Farmakologi

sistem saraf pusat (SSP) dan sistem saraf otonom (SSO)

Tri Widyawati

Blok 6
 Objektif Pembelajaran
• Macam-macam obat yang bekerja pada sistem saraf pusat.
• Farmakologi sedative-hipnotik
• Farmakologi antiepileptik
• Farmakologi antipsikotik
• Farmakologi antidepressan
• Farmakologi NAPZA dan psikoaktif
• Penggolongan obat pada sistem saraf otonom
• Adrenergik dan adrenolitik
• Kolinergik dan antikolinergik
 The ANS comprises of three major
subdivisions:-

a) PARASYMPATHETIC NERVOUS SYSTEM

b) SYMPATHETIC NERVOUS SYSTEM AND

c) ENTERIC NERVOUS SYSTEM (ENS).

 The major receptor systems in the ANS

I. CHOLINERGIC RECEPTORS

II. ADRENERGIC RECEPTORS

III. DOPAMINE RECEPTORS

penggolongan obat pada sistem saraf otonom
1. Simpatomimetik (adrenergik)  efek menyerupai aktivitas susunan s.
simpatis
2. Simpatolitik (penghambat adrenergik)  menghambat timbulnya efek
akibat aktivitas saraf simpatis
3. Parasimpatomimetik ( kolinergik )  efek menyerupai aktivitas susunan
s. parasimpatis
4. Parasimpatolitik (penghambat kolinergik)  menghambat timbulnya
efek akibat aktivitas susunan saraf parasimpatis
Respons Simpatis dan Parasimpatis terhadap Obat

SIMPATIS PARASIMPATIS RESPONS

Simpatomimetik Parasimpatomimetik Berlawanan
Simpatolitik Parasimpatolitik Berlawanan
Simpatomimetik Parasimpatolitik Serupa
Simpatolitik Parasimpatomimetik Serupa
adrenergik dan adrenolitik
Sistem Saraf Simpatis
• Katekolamin : senyawa yang dapat menghasilkan respon
simpatomimetik
• Terdiri dari :
- endogen  adrenalin /epinefrin,
noradrenalin/norepinefrin
dan dopamin
- sintetik  isoproterenol, dobutamin
Sistem Saraf Simpatis
• Katekolamin : senyawa yang dapat menghasilkan
respon simpatomimetik
• Terdiri dari :
- endogen  adrenalin /epinefrin,
noradrenalin/norepinefrin
dan dopamin
- sintetik  isoproterenol, dobutamin

Alpha-adrenergic receptors: respond to NE

Beta-adrenergic receptors: respond to EPI
 COMT MAO

1
2

TYROSINE _METYLDOPA_> NA ___ NA

1

2

3

L-Monoamine oxidases (MAO) Adrenalin

COMT (Catechol-O-Methyltransferase)
 Simpatomimetika
tidak langsung

Note:
Dopamine beta-hydroxylase (DBH)
Normetanephrine (NMN)

Simpatomimetika
langsung
 Pupil Pupil
kontriksi dilatasi

Saliva Saliva
bertambah berkurang

Denyut Denyut
Jantung  Jantung 

Konstriksi Dilatasi
bronkiolus & bronkiolus
sekresi 

Menghambat
M’stimulasi peristaltik &
peristaltik & sekresi
sekresi
Glikogen
menjadi
Stimulasi glukosa
rilis
empedu Sekresi
adrenalin &
Noradrenalin
Kontraksi M’hambat
kandung kontraksi
kemih k.kemih
Transmitter dan reseptor simpatis dan parasimpatis

A B

Ujung saraf terminal Ujung saraf terminal

adrenergik Sel Sel
kolinergik dengan
dengan
alfa reseptor reseptor
NE Ach
nikotinik
NE beta1 Ach

NE beta2 Ach muskarinik

AchE

NE: norepinefrin inaktivasi

Ach : asetilkolin

AchE : asetilkolinesterase
 Respon organ efektor terhadap perangsangan saraf otonom
Organ efektor Perangsangan Adrenergik Perangsangan kolinergik
Reseptor Respons
Jantung β1 Denyut jantung  Denyut jantung 
Kontraktilitas  Kontraktilitas 
Vena 1 Konstriksi
β2 Dilatasi
Arteriol : 1, 2 Konstriksi (kuat)
Kulit & mukosa 1, 2 Konstriksi
Otot rangka β2 Dilatasi (dominan)
Koroner 1, 2 Konstriksi
Paru β2 Dilatasi (dominan)
1 Konstriksi
β2 Dilatasi (dominan)
Paru : β2 Relaksasi Kontraksi
Otot bronkus 1 Sekresi  Sekresi 
Kelenjar bronkus β2 Sekresi 
Saluran cerna : 1, 2 Relaksasi Kontraksi 
Otot polos lambung & β2 Relaksasi Relaksasi
usus Sekresi 
Otot sfingter 1 Kontraksi
Kelenjar 2 Sekresi 
Mata : Kontraksi (midriasis) -
Otot radial iris 1 - Miosis
Otot sfingter β2 Relaksasi untuk melihat jauh Kontraksi utk melihat
Otot siliaris (lemah) dekat
Adrenergik dan Penghambat Adrenergik
 D
A D
NE Simpatomimetik
yang bekerja
NE D reseptor langsung
NE D

D
E/NE

B NE D Adrenergik
Simpatomimetik
NE NE
dan
reseptor yang bekerja tidak
/
langsung
Penghambat
NE NE Adrenergik
amfetamine D

D
C NE
NE
NE reseptor Simpatomimetik
yang bekerja
NE D campuran
D D : obat simpatomimetik
Adrenergik (Simpatomimetik)
 SIMPATOMIMETIKA (KIMIAWI)
CATECHOLAMINE

Endogen: adrenalin
noradrenalin
dopamin

 Nonendogen: -adrenergik : adrenalin

1-adrenergik : phenylephrine, methoxamin
2-adrenergik : clonidine, oxymetazoline

-adrenergik : isoprenaline
1-adrenergik : dobutamine
2-adrenergik : terbutaline, procaterol

Dopamin (D) : dopamin

D1 : fenoldopam
D2 : bromocriptin

NONCATECHOLAMINE : amfetamin, metamfetamin

 Obat-obat adrenergik /simpatomimetik

Adrenergik Reseptor Pemakaian dalam klinik

Epinefrin (Adrenalin) 1, β1, β2 Anafilaktik syok, asma akut, henti jantung

Efedrin 1, β1, β2 Hipotensi, bronkospasme, kongesti hidung

NE 1, β1 Syok  vasokonstriktor kuat

Pseudoefedrin 1, β1 Dekongestan

Fenilefrin 1 Dekongestan

Fenilpropanolamin (PPA) 1, β1 Dekongestan

Dopamin β1 Hipotensi

Isoproterenol β1, β2 Payah jantung kongestif  aliran darah miokardium

dan curah jantung

Metaproterenol Β1, β2 Bronkospasme, blok jantung akut

Albuterol β2 Bronkospasme

Terbutalin β2 Relaksasi uterus

Penghambat Adrenergik
(Simpatolitik)
 1
2

TYROSINE METYLDOPA  NA  NA
1

2

3

Adrenalin
Pr
a
si
n

Pa
sc
a
si
n
 PENGHAMBAT SINTESA

BLOKADE RESEPTOR

Blokade penimbunan

BLOKADE PENGLEPASAN
 Simpatomimetika Simpatolitika

syaraf pasca ganglion perangsangan penghambatan

neurotransmiter
sintesa perangsangan penghambatan
penimbunan penghambatan
penglepasan penghambatan
perombakan penghambatan

reseptor perangsangan penghambatan

Efek Penghambat Adrenergik pada Reseptor

• Reseptor alfa 1 :
- vasodilatasi : menurunkan TD. Dapat terjadi refleks takikardi
- miosis : konstriksi pupil
- menekan ejakulasi
• Beta 1 : menurunkan denyut jantung
• Beta 2 : konstriksi bronkiolus, kontraksi
uterus
 Tyrosine
Tyrosine hydroxylase ↓
DOPA
DOPA carboxylase ↓
Dopamine
Dopamine β- hydroxylase ↓
Noradrenaline
PNMT ↓
Adrenaline
 PENGHAMBAT SINTESA NA

PHENYLALANINE
TYROSINE
TYROSINE

METHYLDOPA
DOPA
 METHYLDOPA

METHYLDOPAMINE
DOPAMINE

METHYLNORADRENALINE
NORADRENALINE

ADRENALINE
SIMPATOLITIKA

PRASINAPS PENGHAMBAT SINTESA

-METHYL DOPA
BLOKADE PENIMBUNAN
RESERPINE
PENGHAMBAT PENGLEPASAN NA
GUANETHIDINE

PASCASINAPS BLOKADE RESEPTOR 

BLOKADE RESEPTOR 
 BLOKADE PENYIMPANAN NA

RESERPINE (RAUWOLFIA SERPENTINE)

KEGUNAAN KLINIK: HIPERTENSI

EFEK SAMPING: SSP DEPRESI

SEDASI
PERIFER NASAL CONGESTI

PENGHAMBAT PENGELEPASAN NA

GUANETHIDINE
 Penghambat Adrenergik / Simpatolitik

Penghambat Adrenergik Reseptor Pemakaian dalam klinik

Tolazolin  Hipertensi

Fentolamin  Hipertensi

Prazosin  Hipertensi

Propanolol β1, β2 Hipertensi, aritmia, angina pectoris, pasca infark

miokardium
Nadolol β1, β2 Hipertensi, angina

Pindolol β1, β2 Hipertensi

Timolol β1, β2 Hipertensi, pasca infark miokardium

Metoprolol β1 Hipertensi, angina, pasca infark miokardium

Atenolol β1 Hipertensi, angina

Asebutolol β1 Hipertensi, aritmia ventrikel

kolinergik dan antikolinergik
DEFINITION
• Cholinomimetic / Parasympathomimetics
• Drugs producing actions similar to Ach – by interacting with
cholinergic receptors or by increasing availability of Ach at these sites.
• The current therapeutic use are limited
• Ubiquitous and complicated nature of cholinergic pathway
 Typical
Receptor Name Responses
Locations
Cholinoceptors
Autonomic ganglia Late EPSP
  Muscarinic M1
CNS Complex: arousal, attention, analgesia
Heart : SA node Slowed spontaneous depolarization
Heart: AV node Decrease conduction velocity
  Muscarinic M2
Heart: atrium Decrease contractile force
Heart: ventricle Slight decrease in contractility

  Muscarinic M3 Smooth muscle Contraction

Muscarinic M4 &
  CNS
M5
Skeletal muscle
End-plate depolarization, skeletal muscle
  Nicotinic NM neuromuscular end
contraction
plate (NMJ)
Depolarization and firing of postganglionic
Autonomic ganglia neuron
  Nicotinic NN Adrenal medulla Secretion of cathecolamine
CNS Complex:at least arousal, attention,
analgesia
PHYSIOLOGIC EFFECT
CHOLINERGIC TRANSMISSION
1. Neuromuscular Junction
2. Autonomic Effect
3. CNS Effect
Effects of Acetylcholine
on Peripheral Tissues
TISSUE EFFECTS OF ACETYLCHOLINE
Endothelial cells Release NO, vasodilation
Eye iris (pupillae sphincter muscle) Contraction and miosis
Ciliary muscle Contraction, accomodation of lens to near
vision
Salivary and lacrimal glands Thin and watery secretion
Bronchi Constriction, increase secretion
Heart Bradycardia, decrease contractility
GI tract Increase tone, secretion
Urinary bladder Contraction detrusor m, relaxation of
sphincter m
Reproductive tract, male Erection
Sweat gland Diaphoresis
PHARMACOLOGIC CLASSES
AND AGENTS
Inhibitor of acetylcholine
synthesis, storage, release
ACETHYLCHOLINESTERASE
INHIBITOR
 Pharmacologic manipulation of AChE: No inhibition
Ca 2+

Na+
Muscarinic
ACH
ACH Receptor

Acetylcholinesterase
ACH
ACH ACH
Action Potential ACH
ACH
ACH

ACH
ACH
ACH
Choline Acetate

Presynaptic neuron
Postsynaptic target
 Pharmacologic manipulation of AChE: Inhibition by drugs

Ca 2+

ACH
ACH
Na+
ACH
Muscarinic
ACH
ACH Receptor

Acetylcholinesterase
ACH ACH
ACH ACH
Action Potential ACH
ACH
ACH ACH
ACH ACH
ACH
ACH

Presynaptic neuron
Postsynaptic target
Signs and Symptoms of
Organophosphate poisonings
- diarhea, abdominal pain, vomitting
- blurred vision

Clinical Findings:
- S alivation
- L acrimation
- U rination
- D iarrhea
- G astroenteric disorders
- E yes pinpoint
Drug name Receptors Pharamacological ADR
approach

Physostigmine Mainly muscarinic - (opthal) glaucoma. More potent than

(M1 toM3) -prevent/break the pilocarpine- highly
adhesion of iris with lipid soluble and
lens or cornea toxic hence rarely
used

Neostigmine Mainly at Nm & direct Myasthenia gravis, . Hypotension ,

agonistic action NMJ Postoperative paralytic bronchospasm
ileus/ urinary retention.
Myasthenia gravis
• Autoimmune disorder affecting 1 in 10,000 population
• Causes: Development of antibodies directed to Nicotinic receptors in muscle end
plate – reduction in number by 1/3rd of NM receptors
• Structural damage to NM junction
• Symptoms: Weakness and easy fatigability
• Treatment:
• Neostigmine – 15 to 30 mg orally every 6 hrly
• Adjusted according to the response
• Dose requirement may fluctuate time to time – adjustment required
• Pyridostigmine – less frequency of dosing
• Other drugs: Corticosteroids (prednisolone 30-60 mg /day)
• Azathioprin and cyclosporin also Plasmapheresis
• Plasmapheresis
Myasthenia Gravis - Images
MUSCARINIC RECEPTOR AGONIST
• Choline esters : hydrophilic, poorly absorbed by the oral route and CNS
1. Methacoline
2. Bethanechol
3.Carbachol
• Alkaloids : amphipatic
- Pilocarpine : miotic agent, sialagogue,
xerostomia
Class of Drug name Receptors Pharamacological ADR
approach
drug
Choline esters Ach Not used

Cholin esters bethanechol Mainly -Post Overdosage-CNS

muscarinic- operative/post stimulation,miosis
bladder & GIT partum non ,spasm of
(M3) obstructive accommodation for
-devoid of urinary retention distance
nicotinic effects & neurogenic vision,bronchoconst
bladder. riction,abd.cramps,
-GIT atony sweating

Alkaloid Pilocarpine Dominant M3 -glaucoma. Above n for

recptors -prevent/break systemic-
Mild action at the adhesion of pul.oedema
ganglia(Nn) iris with lens or
cornea
-sialagogue-
xerostomia
Pilocarpine
• Alkaloid from leaves of Pilocarpus
microphyllus
• Prominent muscarinic actions
• Profuse salivation, lacrimation, sweating
• Dilates blood vessels, causes
hypotension
• On Eyes:
• it produces miosis by contraction of
circular muscles of iris
• Contraction of cilliary muscles
• spasm of accommodation -
fixed for near vision
• Increased outflow of AH
• Lowers intraocular pressure (IOP) in
Glaucoma when applied as eye drops
• Too toxic for systemic use
NICOTINIC RECEPTOR AGONIST
• Succinyl choline
- Depolarized blockade
-Induce paralysis during surgery
MUSCARINIC RECEPTOR ANTAGONIST
• Parasymphatolytic / symphatomimetic
• Atropine:
-mydriasis for opthalmologic examination
-inhibit excessive salivation & mucus secretion: surgery
-Counteract the effect of acetylcholinesterase inhibitor and muscarinic
agonist
- marginal activity at nicotinic receptors: high dose
MUSCARINIC RECEPTOR ANTAGONIST
• Scopolamine: CNS, motion sickness
• Pirenzepine: M1 and M4 receptor, peptic ulcer
• Ipratropium: chronic obstructive pulmonary disease
NICOTINIC RECEPTOR
ANTAGONISTS
Name Indication Mechanism

Tubocurarine Muscle relaxant for surgery Long acting nondepolarizing

neuromuscular blockade

Pancuronium Muscle relaxant for surgery Intermediate acting

nondepolarizing
neuromuscular blockade
Vecuronium Muscle relaxant for surgery Intermediate acting
nondepolarizing
neuromuscular blockade
Rocuronium Muscle relaxant for surgery Intermediate acting
nondepolarizing
neuromuscular blockade
Mivacurium Muscle relaxant for surgery Short-acting nondepolarizing
neuromuscular blockade
sedative-hipnotik
 Sedative & Hypnotics
Sedative : Drugs that calm the patient and reduce
anxiety without inducing normal sleep.

Hypnotic : Drugs that initiate and maintain the normal

sleep.
Classification of Hypnotic Drugs
1. Benzodiazepines ( BDZ )
2. Barbiturates
3. Miscellaneous ( non BDZ non barbiturate drugs).
 Zolpidem
 Zaleplon
 BENZODIAZEPINES (BDZ)
Classifications
According to Duration of Action :

- Short acting: (3-5 hours).

Triazolam
-  Intermediate: (6-24 hours).
Alprazolam
Lorazepam (ALEOT)
Estazolam
Oxazepam
Temazepam
Long acting: ( 24-72 hours)

Chlorazepate Chlordiazepoxide
Diazepam Flurazepam.
Quazepam Prazepam
Nitrazepam
According to uses:
Sedative (Anxiolytics)
Alprazolam Chlordiazepoxide
Diazepam Prazepam

Hypnotics
Triazolam
Lorazepam Estazolam Temazepam
Flurazepam Nitrazepam Quazepam

Preanesthetics
  Diazepam - Midazolam
 Mechanism of Action:

Benzodiazepine:
 facilitation of GABA action on GABA receptors
 chloride channels opening
  chloride influx to the cell
 cell membrane hyperpolarization
  inhibition of propagation of action potential
 inhibitory effect on different sites of the brain especially motor
cortex, and limbic system.
 Barbiturates

• are derivatives of barbituric acid

• second choice as sedative – hypnotic
•Its members end with the suffix (barbital or barbitone)
• Thiobarbiturates are highly lipid soluble.
Classification :
 Long acting( 24-28 h): Phenobarbitone
 Intermediate (8-24h): Amylobarbitone
 Short-acting(3-8h):
• Pentobarbitone
• Secobarbitone
• Amobarbital
 Ultrashort acting (25 minutes): thiopental
Mechanism of Action
1. Facilitation of GABA action on the brain. increase the duration
of the GABA gated channel opening but in large dose, they
can directly activating chloride channels. (not through BZD
receptors).

2. depress excitatory neurotransmitter actions

3. Interfere with Na & K transport across cell membranes (reticular

activating system inhibition).
4. are less selective in action than BZD.
antiepileptik
Seizu
re Kejang disebabkan krn :
Ketidakseimbangan

antara pengaruh inhibisi

(GABA) dan eksitatori
pada otak (Glutamat)
Me  transmisi
inhibitori : paska Tx dg
antagonis GABA,
penghentian pemberian
agonis GABA
(benzodiazepin, alkohol)
Me  transmisi eksitatori :

meningkatnya kasi
glutamat atau aspartat
Tata laksana
Epilepsi
 Non – farmakologik
 cari dan hindari faktor pemicu (jika ada) :
stress, OR, kopi, alkohol, sulit tidur, terlambat
makan

 Farmakologik :
 dengan obat antiepilepsi / antikonvulsi
 Prinsip Mekanisme kerja Antiepilepsi

 Stabilisasi sel saraf dg cara memblok kanal

ion (Na, Ca)
 Me  transmisi inhibitori GABA-ergik
 Me  transmisi glutamat
 SODIUM CHANNEL
BLOCKER

Na terhambat masuk  meningkatkan keadaan

steady state-inactivation  tdk terjaksi potensial

Fenitoin, Karbamazepin, Valproat,, Lamotrigin, Oxcarbazepin

 CALCIUM CHANNEL
BLOCKER

Blok kanal Ca menurunkan ‘ the low-threshold calcium

current (LTCC) ‘ atau ‘ T (transient) current’ Valproat,
Ethosuximide, Dimethadione
Meningkatkan Aksi
GABA

tiagabin

GABAA Receptor
 Agonis GABA :
 Phenobarbital : mengikat allosteric site GABA- barbiturat
receptor  meningktkan aksi GABA- inhibitori :
memperpanjang lama terbukanya kanal Cl 
hiperpolarisasi,
 Benzodiazepin : mengikat allosteric site GABA-
benzodiazepine receptor  aktivasi R/ GABA : me ↑
frekuensi pembukaan kanal ion Cl  hiperpolarisasi
 Me  kdr GABA dlm CSF, mungkin dg menstim relesase
GABA dr non vesikuler pool , Analog GABA, agonis
GABAB, :Gabapentin
 Memfasilitasi glutamic acid decarboxylase (GAD), the enzyme
responsible for GABA synthesis : Valproate
 menghambat re-uotake GABA ke neuron & glia 

GABA di sinap lebih lama : Tiagabin

 Hambat enzim metab GABA-transaminase 

konsentr GABA (GABA-T) : Vigarabin, Valproate

Resume : Sites of action of antiepileptics in
GABAergic synapse
Glutamate
Neurotransmission
 Menghambat Aksi
Glutamat
 Blok R/ NMDA  aksi Glutamat-eksitatori
terhambat Phenobarbital, Valproic
 menurunkan release glutamat di sinap :
Lamotrigine
 Blok R/ kainate: Topiramate
antidepressant
 Symptoms of Symptoms of
Depression Mania
 Changes in mood, sleep, Abnormally and
cognition
 Depressed mood (in children may persistently elevated
be irritability mood
 Diminished Interest or pleasure in Inflated self-esteem or
activities grandiosity
(Anhedonia)
 Significant weight loss or gain Decreased need for
 Insomnia or hypersomnia sleep
 Psychomotor agitation or Talkativeness or
retardation pressure
 Fatigue or loss of energy to keep talking
 Feelings of worthlessness or Flight of ideas
inappropriate guilt
 Diminished ability to think of Distractibility
concentrate Increase in goal-
 Suicidal thoughts or behavior directed behavior
Adapted with permission from Kupfer DJ.Long-term treatment of depression.J
Clin Psychiatry 1991;52 (suppl):28ñ34
Neurotransmitter yg berperan dalam
psikopatologi
 Catecholamine Hypothesis dari
gangguan affective
 Meningkatnya aktifitas catecholaminergic
berkaitan dengan elevated mood

 Agonists (e.g., amphetamine) 

menaikkan mood

 Amine-depleting drugs (e.g., reserpine)

menekan mood
Depresi berkaitan dengan menurunnya aktifitas
catecholaminergic
 Antidepressant

Monoamine Amine reuptake Alpha2 adrenoceptor

Oxidase inhibitors Blocking blockers, NaSSA
-Non selective MAO-A/irreversible drugs -Mirtazapine
(Phenelzine,Tranylcipromine,
Isocarboxacide)
-Selective reversible MAO-
(Meclobemide)
A Nonselective/SNRI SSRIs NRIs, NDRIs
-Selective SARI
irreversible
MA)-B (Deprenyl) -Fluoxetine
-Citalopram
-Paroxetine
-Sertraline

Heterocyclics
Tricyclics

-Amitryptiline
-Imipramine Second generation Atypical
Third generat ion
-Desipramine - Amoxapine -Trazodone
-Mirtazapine - Bupropion
- Maprotilline -Nefazodone
-Venlafaxine
NAPZA
 NAPZA

sebelum sesudah

sebelum sesudah
 NAPZA

• Narkotika, Psikotropika dan Zat Adiktif lainnya

• Narkoba: Narkotika dan obat berbahaya

Cimeng (Bahasa populer di kalangan pengguna)

 MENGAPA NAPZA MEMBAHAYAKAN?

1. Perubahan pikiran, perasaaan, dan tingkah laku pemakainya

2. Gangguan fisik dan psikis dan kerusakan susunan saraf pusat -
kematian
3. Toleransi, depedensi/ketergantungan berupa adiksi dan habituasi,
intoksikasi dan gejala putus obat (withdrawal syndrome).
 DAMPAK PEMAKAIAN NARKOBA
• Secara sosial: pemakai narkoba secara individual cenderung
teralienasi (terpencil) dari masyarakat luas, mengganggu
lingkungan. Sedangkan orang tua akan kerepotan terus-
menerus
• Secara medis: terjadi kerusakan syaraf otak dan kerusakan
fisik (loyo, kurus, tidak bergairah, dll)
• Secara ekonomi: korban narkoba biasanya adalah usia
produktif (di bawah 50 tahun).
• Secara politik: negara akan rusak apabila dikendalikan oleh
para pecandu narkoba
 Narkotika
1.Narkotika Alam:
a. Candu (opium, analgetik kuat)
b. Coca (Kokain, anastesi lokal
dan stimulansia)
2. Semi sintetis:
c. Ganja a.Heroin (diasetilmorfin,
diamorfin): tidak dipakai lagi dalam
terapi medis 3. Narkotika sintetis:
b.Kodein (metal morfin): obat a.Petidin (obat bius, analgetik kuat)
batuk antitusif b.Metadon (analgetik)
c.Dionin (etilmorfin HCl): obat c.Levorvanol
batuk antitusif d.Meskalin
e.Naloxon (antidotum morfin dan
heroin)
f.Fensiklidin
g.Buprenorfin (analgetik kuat)
 1.Depresansia: Psikotropika 3. Halusinogen:
a. Gol.Barbiturat : fenobarbital a.THC (tetra hydro-cannabinol)
b. Gol. Benzodiazepin: diazepam b.LSD ) Lesergic acid diethyl-
c. Gol. Fenotiazin: klorpromazin 2. Stimulansia : amide)
(tranquilizer) a.Amfetamin dan derivatnya: c.Psilosibine
d. Gol.lain: MDMA, extacy. Inex d. Fensiklidin
antiansietas/kecemasan b.Pseudofederin: e. Daun dan bunga kangkung yg
nasaldecongestant-efek energetic- dikeringkan
doping
Mengurangi aktivitas c.antidepresan
f. Daun bunga nusa indah yang
susunan saraf pusat dikeringkan
Mengaktifkan kerja g.Kecubung
(menenangkan)
susunan saraf pusat Zat atau obat yang
(perangsang) menimbulkan perasaan
halusinasi/khayalan.
Stimulan - amfetamin
1.Pelarut organik: Zat Adiktif lainnya
Alkohol,
Metanol. Eter.
Aceton,
Benzen, 2. Tembakau 3. Tanaman Khat:
tinner

Inhalan: Semua zat yang

mudah menguap