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SUBSTANCE USE
DISORDERS
DANA BARTLETT, RN, BSN, MSN, MA
Dana Bartlett is a professional nurse and
author. His clinical experience includes 16 years
of ICU and ER experience and over 20 years as
a poison control center information specialist.
Dana has published numerous CE and journal
articles, written NCLEX material and textbook
chapters, and done editing and reviewing for
publishers such as Elsevier, Lippincott, and
Thieme. He has written widely on the subject of
toxicology
and
was
recently
named
a
contributing editor, toxicology section, for Critical Care Nurse journal. He is currently
employed at the Connecticut Poison Control Center and is actively involved in
lecturing and mentoring nurses, emergency medical residents and pharmacy
students.
ABSTRACT
Substance use in the United States and worldwide is a major health
concern requiring specially trained health professionals in primary
care, public health and treatment centers for the identification of
various categories of substance use and its prevention. There is high
risk of substance use among certain groups in society. Although a
substance use disorder is typically thought of as illicit drug use or
chronic alcohol abuse, commonly occurring within marginalized, crime
ridden sectors of society, in reality, substance use is a wide-spread
societal problem involving alcohol, tobacco, prescription and illicit
drugs, among many individuals indistinguishable from the general
population. Substance use is explained according to the DSM-5
(Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition)
criteria.
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Continuing Nursing Education Course Planners
William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster,
Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner
Policy Statement
This activity has been planned and implemented in accordance with
the policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's
Commission on Accreditation for registered nurses. It is the policy of
NurseCe4Less.com to ensure objectivity, transparency, and best
practice in clinical education for all continuing nursing education (CNE)
activities.
Continuing Education Credit Designation
This continuing education (CE) activity is credited for 2 hours. Nurses
may only claim credit commensurate with the credit awarded for
completion of this course activity.
Statement of Learning Need
Nurses need to understand varying patterns of substance use and the
harm caused by each. As members of the health care team, nurses can
assist individuals needing help begin recovery and, hopefully, succeed.
Course Purpose
This course is designed to provide nurses and health associates with
knowledge about a substance use disorder and the recommended
steps to support patient recovery.
Target Audience
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Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses
and Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Dana Bartlett, RN, BSN, MSN, MA, William S. Cook, PhD,
Douglas Lawrence, MA, Susan DePasquale, MSN, FPMHNP-BC -all have
no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Activity Review Information
Reviewed by Susan DePasquale, MSN, FPMHNP-BC.
Release Date: 1/1/2016
Termination Date: 9/8/2017
Please take time to complete a self-assessment of knowledge,
on page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge
learned will be provided at the end of the course.
1.
The term dependency used in relation to substance use
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means:
a. an intense psychological craving for alcohol or a drug
b. physical need for alcohol or a drug that develops over time.
c. the need for increasing amounts of alcohol or a drug over time.
d. a physical resistance to withdrawal signs and symptoms.
2.
One of the central themes of a substance use disorder
is:
a. continued use despite significant substance related problems.
b. excessive use of alcohol or an illicit drug.
c. a pattern of use of alcohol or a drug that causes medical harm.
d. alcohol or drug use that has social consequences.
3. One of the diagnostic criteria for substance use disorder
is:
a. Self-admitted addiction to alcohol or a drug.
b. Excessive use of alcohol or a drug for > five years.
c. Impaired control relating to use of alcohol or a drug.
d. Use of an illicit drug
4. One of the serious complications of alcohol withdrawal is:
a. Acute renal failure
b. Delirium tremens
c. Rhabdomyolysis
d. Cardiac arrhythmias
5. Withdrawal from benzodiazepines can cause:
a. Seizures
b. Rhabdomyolysis
c. Hepatic damage
d. Pulmonary edema
Introduction
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Substance use is an enormous problem in the United States, and even
the small sample of statistics outlined below illustrates its widespread
and deeply injurious effects.

A 2102 report issued by the U.S. White House Office of National
Drug Control Policy states that, for the period from 2000-2006,
drug users in the United States spent $100 billion each year on
cocaine, heroin, marijuana, and methamphetamine.1

In 2011, nonmedical use of pharmaceuticals was involved in
greater than 1.4 million emergency department encounters.
Additionally, emergency department encounters was reported to
be 505,224 for the use of cocaine, 455,668 for the use of
marijuana, 258,482 for the use of heroin, and 159,840 for the
use of amphetamines, methamphetamine, and other
psychostimulants.2

Alcohol use is the third leading cause of death in the United
States.3

Approximately 17 million American adults and 855,000
adolescents in the United States have an alcohol use disorder.4

Tobacco use is the leading cause of preventable death in the
United States.5
A substance use disorder is typically thought of as illicit drug use or
chronic use of alcohol, and it is often assumed that substance use is
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primarily an issue for those living on or near the fringe of society and a
problem characterized by aberrant behavior and crime. Yet substance
use is a problem that also involves the use of legal substances such as
alcohol and tobacco, prescription drugs such as benzodiazepines and
opioids; moreover, people who are substance users are often
indistinguishable from the general population. This module will discuss
substance use involving cocaine, opioids, amphetamines/stimulants,
sedative/hypnotics, and alcohol.
Note that this module uses the terms substance use and substance
use disorder, not addiction or addict. Both of the former terms are in
common use and there are many professional journals that have the
word addiction as part of their title. But addiction is not a recognized
diagnostic term, and the word addict has negative connotations and
tends to focus attention on the behavior and character of the
individual. The term dependency has also frequently been used when
referring to substance use. Dependency refers to the physical need for
a drug or substance that develops over time and it is just one part of
the clinical picture of a substance use disorder.
Part of the commonly accepted definition of a drug is a substance that
will and is intended to, affect the structure or function of the body.6 A
drug is also defined as a substance intended for the cure, diagnosis,
mitigation, prevention, or treatment of a disease.6 Almost all the
classes of drugs that are involved in substance abuse disorders have
some legitimate, albeit occasionally limited medical use, and alcohol
has in the past been used medicinally. However, alcohol is almost
never used as a drug anymore. The illicit forms of cocaine, opioids,
and stimulants are obviously produced without quality control, and
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there are many well-documented cases of dangerous contaminants
and adulterants being added to them. For practical purposes, when
discussing substance use disorders, alcohol is considered a substance
and all of the rest are considered drugs.
What Is A Substance Use Disorder?
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition
(DSM-5) lists more than 20 separate substance use disorders,7 and a
partial list is provided in Table 1.
Table 1: DSM-5 Substance Use Disorders

Alcohol Use Disorder

Cannabis Use Disorder

Inhalant Use Disorder

Opioid use Disorder

Phencyclidine Use Disorder

Sedative, Hypnotic, or Anxiolytic Use Disorder

Stimulant Use Disorder

Other (or Unknown) Substance Abuse Disorder

Other Hallucinogen Use Disorder
Each of the substance use disorders has its specific features, but the
DSM-5 does point out that all substance use disorders are
characterized by a central theme:
“The essential feature of a substance use disorder is a cluster of
cognitive, behavioral, and physiological symptoms indicating that the
individual continues using the substance despite significant
substance-related problems.”7
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This can be expanded by noting that the person who has a substance
use disorder exhibits the following: 1) has a constant craving for, and
preoccupation with the drug; 2) uses more of the drug than is
necessary to become intoxicated; 3) has a decreased interest in, and
motivation for, normal life activities; 4) develops a tolerance to the
drug so that there is a need for increasingly larger doses and more
frequent use; 5) develops neurological changes that result in craving
and dependency, and; 6) develops withdrawal signs and symptoms if
the drug cannot be obtained.
All of these are further explained by the DSM-5 in the diagnostic
criteria of a substance use disorder. These criteria are divided into five
categories.7
1.
Impaired control:
Impaired control is one of the hallmarks of a substance use
disorder. Someone with a substance use disorder finds that over
time she/he is taking larger amounts of the drug of substance,
despite expressed intentions to cut down or stop use. The life of
a person with a substance use disorder slowly begins to revolve
around drug or substance use, and daily activities become
focused on obtaining, using, and recovering from use. The
individual’s desire for the drug or substance, the craving,
becomes intense and unmanageable.
2.
Social impairment:
The second diagnostic criterion of substance use disorder is
social impairment. Because of impaired control and the priority
on obtaining and using the drug or substance, the substance
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user cannot function at home, at work, or in other areas of
attachment and responsibility. The consequences of the
substance use are often quite serious; i.e., divorce, loss of job
and income, estrangement and isolation from friends and family,
or homelessness. However, despite these consequences, some
substance users cannot or will not change.
3.
Risky use:
A person who has a substance use disorder will continue to use
the drug or substance even if doing so involves significant and
obvious risks to health and life. He/she may do some very risky
things to obtain the drug and get high.
4.
Tolerance:
A substance use disorder is characterized by tolerance.
Tolerance is defined as the need for increasingly higher amounts
of the drug or substance to achieve the desired effect or a
decreased effect from the usual dose or amount. Tolerance is a
complicated phenomenon that involves changes in the central
nervous system (CNS) and the degree of tolerance developed
varies widely from individual to individual
5.
Withdrawal:
Withdrawal is the final diagnostic criterion of substance use
disorders. Withdrawal is defined as specific signs and symptoms
that occur when someone with a substance use disorder abruptly
discontinues or greatly decreases use. The seriousness of
withdrawal depends on the drug or substance that has been
used and the pattern and duration of use.
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Considering these diagnostic criteria, the picture of a substance user
begins to emerge. Drug or substance use is compulsive and causes
intense craving. Acquisition and use can become the sole focus of that
person’s life, and recovery from “highs” can be lengthy and
debilitating. Other areas of life suffer and may be completely
neglected, and the substance abuser may lose his/her home, friends
and family, and job. The health risks and social and personal
consequences of the use are clear, but the substance user feels
compelled to continue and will frequently take ever-increasing risks to
get the drug and get high. The substance user may express a desire to
stop use, but the desire to continue is intense and discontinuation is
discouraged because of withdrawal signs and symptoms - further
reinforcement for continued drug or substance use.
Drugs And Substances With Potential For
A Substance Use Disorder
Certain drugs and substances have strong potential for a substance
use disorder while others do not, and it is not clear why. Drugs such as
cocaine and heroin and substances such as alcohol are intensely
psychoactive - using cruder terms, they provide a powerful high - and
this is certainly one of the reasons for why they are the agents of
choice for people who develop a substance use disorder. However, the
pleasures of intoxication cannot fully explain a substance use disorder,
and research has shown that continued and excessive use of these
harmful agents causes changes in the central nervous system,
changes that both cause and reinforce substance use. Of course, there
are many people who take illicit or prescription drugs and/or drink
alcohol that do not develop a substance use disorder, and these
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individual responses to commonly used drugs and substances further
complicate the efforts at understanding a substance use disorder.
The
mechanism
of
action,
the
signs
and
symptoms
of
acute
intoxication, and the medical consequences of long-term use of
alcohol, amphetamines/stimulants, cocaine, opioids, and sedativehypnotics will be discussed in this section. The mechanisms of action
by which alcohol and these drugs cause a substance use disorder and
the withdrawal syndromes associated with each one will be discussed
in separate sections.
Alcohol
Aside from tobacco, alcohol is the most commonly used psychoactive
drug in our society. There are many types of alcohol, i.e., ethylene
glycol, isopropyl, but the one that is most often consumed for its
intoxicating effects is ethanol.
The exact mechanisms by which ethanol alters consciousness and
causes tolerance and withdrawal are not completely understood. But it
is thought that these effects are due to ethanol changing the activity of
two neurotransmitters and their receptors: a major inhibitory
neurotransmitter called gamma aminobutyric acid (GABA) and a subtype of the major excitatory neurotransmitter glutamate called Nmethyl-d-aspartate (NDMA). Gamma aminobuytric acid acts as an
inhibitory neurotransmitter by increasing intracellular chloride
concentration and decreasing intracellular potassium concentration.
This hyperpolarizes the cells and makes them less able to respond. Nmethyl-d-aspartate increases the movement of calcium and sodium
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across cell membranes, and this increases the cells’ ability to respond
to a stimulus and depolarize.
Ethanol binds to receptors that are associated with GABA and NDMA
receptors on cell membranes in the CNS. This binding increases the
affinity of GABA for GABA receptors and it decreases the affinity of
NDMA for DMA receptors. The result is increased inhibition and
decreased excitation. However, when large amounts of alcohol are
used chronically the body responds by decreasing the number,
sensitivity, and function of GABA receptors and increases the number,
sensitivity, and function of NDMA receptors.11
This effect explains alcohol intoxication as well as tolerance to alcohol,
i.e., the need for larger amounts of alcohol to produce the same
effect; and, it explains withdrawal, the clinical state that is produced
when alcohol intake is stopped. Intoxication is caused by increased
inhibition and decreased excitation in the CNS. Tolerance occurs
because of the effect of chronic alcohol intake on the neurotransmitter
receptors. Furthermore, when the intake of alcohol is stopped,
withdrawal is caused because there are large numbers of highly active
NDMA receptors that can respond to NDMA and a greatly decreased
number of GABA receptors that can respond to GABA.
Alcohol intoxication is characterized primarily by CNS depression and
impairment. Someone who has ingested an excess amount of ethanol
will be drowsy, may be ataxic (incoordination of movement), have
impaired judgment, decreased impulse control, and slurred speech.
Extreme intoxication can cause coma, hypoglycemia, hypotension,
respiratory depression, and death. Long-term use is associated with
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liver disease, heart failure, brain atrophy, gastritis and ulcers, anemia,
and various cancers; it is particularly dangerous to the unborn child.
Amphetamines/stimulants
Amphetamines and stimulants act by directly stimulating the
adrenergic nerve endings. This causes a release into the synapses of
norepinephrine and dopamine, neurotransmitters that stimulate the
peripheral α receptors and β receptors. Acute intoxication causes
anxiety, diaphoresis, hypertension, mydriasis, and tachycardia. More
serious effects such as dysrhythmias, hallucinations, hyperthermia,
myocardial ischemia, myocardial infarction, psychosis, seizures,
stroke, and rhabdomyolysis are possible, as well.
Long-term effects of amphetamine and stimulant use include aortic
and mitral valve regurgitation, cardiomyopathy vasculitis,
cardiomyopathy, pulmonary hypertension, and permanent damage to
the dopaminergic and serotonergic neurons. Amphetamines and
stimulants can be taken as tablets, injected, smoked, or insufflated
(snorted). Probably the most commonly abused amphetamine is
methamphetamine.
Methamphetamine is commercially produced (Desoxyn®), and it has
labeled uses for the treatment of patients who have exogenous obesity
or attention deficit disorder with hyperactivity disorder.
Methamphetamine is lipid-soluble and crosses the blood-brain barrier
more easily than the parent compound amphetamine, making it a
more powerful drug. The great majority of the methamphetamine
involved in substance use is illicitly produced, and this form of the drug
is commonly called crank or speed.
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Cocaine
Cocaine causes the release and blocks the re-uptake of the
neurotransmitters dopamine, epinephrine, norepinephrine, and
serotonin. These actions produce a hyper-adrenergic state, and the
common signs and symptoms of cocaine intoxication are agitation,
anxiety, chest pain, diaphoresis, hypertension, hyperthermia,
mydriasis, tachycardia, and tachypnea. Cocaine also acts to stabilize
the cardiac membrane by an effect on the sodium channels in the
myocardium, and it bocks the movement of potassium through cardiac
membrane ion channels.
Blockade of the sodium channels produces cardiac membrane
stabilization, typically called the quinidine-like effect. This can cause a
prolonged QRS and cardiac dysrhythmias. Blockade of the potassium
ion channels can cause QTc prolongation and cardiac dysrhythmias, as
well.
Cocaine use has also been associated with serious medical problems
affecting essentially every organ system: acute angle-closure
glaucoma, aortic dissection, coronary artery vasospasm, dystonic
reactions, intestinal infarction, myocardial infarction, pneumothorax,
pulmonary infarction, rhabdomyolysis, seizures, stroke, and transient
ischemic attack. Long-term effects of cocaine abuse include
atherosclerosis, cardiomyopathy, endocarditis, malnutrition, and
behavior that can be characterized as virtually identical to personality
disturbances, paranoia, and schizophrenic syndromes.
Cocaine can be ingested, applied to mucous membranes, insufflated,
smoked, or injected. As mentioned previously, there are many well-
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documented cases of dangerous contaminants and adulterants being
added to cocaine, and these can cause significant harm.
Opioids
The opioids are a class of drugs that are derived from chemical
modification of an opiate, an opiate being one of several alkaloids that
are derived directly from the opium poppy. In common practice the
term opioid is the one used for all drugs that have similar structure
and clinical effects including, but not limited to, buprenorphine,
codeine, dextromethorphan, fentanyl, heroin, hydrocodone,
methadone, morphine, oxycodone, and propoxyphene. In the United
States all of these drugs except for heroin are commercially produced
and are commonly prescribed.
In the United States, heroin is classified as a Schedule 1 drug. A
Schedule 1 drug is defined as a drug: 1) with a high potential for
abuse; 2) that has no currently accepted medical use; and, 3) for
which there is a lack of accepted safety for use of the drug while under
medical supervision. Heroin is commercially available in other
countries and is used for treating people who have severe, intractable
pain.
The opioids act by binding to and stimulating opioid receptors in the
brain, spinal cord, and peripheral sites. Opioid receptor stimulation
causes the cells to become hyperpolarized and thus less active and
less able to respond to stimuli. As with alcohol and other drugs
discussed in this module, chronic use of opioids affects the function
and activity of neurotransmitters and their receptors, and this causes
tolerance and the potential for a withdrawal syndrome. The
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therapeutic effects of the opioids are analgesia and an anti-tussive
effect. Constipation, drowsiness, nausea, and vomiting are common
side effects of the opioids.
Opioid intoxication is characterized by ataxia, central nervous system
depression, euphoria, hypotension, miosis, respiratory depression, and
slurred speech. With profound intoxication coma, hypoxic seizures,
hypoxic brain injury, pulmonary edema, and respiratory arrest are
possible. Propoxyphene intoxication can cause myocardium sodium
channel blockade and arrhythmias. Long-term effects of opioid use
include heart valve infections, infectious diseases such as hepatitis B
and C and HIV (human immunodeficiency virus) that occur with
intravenous use, arthritis, collapsed and sclerotic veins, malnutrition,
and a depressed immune system. Opioids can be taken as tablets,
injected, smoked, or insufflated. As mentioned previously, there are
many well-documented cases of dangerous contaminants and
adulterants being added to illicit opioids (typically injectable heroin)
and these can cause significant harm.
Sedative-hypnotics
The sedative-hypnotics are a group of drugs that are used to treat
anxiety and/or agitation (sedatives) or to induce sleep (hypnotics).
There are many drugs that are classified as sedatives or hypnotics, but
the sedative-hypnotics that are most often involved in substance
abuse disorders are the benzodiazepines and the barbiturates.
Table 2A lists the commonly available sedative-hypnotics.
Flunitrazepam is not commercially available in the United States but it
is included here because of its highly publicized status as the date rape
drug, also known as roofies. Midazolam is an injectable benzodiazepine
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that is used for pre-operative sedation. It is seldom a drug of choice
for use but it is included here because it is well known and often used.
The non-benzodiazepine hypnotics (Table 2B) have a similar
mechanism of action as the benzodiazepines.
The barbiturates, listed in Table 3, were at one time the drugs of
choice for treating anxiety/agitation or for inducing sleep, but the
benzodiazepines have been shown to have similar effectiveness for
those purposes and a superior safety profile. The barbiturates are now
used to help induce pre-operative sedation or for the treatment of
seizure disorders. The short-acting barbiturate butalbital is available in
prescription analgesics, compounded in various combinations with
acetaminophen, aspirin, caffeine, and codeine. These drugs are almost
always used and used in tablet or capsule from, but injectable
preparations are available.
Table 2A: Benzodiazepines

Alprazolam (Xanax®)

Chlordiazepoxide (Librium®)

Clonazepam (Klonopin®)

Diazepam (Valium®)

Flunitrazepam (Rohypnol®)

Flurazepam (Dalmane®)

Lorazepam (Ativan®)

Midazolam (Versed®)

Oxazepam (Serax®)

Temazepam (Restoril®)

Triazolam (Halcion®)
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Table 2B: Non-Benzodiazepine Hypnotics

Eszopiclone (Lunesta®)

Zaleplon (Sonata®)

Zolpidem (Ambien®)
Table 3: Barbiturates

Amobarbital (Amytal®)

Butalbital

Pentobarbital (Nembutal®)

Phenobarbital (Luminal®)

Primidone (Mysoline®)

Secobarbital (Seconal®)

Thiopental (Pentothal®)
The mechanism of action differs slightly for the three different
categories, but essentially all these drugs act by binding to specific
receptors that are part of the GABA receptor complex. This binding
increases the affinity of GABA for GABA receptors and, as explained
previously, this increases the inhibitory effect of GABA in the CNS.
Intoxication with a sedative-hypnotic causes ataxia, CNS depression of
varying degrees, from mild drowsiness to coma, hypotension, slurred
speech, and respiratory depression. Death is caused by respiratory
depression. The barbiturates, compared to the benzodiazepines and
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the non-benzodiazepine hypnotics, will produce more severe effects: if
very large amounts are ingested coma and respiratory depression may
last for days.
Compared to alcohol, cocaine, amphetamine/stimulants, and opioids,
the long-term medical consequences of sedative-hypnotic abuse are
relatively mild. Perhaps the biggest risks are the potential for
dependency and development of a substance use disorder. And
although acute intoxication and the long-term medical consequences
of alcohol, cocaine, amphetamines/stimulants, and opioids are much
more severe, the sedative-hypnotic withdrawal from the
benzodiazepines and the barbiturates is comparatively more severe
and can be life threatening.
The Causes Of A Substance Use Disorder
There is no single cause of a substance use disorder, and despite
many years of research there are still no answers to the most pressing
questions about substance use. Why do some people make the use
and acquisition of alcohol, illicit drugs, or certain prescription
medications the sole focus of their lives? Also, why do some people
continue to use substances despite obvious and severe consequences?
Although the term is no longer preferred, another way of asking this
question is, why do some people become addicts while others do not?
There has been a vast amount of effort and research directed towards
uncovering the root cause(s) of substance use disorders. Biological,
psychological, and sociological reasons for these afflictions have all
been advanced, and strong arguments can be made for each of these
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as major contributors to the genesis of, and continued presence of,
substance use disorders.
Current thinking is that there is no single cause of substance use
disorders, and that substance use involves complex neuropsychological phenomena that are behaviorally expressed within a
social context. However, although there has been much research,
more work needs to be done. Much of the published literature involves
animal experiments or a single drug, and it is clear that the true basis
for substance use disorders is not known.
Substance use disorders: the process
A substance use disorder is a multi-factorial process, and the nuances
of how biology, psychology and sociology contribute to it have not
been sorted out. However, although it is not entirely clear what causes
a substance use disorder, there is very strong evidence about how a
substance use disorder develops in, and affects, the neurologic
system.
A substance use disorder involves changes in several areas of the
brain and in neurotransmitters, but perhaps the most important part of
the brain that is affected by substance use is the reward system.
Drugs stimulate areas of the brain that are involved with very
pleasurable survival behaviors such as eating, sex, and bonding. When
these areas of the brain (there are several, but the mesolimbic
pathway is considered to be the most important) are stimulated, they
receive a surge in the neurotransmitter dopamine. Dopamine is a
neurotransmitter that is found in the areas of the brain that control
emotion, motivation, and pleasure, and increases in dopamine levels
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of the CNS have many effects and one of them is the experience of
pleasure.
Cocaine, heroin, etc., stimulate a direct release of dopamine or
prevent its breakdown and, crudely put, the more dopamine the higher
the level of pleasure. Alcohol, and the drugs that are involved in
substance use disorders, cause a higher brain dopamine level than do
natural rewards such as food or sex.
This surge in dopamine and the intensity of the experience - the high is especially strong when it is caused by drugs used and the
information about that experience gets stored and remembered: the
drug is associated with pleasure. However, with succeeding exposures
to these drugs, the dopamine surge become less and less, and the
dopamine levels go lower and lower below normal baseline as less is
produced. There is a reduction in dopamine receptors as well. The
result is that the person who is chemically dependent gets less of a
“high” each time he/she use the drug and he/she feels less happy
when they are not intoxicated, which leads to more drug seeking, and
a vicious cycle because the chemically dependent person has now
developed a tolerance.8
Individuals with an addiction disorder have a term that is called
“chasing the dragon.” It means that there is no high like the first high,
and science is proving that to be correct. There is also evidence that
the faster the increases in dopamine concentration in the brain (which
occurs with early, heavy drug use and with certain drugs such as
cocaine) the stronger the reinforcing effect of the drug. Even worse,
long-term use of addictive drugs produces long-lasting changes in
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brain structure that make the person who has a substance use
disorder susceptible to relapse months and years after successful
rehabilitation and abstinence; a phenomenon that partially explains
the high relapse rate in people who have had a substance use disorder
and they are chemically dependent. Also, these changes in brain
structure make the brain less able to react to the “weaker” pleasure
stimuli such as food, sex, bonding, etc.
However, it has been shown that increases in brain dopamine
concentrations caused by drugs of abuse happen to people who
become addicted and to people who do not, so the short-term increase
in dopamine cannot explain the development of chemical dependency.
It may be that there is a difference in the dopamine circuits between
those who are chemically dependent and those who are not. The
chemically dependent person may have a particularly “weak” circuit
that doesn’t respond to normal pleasurable activities so he/she needs
strong levels of stimulation to feel good, and there is supporting
evidence for this idea in the literature.
It is also possible that people who develop a substance use disorder
have a biological susceptibility to drugs of abuse. Their brains react to
drugs by decreasing the numbers of dopamine receptors and
decreasing the amount of dopamine released, thus inhibiting their
ability to feel pleasure. This may not happen to people who do not
develop a substance use disorder.
Treatment Approaches And Withdrawal
Treatment for substance use disorders is a process as complex as the
disorders themselves. There are many treatment approaches, some
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which have strong supporting evidence in the medical literature and
some that do not. It does seem clear though that early interventions
are more likely to be successful. If someone has had a substance use
disorder for a relatively brief period of time the chances for him/her
successfully discontinuing use are much greater.
However, regardless of the specifics of any approach to treating
substance use disorders the process must involve the following: 1)
stopping the use of alcohol and or the drug; 2) if possible, administer
the patient an equivalent drug that has a more limited potential for
dependency and tolerance; 3) manage the physical signs and
symptoms of withdrawal; and, 4) provide psychiatric and social
support. Treatment for substance use must be a fluid process and be
able to change over time. The patient at times will have a need for
medical support, rehabilitation, and continuing care, and there are a
myriad of personal, social, legal, and medical issues to address.
Withdrawal defined
Discontinuation of alcohol or one of the drugs discussed in this module
will cause withdrawal. Withdrawal is a group of characteristic signs and
symptoms of varying severity, which occur after cessation or reduction
of use of a psychoactive substance. Withdrawal happens when
someone has taken the psychoactive substance in high doses for a
prolonged period of time.9
The intensity and duration of withdrawal depends on many factors. For
some people and for certain drugs the withdrawal process is quite
uncomfortable, but it is self-limiting and poses no serious risk. But for
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certain individuals and with some drugs, the withdrawal process can
be dangerous.
Alcohol withdrawal
The pathophysiology of alcohol withdrawal is not completely
understood, but the primary mechanism is thought to be adaptation
and insensitivity of the CNS to GABA and NDMA.10 In response to
chronic alcohol ingestion and its effects on GABA and NDMA, the body
decreases the number, sensitivity, and function of the GABA receptors
and increases the number, sensitivity, and function of NDMA
receptors.11 When someone who chronically uses alcohol stops
drinking, the stimulation and inhibition respectively of the GABA and
NDMA receptors is removed and the patient experiences an intense
excitatory state which explains, in part, the signs and symptoms of
alcohol withdrawal syndrome.
Alcohol withdrawal syndrome usually starts within six hours or so after
cessation of drinking, but the onset may be delayed for several days.
It is possible for withdrawal to occur even if the patient still has a
relatively high alcohol level.10 The signs and symptoms of alcohol
withdrawal syndrome are primarily cardiac, neurologic, and
gastrointestinal and can be mild to severe. Commonly noted signs and
symptoms include agitation, anxiety, depression, elevated blood
pressure and heart rate, fever, insomnia, nausea, and tremors.10,11
Patients may present with a relatively mild to moderate clinical picture.
However, there are three serious complications of alcohol withdrawal
syndrome that are possible: 1) withdrawal seizures; 2) alcoholic
hallucinations; and, 3) delirium tremens.
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Withdrawal seizures affect approximately 10% of all patients with an
alcohol withdrawal syndrome.11 They typically occur within 12-24 hour
after the last drink is consumed; they are usually single seizures or
several seizures occurring within a short period of time, and they are
self-limiting.10,11
Alcoholic hallucinations (sometimes called alcoholic hallucinosis) are
usually visual, but auditory and tactile hallucinations are possible.
Alcoholic hallucinations are self-limiting and usually resolve within 2448 hours.10 It is important to note that alcoholic hallucinations are a
separate phenomenon from delirium tremens.
Delirium tremens, typically called the DTs, is a specific alcohol
withdrawal syndrome complication. It affects approximately 5% of all
patients who are going through alcohol withdrawal syndrome.10 The
DTs are more likely to occur if the patient 1) has had DTs before, 2)
has been a long-time alcohol abuser, 3) is greater than age 30, 4) is
experiencing alcohol withdrawal and has a high blood alcohol level, 5)
has a concurrent illness, and 6) the onset of alcohol withdrawal is
delayed.10 Delirium tremens produces a clinical picture essentially
identical to mild to moderate alcohol withdrawal syndrome, but the
intensity of the signs and symptoms is much more intense.
Patients who have DTs have severe agitation, confusion and
disorientation, diaphoresis, fluid and electrolyte losses, hallucinations,
fever, hypertension, and tachycardia. Delirium tremens has a mortality
rate of approximately 5%.10 Patients who succumb are those who are
elderly and/or have significant comorbidities.
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Factors that have been correlated with an increased risk of developing
complicated alcohol withdrawal include:12

The use of alcohol within the past 30 days or a measurable blood
alcohol level

Previous episodes of alcohol withdrawal

A history of alcohol withdrawal seizures

A history of DTs

A history of blackouts caused by alcohol ingestion

Prior admission to an alcohol rehabilitation program

The use of alcohol and a CNS depressant drug such as a
benzodiazepine within the past 90 days

The use of alcohol and a substance of abuse within the past 90
days

A blood alcohol level > 200 mg/dL

Evidence of autonomic hyperactivity, i.e., diaphoresis,
tachycardia.
Opioid withdrawal
The pathophysiology of opioid withdrawal is incompletely understood,
but it is thought to be similar to other withdrawal syndromes, i.e.,
continued excessive use of an opioid causes changes to
neurotransmitters and their receptors; in the case of opioids, GABA
and noradrenaline.13 When the opioid is discontinued the changes in
circulating levels of neurotransmitters and the altered function of the
receptors are no longer inhibited by the opioid, resulting in the clinical
picture of withdrawal.
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Opioid withdrawal begins 6-12 hours after last use and the severity of
the signs and symptoms will peak within 24 to 48 hours.14 The clinical
course of opioid withdrawal syndrome often follows the progression
outlined below, starting from the last time the opioid was used.14

6-12 hours: Diaphoresis, lacrimation, mydriasis, rhinorrhea,
yawning

12-18 hours: Anxiety, insomnia, irritability, nausea

18-24 hours: Abdominal cramps, anorexia, piloerection,
restlessness, tremor

> 24 hours: Chills, diarrhea, hyperthermia, muscle spasms,
severe insomnia, tachycardia
The severity of opioid withdrawal can be evaluated by using the
Clinical Opiate Withdrawal Scale (COWS).14 The use of COWS can help
clinicians make an objective assessment of the severity of withdrawal
and it also involves patient input.
Table 4: Clinical Opiate Withdrawal Scale
1. Resting heart rate:
a. 0 - 80 beats/min or below
b. 1 - 81-100 beats/min
c. 2 - 101-120 beats/min
d. 4 - > 120 beats/min
2. Sweating over the past 30 minutes, not caused by ambient
temperature or physical activity:
a. 0 - No chills or flushing
b. 1 - Subjective reporting of chills or flushing
c. 2 - Observed flushing or moistness on the face
d. 3 – Diaphoresis on the brow or face
e. 4 – Sweat streaming from the face
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3. Restlessness:
a. 0 - able to sit still
b. 1 – Reports difficulty sitting still, but can do so
c. 3 – Frequent shifting or extraneous movements of
arms/legs
4. GI upset within past 30 minutes:
a. 0 - No GI symptoms
b. 1 - Stomach cramps
c. 2 - Nausea or loose stools
d. 3 - Vomiting or diarrhea
e. 5 - Multiple episodes of diarrhea or vomiting
5. Anxiety or irritability:
a. 0 - None
b. 1 - Patient reports increasing anxiousness or irritability
c. 2 - Patient is obviously anxious or irritable
d. 4 - Patient is anxious/irritable and difficult to assess
6. Bone or joint aches:
a. 0 - absent
b. 1 - Mild, diffuse discomfort
c. 2 - Patient reports severe, diffuse aching of muscles, joints
d. 4. - Patient is rubbing joints or muscles and cannot sit still
7. Tremor: observation of outstretched arms
a. 0 - No tremor
b. 1 - Tremor can be felt but not observed
c. 2 - Slight tremor observed
d. 4 - Gross tremor or muscle twitching
8. Yawning:
a. 0 - No yawning
b. 1 - Yawning once or twice during assessment
c. 2 - Yawning three or more times during assessment
d. 4 - Yawning several times a minute
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9. Pupils size:
a. 0 - Pupils normal sized for room light or pinned
b. 1 - Pupils possibly (?) than normal size for room light
c. 2 - Pupils moderately dilated
d. 4 - Pupils are dilated to the point that only the rim of the
iris is visible
10. Runny nose or tearing: Not accounted for by allergy or cold:
a. 0 - Not present
b. 1 - Nasal stuffiness or unusually moist eyes
c. 2 - Nose running or tearing
d. 4 - Nose constantly running or tears streaming down
cheeks
11. Gooseflesh skin:
a. 0 - Absent
b. 3 - Skin piloerection can be felt or hair standing up on arms
c. 5 - Prominent piloerection
A score of 5-12 is considered mild; 13-24 is moderate; 25-36 is
moderately severe, and; > 36 is severe.
Benzodiazepine withdrawal
The benzodiazepines are comparatively old drugs; they are commonly
prescribed and commonly abused, and the most of the medical
literature regarding sedative-hypnotic withdrawal has been about
benzodiazepines. Benzodiazepine intoxication is typically mild to
moderate in severity but paradoxically, withdrawal from
benzodiazepines can produce severe signs and symptoms and can be
life-threatening.15
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As with other alcohol and the other drugs discussed in this module,
chronic use of a benzodiazepine changes the affinity of receptors for a
specific neurotransmitter (GABA in the case of benzodiazpines),
causing a compensatory change in the number, function, and activity
of these receptors. When someone who has been chronically using or
abusing a benzodiazepine stops taking the drug, the inhibitory effect of
GABA is removed, causing excess CNS excitation.
Withdrawal from benzodiazepines occurs when use of the drug is
abruptly stopped or tapering of the drug is done too quickly,15 but mild
withdrawal can occur even if the drug is slowly tapered.16 The onset of
signs and symptoms depends on the half-life of the particular
benzodiazepine. The withdrawal syndrome may begin within 24-48
hours after cessation of the drug, but if the benzodiazepine has a long
half-life (> 24 hours) it may be several weeks before signs and
symptoms are observed.15,17 The severity and duration of the
withdrawal syndrome appears to be related to the duration of
use/abuse and how quickly the drug was stopped. However, severe
withdrawal reactions can occur even after short-term use at low
doses.17
The benzodiazepine withdrawal syndrome is characterized by agitation,
anxiety, dysphoria, insomnia, irritability, muscle tremors, and
restlessness. Other, less common signs and symptoms include
abnormal sensory perceptions, delirium, parathesias, tinnitus,
psychotic symptoms, persistent headaches, myoclonic jerks, and
seizures.16,18 The prevalence of seizures has been estimated to be
2.5%-8%.16 They are usually self-limiting, but deaths have been
reported in association with seizures caused by benzodiazepines.19
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The benzodiazepines that have short (< 1 hours) half-lives such as
diazepam and lorazepam are more likely to cause withdrawal
seizures,17,20 and seizures are more likely to occur during withdrawal if
the prescribed dose is high and the duration of use is long.17,20 The risk
of withdrawal seizures is also increased by other factors that are
common to the population of substance abusers such a concomitant
alcohol use.17
Amphetamine/stimulant withdrawal
Compared to the amount of literature published about alcohol
withdrawal and opioid withdrawal there is little data about
amphetamine/stimulant withdrawal and much of the research has
been on methamphetamine. The medical effects of methamphetamine
withdrawal appear to be relatively benign and well tolerated, and
several sources identify an acute phase and a subacute phase.21,22
The acute phase lasts approximately 7 to 10 days and the signs and
symptoms may include diaphoresis, headache, muscle and joint pain,
and mild, self-limiting gastrointestinal distress.21 Psychological effects
during the acute phase include anxiety, depression, an increased
appetite and an increased need for sleep, and craving for the drug.
Psychosis during the acute phase of withdrawal is relatively common.
Patients who have a long history of methamphetamine use, have more
severe depressive symptoms, and are significantly older than other
users, are more likely to have persistent and severe psychotic
symptoms.23
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The subacute phase lasts approximately two weeks and is
characterized by a gradual decrease in the number and intensity of
symptoms.21 Craving may persist for up to five weeks.22
Cocaine withdrawal
Cocaine withdrawal rarely causes serious medical harm or
consequences, and most patients simply have mild, self-limiting signs
and symptoms such as chills, non-specific musculo-skeletal pain, and
tremor.24 However, the psychological effects of cocaine withdrawal can
be intense and debilitating. Patients may experience significant levels
of anxiety, depression, fatigue, inability to concentrate, insomnia, and
intense drug cravings.24 The duration of cocaine withdrawal is typically
one to two weeks.24
Treatment For A Substance Use Disorder
Amphetamine/stimulant use and withdrawal and cocaine use and
withdrawal are considered to be relatively mild and self-limiting and
treated with symptomatic/supportive care.22, 24-26.
Benzodiazepine use and withdrawal is treated by slowly tapering the
use of the drug, administering a long-acting benzodiazepine, and
providing symptomatic/supportive care.15,16 Antihistamines, antipsychotics, beta-blockers, selective serotonin reuptake inhibitors, and
tricyclic anti-depressants have been used to treat benzodiazepine
withdrawal, but they have not been shown to be superior to
benzodiazepines.15,16 There has been some evidence supporting the
use of carbamazepine to treat benzodiazepine withdrawal, but a review
considered the data for its use for this purpose insufficient.27 The
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optimum rate for tapering has not been determined and it may take
weeks to years to successfully withdraw a patient from a
benzodiazepine.28
Treatment of alcohol use and withdrawal has been well studied. The
basic approach is to: 1) make sure the patient is undergoing alcohol
withdrawal by ruling out alternative diagnoses, and; 2) provide
symptomatic/supportive care.10 Symptomatic/supportive care should
consist of frequent assessments, intravenous hydration and nutritional
support, the use of benzodiazepines to control agitation,10 and this
approach is appropriate for all patients who are undergoing alcohol
withdrawal. Patients in severe withdrawal and having a serious
complication such as DTs may need sedation with a long-acting
barbiturate, such as phenobarbital, or a more powerful sedation with
propofol.10
Assessment
One of the most widely used tools for assessing the severity of alcohol
withdrawal is the Clinical Institute Withdrawal Assessment for alcohol
(CIWA).12 The CIWA scale measures 10 symptoms: Agitation, anxiety,
auditory disturbances, clouding of sensorium, headache,
nausea/vomiting, paroxysmal sweats, tactile disturbances, tremor, and
visual disturbances.
The presence of symptoms in the CIWA is scored on a scale of 0-7,
and the total score is used to determine the severity of withdrawal,
i.e., a score of 8-15 indicates the patient is in moderate withdrawal. If
the patient is determined to be in severe withdrawal and needs
intravenous benzodiazepines, an assessment with the CIWA scale may
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be needed every 10-15 minutes.10 If the patient is unable to answer
questions, i.e., he/she is incoherent or endotracheally intubated,
another assessment tool will need to be used.
Intravenous hydration/nutritional support
Careful attention should be given to intravenous (IV) hydration as
patients undergoing alcohol withdrawal are often dehydrated. The IV
fluids provided to patients should contain glucose, supplemental
thiamine, and multivitamins that contain folate.10 Serum levels of
magnesium, phosphate, and potassium should be measured and
replenishment given as needed.
Benzodiazepines
Benzodiazepines are the cornerstone of treating agitation in patients
who are in alcohol withdrawal.10 Many authorities recommend a
symptom-triggered approach in which benzodiazepines are given
based on the result of the CIWA assessment.10 Benzodiazepines such
as diazepam that have a long half-life are preferred, but
chlodiazepoxide and lorazepam can be used, as well. The patient’s
liver function should be evaluated prior to use as compromised hepatic
function could cause decreased metabolism and clearance of a
benzodiazepine, resulting in prolonged effects.
The treatment of opioid use and withdrawal is also well studied and
the treatment approach is relatively standardized. Use of the opioid
should be stopped. A long-acting drug such as methadone that is
pharmacologically similar to the used opioid should be given, and
symptomatic/supportive care should be offered.29
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The pharmacological treatment of opioid use and withdrawal typically
involves three drugs: methadone, buprenorphine/naloxone, and
clonidine. Methadone is the most commonly used drug for the
treatment of opioid withdrawal. It is a longer-acting opioid agonist and
it produces less CNS depression and euphoria than most opioids. The
drug is given as a tablet or oral solution several times a day, and the
amount of time a patient will need to take methadone is highly
variable. Buprenorphine is a partial opioid agonist that can be used to
treat opioid withdrawal.30 It is often combined with naloxone in the
form of Suboxone® in order to discourage abuse. Clonidine is a
centrally acting alpha-agonist that decreases sympathetic outflow. This
mechanism of action makes it useful for treating the signs and
symptoms of opioid withdrawal.30
Anxiolytics and hypnotics can also be used for symptomatic care.
Long-acting opioid antagonists such as naltrexone have been used to
treat opioid use and withdrawal but without a significant degree of
success.30
Psychological treatment
There is a vast and bewildering array of psychological approaches for
treating chemical dependency, and given the diverse multitude of
treatments, it is not surprising that there is no consensus as to what is
the “best” psychological approach for treating chemical dependency.
Also, there are many methods that are widely used that have little
supporting scientific evidence.
Add to the above the fact that research has indicated that many of the
therapeutic approaches have similar success rates and the selection of
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treatment becomes confusing. However, there are common aspects of
successful treatments. The best ones are evidence-based treatments,
and where the practitioners have received extensive training. For
example, there is an organization of physicians who specialize in
treating chemical dependency, the American Society of Addiction
Medicine.
But although there are many ways to address the psychological needs
of the chemically dependent patient, behavioral therapies are most
often used. Behavioral therapies are a group of approaches
characterized by a concern with the patient’s behavior. The therapist
focuses not on past events that may have led to chemical dependency,
but on what is currently occurring in the patient’s life. There are
different behavioral therapies. Cognitive behavioral therapy has been
proven to work, has been thoroughly tested and there is empirical
evidence for its success.
Cognitive behavioral therapy
Cognitive behavioral therapy (CBT) is grounded in social learning
theories and operant conditioning. In this process, the patient
identifies feelings, thoughts, and situations that are associated with
using a substance. The patient sees the thinking – the distorted,
inaccurate, maladaptive thinking – that is the underpinning of negative
emotions that lead to his/her chemical dependency behaviors, and the
therapist helps him/her to replace these with realistic, life-affirming
beliefs. Thus, cognitive behavioral therapy has two parts. The first is a
functional analysis, and the second is skills training. It provides the
chemically dependent patient with motivation for abstinence, teaches
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coping skills, changes reinforcing contingencies, and trains
interpersonal skills that allow the patient to build a support network.
The treatment is a one-on-one encounter with a trained therapist and
12-16 weekly sessions are typically scheduled. It is done on an
outpatient basis (typically) because chemical dependency is intimately
connected with the circumstances of the patient’s life, and this gives
the patient an immediate chance to try new coping skills and get
immediate feedback on their effectiveness. Cognitive behavioral
therapy can be successfully combined with pharmacological treatment
and group, family, and/or couples therapy. It is unique in that it
provides a functional analysis of chemical dependency and concrete
coping skills are taught and practiced during sessions.30
Of course, cognitive behavioral therapy is not the only way to address
the psychological and emotional concerns of the patient with chemical
dependency. Contingency management may be valuable. In this
technique, patients receive rewards for specific behavioral goals, and
there is a lot of very good empirical support for its effectiveness.
However, it should also be noted that there is evidence that the effects
tend to lessen when the contingencies are removed, and that this
approach involves a lot of time and money.
Motivational interviewing is a focused, goal-directed technique that
helps patients explore and resolve ambivalence and helps the patient
towards an acceptable goal. It has been successfully used in treating
chemical dependency on alcohol and research has shown significant
effects, which are very durable. The therapist tries to understand the
patient’s frame of reference, expresses acceptance and affirmation,
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and reinforces the patient’s own concerns, desires, and intentions for
change. Finally, couples and family therapy can be used.
There is much research that indicates these psychological treatments
can be effective in adult and adolescent patients with chemical
dependency.
Nursing Care Of The Chemically Dependent Patient
Nursing care of the patient who is chemically dependent is complex.
Nurses may encounter these patients during acute intoxication, the
withdrawal phase, or during the process of rehabilitation and the
patient’s ongoing attempts to maintain a drug-free state. During these
specific periods, the goals of nursing care will be very different and the
needs of the patient will be very different, so it is difficult to provide a
“one size fits all” approach.
This problem is exacerbated by the fact that nurses often receive little
information about the nursing care of the patient with chemical
dependency during their formal education. There is almost nothing in
the nursing literature on the topic, and as the field of addiction
medicine is relatively new, standards of care are still being formed.
Also, nurses – and other health care personnel – also frequently report
that they do not like caring for the patient with chemical dependency,
and they have negative attitudes towards them. This is not surprising.
The typical heath care paradigm is that the patient seeks help for a
health problem that is out of his/her control and is willing to cooperate
willingly with the recommendations of caregivers. However, many
patients with chemical dependency do not fit this paradigm: quite the
opposite. As a result, nurses caring for them experience impatience,
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resentment, anger, and the feeling that other patients with
“legitimate” health care concerns are being neglected.
Chemical dependency carries a large negative stigma in our society,
and many nurses feel that the patient with chemical dependency is
simply a “bad person.” Nurses often wonder: why can’t they just stop?
The solution is education. Nurses must be taught that chemical
dependency is a chronic disease, and that the health issues of these
patients are legitimate, albeit at times confusing and unfamiliar.
Nurses need specific information about drugs and treatments. They
must familiarize themselves with specific nursing diagnoses (i.e.,
ineffective health maintenance, anxiety, risk for injury, etc.) that will
be used when caring for these patients. In addition, nurses must also
cultivate the following characteristics that have been found to be
important for successful care of someone with a chemical dependency.

Hope and optimism:
Given the seemingly self-inflicted nature of chemical dependency
and the high relapse rate, it can be a challenge to remain
hopeful and optimistic, but these attitudes are essential.

A non-judgmental attitude:
It is very easy to form judgments about the patient with
chemical dependency, to view them as weak or lacking in morals
and/or self-control.
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
A low need to control the patient.

The ability to engage the patient, but still detach.

Patience and tolerance:
Chemical dependency is a chronic disease and relapses are very
common.

Flexibility.

Recognize that people with chemical dependency often have cooccurring psychiatric disorders that must be treated.
Summary
A substance use disorder involves a wide variety of legal and illicit
substances but the essential feature of a substance use disorder is a
cluster of cognitive, behavioral, and physiological symptoms indicating
that the individual continues using the substance despite significant
substance-related problems. In simpler terms, the person who has a
substance use disorder will continue to acquire and use alcohol or
drugs despite very serious consequences. This is further illustrated by
the diagnostic criteria of a substance use disorder, i.e., the person who
has a substance use disorder has impaired control, exhibits risky
behavior regarding acquisition and use, and his/her substance abuse
disorder and its associated behaviors causes social impairment.
The causes of substance abuse disorder are many and varied, but it is
believed that one of the primary effects of continued use of alcohol or
drugs is a significant increase and/or decrease in the activity and
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function of inhibitory and excitatory neurotransmitters. This effect
produces tolerance and withdrawal. The CNS responds by needing
larger amounts of alcohol or drugs to produce the desired effect
(tolerance), and if the alcohol or drug is discontinued the inhibitory
effect of the drug or alcohol is removed and the excitatory effect of
these neurotransmitters is greatly increased, resulting in withdrawal.
Treatment of substance use requires specific interventions and longterm commitment. It involves cessation of alcohol or the drug,
identification and treatment of complications of withdrawal, and, the
use of specific drugs that can help to decrease craving and treat the
signs and symptoms of withdrawal.
Withdrawal is most often a benign and self-limiting process, albeit
physically and psychologically quite uncomfortable. Follow-up care that
involves social and psychological support is crucial after the withdrawal
period is complete. A substance use disorder certainly has a physical
basis but there are emotional and psychological aspects that cause and
reinforce substance use that must be addressed.
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1.
The term dependency used in relation to substance use
means:
a. an intense psychological craving for alcohol or a drug
b. physical need for alcohol or a drug that develops over time.
c. the need for increasing amounts of alcohol or a drug over time.
d. a physical resistance to withdrawal signs and symptoms.
2.
One of the central themes of a substance use disorder
is:
a. continued use despite significant substance related problems
b. excessive use of alcohol or an illicit drug.
c. a pattern of use of alcohol or a drug that causes medical harm.
d. alcohol or drug use that has social consequences.
3.
One of the diagnostic criteria for substance use disorder is:
a. Self-admitted addiction to alcohol or a drug.
b. Excessive use of alcohol or a drug for > five years.
c. Impaired control relating to use of alcohol or a drug.
d. Use of an illicit drug
4.
One of the diagnostic criteria for substance use disorder is:
a. Refusal by the patient to accept professional help.
b. Alcohol or drug use that causes medical harm.
c. Alcohol or drug use that waxes and wanes.
d. Tolerance to alcohol or a drug.
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5.
A substance use disorder is thought to be caused and
reinforced in part by:
a. Changes in neurotransmitters and their receptors.
b. Decreased function of the endocrine system.
c. Changes in microcirculation.
d. Undiagnosed immune system dysfunction.
6.
Withdrawal in most patients who have a substance use
disorder:
a. causes significant morbidity and mortality
b. is relatively benign and self-limiting
c. is less serious if the duration of use has been many years.
d. typically affects males more than females.
7.
One of the serious complications of alcohol withdrawal is:
a. Acute renal failure
b. Delirium tremens
c. Rhabdomyolysis
d. Cardiac arrhythmias
8.
Withdrawal from benzodiazepines can cause:
a. Seizures
b. Rhabdomyolysis
c. Hepatic damage
d. Pulmonary edema
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9. Which of the following is the drug of choice for treating
alcohol withdrawal?
a. Antipsychotics
b. Benzodiazepines
c. Selective serotonin reuptake inhibitors
d. Barbiturates
10. Which of the following drugs are often used to treat opioid
withdrawal?
a. Benzodiazepines, clonidine, and methadone
b. Antipsychotics, barbiturates, and selective serotonin reuptake
inhibitors
c. Non-opioid analgesics, propofol, and tricyclic anti-depressants
d. Buprenorphine/naloxone, clonidine, and methadone
Correct Answers:
1.
B
2.
A
3.
C
4.
D
5.
A
6.
B
7.
B
8.
A
9.
B
10. D
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References Section
The reference section of in-text citations include published works
intended as helpful material for further reading. Unpublished works
and personal communications are not included in this section, although
may appear within the study text.
1.
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on illegal drugs: 2000-2006. February 2014. Retrieved August 29,
2014 from
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2.
Office of National Drug Control Policy. Consequences of illicit drug
use in America. April, 2014. Retrieved August 29, 2014 from
http://www.whitehouse.gov/sites/default/files/ondcp/Fact_Sheets/
consequences_of_illicit_drug_use_-_fact_sheet_april_2014.pdf.
3.
Thompson W. Alcoholism. eMedicine. July 14, 2104. Retrieved
August 29, 2014 from
http://emedicine.medscape.com/article/285913-overview.
4.
National Institute on Alcohol Abuse and Alcoholism. Alcohol use
disorder. Retrieved August 29, 2014 from
http://niaaa.nih.gov/alcohol-health/overview-alcoholconsumption/alcohol-use-disorders.
5.
National Cancer Institute. Tobacco statistics snapshot. Retrieved
August 29, 2014 from
http://www.cancer.gov/cancertopics/tobacco/statisticssnapshot.
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6.
Food and Drug Administration. Glossary of drug terms. Retrieved
August 30, 2014 from
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American Psychiatric Association. Diagnostic and Statistical Manual
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World Health Organization. Management of substance abuse.
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10. Hoffman RS, Weinhouse GL. Management of moderate to severe
alcohol withdrawal syndromes. UpToDate. September 11, 2012.
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11. Stehman CR, Mycyk MB. A rational approach to treatment of
alcohol withdrawal in the ED. American Journal of Emergency
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12. Maldonado JR, Sher Y, Ashouri JF, Hills-Evans K, Swendsen H,
Lolak S, et al. The “Prediction of Alcohol Withdrawal Severity
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new scale for the prediction of complicated alcohol withdrawal
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13. Ashish K. Rehni, Amteshwar S. Jaggi and Nirmal Singh. Opioid
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