Stimulants – Lydia Vezina PDF - CSAM
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CSAM
FUNDAMENTALS
COURSE:
STIMULANTS
Lydia Vezina B.Sc. M.D. C.C.F.P.
OPIOD DEPENDENCY PROGRAM
RENFREW RECOVERY AND DETOX
ADDICTION CENTRE (FOOTHILLS MEDICAL
CENTRE)
ADDICTION NETWORK HOSPITAL
CONSULTANT
October 23rd, 2016
Faculty/Presenter Disclosure
No
relevant disclosures
Learning Objectives
Describe popular
stimulants and how they
are abused.
Understand the neurobiology and
pharmacology of stimulants.
Describe short and long-term effects of
stimulant use.
Understand effective treatment options for
stimulant use disorders.
History of Stimulants
Cocaine: chewing of coca leaves prevalent in
the Andean regions of South America for more
than 2000 years
1860 German Graduate student Albert
Niemann, isolated cocaine as the active
ingredient of coca leaf
Coca-Cola: introduced 1886 (containing 4.5mg
of cocaine per 6 oz.)
1903 cocaine removed from Coca-Cola
History of Stimulants
Amphetamine: first synthesized in 1887
Methamphetamine: first synthesized in 1919
Amphetamines widely used during WWII
Methamphetamine currently available with
a prescription for obesity, attention deficit
hyperactivity disorder, and narcolepsy
ex: Desoxyn
History of Stimulants
Ecstasy: used
unsuccessfully in
psychotherapy in 1970’s, became popular
in rave scene in late 1980’s, early 1990’s
Crack Cocaine: 1984/1985 appears in New
York, Los Angeles and Miami
In late 1980’s smokable form of Crystal
Meth was created in Asia and then
surfaced in California in the 1990’s
Epidemiology Stimulants
2013: 1% (256,000) of Canadians used a stimulant in
the past 12 months, a decrease from 2012 (2%).
Age groups
15 to 19: 3% (or 73,000)
20 to 24: 2% (o 45,000)
25 years and older: 1% (or 138,000)
Gender
No difference in prevalence between males and females:
1% or 139,000 for males and 1% or 117,000 for females.
The Canadian Tobacco, Alcohol and Drugs Survey (CTADS) 2013
Epidemiology Stimulants
Rates of abuse
16% of people who used stimulants (or 39,000
Canadians) reported abusing them, a decrease
from the rate reported in 2012 (40%)
The rate of abuse
15 to 19: 32% (20,000)
20 to 24: 40% (14,000)
25 and older was not reportable.
The Canadian Tobacco, Alcohol and Drugs Survey (CTADS) 2013
Cocaine use
worldwide
UNODC World Drug Report 2016
Amphetamine use
worldwide
UNODC World Drug Report 2016
CURRENT POPULAR
STIMULANTS
Cocaine
Natural plant alkaloid
From the leaves of the coca bush (Andean regions
of South America = Peru, Columbia, Bolivia)
Salt form usually cocaine hydrochloride: powder
Highly water soluble (easy to dissolve for injection
or absorption across mucous membranes for
snorting)
Frequently cut with levamisole (animal dewormer)
Crack Cocaine
Crack Cocaine street name for freebase cocaine
Cocaine hydrochloride can be converted back to
the water insoluble base by heating it in an
organic solvent at base pH
Relatively low melting point, self administered by
smoking it
Absorbed into the blood stream through the lungs
Can be dissolved in vinegar in order to return to
form that can be injected
Cocaine/Crack Cocaine
Amount
used usually reported in grams
Piece: usually refers to crack cocaine (i.e.
a 40 piece)
8 ball: refers to 3.5 grams of cocaine
Speedball: refers to injection of
combination of heroin and cocaine
Crystal Meth
Chemically
similar to amphetamines
White, odourless, bitter-tasting crystalline
powder
Route: oral, smoked, snorted, or injected
Made in illegal labs by chemically altering
OTC medicines (pseudoephedrine)
Ecstasy
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Stimulant and hallucinogen properties
First synthesized by the German pharmaceutical
company Merck in 1912.
Tested by the military in search for the “truth drugs” 1953
Made in illicit labs and may contain other active such as
amphetamine, mephedrone, methamphetamine,
ephedrine, or caffeine
Some tablets sold as ecstasy do not even contain any
MDMA
Street names include “E” , “X”, Molly, Skittles
Prescription Stimulants
Methylphenidate
(Ritalin, Concerta,
Biphentin)
Dextroamphetamine Sulphate (Dexedrine)
Amphetamine and Dextroamphetamine
(Adderall)
Lisdexamfetamine (Vyvanse)
STIMULANTS AND THE BRAIN
The Reward Pathway
When activated by a rewarding stimulus (e.g., food, water,
sex), information travels from the VTA to the nucleus
accumbens and then up to the prefrontal cortex.
The Brain in Stimulant Use Disorders
Cocaine: main mechanism of action
is the blockage of dopamine
reuptake
Cocaine concentrates in the VTA, Nucleus
Accumbens and the Caudate Nucleus
NIDA
Cocaine Blocks Reuptake of Dopamine
NIDA
As a Result of Cocaine’s Actions in the
Nucleus Accumbens, Impulses leaving
the NA activates the Reward System
NIDA
The Brain in Stimulant Use Disorders
Methamphetamines
Inhibit
reuptake of synaptic dopamine AND
promotes direct dopamine release
Ecstasy:
Acutely increases serotonin by blocking
reuptake and directly releasing
Chronically decreases serotonin levels by
depleting serotonin stores and inhibiting the
synthesis of new serotonin
neurotoxicity
Pharmacology of Stimulants
Water soluble
Onset
of action depends on route of
administration: rapid onset of action with
injection or smoking
Duration of action dependent on route of
administration: oral administration
produces longer duration of action
Short term effects of stimulant
use
Stimulant Intoxication
Signs or Symptoms
1. Tachycardia or bradycardia
2. Pupillary dilation
3. Elevated or lowered blood pressure
4. Perspiration or chills
5. Nausea or vomiting
6. Evidence of weight loss
7. Psychomotor agitation or retardation
8. Muscular weakness, respiratory depression, chest pain, or
cardiac arrhythmias
9. Confusion, seizures, dyskinesias, dystonias, or coma
DSM 5
Stimulant Intoxication
Clinically significant problematic behavioural or
psychological changes such as:
euphoria or affective blunting
changes in sociability
hypervigilance
interpersonal sensitivity
anxiety
tension or anger
stereotyped behaviours
impaired judgement
DSM 5
Stimulant Withdrawal
Dysphoric mood and two (or more) of the following
physiological changes, developing within hours to several
days after cessation of prolonged amphetamine-type
substance, cocaine or other stimulant use
1. Fatigue
2. Vivid, unpleasant dreams
3. Insomnia or hypersomnia
4. Increased appetite
5. Psychomotor retardation, or agitation
DSM 5
Acute Consequences of Stimulant Use
Neuro: seizures,
strokes
CVS: tachycardia, arrythmia, MI, HTN
Kidneys: cocaine induced rhabdomyolysis
Heme: Agranulocytosis (levamisole)
Repro: placenta previa
ENT: nosebleeds
Infectious Disease: STI’s, cellulitis, bacterial
endocarditis
ECSTASY: Dehydration, Hyperthermia,
Hyponatremia
Stimulant Induced Mental Health
Disorders
INTOXICATION
WITHDRAWAL
Psychotic
Delusions
Bipolar
Bipolar
Depression
Depression
Anxiety
Anxiety
OCD
OCD
Sleep Disorders
Sleep Disorders
Sexual Dysfunction
DSM 5
Long Term effects of
stimulant use
Long Term Consequences of
Stimulant Use
Tolerance
and Withdrawal
Sensitization
Addiction (Stimulant Use Disorder)
Restlessness, anxiety, irritability, paranoia, panic
attacks, mood disturbances
Insomnia
Sensitization
Sensitization
(opposite of tolerance)
more you use the drugs more likely of
symptoms happening such as:
Seizure
Psychosis (paranoia,
visual, auditory,
and tactile hallucinations)
Stereotypical behaviors
Long Term Consequences of
Stimulant Use
Repro: irregular menses, prematurity
ENT: nasal septum perforation, loss of sense of
smell, chronically runny nose
Infectious Disease: Hep C, HIV
Weight loss
Methamphetamines (neurocognitive
impairment, “meth mouth”)
Psychosocial: homelessness, legal
involvement, trauma
Effects of Crystal Meth
Permission granted by Multnomah County Sheriff’s Office
TREATMENT OF STIMULANT
INTOXICATION, STIMULANT
WITHDRAWAL, AND
STIMULANT USE DISORDER
Treatment of Stimulant Intoxication
Supportive
Phentolamine for
hypertension (no beta blockers
bc unopposed alpha-adrenergic stimulation can
lead to coronary vasoconstriction and ischemia)
Chest pain: ECG, biomarkers, CXR, benzo and
nitro
Treat stimulant induced psychosis if severe
Treat any infections: cellulitis, endocarditis,
infectious diseases (HIV, Hep C, STI’s), abscesses,
septic arthritis
Treatment of Stimulant Withdrawal
Supportive
Suicide prevention
Treatment: Medications for Cocaine
Use Disorders
No evidence
that any of the following are
helpful:
Antidepressants
Dopamine agonists
Modafinil
Cocaine vaccine
Treatment of Stimulant
Use Disorders
SBIRT (Screening, Brief Intervention, Referral to Treatment)
Stages of Change
Harm Reduction (needle exchange/crack pipe programs)
Motivational Enhancement Therapy
Cognitive Behavioural Therapy
Contingency Management
Residential Treatment
Self Help Support
Matrix Model
Treatment of Underlying Mental Health Disorders
Treat any Medical Complications (HIV, HCV)
Risk of Relapse
Re-exposure
to the Drug
Exposure to stress
Exposure to environmental cues
Conditioned response to drug-related
stimuli (e.g. craving on seeing any white
powderlike substance)
Cognitive Behavioural Therapy for
Stimulant Use Disorders
Identification
of high risk situations
Development of coping skills
Development of new lifestyle
behaviours
Development of sense of self-efficacy
References
DSM 5 Diagnostic & Statistical Manual of
Mental Disorders 5th Ed. Text Revision 2013
The ASAM Principles of Addiction Medicine
Fifth Edition. Ries, Fiellin, Miller, Saitz. 2014
The Canadian Tobacco, Alcohol and Drugs
Survey (CTADS) 2013
UNODC, World Drug Report 2016
(http://www.unodc.org/wdr2016/en/mapsand-graphs.html)
National Institute of Drug Abuse (NIDA)
www.drugabuse.gov