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S P Sutama

• Zat psikoaktif : zat kimia yang mampu merubah


suasana hati, pola pikir, perasaan, persepsi, dan
perilaku seseorang.
• Narkoba : narkotika dan obat berbahaya
• NAPZA : Narkotika, Alkohol, Psikotropika, dan Zat
Adiktif lainnya.

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 Fun : untuk kesenangan.
 Forget : untuk melupakan duka lara, mengatasi
stress.
 Functional : untuk dapat berfungsi, ingin
berprestasi, ingin langsing, ingin meningkatkan
kemampuan seksual, ingin meningkatkan
kemampuan kerja.
 Rasa ingin tahu, coba-coba.
 Ikut-ikutan agar dianggap setia kawan, diterima
dalam suatu kelompok.
 Ingin dianggap dewasa, modern atau perkasa.
 Suatu cara menantang ortu.

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Tahap penggunaan NAPZA
1. Eksperimental : coba – coba.
2. Sosial : rame-rame, rekreasional, hiburan.
3. Situasional : pakai pada keadaan tertentu,
misal : sedih, kecewa, tegang.
4. Reguler / habitual : kebiasaan, pola
menyimpang, telah terjadi gangguan fungsi
sosial dan pekerjaan.
5. Ketergantungan : toleransi, gejala putus zat.
6. Berbahaya / hazardous : intoksikasi.

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There are four major diagnostic categories in the Diagnostic and Statistical Manual of
Mental Disorders, fifth edition (DSM-5):
(1) Substance Use Disorder
(2) Substance Intoxication
(3) Substance Withdrawal
(4) Substance-Induced Mental Disorder.

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Substance use disorder is the diagnostic term applied to the specific substance abused
(e.g., alcohol use disorder, opioid use disorder) that results from the prolonged use of
the substance.

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A maladaptive pattern of substance use leading to clinically significant impairment or
distress, as manifested by 2 (or more) of the following, occurring within a 12-month
period:
1. recurrent substance use resulting in a failure to fulfill major role obligations at
work, school, or home (e.g., repeated absences or poor work performance related to
substance use; substance-related absences, suspensions, or expulsions from school;
neglect of children or household)
2. recurrent substance use in situations in which it is physically hazardous (e.g., driving
an automobile or operating a machine when impaired by substance use)
3. continued substance use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of the substance (e.g.,
arguments with spouse about consequences of intoxication, physical fights)
4. tolerance, as defined by either of the following:
a. a need for markedly increased amounts of the substance to achieve intoxication or
desired effect
b. markedly diminished effect with continued use of the same amount of the
substance

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5. withdrawal, as manifested by either of the following:
a. the characteristic withdrawal syndrome for the substance
b. the same (or a closely related) substance is taken to relieve or avoid withdrawal
symptoms
6. the substance is often taken in larger amounts or over a longer period than was
intended
7. there is a persistent desire or unsuccessful efforts to cut down or control substance
use
8. a great deal of time is spent in activities necessary to obtain the substance, use the
substance, or recover from its effects
9. important social, occupational, or recreational activities are given up or reduced
because of substance use
10. the substance use is continued despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused or exacerbated by
the substance
11. craving or a strong desire or urge to use a specific substance.

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Substance intoxication is the diagnosis used to describe a syndrome (e.g., alcohol
intoxication or simple drunkenness) characterized by specific signs and symptoms
resulting from recent ingestion or exposure to the substance.

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A general description of substance intoxication includes the following points:
 The development of a reversible substance-specific syndrome due to recent
ingestion of (or exposure to) a substance. Note: Different substances may produce
similar or identical syndromes.
 Clinically significant maladaptive behavioral or psychological changes that are due
to the effect of the substance on the central nervous system (e.g., belligerence,
mood lability, cognitive impairment, impaired judgment, impaired social or
occupational functioning) and develop during or shortly after use of the substance.
 The symptoms are not due to a general medical condition and are not better
accounted for by another mental disorder.

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Substance withdrawal is the diagnosis used to describe a substance specific syndrome
that results from the abrupt cessation of heavy and prolonged use of a substance
(e.g., opioid withdrawal).

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A general description of substance withdrawal requires the following :
 The development of a substance-specific syndrome due to the cessation of (or
reduction in) substance use that has been heavy and prolonged.
 The substance-specific syndrome causes 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.

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Alcohol is a potent drug that causes both acute and chronic changes in almost all
neurochemical systems. Thus alcohol abuse can produce serious temporary
psychological symptoms including depression, anxiety, and psychoses. Long-term,
escalating levels of alcohol consumption can produce tolerance as well as such
intense adaptation of the body that cessation of use can precipitate a withdrawal
syndrome usually marked by insomnia, evidence of hyperactivity of the autonomic
nervous system, and feelings of anxiety.

COMORBIDITY
The psychiatric diagnoses most commonly associated with the alcohol-related
disorders are other substance-related disorders, antisocial personality disorder, mood
disorders, and anxiety disorders.

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A relation between antisocial personality disorder and alcohol-related disorders has
frequently been reported. Some studies suggest that antisocial personality disorder is
particularly common in men with an alcohol-related disorder and can precede the
development of the alcohol-related disorder. Other studies, however, suggest that
antisocial personality disorder and alcohol-related disorders are completely distinct
entities that are not causally related.

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Depression is more common in women than in men with these disorders. Several
studies reported that depression is likely to occur in patients with alcohol-related
disorders who have a high daily consumption of alcohol and a family history of alcohol
abuse. Persons with alcohol-related disorders and major depressive disorder are at
great risk for attempting suicide and are likely to have other substance-related
disorder diagnoses. Some clinicians recommend antidepressant drug therapy for
depressive symptoms that remain after 2 to 3 weeks of sobriety. Patients with bipolar
I disorder are thought to be at risk for developing an alcohol-related disorder; they
may use alcohol to self-medicate their manic episodes. Some studies have shown that
persons with both alcohol-related disorder and depressive disorder diagnoses have
concentrations of dopamine metabolites (homovanillic acid) and γ-aminobutyric acid
(GABA) in their cerebrospinal fluid (CSF).

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Many persons use alcohol for its efficacy in alleviating anxiety. Although the
comorbidity between alcohol-related disorders and mood disorders is fairly widely
recognized, it is less well known that perhaps 25 to 50 percent of all persons with
alcohol-related disorders also meet the diagnostic criteria for an anxiety disorder.
Phobias and panic disorder are particularly frequent comorbid diagnoses in these
patients. Some data indicate that alcohol may be used in an attempt to self-medicate
symptoms of agoraphobia or social phobia, but an alcohol-related disorder is likely to
precede the development of panic disorder or generalized anxiety disorder.

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Most estimates of the prevalence of suicide among persons with alcohol-related
disorders range from 10 to 15 percent, although alcohol use itself may be involved in
a much higher percentage of suicides. Some investigators have questioned whether
the suicide rate among persons with alcohol-related disorders is as high as the
numbers suggest. Factors that have been associated with suicide among persons with
alcohol-related disorders include the presence of a major depressive episode, weak
psychosocial support systems, a serious coexisting medical condition, unemployment,
and living alone.

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Psychological Theories
A variety of theories relate to the use of alcohol to reduce tension, increase feelings
of power, and decrease the effects of psychological pain. Perhaps the greatest
interest has been paid to the observation that people with alcohol-related problems
often report that alcohol decreases their feelings of nervousness and helps them cope
with the day-to-day stresses of life. The psychological theories are built, in part, on
the observation among nonalcoholic people that the intake of low doses of alcohol in
a tense social setting or after a difficult day can be associated with an enhanced
feeling of well-being and an improved ease of interactions. In high doses, especially
at falling blood alcohol levels, however, most measures of muscle tension and
psychological feelings of nervousness and tension are increased. Thus, tension-
reducing effects of this drug might have an impact most on light to moderate drinkers
or add to the relief of withdrawal symptoms, but play a minor role in causing
alcoholism. The theories that focus on alcohol’s potential to enhance feelings of being
powerful and sexually attractive and to decrease the effects of psychological pain are
difficult to evaluate definitively.

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Psychodynamic Theories
Perhaps related to the disinhibiting or anxiety-lowering effects of lower doses of alcohol is the hypothesis
that some people may use this drug to help them deal with self-punitive harsh superegos and to decrease
unconscious stress levels. In addition, classic psychoanalytical theory hypothesizes that at least some
alcoholic people may have become fixated at the oral stage of development and use alcohol to relieve
their frustrations by taking the substance by mouth. Hypotheses regarding arrested phases of psychosexual
development, although heuristically useful, have had little effect on the usual treatment approaches and
are not the focus of extensive ongoing research. Similarly, most studies have not been able to document an
“addictive personality” present in most alcoholics and associated with a propensity to lack control of
intake of a wide range of substances and foods. Although pathological scores on personality tests are often
seen during intoxication, withdrawal, and early recovery, many of these characteristics are not found to
predate alcoholism, and most disappear with abstinence. Similarly, prospective studies of children of
alcoholics who themselves have no co-occurring disorders usually document high risks mostly for
alcoholism. As is described later in this text, one partial exception occurs with the extreme levels of
impulsivity seen in the 15 to 20 percent of alcoholic men with antisocial personality disorder, because they
have high risks for criminality, violence, and multiple substance dependencies.

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Behavioral Theories
Expectations about the rewarding effects of drinking, cognitive attitudes toward
responsibility for one’s behavior, and subsequent reinforcement after alcohol intake
all contribute to the decision to drink again after the first experience with alcohol
and to continue to imbibe despite problems. These issues are important in efforts to
modify drinking behaviors in the general population, and they contribute to some
important aspects of alcoholic rehabilitation.

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Sociocultural Theories
Sociocultural theories are often based on extrapolations from social groups that have
high and low rates of alcoholism. Theorists hypothesize that ethnic groups, such as
Jews, who introduce children to modest levels of drinking in a family atmosphere and
eschew drunkenness have low rates of alcoholism. Some other groups, such as Irish
men or some American Indian tribes with high rates of abstention but a tradition of
drinking to the point of drunkenness among drinkers, are believed to have high rates
of alcoholism.

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Childhood History
Researchers have identified several factors in the childhood histories of persons with
later alcohol-related disorders and in children at high risk for having an alcohol-
related
disorder because one or both of their parents are affected. In experimental studies,
children at high risk for alcohol-related disorders have been found to possess, on
average, a range of deficits on neurocognitive testing, low amplitude of the P300
wave on evoked potential testing, and a variety of abnormalities on
electroencephalography (EEG) recordings. Studies of high-risk offspring in their 20s
have also shown a generally blunted effect of alcohol compared with that seen in
persons whose parents have not been diagnosed with alcohol-related disorder. These
findings suggest that a heritable biological brain function may predispose a person to
an alcohol-related disorder. A childhood history of attention-deficit/hyperactivity
disorder (ADHD), conduct disorder, or both, increases a child’s risk for an alcohol-
related disorder as an adult. Personality disorders, especially antisocial personality
disorder, as noted earlier, also predispose a person to an alcohol-related disorder.

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Importance of Genetic Influences. Four lines of evidence support the conclusion that
alcoholism is genetically influenced. First, a threefold to fourfold increased risk for severe
alcohol problems is seen in close relatives of alcoholic people. The rate of alcohol
problems increases with the number of alcoholic relatives, the severity of their illness,
and the closeness of their genetic relationship to the person under study. The family
investigations do little to separate the importance of genetics and environment, and the
second approach, twin studies, takes the data a step further. The rate of similarity, or
concordance, for severe alcohol-related problems is significantly higher in identical twins
of alcoholic individuals than in fraternal twins in most investigations, which estimate that
genes explain 60 percent of the variance, with the remainder relating to nonshared,
probably adult environmental influences. Third, the adoption-type studies have all
revealed a significantly enhanced risk for alcoholism in the offspring of alcoholic parents,
even when the children had been separated from their biological parents close to birth
and raised without any knowledge of the problems within the biological family. The risk
for severe alcohol-related difficulties is not further enhanced by being raised by an
alcoholic adoptive family.

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Alcohol Use Disorder

 Patterns of Use
 Phase I. Prealcoholic phase: Characterized by use of alcohol to relieve
everyday stress and tensions of life.
 Phase II. Early alcoholic phase: Begins with blackouts—brief periods of
amnesia that occur during or immediately following a period of drinking;
alcohol is now required by the person.
 Phase III. The crucial phase: Person has lost control; physiological
dependence is clearly evident.
 Phase IV. The chronic phase: Characterized by emotional and physical
disintegration. The person is usually intoxicated more often than sober.
Effects of Alcohol on the Body

 Peripheral neuropathy is characterized by:


 Peripheral nerve damage
 Pain
 Burning
 Tingling
 Prickly sensations of the extremities
 Alcoholic myopathy: thought to result from the same B vitamin
deficiency that contributes to peripheral neuropathy
 Acute: sudden onset of muscle pain, swelling, and weakness; reddish
tinge to the urine; and a rapid rise in muscle enzymes in the blood
 Chronic: gradual wasting and weakness in skeletal muscles

 Wernicke’s encephalopathy
Most serious form of thiamine deficiency in alcoholic patients
 Korsakoff’s psychosis
Syndrome of confusion, loss of recent memory, and confabulation in
alcoholic patients
 Alcoholic cardiomyopathy
Effect of alcohol on the heart is an accumulation of lipids in the
myocardial cells, resulting in enlargement and a weakened
condition.
 Esophagitis
Inflammation and pain in the esophagus occurs because of the toxic
effects of alcohol on the esophageal mucosa and also because of
frequent vomiting associated with alcohol use.
 Gastritis
Effects of alcohol on the stomach include inflammation of the
stomach lining characterized by epigastric distress, nausea,
vomiting, and distention.
 Pancreatitis
 Acute: usually occurs 1 or 2 days after a binge of excessive alcohol
consumption. Symptoms include constant, severe epigastric pain,
nausea and vomiting, and abdominal distention.
 Chronic: leads to pancreatic insufficiency resulting in steatorrhea,
malnutrition, weight loss, and diabetes mellitus
 Alcoholic Hepatitis
 Caused by long-term heavy alcohol use
 Symptoms: enlarged, tender liver; nausea and vomiting; lethargy;
anorexia; elevated white cell count; fever; and jaundice. Also ascites and
weight loss in severe cases.
 Cirrhosis of the Liver
Cirrhosis is the end-stage of alcoholic liver disease and is believed
to be caused by chronic heavy alcohol use. There is widespread
destruction of liver cells, which are replaced by fibrous (scar)
tissue.
 Leukopenia
Impaired production, function, and movement of white blood cells
 Thrombocytopenia
Platelet production and survival are impaired as a result of the toxic
effects of alcohol.
 Sexual Dysfunction
 In the short term, enhanced libido and failure of erection are
common.
 Long-term effects include gynecomastia, sterility, impotence, and
decreased libido.
 Alcohol use during pregnancy can result in fetal alcohol spectrum
disorders (FASDs):
 Fetal alcohol syndrome (FAS): problems with learning, memory,
attention span, communication, vision, and hearing
 Alcohol-related neurodevelopmental disorder
 Alcohol-related birth defects
 No amount of alcohol during pregnancy is considered safe.
 Alcohol can damage a fetus at any stage of pregnancy.
Characteristics of FAS:
 Abnormal facial features  Learning difficulties

 Small head size  Speech and language delays

 Shorter-than-average height  Intellectual disability

 Low body weight  Poor reasoning skills

 Poor coordination  Sleep and sucking problems as a


baby
 Hyperactive behavior
 Vision or hearing problems
 Difficulty paying attention
 Problems with the heart,
 Poor memory kidneys, or bones
 Difficulty in school
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Bind to the mu receptors in the CNS to modulate pain

 Intoxication- pinpoint pupils, sedation, constipation,


bradycardia, hypotension and decreased respiratory rate

 Withdrawal- not life threatening unless severe medical


illness but extremely uncomfortable. s/s dilated pupils
lacrimation, goosebumps, n/v, diarrhea, myalgias,
arthralgias, dysphoria or agitation

 Rx- symptomatically with antiemetic, antacid,


antidiarrheal, muscle relaxant (methocarbamol),
NSAIDS, clonidine and maybe BZD

 Neuroadaptation: increased DA and decreased NE


Opioid Induced Disorder
• Intoxication
– Symptoms are consistent with the half-life of most opioid drugs and
usually last for several hours.
– Symptoms include initial euphoria followed by apathy, dysphoria,
psychomotor agitation or retardation, and impaired judgment.
– Severe opioid intoxication can lead to respiratory depression, coma, and
death.
Opioid Induced Disorder (cont.)
• Withdrawal
– From short-acting drugs (e.g., heroin):
• Symptoms occur within 6 to 8 hours, peak within 1 to 3 days, and gradually
subside in 5 to 10 days
– From long-acting drugs (e.g., methadone):
• Symptoms occur within 1 to 3 days, peak between 4 and 6 days, and subside in
14 to 21 days
– From ultra-short-acting meperidine:
• Symptoms begin quickly, peak in 8 to12 hours, and subside in 4 to 5 days
Opioid Induced Disorder (cont.)
• Symptoms of Opioid Withdrawal
– Dysphoria, muscle aches, nausea and vomiting, lacrimation or
rhinorrhea, pupillary dilation, piloerection, sweating, abdominal
cramping, diarrhea, yawning, fever, and insomnia
 CD treatment
 support, education, skills building, psychiatric and psychological
treatment, NA

 Medications
 Methadone (opioid substitution)
 Naltrexone
 Buprenorphine (opioid substitution)
 Naltrexone
 Opioid blocker, mu antagonist
 50mg po daily

 Methadone
 Mu agonist
 Start at 20-40mg and titrate up until not craving or using illicit opioids
 Average dose 80-100mg daily
 Needs to be enrolled in a certified opiate substitution program

 Buprenorphine
 Partial mu partial agonist with a ceiling effect
 Any physician can Rx after taking certified ASAM course
 Helpful for highly motivated people who do not need high doses
Stimulant Use Disorder
• A Profile of the Substance
– Amphetamines
– Synthetic stimulants
– Nonamphetamine stimulants
– Cocaine
– Caffeine
– Nicotine
Stimulant Use Disorder (cont.)
• Patterns of Use
• Effects on the Body
– CNS effects
– Cardiovascular effects
– Pulmonary effects
– Gastrointestinal and renal effects
– Sexual functioning
 Intoxication (acute)
 psychological and physical signs

 euphoria, enhanced vigor, gregariousness, hyperactivity,


restlessness, interpersonal sensitivity, anxiety, tension, anger,
impaired judgment, paranoia

 tachycardia, papillary dilation, HTN, N/V, diaphoresis, chills, weight


loss, chest pain, cardiac arrhythmias, confusion, seizures, coma
Stimulant Use Disorder (cont.)
• Intoxication
– Amphetamine and cocaine intoxication produce euphoria, impaired
judgment, confusion, changes in vital signs (even coma or death,
depending on amount consumed).
– Caffeine intoxication usually occurs following consumption in excess of
250 mg. Restlessness and insomnia are the most common symptoms.
 Chronic intoxication
 affective blunting, fatigue, sadness, social withdrawal, hypotension, bradycardia, muscle
weakness
 Withdrawal
 not severe but have exhaustion with sleep (crash)
 treat with rest and support
Stimulant Use Disorder (cont.)
• Withdrawal
– Amphetamine and cocaine withdrawal may result in
dysphoria, fatigue, sleep disturbances, and increased
appetite.
– Withdrawal from caffeine may include headache,
fatigue, drowsiness, irritability, muscle pain and
stiffness, and nausea and vomiting.
– Withdrawal from nicotine may include dysphoria,
anxiety, difficulty concentrating, irritability,
restlessness, and increased appetite.
 Route: nasal, IV or smoked
 Has vasoconstrictive effects that may outlast use and
increase risk for CVA and MI (obtain EKG)
 Can get rhabdomyolsis with compartment syndrome from
hypermetabolic state
 Can see psychosis associated with intoxication that resolves
 Neuroadaptation: cocaine mainly prevents reuptake of DA
 CD treatment including support, education, skills, CA
 Pharmacotherapy
 No medications FDA-approved for treatment
 If medication used, also need a psychosocial treatment component
 Similar intoxication syndrome to cocaine but
usually longer
 Route - oral, IV, nasally, smoked
 No vasoconstrictive effect
 Chronic use results in neurotoxicity possibly from
glutamate and axonal degeneration
 Can see permanent amphetamine psychosis with
continued use
 Treatment similar as for cocaine but no known
substances to reduce cravings
 Neuroadaptation
 inhibit reuptake of DA, NE, SE - greatest effect on DA
 CD treatment: including support, education, skills, CA
 No specific medications have been found helpful in treatment although some early
promising research using atypical antipsychotics (methamphetamine)
 Most important preventable cause of death / disease in USA
 25%- current smokers, 25% ex smokers
 20% of all US deaths
 45% of smokers die of tobacco induced disorder
 Second hand smoke causes death / morbidity
 Psychiatric pts at risk for Nicotine dependence-75%-90 % of
Schizophrenia pts smoke
 Drug Interactions
 induces CYP1A2 - watch for interactions when start or
stop (ex. Olanzapine)
 No intoxication diagnosis
 initial use associated with dizziness, HA, nausea
 Neuroadaptation
 nicotine acetylcholine receptors on DA neurons in
ventral tegmental area release DA in nucleus
accumbens
 Tolerance
 rapid
 Withdrawal
 dysphoria, irritability, anxiety, decreased
concentration, insomnia, increased appetite
 Cognitive Behavioral Therapy
 Agonist substitution therapy
 nicotine gum or lozenge, transdermal patch, nasal spray

 Medication
 bupropion (Zyban) 150mg po bid,
 varenicline (Chantix) 1mg po bid
Hallucinogen-Induced Disorder
•A Profile of the Substance
Naturally occurring hallucinogens
Synthetic compounds

•Patterns of Use
Use is usually episodic
Hallucinogen-Induced Disorder
(cont.)
• Intoxication
– Occurs during or shortly after using the drug
– Symptoms include perceptual alteration, depersonalization,
derealization, tachycardia, palpitations
Hallucinogen-Induced Disorder
(cont.)
 Symptoms of PCP intoxication include belligerence and
assaultiveness and may proceed to seizures or coma.
 Physiological  Psychological
 Nausea/vomiting  Heightened response to color,
 Chills sounds
 Pupil dilation  Distorted vision
 Increased BP, pulse  Sense of slowed time
 Loss of appetite  Magnified feelings
 Insomnia  Paranoia, panic
 Elevated blood sugar  Euphoria, peace
 Decreased respirations  Depersonalization
 Derealization
 Increased libido
 Naturally occurring - Peyote cactus (mescaline);
magic mushroom(Psilocybin) - oral
 Synthetic agents – LSD (lysergic acid
diethyamide) - oral
 DMT (dimethyltryptamine) - smoked, snuffed, IV
 STP (2,5-dimethoxy-4-methylamphetamine) –
oral
 MDMA (3,4-methyl-enedioxymethamphetamine)
ecstasy – oral
 Designer club drug
 Enhanced empathy, personal insight, euphoria, increased
energy
 3-6 hour duration
 Intoxication- illusions, hyperacusis, sensitivity of touch,
taste/ smell altered, "oneness with the world", tearfulness,
euphoria, panic, paranoia, impairment judgment
 Tolerance develops quickly and unpleasant side effects with
continued use (teeth grinding) so dependence less likely
 Neuroadaptation- affects serotonin (5HT), DA,
NE but predominantly 5HT2 receptor agonists
 Psychosis
 Hallucinations generally mild
 Paranoid psychosis associated with chronic use
 Serotonin neural injury associated with panic, anxiety,
depression, flashbacks, psychosis, cognitive changes.
 Withdrawal – unclear syndrome (maybe similar
to mild stimulants-sleepiness
and depression due to 5HT depletion)
 Most commonly used illicit drug in America
 THC levels reach peak 10-30 min, lipid soluble; long half life of 50 hours
 Intoxication- Appetite and thirst
increase
Colors/ sounds/ tastes are clearer
Increased confidence and euphoria
Relaxation
Increased libido
Transient depression, anxiety, paranoia
Tachycardia, dry mouth, conjunctival injection
Slowed reaction time/ motor speed
Impaired cognition
Psychosis
Cannabis Use Disorder
 A Profile of the Substance
 Marijuana
 Hashish

 Patterns of Use
Cannabis Use Disorder
• Effects on the Body
– Cardiovascular
– Respiratory
– Reproductive
– Central nervous system
– Sexual functioning
 Neuroadaptation
 CB1, CB2 cannabinoid receptors in brain/ body
 Coupled with G proteins and adenylate cyclase to CA channel
inhibiting calcium influx
 Neuromodulator effect; decrease uptake of GABA and DA

 Withdrawal - insomnia, irritability, anxiety, poor appetite,


depression, physical discomfort
Cannabis Use Disorder
• Intoxication
– Symptoms include impaired motor coordination, euphoria, anxiety,
sensation of slowed time, impaired judgment.
– Physical symptoms include conjunctival injection, increased appetite,
dry mouth, and tachycardia.
– Impairment of motor skills lasts for 8 to 12 hours.
Cannabis Use Disorder
• Withdrawal
– Occurs upon cessation of cannabis use that has been heavy and
prolonged.
– Symptoms occur within a week following cessation of use.
– Symptoms include irritability, anger, aggression, anxiety, sleep
disturbances, decreased appetite, depressed mood, stomach pain,
tremors, sweating, fever, chills, or headache.
 Treatment
-Detox and rehab
-Behavioral model
-No pharmacological treatment but may treat other psychiatric
symptoms
 Dissociative anesthetic
 Similar to Ketamine used in anesthesia
 Intoxication: severe dissociative reactions – paranoid
delusions, hallucinations, can become very agitated/
violent with decreased awareness of pain.
 Cerebellar symptoms - ataxia, dysarthria, nystagmus
(vertical and horizontal)
 With severe OD - mute, catatonic, muscle rigidity, HTN,
hyperthermia, rhabdomyolsis, seizures, coma and death
 Treatment
 antipsychotic drugs or BZD if required
 Low stimulation environment
 acidify urine if severe toxicity/coma

 Neuroadaptation
 opiate receptor effects
 allosteric modulator of glutamate NMDA receptor

 No tolerance or withdrawal
SPECT image 75
SPECT image
76
Scans

Alcohol 25 yrs Cocaine 2 yrs

Normal
Marijuana 12 yrs
Ganja Tembakau
SPECT image 78
 Defined by dysfunctional behaviors that are evident among
members of the family of a chemically dependent person or among
family members who harbor secrets of physical or emotional abuse,
other cruelties, or pathological conditions
 Codependent people sacrifice their own needs for the fulfillment of
others to achieve a sense of control.
 Derive self-worth from others
 Feel responsible for the happiness of others
 Commonly deny that problems exist
 The person keeps feelings in control, and often releases anxiety in
the form of stress-related illnesses, or compulsive behaviors such as
eating, spending, working, or use of substances.
 May have experienced abuse or emotional neglect as a child
 Are outwardly focused on others and know very little about how to
direct their lives from their own sense of self
Gambling Disorder
 Persistent and recurrent problematic gambling
behavior that intensifies when the individual is
under stress.

 As the need to gamble


increases, the individual
may use any means
required to obtain money
to continue the addiction.
Gambling Disorder (cont.)
• Gambling behavior usually begins in adolescence,
although compulsive behaviors rarely occur before
young adulthood.

• The disorder usually runs a chronic course, with periods


of waxing and waning.

• The disorder interferes with


interpersonal relationships,
social, academic, or
occupational functioning.
 Biological Influences
 Genetic

 Increased incidence among family members


 Physiological

 Abnormalities in neurotransmitter systems

 Psychosocial Influences
 Loss of a parent before age 15
 Inappropriate parental discipline
 Exposure to gambling activities as an adolescent
 Family emphasis on material and financial symbols
 Lack of family emphasis on saving, planning, and budgeting
 Behavior Therapy
 Cognitive Therapy
 Psychoanalysis
 Psychopharmacology
 SSRIs
 Clomipramine
 Lithium
 Carbamazepine
 Naltrexone
 Gamblers Anonymous
 Organization modeled after Alcoholics Anonymous
 Only requirement for membership is an expressed desire to stop
gambling
 Reformed gamblers help others resist the urge to gamble
 Related Organizations

 Gam-Anon

 For family and spouses


of compulsive gamblers
 Gam-a-Teen

 For adolescent children of compulsive


gamblers
Penatalaksanaan
ketergantungan NAPZA
 Penatalaksanaan sulit.
 Angka kekambuhan tinggi.
 Perlu motivasi tinggi dari penderita.
 Perlu dukungan keluarga dan masyarakat.
 Tujuan : dapat berfungsi baik tanpa pakai NAPZA.

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 Tidak dapat hanya dilakukan oleh penderita
sendiri.
 Komprehensif dan multidisiplin : medis,
psikososial, spiritual.
 Terpadu dan berkesinambungan → hasil
optimal.

 Langkah – langkah :
 Menegakkan diagnosis
 Detoksifikasi
 Rehabilitasi
 Resosialisasi

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Detoksifikasi :
 Penghentian NAPZA, dapat diberikan substitusi
atau psikofarmaka untuk meringankan gejala
lepas zat.
 Pengembalian pola tidur.
 Pengembalian fungsi kognitif.
 Hanya langkah awal, harus dilanjutkan ke
rehabilitasi.

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Rehabilitasi :
 Tetap mempertahankan stop NAPZA.
 Memantapkan dan meningkatkan kondisi fisik,
emosi, intelegensi, sosial, religi, vokasional,
dsb.
 Pengawasan ketat dan rutin.
 Farmakoterapi untuk rumatan, penyekat, atau
sesuai komorbiditas.
 Psikoterapi : individual, kelompok. Termasuk
terapi perilaku.
Resosialisasi : membina lingkungan sosial baru,
lanjutan terapi vokasional dan psikoterapi.

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