This document summarizes the abuse of central nervous system stimulants like amphetamine. It discusses the toxicity of fatal doses, causes, symptoms and pathology, toxicokinetics, clinical diagnosis, and treatment of amphetamine abuse. A fatal dose is 250mg and can cause convulsions and death. Symptoms include elevated mood, increased activity, and decreased need for sleep. Amphetamine is rapidly absorbed and metabolized in the liver, with a biological half-life of 4-5 hours. Treatment involves stabilization, supportive measures, and drugs like diazepam and amiodarone. Adverse effects include psychosis, kidney disease, seizures, and depression.
3. INTRODUCTION
• Amphetamine was first synthesized in 1887, but began to be therapeutically used
only since the 1930s. Because of its abuse potential, its therapeutic administration
is greatly restricted today
• Chemically, amphetamine is 1-phenylpropan-2-amine.
• Synthetic amphetamines(designer drugs)-methylenedioxy-
methamphetamine(MDA or love drug), methylenedioxy-
methamphetamine(MDMAor ecstacy) and methylenedioxy-
ethamphetamine(MDEA or Eve)
4. CNS STIMULANTS
• DEFINITION:-
• A type of a drug that increases the levels of certain chemicals in the brain and
increases alertness, attention, energy and physical activity. CNS STIMULANTS also
increases respiration, heart rate and bloodpressure
• Ex:-Amphetamine, modanifil.
5. SIGNS AND SYMPTOMS
• 1.Elevated mood
• 2.Increase motor activity
• 3.Increase alertness
• 4.Decrease need for sleep
• Note:
• Overdose leads to convulsion and death
6. FATAL DOSE
• 250mg (addicts can tolerate much larger doses)
CAUSES:
• Amphetamine toxicity generally occurs in the setting of recreational use.
• METH comes in different forms and can be smoked, inhaled, injected or orally
consumed.
• According to the National Institute on drug abuse smoking METH is the most
common way of abuse
7. SYMPTOMS
CNS:
• Euphoria, agitation, headache, paranoia, anorexia, hyperthermia, hypothalamic
dysfunction.
• INTRA CEREBRAL HAEMORRHAGE:
• Abuse of amphetamine and related drugs can increase the risk for cerebrovascular
incidents in young adults
COMA:
• If it occurs is associated with a high mortality rate.
CVS:
• Tachycardia, hypertension, arrythmias, vasospasm, myocardial ischaemia and
cardiomyopathy.
9. damage to GABA interneurons in cortex
loss of GABA interneurons in cortex
GLU dysregulation in cortex
10. Phychosis
TOXICOKINETCS:
ABSORPTION:
• Rapidly absorbed from the gastrointestinal tract
• When smoked it is delivered to the brain via the pulmonary vasculature within approximately
7seconds
DISTRIBUTION:
• Volume of distribution is 3 to 7L/kg
METABOLISM:
• Metabolized in the liver by aromatic hydroxylation, N-dealkylation and deamination
EXCRETION:
• Excretes through urine within 24hrs.
HALF LIFE:
• Biologic half life is 4 to 5hrs
11. CLINICAL DIAGNOSIS
• Urine analysis(TLC, RIA, HPLC and GC-MS).
• A new method (ELECTRON-IMPACT MASS FRAGMENTOGRAPHY) enables
detection and even quantitation of methamphines in hair, nails, sweat and saliva.
• Hair analysis may provide documentation of methamphetamine or other drug
exposure for several months or longer
12. TREATMENT
NON PHARMACOLOGICAL TREATMENT:
• Stabilization- Ivline, oxygen should be provided.
• Supportive measures- airway management, ventilatory support, rapid rehydration, mannitol dieresis and
gatric decontamination
PHARMACOLOGICAL TREATMENT:
• AMIODARONE 300mg-IV
• DIAZEPAM 5-10mg-IV
• NITROGLYCERINE 5-200mg
• LABETALOL 300mg –IV
• Lignocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia
• Diazepam and chlorpromazine have been effective in treating amphetamine-induced chorea
13. ADVERSE EFFECTS
• Psychosis
• Kidney disease
• Seizures
• Muscle weakness
• Panic attacks
• Depression
REFERENCE:
• Anon: Drug alert: Med watch-Inaspine Dear Doctor Letter. U.S.Food and Drug
Administration. Rockville, MD,USA.2001.Available from URL:
http://www.fda/gov/medwatch/SAFETY/2001/inapsine.htm.
