General Principles of Toxicology
Muhammed Malik Al-ani
P. Clinical toxicology
syllabus
1. General Principles of Toxicology
2. Drug toxicity
a. Acetaminophen poisoning.
b. Opiate poisoning.
c. Aspirin Poisoning.
d. Theophylline Poisoning.
3. Digoxin Toxicity
4. Determination of LD50
5. Guidelines for Seminar
Presentations:
a. CCl4
b. Ethanol and methanol
c. Cyanide and carbon monoxide
d. Organophosphorus and Organochlorine
• clinical toxicology: Area of professional of medical
science (clinic) concerned with disease or poisoning by
toxic substance and its treatment.
• Poisons: Are chemicals or chemical products that are
distinctly harmful to humans.
• Toxin: It originally referred to a poison of animal or
plant origin.
• Toxidrome: A group of signs and symptoms and/or
characteristic effects associated with exposure to a
particular substance.
How does the poisoned patient die?
1. Depress the central nervous system (CNS).
2. Cardiovascular toxicity.
3. Cellular hypoxia.
4. Seizures, muscular hyperactivity
5. Other organ system damage.
6. Traumatic injury.
1. Depression of (CNS)
Overdoses
• barbiturates
and
alcohol
airway
obstruction
• by the flaccid
tongue
die
e.g. Narcotics and sedative-hypnotic drugs
2. Cardiovascular toxicity
Hypotension
Peripheral
vascular
collapse
Hypovolemia Depression of
cardiac contractility
temp.
dysregulating
effects
Cardioactive
drugs
Lethal
arrhythmias
n
o
t
c
a
r
d
1. ephedrine, amphetamines, cocaine, digitalis, theophylline.
2. Amitriptyline, amoxapine, antihistamines and some opioid analogs.
• Occur in spite of adequate ventilation and oxygen
administration in case of poisons that interfere
with transport or utilization of oxygen e.g.
1. Cyanide.
2. Carbon monoxide.
• Seizures may cause:
1. Pulmonary aspiration.
2. hypoxia.
3.Brain damage.
• Sustained muscular hyperactivity can lead to:
4. Hyperthermia
5. Muscle breakdown.
6. Myoglobinuria.
7. Lactic acidosis.
• Behavioral effects of ingested drug may result
in traumatic injury.
• e.g intoxication with alcohol and other
sedative-hypnotic drugs is a common
contributing factor to motor vehicle accidents.
1. pulmonary fibrosis:
• Paraquat attacks lung tissue beginning
after several days of ingestion.
2. hepatic necrosis:
poisoning by acetaminophen or certain
mushrooms results in hepatic
encephalopathy and death 48-72 h.
• Initial management of the
poisoned patient
• Patient with coma, seizures, or otherwise
altered mental status should follow the
same approach regardless of the poison
involved.
• Attempting to make a specific
toxicological
diagnosis
supportive
delays
measures
the application
of that
form the basis
("ABCDs") of poisoning treatment.
• A= airway: should be cleared of vomitus or any
other obstruction& oral airway or
endotracheal tube inserted if needed.
• B= Breathing: assessed by observation by oximetry,
measuring arterial blood gases.
• C= circulation: monitoring of pulse rate, BP, urinary
output, evaluation of peripheral perfusion.
• Ds = Dextrose: Alcoholic or malnourished patients
should also receive 100 mg of thiamine I.M or in
I.V infusion solution at this time to prevent
Wernicke's syndrome.
Assessment &management:
1. Clinical assessment: all what mention previous.
2. Laboratory assessment
A-Liver function tests: Acetaminophen.
B- Renal function tests: NSAIDs.
C- ECG: Digoxin toxicity.
D-Imaging findings
• Aplain film of abdomen useful in tablets,
e.g. iron and potassium, may be radiopaque.
• Chest radiographs reveal aspiration pneumonia,
hydrocarbon pneumonia, pulmonary edema.
• (CT) is recommended when head trauma
is suspected,
E. Toxicology Screening Tests:
Benefit:
Help in confirming a suspected intoxication or for
ruling out intoxication as a cause of apparent brain
death.
But: It is time consuming, expensive, and often
unreliable.
Note: They should not delay needed
treatment.
Goals of treatment:
1. Reduce absorption of the toxin.
2. Enhance elimination.
3. Neutralize toxin.
1. Reduce absorption of the
toxin
 Removal from surface skin and eye (wash
with soap and water).
Emesis induction
Gastric lavage
Activated charcoal administration.
Dilution - milk/other drinks for corrosives
 Endoscopic or surgical removal of
ingested chemical
2. Enhance
elimination
Keep a good urine output 150-200 ml/hr
 Alkalinization of urine for salicylate and
phenobarbital poisoning, achieved by IV dose of
bicarb.
Hemodialysis.
3. Neutralise
toxin Neutralise toxin specific antidotes
Acetaminophen N-acetyl cysteine
Anticholinergics Physostigmine
Benzodiazepine Flumazenil
Ca channel blockers Glucagon, insulin + dextrose, calcium
Carbamate Atropine
Digoxin Digoxin antibodies
Opioid Naloxon
Oral hypoglycemic Glucose
Organophosphate Atropine
Warfarin Vitamin K
Iron Desferroxamine
introduction to toxicology principles .pptx

introduction to toxicology principles .pptx

  • 1.
    General Principles ofToxicology Muhammed Malik Al-ani
  • 2.
    P. Clinical toxicology syllabus 1.General Principles of Toxicology 2. Drug toxicity a. Acetaminophen poisoning. b. Opiate poisoning. c. Aspirin Poisoning. d. Theophylline Poisoning. 3. Digoxin Toxicity 4. Determination of LD50 5. Guidelines for Seminar Presentations: a. CCl4 b. Ethanol and methanol c. Cyanide and carbon monoxide d. Organophosphorus and Organochlorine
  • 3.
    • clinical toxicology:Area of professional of medical science (clinic) concerned with disease or poisoning by toxic substance and its treatment. • Poisons: Are chemicals or chemical products that are distinctly harmful to humans. • Toxin: It originally referred to a poison of animal or plant origin. • Toxidrome: A group of signs and symptoms and/or characteristic effects associated with exposure to a particular substance.
  • 4.
    How does thepoisoned patient die? 1. Depress the central nervous system (CNS). 2. Cardiovascular toxicity. 3. Cellular hypoxia. 4. Seizures, muscular hyperactivity 5. Other organ system damage. 6. Traumatic injury.
  • 5.
    1. Depression of(CNS) Overdoses • barbiturates and alcohol airway obstruction • by the flaccid tongue die e.g. Narcotics and sedative-hypnotic drugs
  • 6.
    2. Cardiovascular toxicity Hypotension Peripheral vascular collapse HypovolemiaDepression of cardiac contractility temp. dysregulating effects
  • 7.
    Cardioactive drugs Lethal arrhythmias n o t c a r d 1. ephedrine, amphetamines,cocaine, digitalis, theophylline. 2. Amitriptyline, amoxapine, antihistamines and some opioid analogs.
  • 8.
    • Occur inspite of adequate ventilation and oxygen administration in case of poisons that interfere with transport or utilization of oxygen e.g. 1. Cyanide. 2. Carbon monoxide.
  • 9.
    • Seizures maycause: 1. Pulmonary aspiration. 2. hypoxia. 3.Brain damage. • Sustained muscular hyperactivity can lead to: 4. Hyperthermia 5. Muscle breakdown. 6. Myoglobinuria. 7. Lactic acidosis.
  • 10.
    • Behavioral effectsof ingested drug may result in traumatic injury. • e.g intoxication with alcohol and other sedative-hypnotic drugs is a common contributing factor to motor vehicle accidents.
  • 11.
    1. pulmonary fibrosis: •Paraquat attacks lung tissue beginning after several days of ingestion. 2. hepatic necrosis: poisoning by acetaminophen or certain mushrooms results in hepatic encephalopathy and death 48-72 h.
  • 12.
    • Initial managementof the poisoned patient • Patient with coma, seizures, or otherwise altered mental status should follow the same approach regardless of the poison involved.
  • 13.
    • Attempting tomake a specific toxicological diagnosis supportive delays measures the application of that form the basis ("ABCDs") of poisoning treatment.
  • 14.
    • A= airway:should be cleared of vomitus or any other obstruction& oral airway or endotracheal tube inserted if needed. • B= Breathing: assessed by observation by oximetry, measuring arterial blood gases.
  • 15.
    • C= circulation:monitoring of pulse rate, BP, urinary output, evaluation of peripheral perfusion. • Ds = Dextrose: Alcoholic or malnourished patients should also receive 100 mg of thiamine I.M or in I.V infusion solution at this time to prevent Wernicke's syndrome.
  • 16.
    Assessment &management: 1. Clinicalassessment: all what mention previous. 2. Laboratory assessment A-Liver function tests: Acetaminophen. B- Renal function tests: NSAIDs. C- ECG: Digoxin toxicity.
  • 17.
    D-Imaging findings • Aplainfilm of abdomen useful in tablets, e.g. iron and potassium, may be radiopaque. • Chest radiographs reveal aspiration pneumonia, hydrocarbon pneumonia, pulmonary edema. • (CT) is recommended when head trauma is suspected,
  • 18.
    E. Toxicology ScreeningTests: Benefit: Help in confirming a suspected intoxication or for ruling out intoxication as a cause of apparent brain death. But: It is time consuming, expensive, and often unreliable. Note: They should not delay needed treatment.
  • 19.
    Goals of treatment: 1.Reduce absorption of the toxin. 2. Enhance elimination. 3. Neutralize toxin.
  • 20.
    1. Reduce absorptionof the toxin  Removal from surface skin and eye (wash with soap and water). Emesis induction Gastric lavage Activated charcoal administration. Dilution - milk/other drinks for corrosives  Endoscopic or surgical removal of ingested chemical
  • 21.
    2. Enhance elimination Keep agood urine output 150-200 ml/hr  Alkalinization of urine for salicylate and phenobarbital poisoning, achieved by IV dose of bicarb. Hemodialysis.
  • 22.
    3. Neutralise toxin Neutralisetoxin specific antidotes Acetaminophen N-acetyl cysteine Anticholinergics Physostigmine Benzodiazepine Flumazenil Ca channel blockers Glucagon, insulin + dextrose, calcium Carbamate Atropine Digoxin Digoxin antibodies Opioid Naloxon Oral hypoglycemic Glucose Organophosphate Atropine Warfarin Vitamin K Iron Desferroxamine