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Caffeine Related Disorders

Epidemiologi
Kafein merupakan zat psychoactive yang paling
banyak digunakan
Di USA, orang dewasa rata-rata mengonsumsi
200mg kafein/hari

Etiology
Setelah terekspos terhadap kafein, konsumsi yang berkelanjutan dapat dipengaruhi
beberapa faktor seperti efek pharmacological dari kafein, kafein reinforcing effects,
predisposisi genetic ke penggunaan kafein, dan faktor pribadi konsumen
Neuropharmacology
Kafein
o Class = Methylxantine
o Half-life 3 10 jam, Peak concentration 30 60 menit
o Water & lipid soluble (Dapat melewati BBB)
o Berperan sebagai antagonis adenosine receptors (empat subtype A1, A2a, A2b, A3).
Secara normal, Adenosine receptor mengaktivasi protein inhibitor G (Gi) yang
akan menginhibisi pembentukan second-messenger cyclic adenosine
monophosphate (cAMP). Intake kafein maka akan menyebabkan peningkatan
jumlah intraneuronal cAMP pada neuron yang memiliki adenosine receptor.
o Beberapa penelitian menunjukkan bahwa konsumsi kafein, terutama pada dosis
tinggi atau terkonsentrasi, dapat meningkatkan aktivitas dopamine dan
noradrenergic neurons. Efek dopamine yang meningkat dapat diasosiasikan dengan
laporan kekambuhan pada pasien schizophrenia. Efek noradrenergic diduga
sebagai penyebab gejala withdrawal.
Efek subyektif & reinforcement
o Dosis kafein satuan rendah hingga moderate (i.e. 20 200 mg) dapat menimbulkan
efek subyektif yang menyenangkan pada manusia (energi meningkat, konsentrasi,
termotivasi dll)
o Dosis kafein 300 800mg, menghasilkan efek yang umumnya dinilai tidak nyaman,
seperti anxietas dan nervous
Predisposisi genetik
o Penelitian membandungkan penggunaan kafein pada anak kembar monozygotic dan
dizygotic menunjukkan angka lebih tinggi pada monozygotic untuk total konsumsi,
penggunaan berat, toleransi kafein, withdrawal, dengan heritabilities 35 77%.
Usia, Jenis kelamin, Ras
o Usia paruh baya, perokok, dan orang yang sering meminum alkohol dianggap lebih
banyak mengonsumsi kafein

Diagnosis
Diagnosis tergantung pada anamnesis komprehensif dari intake produk mengandung kafein pada
pasien, apakah pasien pernah mengalami gejala kafein withdrawal saat konsumsi dihentikan atau
dikurangi.
Caffeine Intoxication
Kriteria diagnosis termasuk konsumsi kafein dalam waktu dekat, biasanya melebihi 250
mg. Gejala yang umum terjadi pada kafein intoxication termasuk agitasi psychomotor,
restlessness, irritabilitas, dan keluhan psychophysiological seperti muscle twitching,
flushed face, mual. Diuresis, gastrointestinal distress, keringat berlebih, kesemutan di jari,
dan insomnia
Konsumsi kafein melebihi 1 gr bisa menimbulkan bicara tidak beraturan, bingung, cardiac
arrhythmias, tidak lelah, agitasi, tinnitus, dan halusinasi visual ringan (light flashes).
Konsumsi kafein melebihi 10 gr bisa menyebabkan generalized tonic-clonic seizure, gagal
nafas, dan kematian.
Caffeine Withdrawal
Gejala putus kafein terjadi pada 50 75 % dari pengguna kafein
Gejala paling umum terjadi adalah sakit kepala, lelah, anxietas, irritabilitas, gejala depresif
ringan, psychomotor terganggu, mual, muntah, keinginan konsumsi kafein, nyeri & kaku
pada otot
Gejala putus kafein mulai sejak 12 24 jam setelah dosis terakhir, gejala memuncak pada
24 48 jam kemudian dan menghilang setelah 1 minggu
Caffeine-Induced Anxiety Disorder
Anxietas terkait dengan penggunaan kafein memiliki gejala yang mirip dengan generalized anxiety
disorder. Pasien mungkin terlihat bicara berlebihan, irritable. Keluhan tidak dapat tidur dan
memiliki energi lebih juga dapat muncul. Kafein bisa memicu munculnya serangan panik pada
pasien dengan panic disorder.
Caffeine-Induced Sleep Disorder
Kafein di asosiasikan dengan kesulitan tertidur, sulit mempertahankan tidur, dan terbangun pada
dini hari.
Caffeine Use Disorder
Diagnosis penyalahgunaan kafein diberikan pada pasien dengan konsumsi kafein berlebih dan
kesulitan berhenti meskipun dengan usaha berulang.
Caffeine-Related Disorder Not Elsewhere Classified

Diagnosis Banding
generalized anxiety disorder
panic disorder with or without agoraphobia
bipolar II disorder
attention-deficit/hyperactivity disorder (ADHD)
sleep disorders
Abuse of caffeine-containing over-the-counter medications, anabolic steroids, and other
stimulants, such as amphetamines and cocaine
hyperthyroidism
pheochromocytoma

Treatment
Nonfarmakologi :
Tujuan Mengutang intake kafein secara bertahap
1. Menentukan konsumsi produk mengandung kafein perhari melalu daily food diary
2. Menentukan dosis kafein dalam mg/hari
3. Mengurangi intake 10% tiap beberapa hari
Farmakologi :
Dapat diberikan Analgesics (i.e. Aspirin)
Cannabis-Related Disorders
Merupakan obat illegal yang paling banyak digunakan di dunia, dengan perkiraan 19 juta
pengguna pada tahun 2012.
Neuropharmacology
Berasal dari tanaman Cannabis sativa, mengandung psychoactive molekul yang fat soluble
disebut cannabinoid. 3 jenis cannabinoid adalah Tetrahydrocannabinol (THC), Cannabidiol
(CBD), dan Cannabinol (CBN). CBD cenderung menghasilkan efek seperti menurunkan fungsi
kognitif, perubahan dalam tidur, dan analgesic.
Delta-9-tetrahydrocannabinol (9-THC) merupakan cannabinoid utama yang bertanggung
jawab atas efek psychoactive dari cannabis. Pada manusia, 9-THC di metabolism di liver menjadi
bentuk metabolit aktifnya, yaitu 11-hydroxy-9-THC. Cannabinoid receptor (CB1, CB2)
merupakan bagian dari famili reseptor G-protein-linked, dan terhubung ke inhibitory G protein.
CB1 reseptor banyak ditemukan pada korteks serebral, basal ganglia, cerebellum, anterior
cingulate cortex dan hippocampus. Setelah cannabinoids berikatan akan menstimulasi pelepasan
monoamine dan y-aminobutyric acid (GABA) neurons.
Saat cannabis dikonsumsi dalam rokok, efek euphoria muncul dalam beberapa menit,
memuncak pada 30 menit, dan bertahan selama 2 4 jam. Sebagian efek motor & kognitif dapat
bertahan selama 5 12 jam. cannabis dapat juga dimasukkan dalam makanan dan dikonsumsi
secara oral. Namun, cannabis yang dimasukkan ke makanan harus 2 3 kali lebih banyak agar
menghasilkan efek yang sama dengan inhalasi.
Diagnosis and Gejala Klinis
Efek fisik paling umum dari cannabis adalah dilasi pembuluh darah conjunctival (mata
merah), meningkatnya nafsu makan, mulut kering, dan tachycardia ringan. Gejala biasanya terjadi
dalam 2 jam penggunaan cannabis. Penelitian menunjukkan penggunaan cannabis jangka panjang
diasosiasikan dengan atrofi cerebral, kejang, kerusakan kromosom, birth defects, reaktivitas imun
terganggu, perubahan pada konsentrasi testosterone, dan disregulasi siklus menstruasi.
DSM-V
Cannabis Use Disorder
A problematic pattern of cannabis use leading to clinically significant impairment or distress, as
manifested by at least 2 of the following, occurring within a 12-month period:
Cannabis is often taken in larger amounts or over a longer period than was intended.
There is a persistent desire or unsuccessful efforts to cut down or control cannabis use.
A great deal of time is spent in activities necessary to obtain cannabis, use cannabis, or
recover from its effects.
Craving, or a strong desire or urge to use cannabis.
Recurrent cannabis use resulting in a failure to fulfill major role obligations at work, school,
or home.
Continued cannabis use despite having persistent or recurrent social or interpersonal
problems caused or exacerbated by the effects of cannabis.
Important social, occupational, or recreational activities are given up or reduced because of
cannabis use.
Recurrent cannabis use in situations in which it is physically hazardous.
Cannabis 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 cannabis.
Tolerance, as defined by either a (1) need for markedly increased cannabis to achieve
intoxication or desired effect or (2) markedly diminished effect with continued use of the
same amount of the substance.
Withdrawal, as manifested by either (1) the characteristic withdrawal syndrome for cannabis
or (2) cannabis is taken to relieve or avoid withdrawal symptoms

Cannabis Intoxication
Cannabis intoxication commonly heightens users' sensitivities to external stimuli, reveals new
details, makes colors seem brighter and richer, and subjectively slows the appreciation of time
defined by DSM-5, as the following:
Recent use of cannabis
Clinically significant problematic behavioral or psychological changes (eg, impaired motor
coordination, euphoria, anxiety, sensation of slowed time, impaired judgment, social
withdrawal) that developed during, or shortly after, cannabis use
At least 2 of the following signs, developing within 2 hours of cannabis use:
o Conjunctival injection
o Increased appetite
o Dry mouth
o Tachycardia
Symptoms not due to a general medical condition and not better accounted for by another
mental disorder

Cannabis Intoxication Delirium


diagnosis is appropriate when the following 2 symptoms predominate:
Disturbance in attention (ie, reduced ability to direct focus, sustain, and shift attention) and
awareness (reduced orientation to the environment)
An additional disturbance in cognition (ie, memory deficit, disorientation, language,
visuospatial ability, or perception)

Cannabis Withdrawal
DSM-5 provided criteria for cannabis withdrawal, defined as follows:
Cessation of cannabis use that has been heavy and prolonged (ie, usually daily or almost
daily use over a period of at least a few months).
Three or more of the following signs and symptoms develop within approximately 1 week
after cessation of heavy, prolonged use:
o Irritability, anger or aggression
o Nervousness or anxiety
o Sleep difficulty (ie, insomnia, disturbing dreams)
o Decreased appetite or weight loss
o Restlessness
o Depressed mood
o At least one of the following physical symptoms causing significant discomfort:
abdominal pain, shakiness/tremors, sweating, fever, chills, or headache
The signs or symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, including intoxication or withdrawal from another
substance.

Cannabis Induced Psychotic Disorder


Cannabis-induced psychotic disorder is coded as 292.9 and defined by DSM-5 as follows:
Presence of one or both of the following symptoms:
o Delusions
o Hallucinations
Evidence from the history, physical examination, or laboratory findings of either one of the
following:
o The symptoms in the first criterion developed during or soon after substance
intoxication or withdrawal.
o The involved substance is capable of producing these symptoms.
The disturbance is not better accounted for by a psychotic disorder that is not substance
induced. Evidence that the symptoms are better accounted for by a psychotic disorder that
is not substance induced might include the following:
o The symptoms precede the onset of the substance use (or medication use).
o The symptoms persist for a substantial period (eg, about a month) after the cessation
of acute withdrawal or severe intoxication or are substantially in excess of what
would be expected given the type or amount of the substance used or the duration of
use.
o Other evidence suggests the existence of an independent nonsubstanceinduced
psychotic disorder (eg, a history of recurrent nonsubstancerelated episodes).
The disturbance does not occur exclusively during the course of a delirium.
The disturbance causes clinically significant distress or impairment in social, occupational,
or other important areas of functioning.

Cannabis Induced Anxiety Disorder


Cannabis-induced anxiety disorder , categorized as a cannabis-induced disorder and coded as
292.89, is defined by the DSM-5 as follows:
Panic attacks or anxiety predominate in the clinical picture.
Evidence from the history, physical examination, or laboratory findings of either of the
following:
o The symptoms in the first criterion developed during or soon after substance
intoxication or withdrawal.
o The involved substance is capable of producing the symptoms in the first criterion.
The disturbance is not better accounted for by an anxiety disorder that is not substance
induced. Evidence that the symptoms are better accounted for by an anxiety disorder that is
not substance induced might include the following:
o The symptoms precede the onset of the substance use (or medication use).
o The symptoms persist for a substantial period (eg, about a month) after cessation of
acute withdrawal or severe intoxication or are substantially in excess of what would
be expected given the type or amount of the substance used or the duration of use.
o Other evidence suggests the existence of an independent nonsubstanceinduced
anxiety disorder (eg, a history of recurrent nonsubstancerelated episodes).
The disturbance does not occur exclusively during the course of a delirium.
The disturbance causes clinically significant distress or impairment in social, occupational,
or other important areas of functioning.

Cannabis Induced Sleep Disorder


DSM-5 defines this as follows:
A prominent and severe disturbance in sleep.
There is evidence from the history, physical examination, or laboratory findings of both of
the following:
o The symptoms in the first criterion developed during or soon after cannabis
intoxication or after withdrawal from or exposure to it.
o Cannabis is capable of producing the symptoms in the first criterion. The disturbance
is not better explained by a sleep disorder that is not substance/medication induced.
Such evidence of an independent sleep disorder could include that symptoms precede
the onset of the cannabis use; symptoms persist for a substantial period (ie about a
month) after the cessation of acute withdrawal or severe intoxication; or there is other
evidence suggesting the existence of an independent nonsubstance/medication-
induced sleep disorder (ie, a history of recurrent nonsubstance/medication-related
episodes).
The disturbance does not occur exclusively during the course of delirium.
The disturbance causes clinically significant distress or impairment in social, occupational,
or other important areas of functioning.

Unspecified Cannabis Related Disorder


for cannabis disorders that cannot be classified as cannabis use disorder, cannabis intoxication,
cannabis intoxication delirium, cannabis withdrawal, cannabis-induced psychotic disorder, or
cannabis-induced anxiety disorder

Treatment
Nonpharmacology :
Principles of treatment for substance abuse : Abstinence and support
Abstinence can be achieved through direct interventions, such as hospitalization, or
through careful monitoring on an outpatient basis by the use of urine drug screens
Support can be achieved through the use of individual, family, and group psychotherapies.
Education for patient and support system

Pharmacology :
Anti Anxiety drug for short term relief of withdrawal symptoms

Lorazepam
MOA : Increasing action of GABA
Initial: 2-3 mg PO q8-12hr PRN; not to exceed 10 mg/day
Maintenance: 2-6 mg/day PO divided q8-12hr
Effects usually last 5-8 hours

Stimulant-Related Disorders
AMPHETAMINES
Neuropharmacology
Route of administration : oral (rapidly absorbed), intravenously (classic amphetamines), inhaled
(designer amphetamine)
Onset of action : oral = within 1 hour, IV = immediate
Mechanism of action :
The classic amphetamines (i.e., dextroamphetamine, methamphetamine, and methylphenidate)
produce their primary effects by causing the release of catecholamines, particularly dopamine,
from presynaptic terminals. The effects are particularly potent for the dopaminergic neurons
projecting from the ventral tegmental area to the cerebral cortex and the limbic areas (Reward
circuit pathway)
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.
Adverse effects :
myocardial infarction
severe hypertension
cerebrovascular disease
ischemic colitis
flushing, pallor, cyanosis
fever
headache
tachycardia
nausea, vomiting
bruxism (teeth grinding)
shortness of breath
tremor

COCAINE
Neuropharmacology
Mechanism of action : competitive blockade of dopamine reuptake by the dopamine transporter.
This blockade increases the concentration of dopamine in the synaptic cleft and results in increased
activation of both dopamine type 1 (D1) and type 2 (D2) receptors.
Effect : As a result of actions in the central nervous system (CNS), cocaine can produce a sense of
alertness, euphoria, and well-being. Users may experience decreased hunger and less need for
sleep.
Route of adm : Inhalation (most common), IV, SC
Onset of action : Immediate
Duration of action : 30 60 minute, but metabolites of cocaine can be present in blood and urine
until 10 days
Adverse effects :
nasal congestion
serious inflammation, swelling, bleeding
ulceration of the nasal mucosa, perforation of nasal septa
nonhemorrhagic cerebral infarctions
Diagnosis and clinical features
Stimulant use disorder
DSM-5 diagnostic criteria for stimulant use disorder are similar to the criteria used for other
substance use disorders
Stimulant Intoxication
Stimulant Withdrawal
Symptoms of anxiety, tremulousness, dysphoric mood, lethargy, fatigue, nightmares
(accompanied by rebound rapid eye movement [REM] sleep), headache, profuse sweating, muscle
cramps, stomach cramps, insatiable hunger, and depression.
The withdrawal symptoms generally peak in 2 to 4 days and are resolved in 1 week.
Stimulant Intoxication delirium
Delirium associated with stimulant use generally results from high doses of a stimulant or from
sustained use, and so sleep deprivation affects the clinical presentation
Stimulant Induced Psychotic Disorder
The hallmark of stimulant-induced psychotic disorder is the presence of paranoid delusions and
hallucinations, which occurs in up to 50 percent of stimulant users.
Stimulant Induced Mood Disorder
The DSM-5 allows for the diagnoses of stimulant-induced bipolar disorder and stimulant-induced
depressive disorder, either of which can begin during either intoxication or withdrawal. In general,
intoxication is associated with manic or mixed mood features, whereas withdrawal is associated
with depressive mood features.
Stimulant Induced Anxiety Disorder
The DSM-5 allows for the diagnosis of stimulant-induced anxiety disorder. The onset of stimulant-
induced anxiety disorder can also occur during intoxication or withdrawal. Stimulants can induce
symptoms similar to those seen in panic disorder, and phobic disorders, in particular.
Stimulant Induced Obsessive Compulsive Disorder
Onset can occur during intoxication or withdrawal. After high doses of stimulants, some
individuals develop time-limited stereotyped behaviors or rituals (i.e., picking at clothing, and
arranging and rearranging items purposelessly)
Stimulant Induced Sexual Dysfunction
Stimulants are often misused by persons to enhance sexual experiences. High doses and longterm
use are associated with erectile disorder and other sexual dysfunctions.
Stimulant Induced Sleep Disorder
Can begin during either intoxication or withdrawal, and sleep dysfunction can vary depending on
the onset. Stimulant intoxication can produce insomnia and sleep deprivation, whereas persons
undergoing stimulant withdrawal can experience hypersomnolence and nightmares

Treatment & Rehabilitation


Amphetamine
An inpatient setting and the use of multiple therapeutic methods (individual, family, and group
psychotherapy). Treatment of specific amphetamine-induced disorders (e.g., amphetamine-
induced psychotic disorder and amphetamine-induced anxiety disorder) with specific drugs (e.g.,
antipsychotic and anxiolytics) may be necessary on a short-term basis. Antipsychotics may be
prescribed for the first few days. In the absence of psychosis, diazepam (Valium) is useful to treat
patients' agitation and hyperactivity.
Comorbid conditions, such as depression, may respond to antidepressant medication. Bupropion
(Wellbutrin) may be of use after patients have withdrawn from amphetamine
Cocaine
The cocaine withdrawal syndrome is distinct from that of opioids, alcohol, or sedative-hypnotic
agents, because no physiological disturbances necessitate inpatient or residential drug withdrawal.
Patients withdrawing from cocaine typically experience fatigue, dysphoria, disturbed sleep, and
some craving; some may experience depression.
No pharmacological agents reliably reduce the intensity of withdrawal. Overdose patients can be
given sedative (e.g. diazepam, lorazepam)
Cocaine blocks reuptake dopamine, serotonin, dan norepinephrine