Velez College
F. Ramos Street, Cebu City
Special Topic Report
Substance-Related Disorder and Substance Abuse
Submitted to:
Ms. Adeline C. Famador
Submitted by:
Beloria, Euka Maria
Lagulao, Jermyn Mae
BSOT-IV
I.
Definition
As characterized by the presence of at least one specific symptom
indicating that substance use has interfered with the person’s life. A
maladaptive pattern of substance use leading to clinically significant
impairment or distress, as manifested by one of the following, occurring
within a 12-month period;
a. Recurrent substance use resulting in a failure to fulfill major role
obligations at work, school, or home.
b. Recurrent substance used in which it is physically hazardous.
c. Recurrent substance-related legal problems.
d. Continued substance use despite having persistent or recurrent
social or interpersonal problems caused or exacerbated by the
effects of the substance.
II.
Epidemiology
A large recent survey showed that the life time prevalence of a diagnosis
of substances abuse or dependence among US population older than age
18 was 16.7. The life time prevalence for alcohol abuse or dependence
was 13.8% for non-alcohol substances, it was 6.2%. In 1995, 6.1% of the
population age 12years or older were current elicit drug users are the mist
commonly used, substances but marijuana, hashish and cocaine are also
commonly used. However, for all four of these substances alcohol
marijuana, cigarettes, and cocaine-there has been gradual but consistent
decrease in use from a high around 1980 to 1992. Abuse and dependence
on substances are common in men and women, substances abuse is also
higher among people who are unemployed and among some minority
groups than among people who are employed and among majority
groups, and are not limited to adults. A recent survey of high school
seniors showed that about 30% had tried a non-alcohol substance at least
once and about 16% had tried a non-alcohol, non-marijuana substance
such as amphetamines, inhalants, hallucinogens, sedatives or cocaine at
least once. Substance is more common among medical professionals than
among non-professionals of equal levels of training. Possible explanation
is simply the relatively easy access that medical professionals have to
some classes of substances.
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Illicit Drug Use
- Estimated 12.8 million people in the United States were
current illicit drug users, having used an illicit in the month
preceding the interview. Between 1994 and 1995,the rate
past month illicit drug use among adolescents
increased,from 8.2 to 10.9%.
- An estimated 2.3 million people started using marijuana in
1994.the annual number of marijuana initiates has risen
since 1991.marijuana is the most common illicit drug,used by
77%of current illicit drug users.57% of current illicit drug
users used marijuana only 20% used marijuana and another
illicit drug and the remaining 23% used only an illicit drug
other than marijuana in the past month. However, has
sharply declined from 7.1 million in 1985 to 2.5 million in
1995.
Alcohol Use
- 111 million people in the United States age 12 and older had
used alcohol in the past month. About 32million engaged in
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binge drinking, 11million were heavy drinkers. About
10million current drinkers were under age 21 in 1995.
- Of these, 4.4million were binge drinkers including 1.7million
heavy drinkers.
Cigarette Use
- The rate of current cigarette smoking did not change
between 1994cand 1995. And estimated 20% youths ages
12-17 were current smokers in 1995
- Current smokers are more likely to be heavy drinkers and
illicit drug users than are non-smokers. Among smokers in
1995, 12.6% were heavy drinkers, and 13.6% were illicit
drug users. Among non-smokers, 2.7% were heavy drinkers,
3.0% were illicit drug users.
Women of Child Bearing Age
- Overall, 7.3% of women ages 15-44 in 1995 had used an
illicit drug in the past month. The corresponding age of men
ages 15-44 was 11.6% of the 4.3million ages 15-44 who
were current illicit drug users in 1995, more than 1.6million
had children living with them including 390,000 with at least
one child younger than two years of age.
- Among women ages 15-44 who had no children and were
not pregnant, 9.3% were current illicit drug users. Only 2.3%
of pregnant women were current drug users. Women may
reduce their drug use when they got pregnant but women
who recently gave birth and a rate of used 5.5%. Many
women thus resume their drug used after giving birth.
Ages
- Among adolescent age 12-13, 4.5% were current illicit drug
users. The highest rate was found among young people
ages 16-17 and ages 18-20.
- Rates of use were lower in each successive age group, with
only about 1% of those age 50 and older reporting current
illicit drug use.
Race and Ethnicity
- The rate of current illicit drug use for blacks was 7.9% higher
than for whites was 6.0%, Hispanics 5.1% in 1995. However,
the rates were used about the same for the three groups;
most current illicit drug users were white. Estimated
9.6million whites, 1.9million blacks and 1.0million Hispanics
were current illicit drug users in 1995.
Gender
- As in 1994, men continued to have a higher rate of current
illicit drug use than did women.
Region and Urbanicity
- The current illicit drug use rate changes from 7.8 in the West
to 4.9% in the Northeast.
Education
- Illicit drug use rates remain highly correlated with
educational status. Among young adults’ ages 18 to 34
years in 1995, those who had not completed high school and
the highest rate of use and college graduates had the lowest
rate of use.
Employment
- Current employment status is also highly correlated with
rates of illicit drug use; 14.3%of unemployed adults were
current illicit drug users in 1995, compared with 5.5% of full-
time employed adults. The rate for full-time employed adults
decreased significantly between 1994 and 1995.
III.
Etiology
Substance abuse and substance dependence result from a person’s taking a
particular substance in an abusive pattern. As with all psychiatric disorders,
the initial causative theories grew from psychodynamic models.
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IV.
Psychodynamic Factors
- A masturbatory equivalent, a defense against homosexual
impulses, or manifestation of oral regression. Use to depress
or treat substance use as a reflection of disturbed ego
functions.
- Psychodynamic approaches to people with substance abuse
are more widely valued and accepted than they are in the
treatment of patient with alcohol abuse. In contrast to
alcoholic patient, individuals with poly substance abuse are
more likely to have had unstable childhoods, more likely to
self-medicate with substances and more likely to benefit
from psychotherapy.
Co-addiction/Co-dependence
- When people, usually a couple have a relationship that is
primarily responsible for maintaining addiction behavior in at
least one of the persons. Each behavior that
helpsperpetuates the situation and denial of the situation is a
pre-requisite for such a dyadic relationship to develop.
Behavioral Theories
- A substance seeking behavior has for major principles. The
first two principles are the positive reinforcing qualities and
adverse effect of some substance. According to the third and
fourth principle, a person must be able to discriminate the
substance of abuse from other substance; most of all
substance-seeking behavior is associated with cues that
become connected with the substance-taking experienced.
Genetic Factors
- Genetic pattern in their development.
Neurochemical Factors
- Identified particular neurotransmitter through which, or
neurotransmitter receptors on which the substance has their
effects. The opiates, the long term use of a particular
substance of abuse may eventually modulate receptor
system in the brain, which requires the presence of the
exogenous substance to maintain homeostasis. A receptorlevel may be the mechanism for developing tolerate within
the central nervous system.
Pathophysiology
Several neurobehavioural effects of alcohol have been related to the
development of alcohol dependence. The pleasurable and stimulant effects of
alcohol are mediated by a dopaminergic pathway projecting from the ventral
tegmental area to the nucleus accumbens. Repeated, excessive alcohol
ingestion sensitises this pathway and leads to the development of
dependence. Long-term exposure to alcohol causes adaptive changes in
several neurotransmitter systems, including down-regulation of inhibitory
neuronal gamma-aminobutyric acid receptors, up-regulation of excitatory
glutamate receptors, and increased central norepinephrine (noradrenaline)
activity.
Discontinuation of alcohol ingestion leaves this excitatory state unopposed,
resulting in the nervous system hyperactivity and dysfunction that
characterise alcohol withdrawal. It has also been suggested that withdrawal
symptoms intensify as withdrawal episodes grow in number, a phenomenon
called 'kindling'. Alcohol-dependent patients also experience craving, defined
as the conscious desire or urge to drink alcohol. Craving has been linked to
dopaminergic, serotonergic, and opioid systems that mediate positive
reinforcement, and to the gamma-aminobutyric acid, glutamatergic, and
noradrenergic systems that mediate withdrawal. Long-term use of alcohol is
also proposed to enhance corticotrophin-releasing factor, neuropeptide Y,
and other stress-producing neurotransmitters and hormones, so that
continued alcohol use becomes necessary to relieve chronic stress and
dysphoria.
Continuing to clarify the specific neurotransmitters associated with both the
behavioural effects of alcohol and the development of alcohol dependence
may yield potential targets for drug therapy to treat dependence.
V.
Signs and Symptoms
Alcohol may lead to:
 health problems
 social problems
 morbidity
 injuries
 unprotected sex
 violence
 deaths
 motor vehicle accidents
 homicides
 suicides
 Physical dependence or psychological addiction.
VI.
Course and Prognosis
Individuals who suffer from substance abuse tend to be more successful in
recovery when they are highly motivated to be in treatment, are actively
engaged in their own recovery, and receive intensive treatment services.
Prognosis for substance abuse recovery is further improved by being able to
easily access community-based social supports.
VII.
Medical Management
Formal intervention is necessary to convince the substance abuser to submit
to any form of treatment. Behavioral interventions and medications exist that
have helped many people reduce, or discontinue, their substance abuse.
From the applied behavior analysis literature, behavioral psychology, and
from randomized clinical trials, several evidenced based interventions have
emerged:
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Behavioral marital therapy
Motivational Interviewing
Community reinforcement approach
Exposure therapy
Contingency management
Pharmacological therapy
ALCOHOL-RELATED DISORDER
I.
Definition
The most frequently used brain depressant. Cause of considerable morbidity
and mortality.
II.
Epidemiology
Drinking alcohol-containing beverages is generally considered an acceptable
and common habit in the United States. 85% of all US residents have had an
alcohol-containing drink at least once in their lives. 51% of all US adults are
current users of alcohol. US stated that beer has one half of all alcohol
consumptions, liquor for about one third and wine for about one sixth. About
10% of women and 20% of men have met the diagnostic criteria for alcohol
abuse during their lifetime, and 3 to 5% of women and 10% in men have met
the diagnostic criteria for the more serious diagnosis of alcohol dependence
during their lifetimes. About 200,000 deaths each year are directly related to
alcohol abuse. The common causes of deaths among people with alcoholrelated disorders are suicide, cancer, heart disease and hepatic disease.
Alcohol use and alcohol-related disorders are also associated with about 50%
of all homicides and 25% of all suicides.
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Statistical Factors
- In 1995, approximately 111million people age 12 and over
were current alcohol users; this number was about 52%of
the total population of age 12 and older. About 32million
people engaged in binge drinking and about 11million people
were heavy drinkers. About 10million current drinkers were
under 21 in 1995. Of these, 4.4million were binge drinkers,
including 1.7million heavy drinkers. Alcohol usage rates
were not significantly different between 1994 and 1995.
- Rates of current alcohol use were above 60% for age groups
21 through 25, 26 through 29, 30 through 34, 35 through 39,
and 40 through 44 in 1995. For younger and older age
groups rates were lower. Young adults’ drinkers were the
most likely to binge or drink heavy. About half the drinkers in
this age group were binge drinkers and about one in five was
heavy drinkers.
 Race and Ethnicity
o Rates for Hispanics and blacks were 45% and
41%. Rate for binge use was lower among
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blacks 11.2% and among whites 16.6% and
among Hispanics 17.2%
 Gender
o Men were much more likely than were women
to be binge drinkers 23.8% and 8.5% and
heavy drinkers 9.45 and 2.0%
 Region and Urbanicity
o The rate of current alcohol use was 59% in
North Central Region, 54% in Northeast
Region, 53% in West and 47% in South in
1995. Rates of binge use were 20% in North
Central Region, 16% West and 14% in South
and Northeast. Heavy alcohols were 7% North
Central region, 5.6% West, 4.9 Northeast and
4.8 in South.
 Education
o 68% of adults with college degrees with current
drinkers, 42% of those having less than a high
school education. Rate of heavy alcohol use
was 3.7% who had completed college and
7.1% among not completed high school.
Psychosocial Factors
- People who are stereotypical skid row alcoholics constitute
less than 5% of those with alcohol-related disorders in the
United States.
Comorbidity
 Anti-social Personality Disorder
o Particularly common in men with an alcoholrelated disorder and can precede the
development of alcohol-related disorder.
 Mood Disorder
o Depression is likely to occur in patients with
alcohol-related d/o who have a highly daily
consumption of alcohol and who have family
history of alcohol abuse.
o Depressive symptoms that remain after 2 to 3
weeks of sobriety to be treated with
antidepressant drug. Pt. with bipolar I d/o are
thought to be at risk for developing an alcoholrelated d/o and may use alcohol to selfmedicate their manic episodes. Dopamine
metabolites and y-aminobutyric acid (GABA)
 Anxiety Disorder
o Use alcohol for its efficacy in alleviating
anxiety. Phobias and panic d/o are particularly
frequent comorbid diagnose in this pt.
 Suicide
o Presence of major depressive episode, weak
psychosocial support systems, a serious coexisting medical condition, unemployment and
living alone.
Etiology
All other psychiatric conditions probably represent a heterogeneous group of
disease process. Psychosocial, genetic or behavioral factors may be
important than any other factors. One element, a neurotransmitter receptor
gene, may be more critically involved than other element.
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Childhood History
- Children at high risk for alcohol-related d/o have been found
to possess a range of deficits on neurocognitive testing,
decreased amplitude of the P300 wave on evoked potential
testing. A variety of abnormalities on EEG recordings.
- A childhood history of attention-deficit/hyperactivity d/o or
conduct d/o or both increase a child’s risk for an alcoholrelated d/o as an adult. Anti-social personality d/o
predisposes a person to an alcohol-related d/o.
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Psychodynamic Factors
- According to psychoanalytic theory, people with harsh super
egos’ who are self-punitive turn to alcohol as a way of
diminishing unconscious stress. Anxiety in people fixated at
the oral stage may be reduced by taking substance, such as
alcohol by mouth. The general personality of a person with
an alcohol-related d/o as shy, isolated, impatient, irritable,
anxious, hypersensitive and sexually repressed.
- Alcohol may be abused by some people to reduced tension,
anxiety and psychic pain. Alcohol consumption can also lead
to a sense of power and increased self-worth.
Social and Cultural Factors
- Social settings commonly lead to excessive drinking in
college dormitories and military bases. Colleges and
universities have recently tried to educate students about the
health risks of drinking large quantities of alcohol. Some
cultural and ethnic groups are more restrained than others
about alcohol consumption.
Behavioral and Learning Factors
- Cultural factors can affect drinking habits, so can the habits
within a family, specifically parental drinking habits. The
positive reinforcing aspects of alcohol can induce feelings of
well-being and euphoria and can reduce fear and anxiety
which may further encourage drinking.
Genetic and Other Biological Factors
- The data for the heritability of alcohol-related d/o in men are
stronger than are data for the heritability of alcohol-related
d/o in women.
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IV.
Pathophysiology
Alcohol is metabolized by a normal liver at the rate of about one ounce. An
"abnormal" liver with conditions such as hepatitis, cirrhosis, gall
bladder disease, and cancer will have a slower rate of metabolism.
As drinking increases, people become sleepy, or fall into a stupor. After a
very high level of consumption, the respiratory system becomes depressed
and the person will stop breathing. Comatose patients may aspirate their
vomit. CNS depression and impaired motor co-ordination along with poor
judgement increases the likelihood of accidental injury occurring. It is
estimated that about one third of alcohol-related deaths are due to accidents
(32%), and another 14% are from intentional injury.
In addition to respiratory failure and accidents caused by effects on the
central nervous system, alcohol causes significant metabolic
derangements. Hypoglycaemia occurs due to ethanol's inhibition
of gluconeogenesis, especially in children, and may cause lactic
acidosis, ketoacidosis and acute renal failure. Metabolic acidosis is
compounded by respiratory failure. Patients may also present with
hypothermia.
V.
Signs and Symptoms
Patient will often complain of difficulty of the following
 interpersonal relationships
 problems at work or school
 legal problems
 complain of irritability and insomnia
 Inebriation and poor judgment
 chronic anxiety
 alcohol poisoning
 unintentional injuries
 Suicide
 Hypertension
 Pancreatitis
 sexually transmitted diseases
 Meningitis among other disorders.
VI.
Course and Prognosis
Alcohol abuse during adolescence, especially early adolescence may lead to
long-term changes in the brain which leaves them at increased risk
of alcoholism in later years genetic factors also influence age of onset of
alcohol abuse and risk of alcoholism. College/university students who are
heavy binge drinkers (3 or more times in the past 2 weeks) are 19 times more
likely to be diagnosed with alcohol dependence, and 13 times more likely to
be diagnosed with alcohol abuse compared to non-heavy episodic drinkers,
though the direction of causality remains unclear. Occasional binge drinkers
(one or two times in past 2 weeks), were found to be 4 times more likely to be
diagnosed with alcohol abuse or dependence compared to non-heavy
episodic drinkers.
VII.
Medical Management
Treatment and interventions among youth should focus on eliminating or
reducing the effects of adverse childhood experiences, like childhood
maltreatment, since these are common risk factors contributing to the
development of alcohol abuse approaches like contingency management and
motivational interviewing have shown to be effective means of treating
substance abuse in impulsive adolescents by focusing on positive rewards
and redirecting them towards healthier goals. Educating youth about what is
considered heavy drinking along with helping them focus on their own
drinking behaviors has been shown to effectively change their perceptions of
drinking and could potentially help them to avoid alcohol abuse.
AMPHETAMINE-RELATED DISORDER
I.
Definition
were first synthesized for therapeutic use and are used legitimately to treat a
variety of medical and psychiatric conditions in the treatment of obesity,
although their efficacy and safety for this indication are controversial
preparation the major amphetamines are Dextroamphetamine
(Dexedrine)methamphetamine and methylphenidate (Ritalin) are referred to
as sympathomimetics,stimulants and psychostimulants are used to increased
performance and to induce a euphoric feeling other amphetamine like
substances are ephedrine and propranolamine, which are available as nasal
decongestants.phenylpropranolamine is available as an appetite suppressant
. Ephedrine and propranolamine are subject to abuse both
drugs,propranolamine in particular, can dangerously exacerbate hypertension
precipitate a toxic psychosis or result in death.
II.
Epidemiology
In 1966, about 7 percent of the U.S. population had used stimulants at least
once, althoughless than 1 percent was users. In 1995, about 2 percent of the
US population has tried methamphetamine. The 18 to 25 years old age group
reported the highest level of use, with 9 percent reporting use at least once
and 1 percent describing themselves as current users. Use among the 12 to
17 years old age group appears at an alarming high level, with 3 percent
reporting use et least once and 1 percent reporting current use. Amphetamine
use occurs in all socioeconomic groups, and the trend for amphetamine use
among white professionals is at a high level. Because amphetamine are
available by prescription for specific indication,prescribing physicians must be
aware of the risk of amphetamine abuse by others, including friends and
family members of the patient receiving the amphetamine.
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Amphetamine dependence and Amphetamine Abuse
 Amphetamine Intoxication
o The intoxication syndromes of cocaine and
amphetamines are similar. Because more
rigorous and in-depth research has been done
on cocaine abuse and intoxication than on
amphetamines, the clinical literature on
amphetamine has been strongly influenced by
the clinical findings of cocaine abuse.
o If intact reality testing is absent, a diagnosis of
amphetamine-induced psychotic d/o with onset
during intoxication is indicated. The symptoms
of amphetamine intoxication are mostly
resolved after 24hours and are generally
completely resolved after 48hours.
o Recent use of amphetamine or a related
substance.
o Clinically significant maladaptive behavioral or
psychological changes that developed during,
or shortly after, use of amphetamine or related
substance.
o Two of the following developing, during or
shortly after, use of amphetamine or related
substance:
 Tachycardia and bradycardia
 Papillary dilation
 Elevated or lowered blood pressure
 Perspiration or chills
 Nausea and vomiting
 Evidence of weight loss
 Psychomotor agitation or retardation
 Muscular weakness, respiratory
depression, chest pain, or cardiac
arrhythmias
 Confusion, seizures dyskinesis,
dystonias or coma
o The symptoms are not due to a general
medical condition and not better accounted for
by another mental disorder
 Amphetamine Withdrawal
o A crash occurs with symptoms of anxiet,
tremulousnesss, dysphoric mood,
lethargy,fatigue, nightmares, headache,
profuse,sweating,muscle cramps, and
insatiable hunger. The withdrawal
symptoms generally peak in 2 to 4 days
and are resolved in 1 week. The most
serious withdrawal symptoms is
depressions; which can be particularly
severe after the sustained use of high
doses of amphetamine and which can
be associated with suicidal ideation of
behavior
o Cessation of amphetamine use which
have been heavy and prolonged.
o Dysphoric mood and two of the following
physiological changes, developing
within a few hours to several days
 Fatigue
 Vivid, unpleasant dreams
 Insomnia or hypersomnia
 Increase appetite
 Psychomotor retardation or
agitation
o Cause clinically significant distress or
impairment in social, occupational, or
other important area of functioning
o The symptoms are not due to a general
medical condition and not better
accounted for by another mental
disorder
 Amphetamine Intoxication Delirium
o Associated with amphetamine usually results
from high doses of amphetamine or from its
sustained use so that sleep deprivation affects
the clinical presentation. The combination of
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III.
amphetamines with other substance and the
use of amphetamines by the person with
preexisting brain damage can also cause
delirium to develop.
Amphetamine-Induced psychotic Disorder
o Has a presence of paranoia. Amphetamineinduced psychotic disorder can be
distinguished from paranoid schizophrenia by
several differentiating characteristics
associated with the former, including a
predominance of visual hallucinations,
generally appropriate affects, hyperactivity,
hypersexuality, confusion and incontinence
and incoherence, and little evidence of
disordered thinking.
o However, acute amphetamine induced
psychotic disorder can appear completely
indistinguishable from schizophrenia and only
the resolution of the symptoms in a few days or
a positive finding in a urine drug screen test
eventually reveals the correct diagnosis.
Amphetamine-Induced Mood Disorder
o Onset of amphetamine-induced mood disorder
can occur during intoxication or withdrawal.
Intoxication is associated with manic or mixed
mood features, whereas withdrawal is
associated with depressive mood features.
Amphetamine-Induced Anxiety Disorder
o Onset of amphetamine-induced anxiety
disorder can also occur during intoxication or
withdrawal. Amphetamine, like cocaine can
induce symptoms similar to those seen in
obsessive-compulsive disorder, panic disorder
and phobic disorder in particular.
Amphetamine-Induced Sexual Dysfunction
o Although amphetamine is often used to
enhance sexual experiences, high doses and
long-term use are associated with impotence
and other sexual dysfunctions.
Amphetamine-Induced Sleep Disorder
o The diagnostic criteria for amphetamineinduced sleep disorder with onset during
intoxication. Amphetamine intoxication can
produce insomnia and sleep deprivation,
whereas people undergoing amphetamine
withdrawal can experience hypersomnolence
and nightmares.
Etiology
The familial, social, and psychological factors are relevant in the etiology of
amphetamine misuse. Two-thirds to three-quarters of drug misusers have an
underlying personality disorder, usually of the antisocial type
IV.
Pathophysiology
In general, chronic amphetamine abuse may cause psychiatric symptoms due
to inhibition of the dopamine transporter in the striatum and nucleus
accumbens. The longer the duration of use, the greater the magnitude of
dopamine reduction. Methamphetamine has been suggested to induce
psychosis through inhibiting the dopamine transporter, with a resultant
increase in dopamine in the synaptic cleft.
Amphetamine-induced psychosis often results after increased or large use of
amphetamines, as observed in binge use or after protracted use. Prescription
amphetamines induce the release of dopamine in a dose-dependent manner;
low doses of amphetamines deplete large storage vesicles, and high doses
deplete small storage vesicles. This increase in dopaminergic activity may be
causally related to psychotic symptoms because the use of D2-blocking
agents (eg, haloperidol) often ameliorates these symptoms. Amphetamineinduced psychosis has been used as a model to support the dopamine
hypothesis of schizophrenia, in which overactivity of dopamine in the limbic
system and striatum is associated with psychosis. However, negative
symptoms commonly observed in schizophrenia are relatively rare in
amphetamine psychosis.
MDMA causes the acute release of serotonin and dopamine and inhibits the
reuptake of serotonin into the neuron. MDMA has neurotoxic properties in
animals and, potentially, in humans. Reports suggest that MDMA use is
associated with cognitive, neurologic, and behavioral abnormalities, as well
as hyperthermia, but these reports are confounded by the association with
other factors (eg, heat, exertion, poor diet, other drug use). Serotonergic
damage has been suggested to lead to cognitive impairment.
Delirium caused by amphetamines may be related to the anticholinergic
activity, as observed in different classes of drugs, such as tricyclic
antidepressants, benzodiazepines, sedatives, and dopamine-activating drugs.
Rapid eye movement during the first phase is decreased during intoxication,
and a rebound elevation of rapid eye movement occurs during withdrawal;
this effect eventually alters the circadian rhythm and results in sleep
disturbances.
V.
Signs and Symptoms
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Physical effects
- Hyperactivity
- dilated pupils
- vasoconstriction
- blood shot eyes
- flushing, restlessness
- drymouth
- Bruxism
- Headache
- Tachycardia
- Bradycardia
- Tachypnea
- Hypertension
- Hypotension
- Fever
- Diaphoresis
-
VI.
Diarrhea
Constipation
blurred vision
Aphasia
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Psychological effects
- Euphoria
- Anxiety
- increased libido
- Alertness
- Concentration
- Energy
- self-esteem
- self-confidence
- Sociability
- Irritability and aggression
- psychosomatic disorders, psychomotor agitation
- Grandiosity, repetitive and obsessive behaviors
- paranoia and with chronic and/or high doses
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Withdrawal effects
- mental fatigue
- mental depression
- increased appetite
- anxiety
- Agitation
- excessive sleep
- vivid or lucid dreams
- deep REM sleep and suicidal ideation
Course and Prognosis
Some individuals who develop abuse or dependence on amphetamines
initiate use in an attempt to control their weight. Others become introduced
through the illegal market. Dependence can occur very quickly when the
substance is used intravenously, or is smoked. The few long-term data
available show a tendency for people who have been dependent on
amphetamines to decrease or stop using them after eight to 10 years. This
may result from the development of adverse mental and physical effects that
emerge with long-term dependence. Few data are available on the long-term
course of abuse.
VII.
Medical Management
The treatment of specific amphetamine-induced disorder such as
amphetamine-induced psychotic disorder and amphetamine-induced anxiety
disorder with specific drugs such as antipsychotics and anxiolytics may be
necessary on a short-term basis. A phenothiazine or haloperidol may be
prescribed for the first few days. In the absence of psychosis, diazepam is
useful to treat patients’ agitation and hyperactivity.
Physicians should establish a therapeutic alliance with patients to deal with
the underlying depression or personality disorder or both. Because may
patient are heavily dependent on the drug, however, psychotherapy may be
especially difficult. Haloperidol may used for amphetamine-induced psychotic
disorder.
CAFFEINE-RELATED DISORDER
I.
Definition
Caffeine, usually in the form of coffee or tea, most widely used psychoactive
substance in Western countries. About 80% of North American adults
regularly drink caffeine-containing beverages. It can cause agitation, heart
palpitations and insomnia.
Caffeine can act as a positive reinforce, particularly at low doses. Doses of
100mg induced a mild euphoria in humans and repeated substance-seeking
behavior effects in other animals. Caffeine doses of 300 mg however do not
act as positive reinforces and can produce increased anxiety and mild
dysphoria. Studies in animals and humans have reported that caffeine can be
discriminated from a placebo in blind experimental conditions. Both animal
and human studies have shown that physical tolerance to some effects of
caffeine does develop and that withdrawal symptoms do occur.
II.
Epidemiology
Caffeine is contained in drinks, foods, prescription medicines, and over the
counter medicines. An adult in the United States consumes about 200 mg of
caffeine per day on average, although 20-30% of all adults consume more
than 500mg per day. A cup of coffee generally contains 100-150mg of
caffeine, tea contains about one-third as much. Many over the counter
medications contain one third to one half as much caffeine as that in a cup of
coffee. Migraine medications and over the counter stimulants contain more
caffeine than does a cup of coffee.
Amounts of caffeine are contained in cocoa, chocolate and soft drinks,
enough to cause some symptoms of caffeine intoxication in small children
when they ingest a candy bar and a 12-ounce cola drink. Caffeine can act as
a positive reinforce, particularly at low doses. Doses of 100mg induced a mild
euphoria in humans and repeated substance-seeking behavior effects in
other animals. Caffeine doses of 300 mg however do not act as positive
reinforces and can produce increased anxiety and mild dysphoria. Studies in
animals and humans have reported that caffeine can be discriminated from a
placebo in blind experimental conditions. Both animal and human studies
have shown that physical tolerance to some effects of caffeine does develop
and that withdrawal symptoms do occur

Caffeine Intoxication
- The annual incidence of caffeine intoxication is an estimated
10%, although some clinicians and investigators suspect that
the actual incidence is much higher. The common symptoms
associated with caffeine intoxication include anxiety,
psychomotor agitation, restless, irritability and
psychophysiological complaints, such as muscle twitching,
flushed face, nausea, diuresis, and gastrointestinal distress,
excessive perspiration, tingling in the fingers and toes and
insomnia. The consumption of more than 1g of caffeine can
produce rambling speech, confused thinking cardiac
arrhythmias, inexhaustibleness, mark agitation, tinnitus and



III.
mild visual hallucinations. Consumption of more than 10g of
caffeine can cause generalized tonic-clonic seizures,
respiratory failure and death.
Caffeine withdrawal
- Prolonged daily use of caffeine
- Abrupt cessation of caffeine use, or reduction in the amount
of caffeine used closely followed by headache and one of
the following:
 Marked fatigue or drowsiness
 Marked anxiety or depression
 Nausea and vomiting
- Can cause clinically significant distress or impairment in
social, occupational or other important areas of functioning.
- The symptoms are not due to the direct physiology effects of
a general medical condition and are not better accounted for
by another mental disorder.
Caffeine-Induced Anxiety Disorder
- Patients with the disorder may be perceived as wired, overly
talkative and irritable. They may complain of not sleeping
well of having energy to burn. Although caffeine induces and
exacerbates panic attacks in people with a panic d/o a
causative association between caffeine and a panic d/o has
not yet been demonstrate.
Caffeine-Induced Sleep Disorder
- Caffeine is associated with a delay in falling asleep, an
inability to remain asleep, and early morning awakening.
Etiology
After exposure to caffeine, continued caffeine consumption can be influenced
by several factors, such as pharmacological effects of caffeine, caffeine's
reinforcing effects, genetic predisposition to use caffeine and personal
attributes of the consumer.
IV.
Pathophysiology
Caffeine is a xanthine derivative. It acts by pharmacologically stimulating the
CNS, heart, voluntary muscles, and gastric acid secretion, and it induces
diuresis. Caffeine is rapidly absorbed. Peak plasma levels are achieved in
about 1 hour. Caffeine saturates all body tissues and fluids, including breast
milk. The half-life of caffeine is 4-6 hours.
The amount of caffeine in coffee and tea varies based on brewing times and
methods. General guidelines for beverage caffeine content include the
following:





Brewed coffee (8 oz) - 120 mg
Instant coffee (8 oz) - 70 mg
Iced tea (8 oz) - 60 mg
Hot tea (8 oz) - 60 mg
Caffeinated soft drink (12 oz) - 50 mg
The average daily consumption of caffeine among Americans is 219 mg.
Adults receive nearly three quarters of their daily caffeine from coffee.
Children receive one half of their caffeine from soft drinks. Energy drinks
represent a fast-growing beverage market. A combination of caffeine and
herbal ingredients are touted as providing an energy boost. Energy drinks
vary in the amount of caffeine included in their formulations and can range
from around 50-300 mg. Although it sounds more exotic in some drinks,
guaranine is caffeine. Consumers seeking the activating qualities of caffeine
in pill form can find many preparations, the more well known having 200 mg.
Individuals worldwide consume about 76 mg of caffeine per day.
Caffeine symptoms appear to be dose-related. Most people experience no
behavioral effects with less than 300 mg caffeine. Sleep is more sensitive and
can be disrupted by 200 mg caffeine. At doses exceeding 1 g per day,
susceptible individuals experience toxic effects.
V.
Signs and Symptoms
Include increased alertness, a mild sense of well-being and a sense of
improved verbal and motor performance. Caffeine ingestion is also
associated with diuresis, cardiac muscle stimulation, increased intestinal
peristalsis, increased gastric acid secretion, and usually mild increased in
blood pressure and at risk of cardiovascular disease.
Has mild association between higher daily caffeine uses in women and
delayed and slightly lower birth weight.
-
VI.
restlessness
nervousness
excitement
insomnia
flushed face
gastrointestinal disturbance
muscle twitching
talking or thinking in a rambling manner
tachycardia (speeded-up heartbeat) or disturbances of heart rhythm
periods of inexhaustibility
psychomotor agitation
Course and Prognosis
With the exception of acute episodes of caffeinism, people recover from
caffeine intoxication without great difficulty.
VII.
Medical Management
Is either eliminating or severely reducing the use of caffeine-containing
products.Clinicians advise patient to substitute other beverages such as
water, decaffeinated soft drinks and decaffeinated coffee. Analgesics such as
aspirin are most always sufficient to control the headaches that accompany
caffeine withdrawal, Benzodiazepines to relieve withdrawal symptoms in 4-7
days.
Cannabis-Related Disorders
I.
Definition
Is probably the world’s most common illicit substance. Cannabis, more
commonly called marijuana, refers to the several varieties of Cannabis sativa,
or Indian hemp plant.
II.
Epidemiology
In 1995, an estimated 9.8 million people in the United States were current
(past month) marijuana or hashish users. This figure represents 4.7 percent
of the population age 12 years and older. Marijuana is by far the most
common drug used by illicit drug users; approximately three quarters (77
percent) of the current illicit drug users were marijuana or hashish user in
1995. Trends and demographic differences are generally similar for any illicit
drug use and marijuana hashish user.
Between 1994 and 1995, the rate of marijuana use among adolescents ages
12 to 17 increased from 6.0 to 8.2 percent and continued to a trend that
began during 1992 – 1993. Since 1992, the rate of use among adolescents
has more than doubled. Similar trends are evident among both boys and
girls; among whites, blacks, and Hispanics; in all four geographic regions;
and in metropolitan and nonmetropolitan areas.
Frequent use of marijuana, defined as use on at least 51 days during the post
year, remained unchanged from 1994 to 1995 at just over 5 million users (5.3
million, 2.5 percent of the population in 1995), but frequency of use was
significantly lower than 1985, when there were an estimated 8.4 million
frequent users (4.4 percent of the population).


Cannabis Intoxication
- Commonly heightens users’ sensitivities to external stimuli,
reveals new details, makes colors seem brighter and richer
than in the past, and subjectively slows the appreciation
time. In high doses, users may experience depersonalization
and derealization. Motor skills are impaired by cannabis use,
and the impairment in the motor skills remains after the
subjective, euphoriant effects have resolved. For 8 to 12
hours after using cannabis, users’ impaired motor skills
interfere with the operation of motor vehicles and other
heavy machinery.
 Recent use of cannabis
 Clinically significant maladaptive behavioral or
psychological changes (eg, impaired motor
coordination, euphoria, anxiety, sensation of
slowed time, impaired judgement, social
withdrawal) that develop during, or shortly
after, cannabis use.
 Two (or more) of the following signs,
developing within 2 hours of cannabis use.
- Conjunctival injection
- Increased appetite
- Dry mouth
- Tachycardia
 The symptoms are not due to a general
medical condition and are not better accounted
for by another mental disorder.
Cannabis Intoxication Delirium
-


III.
The delirium associated with cannabis intoxication is
characterized by marked impairment on cognition and
performance tasks. Even modest doses of cannabis result in
impairment in memory, reaction time, perception, motor
coordination, and attention. High doses that also impair
users’ levels of consciousness have marked effects on
cognitive measures
Cannabis – Induced Psychotic Disorder
- Is rare; transient paranoid ideation is more common. Florid
psychosis is somewhat common in countries in which some
people have long-term access to cannabis particularly high
potency. The psychotic episodes are sometimes referred as
to hemp insanity. Cannabis use rarely causes a bad-trip
experience, which is often associated with hallucinogen
intoxication. When cannabis-induced psychotic disorder
does occur, it may be correlated with a pre-existing
personality disorder in the affected person.
Cannabis – Induced Anxiety Disorder
- Is a common diagnosis for acute cannabis intoxication,
which in many people induces short-lived anxiety states
often provoked by paranoid thoughts. In such circumstances,
panics attacks may be induced, based on ill-defined and
disorganized fears. The appearance of anxiety symptoms is
correlated with the dose and the most frequent adverse
reaction to the moderate use of smoked cannabis.
Inexperienced users are much more likely to experience
anxiety symptoms than the experienced user.
Etiology
Intoxication is easiest to diagnose because of clinically observable signs,
including reddened eye membranes, increased appetite, dry mouth, and
increased heart rate. It is also diagnosed by the presence of problematic
behavioral or psychological changes such as impaired motor coordination,
judgment, anxiety, euphoria, and social withdrawal. Occasionally, panic
attacks may occur, and there may be impairment of short-term memory.
Lowered immune system resistance, lowered testosterone levels in males,
and chromosomal damage may also occur. Psychologically, chronic use of
marijuana has been associated with a loss of ambition known as the
"amotivational syndrome."
Cannabis use is often paired with the use of other addictive substances,
especially nicotine, alcohol, and cocaine. Marijuana may be mixed and
smoked with opiates, phencyclidine ("PCP" or "angel dust"), or hallucinogenic
drugs. Individuals who regularly use cannabis often report physical and
mental lethargy and an inability to experience pleasure when not intoxicated
(known as "anhedonia"). If taken in sufficiently high dosages, cannabinoids
have psychoactive effects similar to hallucinogens such as lysergic acid
diethylamide (LSD), and individuals using high doses may experience
adverse effects that resemble hallucinogen-induced "bad trips." Paranoid
ideation is another possible effect of heavy use, and, occasionally,
hallucinations and delusions occur. Highly intoxicated individuals may feel as
if they are out-side their body ("depersonalization") or as if what they are
experiencing isn't real ("derealization"). Fatal traffic accidents are more
common among individuals testing positive for cannabis use.
IV.
Pathophysiology
Any drug that causes euphoria and diminishes anxiety can cause
dependence, and marijuana is no exception. However, heavy use and reports
of inability to stop are unusual. Critics of marijuana cite much scientific data
regarding adverse effects, but most claims of significant biologic effect are
unsubstantiated. Findings are sparse even among relatively heavy users and
in areas intensively investigated (eg, immunologic and reproductive function).
However, high-dose smokers develop pulmonary symptoms (episodes of
acute bronchitis, wheezing, coughing, and increased phlegm), and pulmonary
function may be altered, manifested as large airway changes of unknown
significance. Even daily smokers do not develop obstructive airway disease.
There is no evidence of increased risk of head and neck or airway cancers,
as there is with tobacco. In a few case-control studies, diminished cognitive
function was identified in small samples of long-term high-dose users; this
finding needs to be confirmed. A sense of diminished ambition and energy is
often described.
The effect of prenatal marijuana use on neonates is not clear. Decreased
fetal weight has been reported, but when all factors (eg, maternal alcohol and
tobacco use) are accounted for, the effect on fetal weight appears less. THC
is secreted in breast milk. Although harm to breastfed infants has not been
shown, breastfeeding mothers, like pregnant women, should avoid using
marijuana.
V.
Signs and symptoms
This manual states that the central features of cannabis dependence are
compulsive use, tolerance of its effects, and withdrawal symptoms. Use may
interfere with family, school, and work, and may cause legal problems.
Regular cannabis smokers may show many of the same respiratory
symptoms as tobacco smokers. These include daily cough and phlegm,
chronic bronchitis, and more frequent chest colds. Continued use can lead to
abnormal functioning of the lung tissue, which may be injured or destroyed by
the cannabis smoke.
Recent research indicates that smoking marijuana has the potential to cause
severe increases in heart rate and blood pressure, particularly if combined
with cocaine use. Even with marijuana use alone, however, the heart rate of
subjects increased an average of 29 beats per minute when smoking
marijuana.
A study of heavy marijuana users has shown that critical skills related to
attention, memory, and learning can be impaired, even after use is
discontinued for at least 24 hours. Heavy users, compared to light users,
made more errors on tasks and had more difficulty sustaining attention and
shifting attention when required. They also had more difficulty in registering,
processing, and using information. These findings suggest that the greater
impairment in mental functioning among heavy users is most likely due to an
alteration of brain activity directly produced by the marijuana use.
VI.
Course and prognosis
It may, however, develop more rapidly among young people with other
emotional problems. Most people who become dependent begin using
regularly. Gradually, over time, both frequency and amount increase. With
chronic use, there can sometimes be a decrease in or loss of the pleasurable
effects of the substance, along with increased feelings of anxiety and/or
depression. As with alcohol and nicotine, cannabis use tends to begin early in
the course of substance abuse and many people later go on to develop
dependence on other illicit substances. Because of this, cannabis has been
referred to as a "gateway" drug, although this view remains highly
controversial. There is much that remains unknown about the social,
psychological, and neurochemical basis of drug use progression, and it is
unclear whether marijuana use actually causes individuals to go on to use
other illicit substances.
VII.
Medical management
Treatment is usually unnecessary; for patients experiencing significant
discomfort, treatment is supportive. Management of abuse typically consists
of behavioral therapy in an outpatient drug treatment program.
COCCAINE-RELATED DISORDER
I.
Definition
Cocaine may be abused through a number of different routes. The most
widespread routes of administration include inhaling (snorting), subcutaneous
injection (skin popping), intravenous injection (shooting-up), and smoking
(freebasing or smoking crack).
II.
Epidemiology
Approximately 33.7 million Americans have tried cocaine at least once in their
lifetimes, representing 13.8% of the 12 years and older population.
Approximately 5.5 million (2.3%) used cocaine in the past year and 2.4 million
(1%) used cocaine in the past month.
The incidence of cocaine use generally rose throughout the 1970s to a peak
in 1980 (1.7 million new users) and subsequently declined until 1991 (0.7
million new users). Cocaine initiation steadily increased during the 1990s,
reaching 1.2 million in 2001.
Within the past 12 months of the time the survey was taken, 872,000 persons
used cocaine for the first time. That is a statistically significant reduction from
2002 when there were more than 1 million past-year cocaine initiates.
The National Epidemiologic Survey on Alcohol and Related Conditions
(NESARC) study suggests the transition from use to dependence was highest
for nicotine users, followed by cocaine, alcohol, and cannabis users. [3] An
increased risk of transition to dependence among minorities and those with
psychiatric or dependence comorbidity highlights the importance of promoting
outreach and treatment of these populations.




Mortality/morbidity
- In drug misuse deaths, cocaine was among the top 5
drugs in 28 of the 32 metropolitan areas and in all of the
6 states.
- On average, cocaine alone or in combination with other
drugs was reported in 39% of drug misuse deaths.
- The etiologies of some of the deaths associated with
cocaine abuse include cardiac dysrhythmias, myocardial
infarctions, intractable seizures, strokes, and aortic
dissection.
Race
- In the 2005 Youth Risk Behavior Survey, Hispanic and
white students were significantly more likely than African
American students to report lifetime cocaine use (12.2%
and 7.7%, respectively, vs 2.3%).
- The 1999 Drug Abuse Warning Network data reported
cocaine as an agent in 59%, 36%, and 35% of drugrelated emergency department visits among African
Americans, Hispanics, and whites, respectively.
Sex
- In the 2005 National Youth Risk Behavior Survey, 8.4%
of males and 6.8% of females had used cocaine at least
once in 2005. According to DAWN, males are
disproportionately represented among deaths related to
drug misuse or abuse. After adjusting for population size,
the rate of drug misuse deaths per 1,000,000 population
for males was 2.4 that for females.
Age
- Among students surveyed as part of the 2006 Monitoring
the Future study, 3.4% of eighth graders, 4.8% of tenth
graders, and 8.5% of twelfth graders reported lifetime use
of cocaine. Approximately 8.8% of college students and
14.3% of young adults (aged 19-28) surveyed in 2005
reported lifetime use of cocaine.
 Cocaine Intoxication
o Cocaine intoxication occurs after recent
cocaine use. The person experiences a feeling
of intense happiness, hypervigilance,
increased sensitivity, irritability or anger, with
impaired judgment, and anxiety. The
intoxication impairs the person's ability to
function at work, school, or in social situations.
Two or more of the following symptoms are
present immediately after the use of the
cocaine:







enlarged pupils
elevated heart rate
elevated or lowered blood pressure
chills and increased sweating
nausea or vomiting
weight loss
agitation or slowed movements









weak muscles
chest pain
coma
confusion
irregular heartbeat
depressed respiration
seizures
odd postures
odd movements
 Cocaine Withdrawal
o As mentioned, withdrawal symptoms develop
within hours or days after cocaine use that has
been heavy and prolonged and then abruptly
stopped. The symptoms include irritable mood and
two or more of the following symptoms: fatigue,
nightmares, difficulty sleeping or too much sleep,
elevated appetite, agitation (restlessness), or
slowed physical movements.
 Cocaine-Induced Delirium
o Patients have a disturbance of their level of
consciousness or awareness, evidenced by
drowsiness or an inability to concentrate or pay
attention. Patients also experience a change in
their cognition (ability to think) evidenced by a
deficit in their language or their memory. For
example, these patients may forget where they
have placed an item, or their speech is confusing.
These symptoms have rapid onset within hours or
days of using cocaine and the symptoms fluctuate
throughout the course of the day. These findings
cannot be explained by dementia (state of
impaired thought processes and memory that can
be caused by various diseases and conditions)
and the doctor must not be able to recognize
some other physical reason that can account for
the symptoms other than cocaine intoxication.
 Cocaine-Induced Psychotic Disorder with Delusion
o The person suffering from this disorder has
experienced intoxication or withdrawal from
cocaine within a month from the time he or she
begins to experience delusions (beliefs that the
person continues to maintain, despite evidence to
the contrary). In order for this state to be
considered cocaine-induced psychotic disorder,
these symptoms cannot be due to another
condition or substance.
 Cocaine-Induced Psychotic Disorder with
hallucinations
o This condition is the same as cocaine-induced
psychotic disorder with delusions, except that this
affected individual experiences hallucinations
instead of delusions. Hallucinations can be
described as hearing and seeing things that are
not real.
 Cocaine-Induced Mood Disorder
o The person suffering from this disorder has
experienced intoxication or withdrawal from
cocaine within a month from the time he or she
begins to experience depressed, elevated, or
irritable mood with apathy (lack of empathy for
others, and lack of showing a broad range of
appropriate emotions).
 Cocaine-Induced Anxiety Disorder
o The person suffering from this disorder has
experienced intoxication or withdrawal from
cocaine within a month from the time he or she
begins to experience anxiety, panic attacks,
obsessions, or compulsions. Panic attacks are
discrete episodes of intense anxiety. Persons
affected with panic attacks may experience
accelerated heart rate, shaking or trembling,
sweating, shortness of breath, or fear of going
crazy or losing control, as well as other symptoms.
An obsession is an unwelcome, uncontrollable,
persistent idea, thought, image, or emotion that a
person cannot help thinking even though it creates
significant distress or anxiety. A compulsion is a
repetitive, excessive, meaningless activity or
mental exercise which a person performs in an
attempt to avoid distress or worry.
 Cocaine-Induced Sexual Dysfunction
o The person suffering from this disorder has
experienced intoxication or withdrawal from
cocaine within a month from the time he or she
begins to experience sexual difficulties, and these
difficulties are deemed by the clinician to be due
directly to the cocaine use. Substance-induced
sexual difficulties can range from impaired desire,
impaired arousal, impaired orgasm, or sexual pain.
 Cocaine-Induced Sleep Disorder
o This disorder is characterized by difficulty sleeping
during intoxication or increased sleep duration
when patients are in withdrawal.
III.
Etiology
Cocaine an alkaloid present in the leaves of the coca plant, enhances
norepinephrine, dopamine
and serotonin activity in the central and peripheral nervous systems.
Enhancement of dopamine activity is the likely cause of the drug's intended
effects and thus of the reinforcement that contributes to developing abuse
and dependence.
Norepinephrine activity accounts for the sympathomimetic effects:
tachycardia, hypertension, mydriasis, diaphoresis, and hyperthermia.
Cocaine also blocks Na channels, accounting for its action as a local
anesthetic. Cocaine causes vasoconstriction and thus can affect almost any
organ. MI, cerebral ischemia and hemorrhage, aortic dissection, intestinal
ischemia, and renal ischemia are possible sequelae.
Onset of cocaine's effects depends on mode of use:
 IV injection and smoking: Immediate onset, peak effect after
about 3 to 5 min, and duration of about 15 to 20 min
 Intranasal use: Onset after about 3 to 5 min, peak effect at 20 to
30 min, and duration of about 45 to 90 min
 Oral use: Onset after about 10 min, peak effect at about 60 min,
and duration of about 90 min
Because cocaine is such a short-acting drug, heavy users may inject it or
smoke it repeatedly every 10 to 15 min.
IV.
Pathophysiology
The time to peak effects of cocaine depends on the dose and route of
administration. When cocaine is injected intravenously or crack is smoked,
the onset of action is within seconds and peak effects occur within 5 minutes.
When snorted, the onset of action of cocaine is within the first 5 minutes and
its effects typically peak within 30 minutes. Cocaine can be absorbed across
any mucosal surface, including the respiratory, gastrointestinal, and
genitourinary tracts.
Two major routes account for cocaine's metabolism: (1) enzymatic
metabolism by both liver esterases and plasma cholinesterase to ecgonine
methyl ester and (2) nonenzymatic degradation to benzoylecgonine. The halflife of cocaine is 30-90 minutes. The metabolites ecgonine methyl ester and
benzoylecgonine are excreted in the urine. Drug screens detect the presence
of benzoylecgonine, which may be present in the urine for 2-3 days,
depending on the dose and chronicity of usage. Rare cases of
benzoylecgonine detection in the urine for 22 days following cocaine use
have been reported.
Cocaine has a number of pharmacologic effects on the human body.
Neuronal fast sodium channel blockade produces a local anesthetic effect
that continues to be used in medicine today. During myocardial fast sodium
channel blockade, cocaine blocks fast cardiac sodium channels, which results
in type I antidysrhythmic activity. This may lead to prolongation of the QRS
complex and contribute to the induction of the dysrhythmias associated with
cocaine use.
Blockade of catecholamine reuptake (ie, norepinephrine, dopamine, and
serotonin reuptake blockade) occurs in both the central and peripheral
nervous systems. Blockade of reuptake of norepinephrine leads to the
sympathomimetic syndrome associated with cocaine use. This syndrome
consists of tachycardia, hypertension, tachypnea, mydriasis, diaphoresis, and
agitation. Inhibition of dopamine reuptake in the CNS synapses, such as in
the nucleus accumbens, contributes to the euphoria associated with cocaine.
Norepinephrine release augments norepinephrine reuptake blockade effects.
V.
Signs and symptoms
The following list is a summary of the acute (short-term) physical and
psychological effects of cocaine on the body:












blood vessels constrict
elevated heart rate
elevated blood pressure
a feeling of intense happiness
elevated energy level
a state of increased alertness and sensory sensitivity
elevated anxiety
panic attacks
elevated self-esteem
diminished appetite
spontaneous ejaculation and heightened sexual arousal
psychosis (loss of contact with reality)
The following list is a summary of the chronic (long-term) physical and
psychological effects of cocaine on the body:










VI.
depressed mood
irritability
physical agitation
decreased motivation
difficulty sleeping
hypervigilance
elevated anxiety
panic attacks
hallucinations
psychosis
Course and prognosis
Not all cocaine abusers become dependent on the drug. However, even
someone who only uses occasionally can experience the harmful effects
(interpersonal relationship conflicts, work or school difficulties, etc.) of using
cocaine, and even occasional use is enough to addict. In the course of a
person's battle with cocaine abuse, he or she may vary the forms of the drug
that he or she uses. A person may use the inhaled form at one time and the
injected form at another, for example.
Many studies of short-term outpatient treatment over a six-month to two-year
period indicate that people addicted to cocaine have a better chance of
recovering than people who are addicted to heroin. A study of veterans who
participated in an inpatient or day hospital treatment program that lasted 28
days, revealed that about 60% of people who were abstinent at four months
were able to maintain their abstinence at seven months.
VII.
Medical management
Benzodiazepines are the drugs of choice for acute cocaine intoxication with
extreme agitation.
Dopamine agonists like amantadine and bromocriptine and tricyclic
antidepressants such as desipramine have failed in studies to help treat
symptoms of cocaine withdrawal or intoxication.
Hallucinogen- Related Disorders
I.
Definition
Hallucinogens are natural and synthetic substances that are variously called
psychedelics or psychotomimetics. They induce hallucinations, produce a loss of
contact with reality and an experience of heightened consciousness. They have no
medical use and a high abuse potential.
Naturally-occuring hallucinogens include psilocybin from some mushrooms and
mescaline from peyote cactus. Synthetic hallucinogens are lysergic acid
diethylamide(LSD) and 3,4-methylenedioxyamphetamine(MDMA).
II.
Epidemiology
Hallucinogen use is most common among young (15-35 years old) white men. There
is 2:1 ratio of whites to blacks and 1.5:1 of whites to Hispanics who have used
hallucinogens at least once. 15.5% of persons 26-34 years old have used a
hallucinogen at least once, showing highest use of hallucinogens. Persons 18-25
years old have highest recent use of hallucinogen. Hallucinogen use is associated
with less morbidity and less mortality than that of other substance in which only 1%
of substance-related emergency room visits were related to hallucinogens, more
than 50% were younger than 20 years of age. The lifetime rate of hallucinogen use is
0.6%.
III.
Etiology
Reasons why people take hallucinogens are that they are minimally addictive and
cause no withdrawal symptoms and produce few serious physical side effects.
Deaths from hallucinogen overdoses are rare. They do not usually produce a
delusional state, excessive stupor or excessive stimulation but produce a high that
gives illusion of increased creativity, empathy or self-awareness. Hallucinogens do
not cause memory loss with occasional use. But most of all, they are cheap and
easily available.
IV.
Pathophysiology



V.
LSD, psilocybin, and many designer hallucinogens are serotonin receptor
agonists. For mescaline, a phenylethylamine similar to amphetamines, the exact
mechanism has not been determined.
Most hallucinogens are well absorbed after oral ingestion, although some are
ingested by inhalation, smoking or intravenous injection.
LSD is taken orally from drug-impregnated blotter paper or as tablets. Onset of
action is usually 30 to 60 min after ingestion; duration of effects can be 12 to 24
hours.

Psilocybin is taken orally; effects usually last about 4 to 6 hours.

Mescaline is taken orally as peyote buttons. Onset of effects is usually 30 to 90
min after ingestion; duration of effects is about 12 hours.

DMT, when smoked, has onset in 2 to 5 minutes; duration of effects is 20 to 60
min (accounting for its street name, “businessman's lunch”).
Signs and Symptoms

DSM-IV-TR Diagnostic Criteria for Hallucinogen Dependence
o 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.
DSM-IV-TR Criteria for Hallucinogen Abuse
o A. A maladaptive pattern of substance use leading to clinically significant
impairment or distress, as manifested by one (or more) of the following,
occurring within a 12-month period:
 (1) recurrent substance use resulting in a failure to fulfill major role
obligations at work, school, or home
 (2) recurrent substance use in situations in which it is physically
hazardous.
 (3) recurrent substance-related legal problems (e.g.,arrests for
substance-related disorderly conduct)
 (4) continued substance use despite having persistent or recurrent
social or interpersonal problems caused or exacerbated by the
effects of the substance (e.g., arguments with spouse about
consequences of intoxication, physical fights)
o B. The symptoms have never met the criteria for Substance Dependence
for this hallucinogen.
DSM-IV-TR Diagnostic Criteria for Hallucinogen Intoxication
o A. Recent use of a hallucinogen.
o B. Clinically significant maladaptive behavioral or psychological changes
(e.g., marked anxiety or depression, ideas of reference, fear of losing
one’s mind, paranoid ideation, impaired judgment, or impaired social or
occupational functioning) that developed during, or shortly after,
hallucinogen use.
o C. Perceptual changes occurring in a state of full wakefulness and
alertness
(e.g.,
subjective
intensification
of
perceptions,
depersonalization, derealization, illusions, hallucinations, synesthesias)
that developed during, or shortly after, hallucinogen use.
o D. Two (or more) of the following signs, developing during, or shortly
after, hallucinogen use:
 Pupillary dilation
 Tachycardia
 Sweating
 Palpitations
 Blurring of vision
 Tremors
 Incoordination
o E. The symptoms are not due to a general medical condition and are not
better accounted for by another mental disorder







DSM-IV-TR Diagnostic Criteria for Hallucinogen Persisting Perception Disorder
(Flashbacks)
o A. The re-experiencing, following cessation of use of a hallucinogen, of
one or more of the perceptual symptoms that were experienced while
intoxicated with the hallucinogen (e.g., geometric hallucinations, false
perceptions of movement in the peripheral visual fields, flashes of color,
intensified colors, trails of images of moving objects, positive afterimages,
halos around objects, macropsia, and micropsia).
o B. The symptoms in Criterion A cause clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
o C. The symptoms are not due to a general medical condition (e.g.,
anatomical lesions and infections of the brain, visual epilepsies) and are
not better accounted for by another mental disorder (e.g.,delirium,
dementia, schizophrenia) or hypnopompic hallucinations.
DSM-IV-TR Diagnostic Criteria for Hallucinogen Intoxication Delirium
o A. Disturbance of consciousness (i.e., reduced clarity of awareness of the
environment) with reduced ability to focus, sustain, or shift attention.
o 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 preexisting, established, or evolving
dementia.
o C. The disturbance develops over a short period of time (usually hours to
days) and tends to fluctuate during the course of the day.
o D. 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 ∗Note:
This diagnosis should be made instead of a diagnosis of
substance intoxication only when the cognitive symptoms are in
excess of those usually associated with the intoxication syndrome
and when the symptoms are sufficiently severe to warrant
independent clinical attention. ∗Note: The diagnosis should be
recorded as substance-induced delirium if related to medication
use.
DSM-IV-TR Diagnostic Criteria for Hallucinogen-Induced Psychotic Disorder
o A. Prominent hallucinations or delusions. Note: Do not include
hallucinations if the person has insight that they are substance induced.
o B. There is evidence from the history, physical examination, or laboratory
findings ofeither (1) or (2):
 (1) the symptoms in Criterion A developed during, or within a
month of, substance intoxication or withdrawal
 (2) medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a psychotic disorder
that is not substance induced. Evidence that the symptoms are better
accounted for by a psychotic disorder that is not substance induced might
include the following: the symptoms precede the onset of the substance
use (or medication use); the symptoms persist for a substantial period of
time (e.g., about a month) after the cessation of acute withdrawal or
severe intoxication, or are substantially in excess of what would be
expected given the type or amount of the substance used or the duration
of use; or there is other evidence that suggests the existence of an
independent non–substance-induced psychotic disorder (e.g., a history of
recurrent non–substance-related episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium. Note: This diagnosis should be made instead of a diagnosis of
substance intoxication or substance withdrawal only when the symptoms
are in excess of those usually associated with the intoxication or
withdrawal syndrome and when the symptoms are sufficiently severe to
warrant independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Hallucinogen-Induced Mood Disorder
o


A. A prominent and persistent disturbance in mood predominates in the
clinical picture and is characterized by either (or both) of the following:
(1)depressed mood or markedly diminished interest or pleasure in all, or
almost all, activities (2)elevated, expansive, or irritable mood.
o B. There is evidence from the history, physical examination, or laboratory
findings of either (1) or (2): (1)the symptoms in Criterion A developed
during, or within a month of, substance intoxication or withdrawal
(2)medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a mood disorder that is
not substance induced. Evidence that the symptoms are better accounted
for by a mood disorder that is not substance-induced might include the
following: the symptoms precede the onset of the substance use (or
medication use); the symptoms persist for a substantial period of time
(e.g., about a month) after the cessation of acute withdrawal or severe
intoxication or are substantially in excess of what would be expected
given the type or amount of the substance used or the duration of use; or
there is other evidence that suggests the existence of an independent
non–substance-induced mood disorder (e.g., a history of recurrent major
depressive episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium.
o E. The symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning. Note: This
diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the mood symptoms are
in excess of those usually associated with the intoxication or withdrawal
syndrome and when the symptoms are sufficiently severe to warrant
independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Hallucinogen-Induced Anxiety Disorder
o A. Prominent anxiety, panic attacks, or obsessions or compulsions
predominate in the clinical picture.
o B. There is evidence from the history, physical examination, or laboratory
findings of either (1) or (2): (1)the symptoms in Criterion A developed
during, or within 1 month of, substance intoxication or withdrawal
(2)medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by an anxiety disorder that
is not substance induced. Evidence that the symptoms are better
accounted for by an anxiety disorder that is not substance induced might
include the following: the symptoms precede the onset of the substance
use (or medication use); the symptoms persist for a substantial period of
time (e.g., about a month) after the cessation of acute withdrawal or
severe intoxication or are substantially in excess of what would be
expected given the type or amount of the substance used or the duration
of use; or there is other evidence suggesting the existence of an
independent non–substance-induced anxiety disorder (e.g., a history of
recurrent non–substance-related episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium.
o E. The disturbance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning. Note: This
diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the mood symptoms are
in excess of those usually associated with the intoxication or withdrawal
syndrome and when the symptoms are sufficiently severe to warrant
independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Hallucinogen-Related Disorder Not Otherwise
Specified
o The hallucinogen-related disorder not otherwise specified category is for
disorders associated with the use of hallucinogens that are not
classifiable as hallucinogen dependence, hallucinogen abuse,
hallucinogen intoxication, hallucinogen persisting perception disorder,
hallucinogen intoxication delirium, hallucinogen-induced psychotic
disorder, hallucinogen-induced mood disorder, or hallucinogen-induced
anxiety disorder.
VI.
Course and Prognosis
Because hallucinogens are not physically addictive, many people are able to stop
using these drugs successfully. However, users may be haunted by chronic
problems such as flashbacks or mood and anxiety disorders either brought about or
worsened by use of hallucinogens. It is difficult to predict who will have long-term
complications and who will not.
VII.
Medical Management


Hallucinogen Intoxication
Persons have historically been treated for hallucinogen intoxication by
psychological support for the remainder of the trip, so-called “talking down.”
This is a time-consuming and poten-tially hazardous undertaking, given the
lability of a patient with hallucinogen-related delusions. Accordingly,
treatment of hallucinogen intoxication is the oral administration of 20mg of
diazepam. This medication brings the LSD experience and any associated
panic to a halt within 20 minutes and should be considered superior to
“talking down” the patient over a period of hours or to administering
antipsychotic agents.
Hallucinogen Persisting Disorder
Treatment for hallucinogen persisting perception disorder is palliative. The
first step in the process is correct identification of the disorder.
Pharmacological approaches include long-lasting benzodiazepines, such as
clonazepam (Klonopin) and, to a lesser extent, anticonvulsants including
valproic acid (Depakene) and carbamazepine (Tegretol). But currently, no
drug is completely effective in ablating symptoms. Antipsychotic agents
should only be used in the treatment of hallucinogen-induced psychoses,
because they may have a paradoxical effect and exacerbate symptoms.
A second dimension of treatment is behavioral. The patient must be
instructed to avoid gratuitous stimulation in the form of over-the-counter
drugs, caffeine, and alcohol, and avoidable physical and emotional
stressors. Marijuana smoke is a particularly strong intensifier of the
disorder, even when passively inhaled.
Finally, three comorbid conditions are associated with hallucinogen
persisting perception disorder: panic disorder, major depression, and
alcohol dependence. All these conditions require primary prevention and
early intervention.
Inhalant- Related Disorders
I.
Definition
Inhalant drugs (also called inhalants or volatile substances) are volatile hydrocarbons
such as toluene, n-hexane, methylbutylketone, trichloroethylene, trichloroethane,
dichloromethane, gasoline, and butane. These chemicals are sold in four commercial
classes: (1) solvents for glues and adhesives; (2) propellants for aerosol paint
sprays, hairsprays, frying pan sprays, and shaving cream; (3) thinners; and (4) fuels.
At room temperature, these compounds volatilize to gaseous fumes that can be
inhaled through the nose or mouth, entering the bloodstream by the transpulmonary
route. They are easily available, legal and cheap.
II.
Epidemiology
Among young adults aged 18-25 years, 11% had used inhalants at least once, and
2% were current users. Among adolescents 12-17 years old, 7% had used inhalants
at least once, and 2% were current users. In a study conducted on high school
seniors, 18% reported having used inhalants at least once, and 2.7% reported
having used inhalants within the preceding month. White users are the most
common. Over 80% of inhalant users are male.
III.
Etiology
Peer pressure or social acceptance is one cause of inhalant addiction, especially for
teenagers. It is human nature for a person to feel the need to belong or be accepted.
Many teenagers may face more than peer pressure, as they may be bullied by social
groups. To avoid teasing and humiliation a teen may believe that drug use is the only
solution. Peer pressure occurs at all ages, and many adults find themselves making
decisions in order to be socially accepted.
Another cause of inhalant addiction is boredom. Children are often looking for
something to fill their free time. If children are not stimulated, they will soon begin
searching for something to catch their attention.
Inhalant abuse may develop from genetics or by family influence. Children are more
susceptible to drug abuse if they have witnessed it from a family member, caretaker
or loved one.
An addiction to inhalants may be the result of feelings such as depression, anxiety or
loneliness. Many people may find themselves struggling with these feelings and
getting a quick high can seem like the solution to the pain. Inhalant abuse can act as
an escape from reality for the user. This may numb the pain momentarily but in the
long run leaves the user feeling worse.
IV.
Pathophysiology





V.
Methods of inhalation include breathing the substance straight from the container
or surface (sniffing or snorting), from a soaked rag placed over the face (huffing),
or from a bag filled with the substance (bagging).
The mechanism of action is still unknown, but they are believed to act in the
central nervous system in a manner to volatile anesthetic agents.
Inhalation through the nose or mouth leads to transpulmonary absorption with
very rapid access to the brain.
Inhalants are highly lipid soluble. They easily cross both the alveolar membranes
and the blood-brain barrier. Onset of effect is seen in seconds.
With a few exceptions, elimination occurs primarily through the lungs, with many
inhaled compounds eliminated unchanged by exhalation. Some of the inhalants,
including alkyl nitrites, aromatics, and methylene chloride, undergo significant
hepatic metabolism that can produce damaging free nitrites and toxic carbon
monoxide as byproducts.
Signs and Symptoms

DSM-IV-TR Diagnostic Criteria for Inhalant Dependence
o 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.
DSM-IV-TR Criteria for Inhalant Abuse
o A. A maladaptive pattern of substance use leading to clinically significant
impairment or distress, as manifested by one (or more) of the following,
occurring within a 12-month period:
 (1) recurrent substance use resulting in a failure to fulfill major role
obligations at work, school, or home
 (2) recurrent substance use in situations in which it is physically
hazardous.
 (3) recurrent substance-related legal problems (e.g.,arrests for
substance-related disorderly conduct)
 (4) continued substance use despite having persistent or recurrent
social or interpersonal problems caused or exacerbated by the
effects of the substance (e.g., arguments with spouse about
consequences of intoxication, physical fights)
o B. The symptoms have never met the criteria for Substance Dependence
for inhalants.
DSM-IV-TR Diagnostic Criteria for Inhalant Intoxication
o A. Recent intentional use or short-term, high-dose exposure to volatile
inhalants (excluding anesthetic gases and short-acting vasodilators).
o B. Clinically significant maladaptive behavioral or psychological changes
(e.g., belligerence, assaultiveness, apathy, impaired judgment, impaired
social or occupational functioning) that developed during, or shortly after,
use of or exposure to volatile inhalants.
o C. Two (or more) of the following signs, developing during, or shortly
after, inhalant use or exposure:
 dizziness
 nystagmus
 incoordination
 slurred speech
 unsteady gait
 lethargy
 depressed reflexes
 psychomotor retardation
 tremor
 generalized muscle weakness
 blurred vision or diplopia
 stupor or coma
 euphoria
o D. The symptoms are not due to a general medical condition and are not
better accounted for by another mental disorder.
DSM-IV-TR Diagnostic Criteria for Inhalant Intoxication Delirium
o A. Disturbance of consciousness (i.e., reduced clarity of awareness of the
environment) with reduced ability to focus, sustain, or shift attention.
o 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 preexisting, established, or evolving
dementia.
o



C. The disturbance develops over a short period of time (usually hours to
days) and tends to fluctuate during the course of the day.
o D. 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 ∗Note:
This diagnosis should be made instead of a diagnosis of
substance intoxication only when the cognitive symptoms are in
excess of those usually associated with the intoxication syndrome
and when the symptoms are sufficiently severe to warrant
independent clinical attention. ∗Note: The diagnosis should be
recorded as substance-induced delirium if related to medication
use.
DSM-IV-TR Diagnostic Criteria for Inhalant-Induced Persisting Dementia
o A. The development of multiple cognitive deficits manifested by both
 (1) memory impairment (impaired ability to learn new information
or to recall previously learned information)
 (2)one (or more) of the following cognitive disturbances:
 (a) aphasia (language disturbance)
 (b) apraxia (impaired ability to carry out motor activities
despite intact motor function)
 (c) agnosia (failure to recognize or identify objects despite
intact sensory function)
 (d) disturbance in executive functioning (i.e., planning,
organizing, sequencing, abstracting)
o B. The cognitive deficits in Criteria A1 and A2 each cause significant
impairment in social or occupational functioning and represent a
significant decline from a previous level of functioning.
o C. The deficits do not occur exclusively during the course of a delirium
and persist beyond the usual duration of substance intoxication or
withdrawal.
o D. There is evidence from the history, physical examination, or laboratory
findings that the deficits are etiologically related to the persisting effects of
substance use (e.g., a drug of abuse, a medication).
DSM-IV-TR Diagnostic Criteria for Inhalant-Induced Psychotic Disorder
o A. Prominent hallucinations or delusions. Note: Do not include
hallucinations if the person has insight that they are substance induced.
o B. There is evidence from the history, physical examination, or laboratory
findings ofeither (1) or (2):
 (1) the symptoms in Criterion A developed during, or within a
month of, substance intoxication or withdrawal
 (2) medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a psychotic disorder
that is not substance induced. Evidence that the symptoms are better
accounted for by a psychotic disorder that is not substance induced might
include the following: the symptoms precede the onset of the substance
use (or medication use); the symptoms persist for a substantial period of
time (e.g., about a month) after the cessation of acute withdrawal or
severe intoxication, or are substantially in excess of what would be
expected given the type or amount of the substance used or the duration
of use; or there is other evidence that suggests the existence of an
independent non–substance-induced psychotic disorder (e.g., a history of
recurrent non–substance-related episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium. Note: This diagnosis should be made instead of a diagnosis of
substance intoxication or substance withdrawal only when the symptoms
are in excess of those usually associated with the intoxication or
withdrawal syndrome and when the symptoms are sufficiently severe to
warrant independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Inhalant-Induced Mood Disorder
o


A. A prominent and persistent disturbance in mood predominates in the
clinical picture and is characterized by either (or both) of the following:
(1)depressed mood or markedly diminished interest or pleasure in all, or
almost all, activities (2)elevated, expansive, or irritable mood.
o B. There is evidence from the history, physical examination, or laboratory
findings of either (1) or (2): (1)the symptoms in Criterion A developed
during, or within a month of, substance intoxication or withdrawal
(2)medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a mood disorder that is
not substance induced. Evidence that the symptoms are better accounted
for by a mood disorder that is not substance-induced might include the
following: the symptoms precede the onset of the substance use (or
medication use); the symptoms persist for a substantial period of time
(e.g., about a month) after the cessation of acute withdrawal or severe
intoxication or are substantially in excess of what would be expected
given the type or amount of the substance used or the duration of use; or
there is other evidence that suggests the existence of an independent
non–substance-induced mood disorder (e.g., a history of recurrent major
depressive episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium.
o E. The symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning. Note: This
diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the mood symptoms are
in excess of those usually associated with the intoxication or withdrawal
syndrome and when the symptoms are sufficiently severe to warrant
independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Inhalant-Induced Anxiety Disorder
o A. Prominent anxiety, panic attacks, or obsessions or compulsions
predominate in the clinical picture.
o B. There is evidence from the history, physical examination, or laboratory
findings of either (1) or (2): (1)the symptoms in Criterion A developed
during, or within 1 month of, substance intoxication or withdrawal
(2)medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by an anxiety disorder that
is not substance induced. Evidence that the symptoms are better
accounted for by an anxiety disorder that is not substance induced might
include the following: the symptoms precede the onset of the substance
use (or medication use); the symptoms persist for a substantial period of
time (e.g., about a month) after the cessation of acute withdrawal or
severe intoxication or are substantially in excess of what would be
expected given the type or amount of the substance used or the duration
of use; or there is other evidence suggesting the existence of an
independent non–substance-induced anxiety disorder (e.g., a history of
recurrent non–substance-related episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium.
o E. The disturbance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning. Note: This
diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the mood symptoms are
in excess of those usually associated with the intoxication or withdrawal
syndrome and when the symptoms are sufficiently severe to warrant
independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Inhalant-Related Disorder Not Otherwise
Specified
o The inhalant-related disorder not otherwise specified category is for
disorders associated with the use of inhalants that are not classifiable as
inhalant dependence, inhalant abuse, inhalant intoxication, inhalant
intoxication delirium, inhalant-induced persisting dementia, inhalant-
induced psychotic disorder, inhalant-induced mood disorder, or inhalantinduced anxiety disorder.
VI.
Course and Prognosis
The course of inhalant abuse and dependence differs somewhat depending on the
affected person's age. Younger children who are dependent on or abuse inhalants
use them regularly, especially on weekends and after school. As children get older,
they often stop using inhalants. They may stop substance use altogether or they may
move on to other substances. Adults who abuse or are dependent on inhalants may
use inhalants regularly for years. They may also frequently "binge" on inhalants (i.e.,
using them much more frequently for shorter periods of time). This pattern of use can
go on for years.
The use of inhalants and subsequent dependence on the substance occurs among
people who do not have access to other drugs or are otherwise isolated (such as
prison inmates). Also, as with other substance use disorders, people who have
greater access to inhalants are more likely to develop dependence on them. This
group of people may include workers in industrial settings with ready access to
inhalants.
VII.
Medical Management
Emergency department care begins by protecting the patient's airway as dictated by
level of consciousness and the ability of the patient to control their airway. Intubation
may be required, so have appropriate equipment and personnel available. Place the
patient on supplemental oxygen.
Care primarily involves reassurance, quiet support, and attention to vital signs and
level of consciousness. Sedative drugs, including benzodiazepines, are
contraindicated because they worsen inhalant intoxication. Confusion, panic, and
psychosis mandate special attention to patient safety. Severe agitation may require
cautious control with haloperidol (5mg intramuscularly per 70kg body weight).
Antianxiety medications and antidepressants are not useful in the acute phase of the
disorder; they may be of use in cases of a coexisting anxiety or depressive illness.
Treatment usually takes a long time and involves enlisting the support of the
person's family; changing the friendship network if the individual uses with others;
teaching coping skills; and increasing self-esteem.
Nicotine- Related Disorders
I.
Definition
Nicotine is an alkaloid found in the nightshade family of plants
(Solanaceae); biosynthesis takes place in the roots and accumulation occurs in the
leaves. It constitutes approximately 0.6–3.0% of the dry weight of tobacco. Through
the use of tobacco, nicotine is one of the most heavily used addictive drugs and the
leading preventable cause of disease, disability, and deaths throughout the world.
II.
Epidemiology
The World Health Organization estimates there are 1 billion smokers worldwide, and
they smoke 6 trillion cigarettes a year. WHO also estimates that tobacco kills more
than 3 million persons each year. The mean age of onset is 16 years, and few
persons start smoking after 20.About 20% of population develops nicotine
dependence.
According to the DSM-IV-TR, approximately 85% of current daily smokers are
nicotine dependent. Also, nicotine withdrawal occurs in about 50% of smokers who
try to quit.
Of adults who had not completed high school, 37% smoked cigarettes, whereas only
17% of college graduates smoked.
Approximately 50% of all psychiatric outpatients, 70% of outpatients with bipolar I
disorder, almost 90% of outpatients with schizophrenia, and 70% of substance use
disorder patients smoke.
III.
Etiology
Most people start smoking due to peer pressure and family influence. Sometimes,
because of curiosity. Nicotine is an addictive drug. This means that the use of
nicotine causes changes in the brain that make people want to use more and more
of the drug. In addition, addictive drugs cause unpleasant withdrawal symptoms. The
combination of good feelings caused by the presence of an addictive drug and the
bad feelings when the drug is not present make breaking any addiction very difficult.
The addiction to nicotine has historically been one of the most difficult to break.
IV.
Pathophysiology
When a person inhales smoke from a cigarette, nicotine is distilled from the tobacco
and is carried in smoke particles into the lungs, where it is absorbed rapidly into the
pulmonary venous circulation. It then enters the arterial circulation and moves quickly
to the brain. Nicotine diffuses readily into brain tissue, where it binds to nicotinic
cholinergic receptors (nAChRs), which are ligand-gated ion channels.
Nicotine exerts its neurophysiologic action principally through the brain’s reward
center. This neuroanatomic complex, otherwise known as the mesolimbic dopamine
system, stretches from the ventral tegmental area to the basal forebrain. The nucleus
accumbens, a dopamine-rich area, is an intersection where all addictive behaviors
meet. The release of dopamine at this site promotes pleasure and reinforces the
associated behaviors, such as the use of alcohol and drugs, to replicate the positive
experience.
Other factors may also promote nicotine dependence, such as nicotine’s reduction in
the monoamine oxidase inhibitor enzyme. This enzyme is involved in the metabolism
of catecholamines, including dopamine. The net effect would be a lingering presence
of the stimulating dopamine at the nucleus accumbens.
Nicotine alters the bioavailability of dopamine and serotonin and causes a sharp
increase in heart rate and blood pressure. It acts on brain reward mechanisms, both
indirectly (through endogenous opioid activity) and directly (through dopamine
pathways).
V.
Signs and Symptoms

DSM-IV-TR Diagnostic Criteria for Nicotine Dependence
o 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.



VI.
(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.
DSM-IV-TR Diagnostic Criteria for Nicotine Withdrawal
o A. Daily use of nicotine for at least several weeks.
o 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
o C. The symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
o D. The symptoms are not due to a general medical condition and are not
better accounted for by another mental disorder.
DSM-IV-TR Diagnostic Criteria for Nicotine- Related Disorder Not Otherwise
Specified
o The nicotine- related disorder not otherwise specified category is for
disorders associated with the use of nicotine that are not classifiable as
nicotine dependence or nicotine withdrawal.
Course and Prognosis
Those who are motivated and make persistent efforts to quit using nicotine have a
good chance of success. Once abstinent, the risk for heart disease and cancers
declines with time and may even return to normal. More advanced pulmonary
problems such as chronic bronchitis and emphysema can be slowed down or
arrested, and early damage may be reversible. More than 90% of people who
attempt to quit do so cold turkey; for those seeking treatment to help quit, there is a
20% cessation rate after 1 year.
VII.
Medical Management
Two types of pharmacologic therapy are available as part of a smoking cessation
program nicotine and antidepressants. The goals of pharmacotherapy are to induce
smoking cessation, reduce morbidity, and prevent complications.
The gains in understanding the neuropathology of nicotine addiction have already
opened new frontiers, including effective nicotine replacement therapy (NRT) and
oral therapy.
A critical component of treatment is educating patients about the benefits of smoking
cessation and the cessation process. Provide a description of the expected
withdrawal syndrome. Continue with a discussion of the possible cessation methods,
which include counseling, NRT, antidepressant medications, behavioral training,
group therapy, hypnosis, and quitting “cold turkey.” Successful cessation is
confirmed by measuring cotinine or carbon monoxide levels.
NRT works by making it easier to abstain from tobacco by partially replacing the
nicotine previously obtained from tobacco. There are at least 3 mechanisms by
which NRT could be effective, as follows:
1. Reducing general withdrawal symptoms, thus allowing people to learn to get
by without cigarettes
2. Reducing the reinforcing effects of tobacco-delivered nicotine
3. Exerting some psychological effects on mood and attention states
Nicotine replacement medications should not be viewed as standalone medications
that make people stop smoking; reassurance and guidance from health professionals
are still critical for helping patients achieve and sustain abstinence. There are 6 types
of nicotine replacement products currently on the market, as follows:
1. Transdermal nicotine patch
2. Nicotine nasal spray
3. Nicotine gum
4. Nicotine lozenge
5. Sublingual nicotine tablet
6. Nicotine inhaler
Non-nicotine therapy may help smokers who object philosophically to the notion of
replacement therapy and smokers who fail replacement therapy. Bupropion (Zyban)
is an antidepressant medication that has both dopaminergic and adrenergic actions.
Clonidine (Catapres) decreases sympathetic activity from the locus ceruleus and,
thus, is thought to abate withdrawal symptoms. Whether given as a patch or orally,
0.2 to 0.4mg a day of clonidine appears to double quit rates; however, thescientific
database for the efficacy of clonidine is neither as extensive nor as reliable as that
for nicotine replacement; also, clonidine can cause drowsiness and hypotension.
Some patients benefit from benzodiazepine therapy (10 to 30mg per day) for the first
2 to 3 weeks of abstinence.
Opioid- Related Disorders
I.
Definition
Opioids are among the world's oldest known drugs; the use of the opium poppy for
its therapeutic benefits predates recorded history. Opioid refers to natural and
synthetic narcotics that have the same effects as opiates despite the fact that it is not
obtained from opium. The terms opioid, opiates and narcotics are customarily used
interchangeably. Opioids are among the world's oldest known drugs; the use of
the opium poppy for its therapeutic benefits predates recorded history.
The analgesic (painkiller) effects of opioids are due to decreased perception of pain,
decreased reaction to pain as well as increased pain tolerance.
II.
Epidemiology
Opioid abuse and dependence is a growing public health concern. Approximately 0.4
% of the world's population abuse at least one form of opioid, while 12 million people
abuse heroin globally per year.
An area of concern in the past few years has been a significant increase in the nonmedical use of prescription opioids. In the US, 4.8% of people 12 years of age or
older consumed a prescription pain reliever for non-medical reasons during the years
2002 to 2005. In both 2006 and 2007, an estimated 5.2 million people aged 12 or
older actively used prescription pain relievers for non-medical reasons. In Europe,
about 1.5 million people abused opioids in 2007, with heroin being the primary drug
abused. Strikingly, these data suggest that drug dealers are a relatively small source
of illicitly used prescription opioids. Diversion through family and friends is now the
greatest source of illicit opioids, and the majority of these opioids are obtained from 1
physician, not from "doctor shopping."
III.
Etiology
There are no clear-cut causes of drug use other than the initial choice to use the
drug. This decision to use may be highly influenced by peer group. Typically, the age
of first use of heroin is about 16 years old, but this age has been dropping in recent
years.
Certain social and behavioral characteristics, however, are more commonly seen
among individuals who become dependent on opioids than those who do not. For
instance, many heroin users come from families in which one or more family
members use alcohol or drugs excessively or have mental disorders (such as
antisocial personality disorder). Often heroin users have had health problems early in
life, behavioral problems beginning in childhood, low self-confidence, and antiauthoritarian views.
Among opioid-dependent adolescents, a "heroin behavior syndrome" has sometimes
been described. This syndrome consists of depression (often with anxiety
symptoms), impulsiveness, fear of failure, low self-esteem, low frustration tolerance,
limited coping skills, and relationships based primarily on mutual drug use.
Many people will not become dependent on opioids if they are taken exactly as
prescribed. However, opioids are addictive drugs and it is possible to become
addicted. Chronic use of opioids can result in tolerance for the drugs, which means
that the user must take a higher dose to achieve the same initial effects. Those who
take opioids long-term may become dependent as their body adapts to the presence
of the drug and withdrawal symptoms will occur if they stop using opioids. Long-term
use of opioids will harm the body and will interfere with your daily life. Long-term use
also increases the risk of an overdose.
IV.
Pathophysiology
Opioids act by binding to opioid receptors on neurons distributed throughout the
nervous system and immune system. Four major types of opioid receptors have
been identified: mu, kappa, delta, and the more recently identified OFQ/N.
These receptors are the binding sites for several families of endogenous peptides,
including enkephalins, dynorphins, and endorphins. These endogenous peptides
regulate and modulate several important functions, including the following:
 Pain
 Stress
 Temperature
 Respiration
 Endocrine activity
 Gastrointestinal activity
 Mood
 Motivation
Opioids can be administered by injection, orally, insufflated, transdermally, and by
smoking. Injection is the most potent route because many opioids have significant
first-pass hepatic metabolism; most deaths occur after opioids are injected. The
oral bioavailability of some opioids is 50% or less (morphine and methadone), but
the oral bioavailability of some synthetic opioids is much higher.
V.
Signs and Symptoms



Opioid dependence and abuse are defined in DSM-IV-TR according to general
criteria for these disorders.
DSM-IV-TR Diagnostic Criteria for Opioid Intoxication
o A. Recent use of an opioid.
o B. Clinically significant maladaptive behavioral 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.
o C. Pupillary constriction (or papillary dilation due to anoxia from severe
overdose) and one (or more) of the following signs, developing during, or
shortly after, opioid use:
 (1) drowsiness or coma
 (2) slurred speech
 (3) impairment in attention or memory
o D. The symptoms are not due to a general medical condition and are not
better accounted for by another mental disorder.
o Specify if: With perceptual disturbances
DSM-IV-TR Diagnostic Criteria for Opioid Withdrawal
o


A. Either of the following:
 (1) cessation of (or reduction in) opioid use that has been heavy
and prolonged (several weeks or longer)
 (2) administration of an opioid antagonist after a period of opioid
use
o B. Three (or more) of the following, developing within minutes to several
days after Criterion A:
 (1) dysphoric mood
 (2) nausea or vomiting
 (3) muscle aches
 (4) lacrimation or rhinorrhea
 (5) papillary dilation, piloerection, or sweating
 (6) diarrhea
 (7) yawning
 (8)fever
 (9)insomnia
o C. The symptoms in Criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
o D. The symptoms are not due to a general medical condition and are not
better accounted for by another mental disorder
. DSM-IV-TR Diagnostic Criteria for Opioid Intoxication Delirium
o A. Disturbance of consciousness (i.e., reduced clarity of awareness of the
environment) with reduced ability to focus, sustain, or shift attention.
o 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 preexisting, established, or evolving
dementia.
o C. The disturbance develops over a short period of time (usually hours to
days) and tends to fluctuate during the course of the day.
o D. 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 ∗Note:
This diagnosis should be made instead of a diagnosis of
substance intoxication only when the cognitive symptoms are in
excess of those usually associated with the intoxication syndrome
and when the symptoms are sufficiently severe to warrant
independent clinical attention. ∗Note: The diagnosis should be
recorded as substance-induced delirium if related to medication
use.
DSM-IV-TR Diagnostic Criteria for Opioid-Induced Psychotic Disorder
o A. Prominent hallucinations or delusions. Note: Do not include
hallucinations if the person has insight that they are substance induced.
o B. There is evidence from the history, physical examination, or laboratory
findings ofeither (1) or (2):
 (1) the symptoms in Criterion A developed during, or within a
month of, substance intoxication or withdrawal
 (2) medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a psychotic disorder
that is not substance induced. Evidence that the symptoms are better
accounted for by a psychotic disorder that is not substance induced might
include the following: the symptoms precede the onset of the substance
use (or medication use); the symptoms persist for a substantial period of
time (e.g., about a month) after the cessation of acute withdrawal or
severe intoxication, or are substantially in excess of what would be
expected given the type or amount of the substance used or the duration
of use; or there is other evidence that suggests the existence of an
independent non–substance-induced psychotic disorder (e.g., a history of
recurrent non–substance-related episodes).
o



D. The disturbance does not occur exclusively during the course of a
delirium. Note: This diagnosis should be made instead of a diagnosis of
substance intoxication or substance withdrawal only when the symptoms
are in excess of those usually associated with the intoxication or
withdrawal syndrome and when the symptoms are sufficiently severe to
warrant independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Opiod-Induced Mood Disorder
o A. A prominent and persistent disturbance in mood predominates in the
clinical picture and is characterized by either (or both) of the following:
(1)depressed mood or markedly diminished interest or pleasure in all, or
almost all, activities (2)elevated, expansive, or irritable mood.
o B. There is evidence from the history, physical examination, or laboratory
findings of either (1) or (2): (1)the symptoms in Criterion A developed
during, or within a month of, substance intoxication or withdrawal
(2)medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a mood disorder that is
not substance induced. Evidence that the symptoms are better accounted
for by a mood disorder that is not substance-induced might include the
following: the symptoms precede the onset of the substance use (or
medication use); the symptoms persist for a substantial period of time
(e.g., about a month) after the cessation of acute withdrawal or severe
intoxication or are substantially in excess of what would be expected
given the type or amount of the substance used or the duration of use; or
there is other evidence that suggests the existence of an independent
non–substance-induced mood disorder (e.g., a history of recurrent major
depressive episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium.
o E. The symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning. Note: This
diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the mood symptoms are
in excess of those usually associated with the intoxication or withdrawal
syndrome and when the symptoms are sufficiently severe to warrant
independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Substance-Induced Sexual Dysfunction
o A. Clinically significant sexual dysfunction that results in marked distress
or interpersonal difficulty predominates in the clinical picture.
o B. There is evidence from the history, physical examination, or laboratory
findings that the sexual dysfunction is fully explained by substance use as
manifested by either (1) or (2):
 (1) the symptoms in Criterion A developed during, or within a
month of, substance intoxication
 (2) medication use is etiologically related to the disturbance
o C. The disturbance is not better accounted for by a sexual dysfunction
that is not substance induced. Evidence that the symptoms are better
accounted for by a sexual dysfunction that is not substance induced might
include the following: the symptoms precede the onset of the substance
use or dependence (or medication use); the symptoms persist for a
substantial period of time (e.g., about a month) after the cessation of
intoxication, or are substantially in excess of what would be expected
given the type or amount of the substance used or the duration of use; or
there is other evidence that suggests the existence of an independent
non–substance-induced sexual dysfunction (e.g., a history of recurrent
non–substance-related episodes).
DSM-IV-TR Diagnostic Criteria for Substance-Induced Sleep Disorder
o A. A prominent disturbance in sleep that is sufficiently severe to warrant
in dependent clinical attention.
o B. There is evidence from the history, physical examination, or laboratory
findings of either (1) or (2):
 (1) the symptoms in Criterion A developed during, or within a
month of, substance intoxication or withdrawal
 (2) medication use is etiologically related to the sleep disturbance
C. The disturbance is not better accounted for by a sleep disorder that is
not substance induced. Evidence that the symptoms are better accounted
for by a sleep disorder that is not substance induced might include the
following: the symptoms precede the onset of the substance use (or
medication use); the symptoms persist for a substantial period of time
(e.g., about a month) after the cessation of acute withdrawal or severe
intoxication or are substantially in excess of what would be expected
given the type or amount of the substance used or the duration of use; or
there is other evidence that suggests the existence of an independent
non–substance-induced sleep disorder (e.g., a history of recurrent non–
substance-related episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium.
o E. The sleep disturbance causes clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
DSM-IV-TR Diagnostic Criteria for Opioid-Related Disorder Not Otherwise
Specified
o The opioid-related disorder not otherwise specified category is for
disorders associated with the use of opioids that are not classifiable as
opioid dependence, opioid abuse, opioid intoxication, opioid withdrawal,
opioid intoxication delirium, opioid-induced psychotic disorder, opioidinduced mood disorder, opioid-induced sexual dysfunction, or opioidinduced sleep disorder.
o

VI.
Course and Prognosis
If treatment is rapidly instituted, the outcome is generally good. Complications
include:
- aspiration pneumonia which may be severe,
- haemodynamic disturbances (bradycardia, hypotension and
vasovagal collapse),
- hypothermia,
- rhabdomyolysis
- non cardiac pulmonary oedema,
- convulsions (due to impurities in street drugs)
- hypoxic brain damage.
Death can result from prolonged apnea or a hypersensitivity reaction.
The relapse rate among patients receiving treatment for opioid dependence and
other substance abuse is high, comparable to that of other patients with chronic
relapsing conditions, including hypertension and asthma. Many cases of relapse are
attributable to treatment noncompliance and lack of lifestyle modification.
Duration of agonist replacement therapy is usually recommended as a minimum of 1
year, and some patients will receive agonist replacement therapy indefinitely. Longer
durations of treatment are associated with higher rates of abstinence from illicit
opioids.
Much remains unknown about patient outcomes following termination of long-term
opioid replacement therapy. Some patients aim to achieve total abstinence from all
opioids, but little is known about patient characteristics and strategies used among
those who remain abstinent.
VII.
Medical Management
The first task in overdose treatment is to ensure an adequate airway.
Tracheopharyngeal secretions should be aspirated; an airway may be inserted. The
patient should be ventilated mechanically until naloxone, a specific opioid antagonist,
can be given. Naloxone is administered IV at a slow rate—initially about 0.8mg per
70kg of body weight. Signs of improvement (increased respiratory rate and papillary
dilation) should occur promptly. In opioid-dependent patients, too much naloxone
may produce signs of withdrawal as well as reversal of overdosage. If no response to
the initial dosage occurs, naloxone administration may be repeated after intervals of
a few minutes.
Treatment should initially focus on stabilization of the patient's substance-abuse
disorder, with an initial goal of 2 to 4 weeks abstinence before addressing
comorbidities. Patients who persistently display symptoms of a psychiatric disorder
during abstinence should be considered as having an independent disorder and
should receive prompt psychiatric treatment.
SSRIs are generally safe and well-tolerated, but clinical trials with these agents in
methadone patients have been negative. Therefore, SSRIs may be considered firstline treatment based on their safety profile, but if the patient does not respond, then
TCAs or newer generation agents should be considered. More stimulating
antidepressants, such as venlafaxine and bupropion, may be suitable in patients with
prominent low energy or past or current symptoms consistent with attention deficit
hyperactivity disorder (ADHD). The utility of nonpharmacologic treatments should be
emphasized. Psychosocial therapies are as effective as pharmacotherapy in the
treatment of mild-to-moderate depressive and anxiety symptoms. Treatment of
personality disorders is nonpharmacologic. If depression persists, psychosocial
modalities, such as cognitive therapy, supportive therapy, or contingency
management, have some evidence to support their efficacy in opioid-dependent
patients.
Phencyclidine or Phencyclidine-like-Related Disorders
I.
Definition
PCP is a synthetic, dissociative drug sold as tablets, capsules, or white or colored
powder. It can be snorted, smoked, or eaten. Developed in the 1950s as an IV
anesthetic, PCP was never approved for human use because of problems during
clinical studies, including intensely negative psychological effects. It is known
colloquially as angel dust.
II.
Epidemiology
According to DSM-IV-TR, the actual rate of PCP dependence and abuse is not
known, but PCP is associated with 3% of substance abuse deaths and 32% of
substance-related emergency room visits nationally. Overall, most users are
between 18 and 25 years of age and they account for 50% of cases. Patients are
more likely to be male rather than female, especially those who visit emergency
rooms. Twice as many white as blacks are users, although blacks account for more
visits to hospitals for PCP-related disorders than do whites. PCP use appears to be
rising, with some reports showing a 50% increase, particularly in urban areas.
III.
Etiology
PCP is easy to manufacture and is inexpensively available on the street in most
cities, especially East Coast cities. PCP is a drug that causes hallucinations, which
are profound distortions in a person’s perception of reality. Under the influence
of hallucinogens, people see images, hear sounds, and feel sensations that seem
real but are not. Addiction to PCP is both psychological and physical, as it physically
affects the body by making the user feel as though he or she cannot function without
the drug. Many people become addicted to the feeling of being invincible and the
euphoric feelings associated with PCP. Some abusers continue to use PCP due to
the feelings of strength, power and invulnerability.
IV. Pathophysiology
Phencyclidine and its related compounds are variously sold as a crystalline powder,
paste, liquid, or drug-soaked paper (blotter). It can be snorted, smoked, or eaten. The
primary pharmacodynamic effect of PCP and ketamine is as anantagonist at the
NMDA subtype of glutamate receptors. PCP binds to a site within the NMDAassociated calcium channel and prevents the influx of calcium ions. PCP also activates
the dopaminergic neurons of the ventral tegmental area, which project to the cerebral
cortex and the limbic system. Activation of these neurons is usually involved in
mediating the reinforcing qualities of PCP.
V. Signs and Symptoms


The DSM-IV-TR uses the general criteria for PCP dependence and PCP abuse.
DSM-IV-TR Diagnostic Criteria for Phencyclidine Intoxication
o A. Recent use of phencyclidine (or a related substance).
o B. Clinically significant maladaptive behavioral changes (e.g.,
belligerence,
assaultiveness,
impulsiveness,
unpredictability,
psychomotor agitation, impaired judgment, or impaired social or
occupational functioning) that developed during, or shortly after,
phencyclidine use.
o C. Within an hour (less when smoked, “snorted,” or used intravenously),
two (o rmore) of the following signs:
 (1) vertical or horizontal nystagmus
 (2) hypertension or tachycardia
 (3) numbness or diminished responsiveness to pain
 (4) ataxia
 (5) dysarthria
 (6) muscle rigidity
 (7) seizures or coma
 (8) hyperacusis
o D. The symptoms are not due to a general medical condition and are
not better accounted for by another mental disorder.
 DSM-IV-TR Diagnostic Criteria for PCP Intoxication Delirium
o A. Disturbance of consciousness (i.e., reduced clarity of awareness of
the environment) with reduced ability to focus, sustain, or shift attention.
o 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 preexisting, established, or evolving
dementia.
o C. The disturbance develops over a short period of time (usually hours
to days) and tends to fluctuate during the course of the day.
o D. 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
∗Note: This diagnosis should be made instead of a diagnosis of
substance intoxication only when the cognitive symptoms are in
excess of those usually associated with the intoxication
syndrome and when the symptoms are sufficiently severe to
warrant independent clinical attention. ∗Note: The diagnosis
should be recorded as substance-induced delirium if related to
medication use.
 DSM-IV-TR Diagnostic Criteria for PCP-Induced Psychotic Disorder
o A. Prominent hallucinations or delusions. Note: Do not include
hallucinations if the person has insight that they are substance induced.
o B. There is evidence from the history, physical examination, or
laboratory findings of either (1) or (2):
 (1) the symptoms in Criterion A developed during, or within a
month of, substance intoxication or withdrawal
 (2) medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a psychotic disorder
that is not substance induced. Evidence that the symptoms are better
accounted for by a psychotic disorder that is not substance induced


might include the following: the symptoms precede the onset of the
substance use (or medication use); the symptoms persist for a
substantial period of time (e.g., about a month) after the cessation of
acute withdrawal or severe intoxication, or are substantially in excess of
what would be expected given the type or amount of the substance
used or the duration of use; or there is other evidence that suggests the
existence of an independent non–substance-induced psychotic disorder
(e.g., a history of recurrent non–substance-related episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium. Note: This diagnosis should be made instead of a diagnosis of
substance intoxication or substance withdrawal only when the
symptoms are in excess of those usually associated with the
intoxication or withdrawal syndrome and when the symptoms are
sufficiently severe to warrant independent clinical attention.
DSM-IV-TR Diagnostic Criteria for PCP-Induced Mood Disorder
o A. A prominent and persistent disturbance in mood predominates in the
clinical picture and is characterized by either (or both) of the following:
 (1) depressed mood or markedly diminished interest or pleasure
in all, or almost all, activities
 (2) elevated, expansive, or irritable mood.
o B. There is evidence from the history, physical examination, or
laboratory findings of either (1) or (2):
 (1)the symptoms in Criterion A developed during, or within a
month of, substance intoxication or withdrawal
 (2)medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a mood disorder that
is not substance induced. Evidence that the symptoms are better
accounted for by a mood disorder that is not substance-induced might
include the following: the symptoms precede the onset of the substance
use (or medication use); the symptoms persist for a substantial period
of time (e.g., about a month) after the cessation of acute withdrawal or
severe intoxication or are substantially in excess of what would be
expected given the type or amount of the substance used or the
duration of use; or there is other evidence that suggests the existence
of an independent non–substance-induced mood disorder (e.g., a
history of recurrent major depressive episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium.
o E. The symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning. Note: This
diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the mood symptoms are
in excess of those usually associated with the intoxication or withdrawal
syndrome and when the symptoms are sufficiently severe to warrant
independent clinical attention.
DSM-IV-TR Diagnostic Criteria for PCP-Induced Anxiety Disorder
o A. Prominent anxiety, panic attacks, or obsessions or compulsions
predominate in the clinical picture.
o B. There is evidence from the history, physical examination, or
laboratory findings of either (1) or (2):
 (1) the symptoms in Criterion A developed during, or within 1
month of, substance intoxication or withdrawal
 (2) medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by an anxiety disorder
that is not substance induced. Evidence that the symptoms are better
accounted for by an anxiety disorder that is not substance induced
might include the following: the symptoms precede the onset of the
substance use (or medication use); the symptoms persist for a
substantial period of time (e.g., about a month) after the cessation of
acute withdrawal or severe intoxication or are substantially in excess of
what would be expected given the type or amount of the substance
used or the duration of use; or there is other evidence suggesting the

existence of an independent non–substance-induced anxiety disorder
(e.g., a history of recurrent non–substance-related episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium.
o E. The disturbance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning. Note: This
diagnosis should be made instead of a diagnosis of substance
intoxication or substance withdrawal only when the mood symptoms are
in excess of those usually associated with the intoxication or withdrawal
syndrome and when the symptoms are sufficiently severe to warrant
independent clinical attention.
DSM-IV-TR Diagnostic Criteria for Phencyclidine-Related Disorder Not
Otherwise Specified
o The phencyclidine-related disorder not otherwise specified category is
for disorders associated with the use of phencyclidine that are not
classifiable as phencyclidine dependence, phencyclidine abuse,
phencyclidine intoxication, phencyclidine intoxication delirium,
phencyclidine-induced psychotic disorder, phencyclidine-induced mood
disorder, or phencyclidine-induced anxiety disorder.
VI. Course and Prognosis
Relapse and return to PCP use is common, even among people who have
experienced severe medical and psychiatric complications from the drug. Since
many users also abuse other drugs, their success in renouncing PCP is tied to
their successful treatment for other addictions. Successful treatment takes
persistence, patience, and a functional support system, all of which many users
lack.
VII.
Medical Management
Benzodiazepines are the medication of choice when treating acute PCP
intoxication. People experiencing PCP intoxication or delirium often hurt
themselves or others. They are generally kept in an environment where there is as
little stimulation as possible. They are restrained only as much as is necessary to
keep them from hurting themselves or others until the level of PCP in their bodies
can be reduced. Antipsychotic medications may be used to calm patients in cases
of PCP delirium.
There are no quick ways to rid the body of PCP. If the PCP has been eaten,
stomach pumping or feeding activated charcoal may help keep the drug from being
absorbed into the bloodstream. Physical symptoms such as high body temperature
are treated as needed.
Most people recover from PCP intoxication or delirium without major medical
complications. Many are habitual users who return to use almost immediately.
There are no specific behavioral therapies to treat PCP use. Antidepressants are
sometimes prescribed. Long-term residential treatment or intensive outpatient
treatment along with urine monitoring offers some chance of success. Narcotics
Anonymous, a self-help group, may be helpful for some patients.
Sedative-, Hypnotic-, Anxiolytic- Related Disorders
I.
Definition
The drugs discussed in this section are referred to as anxiolytic or sedative-hypnotic
drugs. The terminology is ambiguous for several reasons: (1) sedatives are drugs
that reduce subjective tension and induce mental calmness; however, the same can
be said of anxiolytics; (2) hypnotics are drugs used to induce sleep; but sedatives
and anxiolytics given in sufficiently high doses also produce sleep; and (3) hypnotics
in low doses, instead of inducing sleep, produce daytime sedation just as do
sedatives and anxiolytics.
The three groups of grugs associated with this class of substance-related disorders
are benzodiazepines, barbiturates and barbiturate-like substances.
II.
Epidemiology
Sedatives, anxiolytics, and hypnotics are commonly prescribed for people in the sixth
and seventh decades of life; however, nonmedical use is highest in people aged 2635 years. The male-to-female ratio is 1:3. Hypnotic usage ratio in whites-to-black is
2:1. In Western Europe and parts of Asia, use of a hypnotic in the course of a year
approaches 25-30%. AccordingtoDSM-IV-TR, about 6% of individuals have used
either sedatives or tranquilizers illicitly, including 0.3% who reported illicit use of
sedatives in the prior year and 0.1% who reported use of sedatives in the prior
month.
III.
Etiology
The therapeutic value of these agents as anxiolytics and hypnotics has been well
established, and they continue to serve an important role in managing many
debilitating anxiety symptoms in the context of both psychiatric disorders and
medical illness. However, the toxic effects of these drugs have also been
established, including various withdrawal syndromes, dependence, and tolerance.
IV.
Pathophysiology
Gamma-aminobutyric acid (GABA) is one of the key inhibitory neurotransmitters
involved in anxiety and in the anxiolytic action of psychotropic drugs used to treat
anxiety disorders. GABA opens chloride (Cl) channels, causing an influx of Cl ions.
The influx of Cl ions causes hyperpolarization of the neuron, subsequently inhibiting
neuronal discharge. The action of hyperpolarization is reversed by the influx of
calcium into the cell. Benzodiazepine-sensitive GABA receptors with alpha-1
subunits may be most important for regulating sleep and are the presumed targets of
sedative-hypnotic agents. On the other hand, benzodiazepine-sensitive GABA-A
receptors with alpha-2 subunits may be most important for regulating anxiety and are
presumed targets of anxiolytic agents. Flumazenil, a benzodiazepine antagonist,
interacts with GABA-A receptors and is used clinically to rapidly reverse the effects
of benzodiazepine overdoses.
V.
Signs and Symptoms


Sedative, hypnotic, or anxiolytic dependence and sedative, hypnotic, or anxiolytic
abuse are diagnosed according to the general criteria in DSM-IV-TR for
substance dependence and substance abuse.
DSM-IV-TR Diagnostic Criteria for Sedative, Hypnotic, or Anxiolytic Intoxication
o A. Recent use of a sedative, hypnotic, or anxiolytic.
o B. Clinically significant maladaptive behavioral or psychological changes
(e.g., inappropriate sexual or aggressive behavior, mood lability, impaired
judgment, impaired social or occupational functioning) that developed during,
or shortly after, sedative, hypnotic, or anxiolytic use.
o C. One (or more) of the following signs, developing during, or shortly after,
sedative, hypnotic, or anxiolytic use:
 (1) slurred speech
 (2) Incoordination
 (3) unsteady gait
 (4) nystagmus
 (5) impairment in attention or memory
 (6) stupor or coma
o D. The symptoms are not due to a general medical condition and are not
better accounted for by another mental disorder




. DSM-IV-TR Diagnostic Criteria for Hallucinogen Intoxication Delirium
o A. Disturbance of consciousness (i.e., reduced clarity of awareness of the
environment) with reduced ability to focus, sustain, or shift attention.
o 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 preexisting, established, or evolving
dementia.
o C. The disturbance develops over a short period of time (usually hours to
days) and tends to fluctuate during the course of the day.
o D. 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 ∗Note:
This diagnosis should be made instead of a diagnosis of
substance intoxication only when the cognitive symptoms are in
excess of those usually associated with the intoxication syndrome
and when the symptoms are sufficiently severe to warrant
independent clinical attention. ∗Note: The diagnosis should be
recorded as substance-induced delirium if related to medication
use.
DSM-IV-TR Diagnostic Criteria for Substance Withdrawal Delirium
o A. Disturbance of consciousness (i.e., reduced clarity of awareness of the
environment) with reduced ability to focus, sustain, or shift attention.
o B. A change in cognition (such as memory deficit, disorientation, language
disturbance) or the development of a perceptual disturbance that is no tbetter
accounted for by a preexisting, established, or evolving dementia.
o C. The disturbance develops over a short period of time (usually hours to
days) and tends to fluctuate during the course of the day.
o 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.
DSM-IV-TR Diagnostic Criteria for Substance-Induced Persisting Dementia
o A. The development of multiple cognitive deficits manifested by both
 (1) memory impairment
 (2) one (or more) of the following cognitive disturbances:
 (a) aphasia (language disturbance)
 (b) apraxia (impaired ability to carry out motor activities despite
intact motor function)
 (c) agnosia
 (d) disturbance in executive functioning (i.e., planning,
organizing, sequencing, abstracting)
o B. The cognitive deficits in Criteria A1 and A2 each cause significant
impairment in social or occupational functioning and represent a significant
decline from a previous level of functioning.
o C. The deficits do not occur exclusively during the course of a delirium and
persist beyond the usual duration of substance intoxication or withdrawal.
o D. There is evidence from the history, physical examination, or laboratory
findings that the deficits are etiologically related to the persisting effects of
substance use (e.g.,a drug of abuse, a medication).
Diagnostic criteria for Substance-Induced Persisting Amnestic Disorder
o The development of memory impairment as manifested by impairment in the
ability to learn new information or the inability to recall previously learned
information.
o The memory disturbance causes significant impairment in social or
occupational functioning and represents a significant decline from a previous
level of functioning.
o The memory disturbance does not occur exclusively during the course of
a Delirium or a Dementia and persists beyond the usual duration of
Substance Delirium or Withdrawal.
o

VI.
There is evidence from the history, physical examination, or laboratory
findings that the memory disturbance is etiologically related to the persisting
effects of substance use (e.g., a drug of abuse, a medication).
DSM-IV-TR Diagnostic Criteria for Hallucinogen-Induced Psychotic Disorder
o A. Prominent hallucinations or delusions. Note: Do not include
hallucinations if the person has insight that they are substance
induced.
o B. There is evidence from the history, physical examination, or
laboratory findings ofeither (1) or (2):
 (1) the symptoms in Criterion A developed during, or within a
month of, substance intoxication or withdrawal
 (2) medication use is etiologically related to the disturbance.
o C. The disturbance is not better accounted for by a psychotic disorder
that is not substance induced. Evidence that the symptoms are better
accounted for by a psychotic disorder that is not substance induced
might include the following: the symptoms precede the onset of the
substance use (or medication use); the symptoms persist for a
substantial period of time (e.g., about a month) after the cessation of
acute withdrawal or severe intoxication, or are substantially in excess
of what would be expected given the type or amount of the substance
used or the duration of use; or there is other evidence that suggests
the existence of an independent non–substance-induced psychotic
disorder (e.g., a history of recurrent non–substance-related episodes).
o D. The disturbance does not occur exclusively during the course of a
delirium. Note: This diagnosis should be made instead of a diagnosis
of substance intoxication or substance withdrawal only when the
symptoms are in excess of those usually associated with the
intoxication or withdrawal syndrome and when the symptoms are
sufficiently severe to warrant independent clinical attention.
Course and Prognosis
Some individuals respond to treatment and stay in remission, while others
experience periods of relapse, in which they begin SHA use/abuse after a period of
remission, and again meet the criteria for substance dependence. Some individuals
are never able to abstain from use and do not experience any periods of remission.
Only a handful of studies have looked into long-term success of benzodiazepine
discontinuation programs. Most studies indicate a high relapse state; however,
outcome is more favorable in those individuals who manage to complete a
discontinuation program. A 4- to 6-year post discharge follow-up study of patients
primarily admitted for primary sedative-hypnotic dependence showed that 84% of the
patients had resumed using sedative-hypnotics, 52% were abusing drugs at followup, and 42% had been readmitted for drug abuse.
Outcome is better in individuals with good social support, absence of psychiatric comorbidity or remission of preexisting psychiatric symptoms, and absence of
dependence on other drugs.
VII.
Medical Management
Initially, treat a patient who has taken an overdose of sedative-hypnotics like any
other patient with drug intoxication.
 Provide an adequate airway and ventilation.
 Stabilize and maintain the hemodynamic status.
 Once initial measures have been carried out, consider inducing emesis,
performing lavage, and administering activated charcoal to a patient who
has orally ingested the drug, depending on the time of ingestion and level of
consciousness.
 Emesis, lavage, and/or activated charcoal prevent absorption of the drug
into the system and absorption of the drug or active metabolites through
enterohepatic recirculation.
 Laxatives may be used to induce catharsis.
Benzodiazepine antagonist, flumazenil, is available for the treatment of
benzodiazepine intoxication.[7] It must be used with some caution; in some cases, it
has not completely reversed respiratory depression, and it can cause seizures in
patients with benzodiazepine dependence.
If the patient overdosed on barbiturates, administer intravenous sodium bicarbonate
to alkalinize the urine, which increases the rate of barbiturate excretion. The dose of
bicarbonate varies depending on the patient's metabolic state. Urine pH should be
monitored and maintained at 7.5. Dialysis may be required, depending on the
severity of the patient's condition.
Address all potential complications, such as aspiration, pulmonary edema, and
respiratory failure due to sedative-hypnotic drug overdose. If a suicide attempt is
suspected, then place the patient on suicide precautions and order a psychiatric
evaluation.
Anabolic-Androgenic Steroid Abuse
I.
Definition
Anabolic steroids are a family of drugs composed of the natural male hormone
testosterone and a group of more than 50 synthetic analogs of testosterone,
synthesized over the last 60 years. These drugs all exhibit various degrees of
anabolic (muscle building) and androgenic (masculinizing) effects.
II.
Epidemiology
Approximately 286,000 men and 26,000 women are estimated to use steroids each
year. Among this number, nearly one third, or 98,000, were between 12 and 17 years
of age.
III.
Etiology
ThemajorreasonfortakingillicitAASistoenhanceeitherathleticperformanceorphysicalappearance.TakingAASisreinforcedbecausetheycanproducetheathleticandphysicaleffectsthatusersdesire,especiall
ywhencombinedwithproperdietandtraining.Furtherreinforcementderivesfromwinningc
ompetitionsandfromsocialadmirationforphysicalappearance.AASusersalsoperceivethattheyc
antrainmoreintensivelyforlongerdurationswithlessfatigueandwithdecreasedrecoveryti
mesbe-tweenworkouts.
IV.
Pathophysiology
High-dose AAS increases the amounts of estrogens produced, which may lead to
irreversible feminising effects in men. Taking testosterone results in a negative
feedback inhibition of the hypothalamic-pituitary-testicular axis and suppression of
GnRH, LH, FSH, and testosterone production. Testicular atrophy and decreased
sperm count and mobility result. Infertility can occur within months. Other adverse
effects due to this hormonal suppression in men include acne, oily skin,
disproportionate muscular development of the upper torso, changes in libido,
testicular atrophy, scrotal pain, impotence, infertility, temporal hairline recession,
irreversible gynaecomastia, and higher voice pitch. In women, adverse effects
include acne, oily skin, muscular development of the upper torso, menstrual
irregularities, and changes in libido. The potential irreversible masculinising effects
include hirsutism, male pattern baldness, deepening of the voice, and clitoral
hypertrophy. Psychiatric effects include aggression, psychosis, anxiety and
depression, physical dependence, and withdrawal.
V.
Signs and Symptoms
The most vital aspects in assessing sedative-hypnotic intoxication or withdrawal
are detailed mental status and neurologic examinations in addition to comprehensive
physical examination.
 Physical findings of intoxication include the following:
o Hypothermia and hypotension
o Eyes - Nystagmus, miosis, and diplopia
o Cardiovascular - Hypotension and bradycardia; patients may develop
tachycardia in response to hypotension
o Pulmonary - Respiratory depression; risk of aspiration
o Gastrointestinal - Variable
o Musculoskeletal - Prolonged unconsciousness resulting in skin necrosis and
rhabdomyolysis
o Neurological - Ataxia, dyskinesia, dysarthria, decreased deep tendon reflexes
 Mental status examination findings of intoxication include the following:
o Appearance - Dependent upon level of intoxication, the patient may be
somnolent and disheveled.
o Behavior - Psychomotor retardation may be seen, but, on occasion, the
patient may show inappropriate sexual or aggressive behavior, usually during
or shortly after sedative use.
o Speech - Speech is often slurred.
o Mood - The patient may report a variety of mood states.
o Affect - Affect is variable, and it can range from flat, blunt, dysphoric, labile,
and even euphoric.
o Thought process and content - Dependent upon the level of intoxication, the
thought content may range from bizarre content to paranoia. Patients may
complain of suicidal ideations.
o Perception - Perception may be altered based on level of intoxication, with a
wide range of disturbances, including illusions and hallucinations.
o Orientation - The patient can be completely disoriented, with obfuscation of
higher functions. Tasks such as computation, abstraction, memory, and
concentration are usually impaired.
o Insight and judgment are usually impaired.
 Physical signs of withdrawal syndromes include the following:
o Vital signs - Hyperthermic temperature above 100°F; pulse rate tachycardic
above 100 beats/minute; respiration rate possibly tachypneic above 20;
blood pressure variable, eg, hypertensive initially, hypotensive from fluid
loses at later stages
o Eyes - Possible dilated pupils as a secondary effect of sympathetic
hyperactivity
o Cardiovascular - Tachycardia and palpitations
o Pulmonary - Tachypnea
o Gastrointestinal - Variable bowel sounds, depending on the type of
autonomic predominance (parasympathetic or sympathetic) at the time of
presentation
o Musculoskeletal - Tremors, potentially leading to muscle spasms and
rhabdomyolysis
o Neurologic - Tremors, increased deep tendon reflexes, ataxia, with or
without dyskinesia
 Mental status examination findings in withdrawal syndromes include the following:
o Appearance - Hygiene may vary, depending on length of time experiencing
withdrawal symptoms. The patient may be alert but high-strung.
o Behavior - The patient may display psychomotor agitation.
o Attitude - The patient may be hostile and irritable.
o Orientation - Depending on the severity of withdrawal symptoms, the patient
may be disoriented to person, place, or time. The patient may have
problems with memory, concentration, abstraction, and performance of
intellectual tasks.
o Perception - The patient may exhibit increased sensory perception (smell,
sight, taste, touch). Depersonalization or derealization is possible.
o Speech - Speech can vary and may be rapid.
o Mood - The patient often reports feeling anxious but may complain of
sadness.
o Affect - Affect may be expansive, labile, dysphoric, and most likely anxious.
o Thought process and content - This may be variable, but the patient may
present with thought disorganization and delusions.
o Hallucinations - Auditory, visual, and tactile hallucinations may be present.
o Judgment - This may be impaired.
o Insight - This may be compromised.
VI.
Course and Prognosis
Anabolic steroid abuse is a treatable condition. Abusers can overcome the problem
with the help of family members, support groups, psychotherapy, medication,
treatment programs, and family counseling. These programs are customized to help
teens and adults lead productive and normal lives. However, heavy steroid use-even
if it is stopped after a few years-may stunt growth and increase the risk of liver
cancer. A steroid user who quits may experience severe depression that can lead to
suicidal thoughts and suicide attempts or completion. The risk of depression and
suicide
is
highest
among
teenage
abusers.
Some physicians recommend that athletes using steroids avoid sudden
discontinuance of all steroids simultaneously because their bodies may enter an
immediate catabolic (metabolic breakdown of compounds) phase. This can lead to a
considerable loss of strength and mass, an increase of fat and water in the body, and
breast enlargement in males. Breast enlargement occurs because the suddenly low
androgen level shifts the hormone balance in favor of estrogen compounds, which
suddenly become the dominant hormone.
VII.
Medical Management
Few studies of treatment for anabolic steroid abuse have been conducted.
Knowledge as of 2009 is based largely on the experiences of a small number of
physicians who have worked with individuals undergoing steroid withdrawal. The
physicians have found that supportive therapy is sufficient in some cases. Patients
are educated about what they may experience during withdrawal and are evaluated
for suicidal thoughts. If symptoms are severe or prolonged, medications or
hospitalization may be needed. Depression needs to be monitored closely.
Sometimes medications are used to restore hormone balance after its disruption by
steroid abuse. Other medications target specific withdrawal symptoms, for example,
antidepressants to treat depression, and analgesics (pain killers) for headaches,
muscle, and joint pains. Some individuals are psychologically addicted to steroids
and benefit from behavioral therapies.
VIII.
OT Application
a. FOR
The first frame of reference that may be applicable is the Object Relations
FOR which views persons, media and activities as objects invested with
psychic energy and thus studies the interaction of these objects. The
process of therapy would seek to free up libidinal energy, allowing it to be
voluntarily invested in a variety of socially acceptable, need-satisfying
object relationships. The therapist would like to explore and understand
with the patient the feeling side of personal experiences. Basically,
through this frame of reference, the therapists aim to identify and attempt
to resolve the patient’s inner conflicts that may have triggered their
dependence and attachment to substances.
Another frame of reference that a therapist may plan to employ is the
Behavioral FOR. With this approach, the aim is to help the client in
conditioning and disciplining himself in an effective manner so that he may
abstain from consuming the addictive substance as well as reward himself
appropriately to avoid relapse.
The last proposed frame of reference for treating substance abuse is the
Model of Human Occupation which seeks to explain how occupation is
motivated, patterned and performed. Therefore, this model aims to
understand occupation and problems of occupation that occur in terms of
its primary concepts of volition, habituation, performance capacity, and
environmental context. Substance abuse can begin as an attempt to
satisfy an unmet need, such as providing temporary stress relief from
difficult relationships or financial problems, or it may be an artificial means
to achieving pleasure because the individual's roles and routines are not
providing satisfactory pleasure experiences. So a goal is to redirect the
client’s time and energy into more wholesome pleasurable activities and
not on substance abuse. When the individual attains sufficient volition to
make the needed change and break the substance abuse pattern, he
needs to increase her performance capacity in the replacement skills to a
level high enough to overcome the habituation. When he has done that to
a level that is beginning to be more stable, he can maintain it by building
successful experiences and developing further resources to sustain the
change. Although a client may habituate new behavior, the environments
in which he or she lives and engages will continue to contain incentives to
return to substance abuse. Clients must be prepared to withstand these
challenges. The goal in terminating the process is to ensure that clients
have sufficient resources readily available.
To assess the client’s inner conflicts, projective instruments should be
used such as the Azima battery, Shoemyen battery, Goodman battery or
the Magazine Picture Collage. To evaluate the client’s functionality and
performance skills, the Bay Area Functional Performance Evaluation,
Kohlman Evaluation of Living Skills, Milwaukee Evaluation of Daily Living
Skills and Work Tolerance Screening may be utilized.
In identifying the client’s roles and interests that may be utilized during the
therapy process, the Role Checklist, Adolescent Role Assessment and
NPI Interest Checklist may be used.
b. Evaluation and Assessment
To assess the client’s inner conflicts, projective instruments should be
used such as the Azima battery, Shoemyen battery, Goodman battery or
the Magazine Picture Collage. To evaluate the client’s functionality and
performance skills, the Bay Area Functional Performance Evaluation,
Kohlman Evaluation of Living Skills, Milwaukee Evaluation of Daily Living
Skills and Work Tolerance Screening may be utilized.
In identifying the client’s roles and interests that may be utilized during the
therapy process, the Role Checklist, Adolescent Role Assessment and
NPI Interest Checklist may be used.
c. OT Management
All alcohol related substance or substance can be managing trough the
use of therapeutic activities and therapy. These are the following:

Individual psychotherapy
 Patient can address the cause of the abuse.
 Establishing trust to one self

Group therapy
 They may attend group OT session and through that they
can be able express their true feelings and the reason why
did they use such substance.
 They may also value friendship and trust

Family therapy
 They can help the patient through opening and asking them
questions, sharing their problems
 Can have get together, going out of town sometime, building
up bonding relationship to their children
 Family reunions