chemical dependency - nursece4less.com · web viewboth of the former terms are still in common use...

SUBSTANCE ABUSE 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 abuse and its prevention. There is high risk of substance abuse among certain groups in society. Although substance abuse is typically thought of as illicit drug use or chronic alcohol abuse, commonly occurring within marginalized, crime ridden sectors of society, in reality, substance abuse is a wide-spread societal problem involving alcohol, tobacco, prescription and illicit drugs, among many individuals indistinguishable from the general population. Substance abuse 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 Director & Planners:William A. Cook, PhD, Director; Douglas Lawrence, MS, Webmaster;

Susan DePasquale, CGRN, MSN, FPMHNP-BC, Lead Nurse Planner

Accreditation 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.

Credit Designation:This continuing education (CE) activity is credited for 3.5 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity.

Course Author & Planner Disclosure Policy Statements:It is the policy of NurseCe4Less.com to ensure objectivity, transparency, and best practice for all continuing nursing education (CNE) activities. All authors and course planners participating in the planning or implementation of a CNE activity are expected to disclose to course participants any relevant conflict of interest that may arise.

Statement of 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 substance abuse and the recommended steps to support patient recovery. Learning Objectives:


1. Identify the diagnostic criteria of a substance abuse disorder. 2. Identify a mechanism of action by which substance abuse occurs. 3. Identify behaviors commonly associated with a substance abuse disorder.4. Identify signs/symptoms of substance abuse withdrawal. 5. Identify drugs used for treating substance abuse withdrawal.

Target Audience:Advanced Practice Registered Nurses, Registered Nurses, Licensed Practical Nurses, and Associates

Course Author & Director Disclosures: Dana Bartlett, RN, MA, MSN, William S. Cook, PhD,

Douglas Lawrence, MS, Susan DePasquale, CGRN, 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, CGRN, MSN, FPMHNP-BC.

Release Date: 9/8/2014 Termination Date: 9/8/2017

Please take time to complete the self-assessment Knowledge Questions before reading the article. Opportunity to self-assess knowledge learned will

be provided at the end of the course.

1. The term dependency used in relation to substance abuse 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 abuse 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 abuse 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 abuse 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.

5. Substance abuse 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 abuse 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

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. Anti-psychotics, barbiturates, and selective serotonin reuptake inhibitors c. Non-opioid analgesics, propofol, and tri-cyclic anti-depressants d. Buprenorphine/naloxone, clonidine, and methadone

INTRODUCTION

Substance abuse 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

Substance abuse is typically thought of as illicit drug use or chronic abuse of alcohol, and it is often assumed that substance abuse is primarily an issue for those living on or near the fringe of society and a problem characterized by aberrant behavior and crime. Yet substance abuse 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 abusers are often indistinguishable from the general population. This module will discuss substance abuse involving cocaine, opioids, amphetamines/stimulants, sedative/hypnotics, and alcohol.


Note that this module uses the terms substance abuse and substance abuse disorder, not addiction or addict. Both of the former terms are still 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 is also frequently used when referring to substance abuse. 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 substance abuse.

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 there are many well-documented cases of dangerous contaminants and adulterants being added to them. For practical purposes, when discussing substance abuse disorders, alcohol is considered a substance and all of the rest are considered drugs.

WHAT IS SUBSTANCE ABUSE? 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 Abuse Disorders

Each of the substance abuse disorders has its specific features, but the DSM-5 does point out that all substance abuse 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

This can be expanded by noting that the person who has a substance abuse 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.


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

http://dsm.psychiatryonline.org.online.uchc.edu/content.aspx?bookid=556&sectionid=41101782&resultclick=1#103440850



All of these are further explained by the DSM-5 in the diagnostic criteria of substance abuse. These criteria are divided into five categories.7

1. Impaired control: Impaired control is one of the hallmarks of a substance abuse disorder. Someone with a substance abuse 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 abuse 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 abuse disorder is social impairment. Because of impaired control and the priority on obtaining and using the drug or substance, the substance abuser cannot function at home, at work, or in other areas of attachment and responsibility. The consequences of the substance abuse are often quite serious; e.g., divorce, loss of job and income, estrangement and isolation from friends and family, or homelessness. However, despite these consequences, some substance abusers cannot or will not change.

3. Risky use:

A person who has a substance abuse 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 abuse 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 abuse disorders. Withdrawal is defined as specific signs and symptoms that occur when someone with a substance abuse 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.

Considering these diagnostic criteria, the picture of a substance abuser 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 abuse are clear, but the substance abuser feels compelled to continue and will frequently take ever-increasing risks to get the drug and get high. The substance abuser 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 abuse.


DRUGS AND SUBSTANCES THAT ARE ABUSED

Certain drugs and substances have strong potential for abuse 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 abuse disorder. However, the pleasures of intoxication cannot fully explain substance abuse, 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 abuse. Of course, there are many people who take illicit or prescription drugs and/or drink alcohol that do not develop a substance abuse disorder, and these individual responses to commonly abused drugs and substances further complicate the efforts at understanding substance abuse. 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 sedative-hypnotics will be discussed in this section. The mechanisms of action by which alcohol and these drugs cause substance abuse disorder and the withdrawal syndromes associated with each one will be discussed in separate sections. Alcohol

Aside from tobacco, alcohol is the most commonly abused psychoactive drug in our society. There are many types of alcohol, e.g., 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 sub-type of the major excitatory neurotransmitter glutamate called N-methyl-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. N-methyl-d-aspartate increases the movement of calcium and sodium 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 abused 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, e.g., 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 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 abuse is illicitly produced, and this form of the drug is commonly called crank or speed.

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 abuse 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-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 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 abuse 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 that is used for pre-operative sedation. It is seldom a drug of choice for abuse 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 abused 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®)

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 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 substance abuse. 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 SUBSTANCE ABUSE

There is no single cause of substance abuse, and despite many years of research there are still no answers to the most pressing questions about substance abuse. 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 abuse 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 abuse disorders. Biological, psychological, and sociological reasons for these afflictions have all


been advanced, and strong arguments can be made for each of these as major contributors to the genesis of, and continued presence of, substance abuse disorders. Current thinking is that there is no single cause of substance abuse disorders, and that substance abuse involves complex neuro-psychological 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 abuse disorders is not known.

Substance abuse: the process

Substance abuse 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 substance abuse, there is very strong evidence about how substance abuse develops in, and affects, the neurologic system.

Substance abuse 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 abuse is the reward system. Drugs of abuse 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 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 abuse 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 of abuse 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

Addicts 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 brain structure that make the person who has a substance abuse 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 abuse 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 she/he 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 abuse 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 abuse disorder.

TREATMENT APPROACHES AND WITHDRAWAL

Treatment for substance abuse disorders is a process as complex as the disorders themselves. There are many treatment approaches, some 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 abuse 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 abuse 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 abuse 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 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 abuses 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.

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 24-48 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 co-morbidities.

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, e.g., 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.

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 Scale1. Resting heart rate:

a. 0 - 80 beats/min or belowb. 1 - 81-100 beats/minc. 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 flushingb. 1 - Subjective reporting of chills or flushingc. 2 - Observed flushing or moistness on the faced. 3 – Diaphoresis on the brow or face

e. 4 – Sweat streaming from the face 3. Restlessness:

a. 0 - able to sit stillb. 1 – Reports difficulty sitting still, but can do soc. 3 – Frequent shifting or extraneous movements of arms/legs

4. GI upset within past 30 minutes:a. 0 - No GI symptomsb. 1 - Stomach crampsc. 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 - absentb. 1 - Mild, diffuse discomfort c. 2 - Patient reports severe, diffuse aching of muscles, jointsd. 4. - Patient is rubbing joints or muscles and cannot sit still

7. Tremor: observation of outstretched armsa. 0 - No tremorb. 1 - Tremor can be felt but not observedc. 2 - Slight tremor observed d. 4 - Gross tremor or muscle twitching

8. Yawning: a. 0 - No yawningb. 1 - Yawning once or twice during assessmentc. 2 - Yawning three or more times during assessment d. 4 - Yawning several times a minute

9. Pupils size:a. 0 - Pupils normal sized for room light or pinned b. 1 - Pupils possibly (?) than normal size for room lightc. 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 presentb. 1 - Nasal stuffiness or unusually moist eyesc. 2 - Nose running or tearingd. 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

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 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 sub-acute 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

The sub-acute phase lasts approximately to 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 SUBSTANCE ABUSE

Amphetamine/stimulant abuse and withdrawal and cocaine abuse and withdrawal are considered to be relatively mild and self-limiting and treated with symptomatic/supportive care.22, 24-26.


Benzodiazepine abuse 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, anti-psychotics, 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 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 abuse 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, e.g., 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 be needed every 10-15 minutes.10 If the patient is unable to answer questions, e.g., 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 abuse 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/abused opioid should be given, and symptomatic/supportive care should be offered.29

The pharmacological treatment of opioid abuse 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 abuse 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 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 the substance of abuse. 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 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, 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, 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 (e.g., 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.

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 co-occurring psychiatric disorders that must be treated.

SUMMARY

Substance abuse 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 abuse 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 abuse disorder, e.g., the person who has a substance abuse 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 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 abuse requires specific interventions and long-term 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. Substance abuse disorder certainly has a physical basis but there are emotional and psychological aspects that cause and reinforce substance abuse that must be addressed.

Please take time to help NurseCe4Less.com course planners evaluate the nursing knowledge needs met by completing the self-assessment

Knowledge Questions after reading the article, and providing feedback in


the course evaluation.

Correct Answers, pg. 46

1. The term dependency used in relation to substance abuse 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 abuse 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 abuse 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 abuse 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.


5. Substance abuse 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 abuse 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


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. Anti-psychotics, barbiturates, and selective serotonin reuptake inhibitors c. Non-opioid analgesics, propofol, and tri-cyclic anti-depressants d. Buprenorphine/naloxone, clonidine, and methadone

CORRECT ANSWERS:

1. B2. A3. C4. D5. A6. B7. B8. A9. B10. D


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7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA; American Psychiatric Publishing: 2013.

8. Hoffman J, Froemke S, ed. Addiction: Why Can’t They Just Stop? Emmaus, PA: Rodale; 2007.

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http://www.ncbi.nlm.nih.gov/pubmed?term=Donoghue%20J%5BAuthor%5D&cauthor=true&cauthor_uid=19062773

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http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed?term=Pennay%20AE%5BAuthor%5D&cauthor=true&cauthor_uid=21355922

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chemical dependency - nursece4less.com · web viewboth of the former terms are still in common use...

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