Transcript Erickson-DrugsHandout

Ecstasy: The drug of a new
generation.
Ecstasy = MDMA
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3,4 methylenedioxymethamphetamine
X, E, M, XTC, Rolls, Adam, Bean, Hug Drug
MDMA History
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1912 – first synthesized by Merck
1914 – patented by Merck –
manufactured as an appetite
suppressant, never marketed
1950’s- studied by US Army as potential
agent in psychological warfare
1970 – used in psychotherapy,
“penicillin for the soul”
1977 – class A illegal drug in UK
1985 – Schedule I illegal drug in U.S.
Areas of Usage
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Highest at raves,
dance clubs (as
high as 91% of
clubbers in dance
scene in Scotland)
Dramatic increase
in college use,
suburban teens,
house parties
Millroy, CM, JRSM February 1999
Physical CLUES
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Glowsticks or lights
Lollipops
Pacifiers
Vick’s Vapor Rub
and Nasal Inhaler
Fuzzy Mittens
Most Predictive Factor of
Drug Use = CLUB MUSIC!
Methods of
Administration
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Mainly PO – stamped tablets, capsules
Intra-nasal – rapid absorption of
crushed tablets or opened capsules
Intra-rectal – faster absorption than PO
Recreational usage varies from ½ pill to
as much 15 pills in a 6 hour span
MDMA Adulterants
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MDEA
MBDB
MDA
PMA
Caffeine
Dextromorphan
Aspirin
Piracetam
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Methamphetamine
PCP
Ketamine
Heroin
Quinine
LSD
Marijuana
Ephedrine
MDMA
Onset
20-90
min
Rise up 5-20
min
Plateau 2-3
hours
Come
1-2
down
hours
After
3-24
Effects hrs
Positive Effects
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Extreme euphoria
Increased energy
Feelings of
belonging and
closeness
Heightened
sensations (touch,
taste, smell,
hearing)
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Increased openness
Feelings of love and
empathy
Bright, intense
visual perceptions
Musical
appreciation
Fear dissolution
“Profound” thought
Other Effects
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Appetite loss
Vertical nystagmus
(rolling)
Moderate increases
in HR and BP
Mild visual
hallucinations
Mind racing
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Changes in
thermoregulation
Restlessness,
nervousness,
shivering
Strong desire to
take more drug
during come down
Mydriasis
Negative Side Effects
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Mild to extreme
trisma and bruxism
Short-memory loss
Confusion
Vertigo, ataxia
Muscle tension
Nausea & vomiting
Concentration
difficulties
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“Crash” come down
Hangover lasting
days to weeks
Depression and
fatigue for up to a
week
Psychological
addiction
Panic attacks
Major Toxic
Complications
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Hyperthermia/Heat Stroke
Dehydration
Hyponatremia
SIADH
Hepatitis/Liver Failure
Rhabdomyolysis/Renal Failure
Neurotoxic Effects
Acute Psychotic Break/Severe Depression
 Death!
Ecstasy Related Fatalities
87 cases reported in the literature
caused by:
 Hyperpyrexia – 30
 Hepatic – 4
 Cardiovascular/Cerebrovascular – 8
 Cerebral, including Hyponatremia – 9
 Drug Related Accidents or Suicide – 14
 Unknown – 22
Kalant, H; Canadian Medical Association Journal, October, 2001
Major Physical Toxicity Hepatic
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Mild viral hepatitis – jaundice, enlarged
tender liver, elevated LFT’s/Coags – self
limited, 2 wks-3 mo, related to glutathione
decrease and oxidative cell destruction
Prolonged hepatitis – slow recovery with
potential permanent fibrosis
Fulminant liver failure – fatal without liver
transplant
Kalant, H; Canadian Medical Association Journal, October, 2001
Major Physical Toxicity Cardiovascular
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NE responsible: HTN and tachycardia
Major intracranial hemorrhage
Petechial hemorrhages – brain and other
organs
Retinal hemorrhage at autopsy
Intravascular thrombosis and CVA
Serious cardiac dysrhythmias
Pulmonary edema/heart failure
Major Physical ToxicityCerebral
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Hyponatremia- result of vigorous physical
activity, profuse sweating, large Na+ loss,
excessive water consumption
SIADH – less common mechanism of water
retention, but can complicate picture
Cerebral edema w/hyponatremic seizures –
therapy includes BZD’s and cautious
replacement of Na with hypertonic saline
Brain stem and cerebellum compression
Hyperpyrexic Pattern of
Toxicity
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Most dangerous form of ecstasy induced
toxicity
Results from a combo of drug action,
intense physical activity, and hot
environment
Adulterants such as dextromorphan can
inhibit sweating leading to further heat
retention
Changes resemble those seen
in severe heatstroke
Features of Hyperpyrexia
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Rhabdomyolysis – heat production
and muscle necrosis
Myoglobinuria and renal failure –
secondary to rhabdomyolysis
Hepatic necrosis
DIC
PMA
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Paramethoxyamphetamine
Pills contain 50mg of PMA, look like MDMA
tablets
Longer duration to onset – toxic in doses of
60-80mg
Rapid rise in BP and temp leading to
convulsions, coma, and death
Responsible for 10 deaths (3 in suburbs of
Chicago)
Gamma Hydroxybutyrate Acid
(GHB)
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Liquid ecstacy
Liquid G
Gamma Oh
Grievous bodily harm
Scoop
Samatomax
Bioski
Cow Growth Hormone
Georgia Home Boy
GHB
Analogue
of inhibitory neurotransmitter
gamma-aminobutyirc acid- CNS depressant
Synthesized
in 1960 and used in 1970’s for
sleep disorders because it induces REM sleep
Used
in Europe as anesthetic agent until found
that it caused seizures
1977,
study claimed it stimulated effects of
Growth Hormone
GHB
Unapproved
drug in US, but
legally obtainable under FDA
investigational New Drug
exemption for treatment of
narcolepsy
–20 states have controlled its
use with penalties similar to
marijuana possession
Gamma Hydroxybutyrate Acid
(GHB)
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Readily available in drug market and
inexpensive and relatively easy to make
– recipes are obtainable on the internet
Obtainable as clear and odorless liquid,
gel, or powder which have a salty taste
– however, taste is masked by ETOH
which increases its clinical effects
GHB
Used
in date rape because:
–quick onset of effect
– easily obtainable
– small quantities are needed
–causes hallucinations and amnesia
making the patient an unreliable
witness
GHB
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GHB - Toxicity
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Acts as neurotransmitter affecting GHB and
GABA- B receptors causing CNS depression
– takes effects in 15-30 minutes causing
drowsiness, dizziness, and disorientation
– duration of action up to 3 hours
– half life of 20 min to 1 hour
– hallmark is marked agitation upon
stimulation despite apnea and hypoxia
10mg/kg
causes vomiting, rapid
onset of coma and amnesia
20-30mg/kg
cause rapid cycles of
REM and non-REM sleep
50mg/kg
can cause resp
depression, bradycardia, clonic
muscle contractions, and decreased
cardiac output
GHB - Other forms
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Gamma butyrolactone (GBL) - can be
purchased from chemical supply stores or
catalogues and converted to GHB with
NaOH
– GBL is rapidly converted to GHB by
peripheral lactonases within minutes
1,4-Butanediol
- can be purchased in
similar manner as GBL
–converted to gamma
hydroxybutyaldehyde by alcohol
dehydrogenase
–then, converted to GHB by aldehyde
dehydrogenase
Ketamine
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Ketamine
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AKA: Special K, Super Acid, Super C
used as an anesthetic in EM and veterinary
medicine
Ketamine is a controlled substance in 18
states as schedule III drug
Used in date rape because:
– rapid onset
– dissociative hallucinogenic
Ketamine - Toxicity
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Chemically related to PCP
takes effect 15-20 minutes, producing
analgesia
Higher doses produces dissociative
hallucinations, delirium, resp depresion,
Sz, arrythmias and cardiac arrest
Effects last 20-45min
Ketamine - Treatment
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Mainly supportive
No antidote
Pt should be placed in quiet room with
minimal stimulation
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