Substance Use Disorders

Dr. S. K. Vijayachandran
For Nursing
Students
What are drugs?

 A drug is any
substance other
than food that can
change the way
the mind and body
works.
 Mood altering
substances

SRO Greg Newton,Liberty Police Department

Who invented drugs?

 From earliest
times, men used
preparations from
plants and herbs to
make medicines to
relieve pain.

SRO Greg Newton,Liberty Police Department

Clay tablets from 2000 B.C. list
drugs and prescriptions.
 The early Greeks and
Romans found opium
relieved pain.
 The ancient Chinese
also used opium.
 The Inca Indians in
America chewed cocoa
leaves to relieve pain
and alleviate fatigue.

SRO Greg Newton,Liberty Police Department

During the 1800’s morphine became the
first drug to be isolated.

 Many wounded
soldiers during the
Civil War became
addicted to
morphine given for
pain
 Why People Use
Drugs?

The Psychopharmacology of
Drugs of Abuse
 Neuroanatomical Structures

Planning PFC
Judgement
FC

NAc

REWARD MFB

VTA

EMOTIONS A
conditioned effect
Mesolimbic Dopamine Pathway

Activation of mesocorticolimbic system

Vijay A. Ramchandani, Ph.D.
Indiana University School of Medicine
Final Common Pathway or Reward
 ‘Pleasure centre’
 “Pleasure Neurotransmitter”
 Natural ways to trigger- intellectual to
athletic achievements,symphony to
orgasm- ‘natural highs’
 Pharmacy of naturally occurring substances
in brain
 Endorphins (morphine/heroin)
 Anandamide (marijuana)
 Acetyl choline (nicotine)
 Dopamine (cocaine and amphetamine)
Mesolimbic Dopamine Pathway

Yes Yes
Psychotropics in Nature
 Psychotropics occurring in nature
 Bypass brain’s natural neurotransmitters
directly stimulates D2 receptors
 Not necessary to earn one’s rewards naturally –
more intense reward
 Furious craving
 Risk may depend on how many receptors a
person has
 Fewer receptors – internal reward system not
working properly
 Low initial response – high risk of later abuse
 Large number of receptor – initial response
aversive – will not try again
Some Neurotransmitters
 Glutamate
 G A B A- gamma amino butyric
acid
 Dopamine - DA
 Serotonin- 5-HT
 Noradrenaline – NA
 Acetyl Choline- Ach
 GABA
Alcohol

Amphetamine
Opioid

Acetyl choline Dopamine

Hallucinogen Alcohol
Cocaine
Cannabis

Serotonin PCP
Glutamate
Stimulants

Cocaine and Amphetamine

Stimulants:
Cocaine and Amphetamine

 Cocaine
 Local anaesthetic
 Inhibitor of Monamine transportation,
especially dopamine (also 5HT and NA)
 Freud

 Also release DA – (reversing transport)

 DA

DA

5HT NE

Amphetamine
Methamphetamine

Caine
 Dopaminergic
Neurotransmission
 D5

D4

D3

D2

D1
 D5

D4

D3

D2

D1
Blocking Reuptake
Mechanism
Cocaine Blocking
Dopamine Reuptake
Cocaine
 D5

D4

D2

D3

D2

D1

D2
 D5

D4

D2

D3

D2

D1

D2
 Delusions
Thought disorder

hallucinations
53
Hallucinogens

Hallucinogens, Designer Drugs and

Phencyclidine
Hallucinogens, Designer Drugs and
Phencyclidine
 Intoxication – a “trip”
 Visual illusions, hallucinations, enhanced awareness of external
stimuli and internal thoughts and stimuli, in full wakeness and
alertness
 Psychedelic – like religious experience
 Psychotomimetic – superficial resemblance
 “Bad trip” – like a panic attack
 Delirium – later psychosis
 Common hallucinogens
 LSD (d-lysergic acid dimethyl amine), psilocybin and DMT
(dimethyl tryptamine)
 Phenylalkyl amines- resemble NA and DA - mescaline, DOM
(dimethoxymethylamphetamine)
 Designer drugs–MDMA [ecstasy]
(Mehtyldioxymethamphetamine)
 Complex actions – common action-agonists of serotonin 2A
flash backs
Cannabinoids
Getting Stoned :
Marijuana
 THC- tetrahydrocannabinoids
 Cannabinoid receptors- trigger DA release
 Two types – CB1 in the brain and CB2 in the immune
system
 Endocannabinoid system – anandamide
 Stimulant and sedative properties
 Intoxicating doses
 Well-being, relaxation, friendliness, loss of
temporal awareness (including confusing the
past with the present) slowing of thought,
impairment of STM, feeling of achieving special
insights
 High doses – panic, toxic delirium, rarely psychosis
 Heavy Long term use – amotivational syndrome
Opioids
Effects
 Very intense, brief euphoria [rush],  tranquility [several
hours] drowsiness [nodding], mood swings, mental
clouding, apathy and slowed motor movements
 In overdose resp. depression and coma
 Tolerance and dependence – later little room between
euphoric dose and toxic dose – later very little euphoria
 Withdrawal- dysphoria, craving, irritability, tachycardia,
tremor, sweating, ‘goose bumps’, ‘cold turkey’- subjectively
horrible- stop at nothing
 Treatment
 Clonidine – alpha2 adrenergic agonist
 Methadone substitution
 Naloxone and naltrexone- competitive antagonists
 Buprenorphine
Benzodiazepines and
Sedative-hypnotics
 Alcohol

Major
Public
Health
Problem
Alcohol
 Not understood very well
 Effect on a wide variety of neurotransmitter systems –
‘a depressant of CNS neuronal functioning
 Enhances inhibition- enhancing GABA-A
 Reducing excitation – inhibiting NMDA subtype of
glutamate receptors
 DA release
 Release both opioids and cannabinoids
 Naltrexone- first 90 days, up to 1 year
 Acamprosate –interacts with NMDA receptors, substitute
for this effect of alcohol during abstinence reduce the
neuronal hyperexcitabilty of AWD – reduce distress and
craving
Classification
Classification:
ICD-10 F 10 - F 19 Mental and behavioural disorders
due to psychoactive substance use

10.Alcohol 16.Hallucinogens
11.Opioids 17.Tobacco
12.Cannabinoids 18.Volatile solvents
13.Sedative hypnotics 19.Multiple drug use and
use of other
14.Cocaine
psychoactive
15.Other stimulants substances
including caffeine
Dependence
Substance use + impaired function + three or
more of the following

 Tolerance (  amount or  effect)

 Withdrawal ( WDS on stopping or reducing or
substance used to relieve WDS)
 Loss of control
 Craving , failed effort to cut down
 Much time spent on drug / obtaining drug
 Necessary activities given up
 Continues use despite problems
Alcohol
How Common?
 Alcohol
 Point prevalence – 1.7% (2.8
for men and 0.5% for women)-
varies – in US 5%
 1.5% of all deaths
 3.5% of total DALY
 Life-time risk for alcohol
dependence 10% for men
 20% - dependence + abuse
 20-30% of psychiatric patients
Among users:
 15.4% will become dependent
(21.4% for men)
Patterns of Alcohol Use In
Karnataka
 Men far > women, but
women’s rising
 Start earlier ,develop
problems earlier
 One out of two who drink
develops problem drinking
 44% of users prefer to drink
to intoxication
 Only 24% drink at home, the
rest in bars, arrack shops
 Only 27 % have ever drunk
along with other family
members.
 Drinking is not normally done
at home
The drink industry
In UK alone:
 40,000 premature deaths

 1/5 of all hospital bed occupancy

 2/3 attempted suicides

 ½ of all crimes
 ½ of all murders
 ½ of battered wives
 2/5 of fires

 2/3 Road Traffic Accidents

Is It only a
Private
Pleasure?
Alcohol
and
Violence
The Drink Industry (cont)
 The drink industry in
UK spends around 200
million pounds each
year on advertising
and sponsorships. The
government spends
less than 0.5 % of
that figure for alcohol
education.
 Affect the course of
most psychiatric
illnesses
 Alter the metabolism
of most drugs
What is alcohol?
 Ethanol
 Beer -3.6% Wine
-12%
 Spirits-40%

 ½ pint of beer =

1 glass of wine =
1 measure of spirts
How it is made?
Fermentation
 Food  poison

Absorption
Mouth, oesophagus and stomach
Most prominent from proximal small
intestine
How Disposed Off?
 90 % by oxidation- oxidative metabolism
in liver- 4 pathways Acetaldehyde. Most
by ADH (alcohol dehydrogenase)- rate
limiting enzyme.
 Acetaldehyde  Acetate by ADH
(aldehyde dehydrogenase)-blocked by
disulfiram
 Elimination 6 %-lungs, kidneys, sweat
Mechanism of Action
 Old idea- dissolving the neuronal
membrane
 Effect on NT funcions
 Increases Dopamine concentration
 Stimulates Opiate Neuropeptide
Release
 Potentiates GABA receptor function
 Decreases Serotonin neurotransmission
 Inhibits Glutamate receptor function
Aetiology of Alcoholism
Cause unknown
Dopamine D2 receptor (DRD2)
gene linked to susceptibility
Evidence from adoption studies:
Children with alcoholic biological
parents more likely to misuse
alcohol
Bottle Training
Dependence …
Disposition to use drugs

Learning (Conditioning)

DRUG USE

Brain Changes

Tolerance Withdrawal

Consequences
Consequences
1. Negative 2. Positive

consequences consequences
Toxic effects Mood
enhancement
Organic damage
Psychosocial
Psychosocial facilitation
dysfunction
Avoidance / relief
Decreased effect of of withdrawal
drugs symptoms
 
Comorbidity
 Personality disorder
(dyssocial personality disorder )
 Mood disorders

 Anxiety disorders

Be careful in diagnosing psychiatric

disorder during intoxication / within
one month of withdrawal
Complications
Complications of Alcohol
Dependence
1. Brain and mind
 Intoxication
 Coma
 Violence
 Head injury
 Convulsions

Contd..
Complications (cont.)
Acute withdrawal symptoms
12 – 48 hours after
cessation of intake
 tremor, sweating,
nausea, anxiety,
weakness, depression
Severe Withdrawal Symptoms
Delirium tremens
48 – 72 hours after alcohol
cessation
Mild delirium
Anxiety attacks,
confusion, nightmares,
sweating
Pulse: 100-120 bpm,
temp: 99-100°F
Complications (cont.)
Severe delerium
Gross disorientation,
cognitive disruption
Hypersensitivity of
sensory stimuli
Pulse: >120 bpm,
temp: >100 °F
Self-limiting, resolves
in 12-24 hours
Alcoholic hallucinosis
Hallucinations, illusions,
vivid nightmares  like
schizophrenia
Usually subsides after
1-3 weeks of abstinence
Complications (cont.)
 Alcoholic delusional  Sleep disorders-
disorder fragmented non-restful
 Dementia sleep, nightmares and
 Psychosis recurrent awakenings
 Peripheral neuritis  Suicide- 15-25 % in
 Cerebellar alcoholics
degeneration  55 % consumed
 Anxiety (generalised, alcohol at the time of
panic attacks, phobias the attempt
 Depression
Complications (cont.)
CVS GIT
 Arrythmias  APD, Ca tongue,
 Hypertension oesophagus
 Cardiomyopathy
 Hypoglycemia
 Diarrhoea and
RS vomiting
 Infections  Liver disease
 Cancer, chronic  Pancreatitis
bronchitis ( assn with Nutrition
smoking)  Malnutrition
 Pulmonary tuberculosis  Anaemia
 ‘Café coronary’  Vitamin deficiencies
Complications (cont.)
Sexual dysfunction
 Infertility
 Impotence,  sexual
desire
Work
Intoxication during work,
absences, sick leave, 
illnesses, smell of alcohol
during work, keeping
bottles in the bag/table,
arguments, aggression,
crime, coming late,
sleeping at work,
quarrels with authority
and colleagues,
unreliability.
Complications (cont.)
Financial
 Debts, taking advances,
poor clothing, non-
payment of rent etc.
Legal
 Murder, assaults,
drunken driving, shop
lifting, sexual offences.
Accidents
 At home, office, work
place, fire, drowning,
road traffic accidents.
Complications (cont.)
Family
 Marital disharmony,
separations, divorces,
spouse abuse, child abuse
 In wife- anxiety and
depression
 In children- aggression,
anxiety, poor school
performance.
Social
 Some unable to marry,
Social isolation, loss of
hobbies, interests and
creativity
Diagnosis
 If affects
self/others, health,
finance, law, work,
interpersonal
relationships 
Treatment is needed.
 Awareness in
professionals
 Early identification
 History taking-
tactful, confidential, in
privacy, without
degrading patient
The Cage Questionnaire
 Have you tried to Cut
down on alcohol?
 Have you been Annoyed
when someone criticized
your drinking?
 Have you felt Guilty
about your drinking?
 Have you used alcohol as
an Eye-opener by having
a drink in the morning?
More than one positive
answer denotes
dependence.
1. Medical Management

Medical Management
Where are treatment efforts
focused?

• Management of alcohol withdrawal

• Amelioration of comorbid
psychiatric condition
• Long-term treatment of alcoholism
Medical Management

Detoxification
a.Medication
Mild to moderate-
 25 mg Chlordiazepoxide (librium) 3-4
times daily on the first day-
 Skip if the patient is drowsy / asleep
 Add 1-2 tablets in first 24 hours if patient
jittery/  tremor / autonomous
dysfunction.
Cont..
Detoxification (cont)
Calculate total dose

reduce by 20 % each day from 2nd day

Stop in 5 days.
 If long acting BDZ is used  avoid
excessive sleepiness
 If short acting BDZ is used  do not
miss dose.
Severe -Higher doses .

Cont..
Detoxification (cont)
b. Diet
c. Hydration
d. Monitor vital signs
e. Thiamine by
injection
f. Folic acid
g. Multivitamins
h. Antibiotics, antacids
etc. as needed
Medications for Relapse Prevention
in Alcoholics

 Naltrexone
(1994)
 Disulfiram (1950)
 Acamprosate (...)
 Nalmefene (...)
Pharmacological Management
Alcohol Acetaldehyde Acetate
aldehyde
dehydrogenase
 Disulfiram
 Irreversible inhibitor of aldehyde
dehydrogenase (many other enzymes
also)
 Ingestion of alcohol  acetaldehyde
accumulation
 Tachycardia, flushing, dyspnoea,
nausea & vomiting
  DETERRENT
 250mg once daily
Disulfiram
 A deterrant to further drinking
 Reaction
 Ranges from mild discomfort to a severe reaction-
flushing, throbbing in the head, respiratory
difficulty,nausea and vomiting, sweating, chest pain,
palpitations, dyspnoea, hypotension, syncope,
vertigo, confusion and blurred vision
 In severe cases unconsciousness, respiratory arrest,
cardiovascular collapse, convulsions and death can
occur
 The decision not to drink is taken once a day when
the tablet is taken, not when craving occurs
 Duration of action is 5-14 days
2. Psychological
Management
The Cycle of Change

6.Drug free
life
4. Maintenance 3.Action

5. Relapse 2. Contemplation

I.
Precontemplation
Cycle of Change(cont)
Later in dependence-
 negative consequences
 positive consequences

Changing balance

Conflict
 Intervention should be
matched to the
stage
1. Precontemplation Stage
Patient : “not a problem”,  staying in contact
“nothing I can do”  active listening
Approach-  information giving
 damage limiting- safe
drinking
 helping with problems
 positive relationship  supporting the family
 motivational change  Goals are set by the
strategies patient
 positive regard
 feedback
2. Contemplation and
3. Action
Contemplating phase
 Self monitoring

 Decision balance sheet( advantages vs.

disadvantages of drinking)
Action
 cover withdrawal (detoxification)

 attend to need for relaxation, stress

reduction, excitement, peer relationship)
 cue avoidance

 cue exposure
Maintenance and Relapse
Maintenance Phase
 Life style change
 Balance ‘shoulds’ (activities necessary to exist) and
‘wants’ ( activities necessary to increase pleasures of
living)
 Encourage positive addictions
e.g.- Exercising vs. drinking
Relapse prevention
 lapse vs. relapse
 Relapse part of alcoholism
 Relapse should be used as learning experience
Process of Relapse
Lifestyle imbalance
(shoulds > wants)

Craving and urges

Seemingly irrelevant decisions(SID)

High risk situations ( HRS)
1.       negative emotions (anger etc)
2.       Rows( interpersonal relationships)
3.       Peer group pressure
Process of Relapse (cont.)

lapse

Rule Violation Effect (RVE)

Guilt
 self-confidence
Poor coping skills

Relapse
Relapse Prevention

 Anticipate relapse.
 Identify HRS.
 Teach - assertive skills.
 Problem solving skills.
 ‘Fire drill’- role play.
 Involve family
 Most important-
 Relapse anticipated.

 Explained to relatives and

patient.
 Accept relapse like exacerbation
of any other diseases like
diabetes, asthma or rheumatoid
arthritis.
\µn