DOCSLIB.ORG

Cocaine Use Disorder

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

COCAINE USE DISORDER ABSTRACT Cocaine addiction is a serious public health problem. Millions of Americans regularly use cocaine, and some develop a substance use disorder. Cocaine is generally not ingested, but toxicity and death from gastrointestinal absorption has been known to occur. Medications that have been used as substitution therapy for the treatment of a cocaine use disorder include amphetamine, bupropion, methylphenidate, and modafinil. While pharmacological interventions can be effective, a recent review of pharmacological therapy for cocaine use indicates that psycho-social efforts are more consistent over medication as a treatment option. Introduction Cocaine is an illicit, addictive drug that is widely used. Cocaine addiction is a serious public health problem that burdens the healthcare system and that can be destructive to individual lives. It is impossible to know with certainty the extent of use but data from public health surveys, morbidity and mortality reports, and healthcare facilities show that there are millions of Americans who regularly take cocaine. Cocaine intoxication is a common cause for emergency room visits, and it is one drug that is most often involved in fatal overdoses. Some cocaine users take the drug occasionally and sporadically but as with every illicit drug there is a percentage of people who develop a substance use disorder. Treatment of a cocaine use disorder involves psycho-social interventions, pharmacotherapy, or a combination of the two. 1 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Pharmacology of Cocaine Cocaine is an alkaloid derived from the Erthroxylum coca plant, a plant that is indigenous to South America and several other parts of the world, and is cultivated elsewhere. Chemical processing of the plant yields the alkaloid in the form of a cocaine powder that can be injected, insufflated (snorted), applied to mucous membranes, or smoked. Cocaine is well-absorbed by all these routes but absorption through the mucous membranes of the oral and nasal cavities may be delayed due to local vasoconstriction. Cocaine is generally not ingested, but toxicity and death from gastrointestinal (GI) absorption can occur when people try to smuggle packages of cocaine (body packers or body pushers) or swallow cocaine packages while attempting to avoid arrest (body stuffers).1,2 Crack cocaine is powdered cocaine that is mixed with baking soda or ammonia and water and then heated. Heat separates out the cocaine and the result is small, solid nuggets (often called rocks) of cocaine that unlike powdered cocaine is not destroyed by heat. Crack cocaine rocks are put into a pipe, heat is applied to the bowl with a cigarette lighter, and the cocaine fumes/vapors are inhaled. The term crack is used because the cocaine rocks make a crackling sound when they are heated.3 Cocaine is essentially a stimulant, and there are three primary mechanisms of action that underlie cocaine intoxication and toxicity: 1) Neurotransmitter blockade and release, 2) Ion channel blockade, and 3) Excitatory neurotransmitter release.3 Neurotransmitter Blockade and Release Cocaine blocks the pre-synaptic re-uptake of the neurotransmitters dopamine, epinephrine, norepinephrine, and serotonin in the central and 2 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com peripheral nervous systems. This results in a hyper-adrenergic state and stimulation of alpha1, and alpha2, beta1, and beta2 adrenoreceptors, and it explains many of the acute and chronic effects of cocaine intoxication. Cocaine may also cause the release of catecholamines from storage sites. Ion Channel Blockade Cocaine also blocks the sodium ion channels in the myocardium and peripheral nerves, and blocks potassium in channels in the myocardium. Sodium ion channel blockade in the myocardium produces a membrane depressant effect and may cause a prolonged QRS, arrhythmias, and hypotension, sodium ion channel blockade in peripheral nerves prevents transmission of pain impulses, a local anesthetic effect, and potassium ion channel blockade in the myocardium produces QTc prolongation and can cause torsades de pointes.1,4 Excitatory Neurotransmitter Release There is some evidence that cocaine causes an increase in brain levels of the excitatory neurotransmitters glutamate and aspartate. The onset of action of cocaine is very rapid and the duration of action is short; the effects typically begin within 1-5 minutes and the duration of action is usually 30-60 minutes. Cocaine is metabolized by serum cholinesterase, and a considerable amount of the metabolites are excreted in the urine, primarily in the form of benzoylecogonine and ecgonine methyl ester. Benzoylecgonine is the metabolite that is measured in a urine drug screen (UDS); it can be detected several hours after cocaine use and if someone is using large amounts of cocaine on a regular basis, the UDS may be positive for up to 10 days after use.3 A false positive UDS for cocaine is possible but rare3 but as with any 3 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com UDS result the metabolites of cocaine can be detected long after intoxication and impairment occurred.5 Ingestion of drinking alcohol (ethanol) and the use of cocaine, which is a very common situation,6 produces a metabolite called cocaethylene.3,6 Cocaethylene is more toxic than cocaine alone,7 it has a long duration of action (up to 13 hours), and it also prolongs the duration of action of cocaine.6 Acute Cocaine Intoxication Acute cocaine intoxication affects essentially every organ system, and it can cause serious morbidity and death. Cardiovascular Elevations of blood pressure and heart rate are common.3,8,9 Cocaine increases myocardial oxygen demand but because of coronary artery vasoconstriction it reduces oxygen delivery to the myocardium. Chest pain is a common occurrence as is myocardial ischemia but fortunately only approximately 6% of patients with cocaine intoxication will have a myocardial infarction.8 Relatively benign arrhythmias like supraventricular tachycardia are common while serious arrhythmias like ventricular tachycardia are not. Aortic aneurysm and dissection and rupture and heart failure can occur but they are rare.9 Central Nervous System 4 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Agitation, anxiety, headache and tremor are common, and patients can be confused and delirious, as well.10 Coma, intracranial hemorrhage, seizures, and stroke can occur but seldom do.3,10 Elevation of body temperature and hyperthermia (body temperature up to 40° C/104° F) can occur.1 Pulmonary Cocaine that is smoked can cause thermal injury to the upper airway, shortness of breath, and exacerbation of reversible airway disease. Less common but more dangerous effects of smoking cocaine include pneumothorax, pneumomediastinum, and pneumopericardium.3,12-14 Other Organ System Toxicity Acidosis, perforated gastric ulcer, intestinal infarction, renal infarction, rhabdomyolysis can occur as consequences of cocaine intoxication.3,15,16 Cocaine Use Disorder Diagnosis Chronic cocaine use causes inflammation and damage to the vascular system by way of inflammation, increased shear stress, stress on the myocardium, increased platelet aggregation, and thrombus formation.3,8,17,18 Atherosclerosis, bradycardia, coronary artery thrombosis, dilated cardiomyopathy, left ventricular hypertrophy, and myocarditis are all possible consequences of long-term cocaine use.3,8,19-21 Chronic cocaine users are at risk for infection with hepatitis and human immunodeficiency virus (HIV), psychosis,22 chronic kidney disease,23 structural brain damage and cognitive impairment,24 stroke, impaired sexual function in men,24 and suicide.24 Cocaine use disorder is a substance use disorder. A substance use disorder is defined by specific diagnostic criteria and categorized as mild, moderate, 5 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com or severe, and characterized by recurrent use of alcohol or a drug, use that results in impaired functioning, health problems, and adverse personal, occupational, and social consequences.25 The Diagnostic And Statistical Manual of Mental Disorders, 5th edition (DSM- 5) diagnosis for a substance use disorder are that 2 of these 11 symptoms must be present within the prior 12 months.26 • Consuming more alcohol or other substance than originally planned • Concern about stopping or having consistently failed efforts to control or stop use • Spending a large amount of time using drugs/alcohol, or in activities needed to obtain them • Substance use causes failure to meet significant obligations at home, school, and/or work • The person with a substance use disorder has craving for alcohol or the drug. (Craving in the context of substance use disorder is complex, but it is essentially a strong desire to use alcohol and/or a drug and often the inability to resist the desire.) • Continuing to use a substance despite mental or physical health problems caused or worsened by it substance use • Continuing the use of a substance despite its having negative effects on relationships with others • Repeated use of the substance in dangerous situation, i.e., driving a car) • Giving preference to alcohol or substance use over other life activities • Developing to a tolerance to the alcohol or drug. Tolerance is defined by the DSM-5 as needing to use noticeably larger amounts over time to get the desired effect or experienced a diminished effect
Recommended publications
  • Smoking Cessation Treatment at Substance Abuse Rehabilitation Programs

    Smoking Cessation Treatment at Substance Abuse Rehabilitation Programs

    SMOKING CEssATION TREATMENT AT SUBSTANCE ABUSE REHABILITATION PROGRAMS Malcolm S. Reid, PhD, New York University School of Medicine, Department of Psychiatry; Jeff Sel- zer, MD, North Shore Long Island Jewish Healthcare System; John Rotrosen, MD, New York University School of Medicine, Department of Psychiatry Cigarette smoking is common among persons with drug and alcohol n Nicotine is a highly use disorders, with prevalence rates of 80-90% among patients in sub- addictive substance stance use disorder treatment programs. Such concurrent smoking may that meets all of produce adverse behavioral and medical problems, and is associated the criteria for drug with greater levels of substance use disorder. dependence. CBehavioral studies indicate that the act of cigarette smoking serves as a cue for drug and alcohol craving, and the active ingredient of cigarettes, nicotine, serves as a primer for drug and alcohol abuse (Sees and Clarke, 1993; Reid et al., 1998). More critically, longitudinal studies have found tobacco use to be the number one cause of preventable death in the United States, and also the single highest contributor to mortality in patients treated for alcoholism (Hurt et al., 1996). Nicotine is a highly addictive substance that meets all of the criteria for drug dependence, and cigarette smoking is an especially effective method for the delivery of nicotine, producing peak brain levels within 15-20 seconds. This rapid drug delivery is one of a number of common properties that cigarette smok- ing shares with hazardous drug and alcohol use, such as the ability to activate the dopamine system in the reward circuitry of the brain.
  • Treatment of Stimulant Use Disorders

    Treatment of Stimulant Use Disorders

    UW PACC Psychiatry and Addictions Case Conference UW Medicine | Psychiatry and Behavioral Sciences TREATMENT OF STIMULANT USE DISORDERS Matt Iles-Shih, MD Addiction Psychiatry Fellow University Of Washington & VA Puget Sound Health Care System UW PACC ©2017 University of Washington GENERAL DISCLOSURES The University of Washington School of Medicine also gratefully acknowledges receipt of educational grant support for this activity from the Washington State Legislature through the Safety-Net Hospital Assessment, working to expand access to psychiatric services throughout Washington State. UW PACC ©2017 University of Washington SPEAKER DISCLOSURES No conflicts of interest/disclosures UW PACC ©2017 University of Washington OBJECTIVES 1. Brief overview of stimulant-related physiology & epidemiology 2. Recognizing & treating stimulant use disorders: . Diagnosis & management of acute effects (brief) . Psychotherapies (brief) . Pharmacotherapies 3. Special populations – ADHD in stimulant-abusing pts: to Rx, and how? UW PACC ©2017 University of Washington STIMULANTS: What Substances Are We Talking About? Cocaine Amphetamines: – Prescription Meds – Methamphetamine – Multiple other modified amphetamines MDMA (3,4-methylenedioxy-methamphetamine) [Note: mixed stimulant-psychodelic properties, w/↑serotonin > dopamine and abuse >> addiction.] Others: – Cathinones: Khat & Synthetics (e.g., “Bath Salts”) – Piperazine-like substances (various) – Phenylaklylpyrrolidines (various) UW PACC ©2017 University of Washington COMMONALITIES (WHAT MAKES A STIMULANT
  • Medications to Treat Opioid Use Disorder Research Report

    Medications to Treat Opioid Use Disorder Research Report

    Research Report Revised Junio 2018 Medications to Treat Opioid Use Disorder Research Report Table of Contents Medications to Treat Opioid Use Disorder Research Report Overview How do medications to treat opioid use disorder work? How effective are medications to treat opioid use disorder? What are misconceptions about maintenance treatment? What is the treatment need versus the diversion risk for opioid use disorder treatment? What is the impact of medication for opioid use disorder treatment on HIV/HCV outcomes? How is opioid use disorder treated in the criminal justice system? Is medication to treat opioid use disorder available in the military? What treatment is available for pregnant mothers and their babies? How much does opioid treatment cost? Is naloxone accessible? References Page 1 Medications to Treat Opioid Use Disorder Research Report Discusses effective medications used to treat opioid use disorders: methadone, buprenorphine, and naltrexone. Overview An estimated 1.4 million people in the United States had a substance use disorder related to prescription opioids in 2019.1 However, only a fraction of people with prescription opioid use disorders receive tailored treatment (22 percent in 2019).1 Overdose deaths involving prescription opioids more than quadrupled from 1999 through 2016 followed by significant declines reported in both 2018 and 2019.2,3 Besides overdose, consequences of the opioid crisis include a rising incidence of infants born dependent on opioids because their mothers used these substances during pregnancy4,5 and increased spread of infectious diseases, including HIV and hepatitis C (HCV), as was seen in 2015 in southern Indiana.6 Effective prevention and treatment strategies exist for opioid misuse and use disorder but are highly underutilized across the United States.
  • Barriers and Solutions to Addressing Tobacco Dependence in Addiction Treatment Programs

    Barriers and Solutions to Addressing Tobacco Dependence in Addiction Treatment Programs

    Barriers and Solutions to Addressing Tobacco Dependence in Addiction Treatment Programs Douglas M. Ziedonis, M.D., M.P.H.; Joseph Guydish, Ph.D., M.P.H.; Jill Williams, M.D.; Marc Steinberg, Ph.D.; and Jonathan Foulds, Ph.D. Despite the high prevalence of tobacco use among people with substance use disorders, tobacco dependence is often overlooked in addiction treatment programs. Several studies and a meta-analytic review have concluded that patients who receive tobacco dependence treatment during addiction treatment have better overall substance abuse treatment outcomes compared with those who do not. Barriers that contribute to the lack of attention given to this important problem include staff attitudes about and use of tobacco, lack of adequate staff training to address tobacco use, unfounded fears among treatment staff and administration regarding tobacco policies, and limited tobacco dependence treatment resources. Specific clinical-, program-, and system-level changes are recommended to fully address the problem of tobacco use among alcohol and other drug abuse patients. KEY WORDS: Alcohol and tobacco; alcohol, tobacco, and other drug (ATOD) use, abuse, dependence; addiction care; tobacco dependence; smoking; secondhand smoke; nicotine; nicotine replacement; tobacco dependence screening; tobacco dependence treatment; treatment facility-based prevention; co-treatment; treatment issues; treatment barriers; treatment provider characteristics; treatment staff; staff training; AODD counselor; client counselor interaction; smoking cessation; Tobacco Dependence Program at the University of Medicine and Dentistry of New Jersey obacco dependence is one of to the other. The common genetic vul­ stance use was considered a potential the most common substance use nerability may be located on chromo­ trigger for the primary addiction.
  • Alcohol Use Disorder

    Alcohol Use Disorder

    Section: A B C D E Resources References Alcohol Use Disorder (AUD) Tool This tool is designed to support primary care providers (family physicians and primary care nurse practitioners) in screening, diagnosing and implementing pharmacotherapy treatments for adult patients (>18 years) with Alcohol Use Disorder (AUD). Primary care providers should routinely offer medication for moderate and severe AUD. Pharmacotherapy alone to treat AUD is better than no therapy at all.1 Pharmacotherapy is most effective when combined with non-pharmacotherapy, including behavioural therapy, community reinforcement, motivational enhancement, counselling and/or support groups. 2,3 TABLE OF CONTENTS pg. 1 Section A: Screening for AUD pg. 7 Section D: Non-Pharmacotherapy Options pg. 4 Section B: Diagnosing AUD pg. 8 Section E: Alcohol Withdrawal pg. 5 Section C: Pharmacotherapy Options pg. 9 Resources SECTION A: Screening for AUD All patients should be screened routinely (e.g. annually or when indicators are observed) with a recommended tool like the AUDIT. 2,3 It is important to screen all patients and not just patients eliciting an index of suspicion for AUD, since most persons with AUD are not recognized. 4 Consider screening for AUD when any of the following indicators are observed: • After a recent motor vehicle accident • High blood pressure • Liver disease • Frequent work avoidance (off work slips) • Cardiac arrhythmia • Chronic pain • Rosacea • Insomnia • Social problems • Rhinophyma • Exacerbation of sleep apnea • Legal problems Special Patient Populations A few studies have reviewed AUD in specific patient populations, including youth, older adults and pregnant or breastfeeding patients. The AUDIT screening tool considered these populations in determining the sensitivity of the tool.
  • DIAGNOSIS REFERENCE GUIDE A. Diagnostic Criteria for Substance

    DIAGNOSIS REFERENCE GUIDE A. Diagnostic Criteria for Substance

    ALCOHOL & OTHER DRUG SERVICES DIAGNOSIS REFERENCE GUIDE A. Diagnostic Criteria for Substance Use Disorder See DSM-5 for criteria specific to the drugs identified as primary, secondary or tertiary. P S T (P=Primary, S=Secondary, T=Tertiary) 1. Substance is often taken in larger amounts and/or over a longer period than the patient intended. 2. Persistent attempts or one or more unsuccessful efforts made to cut down or control substance use. 3. A great deal of time is spent in activities necessary to obtain the substance, use the substance, or recover from effects. 4. Craving or strong desire or urge to use the substance 5. Recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home. 6. Continued substance use despite having persistent or recurrent social or interpersonal problem caused or exacerbated by the effects of the substance. 7. Important social, occupational or recreational activities given up or reduced because of substance use. 8. Recurrent substance use in situations in which it is physically hazardous. 9. Substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance. 10. Tolerance, as defined by either of the following: a. Markedly increased amounts of the substance in order to achieve intoxication or desired effect; Which:__________________________________________ b. Markedly diminished effect with continued use of the same amount; Which:___________________________________________ 11. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome for the substance; Which:___________________________________________ b.
  • Cocaine Intoxication and Hypertension

    Cocaine Intoxication and Hypertension

    THE EMCREG-INTERNATIONAL CONSENSUS PANEL RECOMMENDATIONS Cocaine Intoxication and Hypertension Judd E. Hollander, MD From the Department of Emergency Medicine, University of Pennsylvania, Philadelphia, PA. 0196-0644/$-see front matter Copyright © 2008 by the American College of Emergency Physicians. doi:10.1016/j.annemergmed.2007.11.008 [Ann Emerg Med. 2008;51:S18-S20.] with cocaine intoxication is analogous to that of the patient with hypertension: the treatment should be geared toward the Cocaine toxicity has been reported in virtually all organ patient’s presenting complaint. systems. Many of the adverse effects of cocaine are similar to When the medical history is clear and symptoms are mild, adverse events that can result from either acute hypertensive laboratory evaluation is usually unnecessary. In contrast, if the crisis or chronic effects of hypertension. Recognizing when the patient has severe toxicity, evaluation should be geared toward specific disease requires treatment separate from cocaine toxicity the presenting complaint. Laboratory evaluation may include a is paramount to the treatment of patients with cocaine CBC count; determination of electrolyte, glucose, blood urea intoxication. nitrogen, creatine kinase, and creatinine levels; arterial blood The initial physiologic effect of cocaine on the cardiovascular gas analysis; urinalysis; and cardiac marker determinations. system is a transient bradycardia as a result of stimulation of the Increased creatine kinase level occurs with rhabdomyolysis. vagal nuclei. Tachycardia typically ensues, predominantly from Cardiac markers are increased in myocardial infarction. Cardiac increased central sympathetic stimulation. Cocaine has a troponin I is preferred to identify acute myocardial13 infarction. cardiostimulatory effect through sensitization to epinephrine A chest radiograph should be obtained in patients with and norepinephrine.
  • Why Does Smoking So Often Produce Dependence? a Somewhat Diverent View

    Why Does Smoking So Often Produce Dependence? a Somewhat Diverent View

    62 Tobacco Control 2001;10:62–64 Tob Control: first published as 10.1136/tc.10.1.62 on 1 March 2001. Downloaded from COMMENTARY Why does smoking so often produce dependence? A somewhat diVerent view John R Hughes Abstract These explanations often give little emphasis The usual explanation for why smoking to the possibility that nicotine induces depend- produces dependence focuses on the ence because it produces beneficial eVects that eVects of nicotine on dopamine and other can help smokers cope with their environ- neurobiological explanations. This review ment.89 By beneficial eVects, I mean positive oVers four somewhat diVerent explana- eVects that are not due to relief of withdrawal tions: (1) nicotine can oVer several but rather are eVects above and beyond a “nor- psychopharmacological benefits at the age mal” baseline functioning.10 when such benefits are especially needed; Whether nicotine via smoking causes true (2) cigarettes provide for a rapid, beneficial eVects is, to many, debatable.891112 frequent, reliable and easy-to-obtain My belief (and that of others before me89) that reward; (3) nicotine is not intoxicating, nicotine can cause true beneficial eVects is allowing chronic intake; and (4) the long based on three sets of data. First, nicotine often duration of the nicotine withdrawal causes improvements in animals with no syndrome eVectively undermines cessa- history of nicotine exposure, in never smokers, tion. This article reviews the evidence for and in non-deprived smokers.8911 Second, the above views and the tobacco control most other drugs of dependence produce ben- activities these views suggest. eficial eVects—for example, cocaine produces (Tobacco Control 2001;10:62–64) stimulation and alcohol produces relaxation http://tobaccocontrol.bmj.com/ Keywords: nicotine; substance use disorder; substance and increased confidence.
  • Treatment of Patients with Substance Use Disorders Second Edition

    Treatment of Patients with Substance Use Disorders Second Edition

    PRACTICE GUIDELINE FOR THE Treatment of Patients With Substance Use Disorders Second Edition WORK GROUP ON SUBSTANCE USE DISORDERS Herbert D. Kleber, M.D., Chair Roger D. Weiss, M.D., Vice-Chair Raymond F. Anton Jr., M.D. To n y P. G e o r ge , M .D . Shelly F. Greenfield, M.D., M.P.H. Thomas R. Kosten, M.D. Charles P. O’Brien, M.D., Ph.D. Bruce J. Rounsaville, M.D. Eric C. Strain, M.D. Douglas M. Ziedonis, M.D. Grace Hennessy, M.D. (Consultant) Hilary Smith Connery, M.D., Ph.D. (Consultant) This practice guideline was approved in December 2005 and published in August 2006. A guideline watch, summarizing significant developments in the scientific literature since publication of this guideline, may be available in the Psychiatric Practice section of the APA web site at www.psych.org. 1 Copyright 2010, American Psychiatric Association. APA makes this practice guideline freely available to promote its dissemination and use; however, copyright protections are enforced in full. No part of this guideline may be reproduced except as permitted under Sections 107 and 108 of U.S. Copyright Act. For permission for reuse, visit APPI Permissions & Licensing Center at http://www.appi.org/CustomerService/Pages/Permissions.aspx. AMERICAN PSYCHIATRIC ASSOCIATION STEERING COMMITTEE ON PRACTICE GUIDELINES John S. McIntyre, M.D., Chair Sara C. Charles, M.D., Vice-Chair Daniel J. Anzia, M.D. Ian A. Cook, M.D. Molly T. Finnerty, M.D. Bradley R. Johnson, M.D. James E. Nininger, M.D. Paul Summergrad, M.D. Sherwyn M.
  • Substance Use Disorder Defined by NIDA and SAMHSA

    Substance Use Disorder Defined by NIDA and SAMHSA

    Substance Use Disorder defined by NIDA and SAMHSA: NIDA (National Institute on Drug Abuse) defines SUD/Addiction as: What is drug addiction? Addiction is defined as a chronic, relapsing disorder characterized by compulsive drug seeking, continued use despite harmful consequences, and long-lasting changes in the brain. It is considered both a complex brain disorder and a mental illness. Addiction is the most severe form of a full spectrum of substance use disorders, and is a medical illness caused by repeated misuse of a substance or substances. Why study drug use and addiction? Use of and addiction to alcohol, nicotine, and illicit drugs cost the Nation more than $740 billion a year related to healthcare, crime, and lost productivity.1,2 In 2016, drug overdoses killed over 63,000 people in America, while 88,000 died from excessive alcohol use.3,4 Tobacco is linked to an estimated 480,000 deaths per year.5 (Hereafter, unless otherwise specified, drugs refers to all of these substances.) How are substance use disorders categorized? NIDA uses the term addiction to describe compulsive drug seeking despite negative consequences. However, addiction is not a specific diagnosis in the fifth edition of The Diagnostic and Statistical Manual of Mental Disorders (DSM-5)—a diagnostic manual for clinicians that contains descriptions and symptoms of all mental disorders classified by the American Psychiatric Association (APA). In 2013, APA updated the DSM, replacing the categories of substance abuse and substance dependence with a single category: substance use disorder, with three subclassifications—mild, moderate, and severe. The symptoms associated with a substance use disorder fall into four major groupings: impaired control, social impairment, risky use, and pharmacological criteria (i.e., tolerance and withdrawal).
  • DSM-5 Diagnoses and New ICD-10-CM Codes

    DSM-5 Diagnoses and New ICD-10-CM Codes

    DSM-5 DiAgnoses And New ICD-10-CM Codes As Ordered in the DSM-5 Classification DSM-5 Recommended DSM-5 Recommended Disorder ICD-10-CM Code for use ICD-10-CM Code for use through September 30, 2017 beginning October 1, 2017 Avoidant/Restrictive Food Intake Disorder F50.89 F50.82 Alcohol Use Disorder, Mild F10.10 F10.10 Alcohol Use Disorder, Mild, In early or sustained remission F10.10 F10.11 Alcohol Use Disorder, Moderate F10.20 F10.20 Alcohol Use Disorder, Moderate, In early or sustained F10.20 F10.21 remission Alcohol Use Disorder, Severe F10.20 F10.20 Alcohol Use Disorder, Severe, In early or sustained F10.20 F10.21 remission Cannabis Use Disorder, Mild F12.10 F12.10 Cannabis Use Disorder, Mild, In early or sustained F12.10 F12.11 remission Cannabis Use Disorder, Moderate F12.20 F12.20 Cannabis Use Disorder, Moderate, In early or sustained F12.20 F12.21 remission Cannabis Use Disorder, Severe F12.20 F12.20 Cannabis Use Disorder, Severe, In early or sustained F12.20 F12.21 remission Phencyclidine Use Disorder, Mild F16.10 F16.10 Phencyclidine Use Disorder, Mild, In early or sustained F16.10 F16.11 remission Phencyclidine Use Disorder, Moderate F16.20 F16.20 Phencyclidine Use Disorder, Moderate, In early or F16.20 F16.21 sustained remission Phencyclidine Use Disorder, Severe F16.20 F16.20 Phencyclidine Use Disorder, Severe, In early or sustained F16.20 F16.21 remission Other Hallucinogen Use Disorder, Mild F16.10 F16.10 Other Hallucinogen Use Disorder, Mild, In early or F16.10 F16.11 sustained remission Other Hallucinogen Use Disorder,
  • Stimulant Use Disorder

    Stimulant Use Disorder

    Public Meeting on Patient-Focused Drug Development for Stimulant Use Disorder Tuesday, October 6, 2020 FDA will be streaming a live webcast of the meeting with the presentation slides, which is open to the public at: http://fda.yorkcast.com/webcast/Play/89f7acb8d56e4de8827d1ade8efa42661d. The webcast recording and presentation slides, along with a meeting transcript and summary report, will also be made publicly available after the meeting. #PFDD Welcome Robyn Bent, RN, MS | CAPT, U.S. Public Health Service Director, Patient-Focused Drug Development Program Office of Center Director Center for Drug Evaluation and Research U.S. Food and Drug Administration Agenda • Opening Remarks • Setting the Context • Overview of FDA’s Patient-Focused Drug Development Initiative • Overview of Stimulant Use Disorder • Overview of Discussion Format • Discussion Topic 1: Health Effects and Daily Impacts • Break • Discussion Topic 2: Current Approaches to Management • Discussion Topic 3: Impact of COVID-19 Pandemic on Stimulant Use Disorder • Closing Remarks www.fda.gov 3 Opening Remarks Admiral Brett P. Giroir, MD Assistant Secretary for Health United States Department of Health and Human Services Overview of FDA’s Patient-Focused Drug Development Initiative Theresa Mullin, PhD Associate Director for Strategic Initiatives Center for Drug Evaluation and Research U.S. Food and Drug Administration FDA’s role in medical product development and evaluation Review divisions at FDA (e.g., Division of Neurology, Division While FDA plays a critical of Psychiatry, etc.) provide FDA’s mission is to protect and oversight role in drug regulatory oversight during promote public health by development, it is just one part drug development, make evaluating the safety and of the process.