Skizofrenia

If you talk to God, you are praying;

if God talks to you, you have schizophrenia.
Thomas Szasz
 Takrif dan pengertian
 Istilah Skizoprenia diciptakan oleh Bleuler (psikiater dari
Swiss)  dari bahasa Yunani skhizo = split / membelah,
dan phren = mind / pikiran  berarti : terbelahnya/
terpisahnya antara emosi dan pikiran/intelektual
 (people with schizophrenia are split off from reality and
can’t distinguish what is real from what is not real)
 Merupakan penyakit psikiatrik kronik pada pikiran
manusia  mempengaruhi seseorang sehingga
mengganggu hubungan antarpersonal dan kemampuan
untuk menjalani kehidupan sosial

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 Some Facts About Schizophrenia
 Schiz: “Split” with reality
 Occurs in all cultures
 Affects 1.5% of American population at
any one time, 10-15X more vulnerable
 1/2 of psychiatric hospitalizations
 M=F; more common in lower SES
(downward drift)
 Blacks less severely impaired than whites;
females less severely impaired than males
 Onset typically in late adolescence/early
adulthood
 The “cancer of mental illness”
 Types of Schizophrenia
 Disorganized (hebephrenic) -- silly and
incoherent (most severe)
 Catatonic -- grossly abnormal motor
behavior and negativism (least common)
 Paranoid -- grossly delusional but better
prognosis (most common)
 Undifferentiated -- All others
 Residual -- After it’s all over
 Predisposing factors
 Combination of genetic and environmental factors
 Neurobiological factors –imaging studies show
decreased brain volume (white matter). Findings
include atrophy in the frontal lobe, cerebellum and
limbic structures. There are also alterations in
neurotransmitters (dopamine, serotonin, and
glutamate)
 Genetic Risk for Schizophrenia
 Fraternal twin 50 % risk
 Identical twin 15 % risk
 Sibling 10 % risk
 One parent affected 15% risk
 Both parents affected 35% risk
 No affected relative 1% risk
Zullies Ikawati's Lecture Notes 10/03/2020
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 A graph to show the genetic
risk of developing
schizophrenia.
Source: Zimbardo et al
(1995)

Q) What does this suggest about

schizophrenia?
 Theories regarding causes of schizophrenia
 Dysregulation Hypothesis- neurotransmitters
causing unstable neurotransmission regarding
dopamine and serotonin.
 Neurodevelopment theory-several brain
structures are abnormal that interfere with
memory (prefrontal cortex and hippocampus)
ETIOLOGI
 Theories regarding causes of schizophrenia
 Viral Theories-mixed evidence that prenatal
exposure to the influenza virus during the 2 nd
trimester of pregnancy may influence the
etiology.
 Sociocultural theory-stress related to poverty,
society, and environment may be a factor.
 Biological Stressors

 Information-processing overload

 Abnormal “gating mechanisms” refers to nerve

potentials and feedback systems within the
nervous system.
 Some Common Triggers
 Poor nutrition
 Lack of sleep
 Infection
 Hostile environment
 Social isolation
 “Hopeless” attitude
 Poor social skills
 Stress Diathesis Model

 Schizophrenia is made worse by stress and

causes stress.
 Liberman (1994)
 Schizophrenia symptoms develop based on the
amount of stress a person experiences and an
internal stress threshold.
Etiology of Schizophrenia: Neurotransmitters
 Dopamine Theory
• Disorder due to excess levels of dopamine
 Drugs that alleviate symptoms reduce dopamine activity
 Amphetamines, which increase dopamine levels, can
induce a psychosis
 Theory revised
• Excess numbers of dopamine receptors or
oversensitive dopamine receptors
• Localized mainly in the mesolimbic pathway
 Dopamine abnormalities mainly related to
positive symptoms

Copyright 2009 John Wiley & Sons, NY

16
 Patofisiologi
 Patofisiologi skizoprenia melibatkan system dopaminergik dan
serotonergik (more recently : glutamat)
 Hipotesis/teori tentang patofisiologi skizoprenia :
• Pada pasien skizoprenia terjadi hiperreaktivitas sistem
dopaminergik
• Hiperdopaminergia pada sistem mesolimbik  berkaitan
dengan gejala positif
• Hipodopaminergia pada sistem mesocortis dan nigrostriatal
 bertanggungjawab thd gejala negatif dan gejala
ekstrapiramidal

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1. Jalur nigrostriatal: dari substantia nigra ke basal ganglia  fungsi gerakan,
EPS
2. jalur mesolimbik : dari tegmental area menuju ke sistem limbik  memori,
sikap, kesadaran, proses stimulus
3. jalur mesocortical : dari tegmental area menuju ke frontal cortex  kognisi,
fungsi sosial, komunikasi, respons terhadap stress
4. jalur tuberoinfendibular: dari hipotalamus ke kelenjar pituitary  pelepasan
Zullies Ikawati's Lecture Notes 10/03/2020
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-Basal Ganglia – involved in the movement of emotions and sensory info.
Abnormal function is thought to contribute to paranoia and hallicinations
-Frontal Lobe – critical to problem solving. Leads to difficulty planning
actions and organizing thoughts
-Limbic System – involved in emotion, contributes to agitation
-Auditory System - hear and understand speech. Overactivity in
Weirnickes area can cause auditory hallucinations.
-Occipital lobe – process info about visual world. Difficulties interpreting
complex images, recognizing motion and reading emotions on others.
-Hippocampus - learning and memory function – both severely impaired
by Chilhood Onset of Schizophrenia.
 In human anatomy, the
extrapyramidal system is a neural
network located in the brain that is
part of the motor system involved
in the coordination of movement.
 The system is called
"extrapyramidal" to distinguish it
from the tracts of the motor cortex
that reach their targets by traveling
through the "pyramids" of the
medulla.
 The pyramidal pathways
(corticospinal and some
corticobulbar tracts) may directly
innervate motor neurons of the
spinal cord or brainstem (anterior
horn cells or certain cranial nerve
nuclei), whereas the
extrapyramidal system centers
around the modulation and
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regulation (indirect control) of
• serotonergic neurons from the dorsal and median raphe nuclei project to
dopaminergic cell bodies within the VTA and SN of the midbrain.
• Serotonergic neurons primarily from the dorsal raphe project to the terminal
fields of the striatum, nucleus accumbens, and cortex.
• Serotonergic neurons have been reported to directly terminate on dopaminergic
cell bodies and exert an inhibitory influence on mesolimbic and nigrostriatal
Zullies Ikawati's Lecture Notes 10/03/2020
dopamine activity through 5-HT2A receptors 22
reductions in serotonin activity are associated with
enhancements in dopamine activity

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 lanjutan

 Reseptor dopamine yang terlibat adalah reseptor

dopamine-2 (D2)  dijumpai peningkatan
densitas reseptor D2 pada jaringan otak pasien
skizoprenia
 Peningkatan aktivitas sistem dopaminergik pada
sistem mesolimbik  bertanggungjawab terhadap
gejala positif
 Peningkatan aktivitas serotonergik  menurunkan
aktivitas dopaminergik pada sistem mesocortis 
bertanggung-jawab terhadap gejala negatif
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More recent data implicate dysfunctions in glutamatergic
neurotransmission in the pathophysiology of psychosis 
deficiency of glutamate lead to psychotic effects
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 Gejala dan tanda
 gambaran klinis skizoprenia sgt bervariasi tidak ada
stereotip yg pasti
 skizoprenia bukan “split personality”  tetapi
gangguan pikiran yang kronis dan mempengaruhi
hubungan interpersonal dan kemampuan untuk
berfungsi sosial sehari-hari  pada fase normal, pasien
memiliki kontrol yang baik terhadap pikiran, perasaan,
tindakannya.
 episode psikotik yang pertama kali mungkin terjadi
secara tiba-tiba, atau biasanya diawali dengan kelakuan
yang menarik diri, pencuriga, dan aneh
 pada episode akut, pasien kehilangan kontak dengan
realitas, dalam hal ini otak menciptakan realitas palsu
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 From memoir of Prof. Elyn Sacs (Majalah Time, 27 Agst 2007)
 When was your first episode?
 At seven or eight. I asked my dad, 'can't we go to the cabana?' He kind of
snapped at me, 'I already said no, and the weather's not great. I need to go back
to work.' And at that moment, I disappointed my dad. It felt like falling apart,
my self losing coherence. Imagine a sand castle with all the sand sliding away
in the receding surf. So in the end, there's no center to take things in and
process them and view the world. That was the first kind of scary, weird thing.
Even more alarming, when I was 16 or 17, I suddenly, having just read Sylvia
Plath and identifying with her, got up in the middle of the day [at school] and
started walking home several miles away, something I'd never done before. I
was a good girl — I never skipped school. And as I was walking, the houses
got very ominous and foreboding, and I started to think that they were sending
me messages. 'Look! See! You must see! You are bad! You are evil!' I didn't
hear it as voices; they were thoughts, but I thought they were thoughts put in
my head by the houses. It was very scary.

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 Diagnostic and Statistical Manual of Mental Disorders edisi 4 (DSM-IV) membagi
gejala skizoprenia menjadi 2 katagori  berkembang menjadi 3 kategori (APA)

Gejala positif Gejala negatif Gejala kognisi

Delusion (khayalan) Alogia (Kehilangan Gangguan perhatian
kemampuan berpikir atau
bicara)
Halusinasi Perasaan/emosi menjadi Gangguan ingatan
tumpul
Perilaku aneh, tidak Avolition (Kehilangan Gangguan fungsi
terorganisir motivasi) melakukan pekerjaan
tertentu
Bicara tidak teratur, Anhedonia/asosiality
topik melompat- (kurangnya kemampuan
lompat tidak saling untuk merasakan kesenangan,
berhubungan mengisolasi diri dari
kehidupan sosial
Ilusi, pencuriga Tidak mampu berkonsentrasi
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 Diagnosis
 Pasien didiagnosis menderita skizoprenia jika terdapat 2
atau lebih tanda-tanda seperti :
• delusi
• halusinasi
• disorganized speech
• perilaku katatonik (aktivitas motorik berlebihan)
• gejala negatif
secara terus menerus sedikitnya dalam waktu enam
bulan, dengan sedikitnya ada satu bulan di mana pasien
menunjukkan gejala-gejala tersebut secara intensif
Note : 6 bln meliputi gejala prodromal dan residual

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Diagnostic Criteria for Schizophrenia (DSM-IV)
A. Characteristic symptoms: Two (or more) of the following, each
present for a significant portion of time during a 1-month period
(or less if successfully treated):
(1) delusions
(2) hallucinations
(3) disorganized speech (e.g., frequent derailment or incoherence)
(4) grossly disorganized or catatonic behavior
(5) negative symptoms, i.e., affective flattening, alogia, or avolition
B. Social/occupational dysfunction: For a significant portion of the
time since the onset of the disturbance, one or more major areas of
functioning such as work, interpersonal relations, or self-care are
markedly below the level achieved prior to the onset (or when the
onset is in childhood or adolescence, failure to achieve expected
level of interpersonal, academic, or occupational achievement).
C. Duration: Continuous signs of the disturbance persist for at least 6
months. This 6-month period must include at least 1 month of
symptoms (or less if successfully treated) that meet Criterion A (i.e.,
active-phase symptoms) and may include periods of prodromal or
residual symptoms. During these
American Psychiatric Association: Diagnostic and Manual of Mental Disorders, 4th ed, Text Revision
(DSM-IV-TR)
Schizophrenia
prodromal or residual periods, the signs of the disturbance may be
manifested by only negative symptoms or two or more symptoms
listed in Criterion A present in an attenuated form (e.g., odd beliefs,
unusual perceptual experiences).
D. Schizoaffective and Mood Disorder exclusion: Schizoaffective
Disorder and Mood Disorder With Psychotic Features have been
ruled out because either (1) no Major Depressive, Manic, or Mixed
Episodes have occurred concurrently with the active-phase
symptoms; or (2) if mood episodes have occurred during active-phase
symptoms, their total duration has been brief relative to the duration
of the active and residual periods.
E. Substance/general medical condition exclusion: The disturbance is
not due to the direct physiological effects of a substance (e.g., a drug
of abuse, a medication) or a general medical condition.
F. Relationship to a Pervasive Developmental Disorder: If there is a
history of Autistic Disorder or another Pervasive Developmental
Disorder, the additional diagnosis of Schizophrenia is made only if
prominent delusions or hallucinations are also present for at least a
month (or less if successfully treated).
 Prognosis
 Prognosis cukup baik jika : onset lebih lambat,
pemicunya diketahui, sejarah pre-morbid bagus, dan ada
dukungan keluarga  20-30% mungkin bisa kembali
normal
 Kurang lebih 20-30 % mungkin akan mengalami gejala
sedang
 40 – 60% mungkin tidak akan kembali normal seumur
hidupnya

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 Schizophrenia
Prognostic Features
Good Prognosis Poor Prognosis
Later onset Early onset
Obvious precipitating factors No precipitating factors
Acute onset Insidious onset
Good premorbid social and work history Poor premorbid social and work history
Preponderant positive symptoms Preponderant negative symptoms
Depressive symptoms Absence of depressive symptoms
Preservation of adequate affective expression Blunted or inappropriate affect
Paranoid or catatonic features Undifferentiated or disorganized features
Variable course Chronic course
Absence of neuropsychological impairment Presence of neuropsychological impairment
Absence of structural brain abnormalities Presence of structural brain abnormalities
Good social support systems Poor social support systems
Early adequate treatment No treatment or delayed/ inadequate treatment

Adapted from: Sadock BJ, Sadock VA: Kaplan and Sadock’s Comprehensive Textbook of Psychiatry, 7th ed, Philadelphia,
Lippincott Williams & Wilkins, p. 1197
 Schizophrenia
Complications
 Suicide – 5-10% of deaths
 Depression - occurs in 50% of cases, often
after an acute episode
 Homelessness – 30-35% of homeless
 Crime: 4-fold increase in acts of violence
compared with the general population. These
patients are more frequently victims of both
violent and nonviolent crimes.
 Substance abuse
 Sasaran terapi
 Sasaran terapi: bervariasi, berdasarkan fase
dan keparahan penyakit
 Pada fase akut : mengurangi atau
menghilangkan gejala psikotik dan
meningkatkan fungsi
 Pada fase stabilisasi: mengurangi resiko
kekambuhan dan meningkatkan adaptasi
pasien terhadap kehidupan dalam masyarakat

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 Strategi terapi
Non-farmakologi :
 program rehabilitasi : living skills, social skills,

basic education, work program,supported housing

 Psikoterapi : terapi tambahan, terutama jika pasien

sudah berespon thd obat

 Family education

Farmakologi : menggunakan obat antipsikotik

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Non pharmacological treatment
 Psychosocial interventions

• Social skills training

• Vocational rehabilitation
• Family psychoeducation – especially for
families with high levels of “expressed
emotion”
• Supportive psychotherapy
 Psychological Treatments
 Cognitive behavioral therapy
• Recognize and challenge delusional beliefs
• Recognize and challenge expectations associated with
negative symptoms
 e.g., “Nothing will make me feel better so why bother?”
 Cognitive enhancement therapy (CET)
• Improve attention, memory, problem solving and other
cognitive based symptoms

Copyright 2009 John Wiley & Sons, NY

38
 Terapi Farmakologi
Menggunakan obat-obat antipsikotik untuk memodulasi
neurotransmiter yang terlibat

Antipsikotik
Tipikal/FGA Atipikal/SGA

- Generasi lama - Generasi lebih baru (th

- Memblok reseptor dopamin
D2
- Efek samping EPS besar
- Efektif untuk mengatasi
gejala positif
1990an)
- Memblok reseptor 5-HT2, efek
blokade dopamin rendah
- Efek samping EPS lebih kecil
- Efektif untuk mengatasi gejala
baik positif maupun negatif
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 Antipsikotik tipikal (FGA)
 Klorpromazin
 Tioridazin Low potency
 Mesoridazin
 Flufenazin
 Perfenazin
 Thiotixene
 Haloperidol
 Loxapin High potency
 Molindon

Pada dasarnya potensi tidak berhubungan dengan efektifitas obat

 hanya menunjukkan miligram equivalency (contoh : haloperidol
15 mg equivalent dengan klorpromasin 750 mg)  jika digunakan
dalam dosis yang ekuipoten semua antipsikotik tipikal sama
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 Antipsikotik atipikal (SGA)
 Clozapin
 Risperidon
 Olanzapin
 Quetiapin Antagonis reseptor 5-HT,
Blokade dopamin rendah
 Ziprasidon
 Aripiprazol

• terdapat hubungan kuat antara system dopaminergik dan

serotonergik  serotonin memodulasi fungsi dopamine
(reductions in serotonin activity are associated with
enhancements in dopamine activity)
• Saat ini lebih banyak digunakan sebagai “drug of choice”
karena relatif lebih aman dari efek samping
ekstrapiramidal
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 Terapi pada episode akut skizoprenia :
 Tujuan terapi 7 hari pertama : mengurangi agitasi, hostility,
agresi, anxiety
 jika seorang pasien terkena serangan psikotik akut, lebih baik
diatasi dengan “meng-imobilisasi” pasien dulu dan
mengajaknya bicara, kemudian diberi benzodiazepine untuk
penenang dan atau suatu obat antipsikotik
 benzodiazepine (exp: lorazepam 2 mg i.m setiap 30 menit)
terbukti efektif mengurangi agitasi  shg mengurangi dosis
antipsikotik yang dibutuhkan  mengurangi efek samping
 Jika dibutuhkan antipsikosis utk agitasi yang berat  obat
potensi tinggi bisa digunakan, exp: haloperidol 2-5 mg IM
setiap 60 min
 Selanjutnya dapat digunakan antipsikotik lain sesuai algoritma

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 Terapi stabilisasi
 Terapi minggu ke 2-3  terapi stabilisasi  tujuannya:
meningkatkan sosialisasi dan perbaikan kebiasaan (self-
care habits) dan perasaan
 Mungkin perlu waktu 6-8 minggu utk mendapat respon
yang diharapkan, pada pasien kronis  mungkin butuh
waktu 3-6 bulan
 Pengobatan : menggunakan antipsikotik atipikal (if any);
jika menggunakan obat tipikal: dosis yang ekuivalen
dengan klorpromasin 300-1000 mg dapat digunakan
 Terapi tidak bisa menyembuhkan, hanya mengurangi
gejala

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 Terapi pemeliharaan
 Tujuan : mencegah kekambuhan
 harus diberikan sedikitnya sampai setahun sejak sembuh dari
episode akut
 bahkan untuk bisa lebih berhasil  perlu terapi selama
sedikitnya 5 tahun, kemudian dosis pada diturunkan perlahan-
lahan
 terapi pemeliharaan dapat diberikan dalam dosis setengah dari
dosis akut
 bagi pasien yang kepatuhannya rendah  ada obat yang dibuat
dalam formulasi depot  contoh : flufenazin dekanoat atau
haloperidol dekanoat  dapat diberikan setiap 2 -4 minggu
sekali secara i.m.  tetapi formulasi depot ini hanya dapat
diberikan jika pasien telah memiliki dosis efektif p.o yang
stabil
 Recently : Risperidon long acting dg dosis 25-50 mg IM every
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 Penatalaksanaan pasien yang resisten
terhadap pengobatan

 Satu-satunya obat yang terbukti superior dalam uji

klinik pada pasien resisten adalah Clozapin
 Namun karena CLZ memiliki efek samping
hipotensi ortostatik, dosis harus dititrasi
 Obat penguat dapat diberikan jika pasien tidak
berespon baik  contoh: Li, Carbamazepin, asam
valproat

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TIMA
Algoritma terapi skizoprenia
Serangan pertama Tahap 1:
atau belum pernah Coba SGA tunggal:
menggunakan SGA max 12 minggu
Aripiprazol, olanzapin,
sebelumnya quetiapin, risperidon, atau
ziprasidon
Respon parsial atau tidak ada
Tahap 2:
Coba SGA tunggal yang lain max 12 minggu
selain yang dipakai pada tahap 1

Respon parsial atau tidak ada Respon parsial atau tidak ada

6 bulan
Tahap 2A Tahap 3
Coba FGA atau SGA yg lain Respon parsial Coba FGA atau SGA yg lain
atau tidak ada

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Respon parsial atau tidak ada

Tahap 4
Klozapin Menolak klozapin

tidak ada respon

Tahap 5
Coba satu obat
FGA atau
SGA
yg belum
tidak ada respon dicoba

Tahap 6
Terapi kombinasi
SGA + FGA, kombinasi SGA,
(FGA atau SGA) + ECT,
(FGA atau SGA) + agen lain
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 Algoritma tatalaksana terapi
Tidak ada riwayat Ada riwayat
Kegagalan terapi AT Kegagalan terapi AT
Olanzapin or Gunakan Olanzapin or Gunakan
Stage 1 Quetiapin or salah satu Quetiapin or salah satu
Risperidon Risperidon
Tidak ada respon Tidak ada respon
Tidak Tidak
Stage 2 Gunakan yang lain patuh Haloperidol dekanoat Gunakan yang lain
atau flufenazin dekanoat patuh
Tidak ada respon Tidak ada respon
Tidak ada respon
Stage 3 Gunakan yang lain Gunakan yang lain
Gunakan yang lain
Tidak ada respon Tidak ada respon
Stage 4 Gunakan AP tipikal Tidak ada respon

Tidak ada respon

Stage 5 Clozapin Cont’d

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 lanjutan

Stage 5 Clozapin

Respon parsial

Stage 5a Clozapin + obat

pendukung Tidak ada respon
(AP tipikal/atipikal, atau menolak klozapin
mood stabilizer, ECT,
antidepresan
Tidak ada respon

Stage 5b
Kombinasi Atipikal+tipikal, atau kombinasi tipikal,
atau kombinasi atipikal, atau atipikal + ECT

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 Efek samping relatif
Obat sedasi ekstrapiramidal antikolinergi ortostatik
k
Klorpromaz ++++ +++ +++ ++++
in
Flufenazin + ++++ + +
Haloperidol + ++++ + +
Loksapin +++ +++ ++ +++
Perfenazin ++ +++ ++ ++
Tioridazin ++++ +++ ++++ ++++
Tiotiksen + ++++ + +
Molindon + +++ ++ ++
Klozapin ++++  ++++ ++++
Olanzapin ++ ++ ++ ++
Quetiapin ++ + + ++
Risperidon + ++ + ++
Zullies Ikawati's Lecture Notes 10/03/2020
Ziprasidon ++ ++ + ++ 50
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 Rentang dosis oral efektif dan potensi anti psikotik
Obat Dosis akut Dosis pemeliharaan Potensi
(mg/hari) (mg/hari)
Klorpromasin 400 – 1000 100 – 300 100
Tioridazin 400 – 800 100 – 200 100
Flufenazin 10 – 60 3 – 20 2
Perfenazin 8 – 64 4 – 32 8
Trifluoperazin 20 – 80 5 – 20 5
Tiotiksen 20 – 80 5 – 30 4
Haloperidol 10 – 60 3 – 20 2
Loxapin 40 – 160 20 – 80 10
Molindon 50 – 200 20 – 100 10
Klozapin 300 – 600 150 – 400 -
Risperidon 4–6 2–4 -
Olanzapin 10 – 20 5 – 50 -
Quetiapin 300 – 600 150 – 300 -
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 Antipsikotik yang beredar di Indonesia
(ISO 2004, IONI 2000)

 Klorpromazin (generik,  Trifluoperazin (generik,

Meprosetil, Largactil,
Largazine, Promactil)
 Haloperidol (Lodomer,
Govotil, Halonace, Haldol,
Seradol, Serenace)
 Flufenazin (Anatensol)
 Perfenazin (generik,
Trilafon)
 Proklorperazin (Stemetil)
 Tioridazin (Melleril)
Stelazine, Trizine)
 Levomepromazin
(Nozinan)
 Flufenazin dekanoat
(Modecate)
 Haloperidol dekanoat
(Haldol decanoas)
 Risperidon (Persidal,
Rizodal, Zofredal)
 Klozapin (Clozaril)
 Quetiapin
 Olanzapin

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 Masalah dalam penggunaan obat antipsikotik : ketidakpatuhan
akibat efek samping obat

 efek samping ekstrapiramidal  dijumpai pada obat antipsikotik

tipikal
 efek antikolinergik (mulut kering, pandangan kabur, konstipasi,
retensi urin, penurunan memori)  pada antipsikotik potensi rendah
(exp: klorpromazin)
 tardive dyskinesia  gerakan yg tidak terkontrol, terutama pada
mulut, lidah
 efek pada kardiovaskuler (hipotensi ortostatik)  pada obat tipikal
dan atipikal
 efek pada fungsi seksual dan endokrin
 kejang  potensi tertinggi pada pemakaian klorpromazin atau
klozapin
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 Efek samping utama ?
Gejala ekstra piramidal
 dystonic reaction (kekejangan otot yang nyeri)
- banyak dijumpai pada obat antipsikotik potensi tinggi
- diatasi dengan obat antikolinergik (benztropin, THF, atau
difenhidramin)
 Pseudoparkinsonism
- adanya blockade dopaminergik di striatum  muncul gejala mirip
Parkinson
- diatasi dengan antikolinergik (benztropin) atau amantadin
 akathisia ( tidak bisa duduk tenang, dan gerakan-gerakan yang tidak
bisa berhenti)
- paling tidak responsive terhadap terapi  turunkan dosis, atau
- diatasi dengan propanolol atau benzodiazepine (lorazepam,
klonazepam)

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Zullies Ikawati's Lecture Notes 10/03/2020
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 Prevention ?
Recent study : schizophrenia is due to a genetic predisposition and
environmental stressors early in a child's development (during
pregnancy and birth, and/or early childhood) which lead to
subtle alterations in the brain that make a person susceptible to
developing schizophrenia.
Additional environmental factors and stresses later in life (during
childhood, adolescence and young adulthood) can either damage
the already vulnerable brain further or lessen the expression of
neurodevelopmental defects and decrease the risk of
schizophrenia

There is no specific amount of genetic or environmental input that

has been identified that will ensure someone will or will not
develop schizophrenia so it is never to late or too early to begin
planning for your mental health and that of your children
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 Evaluasi outcome terapi
 Pemantauan dapat dilakukan dgn berbagai alat bantu,
misal: Brief Psychiatric Rating Scale (BPRS),
Positive and Negative Symptom Scale (PANSS), dll
 Pemantauan juga dilakukan terhadap ESO, spt: EPS
(utama), weight gain, antikolinergik, hipotensi
ortostatik, dll.
 Khusus utk clozapin : check WBC setiap minggu
selama terapi.

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 Agranulocytosis Monitoring Guidelines
 Check WBC before starting clozapine. Do not start the drug if the WBC
is less than 3500/mm3.
 Teach patient to immediately report any sign of infection, such as sore
throat, fever, weakness, lethargy.
 Measure WBC level every week during treatment and for 4 weeks after
treatment ends.

If laboratory results reveal a WBC of:

• < 2000/mm3 or an absolute neutrophil count (ANC) < 1000/mm3
 stop clozapine, check WBC and differential daily, consider bone
marrow aspiration and protective isolation.
• 2000 - 3000/mm3 or ANC is 1000-1500/mm3  stop clozapine,
check WBC and differential daily, monitor for signs of infection;
clozapine may be resumed if infection absent, WBC rises above
3000/mm3, and ANC above 1500 mm3, but continue checking
WBC and differential twice weekly.
• 3000-3500/mm3, a drop of 3000/mm3 over 1-3 weeks, or immature
forms, repeat WBC with a differential count. If the repeat WBC is
still 3000-3500/mm3 and the ANC is more than 1500/mm3, repeat
WBC with differential twice weekly until 10/03/2020
the count rises above
3500/mm3. 59
 Key points:
Key points:Key

• skizoprenia adalah penyakit kronis yang memerlukan terapi

pemeliharaan untuk mencegah kekambuhan
• perbedaan antara gejala negative dan positif mempengaruhi
pemilihan obat, selain pertimbangan profil efek samping dan
sejarah respon thd obat
• pada pengatasan episode akut, penggunaan kombinasi
benzodiazepin dengan suatu obat antipsikotik yang tepat
lebih baik daripada menggunakan antipsikotik dosis tinggi
• Tanpa pemeliharaan dengan obat, 70% pasien dapat kambuh
dalam waktu satu tahun
• Terapi pemeliharaan yang terus menerus menggunakan
antipsikotik dosis rendah diperlukan, karena terapi yang
terputus-putus tidak dapat mencegah kekambuhan
Zullies Ikawati's Lecture Notes 10/03/2020
60
 lanjutan
• Efek samping gejala ekstra pyramidal dan tardive
dyskinesia merupakan efek samping tersering dan
serius dari obat antipsikotik dan merupakan
penyebab utama ketidak patuhan pasien terhadap
pengobatan
• Obat antipsikotik atipikal merupakan revolusi
dalam pengobatan skizoprenia  th 1990, untuk
pertama kalinya gejala negative dapat diobati
secara efektif
• Risperidon, olanzapin, dan quetiapin merupakan
pemula generasi obat atipikal  menjadi first line
treatment untuk skizoprenia
Zullies Ikawati's Lecture Notes 10/03/2020
61
 SCHIZOFRENIA 6 (Sebuah kata motivasi)
  
 jiwa –jiwa yang terasa terbelenggu
 tak harus merasa kelu dan sendu
 karena sesungguhnya bisa terasa syahdu
  
 jiwa-jiwa yang terasa berbeda
 tak harus merasa menderita dan merana
 karena sejatinya setiap jiwa adalah sama
  
 jiwa-jiwa yang terasa asing
 tak harus merasa berpaling
 karena kita adalah pemilik jiwa kita sendiri yang sejati
  
 jiwa-jiwa yang terasa terjajah
 tak harus merasa kalah dan menyerah
 karena sebenarnya setiap jiwa adalah merdeka
  
 schizofrenia yang syahdu, sejati, tak berbeda dan merdeka
 sesungguhnya adalah sebuah jiwa indah yang nyata…
  
 Djogja, 2 Agustus 2011
Thank you