1. AMPHETAMINES- Expected Lecture Outcomes
Respond to the threat of amphetamine intoxication.
List various means of possible exposure.
Develop protocol for managing toxic ingestions of amphetamines and treatments associated with their pathology.

2. AMPHETAMINES OVERVIEW
Dextroamphetamine (Dexedrine) and methylphenidate
(Ritalin) are used for the treatment of narcolepsy
and for attention-deficit disorders in children.
Several amphetamine-related drugs (benzphetamine,
diethylpropion, phendimetrazine, phenmetrazine,
and phentermine) are marketed as prescription
anorectic medications for use in weight reduction.

3. AMPHETAMINES Methamphetamine (crank, speed),
Methylenedioxymethamphetamine (MDMA, ecstasy),
Paramethoxyamphetamine (PMA), and several other
amphetamine derivatives ( LSD and
Other Hallucinogens), are used orally and intravenously
as illicit stimulants and hallucinogens.
"Ice" is a smokable form of Methamphetamine.

4. AMPHETAMINE LIKE DRUGS

5. Amphetamine and related drugs activate the
MECHANISM OF TOXICITY
Amphetamine and related drugs activate the
sympathetic nervous system by CNS stimulation,
peripheral release of catecholamines,
inhibition of neuronal reuptake of catecholamines,
inhibition of monoamine oxidase.
Low therapeutic index
1mg/kg considered as life-threatening dose

6. CLINICAL PRESENTATION
Acute CNS effects of intoxication include euphoria,
talkativeness, anxiety, restlessness, agitation, seizures,
and coma. Intracranial hemorrhage may occur owing
to hypertension or cerebral vasculitis.
Other effects include sweating, tremor,
muscle fasciculation and rigidity, tachycardia,
hypertension, acute myocardial ischemia, and
infarction (even with normal coronary arteries).
Inadvertent intra-arterial injection may cause
vasospasm resulting in gangrene;

7. CLINICAL PRESENTATION
Chronic effects of amphetamine abuse include
weight loss, cardiomyopathy, pulmonary hypertension,
dental changes, stereotypic behavior, paranoia, and
paranoid psychosis.
Death may be caused by ventricular arrhythmia,
status epilepticus, intracranial hemorrhage, or
hyperthermia.
Hyperthermia frequently results from seizures and
muscular hyperactivity and may cause brain damage,
rhabdomyolysis, and myoglobinuric renal failure.

8. TREATMENT Maintain an open airway and assist ventilation if necessary.
Treat agitation, seizures, coma and hyperthermia if they
occur.
Benzodiazepines are usually satisfactory for treatment of
agitation, although butyrophenones (e.g, Haloperidol and
Droperidol) may also be used.
Continuously monitor the temperature, other vital signs,
and the ECG for a minimum of 6 hours.
There is no specific antidote.

9. TREATMENT Hypertension is best treated with sedation and,
if this is not effective, a parenteral vasodilator
such as phentolamine or nitroprusside.
Treat tachyarrhythmias with propranolol or esmolol.
Treat arterial vasospasm as described for ergots
(Ergot Derivatives).
Administer activated charcoal only if
conditions are suitable.

10. ETHANOL- Expected Lecture Outcomes
Respond to the threat of ethanol intoxication.
List various means of possible exposure.
Develop protocol for managing toxic ingestions, and the antidotes and treatments associated with their pathology.

11. ETHANOL Commercial beer, wine, and liquors contain various
amounts of ethanol.
Ethanol also is found in a variety of colognes,
perfumes, aftershaves, mouthwashes; some rubbing
alcohols; many food flavorings (eg, vanilla, almond,
and lemon extracts); pharmaceutical preparations
(eg, elixirs); and many other products.

12. ETHANOL
Ethanol is frequently ingested recreationally and is the most common co-ingestant with other drugs in suicide attempts.
Ethanol may also serve as a competitive substrate in the emergency treatment of methanol and ethylene glycol poisonings.

13. MECHANISM OF TOXICITY
CNS depression is the principal effect of acute ethanol
intoxication.
Ethanol has additive effects with other CNS depressants
such as barbiturates, benzodiazepines,
opioids, antidepressants, and antipsychotics.
Hypoglycemia may be caused by impaired gluconeogenesis
in patients with depleted or low glycogen stores
(particularly small children and poorly nourished persons).

14. may be awake with levels of 500-600 mg/dL or higher.
MECHANISM OF TOXICITY
The level sufficient to cause deep coma or respiratory depression is highly variable, depending on the individual's degree of tolerance to ethanol.
Although levels above 300 mg/dL usually cause coma in novice drinkers, chronic alcoholics
may be awake with levels of mg/dL or higher.

15. CLINICAL PRESENTATION
WITH ACUTE INTOXICATION
With deep intoxication, coma, respiratory depression, and pulmonary aspiration may occur.
In these patients, the pupils are usually small and the temperature, blood pressure, and pulse rate
are often decreased.
Rhabdomyolysis may result from prolonged immobility.

16. CLINICAL PRESENTATION
WITH CHRONIC ABUSE
1.Hepatic toxicity includes fatty infiltration of the liver, alcoholic hepatitis, and eventually cirrhosis. hyponatremia from fluid retention; and bacterial peritonitis.
Production of clotting factors is impaired, leading to prolonged prothrombin time. Hepatic metabolism of drugs and endogenous toxins is impaired and may contribute to hepatic encephalopathy.
2. Gastrointestinal bleeding may result from alcohol-induced gastritis, esophagitis, and duodenitis. Acute pancreatitis is a common cause of abdominal pain and vomiting.

17. CLINICAL PRESENTATION
3. Cardiac disorders include various dysrhythmias such as atrial fibrillation that may be associated with potassium and magnesium depletion and poor caloric intake ("holiday heart").
Cardiomyopathy has been associated with long-term alcohol use. (Cardiomyopathy was also historically associated with ingestion of cobalt used to stabilize beer.)
4.Neurologic toxicity includes cerebral atrophy, cerebellar degeneration, and peripheral neuropathy. Nutritional disorders such as thiamine (vitamin B1) deficiency.
5.Alcoholic ketoacidosis.

18. TREATMENT
a. Protect the airway to prevent aspiration and intubate and assist ventilation if needed (Airway).
b. Give glucose and thiamine , and treat coma and seizures if they occur.Glucagon is not effective
for alcohol-induced hypoglycemia.
c. Correct hypothermia with gradual rewarming .
d. Most patients will recover within 4-6 hours. Observe children until their blood alcohol level
is below 50 mg/dL and there is no evidence of hypoglycemia.
Alcoholic ketoacidosis. Treat with volume replacement, thiamine , and supplemental glucose. Most patients recover rapidly.

19. TREATMENT
Alcohol withdrawal. Treat with benzodiazepines (eg, diazepam, 2-10 mg i.v initially and repeat as needed).
Specific drugs and antidotes:There is no available specific ethanol receptor antagonist despite anecdotal reports of arousal after administration of naloxone.
Decontamination Consider aspirating gastric contents with a small flexible tube if the alcohol ingestion was massive and recent (within minutes).
Activated charcoal does not effectively adsorb ethanol but may be given if other drugs or toxins were ingested.

20. BARBITURATES- Expected Lecture Outcomes
Respond to the threat of Barbiturate intoxication.
List various means of possible exposure.
Develop protocol for managing toxic ingestions, and the antidotes and treatments associated with their pathology.

21. BARBITURATES CLINICAL USES: Hypnotic and sedative,
In the induction of anaesthetic,
To treat epilepsy and status epilepticus
TYPES:
Ultra short acting:Methohexital,Thiopental
Short acting:Pentobarbital,Secobarbital
Intermediate acting:Amobarbital,Apobarbital
Long acting:Mephobarbital,Phenobarbital

22. CLINICAL PRESENTATION
Slurred speech,nystagmus,ataxia at lower doses.
Hypotension coma and respiratory arrest.
Partial or complete renal shutdown.
During coma,The patient may lose all reflex activity.
Hypothermia in patients with coma and hypotension and bradycardia accompany hypothermia

23. MECHANISM OF TOXICITY:
Attach with barbiturate receptors
Potentiation of GABA release
Chloride channels open
Depression of neuronal activity

24. TREATMENT:
Leave a suspension of activated charcoal in stomach to prevent absorption of drug from intestine.
Take supportive measures such as assure airway,respiration,maintain blood volume by fluid infusion and use of vasopressors.
Forced alkaline diuresis should be done with mannitol and sodiumbicarbonate in case of poisoning with long acting agents

25. TREATMENT
Haemodialysis and Haemoperfusion is highly effective in poisoning with short acting and long acting barbiturates.
Dopamine can be used to increase renal blood flow.
No specific antidote.
In the past analeptics like metrazol and bemegride were used to awaken the patients but later stopped because these agents precipitate seizures in patients
with coma.

26. BENZODIAZEPINES- Expected Lecture Outcomes
Respond to the threat of Benzodiazepine intoxication.
List various means of possible exposure.
Develop protocol for managing toxic ingestions, and the antidotes and treatments associated with their pathology.

27. BENZODIAZEPINES
CLINICAL USES:
Anxiety disorders.
Muscular disorders including spasticity due to multiple sclerosis and cerebral palsy.
Seizures.
Sleep disorders.

28. SYMPTOMS:
Respiratory arrest is more likely with newer short-acting benzodiazepines such as triazolam, alprazolam, and midazolam. It has also been reported with zolpidem.
Cardiopulmonary arrest has occurred after rapid injection of diazepam, possibly because of CNS depressant effects or because of the toxic effects of the diluent propylene glycol.

29. Mechanism of Toxicity
Benzodiazepines enhance the release of GABA.
Generalized neuronal depression of spinal reflexes and the reticular activating system.
Coma and respiratory arrest.

30. Protect the airway and assist ventilation if necessary.
TREATMENT
Protect the airway and assist ventilation if necessary.
Treat coma, hypotension , and hypothermia if they occur.
Hypotension usually responds promptly to supine position and intravenous fluids.
Flumazenil is a specific benzodiazepine receptor antagonist that can rapidly reverse coma.
However, benzodiazepine overdose by itself is rarely fatal.

31. Problems with flumazenil:
It may induce seizures in patients with tricyclic antidepressant overdose.
It may induce acute withdrawal, including seizures and autonomic instability, in patients who
are addicted to benzodiazepines.
Resedation is common when the drug wears off after 1-2 hours, and repeated dosing or a
continuous infusion is often required.

32. Cocaine- Expected Lecture Outcomes
Respond to the threat of Cocaine intoxication.
Acquire knowledge about the various means of possible exposure.
Understand an overview of protocol for managing toxic ingestions, and the antidotes and treatments associated with their pathology.

33. COCAINE MOA of Toxicity
Cocaine [koe KANE] is an inexpensive, widely available, and highly addictive drug that is currently abused daily by over 3 million people in the United States.
MOA of Toxicity
Cocaine has a local anesthetic action .Cocaine is applied topically
as a local anesthetic during eye, ear, nose, and throat surgery.
While the local anesthetic action of cocaine is due to a block of
voltage-activated sodium channels, an interaction with
potassium channels may contribute to cardiac arrhythmias.

34. Symptoms of cocaine overdose

35. TREATMENT
1. Maintain an open airway and assist ventilation if necessary .
2. Treat coma, agitation, seizures , hyperthermia, arrhythmias, and hypotension if they occur.
Benzodiazepines are a good choice for initial management of hypertension and tachycardia associated with agitation.
3. Angina pectoris may be treated with benzodiazepines, aspirin, nitrates, or calcium channel blockers.

36. TREATMENT
4. Monitor vital signs and ECG for several hours. Because of reports of persistent or recurrent
coronary spasm up to several days after initial exposure, consider the use of an oral calcium
antagonist and/or cardiac nitrates for 2-4 weeks after discharge.
B. Specific drugs and antidotes. There is no specific antidote.
1. Esmolol may be also be used in combination with a vasodilator such as phentolamine for management of hypertension.
2. QRS prolongation caused by sodium channel blockade can be treated with sodium bicarbonate (Bicarbonate, Sodium).