alcohol SUD/stimulant use DISORDER
what psychoactive drugs are canadians using?
alcohol
tobacco
marijuana
other
men consume more drugs compared to women
true
nova scotia consumes more alcohol than other province in canada
true
alcohol harms highest in least affluent groups despite high drinking rates in affluent groups
true
Canada’s Guidance on Alcohol and
Health
Update published
January 2023
Much chatter in the press/social media about the
severe change in
recommendations from earlier iterations
Previous recommendations:
10 drinks per week for women, no
more than 2 drinks on any given day most days
15 drinks per
week for men, no more than 3 drinks on any given day most days
Canada’s Guidance on Alcohol and
Health
it is recommended that people living in canada consider reducing their alcohol use.
because there is a continuum of risk associated with weekly alcohol consumption
the risk of harm from alcohol is...
low for individuals who consume 2 standard drinks or less per week.
and moderate for those who consume between 3 and 6 standard drinks per week.
risks increase for those that consume 7 standard drinks or more per week.
consuming more than 2 standard drinks per occassion is associated with an increased risk of harms to self an others.
true
when trying to get prego or prego there is no known safe amt of alcohol use
true
sex and gender
above the upper limit of the moderate risk zone for alcohol consumption-the health risks increase steeply for females than males.
DSM-V
Criteria:
Substance Use
Disorder
“A problematic pattern of
[substance] use leading to
clinically
significant impairment or distress,
as manifested
by at least 2 of the
following, occurring within a 12-
month
period:”
-Impaired control
- Social impairment
- Risky
use
- Pharmacological criteria
DSM-V Diagnostic Criteria- Alcohol Use Disorder
1. Alcohol is often taken in larger amounts or over a longer period
than was intended.
2. There is a persistent desire or
unsuccessful efforts to cut down or control alcohol use.
3. A
great deal of time is spent in activities necessary to obtain alcohol,
use alcohol, or recover from its effects.
4. Craving, or a strong
desire or urge to use alcohol.
5. Recurrent alcohol use resulting
in a failure to fulfill major role obligations at work, school, or
home.
6. Continued alcohol use despite having persistent or
recurrent social or interpersonal problems caused or exacerbated by
the effects of
alcohol.
7. Important social, occupational,
or recreational activities are given up or reduced because of alcohol
use.
8. Recurrent alcohol use in situations in which it is
physically hazardous.
9. Alcohol use is continued despite
knowledge of having a persistent or recurrent physical or
psychological problem that is likely to have
been caused or
exacerbated by alcohol.
10. Tolerance, as defined by either of
the following:
1. A need for markedly increased amounts of
alcohol to achieve intoxication or desired effect.
2. A markedly
diminished effect with continued use of the same amount of
alcohol.
11. Withdrawal, as manifested by either of the
following:
1. The characteristic withdrawal syndrome for alcohol
(refer to Criteria A and B of the criteria set for alcohol
withdrawal).
2. Alcohol (or a closely related substance, such as
a benzodiazepine) is taken to relieve or avoid withdrawal symptoms.
1) Have you ever felt you should Cut down on your
drinking?
2) Have people Annoyed you by
criticizing your drinking?
3) Have you ever felt bad or
Guilty about your drinking?
4) Have you ever had
a drink first thing in the morning to steady your nerves or to get rid
of a hangover (Eye-opener)?
Assessment Tool: CAGE
Scoring: Item responses on the CAGE questions are scored 0 for "no" and 1 for "yes" answers, with a higher score being an indication of alcohol problems. A total score of two or greater is considered clinically significant.
Assessment
Tool: AUDIT
AUDIT = Alcohol Use Disorders IdentificationTest
10 questions
Interview or Self-Reported
Developed by the
World Health Organization
Must be answered based on STANDARD drinks
Assessment Tool:
AUDIT
- Score 8 or more: Hazardous
Drinking
- Score 13 for
females, 15 for
males: Likely presence of
alcohol use disorder
Why the
difference
between sexes?
- Answer lies in physiological difference
between the
sexes
- Cis-women and people who were Assigned
Female at
Birth (AFAB) generally have a
lower % water in their
bodies
- Alcohol is water soluble
- Therefore, less alcohol
is needed to cause
intoxication
- New research suggests
cis-women and
AFAB may produce less alcohol
dehydrogenase
than cis-men or people
assigned male at birth (AMAB)
MOA of Alcohol
Alcohol
Ingestion
-incr GABA (+ incr Glutamate to compensate)
-Disinhibition/
CNS
depression
under normal circumstances
inhibition =excitation
GABA and excitation= glutamate
alcohol causes GABA to .....
increase
with long term alcohol exposure, the brain attempts to restore eqbm by...
compensating for the depressant effects of alcohol aka the brain decreases inhibitory neurotransmission and enhances excitatory neurotransmission.
how does short term alcohol exposure tilt the balance towards inhibition?
by enhancing the function of inhibitory neurotransmitters and neuromodulators i.e GABA, glycine and adenosine
what happens during withdawal?
compesatory changes are no longer opposed by the presence of alcohol-balance shifts towards excessive excitation.
what are the characteristics of the state of hyperexcitation?
seizures
delirium and anxiety
→ Chronic alcohol use leads to chronically elevated
GABA and glutamate
When alcohol quickly removed:
GABA levels drop quickly
glutamate levels remain elevated
Can lead to Delirium Tremens
ALCOHOL ADME
Absorption- oral absorption is rapid- 5-10 mins after ingestion
Peak = 30-90 mins after last drink depending on type
of drink
Food slows absorption and increases
time to peak
-Distribution- Vd = 0.6-0.7L/kg,
less in women
Metabolism
Ethanol
(worked on by Alcohol Dehydrogenase) to acetaldehyde which is worked
on by Acetaldehyde dehydrogenase to become
acetate CO2 + H2O
▪ Elimination-
Primarily renal. Lungs can eliminate up to 10% (rely
on this for breathalyzer tests)
▪ Elimination rate =
15-20mg/dL/hour (longer in AUD)
Symptoms: Acute
Intoxication
Slurred speech
Ataxia
Disinhibition
Euphoria
(via reward pathway)
Aggression
Flushing
Nausea/vomiting
Severe
Intoxication/Overdose
Severe intoxication/overdose:
Blackouts- not creating
new
memories
Coma
Respiratory depression
Hypoglycemia
Hypothermia
Death
Management:
Acute Intoxication
Provide a safe space
Fluid balance is very important- oral or
IV fluids as
tolerated
Glucose monitoring
TIME is
the main cure for acute alcohol intoxication
Antagonists not
used
Alcohol poisoning- the person may pass out and not
be
able to vomit→ MAY require stomach pumping etc. No
longer
routinely done
Alcohol Withdrawal
More than just a hangover
Can be life threatening
Body
has compensated for chronically
high levels of GABA by increasing
release
of excitatory neurotransmitters
like
glutamate
Abrupt removal of alcohol leads to
a
rapid drop in inhibitory neurotransmitters
Excitatory
neurotransmitters take time to
down-regulate and reduce
CNS in an excitatory state
Delirium tremens, seizures, death
CIWA-Ar
Clinical Institute
Withdrawal
Assessment- Alcohol (revised)
Pulse
Nausea/vomiting
Tremor
Paroxysmal
sweating
Anxiety
Agitation
Tactile disturbances
Auditory disturbances
Visual
disturbances
Headache/fullness
Orientation/clouding of
sensorium
Clinician assessment tool used to
evaluate the level of
alcohol
withdrawal
Helps dictate treatment of
alcohol
withdrawal
Combines clinician observation
and patient
reporting
Validated tool
CIWA-Ar score of less than ....is the goal
discontinue protcol if score less than 10 for....
10
3 consectutive assessments.
hold benzos and notify prescriber if benzo intoxication occurs e.g..
ataxia
nystagmus
disorientation, RRless than 10/min or systolic BP less than 100mmhg.
notify prescriber if patient has recieved more than....or if sx of wwithdrawal worsen after 2 consecutive doses
60mg diazepam or 12mg lorazepam in a 12h period
Delirium Tremens
Life threatening condition
caused by severe
alcohol
withdrawal due to acute
abstinence or reduction
in
consumption of alcohol
Occurs in ~5%
of alcohol
withdrawal patients
Starts
~48-96 hours after last
drink and lasts ~5 days
Delusions
Hallucinations requirement
Tachycardia
Hyperthermia
Hypertension
Diaphoresis
Elevated cardiac markers
Increased O2
Hyperventilation → respiratory
alkalosis
Hypophosphatemia
Rhabdomyolysis
Cardiac failure
Risk factors for DTs
Previous DT
Sustained heavy drinking
>30y/o
Concurrent illness
Significant alcohol withdrawal in
the
presence of elevated BAC
Longer period since last
drink (ex.
Person presenting >2 days since
last
drink)
Treat with supportive care,
benzos,
treatment of underlying conditions, and
frequent
monitoring of symptoms
NO SUCH THING AS MILD DTs(Delirium Tremens)
DTs are the most
severe form
of withdrawal
Occur after other
withdrawal
symptoms
Withdrawal hallucinosis can
occur
well before DTs set in
true
Non-Beverage
Alcohol
Non-beverage alcohol is alcohol that is not intended for
human
consumption as a beverage.
E.g. hand sanitizer, mouth wash,
aftershave, vanilla
extract
Marginalized people with
severe AUD are often forced to
turn to these forms of alcohol due
to inability to afford
beverage alcohol
Can lead to many
harms, including severe intoxication,
blindness, and death
(especially if it is not ethanol that is
being consumed)
A
harm reduction approach here would be to provide them
with
beverage alcohol.
More on this later
Chronic
Alcohol Use
Alcohol use disorder
Different than treating acute
withdrawal or
intoxication
Non-pharm= CBT, group therapy,
AA and other
abstinence-based therapies
Pharmacological =
disulfiram, acamprosate,
naltrexone
All used to help
promote prolonged abstinence and
recovery
A Word About AA/NA
Created in USA by Bill Wilson and Bob Smith
Originally a
faith-based program
Abstinence- based: believe that use of
drugs to
help with abstinence (ex. Diazepam for
alcoholism
or methadone for opioid use
disorder) dose not constitute true
abstinence
Historically, people who used medications
like
above were not allowed in AA/NA
Newer groups forming
with less emphasis on the
“God” aspect and with medications allowed
Naltrexone
Aka Revia®
Mechanism of action: blocks central µ
opioid
receptors
Doing so blocks the reinforcing nature
of
alcohol in the nucleus acumbens (reward
pathway) in the
brain
Also has effect on HPA-axis to suppress
alcohol
use
DOES NOT CAUSE PHYSICAL AVERSION TO
ALCOHOL
If the person drinks, they will not vomit etc
Rather, helps reduce cravings for, and euphoria
caused by alcohol
Naltrexone
Dosing:
50mg daily (often will see
starting dose of 25mg)
Efficacy:
Found to reduce alcohol use in
people with AUD
better than
placebo in several SR/MA
E.g. A 2010 Cochrane
review
found the RR to be 0.83 (0.76-
0.9) for heavy
drinking for
naloxone compared to placebo.
Also reduced
drinking days by 4%
Naltrexone
IMPORTANT:
THIS IS AN OPIOID ANTAGONIST
Therefore,
opioid analgesia will be
ineffective
CONTRAINDICATED IN
COMBINATION
WITH METHADONE- several dangerous
cases have
occurred as a result of
naltrexone+methadone combination
THERE IS NO SITUATION IN WHICH THE
COMBO IS WORTH THE RISK
ADRs: Nausea, headache, dizziness. Can
cause elevation in LFTs-
measure at
baseline and then monthly
Acamprosate Aka Campral®
Mechanism of action: not 100% clear
Postulated to restore
glutamate “tone”
Modulates the neurotransmission
of
glutamate upon alcohol use cessation
DOES NOT DECREASE
WITHDRAWAL
SYMPTOMS- pt is still at risk of DTs
Patients
may do better if already
abstinent x 7 days or so- evidence
on
this unclear
Acamprosate
Dose
2x333mg TID (ADHERENCE ISSUE)
Evidence:
Murky here
too
Cochrane Review in 2010 of acamprosate vs
placebo
showed NNT of 9 for return to ANY
drinking and increased
abstinence duration
by 11%. NO effect on heavy drinking
Other studies have found it to be less
effective
ADRs:
Diarrhea, flatulence, insomnia, anxiety,
depression
CI in
CrCl <30ml/min
DisulfiramAka Antabuse
▪ Irreversible inhibition of acetaldehyde dehydrogenase (DOA up to 14
days)
▪ Produces severe reaction in combination with alcohol due
to build-up of acetaldehyde → approximately 30mins after ethanol
exposure
▪ Vomiting, flushing, tachycardia, hypotension,
syncope
▪ Reaction severity depends on dose of disulfiram and ethanol
Disulfiram
Considered aversion therapy
Helps eliminate positive
conditioning
associated with drinking- no longer
associated
with euphoria but with negative
consequences
Best if given
under supervision or in highly
motivated patients
Dosing:
125-500mg daily. often done as
500mg daily for 2 weeks then 250mg
once
daily thereafter
Disulfiram
Evidence
Evidence = mixed at best
2014 meta-analysis =
disulfiram
no better than placebo for
return to drinking
(JAMA. 2014
May;311(18):1889-900)
Other SR/MA have found
time to
first drink and other measures of
abstinence to be
no better with
disulfiram than placebo
No longer
commercially
available- must be compounded
Other Anti-Craving
Treatment
Anti-craving treatments work to reduce reward
pathway
activity
Gabapentin- modulates dopamine. Has good
evidence,
especially in combination with naltrexone
Baclofen- GABA agonist
Topiramate- modulates GABA system
Complications of Alcohol Use
MANY
Liver disease: hepatitis, fatty
liver,
cirrhosis
Wernicke’s encephalopathy,
Korsakoff’s
dementia
Peripheral neuropathy
Stroke
(hemorrhagic)
Cardiomyopathy
Arrhythmia
Cancer
Impotence
Esophageal varices
Complications
Chronic AUD
MANY
Liver disease: hepatitis, fatty
liver,
cirrhosis
Wernicke’s encephalopathy,
Korsakoff’s
dementia
Peripheral neuropathy
Stroke
(hemorrhagic)
Cardiomyopathy
Arrhythmia
Cancer
Impotence
Esophageal varices
Chronic Alcohol Use: The Reality
Many of these people are homeless or have experienced
homelessness
“Listerine Bums”
Imagine how awful the
disease must be to have a person stealing mouth wash,
cologne,
vanilla extract etc. to support stave off cravings and feed their use
disorder
As pharmacists, we need to get away from this
demeaning language and refer to
these people as what they are,
PEOPLE WHO NEED OUR HELP
Will be in and out of the justice
system- there is little help available to these
folks
Often spend many nights in the “drunk tank”
Given a Cliff bar
and a bottle of water
“dry out”
Sent back out to the
street once sober
What Can Pharmacists Do?
ASK, in a non-judgemental way, about people’s drinking
ASK
if they feel they would like to change their drinking habits
USE the CAGE screening tool to aid your discussions
KNOW where
to refer people when they come to you for help
Difficult to get a true picture of stimulant use in Canada
CTADS historically combined them into “illicit drugs”
-Cocaine/crack
- MDMA
- Hallucinogens
-
Methamphetamine
- Heroin
- Past year use of those 5 drugs
was 3% in the 2017 CTADS
However, methamphetamine use is
escalating across the country
trauma..>dusconnection...>drug use numb pain....>criminal activity to get access to drug.>arest incarcerate &bac
true
Substance Use Disorder Risk Factors
Personal history of substance use disorder
Family history of
substance use disorder
History of psychiatric illness
History of pre-adolescent sexual abuse
DSM-V Criteria: Substance Use Disorder
“A problematic pattern of [substance] use leading to
clinically
significant impairment or distress, as manifested
by at least 2
of the following, occurring within a 12-month
period:”
Impaired control
Social impairment
Risky use
Pharmacological criteria
Impaired control
Using higher doses and/or
using substance over a
longer
period of time than initially
intended.
e.g Taking more hydromorphone
pills than prescribed or
continuing to seek them out after rx is finished
“I really need
to cut back”
Social impairment
Failure to fulfill major roles
(home, school, work
etc)
Avoiding family activities in
order to use
Risky use
Using in situations that are
physically dangerous or
using
despite knowledge of serious
harm
Drinking and
driving.
Continued use of cocaine
despite knowledge of
arrhythmia
Pharmacological criteria
(tolerance and withdrawal)
Increasing doses required to
achieve desired
effect
(tolerance). Withdrawal
symptoms occurring when
use
abruptly stopped.
e.g Escalating doses
of
hydromorphone required to
achieve the “high.”
Alcohol
withdrawal syndrome and DTs.
SUD etiology
we find SUD at the intersection of
-learned maladaptive coping
-environment
-drug
-genetics
“Abuse liability
refers to the tendency of a drug to be used in nonmedical situations,
even sporadically, due to underlying psychoactive effects it produces
(such as euphoria, sedation, or mood changes)” –
Cambridge Cognition
A drug needs to have abuse liability to .....
reinforce the neural
pathways/reward system
SUD is ......whereby the drug “hijacks” the normal
reward
pathway and the brain learns that that is easier than
normal coping
strategies.
a learning disorder
Lays down neural pathways that say “stress is more easily managed
by
using drug X”
CNS Depressants
Alcohol
Benzodiazepines/barbiturates
Opioids
Volatile Solvents
Stimulants
Cocaine/crack
Amphetamines
Caffeine
Nicotine
Hallucinogens
LSD
Psilocybin (mushrooms)
Mescaline
Phencyclidine (PCP)
Ecstasy (MDMA) (also stimulant)
Cannabis (also depressant)
natural rewards elevate dopamine levels.
food and sex
Basic Pharmacology: Stimulants
Lead to release of ++ neurotransmitters
Especially NE,
Dopamine, Serotonin
Hijack the reward pathway
Cocaine:
Other names: Blow, snow, rock, coke, crack
Available in 2 main forms:
Crack= crystalline, smokable
form→cheaper than pure cocaine
Cocaine= pure form→ water
soluble. Injected or snorted.
MOA: blocks reuptake of catecholamines to the
presynaptic neuron
leading to increased concentrations of 5HT,
NE, dopamine and
epinephrine in the synapse.
cocaine use leads to....
Exogenous activation of the reward pathway→euphoria,
insomnia,
increased heart rate, reduced appetite
Directly
cardiotoxic- overdose deaths usually caused by cardiac arrest
Can lead to extreme increases in core body temperature, which is very
dangerous
cocaine kinetics
intravenous onset
<1 minute
peak 3-5 minutes
duration of action 30-60mins
nasal route onset
1-5 mins
peak 20-30mins
duration of action 60-120
smoking onset
< 1 min
peak 3-5 minute
duration 30-60 minutes
gastrointestinal route
onset
onset 30-60minutes
peak 60-90
duration - unknown.
Cocaine: Acute Effects
Euphoria/extreme happiness
++ Energy
Mental
alertness
Irritability
Paranoia
Bizarre,
unpredictable behaviour
Insomnia
Vasoconstriction
Dilated pupils
Nausea
Increased BT and BP
Tachycardia
Tremors/restlessness
Muscle twitches
Cocaine: Long Term Effects
Of snorting: nosebleeds, frequent runny nose, loss
of smell, trouble
swallowing
Of smoking:
Cough, asthma, respiratory distress, increased risk
of
pneumonia
Of injection: Increased risk
of HIV and Hep C, other bloodborne illness,
endocarditis,
skin/soft tissue infections, collapsed veins
General:
Malnourishment due to chronic appetite
suppression
Parkinson’s disease after years of
use
Insomnia/restlessness after binges
Severe paranoia
Cocaine: Overdose
Overdose:
Tachycardia
Hypertensive crisis
Fever/hyperthermia
MI
Death
Risk of death
increases when mixed with other drugs
Often mixed with EtOH→
party drug
Heroin + cocaine = speedball = very dangerous and
deadly
No antidote to cocaine overdose- supportive care only
Cocaine: Withdrawal
Withdrawal:
Anhedonia
Depression
Fatigue
Increased appetite
Slowed thinking
Scary
dreams and insomnia
Anhedonia and depression and persist for
YEARS after drug
use stops
Brain needs to re-learn how to
experience normal
pleasure
Methamphetamine:
AKA Crystal Meth, Crystal, Ice, Speed, Blue,
Meth
ROA: Smoked, swallowed, Snorted, Injecting (powder
dissolved in water or
EtOH)
wat is the MOA?
MOA: ++++ dopamine, serotonin, norepinephrine, and epinephrine release in the nucleus acumbens
Also blocks neurotransmitter reuptake.
Methamphetamine: Pharmacokinetics
Absorption:
rapid via any route (PO, IN,
Inhaled, IM, IV, PR, PV)
Methamphetamine: Pharmacokinetics Distribution:
Quickly and easily crosses BBB
Large Vd of 3-4L/kg
Methamphetamine: Pharmacokinetics Onset of action:
Injection or smoking: seconds
Intranasal: 5 mins
Oral: 20 mins
Methamphetamine: Pharmacokinetics Peak plasma [ ]:
Injection or smoking: 30 mins
Oral: 2-3 hours
Methamphetamine: Pharmacokinetics Duration of action:
Plasma T1/2 : 12-34 hours
Effects commonly persist for
>24 hours
Methamphetamine: Acute Effects
Adrenergic activity:
Adrenergic activity:
Tachycardia
Hypertension
Hyperthermia
Wakefulness
Dopaminergic activity:
Increased movement
“Tweaking”
Euphoria/rewarding feeling
Methamphetamine: Acute Effects Serotonergic activity:
Changes in appetite
Changes in thirst
signal
response
Changes in mood
(expansive)
Methamphetamine: Acute Effects
Dopaminergic activity:
Increased movement
“Tweaking”
Euphoria/rewarding feeling
Methamphetamine: Long Term Effects
Increased risk HIV and Hep B&C
Risky behaviours
Injury to nerve cells (worsening of
HIV as a result)
Dental complications (“meth
mouth” see pic)
Changes in
brain structure and
functioning; changes in
dopaminergic
pathways
May be irreversible or may not
recover for a long
time after drug
use stops
Psychosis/hallucinations
Violent behaviour
Sleeping problems
Changes in bone
structure
Overdose = death from cardiac
arrest or due to hallucination
Methamphetamine: Formication
sense of bugs crawling all over the
skin accompanied by
extreme
itchiness.
Leads to intense sessions
of
scratching and subsequent
scabbing and scars.
MDMA (Ecstasy): AKA: Ecstasy, Molly (slang for molecular,
implying purity/scientific)
3,4-Methylenedioxymethamphetamine
is a ....
A sympathomimetic amphetamine
MDMA (Ecstasy):
Considered a social/party drug- people report feeling close to
others,feeling loved, feeling more social and having improved sensory
perception
Often sold at parties and in bars, part of “rave”
culture
Sold in pill form with “cute” designs to appeal to
party goers
MOA: Indirect serotonergic agonist- leads to increased
concentration of
serotonin in the synapse. Also leads to release
of NE and dopamine.
Similar effects to amphetamines- euphoria
MDMA Pharmacokinetics
Absorption: readily absorbed from GI tract
Distribution:
Peak within 2 hours
Duration: 4-6 hours
Elimination:
75% excreted intact via urine
Remainder metabolized via
CYP 2D6
MDMA: Short Term Effects
With onset of action comes:
Increased energy/activity
HTN/tachycardia
Euphoria/expansive mood
Closeness with others and increased
sexual libido
Increased trust/empathy
Nausea
Muscle cramping
Chills
MDMA: Short Term Effects
Hyponatremia:
+++sweating
+++thirst
MDMA
causes persistent secretion of antidiuretic
hormone which slows
water excretion
MDMA users also often believe that drinking
lots of
water will reduce risk of hyperthermia
All leads
to hyponatremia which can be very dangerous
MDMA: Short Term Effects
Serotonin Syndrome:
MDMA is ++
serotonergic
Characterized by a triad of
symptoms:
Autonomic dysfunction
Abnormal neuromuscular
activity
Altered mental status
Potentially life threatening
MDMA: Long Term Effects
Many of these can persist for YEARS
Especially anything to
do with
pleasure
Brain needs to re-learn how
to
experience pleasure in response to
normally pleasurable
experiences
like yummy food, a hug from a
loved one, or sex.
Irritability
Impulsivity
Aggression
Depression
Sleep problems
Anxiety
Memory and
attention issues
Decreased appetite
Decreased interest
in and pleasure
from sex
MDMA Overdose
Serotonin syndrome
Hyponatremia
Hepatotoxicity
Life-threatening increases in HR, BT, and BP
No antidote
Supportive measures only
Stimulant Use Disorder Treatment
Not much to offer folks
Not a lot of evidence on what to
use
Non-Pharm: CBT, CBT,
Group Therapy, Motivational incentives
(aka $$)
Pharmacological trtment for stimulant use disorder
(May see):
Benzodiazepines (diazepam)- issues with efficacy
and risk of
developing BZD use disorder
Methylphenidate or
dextroamphetamine (Dexedrine)
Some emerging evidence that these
MAY help with stimulant
withdrawal
Hallucinogens
Drugs:
LSD
Psilocybin
Peyote
Dextromethorphan
Salvia
PCP and Ketamine (dissociative
hallucinogens)
Hallucinogens-effects
Sleep changes
Hallucinations/delusion
Change in
sexual behaviour
Changes in perception of time
and
place
Spiritual experiences
Relaxation
Paranoia and overt psychosis (short
and long term
hallucinogen Dissociative:
changes in pain
perception, perception of
past
trauma
Some being studied for tx of
tx resistant
depression etc
Hallucinogen Persisting
Perception Disorder (HPPD):
Flashbacks to when patient
was on hallucinogen
Happen
without warning
Can happen days to years
after last drug use
Hallucinogen “Abuse Liability”
Hallucinogen use disorders are in the DSM-V
However, there
is some debate about whether a true hallucinogen use disorder can
occur at a brain level
They do not cause a release of NTs in
the nucleus acumbens
They do not then “hijack” the reward
pathway
Without doing that, can a person have a true use
disorder?
Rarely hear of someone using LSD over and over again
to the detriment of their
family, work, or school
commitments
Hallucinogens are often taken in addition to other
substances
Those substances are usually the ones for which the
person has the true use disorder
Food for thought!
Volatile Solvents/Inhalants
Solvents (become gas at RT)
Aerosol sprays
Gases
(including petroleum gas)
Nitrites (ex. Nitroglycerine)
Work to slow/reduce brain activity
Volatile Solvents/Inhalants
Acute Effects:
Slurred speech
Ataxia
Euphoria
Dizziness
Long term effects:
Liver and kidney damage
Hearing loss
Bone marrow
damage
Loss of coordination
Muscle damage
Delayed
behavioural development
Brain damage
Hallucinogen/Solvent Use Disorder
Treatment
Not much to offer folks
Not a lot of evidence on what to
use
Non-Pharm: CBT, CBT, Group Therapy,
Motivational
incentives (aka $$)