odor of vinegar

WHITISH BLEACHING BURNS CAUSED BY PHENOL

YELLOW STAIN ON SKIN CAUSED BY NITRIC ACID

MOUTH SCALDED APPEARANCE CAUSED BY ACETIC ACID

ORIGIN OF POISON - MINERALS

SOURCE SYNONYMS REMARKS

Sulfuric acid

Oil of vitriol

GROUND COFFEE VOMITUS severe corrosion with blackening

SEVERE CORROSION WITHOUT BLACKENING, acid penetrating odor Saponification effects on lipids and dehydrating action on tissue cells which become gelatinous Same as NaOH

Hydrochloric acid

Muriatic acid, spirits of salt Caustic soda, lye

Sodium hydroxide

Potassium hydroxide

Caustic potash

EFFECT OF KOH and NaOH ON SKIN

ORIGIN OF POISON - SYNTHETIC

SOURCE Aluminum Eosin Methanol Formaldehyde SYNONYMS REMARKS Found in deodorant product, tawas Lipsticks Permanent blindness Protein precipitant, coagulation of albumin, hardening of tissue Crude oil, very toxic (120ml)

Wood alcohol, denatured alcohol Formalin

Isopropyl alcohol

Rubbing alcohol

ORIGIN OF POISON - SYNTHETIC

SOURCE Phencyclidine (PCP) Asbestos SYNONYMS Angel dust REMARKS Psychedelic, hallucinogen, causes hypersalivation Fire retardant, fire proof clothing of firemen, causes ASBESTOSIS and lung CA

Carbon tetrachloride
Naphthalene

Tetrachlorometh Decomposes to PHOSGENE ane + HCL. Causes cellular necrosis in kidney and liver Moth balls, tar Hemolysis of glucose-6camphor phosphate dehydrogenase

This is a 4-year old boy diagnosed with Glucose-6phosphate Dehydrogenase Deficiency showing Jaundice in the sclera

ORIGIN OF POISON - SYNTHETIC

SOURCE Hydrogen sulfide SYNONYMS Stink damp, sulfur hydride, sulfurated hydrogen REMARKS Colorless gas with rotten egg odor, causes gas eyes for SEWER WORKERS inhibition of cytochrome oxidase leading to ANOXIA. Antifreeze liquid

Ethylene glycol

Chloral hydrate

Knock out drops

Odor of pear or banana causes sedation or hypnotics

CNS stimulant

Amphetamine

PEP pills , coke

I live smelling death, but it is fine. Rewa Ram, sewer worker

ORIGIN OF POISON - SYNTHETIC

SOURCE
Carbon disulfide Picric acid Aniline trinitrophenol Blue oil

SYNONYMS

REMARKS
Decomposition of RBC Colorant in textile industries Methemoglobinemia (changes RBC to chocolate brown) Same effect with aniline Obtained from ergot causes hallucination

Nitrobenzene

LSD (Lysergic acid diethylamide)

Essence of mirbane/ oil of mirbane Morning glory

CLASSIFICATION OF POISON

CLASSIFICATION OF POISON
According to characteristics effects or properties
A. CORROSIVE POISONS Physically damages flesh ex. Strong acids (HNO3, H2SO4, HCl) strong bases (NaOH, KOH) B. SYSTEMIC POISONS Effect is not localized in one spot but spread to all body systems in varying degress. Ex. mercury C. BIOLOGICAL POISONS Contact or absorption of poisons can cause rapid death or impairment. Ex. Nerve gas

CLASSIFICATION OF POISON
According to autenrieth classification
A. Volatile poisons
Examples: camphor, eucalyptus, turpentine Example: cyanide Example: lead, mercury, arsenic, and cadmium.

B. Non-volatile poisons C. Metallic poisons

CLASSIFICATION OF POISON
According physiological classification A. Corrosive poisons B. Irritants
Irritants are chemicals that can cause a reversible inflammation of your nasal passages, tear ducts, or skin.

C. Asphyxiants
Substance capable of reducing the level of oxygen in the body to dangerous levels

D. Anesthetics and narcotics

CLASSIFICATION OF POISON
According physiological classification E. Neurotic poisons
Neurotic poisons either produce stupor or otherwise damage the nervous. Ex. chloroform

F. Tetanics G. Deliriant
substances that may impair the intellect, memory and concentration

H. Depressants or sedatives I. Asthenic or exhaustives

Produce exhaustion and caused by marked loose of muscle powers

CLASSIFICATION OF POISON
CHEMICAL CLASSIFICATION
A. INORGANIC Volatile non metallic, metallic poisons, mineral acids mineral alkalis.

A. ORGANIC

Volatile organic poisons, alkaloids, animal poisons, bacterial, glucosides, organic acids.

EFFECTS OF POISONS
A. LOCAL EFFECTS
refers to an adverse health effect that takes place at the point or area of contact. The site may be skin, mucous membranes, the respiratory tract, gastrointestinal system, eyes, etc. Absorption does not necessarily occur. Examples: strong acids or alkalis.

B. REMOTE EFFECTS C. COMBINED EFFECTS

ORGANIC POISONS

ORGANIC POISONS
POISON Boric acid Aspartame Saccharin BHA/BHT Nitrite REMARKS Causes the boiled lobster appearance, used in astringent preparation Artificial sweetener Artificial sweetener Carcinogenic anti-oxidant Food preservatives

BOILED LOBSTER APPEARANCE

ORGANIC POISONS
POISON
Tannic acids Monomethyl hydrazine Tartrazine Potassium bromate

REMARKS
Carcinogen found in iced tea From poisonous mushroom Gyromitra esculenta Food colorant Found in cold wave neutralizers, dough improver

INORGANIC POISON
POISON Arsenic (As) Manganese (Mn) Osmium (Os) Lithium (Li) Gold (Au) REMARKS Used in the manufacture of insecticides Used as a cofactor in enzymatic reaction Densest metal, used in the preparation of slides for electron microscope Used in the treatment of mania Used in the treatment of lupus erythematosus and act as antiinflammatory agent.

INORGANIC POISON
POISON
Lead (Pb) Aluminum (Al)

REMARKS
Causes plumbism Causes shavers disease 3rd most abundant element on earths crust Has constipating and astringent effects. Glucose tolerance factor Toxicity resembles DM Used in bacterial fixation of atmospheric nitrogen Causes Wilson's disease. Used in water purification

Chromium (Cr) Molybdenum (Mo) Copper (Cu)

BAUXITE ROCK

A KAYSER-FLEISCHER RING (THE BROWN RING ON THE EDGE OF THE IRIS) IS COMMON IN WILSON'S DISEASE, ESPECIALLY WHEN NEUROLOGICAL SYMPTOMS ARE PRESENT

INORGANIC POISON
POISON
Magnesium (Mg) Iron (Fe) Nickel (Ni)

REMARKS
Second most abundant intracellular cation Possess cathartic and anticonvulsive activities Hematinic Causes contact dermatitis Most powerful inorganic carcinogen Produced in fossil fuel combustion. Causes iodinism signs of iodinism include lacrimation, salivation, increased respiratory secretions, coughing, inappetence, dry scaly skin, and tachycardia. Found in canned milk and other canned product

Iodine (I)

Tin (Sn)

INORGANIC POISON
POISON
Boron (B) Beryllium (Be)

REMARKS

Used in the vulcanizing of rubber Most toxic metal Found in fluorescent and neon lamps Cadmium (Cd) Metal responsible for itai-itai poisoning Found in smoke/stink bombs and solder and anti-dandruff shampoo. Chlorine (Cl) Tear gas, used in water purification Phosphorous (P) Used as rat poison. Found in matches and firecrackers Produced lucifers law and also known as St. Elmos fire

Itai-itai disease induced by long-term Cadmium-exposure It is also known as ouch ouch sickness SOURCE: Mining in Toyama Prefecture Manifested by severe pain in joints and spine

St. Elmos fire

INORGANIC POISON
POISON
Bromine (Br)

REMARKS
Dark brownish volatile liquids with suffocating odor Causes brominism Causes fluorosis in children Found in drinking supplies and tooth paste Causes baratosis Found in depilatories and green colored fire works Also known as quick silver Causes minamata disease, hydraryism Found in thermometer and merthiolate

Flourine (F) Barium (Ba)

Mercury (Hg)

A MILD CASE OF DENTAL FLUOROSIS (THE WHITE STREAKS ON THE SUBJECT'S UPPER RIGHT CENTRAL INCISOR) OBSERVED IN DENTAL PRACTICE

A SEVERE CASE OF DENTAL FLUOROSIS, OR "MOTTLED DENTAL ENAMEL."

THE CRIPPLED HAND OF A MINAMATA DISEASE VICTIM

INORGANIC POISON
POISON
Silver (Ag)

REMARKS
Causes argyria Found in indelible ink Protein precipitant. Also known as beautiful meadows Used in silvering of mirrors Used in galvanizing iron and as container for battery cells Causes parakeratosis, Metal fume fever

Bismuth (Bi) Zinc (Zn)

BLUE OR BLUISH-GREY COLORED SKIN IS THE DRAMATIC SYMPTOM OF ARGYRIA

Para keratosis characterized by red to brown keratotic papules and plaques.

CONDITIONS INFLUENCING THE RAPIDITY OF ABSORPTION

1. Solubility of poison 2. Character of the surface to which the poison is applied 3. Quantity of blood in the blood vessels

ADMINISTRATION OF POISON
Orally Topically Inhalation Parenteral Nasally

TYPES OF POISONING
1. Medical point of view
Acute poisoning Chronic poisoning

2. legal point of view

accidental suicidal homicidal undetermined

ELIMINATION OF POISON
saliva sweat urine feces respiration tears bile pancreatic juice emesis

EVIDENCES OF POISONING
circumstantial or moral evidence symptomatic evidence chemical evidence post mortem evidence experimental evidence

CHEMICAL TEST

CHEMICAL TEST Lead acetate or xanthogenate Tollens Schwartz resorcinol Schonbienpagenstecher Scheren/mitscherich

POISON DETECTED Differentiate CS from H2S Reducing sugar Chloroform Prussic acid Phosphorous

CHEMICAL TEST Rodillion/Millon Potassium iodide Phenylisocyanide Nylander Nessler

POISON DETECTED Phenol Mercury Nitrobenzene reduction, Aniline and chloroform Bismuth Differentiation of chloral hydrate from chloroform

CHEMICAL TEST POISON DETECTED Modified Duquenols Marijuana Liebens iodoform Differentiation from ethanol from methanol Bromine water Aniline Benzoid gunning Acetone Beilstein Halogens

STAINING AND DISCOLORATION OF SKIN

POISON Picric acid, Nitric acid Phenol Boric acid Arsenic Opium, aniline, sulfides

COLOR OF STAIN ON SKIN Yellow Bleaching white Boiled lobster appearance Pale binds on fingernails Blue

POISON Silver salts Sulfuric acid, iodine, silver nitrate Bromine Mercuric chloride, physostigmine

COLOR OF STAIN ON SKIN Bluish gray Brown black Deep brown Ash gray

EFFECT OF SULFURIC ACID ON SKIN

EFFECT OF MERCURIC CHLORIDE ON SKIN

URINARY CHANGES

POISON Picric acid Aloe, senna Turpentine Phenol and its derivatives, methylene blue Caffeine, lead, mercury, benzene, carbon tetrachloride and rifampicin

COLOR CHANGES IN URINE Dark yellow Yellow burn Odor of violets Green/blue Wine red or red brown

BLOOD CHANGES

POISON

Heparin, coumarin, benzene, fluorine, phosphorous Carbon monoxide, cyanide Nicotine Aniline nitrates, nitroderivatives

COLOR/CHANGES IN BLOODS Decreased blood coagulability

Cherry red blood Dark red blood Chocolate brown blood

DISCOLORATION OF GUMS

POISON Bismuth, lead Mercury

GUM LINE COLOR Blue gum line Black gum line

VISUAL DISTURBANCES

POISON Digitalis, marijuana Marijuana Ethambutol Methanol, formic acid, sclanine Anticholinergic

VISUAL CHANGES Purple Vision Blood shot eyes Optic neuritis Partial/total blindness

Blurred vision

ODOR OF BREATH

POISON Chloroform Cyanide Nicotine Coniine Phosphorous, arsenic, malathion Ethanol Nitrobenzene

ODOR OF BREATH Sweet penetratingodor Bitter almond Stale tobacco Mouse urine Garlic Odor

Fruity Shoe polish

RESPIRATORY CHANGES

POISON Sulfur dioxide Carbon monoxide Veratrine Opium, barbiturates, cyanides, benzodiazepine

RESPIRATORY CHANGES Irritation Dyspnea Violent sneezing General respiratory depression

OTHER CHANGES

POISON Cantharidin Strychnine

REMARK/S Blister formation Loose teeth, bleeding gum, risus sardonicus Barium Muscular twitching, loss of voice Sulfuric acid Ground coffee vomitus Copper Blue green vomitus Anticholinergic Xerostomia Aminoglycosides, loop diuretic Ototoxicity Salicylates, quinine Tinnitus Arsenic Alopecia Arsenic alopecia

MODES OF DEATH
Death beginning at brain (COMA) Death beginning at heart (SYNCOPE) Death beginning at lungs (ASPHYXIA or APNEA}

ANTIDOTES
The word "antidote" is from the Greek antidotos which came from anti, against, + dotos, what is given. what is given against (something) An agent that counteracts a poison and neutralizes its effects.

TYPICAL ANTIDOTE SHOULD POSSESS THE FOLLOWING PROPERTIES:

1. It should be capable of being taken in large doses without danger 2. It should act upon the poison, whether liquid or solid 3. It should be capable of combining with the poison immediately at a temperature equal or below that of the body 4. Its action should be quick 5. It should deprive the poison of its deleterious properties

UNIVERSAL ANTIDOTE
2 parts activated charcoal
Used as adsorbent

1 part tannin or strong tea

Used as precipitating agent

1 part MgO or milk of magnesia

Used as neutralizer

GENERAL MANAGEMENT
1. Supportive care and ABCs 2. Obtaining history of exposure 3. Routine laboratory assessment 4. Toxicology laboratory tests 5. Skin decontamination 6. Gastric decontamination 7. Whole bowel Irrigation 8. Forced diuresis and urinary pH manipulation 9. Dialysis 10. Hemoperfusion

SUPPORTIVE CARE & ABCs

1. Evaluating and supporting vital functions:
AIRWAY BREATHING CIRCULATION

2. Mandatory first step in the initial management of drug Ingestion 3. After the patient is stabilized, the specific issue/s of poison management should be addressed

OBTAINING A HISTORY OF EXPOSURE

1. 2. 3. 4. 5. Identify Neurologic examination Cardiopulmonary examination GI examination Past medical history

ROUTINE LABORATORY ASSESSMENT

1. 2. 3. 4. 5. 6. 7. CBC Serum electrolytes BUN and serum creatinine Blood glucose Urinalysis ECG Chest x-ray

TOXICOLOGY LABORATORY TESTS

1. Qualitative determination
To determine the poison

2. Quantitative determination
To determine the amount of poison

ADVANTAGES OF TOXICOLOGICAL LABORATORY TESTS

1. Confirm or determine the presence of a particular agents 2. Predict the anticipated toxic effects or severity of exposure to some poison 3. Confirm or distinguish or contributing diagnosis 4. Occasionally help guide therapy

LIST OF POISON AND ANTIDOTE

POISON Digitalis Benzodiazepine Barbiturate Phencyclidine Paraquat

ANTIDOTE FAB fragments Flumazenil Urine alkalizers Propranolol, Diazepam Sodium sulfate

POISON Amphetamine Ammonia Formaldehyde Heparin Warfarin

ANTIDOTE Chlorpromazine, vitamin C Formaldehyde Ammonia, sodium bicarbonate Protamine sulfate Vitamin K

POISON Nitrite, chlorate, nitrobenzene, aniline Oxalate Lomotil (diphenoxylate + atropine) Narcotics Isoniazid

ANTIDOTE Methylene blue

Calcium gluconate Naloxone/naltrexone, charcoal Naloxone/ naltrexone Vitamin B6 (pyridoxine)

POISON ANTIDOTE Fluoride Calcium gluconate Cardon monoxide 100% oxygen, hyperbaric oxygen Sulfur dioxide Oxygen TCA Physostigmine Alkaloids Activated charcoal

POISON Barium

Phosporous
Acids Alkali Silver

ANTIDOTE Magnesium sulfate, benzodiazepines Copper sulfate (as gastric lavage) Diluted alkali Diluted acid Saline solution

ANTIDOTE Iodine Starch solution Copper Penicillamine Iron Deferoxamine Pb, Cd, Hg, Se, Ra, U EDTA As, Hg, Au, Ni, Bi, W, Zn BAL

POISON

POISON Thallium

ANTIDOTE Prussian blue or diphenyldithiocarbanate Cyanide Nitrites, sodium thiosulfate Paracetamol N-acetylcysteine Petroleum products Mineral oil Ethanol Disulfiram, caffeine

POISON ANTIDOTE Methanol, ethylene Ethanol glycol Strychnine Diazepam, neumuscular blockers Anticholinergic Physostigmine Anticholinesterase Atropine, 2-PAM Antihistamine Anticholinergic

DISADVANTAGES OF TOXICOLOGICAL LABORATORY TEST

1. These tests cannot provide a specific diagnosis for all patients 2. All possible intoxicating agents cannot be screened 3. In critically ill patients, supportive treatment is needed before laboratory results of the toxicology screen are available 4. Laboratory drug detection abilities differ

TOXICOLOGICAL LABORATORY TEST

ACETAMINOPHEN ARSENIC CARBOXYHEMOGLOBIN DIGOXIN ETHANOL ETHYLENE GLYCOL IRON LEAD

TOXICOLOGICAL LABORATORY TEST

LITHIUM MERCURY METHANOL METHEMOGLOBIN PHENOBARBITAL SALICYLATE THEOPHYLLINE

SKIN DECONTAMINATION
It is performed where percutaneous absorption of a substance may result in systemic toxicity when the contaminating substance may produce local toxic effects

GASTRIC DECONTAMINATION
Attempted when supportive care begun Involves removal of the ingestant with EMESIS or LAVAGE, the USE OF ACTIVATED CHARCOAL potentially to bind the ingestants and the USE OF CATHARTIC to hasten the excretion and thereby limit absorption

GASTRIC DECONTAMINATION - EMESIS

1. Induce vomiting 2. syrup of lpecac
derived from the roots of a plant called ipecacuanha (Psychotria ipecacuanha) Active ingredient: EMETINE

GASTRIC DECONTAMINATION - EMESIS

CONTRAINDICATIONS 1. Children less than 6 months old 2. Patients with CNS depression or seizure 3. Patients who have ingested a strong acid, alkali or sharp object 4. Patients with compromised airway protective reflexes 5. Patients who have ingested some types of hydrocarbons or petroleum distillates 6. Patients who have ingested substances with extremely rapid onset of action 7. Patients with emesis following ingestion

GASTRIC DECONTAMINATION - LAVAGE

Used in patients who are not alert or have a diminished gag reflex Should also be considered in patients who are seen early following massive ingestion or individuals who have contraindication to syrup of ipecac

GASTRIC DECONTAMINATIONACTIVATED CHARCOAL

Adsorbs almost all commonly ingested drugs and chemicals Usually administered to most overdosed patients as quickly as possible

WHOLE BOWEL IRRIGATION

Shown to be effective under certain conditions, particularly when activated charcoal lacks efficacy isosmotic cathartic solution such as polyethylene glycol is used

FORCED DIURESIS
Used to enhance the elimination of substance whose elimination is primarily renal Substance has a relatively small volume of distribution with little protein binding

FORCED DIURESIS
1. Alkaline diuresis
POISON (weak acid) + NaHCO3 promotes ionization of weak acids, thereby preventing reabsorption by the kidney which facilitates the excretion of the weak acid Used in the management of patients who have ingested long acting barbiturates such s phenobarbital or salicylic acid COMPLICATIONS: metabolic alkalosis, hypernatremia, hyperosmolarity and fluid overload

FORCED DIURESIS
2. Acid diuresis
POISON (weak base) + ascorbic acid or NH4Cl Used for weak bases such as amphetamine, phencyclidine and quinidine derivative.

DIALYSIS
Given to patients who fail to respond to the previously mentioned measures of decontamination Hemodialysis and to a lesser extent peritoneal dialysis may enhance drug elimination Water-soluble substances, low molecular weight not significantly bound to plasma protein Enhance the elimination of ethanol, theophylline, lithium, salicylates, long-acting barbiturate.

HEMOPERFUSION
Anticoagulated blood is passed through a column containing activated charcoal or resin particles Clears substances from the blood more rapidly than hemodialysis BUT it does not correct fluid and electrolyte abnormalities as hemodialysis does Less effective in removing ethanol or methanol

GENERAL TYPES OF ANTIDOTES

1. Chemical or true antidotes 2. Mechanical Antidotes
Gastric lavage Emetic Cathartic Demulcents Precipitants

3. Physiologic or antagonist

MANAGEMENT OF SPECIFIC POISON

ACETAMINOPHEN
Antipyretic-analgesic that can produce FATAL HEPATOTOXICITY in untreated patients through the generation of a toxic metabolite TOXICOKINETIC: It is well absorbed from the GI tract and a half-life between 2-3 hour and has less than 5% excreted unchanged in the urine, with the remainder metabolized in the liver by the cytochrome P450 system

ACETAMINOPHEN
CLINICAL PRESENTATION: Phase 1 (12-24 hours post ingestion)
nausea, vomiting, anorexia and diaphoresis

Phase 2 (1-4 days post ingestion)

Asymptomatic

Phase 3: (2-3 days in untreated patients)

nausea, abdominal pain, progressive evidence of hepatic failure, coma and death

ACETAMINOPHEN
LABORATORY DATA: serum acetaminophen levels (based on Rumack-Matthews nomogram graph - used to indicate possible hepatotoxicity, and the need for antidotal therapy based on the patient's serum acetaminophen level); baseline liver function tests; renal function tests; coagulation studies TREATMENT: gastric lavage within 2 hours; activated charcoal administration; administration of NACETYLCYSTEINE LOADING DOSE: 140 mg/kg orally, MAINTENANCE DOSE: 70 mg/kg orally every 4 hours for 17doses

AIR POLLUTANTS
POLLUTANTS CHARACTERISTIC SOURCE MECHANISM TREATMENT

CO

Color less, odorless

Combustio n of fossil fuels and cigarette smoking

CO causes tissue hypoxia because the affinity of CO for hemoglobin is more than 200 folds greater than that of oxygen

100% oxygen, hyperbaric oxygen

AIR POLLUTANTS
POLLUTANTS CHARAC. SOURCE MECHANISM TREATMENT

Sulfur oxides Colorless

combustion of fossil fuels, manufacturing of sulfuric acid; refrigerants

It forms Supportive sulfurous acid on therapy contact with moist membranes MANIFESTATION: conjunctival and bronchial irritation, epistaxis, pulmonary edema

AIR POLLUTANTS
POLLUTANTS CHARACTERISTIC SOURCE MECHANISM TREATMENT

Nitrogen oxide

Brownish gas

Farming Causes deep Supportive and lung irritation treatment firefighting and pulmonary edema and may cause irritation of the eye nose and throat.

AIR POLLUTANTS
POLLUTANTS CHARAC. SOURCE produced in water and air purification devices as well as arc welding MECHANISM TREATMENT

Ozone

CLINICAL Supportiv PRESENTATION e measure ACUTE EXPOSURESirritation and dryness of mucous membranes; CHRONIC EXPOSURESemphysema, bronchitis , bronchiolitis, pulmonary fibrosis

AIR POLLUTANTS
POLLUTANTS CHARAC. SOURCE MECHANISM TREATMENT

Hydrocar bon

Industrial and cleaning solvents Commonly used: Benzene, Toluene, Carbon tetrachloride

CLINICAL Supportive PRESENTATI measures ON: CNS depressants. nausea, vertigo, headache, coma

ETHYLENE GLYCOL
USE:
Anti freeze and windshield de-icing solution

CHARACTERISTIC:
odorless and has sweet taste

TOXICOKINETICS:
It is hepatically metabolized by alcohol dehydrogenase to glycoaldehyde, which is metabolized by aldehyde dehydrogenase to glycolic acid. Glycolic acid is converted to glyoxylic acid whose toxic metabolite is oxalic acid

ETHYLENE GLYCOL
TREATMENT: gastric lavage within 30 minutes of ingestion Iv ethanol Fomepizole ( a potent alcohol dehydrogenase inhibitor) pyridoxine and thiamine Na bicarbonate Hemodialysis

METHANOL
USE:
found in anti- freeze, solvents, bootleg (homemade) alcohol, windshield washer

TOXICOKINETICS
Alcohol dehydrogenase converts methanol to formaldehyde which is then converted to formic acid

TREATMENT
IV Ethanol, folic acid, fomepizole, sodium bicarbonate and hemodialysis Activated charcoal is not effective in adsorbing methanol

ISOPROPYL ALCOHOL
USE
Rubbing alcohol and anti-freeze

CLINICAL MANIFESTATION
nausea, vomiting, abdominal pain, ataxia, .respiratory depression

TREATMENT
gastric lavage, supportive therapy (IV fluids and bicarbonate administration, hemodialysis Activated charcoal is not effective in adsorbing isopropyl alcohol
Y

HEPARIN
DOSAGE FORM Parenteral dosage for IV and SQ administration TOXICOKINETICS It has a half-life of 1-1.5 hours and is primarily metabolized in the liver CLINICAL PRESENTATTON Bleeding or bruising LABORATORY aPTT, bleeding time and platelet counts TREATMENT protamine combines with heparin and neutralizes it. 1 mg protamine neutralizes 100 units of heparin

HEPARIN
DOSAGE FORM oral tablets and solution for parenteral administration TOXICOKINETICS
well absorb following oral administration. Its mean half-life is 35 hours; protein binding is 99% with a 5-day duration of activity. Vitamin K dependent clotting factor begin to decline 6 hours after administration but therapeutic anticoagulation may require several days

HEPARIN
CLINICAL PRESENTATTON Bleeding or bruising LABORATORY PT, INR, bleeding time TREATMENT Phytonadione (vitamin K)

TRICYCLIC ANTIDEPRESSANTS
MEMBERS
include amitriptyline, nortriptyline, imipramine, desipramine, doxepin, protriptyline, clomipramine

TOXICOKINETICS
hepatically metabolized, undergo enterohepatic re-circulation, are highly bound to plasma protein and have an elimination half-life of approxjznately 24 hours

TRICYCLIC ANTIDEPRESSANTS
CLINICAL PRESENTATION Anticholinergic, cardiopulmonary toxicity, CNS manifestations range from agitation and confusion to hallucinations, seizures and coma LABORATORY DATA Serum levels can be used for diagnosis as well as determining the severity therapeutic :serum level < 1000 nmoL/L severe overdose: serum level > 3300 nmol/L

TRICYCLIC ANTIDEPRESSANTS
TREATMENT GI decontamination (activated charcoal) Alkalinization with sodium bicarbonate Phenytoin or BZD may be required to control seizures physostigmine to reverse anticholinergic toxicity

SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRI)

MEMBERS defluoxetine, sertraline and paroxetine TOXICOKINETICS they are well absorbed following oral administration. Peak levels occur within 2 to 6 hours. They are hepatically metabolized with a half-life between 8 to 30 hours

SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRI)

CLINICAL PRESENTATION agitated, drowsy or confsed LABORATORY DATA ECG monitoring TREATMEN gastric lavage and supportive treatment

BENZODIAZEPINE
MEMBERS include chlordiazepoxide, diazepam, flurazepam. midazolam, lorazepam, alprazolam and triazolam TOXICOKINETICS these drugs are hepatically metabolized CLINICAL PRESENTATION drowsiness, ataxia and confusion LABORATORY DATA drug level monitoring is not indicated TREATMENT supportive treatment (gastric emptying, activated charcoal, cathartic); Flumazenil

BETA-ADRENERGIC ANTAGONIST
MEMBERS
Include propanolol, metoprolol, atenolol

TOXICOKINETICS
All of the members within this class differ with regard to renal versus hepatic elimination, lipid solubility and protein binding. Patients may become toxic due to changes in organ function

CLINICAL PRESENTATION
hypotension, bradycardia, atrioventricular block.

LABORATORY DATA
serum electrolytes, blood glucose

TREATMENT
Gl decontamination (gastric lavage, activated charcoal); epinephrine

CALCIUM CHANNEL ANTAGONIST

MEMBERS include verapamil, diltiazem, and the dihydropyridine class TOXICOKINETICS onset of action is approximately 30 minutes, whereas the duration is 6-8 hours. CLINICAL PRESENTATION hypotension, bradycardia and atrioventicular block LABORATORY DATA ECG and serum electrolytes TREATMENT GI decontamination (gastric lavage, activated charcoal and whole bowel irrigation); 10% calcium chloride; glucagons

COCAINE
MEMBERS alkaloid from Erythroxylom coca TOXICOKINETICS It is well absorbed following oral, inhalational, intranasal, IV administration. It is metabolized in the liver and excreted in the urine

COCAINE
CLINICAL PRESENTATION CNS and Sympathetic stimulation, death may result from respiratory failure, myocardial infarction or cardiac arrest LABORATORY DATA cocaine and cocaine metabolite urine screes TREATMENT benzodiazepines for seizures, labetalol for hypotension and neuroleptics for psychosis

CORROSIVES
MEMBERS include strong acids or alkalis TOXICOKINETICS Corrosives are well absorbed following oral and inhalational administration CLINICAL PRESENTATION these compounds produce burns on contact . LABORATORY DATA Chest radiograph and at least 6 hours of observations are required for inhalation exposure TREATMENT Decontamination: Exposed skin must be irrigated with water

CYANIDES
MEMBERS found in industrial chemicals and some nail polish removers TOXICOKINETICS

the drug is rapidly absorbed following oral or inhalational exposure. It inhibits cytochrome oxidase therefore blocks electron transport which results in decreased aerobic energy production

CYANIDES
CLINICAL PRESENTATION headache, dyspnea, nausea, vomiting, ataxia, coma, seizures and death (bitter almond odor) LABORATORY DATA cyanide levels, electrolytes, ECG TREATMENT cyanide antidote kit (amyl nitrite, sodium nitrite, sodium thiosulfate, oxygen, sodium bicarbonate hyperbaric oxygen)

DIGOXIN
MEMBERS available dosage form include oral and parenteral TOXICOKINETICS Digoxin is well absorbed is primarily renally eliminated has a half-life of 3.6-48 hours. Its volume of is distribution: 7-10 L/kg

DIGOXIN
CLINICAL PRESENTATION
anorexia, nausea and vomiting in mild cases. In more severe cases, cardiac dysrhythmia are seen

LABORATORY DATA
serum digoxin levels, electrolytes (particularly serum potassium levels) and ECG

TREATMENT
decontamination (ipecac, activated charcoal): supportive therapy and Digoxin- specific FAB antibodies

ELECTROLYTE - Magnesium
MEMBERS available dosage forms includes oral, rectal, parenteral. Magnesium containing cathartics (e.g. magnesium citrate) have been reported to produce hypermagnesemia in patients receiving repetitive doses with activated charcoal TOXICOKINETICS lt is found intracellularly and is renally eliminated

ELECTROLYTE - Magnesium
CLINICAL PRESENTATION Mild deep tendon reflexes may be depressed, lethargy and weakness, severe respiratory paralysis and heart block; prolonged PR, QRS and QT intervals LABORATORY DATA Mild-more than 4 mEq/L severe -more than 10 mEq/L TREATMENT 10%, calcium chloride; hemodialysis

ELECTROLYTE - Potassium
MEMBERS
Oral and parenteral

TOXICOKINETICS
It is primarily an intracellular cation. Changes in acid-base balance produce shifts in serum potassium values

ELECTROLYTE - Potassium
CLINICAL PRESENTATION
cardiac irritability and peripheral weakness with minor increases. Cardiac dysrhythmias

LABORATORY DATA ECG TREATMENT

10% calcium chloride; sodium bicarbonate; glucose and insulin; cation exchange resin; hemodialysis

HEAVY METALS - As
SOURCE
found as organic arsenic (ubiquitous in the environment): inorganic arsenic (insecticides, fungicides, rodenticides and compounds used in glass manufacturing); arsine gas (produced in smelting of metals and making of silicon microchips and lead plating)

TOXICOKINETICS
it interferes with oxidative phosphorylation

HEAVY METALS - As
CLINICAL PRESENTATION ACUTE Gl distress, Cardiovascular effects (hypotension, arrhythmia) CNS effects (seizure, coma) Hematologic effects (hemolysis and bone marrow depression) renal effects (acute tubular necrosis and oliguria CHRONIC Polyneuritis, skin changes (erythrooderma, hyperkeratosis, Aldrich-Mees lines). Sweet garlic odor

Aldrich-Mees' lines are lines of discoloration across the nails of the fingers and toes.

HEAVY METALS - As
LABORATORY DATA
Serum arsenic levels

TREATMENT
Gastric lavage Dimercaprol (BAL) Penicillamine Hemodialysis

HEAVY METAL - Pb
SOURCE
lead-containing paint or gasoline fume inhalation

TOXICOKINETICS
lead has slow distribution with a half-life of approximately 2 months

HEAVY METAL - Pb
CLINICAL PRESENTATION ACUTE
Nausea, vomiting, abdominal pain, peripheral neuropathies, convulsions and coma

CHRONIC- Childhood form

abdominal pain, anemia, and subclinical CNS effects, such as mental retardation and learning disabilities.

CHRONIC- Adult form

abdominal pain, anemia, peripheral neuropathy, ataxia, memory loss, renal disease

HEAVY METAL - Pb
LABORATORY DATA
Anemia and elevated blood lead level

TREATMENT
Calcium EDTA Dimercaprol

HEAVY METALS - Hg
SOURCE
Batteries, thermometer and dental fillings

TOXICOKINETICS
mercury intoxication occur through inhalation. However, this metal may be ingested or absorbed through the skin

HEAVY METALS - Hg
CLINICAL PRESENTATION Acute Gl distress, chest pain and shortness of breath secondary to inflammation of airways and interstitial pneumonitis, CNS effects (intention tremor, increased excitability, delirium). Chronic CNS effects {same as acute) loosening of the teeth, gingivitis, stomatitis, excessive salivation LABORATORY DATA serum mercury levels TREATMENT gastric lavage, dimercaprol, penicillamine or succimer

IRON
SOURCE:
Toxicity is based on the amount of elemental iron ingested Sulfate salt-20% elemental iron Fumarate salt 33% elemental iron Gluconate salt 12% elemental iron

TOXICOKINETICS
Absorbed in the duodenum and jejunum

IRON
CLINICAL PRESENTATION Phase I nausea, vomiting, diarrhea, GI bleeding, hypotension Phase II clinical improvement seen 6-24 hours after ingestion Phase III- metabolic acidosis, renal and hepatic failure, sepsis, pulmonary edema and death

IRON
LABORATORY DATA Serum iron levels, total iron binding capacity, ABG, hemoglobin and hematocrit TREATMENT Decontamination, supportive treatment, deferoxamine

ISONIAZID (INH)
DOSAGE FORM
Oral and parenteral

TOXICOKINETICS
INH is well absorbed orally Peak levels are within 1-2 hours after ingestion INH is hepatically metabolized

ISONIAZID (INH)
CLINICAL PRESENTATION
Nausea, vomiting, slurred speech, ataxia, generalized tonic clonic seizure and coma

LABORATORY DATA
Severe lactic acidosis, hypoglycemia, mild hyperkalemia, leukocytosis

TREATMENT
Decontamination, pyridoxine and sodium bicarbonate

LITHIUM
DOSAGE FORM
Liquids, capsules and tablets

TOXICOKINETICS
Well absorbed following oral administration It is not appreciably found to plasma protein and has small Vd Elimination is renal with a half-life of 14-24 hours

LITHIUM
CLINICAL PRESENTATION MILD INTOXICATION
Polyuria, blurred vision, weakness, slurred speech, ataxia, tremor, myoclonic jerks

SEVERE INTOXICATION
Delirium, coma, seizure, hyperthermia

LITHIUM
LABORATORY DATA
Therapeutic range: 0.6 to 1.2 mEq/L Mild toxicity : 1.5-2.5 mEq/L Moderate: 2.5-3 mEq/L Severe: > 3 mEq/L

TREATMENT
Decontamination (ipecac, sodium polystyrene sulfonate, whole bowel irrigation, HD Supportive care

OPIATES
DOSAGE FORMS
Oral immediate release, SR preparations as well as parenteral agents

TOXICOKINETICS
Some agents have prolonged elimination halflives (e.g. heroine, methadone)

OPIATES
CLINICAL PRESENTATION
Respiratory depression, decreased level of consciousness

LABORATORY DATA
Baseline ABGs and toxicology screen

TREATMENT naloxone and nalmefene

SALICYLATES
DOSAGE FORM
Oral, rectal, and topical prducts

TOXICOKINETICS
Well absorbed following oral administration Half is 6-12 hours at lower dose In over dose situations, the half life may be prolonged to more than 20 hours

SALICYLATES
CLINICAL PRESENTATION MILD TOXICITY
Nausea, vomiting, tinnitus and malaise

SEVERE TOXICITY
- lethargy, convulsions, coma, metabolic acidosis. - Potential complications from therapeutic and toxic doses include Gl bleeding, increased prothrombin time, hepatic toxicity, pancreatitis, proteinuria

SALICYLATES
LABORATORY DATA
for the following 6 hour post ingestion levels: Tinnitus: 40-60 mg/dL moderate toxicity: 60-95 mg/dl Severe toxicity: More than 95 mg/dl. With the presence of acidemia and aciduria, evaluate ABGs additional laboratory evaluation may show leukocytosis, thrombocytopenia, increased or decreased serum glucose and sodium, hypokalemia, and increased serum BUN, creatinine and ketones

TREATMENT
Decontamination, alkaline diuresis, hemodialysis, fluid and electrolyte replacement, vitamin K and FFP

THEOPHYLLINE
DOSAGE FORM
liquid, sustained release tablet, capsules, as well as parenteral forms

TOXICOKINETICS
Well absorbed orally with a Vd approximately 0.5 L/kg. It is hepatically metabolized and has a half-life of approximately 4-8 hours. Theophylline clearance is highly dependent on age, concomitant disease states, and interacting drugs

THEOPHYLLINE
CLINICAL PRESENTATION
Nausea, vomiting, seizures and cardiac dysrhythmias Chronic toxicity carries a poorer prognosis than acute toxicity.

LABORATORY DATA
therapeutic levels are 5-20 ug/ml. Hyperglycemia and hypokalemia are seen with acute ingestions. Other useful laboratory tests include serum electrolyte, BUN, creatinine, hepatic function and ECG monitoring

TREATMENT
supportive therapy, decontamination, a-adrenergic antagonist (e.g. esmolol)

CHELATORS
Molecules with two or more electronegative groups that is used to BIND TOXIC METALS in STABLE COMPLEXES The complexes are relatively LOW TOXICITY and ENHANCED FECAL and RENAL EXCRETION Chelators are used in the treatment of HEAVY METAL toxicities

EDTA (Ethylenediaminetetraacetic acid)

administered pareterally (IM or IV) used to treat LEAD poisoning nephrotoxicity (adverse effect)- reversible calcium EDTA is used instead of sodium EDTA, because the sodium salt of EDTA can cause severe hypocalcemia

DIMERCAPROL
As an antidote for lewisite, an arsenical war gas. It was first named BAL (british anti lewisite) Used to treat MERCURY, ARSENIC, LEAD and CADMIUM toxicities Administered parenterally (IM) CONTRAINDICATIONS TO DIMERCAPROL:
concurrent use of iron therapy, glucose -6-phosphate dehydrogenase deficiency allergy to peanut oil

PENICILLAMINE
used to treat LEAD, ARSENIC, MERCURY and GOLD toxicities, as well as RHEUMATOID ARTHRITIS and CYSTINURIA Administered orally Adverse effects
Rash fever Leukopenia thrombocytopenia resembling a penicillin hyper sensitivity reaction

DEFEROXAMINE
used to treat acute iron Intoxication administered parenteraIIy Compete for the heme iron in hemoglobin and cytochrome ADVERSE EFFECTS
Neurotoxicity, hepatic and renaI dysfunction, severe coagulopathies, histamine-release and hypotensive shock when given by rapid IV infusion

SUCCIMER
oral congener of dimercaprol used to treat childh00d lead intoxication with serum levels >45 ug/dL ADVERSE EFFECTS
transient increase in hepatic transaminase levels skin rash GI distress