SUBSTANCE RELbddddddddATED DISORDER.pptx

Jasleen K Brar
Assistant Prof.
DMCH CON, Malakpur

The substance related disorders are composed of
two groups:-
 Substance use disorders ( dependence and abuse)
 Substance induced disorder (intoxication, withdrawal,
delirium, dementia, amnesia, psychosis, mood disorders,
anxiety disorder, sexual dysfunction and sleep disorders)

 According to Bennett and Woolf
Substance abuse as psychoactive drug use of any class
or type, used alone or in combination, that poses
significant hazards to health.
 According to American Psychiatric Association
Substance abuse is defined as a maladaptive pattern of
substance use manifested by recurrent and significant
adverse consequences related to repeated use of the
substance.

 A pattern of psychoactive substance use that is causing
damage to health. The damage may be physical (as in
cases of hepatitis from the self administration of injected
drugs) or mental (e.g. episodes of depressive disorder
secondary to heavy consumption of alcohol).

 According to ICD-10
The diagnosis requires that actual damage should have
been caused to the mental or physical health of the user.

 The repeated use of a drug or chemical substance
with or without physical dependence. It is mainly of
two types:-
 Physical dependence
 Psychological dependence

Physical dependence – According to American Psychiatric
Association
 Physical dependence on a substance is evidenced by a
cluster of cognitive, behavioural and physiological symptoms
indicating that the individual continues use of substance
despite significant substance related problems.
 It occurs when there is biological need in the body for abused
substance, if the substance is not supplied, physical
withdrawal symptoms appear.

 Psychological dependence – According to Hermes
An individual is considered to be psychologically
dependent on a substance when there is an
overwhelming desire to repeat the use of particular drug
to produce pleasure or avoid discomfort.
 It is the craving for the subjective effect of the substance
to experience the psychic effects and to avoid discomfort.

 According to ICD-10
The dependence syndrome is a cluster of physiological,
behavioural and cognitive phenomena in which the use
of a substance or a class of substances takes on a much
higher priority for a given individual than other behaviours
that once had great value.

A definite diagnosis of dependence should be made only
if three or more of the following have been present
together at some time during the previous year:
 A strong desire or sense of compulsion to take the
substance;
 Difficulties in controlling substance taking behaviour in
terms of its onset, termination or levels of use;

 A physiological withdrawal state when substance use has
ceased or been reduced, as evidenced by: the
characteristic withdrawal syndrome for the substance; or
use of the same (or closely related) substance with the
intention of relieving or avoiding withdrawal symptoms.
 Evidence of tolerance, such that increased doses of the
psychoactive substance are required in order to achieve
effects originally produced by lower doses;

 Progressive neglect of alternatives or interests because of
psychoactive substance use, increased amount of time necessary
to obtain or take the substance or to recover from its effects;
 Persisting with substance use despite clear evidence of overtly
harmful consequences, such as harm to the liver through
excessive drinking, depressive mood states consequent to periods
of heavy substance use, or drug related impairment of cognitive
functioning; efforts should be made to determine that the user was
actually, or could be expected to be, aware of the nature and
extent of harm.

 Misuse- Similar to abuse, but usually applies to drugs
prescribed by physicians that are not used properly.
 Intoxication- A reversible syndrome caused by a specific
substance (e.g. alcohol) that affects one or more of the
following functions: memory, orientation, mood,
judgement and behavioural, social or occupational
functioning.

 Withdrawal –A substance specific syndrome that occurs
after stopping or reducing the amount of the drug or
substance that has been used regularly over a prolonged
period of time. The syndrome is characterized by
physiologic signs and symptoms in addition to
psychological changes, such as disturbances in thinking,
feeling and behaviour.

 Withdrawal state is one of the indicators of dependence
syndrome. This too, is a short lasting syndrome with
usual duration of few hours to few days. Typically, the
patient reports that withdrawal symptoms are relieved by
further substance use.
 The withdrawal state is further classified as:
 Uncomplicated
 With convulsions
 With delirium

 Tolerance – Phenomenon in which, after repeated
administration, a given dose of drug produces a
decreased effect or increasingly large doses must be
administered to obtain the effect observed with the
original dose.
 It is the state when an individual requires repeated and
increased doses of a drug to experience the effects, as
he has lost his sensitivity to a particular drug.

 Co-dependence – Term used to refer to family
members affected by or influencing the behaviour of
the substance abuser.
 Habituation - It results from the repeated
consumption of a drug,a desire to continue taking
the drug for the sense of improved well being; it will
have some degree of psychic dependence, but
absence of physical dependence.

 POLYSUBSTANCE ABUSE:-it refers to abuse of two or more
drugs or of alcohol & drugs.
 POTENTIATION:-two or more substance interact in the body
to produce an effect greater than the sum of the effects of
each substance taken alone.
 CROSS TOLERANCE :-the ability of one drug to produce the
effect of another when the body has developed a tissue
tolerance for effect of the first substance.

1) Alcohol
2) Amphetamines and related disorder
3) Caffeine
4) Cannabis
5) Cocaine
6) Hallucinogens
7) Inhalants
8) Nicotine
9) Opioids
10) Phenylcyclidine (PCP) and related substances
11) Sedatives, hypnotics or anxiolytics

 A number of factors have been implicated in the
predisposition to abuse of substances. At present, no
single theory can adequately explain the etiology of the
problem. These are:-
(a) Biological Factors
(a) Psychological Factors
(a) Socio-cultural Factors

BIOLOGICAL FACTORS
Genetics
 An apparent hereditary factor is involved in the
development of substance-use disorders.
 This is especially evident with alcoholism, less so with
other substances.
 Children of alcoholics are three times more likely than
other children to become alcoholics.
 Monozygotic twins have a higher rate for concordance of
alcoholism than dizygotic twins.

Biochemicals
Alcohol may produce morphine like substances in the brain
responsible for
alcohol addiction
Reaction of active amines + products of = Morphine like
alcohol substances
(Dopamine & Serotonin) (Aldehyde)

 PSYCHOLOGICAL FACTORS
Developmental Influences
 Punitive superego
 Diminish unconscious anxiety
 Fixation at oral stage
 Self medication
Alcoholism may be used to control panic
opioids to diminish anger
amphetamines to alleviate depression.

 Personality Factors
 Certain personality traits like a:-
 low self-esteem Increase the
 frequent depression tendency towards
 passivity addictive
 the inability to relax behaviour
 inability to communicate effectively
 antisocial personality
 depressive response styles.

 Personality disorders – persons who have harsh super
ego and who are self puncture turn to alcoholics to
diminish their stress.
 Childhood history of antisocial personality disorder.
 Common in cyclothemic personalities.
 Poor social support, fashion- a sign of modernity, social
inadequacy, isolation.
 Some settings as colleges and military settings where
alcohol is considered as a status symbol.

 Social factors – over crowding, influence of bad
company, cinemas, literature.
 Peer pressure, urbanization, religious reasons,
unemployment.
 To forget miseries and problems of life.
 Unhealthy environment, sudden loss in property or
closed ones.
 Parental disharmony.
 Occupational – heavy vehicle drivers, labourers, manual
workers, Physical exhaustion or hard physical labour.

 Conditioning
 Many substances create a pleasurable experience
encourages

user to repeat it.
 Thus, it is intrinsically reinforcing properties of addictive
drugs that “condition” the individual to seek out their use
again and again.
 The environment in which the substance is taken also
contributes to the reinforcement. If the environment is
pleasurable, substance use is usually increased.

 Cultural and Ethnic Influences
 Factors within an individual’s culture help to establish
patterns of substance use by moulding attitudes,
influencing patterns of consumption based on cultural
acceptance and determining the availability of the
substance.

 Economic causes :
 Poverty
 Unemployment
 Professions like poets, painters, waiters, journalists,
commercial, musicians, reporters are at greater risk.
 Others :
 Marital disharmony
 Easy availability
 Free time and boredom
 Loneliness.
 Psychiatric disorders

Physical warning signs of drug abuse
 Bloodshot eyes, pupils larger or smaller than usual.
 Changes in appetite or sleep patterns. Sudden weight
loss or weight gain.
 Deterioration of physical appearance, personal grooming
habits.
 Unusual smells on breath, body, or clothing.
 Tremors, slurred speech, or impaired coordination

Behavioral signs of drug abuse
 Drop in attendance and performance at work or school.
 Unexplained need for money or financial problems. May
borrow or steal to get it.
 Engaging in secretive or suspicious behaviors.
 Sudden change in friends, favorite hangouts, and
hobbies.
 Frequently getting into trouble (fights, accidents, illegal
activities).

Psychological warning signs of drug abuse
 Unexplained change in personality or attitude.
 Sudden mood swings, irritability, or angry outbursts.
 Periods of unusual hyperactivity, agitation.
 Lack of motivation; appears lethargic or “spaced out.”
 Appears fearful, anxious, or paranoid, with no reason.

 Alcohol dependence was earlier called as alcoholism.
This term like addiction has been dropped due to its
derogatory meaning.

Jellinek outline four phases through which the
alcoholic’s pattern of drinking progresses.
Phase I – The Pre-alcoholic Phase
This phase is characterized by the use of alcohol to
relieve the everyday stress and tensions of life.
 As a child, the individual may have observed parents or
other adults drinking alcohol and enjoying the effects.
The child learns that use of alcohol is an acceptable
method of coping with stress.
Tolerance develops, and the amount required achieving
the desired effect increases steadily.

Phase II -The Early Alcoholic Phase
•This phase begins with blackouts.
•Brief periods of amnesia that occurs during or
immediately following a period of drinking.
•Now the alcohol is no longer a source of pleasure or relief
for the individual but rather a drug that is required by the
individual.
Common behaviour includes – secret drinking,
preoccupation with drinking and maintaining the supply of
alcohol and further blackouts. Excessive use of denial and
rationalization is evident.

Phase III – The Crucial Phase
In this phase, the individual has lost control.
Physiological dependence is clearly evident.
Binge drinking, lasting from a few hours to several weeks
is common.
This phase is characterized by sickness, loss of
consciousness and degradation. Anger and aggression are
common manifestations.
By this phase of illness, individual experienced the loss
of job, marriage, family, friends and most especially self
respect.

Phase IV- The Chronic Phase
•This phase is characterized by emotional and
physiological disintegration.
•Emotional disintegration is evidenced by profound
helplessness and self pity.
•Impairment in reality testing may result in psychosis.
•Abstention from alcohol results in a terrifying syndrome of
symptoms that include hallucinations, tremors,
convulsions, severe agitation and panic.
•Depression and ideas of suicide are common.

 EXPERIMENTAL: Due to peer pressure and curiousity,
individual starts consuming alcohol.
 RECREATIONAL : Gradually the frequency of alcohol
consumption will increase as an enjoyment.
 RELAXATIONAL : During weekends or on holiday, it
may work out to release the tension ,relax mind and to
sedate the brain from painful emotions and promotes a
sense of well being and pleasure.
 COMPULSIVE: Person becomes addict to overcome the
discomfort of withdrawal symptoms.

Medical complications
 Gastrointestinal system
 Fatty liver
 Cirrhosis of liver
 Hepatitis
 Liver cell carcinoma
 Gastritis
 Reflux esophagitis
 Esophageal varices
 Peptic ulcer
 Carcinoma of stomach
and esophagus
 Malabsorption syndrome
 Pancreatitis
Central nervous system
 Peripheral neuropathy
 Delirium tremens
 Rum fits
 Alcoholic hallucinosis
 Wernicke-Korsakoff
psychosis
 Alcoholic dementia
 Suicide
 Cerebellar degeneration

Miscellaneous
 Parotid enlargement
 Ascites
 Fetal alcohol syndrome
 Alcoholic hypoglycaemia
 Cardiomyopathy
 Anemia,
thrombocytopenia
 Vitamin K deficiency
 Malnutrition
 Decreased immune
function
 Sexual dysfunction
 Social complications
 Accidents
 Marital disharmony
 Divorce
 Occupational problems
 Increased incidence of
drug dependence
 Criminality
 Financial difficulties

According to WHO
 The harmful use of alcohol results in 2.5 million deaths
each year.
 320,000 young people between the age of 15 and 29 die
from alcohol-related causes, resulting in 9% of all deaths
in that age group.
 Prevalence among male 15 + years 3.47% in India
 Prevalence among female 15 + years 0.47% in India

PSYCHIATRIC
DISORDERS
DESCRIPTION
Antisocial
personality
disorder
Some studies suggest that antisocial
personality disorder is particularly
common in men with an alcohol related
disorder.
Mood disorders About 30-40% of persons with an
alcohol related disorder meet the
diagnostic criteria for major depressive
disorder.

PSYCHIATRIC
DISORDERS
DESCRIPTION
Anxiety
disorders.
25-50% of all persons with alcohol
related disorders also meet the criteria
for an anxiety disorder. Phobia and
panic disorder are particularly frequent
co-morbid diagnosis in these patients.
Suicide Most estimates of the prevalence of
suicide among persons with alcohol
related disorders range from 10 to
15%,

The DSM IV- TR diagnostic criteria for alcohol intoxication are
based on evidence of recent ingestion of ethanol, maladaptive
behaviour and at least one of the six possible physiological
correlates of intoxication.
(A) Recent ingestion of alcohol
(B) Clinically significant maladaptive behavioural or
psychological changes(e.g. aggressive behaviour, mood
liability, impaired judgement, impaired social or occupational
functioning) that developed during, or shortly after alcohol
ingestion.

C)One of the following signs developing during or shortly
after alcohol use:-
(1) Slurred speech
(2) In coordination
(3) Unsteady gait
(4) Nystagmus
(5) Impairment in attention or memory
(6) Stupor or coma
D).The symptoms are not due to a general medical
condition and are not better accounted for by another
mental disorder.

Level Impairment
20-30 mg/dl slowed motor performance and
decreased thinking ability
30-80 mg/dl increases in motor and cognitive ability
80-200
mg/dl
increases in incoordination and
judgement errors
mood lability
deterioration in cognition
200-300
mg/dl
nystagmus, marked slurring of
speech and alcohol blackouts
>300 mg/dl impaired vital signs and possible death

The DSM-IV-TR criteria for alcohol withdrawal is as
follows:-
A. Cessation of (or reduction in) alcohol use that has been
heavy and prolonged.
B. Two or more of the following, developing within several
hours to a few days after criterion A.

(1) Autonomic hyperactivity (e.g. sweating or pulse
rate greater than 100)
(2) Increased hand tremor
(3) Insomnia
(4) Nausea or vomiting
(5)Transient or visual, tactile or auditory
hallucinations or illusions
(6) Psychomotor agitation
(7) Anxiety
(8) Grand mal seizures
C. The symptoms in criteria B cause clinically significant
distress or impairment in social, occupational or other
important areas of functioning
D. The symptoms are not due to general medical condition
and are not better accounted for by another mental
disorder.

 Delirium tremens is the most severe alcohol withdrawal
syndrome. It occurs usually within 2-4 days of complete
abstinence from heavy alcohol drinking. The main clinical
features are:-
 Clouding of consciousness with disorientation in time and
place.
 Poor attention span and distractibility
 Visual or auditory hallucination or illusions, Tactile
hallucinations of insects crawling over body may occur.

Marked autonomous disturbance with tachycardia, fever,
sweating, hypertension and pupillary dilation.
Psychomotor agitation and ataxia
Insomnia, with a reversal of sleep-wake pattern.
Dehydration with electrolyte imbalance
Treatment
The best treatment for DTs is prevention.
Patients withdrawing from alcohol who exhibit withdrawal
phenomena should receive a benzodiazepine, such as 25
to 50 mg of chlordiazepoxide every 2 to 4 hours.
Once the delirium appears, however 50 to 100mg of
chlordiazepoxide should be given every 4 hours orally.
Lorazepam should be given IV.

Management
 Monitor vital signs, observe the patient carefully.
 Decrease stimulation.
 Provide general nursing care.
 Evaluate the patient’s hydration and serum electrolytes.
 Maintain intake output chart.
 Institute high calorie and high carbohydrate diet.
 Add vitamins, thiamine 100 mg IM, then orally daily folic
acid 1 mg orally daily 7-10 days.
 Initiate pharmacotherapy such as benzodiazepines.

DSM –IV-TR Diagnostic Criteria for Substance
Intoxication Delirium
A. Disturbance of consciousness (i.e. reduced clarity of
awareness of the environment) with reduced ability to
focus, sustain or shift attention.
B. A change in cognition (such as memory deficit,
disorientation, language disturbance) or the development
of a perceptual disturbance that is not better accounted for
by a pre-existing, established or evolving dementia.
C. The disturbance develops over a short period of time
(usually hours to days) and tends to fluctuate during the
course of the day.

There is evidence from the history, physical examination or
laboratory findings of either (1) or (2):
(1) The symptoms in criteria A and B developed
during substance intoxication
(2) Medication use is etiologically related to the
disturbance.

DSM –IV-TR Diagnostic Criteria for Substance
Withdrawal Delirium
A. Disturbances of consciousness (i.e. reduced clarity of
awareness of the environment) with reduced ability to
focus sustain or shift attention.
B. A change in cognition (such as memory deficit,
disorientation, language disturbance) or the development
of a perceptual disturbance that is not better accounted for
by a pre-existing established or evolving dementia.

C. The disturbance develops over a short period of time
(usually hours to days) and tends to fluctuate during the
course of the study.
D. There is evidence from the history, physical examination
or laboratory findings that the symptoms in criteria A and B
developed during, or shortly after a withdrawal syndrome.

Alcoholic Seizures (Rum fits)
Seizures associated with alcohol withdrawal are
stereotyped, generalized and tonic-clonic in character
usually 12-48 hours after a heavy bout of drinking. Multiple
seizures, 2-6 at one time, are more common than single
seizures.
Treatment
The primary medication to control alcohol withdrawal
symptoms are the benzodiazepines.

Alcoholic Hallucinosis
This is characterized by the presence of hallucinations
(usually auditory) usually abstinence, following regular
alcohol intake.
Wernicke’s Encephalopathy
This is an acute reaction to severe thiamine deficiency, the
commonest cause being chronic alcohol use.
Characteristically the onset occurs after a period of
persistent vomiting. The important clinical signs are:-
Ocular signs – nystagmus and opthalmoplegia, papillary
irregularities, retinal haemorrhage., papilledema.
Higher mental function disturbance – disorientation,
confusion, recent memory disturbances, poor attention
span, distractibility, apathy, ataxia

Koroskoff psychosis
Clinically Koroskoff psychosis presents as an amnestic
syndrome, characterized by gross memory disturbances
with confabulation, insight is often impaired.
The cause is severe, untreated, thiamine deficiency
secondary to alcohol use.
Treatment
The dosage of thiamine is initiated at 100 mg by mouth two
to three times daily and is continued for 1 to 2 weeks. In
case of Koroskoff psychosis the treatment regimen should
be continued for 3 to 12 months.

 The aim of detoxification is the symptomatic
management of the emergent withdrawal symptoms.
 Benzodiazepines are the drug of choice in management
of alcohol withdrawal.
 Usually divided doses of 20 – 40 mg of diazepam or 40 -
80 mg of chlordiazepoxide are required.
 The dose of benzodiazepines is gradually tapered off
over next 7-10 days.
 Oral administration of thiamine is necessary in all the
patients for prevention of alcohol related disorders.

Medications for maintenance phase
Deterrent – disulfiram, calcium carbimide
Anticraving – acamprosate, naltrexone
Acmprosate
Reduce craving
333 mg 4-6 tab/day
Side effects – nausea, diarrhoea, abdominal pain,
irregular heart beat
Not to be given in kidney function
Naltrexone
Reduces craving
50mg/day
Monitor for hepatotoxicity

 Disulfiram is used to treat alcohol dependence.
Disulfiram is an alcohol sensitizing agent. It deters
use of alcohol by producing a rapid and violently
unpleasant reaction in a person who ingests even a
small amount of alcohol.
 Mechanism of Action
It inhibits the intermediate metabolism of alcohol and
this leads to accumulation of acetaldehyde in blood.

Ethyl alcohol acetaldehyde acetate CO2 + H2O
( Aldehyde Dehydrogenase
Enzyme)
Disulfiram

Dosage- Disulfiram is supplied in 250 and 500 mg tablets.
Initial dose is 500 mg a day taken by mouth for the first 1
or 2 weeks, followed by a maintenance dosage of 250 mg
a day. The dosage should not exceed 500 mg a day.
Contraindications
Concomitant use of alcohol or alcohol containing
preparations or metronidazole
Coronary artery disease
Severe myocardial infarction

Precautions
High impulsivity-likely to drink while using it.
Psychoses
Diabetes mellitus
Epilepsy
Hepatic dysfunction
Hypothyroidism
Renal impairment
Contact dermatitis
Serious side effects
Hepatitis
Optic neuritis
Peripheral neuropathy
Metallic taste
Dermatitis

Disulfiram ethanol reaction
Flushing, tachycardia, hypotension, tachypnea,
palpitations, headache, sweating, nausea, vomiting,
giddiness.
Onset of reaction – Within 30 minutes, become full blown
within 1 hour, and subsides usually within 2 hours of
ingestion of alcohol.
Before prescribing
Warn that the patient should not take disulfiram for at least
12 hours after drinking and that a disulfiram alcohol
reaction can occur up to 2 weeks after the last dose
Warn about alcohol in the diet (e.g. sauces and vinegars).
Follow up
Monitor liver function tests periodically.

Naltrexone
Naltrexone is a long acting opioid antagonist.
Mechanism of action
It blocks the opioid receptors, resulting in reduced craving
and reduced reward in response to drinking.
Dose – 50 mg daily
Contraindications
Liver failure Side effects
Nausea
Abdominal pain
Constipation
Dizziness
Headache
Anxiety
Fatigue

Treatment of alcohol dependence
1. Behaviour therapy-
aversion therapy
covert sensitization
relaxation techniques
assertiveness training
positive reinforcements
2. Individual psychotherapy – The patient should be
educated about the risks of continuing alcohol use.

Self help groups – The best known self help group is the
alcoholic anonymous. Small groups of 10-20 people with
problems of drinking met regularly. In closed meetings only
AA members are allowed whereas in open meetings family
members and friends also can join. It is a voluntary group
spread all over the world and follows a standard routine in
its functioning. The members are required to acknowledge
that they are alcoholics, that alcoholism is a disease and
that abstinence is the only way to recovery.

 Alcoholism is characterized by a high frequency of
comorbid depression, and both diseases have a mutual
negative impact. The frequent comorbidity
of alcoholism and depression (as well as disorders
related to anxiety) serves as the basis for use of
antidepressants for individuals suffering from alcohol
dependence. Among the drugs of choice in the treatment
of alcohol dependence complicated by depression and
anxiety disorders, is escitalopram.

 Alcohol intoxication results in marked reductions in brain
glucose metabolism, which we hypothesized reflect not
just its GABAergic enhancing effects but also the
metabolism of acetate as an alternative brain energy
source. To test this hypothesis we separately assessed
the effects of alcohol intoxication on brain glucose and
acetate metabolism using Positron Emission Tomography
(PET). We found that alcohol intoxication significantly
decreased whole brain glucose metabolism (measured
with FDG) with the largest decrements in cerebellum and
occipital cortex and the smallest in the thalamus.

 In contrast, alcohol intoxication caused a significant
increase in [1-(11)C]acetate brain uptake (measured as
standard uptake value, SUV), with the largest increases
occurring in the cerebellum and the smallest in the
thalamus.

 Stage One: Experimentation
 The first stage is the voluntary use of alcohol or other
drugs.
 People will often take drugs the first time out of curiosity.
 They have heard all about them, and just want to see
what the fuss is about.
 They might also have friends that use these substances
and feel peer pressure to join in.

 Stage Two: Regular Use
 The individual enjoyed their early experimentation with
drugs so has now start to use this substance regularly.
 Some people will never go beyond this stage of
substance abuse. So they will not develop a problem,
and stop by themselves.

 Stage Three: Substance abuse
 Substance abuse is when the individual starts to use
alcohol or drugs so much that it leads to harmful
consequences.
 Some will respond to these negative consequences by
cutting down or by completely abstaining from the
substance.
 Other people will ignore these warning signs and
continue to abuse the drug.

 Stage Four: Dependence
 Characteristics of dependence include: Repeated use of
alcohol or other drugs that leads to failure to fulfil major
responsibilities related to work, family, school or other
roles. Or, repeatedly drinking or using drugs in situations
that are physically hazardous, such as driving while
intoxicated or using heavy machinery when intoxicated.
Or repeated legal problems. Or any combination of
these.

 The last phase of the spectrum of substance use
problems is addiction. Addiction is a medical condition
involving serious psychological and physical changes
from repeated heavy use of alcohol, other drugs, or both.
 Symptoms include uncontrollable alcohol or other drug
craving, seeking, and use, that persists even in the face
of negative consequences.
 Addiction is a progressive illness. If left untreated, it gets
worse. It is also chronic, or long-standing (versus acute,
or short-term).

 Addiction is when the individual is not only
psychologically dependent on the drug, but also
physically dependent. Their tolerance for the substance
will have increased, and they will suffer withdrawal
symptoms should they try to stop.

 Amphetamine is one of the CNS stimulants.
Amphetamine and amphetamine related substances
are the second most widely misused drug in Asia
and many other countries.
 The typical amphetamines are used to increase
performance and to induce a euphoric feelings, for
example by students studying for exams, by long
distance truck drivers on trip.
 Methamphetamine is a potent form of amphetamine
that abusers of the substance inhale, smoke or inject
intravenously.

Categories Trade Name Street Name
Amphetamines Dextroamphetamine
(Dexedrine)
Methamphetamine
(Desoxyn)
Amphetamines +
Dextroamphetamine
Dexies, Uppers,
Truck Drivers
Meth, Speed,
Crystal, Ice

Non
Amphetamines
Phendimetrazine
Benzphetamine
Diet Pills
Cocaine Cocaine Hydrochloride Coke, Blow, Toot,
Snow, Flake,
Crack
Caffeine Coffee, Tea, Colas,
Chocolate
Java, Mud, Brew,
Cocoa
Nicotine Cigarettes, Cigars, Pipe
Tobacco, Snuff
Weeds, Fags,
Butts, Chaw,
Cancer Sticks

SYSTEM EFFECTS
CNS effects Tremors, restlessness, anorexia,
insomnia, agitation and increased
psychomotor activity, decrease in
fatigue, elation and euphoria.
Cardiovascular Increased systolic and diastolic blood
pressure, increased heart rate, cardiac
arrhymias.

SYSTEM EFFECTS
Gastrointestinal Constipation, decreased GI tract
motility,
Renal effects contraction of bladder sphincter makes
urination difficult.
Sexual functioning Promotes the coital urge in both men
and women.

CNS stimulant intoxication produces :-
 Maladaptive behavioure
 Psychological changes that develop during or shortly
after use of these drugs.
 Euphoria or affect blunting
 Changes in sociability
 Hypervigilance
 Interpersonal sensitivity
 Anxiety, tension or anger, impaired judgement.

DSM-IV-TR Diagnostic Criteria for Amphetamine
Intoxication
A. Recent use of amphetamine or a related substance
(e.g., methylphenidate).
B. Clinically significant maladaptive behavioural or
psychological changes (e.g. euphoria or affective blunting;
changes in sociability; hypervigilance; interpersonal
sensitivity; anxiety, tension, or anger; stereotyped
behaviours; impaired judgment; or impaired social or
occupational functioning) that developed during, or shortly
after, use of amphetamine or a related substance.

C. Two (or more) of the following, developing during, or
shortly after, use of amphetamine or a related substance:
(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
D. The symptoms are not due to a general medical
mental disorder.

 Withdrawal syndrome develops within a few hours to
several days after cessation of or reduction in heavy and
prolonged use.
 Withdrawal from amphetamines – A crash occurs with
symptoms of anxiety, dysphoria, fatigue, vivid unpleasant
dreams, insomnia or hypersomnia, increased appetite
and psychomotor retardation or agitation.
 It will be peak in 2-4 days and are resolved with in one
week.
 The most serious withdrawal symptom is depression
which can be severe after the continuous use of the drug
and also associated with suicidal ideations.

DSM-IV-TR Diagnostic Criteria for Amphetamine
Withdrawal
A maladaptive pattern of substance use, leading to
clinically significant impairment or distress, as manifested
by three (or more) of the following, occurring at any time in
the same 12-month period:
(1) Tolerance, as defined by either of the following:
(a) a need for markedly increased amounts of the
substance to achieve Intoxication or
desired effect
(b) markedly diminished effect with continued use of
the same amount of the substance

(2) Withdrawal, as manifested by either of the following:
(a) the characteristic withdrawal syndrome for the
substance (refer to Criteria A and B of the
criteria sets for Withdrawal from the specific
substances)
(b) the same (or a closely related) substance is
taken to relieve or avoid withdrawal
symptoms
(3) The substance is often taken in larger amounts or over
a longer period than was intended
(4) There is a persistent desire or unsuccessful efforts to
cut down or control substance use

(5) A great deal of time is spent in activities necessary to
obtain the substance (e.g., visiting multiple doctors or
driving long distances), use the substance (e.g., chain-
smoking), or recover from its effects
(6) Important social, occupational, or recreational activities
are given up or reduced because of substance use
(7) The substance 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 the substance (e.g., current cocaine use despite
recognition of cocaine-induced depression, or continued
drinking despite recognition that an ulcer was made worse
by alcohol consumption)

Specify if:
With Physiological Dependence: evidence of tolerance or
withdrawal (i.e., either Item 1 or 2 is present)
Without Physiological Dependence: no evidence of
tolerance or withdrawal (i.e., neither Item 1 nor 2 is
present)

 Delirium associated with amphetamine use generally
result of high doses or of sustained use of the drug.
 The combination of amphetamine with other drugs and
the use of amphetamine by the persons with pre existing
brain damage also will lead to the development of
delirium.

 Amphetamine induced psychotic disorder are similar to
the clinical presentation of paranoid schizophrenia.
 The hall mark of amphetamine induced psychosis is
paranoia.
 The amphetamine induced psychosis can be
distinguished from paranoid schizophrenia by the clinical
features such as visual hallucinations, ambivalence,
association disturbances which are evident
schizophrenia.
 The treatment of choice for this condition is the use of
antipsychotics such as haloperidol.

 According to DSM- IV-TR the mood disorders associated
with amphetamine are during the intoxication and
withdrawal states.
 Intoxication is associated with manic or mixed mood
states
 Withdrawal is associated with depressive symptoms.

 Amphetamine induced anxiety disorders can also occur
during intoxication and withdrawal periods.
 Amphetamines can induce symptoms which are similar
to OCD, panic disorders, and phobia.

 Amphetamines can be use as an antidote to the sexual
side effects of serotonergic agents such as fluoxetine,
but they often misuse to enhance sexual experience.
High doses and long term use are associated with
erectile problems and other sexual problems. It is more
evident in the intoxication states also.

 Sleep disorders are present in intoxication as well as
withdrawal states.
 Intoxication can cause insomnia and sleep deprivation.
 Withdrawal can cause hyper somnolence and
nightmares.

1. Acute intoxication is treated by symptomatic
management. For example:-
 Hyperpyrexia - cold sponging
 Seizures - diazepam
 Psychotic symptoms - haloperidol
 Hypertension - antihypertensive
2. Acidification of urine with oral NH4CL 500mg every 4
hours facilitates the elimination of amphetamines

 The presence of suicidal depression requires
hospitalization.
 The treatment includes symptomatic management, use
of antidepressants and supportive psychotherapy.
 The management of withdrawal syndrome is the first step
of treatment of amphetamine dependence.
 Physicians should establish therapeutic alliance with the
clients to treat the underlying depression and personality
problems
 Bupropion can be use once the patient recover from the
withdrawal symptom to enhance the feeling of well
being.

 Caffeine is the most widely consumed psychoactive
substance in the world.
 Psychiatric symptoms and disorders can be associated
with its excessive use.
 DSM-IV-TR lists several caffeine related disorders, e.g.-
caffeine intoxication, caffeine induced anxiety disorder
and caffeine induced sleep disorder. Other caffeine
related disorders are caffeine withdrawal and caffeine
dependence.

 Caffeine is contained in drinks, foods, prescription
medicines and over the counter medications.
 An adult consumes about 200 mg of caffeine per
day on an average .
 20-30% of adults consumes more than 500mg of
caffeine per day.
 A cup of coffee contains around 100 to 150mg of
caffeine.
 Cocoa, chocolate and soft drinks also contain
significant amount of caffeine, enough to cause
some symptoms of caffeine intoxication
 The average daily caffeine consumption of caffeine
consumers of all age is 2.79 mg/kg body weight.

 Caffeine is more potent.
 The half life of caffeine in human body is 3 to 10 hrs.
 The time of peak concentration is 30-60 min.
 Caffeine readily crosses the blood brain barrier. Caffeine
acts primarily as an antagonist of adenosine receptors.

Adenosine receptors
activate
an inhibitory G protein
thus inhibit the formation of the second messenger cyclic
adenosine monophosphate (cAMP).
Caffeine intake result in an increase in intraneuronal cAMP
concentrations in neurons with adenosine receptors.

 High doses of caffeine can affect the dopaminergic and
noradrenergic system.
 Dopamine activity is enhanced by the caffeine activity, so
it may be the reason of exacerbation of clinical symptoms
in patients with schizophrenia in increased caffeine
intake.

Effects on cerebral blood flow
Caffeine
results in
cerebral vasoconstriction
decrease in cerebral blood flow
Cerebral blood flow improves after withdrawal from the
caffeine.
Many other studies reveals that caffeine can cause
coronary artery constriction.

 Diagnostic criteria includes the recent consumption of
caffeine, usually more than 250 mg.
 Common symptoms associated with caffeine intoxication
are anxiety, psychomotor agitation, restlessness, muscle
twitching, psychophysiological complaints, nausea ,
diuresis, GIT upset, tingling in the fingers and toes.
 Consumption of more than one gram of caffeine can
cause rambling of speech, confused thinking, cardiac
arrhythmias, agitation, tinnitus and visual hallucinations.

DSM- IV- TR Diagnostic Criteria for Caffeine
Intoxification
A. Recent consumption of caffeine intake usually more
than 250 mg(more than 2-3 cups of brewed coffee)
B. Five or more of following signs, developing during,
shortly and after the caffeine use:
1. Restlessness
2. Nervousness
3. Excitement
4. Insomnia
5. Flushing of face
6. Diuresis
7. GIT disturbances
8. Rambling flow of thought and speech
9. Tachycardia or cardiac arrhythmia
10. Periods of inexhaustibility
11. Psychomotor agitation

C. The symptom in criteria B causes significant distress or
impairment in social, occupational, or other important
areas of functioning.
D. The symptoms are not due to general medical
conditions and are not better account for any other mental
disorders.
Withdrawal from caffeine – Headache, fatigue, anxiety,
irritability, depression, impaired psychomotor performance,
nausea, vomiting, craving for caffeine, muscle pain and
stiffness.

 Caffeine induced anxiety disorder can occur during
caffeine intoxication.
 The anxiety related to caffeine use can resemble the
generalized anxiety disorder.
 The patient may be over talkative, and irritable. They
may complaint of reduced sleep.
 Caffeine can induce and exacerbate panic attacks in
persons with panic anxiety disorder.

 Caffeine induced sleep disorder can occur in acute
intoxication.
 Caffeine is associated with delay in falling sleep, inability
to remain in sleep, and early morning awakening.

 Analgesics such as aspirin can be used to control the
headache because of caffeine withdrawal.
 Rarely patients need benzodiazepines to manage the
withdrawal effects.
 Person should recognize all sources of caffeine in his diet and
control the caffeine intake.
 Caffeine is used in the beverage form, it can be substituted
with beverages which are non-caffeinated.
 The patient should avoid stopping the caffeine intake abruptly.

 The psychoactive component of tobacco is nicotine
which affects the CNS.
 About 25% of the nicotine inhaled during smoking
reaches blood stream, through which nicotine reaches
the brain within 15 seconds.
 The half life of the nicotine is 2 hours.

Nicotine is believed to produce its positive reinforcing
and addictive properties by activating the dopaminergic
pathway projecting from the ventral segmental area to the
cerebral cortex and limbic system.
It also causes an increase in the concentration of
norepinephrine and epinephrine and an increase in the
release of vasopressin, beta endorphins, ACTH and
cortisol. These hormones are thought to cause stimulatory
effects of nicotine on the CNS.

 Withdrawal symptoms can develop within 2 hours of
smoking the last cigarette.
 They generally peak in the first 24 to 48 hours and can
last for weeks or months.

Symptoms : The common symptoms are:-
 An intense craving for nicotine
 Tension,
 Irritability,
 Difficulty concentrating,
 Drowsiness
 Paradoxical trouble sleeping,
 Decreased heart rate and blood pressure,
 Increased appetite
 Weight gain,
 Decreased motor performance
 Increased muscle tensions.

DSM- IV-TR Diagnostic Criteria for Nicotine
Dependence
A. Daily use of nicotine for at least several weeks.
B. Abrupt cessation of nicotine use, or reduction in the
amount of nicotine used, followed within 24 hours by four
(or more) of the following signs:
dysphoric or depressed mood
insomnia
irritability, frustration, or anger
anxiety
difficulty concentrating
restlessness
decreased heart rate
increased appetite or weight gain

C. The symptoms in Criterion B cause clinically significant
distress or impairment in social, occupational, or other
important areas of functioning.
mental disorder.

Nicotine Related Disorders Not Otherwise Specified
Nicotine related disorders not otherwise specified is a
diagnostic category for nicotine-related disorders that do
not fit into one of the categories discussed above.
Such diagnoses may include nicotine intoxication, nicotine
abuse, mood disorders and anxiety disorders associated
with nicotine use.

 Nicotine is highly toxic alkaloid.
 Doses of 60 mg in an adult are fatal secondary to
respiratory paralysis.
 Doses of 0.5 mg are delivered by smoking an average
cigarette.

In low doses the signs and symptoms include:-
 Nausea and vomiting,
 salivation
 pallor (due to peripheral vasoconstriction)
 weakness
 abdominal pain (caused by increased peristalsis)
 diarrhea
 dizziness
 headache
 increased blood pressure
 tachycardia
 tremors and cold sweats
Toxicity is also associated with an inability to concentrate,
confusion and sensory disturbances.

 Nicotine replacement therapies
 All nicotine therapies double the cessation rates because
they reduce the nicotine withdrawal. These therapies can
also be used to reduce withdrawal in patients on smoke
free ward.
 Replacement therapies use a short period of
maintenance of 6 to 12 weeks often followed by a
gradual reduction period of another 6 to 12 weeks.
 Nicotine polacrilex gum (Nicorette) is an OTC product
that release nicotine via chewing and buccal absorption.

Dose:
•A 2 mg variety for those who smoke fewer than 25
cigarettes.
•4 mg variety for those who smoke more than 25 cigarettes
a day.
•Smokers are to use one to two pieces of gum per hour up
to maximum 25 pieces per day after abrupt cessation.
•Acidic beverages(coffee, tea, soda and juice) should not
be used before during or after gum use because they
decrease absorption.
•Adverse effects are minor include bad taste and sore
jaws.

Nicotine lozenges (Commit)
Dose: available in 2mg and 4mg. Generally 9 to 12
lozenges a day are used during the first 6 weeks with
decrease in dosage there after.
Use: They are useful for patients who smoke cigarette
immediately on awakening. They offer the highest level of
nicotine of all nicotine replacement products.
Method of administration : users suck the lozenges until
it dissolved and not swallow it.
Side effects : Insomnia , nausea, heartburn, headache
and hiccups.

Nicotine patches
These are also sold OTC, are available in a 16 hours no-
taper preparation (Nicotrol) and a 24 or 16 hours tapering
preparartion (Nicoderm CQ).
Method of administration: Patches are administered
each morning
Compliance is high and the only major adverse effect are
rashes and with 24 hour wear, insomnia. After 6 to 12
week, the patch is discontinued because it is not for long
term use.

Nicotine nasal spray (Nicotrol): Available only by
prescription, produces nicotine concentrations in the blood
that are more similar to those from smoking a cigarette and
is helpful for heavily dependent smokers.
The spray causes rhinitis, watering eyes and coughing
more than 70 percent of patients.

Nicotine inhaler: It designed to deliver nicotine to the
lungs. It delivers 4mg per cartridge and resultant nicotine
levels are low.
Major advantage is that it provides a behavioural substitute
for smoking. It doubles the quit rates.
These devices requires frequent puffing -about 20 minutes
to extract 4mg of nicotine.
It has got minor adverse effects.

 It is useful to those smokers who object the notion of
replacement therapy and smokers who fail
replacement therapy.
 Bupropion which is an antidepressant is used as non
nicotine medication.
 Dose: It is started at 150 mg per day for 3days.
 Increased to 150 mg twice a day for 6 to 12 weeks.

 Second line of drug is Nortriptyline. It is found to be
effective in smoking cessation.
 Some patients benefit from benzodiazepine therapy (10
to 30 mg per day) for the first 2 to 3 weeks of abstinence.

 Clonidine (Catapress) decreases sympathetic activity.
 It decreases the withdrawal symptoms.
 Whether given as a patch or orally, 0.2 to 0.4 mg a day
 It is not much effective as other drugs.
 It causes drowsiness and hypotension.

 The term opioid refers to a group of compounds include
opium, opium derivatives and synthetic substitutes.
 Opioid exerts both a sedative and an analgesic effect,
and their major medical uses are for the relief of pain, the
treatment of diarrhoea, and the relief of coughing.
 These drugs have addictive qualities; that is they are
capable of inducing tolerance and physiological and
psychological dependence.

Categories Trade Names Common Street Names
Opioids of
natural origin
Opium
Morphine
Codeine
Black stuff, poppy, tar,
big O
M, white stuff, Miss
Emma
Terp, schoolboy, syrup,
cody
Opioid
derivatives
Herion
Hydromorphine
Oxycodone
Hydrocodone
H, horse, junk, brown
sugar, smack, skag
DLs, 4s, lords, little D
Perks, perkies, oxy, O.C.
Vike

Synthetic
opiate like
drugs
Meperidine
Methadone
Propoxyphene
Pentazocine
Fentanyl
Doctors
Dollies, done
pinks and grays
Ts
Apache, china girl,
Chinatown, dance
fever, goodfella,
jackpot

 It includes:-
 Oral, snorting
 Subcutaneous
 Intramuscular
 Intravenous injections .

 The development of opioid abuse and the dependence
may follow one of two typical behaviour patterns.
 The first occurs in the individual who has obtained the
drug by prescription from a doctor for the relief of a
medical problem.
 Abuse and dependency occur when the individual
increases the amount of the substance and frequency of
use, justifying the behaviour as symptom treatment.
 He or she becomes obsessed with obtaining increasing
amount of the substance, seeking out several physicians
in order to replenish and maintain supplies.

 The second pattern of behaviour associated with abuse
and dependency of opioids occurs among individuals
who use the drugs for recreational purposes and obtain
them from illegal sources.
 Opioids may be used alone to induce the euphoric
effects or in combination with stimulants or other drugs to
enhance the euphoria or to counteract the depressant
effects of the opioid.
 Tolerance develops and dependency occurs, leading the
individual to procure the substance by whatever means is
required to support the habit.

 The primary effects of the opioid are mediated through
the opioid receptors.
 The µ -opioid receptors are involved in the regulation and
mediation of analgesia, respiratory depression,
constipation and dependence.
 The k -opioid receptors with analgesia, diuresis and
sedation.
 The δ -opioid receptors possibly with analgesia.

 The DSM IV TR defines the opioid intoxication as
including:-
 maladaptive behavioral changes and some specific
physical symptoms of opioid use.
 In general ,altered mood, psychomotor retardation,
drowsiness, slurred speech and impaired memory and
attention suggest a diagnosis of opioid intoxication.

Diagnostic criteria for Opioid Intoxication
A. Recent use of an opioid.
B. Clinically significant maladaptive behavioural or
psychological changes (e.g., initial euphoria followed by
apathy, dysphoria, psychomotor agitation or retardation,
impaired judgment, or impaired social or occupational
functioning) that developed during, or shortly after, opioid
use.
C. Pupillary constriction (or pupillary dilation due to anoxia
from severe overdose) and one (or more) of the following
signs, developing during, or shortly after, opioid use:
drowsiness or coma
slurred speech
impairment in attention or memory

D.The symptoms are not due to a general medical
mental disorder.
Specify if:
With perceptual disturbances

DSM-IV-TR Diagnostic criteria for opioid withdrawal
A. Either of the following:
• cessation of (or reduction in) opioid use that has been
heavy and prolonged (several weeks or longer)
• administration of an opioid antagonist after a period
opioid use
B. Three (or more) of the following, developing within
minutes to several days after Criterion A:

dysphoric mood
nausea or vomiting
muscle aches
lacrimation or rhinorrhea
pupillary dilation, piloerection, or sweating
diarrhea
yawning
fever
insomnia
C. The symptoms in Criterion B cause clinically significant
distress or impairment in social, occupational, or other
important areas of functioning.

mental disorder.
The general rule about the onset and duration of
withdrawal symptoms is that substances with short
duration of action tend to produce short, intense
withdrawal syndromes and substances with long duration
of action produce prolonged but mild symptoms.

 Severe bone aches
 Profuse diarrhoea
 Abdominal cramps,
 Rhinorrhea
 Lacrimation
 Piloerection
 Yawning
 Pupillary dilatation
 Hypotension
 Tachycardia
 Insomnia
 Bradycardia
 Restlessness
 Irritability
 Depression
 Tremor
 Weakness
 Nausea and vomiting.
 Temperature
dysregulation including
hypothermia and
hyperthermia.
 Craving for opioids -can
persists for months after
withdrawal.

Morphine and Heroine : The withdrawal symptoms begin
6 to 8 hours after the last dose.
The withdrawal symptoms reaches its peak during the
second or third day and subsides during the next 7 to 10
days, but some symptoms may persists for 6months or
longer.
Meperidine: Withdrawal symptoms begins quickly,
reaches a peak in 8 to 12 hours and ends in 4 to 5 days .

Methadone : Withdrawal symptoms begins 1 to 3 days
after the last dose and ends in 10-14 days.

 It is more likely to happen when:-
 opioids are used in high doses
 opioids are mixed with other psychoactive compounds
 opioids are used by a person with pre-existing brain
damage or CNS disorder like epilepsy.

 It can begin during opioid intoxication. Clinicians can specify
whether hallucinations or delusions are the predominant
symptoms.
OPIOID INDUCED MOOD DISORDER
 It can begin during intoxication the symptom can have
manic, depressed or mixed nature, depending on a
person’s response to opioids.
 A person coming to psychiatric attention with opioid
mood disorder usually has mixed symptoms, combining
irritability, expansiveness and depression.

Opioid Induced Sleep Disorder And Opioid Induced
Sexual Dysfunction
The most common sexual dysfunction is impotence.
Opioid Related Disorder Not Otherwise Specified
The DSM IV TR includes diagnoses for opioid -related
disorders with symptoms of delirium, abnormal mood,
psychosis, abnormal sleep and sexual dysfunction.
Clinical situation that do not fit into those will be placed
under this category.

 Death from an overdose of an opioid
 Respiratory depression.
 Unresponsiveness,
 Coma
 Hypothermia,
 Hypotension
 Bradycardia.
 When presented with the clinical triad of coma, pinpoint
pupils and respiratory depression ,clinician should
consider opioid overdose as a primary diagnosis.

 Ensure an adequate airway: Tracheopharyngeal
secretions should be aspirated, an airway may be
inserted.
 The patient should be ventilated mechanically until
naloxone is given
 Naloxone is administered IV at a slow rate -initially about
0.8mg per 70 kg of body weight. Signs of improvement
(increased respiratory rate and papillary dilation )should
occur promptly.
 The duration of action of naloxone is short compared with
that of many opioids, repeated administration may be
required to prevent recurrence of opiod toxicity.

 Methadone : It is a synthetic narcotic that
substitutes for heroin and can be taken orally.
 A daily doses of 20 to 80mg is sufficient, although
daily dose of 120mg can be given.
 Methadone maintenance is continued until the
patient can be withdrawn from methadone, which
itself causes dependence.
 An abstinence syndrome occurs with methadone
withdrawal but patients are detoxified methadone
more easily than from heroin.
 Clonidine (0.1 to 0.3mg three to four time a day) is
usually given during the detoxification period.

 It frees the persons with opioid dependence from using
injectable heroin and reduces the chance of spreading
HIV infection through contaminated needles.
 Methadone produces minimal euphoria and rarely
causes drowsiness or depression when taken for a long
time.
 It allows patients to engage in gainful employment
instead of criminal activity.

 Patient remain dependent on methadone.

 Levomethadyl (LAAM): It is an opioid agonist that
suppresses opioid withdrawal.
 It is no longer used because some patients developed
prolonged QT interval with arrhythmias.
 Buprenorphine: It can be dispensed on an outpatient
basis.
 It is effective in thrice weekly dosing.
 Daily use of 8-10mg appears to reduce heroin use.
 After repeated administration, it blocks the subjective
effect of parenterally administered opioid such as heroin
or morphine.
 A mild withdrawal syndrome occurs if the drug is abruptly
discontinued after chronic administration.

Sublingual tablet formulations of buprenorphine containing
buprenorphine only or buprenorphine combined with
naloxone in a 4:1 ratio are used for opioid maintenance
treatment.
Opioid antagonists:- Opioid antagonists block the effects
of opioids.
They do not exert narcotic effects and do not cause
dependence.
Opioid antagonists include naloxone which is used to treat
opioid overdose because it reverse the effects of narcotics
and naltrexone .

Opioid detoxification programs
when patient weaned from potent opioid agonists (heroin)
appear
adrenergic withdrawal effects
treated with
clonidine.

Detoxification protocol includes:-
potent agonists (Herion)
gradually replaced by
weaker agonists (Methadone)
followed by
mixed agonist antagonist (Buprenorphine)
finally by
pure antagonists (Naltrexone)

Because opioid receptor antagonists are used to
maintain a drug free state after opioid detoxification.
Great care must be taken to ensure that an adequate
washout period elapses after the last dose of opioids and
before the first dose of an opioid receptor antagonists.
If any question persists of whether opioids are in the
body despite a negative urine screen result, naloxone
challenge test should be performed.

The naloxone challenge test can be administered by
either the intravenous (IV) or subcutaneous route.
Intravenous challenge – Following appropriate screening
of the patient, 0.8 mg of naloxone should be drawn into a
sterile syringe.
•If the IV route of administration is selected, 0.2 mg of
naloxone should be injected
•while the needle is in patient’s vein, the patient should be
observed for 30 seconds for evidence of withdrawal
symptoms.
•If no evidence of withdrawal is seen, the remaining 0.6 mg
of naloxone should be injected and the patient observed
for an additional 20 minutes for signs and symptoms of
withdrawal.

Withdrawal signs – stuffiness or running of nose, tearing,
yawning, sweating, tremor, vomiting or piloerection.
Withdrawal symptoms – feeling of temperature change,
joint or bone and muscle pain
The theory for using an antagonists is that it blocks the
agonist effect, particularly euphoria, discourages the
person with opioid dependence from substance seeking
behaviors and thus deconditions this behavior.

 Inhalant drugs (also called inhalants or volatile
substances) are volatile hydrocarbons such as toluene,
trichloroethylene, trichloroethane, dichloromethane,
gasoline and butane. These chemicals are sold in four
commercial classes:
• Solvents for glues and adhesives.
• Propellants for aerosol paint sprays, hairsprays, frying
pan sprays, and shaving cream, Thinners( paint
products)
• Fuels

 Methods of use include huffing"- a procedure in which a
rag soaked with the substance is applied to the mouth
and nose and the vapours breathed in.
 Another common method is called "bagging" in which the
substance is placed in a paper or plastic bag and inhaled
from the bag by the user. They may also be inhaled
directly from the container or sprayed in the mouth or
nose.

 Inhalants usually act as a central nervous system
depressant.
 Tolerance for inhalants can develop, although withdrawal
symptoms are usually fairly mild and are not classified as
disorders in DSM-IV-TR.
 Inhalants are rapidly absorbed through the lungs and
rapidly delivered to the brain.
 The effects appear within 5 minutes and can last for 30
minutes to several hours, depending on the inhalant
substance and the dose.
 The concentration of the many inhalant substances is
increased when used in combination with alcohol.

A) Recent intentional use or short term, high dose
exposure to volatile inhalants(excluding anaesthetic
gases and short acting vasodilators)
B) Clinically significant maladaptive behavioural or
psychological changes ( e.g: belligerence, assultiveness,
apathy, impaired judgement, impaired social or
occupational functioning) that developed during, or
shortly after, use of or exposure to volatile inhalants.

Two (or more) of the following signs, developing during, or
shortly after, inhalant use or exposure:
Dizziness
Nystagmus
In coordination
Slurred speech
Unsteady gait
Lethargy
Depressed reflexes
Psychomotor retardation
Tremor
Generalized muscle weakness
Blurred vision or diplopia
Stupor or coma
Euphoria

Inhalant Intoxication Delirium
Delirium can be induced by the effects of the inhalants
themselves, by pharmacodynamic interactions with other
substances, and by hypoxia, that may be associated with
either the inhalant or its method of inhalation.
If the delirium results in severe behavioural disturbances,
short term treatment with a dopamine receptor antagonist,
such as haloperidol may be necessary.
Benzodiazepines should be avoided because of the
possibility of increasing the patient's respiratory
depression.

Inhalant Induced Psychotic Disorder
Clinicians can specify hallucinations or delusions as the
predominant symptoms. Paranoid states are probably the
most common psychotic syndromes during inhalant
intoxication.
Inhalant Induced Mood Disorder and Inhalant Induced
Anxiety Disorder
Inhalant induced mood disorder and inhalant induced
anxiety disorder are DSM IV TR diagnoses that allow the
classification of inhalant related disorders characterized by
prominent mood and anxiety symptoms.
Depressive disorders are the most common mood
disorders associated with inhalant use, and panic
disorders and generalized anxiety disorder are the most
common anxiety disorders.

DSM- IV Diagnostic Criteria For Inhalant Disorder Not
Otherwise Specified.
This category is for disorders associated with the use of
inhalants and is not classifiable as inhalant dependence,
inhalant abuse, inhalant intoxication, Inhalant abuse,
Inhalant intoxication, Inhalant intoxication delirium,
Inhalant induced persisting dementia, Inhalant induced
psychotic disorder, with delusions, Inhalant induced
psychotic disorder, with hallucinations, Inhalant induced
mood disorder, and Inhalant induced anxiety disorder.

 In small initial doses, inhalants can produce feelings of
euphoria and excitement and pleasant floating
sensations, the effects for which persons presumably use
the drugs.
 High doses of inhalants can cause psychological
symptoms of fearfulness, sensory illusions, auditory and
visual hallucinations, and distortions of body size.

The neurological symptoms can include slurred speech,
decreased speed of talking, and ataxia.
Long term can be associated with irritability, emotional
liability and impaired memory.
Tolerance for inhalants does develop; although not
recognized by DSM-IV TR, a withdrawal syndrome can
accompany the cessation of inhalant use.
The withdrawal syndrome does not occur frequently; when
it does it can be characterized by sleep disturbances,
irritability, jitteriness, sweating, nausea, vomiting,
tachycardia, and delusions and hallucinations.

 Inhalants are absorbed from the lungs and reach the
CNS very rapidly. Inhalants generally act as a CNS
depressant. The effects are relatively brief, lasting from
several minutes to a few hours, depending on the
specific substance and amount consumed.
 Central nervous system:
Inhalants can cause both central nervous system and
peripheral nervous system damage, which may be
permanent. Neurological deficits, such as generalized
weakness and peripheral neuropathies, may be evident.

SYSTEM EFFECTS
Respiratory Upper or lower airway irritation, pulmonary
hypertension, acute respiratory distress,
coughing, sinus discharge, dyspnoea, rales,
or rhonchi, pneumonitis or asphyxia.
Gastrointestinal Abdominal pain, nausea and vomiting,
Rashes around the individual's nose or
mouth, Unusual breath odour
Renal system Chronic renal failure, hepatorenal
syndrome, and proximal renal tubular
acidosis

 Inhalant intoxication, as with alcohol intoxication
 It usually requires no medical attention and resolves
spontaneously.

 The sedative hypnotic compounds are the drugs of
diverse chemical structures that are capable of inducing
varying degree of CNS depression from tranquilizing
relief of anxiety to anestheisa, coma and even death.
 They are generally categorised as:-
 Barbiturates
 Non-barbiturates
 Antianxiety agents

Categories Trade Name Street Name
Barbiturates Pentobarbital
Secobarbital
Phenobarbital
Amobarbital
Yellow Jackets, Yellow
Birds
Gbs, Red Birds, Red
Devils
Blur Birds, Blue
Angles

Non-Barbiturates
Hypnotics
Chloral Hydrate
Triazolam
Flurazepam
Temazepam
Peter, Mickey
Sleepers
Sleepers
Sleepers
Antianxiety Agents Diazepam
Chlordiazepoxide
Meprobamate
Alprazolam
Lorazepam
Vs (Color Designates
Strength)
Green And Whites,
Roaches
Dolls, Dollis

Club Drugs Flunitrazepam (Rohypnol)
Gamma Hydroxybutyric
Acid
Date Rape Drug,
Roofies
G, Liquid X, Easy
Lay

 Two patterns use:-
 The first pattern is one of an individual whose physician
originally prescribed the CNS depressant as treatment
for anxiety or insomnia. Independently, the individual has
increased the dosage or frequency from that which was
prescribed.
 The second pattern involves young people in their teens
or early 20s who, in company of their peers, use
substances that were obtained illegally.

 The sedative hypnotic compounds induce a general
depressant effect.
 They depress the activity of the brain, nerves, muscles
and heart tissue.
 They reduce the rate of metabolism in a variety of tissues
throughout the body and in general they depress any
system that uses energy.

SYSTEM EFFECTS
Effects on sleep
and dreaming
Barbiturates use decreases the amount of
sleep time spent in dreaming.
During drug withdrawal, dreaming
becomes vivid and excessive.
Respiratory
system
Respiratory depression.
Cardiovascular
effect
Hypotension , decreased cardiac output,
decreased cerebral blood flow, impaired
myocardial contractility.

SYSTEM EFFECTS
Renal effects In high doses- suppress urine function.
Hepatic effects Jaundice, liver damage
Body
temperature
Decrease body temperature.
Sexual
functioning
Initially increase in libido, decrease in ability
to maintain an erection.

 Inappropriate sexual or aggressive behaviour
 Mood lability
 Impaired judgement
 Impaired social or occupational functioning
 Slurred speech
 In-coordination and unsteady gait
 Nystagmus
 Impairment in attention or memory
 Stupor or coma.

 Sweating
 Pulse rate higher than 100
 Increased hand tremor
 Insomnia
 Nausea or vomiting
 Hallucinations
 Illusions
 Psychomotor agitation
 Anxiety
 Grand mal seizures

 Assessment is a process of gathering information about
a person’s substance use status and health and is an
going process.
Types of assessment
 Screening
 Basic assessment
 Specialized assessment

For detection of problem drinkers in the community,
several screening instruments are available:-
CAGE questionnaire
It consists of 4 questions:-
Have you ever had to Cut down on alcohol (amount).
Have you ever been Annoyed by people’s criticsm of
alcoholism.
Have you ever felt Guilty about drinking.
Have you ever needed Eye opener drink (early morning
drink).

Certain laboratory markers of alcohol dependence have
been suggested . These include:-
i. GGT (gamma glutyl transferase) is raised to about 40
IU/L in about 80 % of the alcohol dependent individuals.
GGT returns to normal rapidly (i.e. within 48 hours) on
abstinence from alcohol. An increase of GGT of more
than 50% in an abstinent individual signifies a
resumption of heavy drinking.
ii. MCV (mean corpuscular Volume) is more than 92 fl
(normal = 80 -90 fl) in about 60% of the alcohol
dependent individuals. MCV tales several weeks to
return to normal values after abstinence.
iii. Other lab markers include alkaline phosphate, AST,
ALT, uric acid, blood triglycerides and CK.

 This includes clinical interview and physical examination
supported with or without laboratory investigations to
arrive at a diagnosis.
 Clinical interview – it involves eliciting answers by
enquiring into specific issues regarding substance use
i.e. initiation, progression, complications associated with
its use and motivation.

 This is done by a specialist to assess personality, coping
skills, social supports, risk factors for relapse, presence
of concurrent physical illness and psychiatric illness in-
depth.

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