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PHARMACOLOGY
ELLY NURUS SAKINAH
NEUROTRANSMITTER
Neurotransmitte
r
Asetilkolin
Dopamine
Kelebihan
Kekurangan
Delirium, psikosis
Psikosis,
sindrom
Tourette, chorea
Penyakit alzeimer
Parkinson, depresi
GABA
Glutamat
Kejangn
neuron
Kejang,
gangguan
gerak
Skizofren,
depresi,
gangguan kognitif
Norepinefrin
Ansietas,
panic,
anoreksia, insomnia
Depresi
Serotonin
Tidur,
halusinasi,
penurunan
nafsu
makan, ansietas
Depresi,
sensitive
nyeri,ansietas
degenerasi
SEDATIF HIPNOTIK
ELLY NURUS SAKINAH
PENGERTIAN
Anxiolytic (sedative) adalah obat yang
Barbiturat dan
alkohol
Benzodia
zepin
NT noradrenergic
Kekurangan GABA
Kelebihan Glutamat
Penurunan BDNF (Brain-derived neurotropic
factor)
OBAT SEDATIF-HIPNOTIK
BENZODIAZEPINE (BZD)
BARBITURAT
Z DRUG
RAMELTEON
BUSPIRON
BENZODIAZEPINE
FARMAKOKINETIK
Rates of oral absorption : lipophilicity major role
Drug
Tmax(hr)
T1/2 (hr)
Comments
Alprazolam
1-2
12-15
Chloediazepoxide
2-4
15-40
Active metabolite
Clorazepate
1-2
(nordiazepa
m)
50-100
Diazepam
1-2
20-80
Active metabolic
Eszoplicone
Flurazepam
1-2
40-100
Lorazepam
1-6
10-20
No active metabolites
Oxazepam
2-4
10-20
No active metabolites
Temazepam
2-3
10-40
Triazolam
2-3
Zaleplon
<1
1-2
Zolpidem
1-3
1,5-3,5
No active metabolite
Pharmacodynamics of
BZD
The GABAA-receptors is a ligand-gated ion
BZD
EFEK SAMPING
drowsiness, confusion, amnesia, impaired
II. BARBITURAT
Mekanisme kerja: potensiasi efek GABA,
MEKANISME KERJA
Penguatan
Epilepsi
Type of seizure
First line
Second line
Partial Seizure
Phenytoin
Carbamazepine
Valproate
Lamotrigine
topiramate
Phenobarbital, primidone
Clonazepam / clobazam
Gabapentin
Vigabatrin
Zonisamide
Tonic clonic
Carbamazepine
Valproate
Lamotrigine
Phenytoin
Phenobarbital / primidone
Vigabatrine
Phenytoin
Myoclonic
Valproate
Ethosuximide
Clonazepam
absence
Ethosuximide
Valproat
Generalized seizure
Clonazepam
lamotrigine
Adverse effect
BZD
Carbamazepine
Ethosuximide
Gabapentin
Lamotrigine
Phenobarbital
Phenytoin
Tiagabine
Topiramate
Valproate
lamotrigine, phenytoin
Anti Parkinson
PARKINSON
Pathophysiology: degeneration of
substantia nigra neurons, which results in
loss of dopamine (DA) to striatum
www.nwabr.org/.../pictures/whthppn
s.jpg
Dopamine agonists
bromocriptine
pergolide
pramipexole
ropinerole
Dopamine Releaser
amantadine
Menghambat
perusakan Dopamin
COMT inhibitors
entacapone, tolcapone
MAO-B inhibitor
Selegiline
Menurunkan ACh
Anticholinergics
trihexyphenidyl (Artane)
benztropine (Cogentin)
Levodo
pa
Bromocript
ine,
pergolide
Amanta
dine
1. Levodopa
Mechanism:
(1) Because dopamine does not cross the blood-brain
barrier, levodopa the precursor of dopamine, is given
instead.
(2) Levodopa itself has minimal pharmacologic activity,
in contrast to its decarboxylated product, dopamine.
(3) Levodopa is rapidly decarboxylated in the
gastrointestinal tract. Prior to the advent of
decarboxylase inhibitors (carbidopa), large oral
doses of levodopa were required; thus, toxicity from
dopamine was a limiting factor.
Adverse effect
DRUG
MOA
LEVODOPA
DA precursor
BROMOCRIPTINE
Agonis DA parsial
Hipertensi,nausea, fatigue
PERGOLIDE
DA agonis (D1/D2)
Hipertensi,nausea, fatigue
ROPINIROLE
DA agonis (D2selective)
PRAMIPEXOLE
DA agonis (D2selective)
SELEGILINE
MAO-B inhibitor
RASAGILINE
= selegiline
= selegiline
ENTACAPONE/
TOLCAPONE
COMT inhibitor
TRIHEXYPHENIDYL
Antagonis
muskarinik
Levodopa
Adverse effect:
On-off phenomena
On-off Effect fluctuations in clinical response to
levodopa.
Off = marked akinesia.
On = improved mobility but marked dyskinesia.
Thought to be related to fluctuations in levodopa
plasma concentrations.
Fluctuations can be smoothed out by
incorporating a dopamine receptor agonist into
pharmacotherapy.
Pramipexole.
Ropinirole.
Apomorphine.
Selegiline
tolcapone
Anti Psikosis
ANTI
PSYCHOTIC
TYPICAL
Dopamine Pathways
Mesolimbic dan mesokortikal efek psikologis
Nigrostriatal voluntary movement
Tuberoinfundibular hambat pelepasan prolaktin
D2
BLOCK
D4
BLOCK
1
BLOCK
5HT2
BLOCK
M
BLOCK
H1
BLOCK
Most
phenothia
zine dan
tioxanthin
e
++
++
Thioridazi
ne
++
++
+++
Haloperido +++
l
Clozapine
++
++
++
++
Molindone
++
Olanzapin
e
++
++
Risperidon ++
e
ADVERSE EFFECT
Gejala
akathisia
Gejala
Acute
Acute
akathisia
Antidepressants drugs
Department of Pharmacology
2012
Pathophysiology of
depression
Neurotrophic Hypothesis
Monoamines and other
neurotransmitters
Neuroendocrine factors
brain-derived
neurotrophic
factor (BDNF)
nerve growth factors
regulation of neural
plasticity, resilience,
and neurogenesis
depression is
associated with the
loss of neurotrophic
support atrophic
structural changes in
the hippocampus,
frontal cortex, anterior
cingulate
Monoamine
hypothesis
depression is
related to a
deficiency in the
amount or
function of
cortical and
limbic serotonin
(5-HT),
norepinephrine
(NE), and
dopamine
(DA)
(Redrawn, with permission, from Belmaker
R, Agam G:
Major
depressive disorder. N Engl J Med 2008;358:59.)
The purpose of
antidepressants
is the increase
the [monoamine
neurotransmitter
s] in the synapse
by one of several
mechanisms
Anti Depresan
Heterocyclic
Mekanisme kerja
Heterocyclic
How to choose an
antidepressant
Rationale should be based on side
effects, not efficacy
Tremors
Tachycardia
Gastrointestinal disturbances
Anxiety (dose dependent)
Sexual dysfunction
Psychomotor activation
Antiparkinsonian effects
Psychoses
Increased attention/concentration
Histamine H1 blockade
Possible clinical consequences
Sedation, drowsiness
Weight gain
hypotension
Blurred vision
Dry mouth
Sinus tachycardia
Constipation
Urinary retention
Memory dysfunction
Postural hypotension
Reflex tachycardia
Dizziness
Drug interaction