1. OPIOIDS Dr. Hisham Zein Alabdin

2. Plant origin  It is the dried extract of the poppy plant: Popover somniferum.  Raw opium typically is composed of at least 10% morphine.

3. Opioids The term opioids are compounds that exert pharmacologic activity at opioids receptors. Opium derivatives:  Natural: morphine, codeine.  Semi- synthetic: heroin (Diacetyl morphine), apomorphine.  Wholly synthetic: methadone, pethidine.

4. Uses  Medical: Analgesic,  Surgical.  Toxicological uses: in corrosive. Contraindications:  Age: patient less than twelve (very sensitive respiratory center).  Head injury: it masks the pupil change, it leads to increased intracranial pressure by producing vasodilatation.

5.  Acute abdomen: it masks the sign and symptom.  Bronchial asthma:(it cause bronchospasm).  Pregnancy and delivery: (crosses placental barrier)  Liver & kidney disease.

6. Toxicokinetics Absorption: are well absorbed from GIT, IM, subcutaneous. Metabolism: it takes place in the liver undergo hepatic conjugation with glucoronic acid. Excretion: stomach is the main excretory organ (reexcetion).

7. Clinical picture A-CNS Are combination of stimulation and depression. There is transient euphoria followed by dysphoria. Stimulant effects:  Chemoreceptor trigger zone nausea, vomiting  Vagus nucleus slow full pulse.  Third nerve nucleus pin point pupils.

8. Depressant effects:  on cerebral cortex: o Analgesia :by increasing pain tolerance and altering psychological response to pain. o Suppression of anxiety sedation. o Drowsiness, mood changes and mental cloudiness followed by sleep.

9.  On the cough centre suppression of cough reflex.  On the respiratory centre slow, shallow (by reducing the sensitivity of respiratory centre to raised arterial CO2 tension) and apnea.  On the heat regulating centre hypothermia

10.  On the cough centre suppression of the cough reflex e.g. codeine.  On respiratory centre slow, shallow respiration (by reducing the sensitivity of respiratory centre to raised arterial Co 2 tension) and apnea.  On the heat regulating centre hypothermia

11. B) Cardiovascular effects: Peripheral vasodilatations orthostatic hypotension and syncope due to release of histamine and central depression of vasomotor centre.

12. C) Gastrointestinal effects Mainly constipation due to: 1- Decreased gastrointestinal motility. 2- Decreased HCL secretion 3- Increased antral muscle tone and duodenal muscle tone. 4- Increased iliocecal valve and sphincter tone.

13. D) Biliary tract: Aggravates biliary colic by: 1- Constriction of sphincter of Oddi. 2- Increased biliary tract pressure. 3-Decreased biliary secretion.

14. E) Genito- urinary tract: Increased detrusor muscle tone and increased vesicle sphincter tone urgency and retention of urine, it is aggravated by increased secretion of ADH. F) Skin: Flushing, urticaria, and skin rash.

15. Diagnosis  By circumstantial evidence  History  Clinical examination: o CNS depression, miosis, hypothermia and respiratory depression.

16. Differential diagnosis  Other toxic coma (parathione).  Traumatic and pathological coma with miosis the most important is coma due to pontine haemorrhage.

17. Investigation  TLC It gives a positive result about 30 minutes after a single dose and remains +ve up to 36 hrs and up to 72 hrs after repeated doses.

18. Treatment  A B C  Prevent further absorption  Narcotic antagonists:  Pure narcotic antagonist: Naltrexone, Naloxone(Narcan).  Mixed narcotic agonist-antagonist: Not used

19. Disadvantages of mixed agonist-antagonist  So they can produce synergism with opiates and aggravate respiratory depression.  In non opiate poisoning, they produce symptoms and signs like opiate toxic effects.  In addicts they produce severe withdrawal syndrome.

20. Cause of death Central asphyxia