Presentation on theme: "دکتر طاهره صادقیه فوق تخصص روانپزشکی کودک ونوجوان"— Presentation transcript:
1 دکتر طاهره صادقیه فوق تخصص روانپزشکی کودک ونوجوان Metamphetamineدکتر طاهره صادقیهفوق تخصص روانپزشکی کودک ونوجوان
2 12-14,%15-17,%18-20,%None18.104.22.168Alcohol17.719.930.6Crack/cocaine22.214.171.124Marijuana/hashish66.766.937.9Heroin0.29.8Nonprescription methadone0.1Other opiates and synthetics0.40.62.5PCPHallucinogens0.3Methamphetamine2.148.4Other amphetamines1.4Other stimulantsBenzodiazapinesOther tranquilizersBarbituratesOther sedatives or hypnoticsInhalantsOver-the-counter medicationsOther0.5Total percent100(Total N)(24,911)(123,496)(119,138)(From TEDS: Treatment Episode Data Set: 2003 Highlights. National Admissions to Substance Abuse Treatment Services, DASIS Series: S-27. Rockville, MD; Services DoHaH, ed.; DHHS Publication No. SMA 05â€“4043, with permission.)
3 The prevalence of substance use and SUDs increases almost linearly from early to late adolescence. Approximately one in four older adolescents meets criteria for abuse for at least one substance, and one in five meets criteria for SD.
4 Etiology Genetic and Environmental Influences Twin and adoption studies have demonstrated that considerable shared environmental influences exist for the initiation of substance use, and that genetic influences become more apparent when environments allow for their expression
5 Genetic influences on the development of adolescent SUDs may act through a direct effect on psychophysiological reactions to substances or their metabolism,or indirectly through genetic effects on personality traits such as behavioral disinhibition, which leads to substance experimentation
6 Externalizing Disorders Conduct disorder has consistently been shown to be a predictor of substance use initiation and progression toward SUDs.Oppositional defiant disorder (ODD) and attention-deficit hyperactivity disorder (ADHD) appear to increase risk for developing SUDs somewhat, although there is controversy about the magnitude of the effect of ODD or ADHD due to their comorbidity with CD.
7 Stage Theory and the Gateway Theory Thus, typically a licit substance, such as alcohol or cigarettes, is used first in a sequence, followed by marijuana, which is usually the first illicit substance before progressing on to use of other illicit substances
8 Family and Peer Effects Parental drug use, as well as drug use by older siblings, is a significant risk factor for the development of adolescent substance use. However, the mechanism of transmission is complex, with individual personality dimensions mediating the effect of sibling and parent influences
9 Family and Peer Effects while the common notion has been that peers create peer pressure to consume substances, most studies support the notion that there exists a complex process by which individuals select peer groups, and then in turn influence these, as well as are influenced by them
10 Biological Mechanisms in the Etiology of Substance Use Disorders neural adaptations altering the hedonic tone of individuals. This tone is reset by substance use so that it is lower over time, resulting in dysphoria and craving when not using, and driving the substance dependence cycle
11 Substance-Specific Risks there are differences between substances in terms of their addictive potential. The time course toward the development of dependence varies by individual, by substance, and by route of administration. Some substances,Cocaine—15-16% Alchol %AMPHETAMINMarijuana %
12 Table 49.9-1 Domains of Facters Associated with Drug Use I. Cultural/societal Laws favorable to drug use Social norms favorable to drug use Availability of drugs Extreme economic deprivations Neighborhood disorganization
13 II. Interpersonal Childhood interpersonal factors Family alcohol and drug behavior and attitudes Poor and inconsistent family management practices Parent personality and other characteristics Family conflicts Physical or sexual abuse Adolescent interpersonal factors General stressful life events (i.e., relocation) Peer rejection in school and other contexts Association with drug-using peers
14 III. Psychobehavioral Child and adolescent psychobehavioral influences Age Early and persistent behavior problem (including drug use) Academic failure Low degree of commitment to school Postadolescent psychobehavioral factors Occupational satisfaction and success Child-rearing demands Multiple role obligations Achievement of sex role expectations Intimate relationship functioning Educational/financial attainment and security Psychobehavioral antecedents and consequences throughout life Alienation, rebelliousness, or antisocial personality Sensation seeking Psychopathology (depression, anxiety) Attitudes favorable to drug use Cognitive motivations or expectancies for drug use Inability to delay gratification
15 IV. Biogenetic Inherited susceptibility to drug use Psychophysiological vulnerability to drug effects
16 Difficulties with risk assessment Cognitive immaturity in early adolescenceDifficulty hypothesising alternative futures hampers risk assessmentNarrow range of solutionsAvoidant coping style – early teensAdolescent omnipotence (Elkind, 1967)Invulnerability to adverse consequences of risk behaviourLack of life experienceRisk taking is also a normative, healthy behaviour, used to achieve task of sep/indiv, identity formation and establishment of peer relationships
17 ADOLESCENT DRUG USEWHO: Adolescence is a period between the agesAdolescence is a stage of searching;Searching for identity..Searching for joy ...Searching for excitement…Searching for difference…Searching for independence……
18 Adolescence and Brain Immaturity The last brain structures to fully mature are the areas of the cortex related to so-called executive functions:- decision making- inhibition of behaviour- selective attention- problem solving and reasoning
19 Normal brain development : function of different stages of development Proliferation of pathways- makes the brain versatile and able to adapt to different environmentsPruning of these pathways- with experience the unused pathways are eliminated, narrowing the options for behaviourMyelination (white matter)- makes the remaining pathways faster and more efficientAs a result brain has become adapted to environment and efficient in functioning, but is less able to change in future.
21 DDThe most frequent of these are externalizing disorders, but internalizing disorders are also more prevalent than in the general population76%--COMORBIDITY68%--disruptive behavior dis32%---mood dis20%---anxiety disComorbidity rule
23 The racemate amphetamine sulfate (Benzedrine) treatment of nasal congestion and asthma. In 1937, amphetamine sulfate tablets were introduced for the treatment of narcolepsy, postencephalitic parkinsonism, depression, and lethargy.
24 FDA)-approved indications for amphetamine are limited to attention-deficit/hyperactivity disorder (ADHD) and narcolepsy; however, amphetamines are also used in the treatment of obesity, depression, dysthymia, chronic fatigue syndrome, acquired immune deficiency syndrome (AIDS), dementia, and neurasthenia.
25 PreparationsThe major amphetamines currently available and used in the United States are dextroamphetamine (Dexedrine), methamphetamine (Desoxyn), a mixed dextroamphetamine-amphetamine salt (Adderall), and theThese drugs go by such street names as ice, crystal, crystal meth, and speed.the amphetamines are referred to as analeptics, sympathomimetics, stimulants, and psychostimulants.
26 The typical amphetamines are used to increase performance and to induce a euphoric feeling, for example, by students studying for examinations, by long-distance truck drivers on trips, by business people with important deadlines, by athletes in competition, and by soldiers during wartime. Although not as addictive as cocaine, amphetamines are nonetheless addictive drugs.
27 Other amphetamine-like substances are ephedrine, pseudoephedrine, and phenylpropanolamine (PPA). These drugs, PPA in particular, can dangerously exacerbate hypertension, precipitate a toxic psychosis, cause intestinal infarction, or result in death.
28 The safety margin for PPA is particularly narrow, and three to four times the normal dose can result in life-threatening hypertension.
29 methamphetamine is a potent form of amphetamine that abusers of the substance inhale, smoke, or inject intravenously (IV). Its psychological effects last for hours and are described as particularly powerful. Unlike cocaine (which must be imported, methamphetamine is a synthetic drug that can be manufactured domestically in illicit laboratories.
31 EpidemiologyThe National Household Survey on Drug Abuse (NHSDA) conducted in 2001 found that 7.1 percent of persons (12 years of age and older) reported lifetime nonmedical use of stimulants,a significant increase since the 4.5 percent found in the 1997 survey. The highest rates of use in the past year (1.5 percent) were among 18- to 25-year-olds, followed by 12- to 17-year-olds.The treatment admission rate for primary amphetamine abuse in the United States is about 30 per 100,000 people 12 years of age or older.
32 AmphetaminesNonmedical use of stimulants is reported by approximately 2% of year-olds, with 0.6% reporting methamphetamine use
33 all socioeconomic groups white professionalsabuse by others, including friends and family members of the patient receiving the amphetaminethe lifetime prevalence of amphetamine dependence and abuse is 1.5 percent, and the male to female ratio is 1.
34 NeuropharmacologyThe classic amphetamines (i.e., dextroamphetamine, methamphetamine, and methylphenidate) produce their primary effects by causing the release of catecholamines, particularly dopamine, from presynaptic terminalsThe effects are particularly potent for the dopaminergic neurons projecting from the ventral tegmental area to the cerebral cortex and the limbic areas. This pathway has been termed the reward circuit pathway, and its activation is probably the major addicting mechanism for the amphetamines
35 The designer amphetamines cause the release of catecholamines (dopamine and norepinephrine) and of serotonin, the neurotransmitter implicated as the major neurochemical pathway for hallucinogens. Therefore, the clinical effects of designer amphetamines are a blend of the effects of classic amphetamines and those of hallucinogens.
36 Substituted Amphetamines MDMA (3,4-methylene-dioxymethamphetamine) is one of a series of substituted amphetamines that also includes MDEA, MDA (3,4-methylene-dioxyamphetamine), DOB (2,5-dimethoxy-4-bromoamphetamine), PMA (paramethoxyamphetamine), and others. These drugs produce subjective effects resembling those of amphetamine and LSD (lysergic acid diethylamide), and in that sense, MDMA and similar analogues may represent a distinct category of drugs
37 Club DrugsThe use of a certain group of substances popularly called club drugs is often associated with dance clubs, bars, and all-night dance parties (raves). The group includes LSD, خ³-hydroxybutyrate (GHB), ketamine, methamphetamine, MDMA (ecstasy), and Rohypnol or â€œroofiesâ€ (flunitrazepam). These substances are not all in the same drug class, nor do they produce the same physical or subjective effects. GHB, ketamine, and Rohypnol have been called date rape drugs because they produce disorienting and sedating effects, and often users cannot recall what occurred during all or part of an episode under the influence of the drug. Hence, it is alleged that these drugs might be surreptitiously placed in a beverage, or a person might be convinced to take the drug and then not recall clearly what occurred after ingestion.
40 Its use is associated with major health consequences, including memory loss, aggression, violence and psychotic behavior, and neuropsychological deficitsSimilar to cocaine, dependence can develop quickly and be associated with rapid psychosocial decline.The physical effects of acute. Convulsions and seizures may occur.
41 Table 12.3-2 DSM-IV-TR Diagnostic Criteria for Amphetamine Intoxication Recent use of amphetamine or a related substance (e.g., methylphenidate).Clinically significant maladaptive behavioral or psychological changes (e.g., euphoria or affective blunting; changes in sociability; hypervigilance; interpersonal sensitivity; anxiety, tension, or anger; stereotyped behaviors; impaired judgment; or impaired social or occupational functioning) that developed during, or shortly after, use of amphetamine or a related substance.Two (or more) of the following, developing during, or shortly after, use of amphetamine or a related substance:tachycardia or bradycardiaapillary dilationelevated or lowered blood pressureperspiration or chillsnausea or vomitingevidence of weight losspsychomotor agitation or retardationmuscular weakness, respiratory depression, chest pain, or cardiac arrhythmiasconfusion, seizures, dyskinesias, dystonias, or comaThe symptoms are not due to a general medical condition and are not better accounted for by another mental disorder.Specify if: With perceptual disturbances (From American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Text rev. Washington, DC: American Psychiatric Association; copyright 2000, with permission.)
42 Table 12.3-3 DSM-IV-TR Diagnostic Criteria for Amphetamine Withdrawal Cessation of (or reduction in) amphetamine (or a related substance) use that has been heavy and prolonged.Dysphoric mood and two (or more) of the following physiological changes, developing within a few hours to several days after Criterion A:fatiguevivid, unpleasant dreamsinsomnia or hypersomniaincreased appetitepsychomotor retardation or agitationThe symptoms in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.The symptoms are not due to a general medical condition and are not better accounted for by another mental disorder
43 Amphetamine Withdrawal After amphetamine intoxication, a crash occurs with symptoms of anxiety, tremulousness, dysphoric mood, lethargy, fatigue, nightmares (accompanied by rebound rapid eye movement [REM] sleep), headache, profuse sweating, muscle cramps, stomach cramps, and insatiable hunger. The withdrawal symptoms generally peak in 2 to 4 days and are resolved in 1 week. The most serious withdrawal symptom is depression, which can be particularly severe after the sustained use of high doses of amphetamine and which can be associated with suicidal ideation or behavior
44 MYTHS ABOUT DU/DADrug addiction occurs as a result of free will. You choose to become addicted.Drug addiction happens in people who have a ‘weak’ character or lack self-disciplineMarijuana is not addictingPeople who carry on taking drugs after treatment are a waste of time and will never beat their addiction
45 TABLE 17–5. Urine toxicology SubstanceHalf-life, hrsDetection after last use, daysAmphetamines10–151–2Barbiturates20–963–21Benzodiazepines20–902–9Cocaine0.8–6.00.2–4 (metabolites)Methaqualone20–607–24Opiates2–4Phencyclidine7–162–8Cannabinoids10–402–8 (acute); 14–42 (chronic)Alcohol12 hoursHeroin2–31–3Methadone15–607–10
46 Amphetamines Detection period: 1-2 days Positive screening test with: amphetamine, dextroamphetamine, methamphetamine, pseudoephedrine, phentermine, ephedrine, phenylpropanolamine, phenylephrine, selegiline(Parkinson’s med)some will dectect MDMA (ecstacy) most will not
47 AmphetaminesUrinary excretion is pH dependent; acidification can reduce plasma 1/2-life to 7-8 hours, alkinization may increase the 1/2-life to over 33 hoursLack of specificity of screening test makes confirmatory test essential
49 Levels of AssessmentScreening identifies the need for a comprehensive assessment and is not a substitute for an assessment.
50 Validity of Adolescent Report Most youth in drug treatment settings admit to use of substances; few treatment-seeking adolescents endorse questions that indicate blatant faking of responses (e.g., admit to the use of a fictitious drug).Specific populations, especially extremely antisocial youth, have much higher responses of "faking good" than clinical samples (Winters et al. 1991).
51 factors at intake such as denial, reluctance to self-disclose due to embarrassment, and wish to avoid sanctions for use, as well as ability of the adolescent in treatment to more carefully examine the extent of substance use.
52 The Interviewclinician to be direct, persistent, but nonjudgmental and respectful of confidentiality issues.
53 The Interviewage at onset, duration, frequency, and route of ingestion for each individual drug, including alcohol, tobacco, illicit drugs, inhalants, over-the-counter medications, and prescription drugs such as benzodiazepines, opiates, and stimulants.Additional inquiry should cover negative consequences as well as attempts and motivation to control use or quit.
54 setting of use (time and place), alone or with peers,and the attitudes of these peers about substance use.Variability in quantity and frequency of periods of abstinence as well as periods of rapid acceleration of use and heavy use of particular agents.A timeline drug chart or calendar is often useful to allow the adolescent to report quantity, frequency, and variability data across time with important dates, holidays, and other time cues as a guide.
55 attitudes and/or expectancies of use, and motivation(s) or perceived benefits to use. usual antecedents to use and consequences of use.Such an analysis may allow a more specific targeting of relevant antecedents during treatment. Along with specific attitudes and beliefs about substance use, the clinician should also inquire about the adolescent's values and attitudes in general.
56 depression, suicidality, aggression, psychosis, and treatment history may be sufficient in order to augment other information in determining when an adolescent should be referred for a more detailed, comprehensive psychiatric evaluation
57 The medical history and possible physical exam search for symptoms and illnesses that may be related to SUDs and behaviors, including trauma, pregnancies, HIV/AIDS, sexually transmitted diseases, infections or wounds, and possible liver diseases
58 School/vocational, peer, and family domains would emphasize family and peer substance use and attitudes toward use,parental monitoring and supervision,family history of SUDs and psychiatric disorders, and the effect of substance use on academic and/or vocational functioning.
59 Inquiry into recreational or prosocial activities such as sports, interests, and hobbies will provide the clinician with information about the adolescent's social repertoire and whether this will have to be targeted for change.
60 ConfidentialityAdolescents are more likely to provide truthful information if they believe that their information, at least the details, will not be shared. Prior to the adolescent interview, the clinician should review exactly what information the clinician is obliged to share and with whom
61 Typically, a clinician should inform the adolescent that a threat of danger to self or others will force the clinician to inform a responsible adult, usually the parents.
62 The clinician should be knowledgeable about state and federal laws that limit what information may be released from drug and alcohol treatment programs.Confidentiality statutes include information about illegal behavior such as selling drugs, who sells the adolescent drugs, and peer behaviors. In order for the assessment team to speak with the adolescent's family, school, or legal staff members, the adolescent must sign a consent form.
63 Table 52.5-1. The CRAFFT Questions: A Brief Screening Test for Adolescent Substance Abuse C Have you ever ridden in a Car driven by someone (including yourself) who was “high” or had been using alcohol or drugszR Do you ever use alcohol or drugs to Relax, feel better about yourself, or fit in?A Do you ever use alcohol/drugs while you are by yourself, Alone?F Do your family or Friends ever tell you that you should cut down on your drinking or drug use?F Do you ever Forget things you did while using alcohol or drugs?T Have you gotten into Trouble while you were using alcohol or drugs?
65 TreatmentThe primary goal for the treatment of adolescents with SUDs is achieving and maintaining abstinence from substance use. While abstinence should remain the explicit long-term goal for treatment, a realistic view recognizes both the chronicity of SUDs in some populations of adolescents and the self-limited nature of substance use and substance use–related problems in others
66 psychoeducation about SUDs, which decreases familial resistance to treatment and increases motivation and engagement; assisting parents and family to initiate and maintain efforts to get the adolescent into appropriate treatment and achieve abstinence;assisting parents and family to establish or reestablish structure with consistent limit setting and careful monitoring of the adolescent's activities and behavior;improving communication among family members; and getting other family members into treatment and/or support programs.
67 The Course of Substance Use Disorders in Adolescents There is considerable individual variability in the rate of return and extent of posttreatment substance use among adolescents following treatment. Although most treated adolescents return to some substance use following treatment, treated adolescents generally show reductions in substance use and problems over both short- and longer-term follow-up
68 Longer-term outcome studies report that most adolescents show developmentally limited patterns of substance use and related problems, although small proportions show more-chronic high levels of substance involvement through young adulthood.
69 Non pharmacologicalEntranceDiscontinutionMaintanceMotivation/family/12 steps/CBT/MATRIX
70 The clinician should also consider alternative agents to psychostimulants, such as atomoxetine or bupropion, which do not have abuse potential.RITALINE