OBAT NEUROLOGI OBAT NEUROLOGI dan dan NEUROMUSKULAR NEUROMUSKULAR M. M. Bakhriansyah Bakhriansyah, H., dr., , H., dr., M.Kes M.Kes , , M.Med.Ed M.Med.Ed Bagian Bagian Farmakologi Farmakologi Banjarbaru Banjarbaru Sasaran Sasaran Belajar Belajar Di Di akhir akhir pembelajaran pembelajaran, , mahasiswa mahasiswa mampu mampu memahami memahami mekanisme mekanisme kerja kerja, , indikasi indikasi dan dan efek efek samping samping obat obat: 1. 1. Antikonvulasi Antikonvulasi 2. 2. Hipnotik Hipnotik sedatif sedatif 3. 3. Parkinson Parkinson 4. 4. Pelemas Pelemas Otot Otot 5. 5. Anestesi Anestesi Umum Umum 6. 6. Anestesi Anestesi Lokal Lokal
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OBAT NEUROLOGI OBAT NEUROLOGI dandan
NEUROMUSKULARNEUROMUSKULAR
M. M. BakhriansyahBakhriansyah, H., dr., , H., dr., M.KesM.Kes, , M.Med.EdM.Med.Ed
►► SE : SE : �� Continues seizures Continues seizures occuringoccuring 30 minutes 30 minutes ((epilepsiepilepsi foundation)foundation)
�� More than 30 minutes More than 30 minutes of continues seizures of continues seizures activity or 2 or more activity or 2 or more sequential seizures sequential seizures without full recovery of without full recovery of consciousness between consciousness between seizures (Dodson, seizures (Dodson, 1993)1993)..
►► Systemic and primary brain changes Systemic and primary brain changes �� related to related to
morbidity and mortality ratesmorbidity and mortality rates
►► Goal of therapy: to treat the epilepsy and to Goal of therapy: to treat the epilepsy and to minimaliseminimalise the side effectsthe side effects
Principal therapy:Principal therapy:
►►MonotherapyMonotherapy is better than is better than polypharmacypolypharmacy
►► Dosage is increased until the therapeutic effect or Dosage is increased until the therapeutic effect or toxicity effect are met. toxicity effect are met.
►► PolypharmacyPolypharmacy is introduced when is introduced when monotherapymonotherapydoes not workdoes not work
►► Avoiding the sudden withdrawal Avoiding the sudden withdrawal
Treatment flowchart for status Treatment flowchart for status
epilepticusepilepticus
Medications Medications
BarbituratBenzodiazepinAsam valproatGabapentin
Lamotrigin
FenitoinKarbamazepinAsam valproatEtosuksimid
FenitoinKarbamazepin
GABA
Glutamate
Ca
Na
STATUS EPILEPTICUS
KarbamazepinKarbamazepin
►► Stabilize neural Stabilize neural
membrane by membrane by
decreasing Na, Ca and decreasing Na, Ca and
K flows through it.K flows through it.
►► avoid to be given with avoid to be given with
MAO inhibitor MAO inhibitor
consecutivelyconsecutively
FenitoinFenitoin
►► DifenilhidantoinDifenilhidantoin
derivatederivate
►►Mechanism of actions Mechanism of actions
are similar to are similar to
KarbamazepinKarbamazepin
►► Could be given orally, Could be given orally,
intra venous and intra intra venous and intra
muscularmuscular
ValproicValproic AcidAcid
►► Increasing GABA Increasing GABA
transmission transmission
►► Sedation effect is Sedation effect is
minimalminimal
EtosuksimidEtosuksimid
►►Mechanism of action Mechanism of action is is
unknownunknown
►► Probably by inhibiting Probably by inhibiting
Ca channelCa channel
PhenobarbitalPhenobarbital
►► Stimulating GABA Stimulating GABA
receptorreceptor
►► SE: sedation, SE: sedation,
nistagmusnistagmus, ataxia and , ataxia and
allergyallergy
►► Inducing Inducing enzymenzym P450 P450
PrimidonPrimidon
►►Mechanism of actions Mechanism of actions
are unknownare unknown
►► Its active Its active metabolitmetabolit
has long half lifehas long half life
GabapentinGabapentin
►► GABA agonist GABA agonist
►► Adjuvant therapyAdjuvant therapy
LamotriginLamotrigin
►► Stabilizing neuron and Stabilizing neuron and
affecting glutamate affecting glutamate
releaserelease
►► Adjuvant therapyAdjuvant therapy
►► SE: rash (prominent)SE: rash (prominent)
KlonazepamKlonazepam
►► Stimulating GABA Stimulating GABA
receptor receptor
FelbamatFelbamat
►► Stimulating GABA Stimulating GABA
receptor and inhibiting receptor and inhibiting
NMDA receptorNMDA receptor
►► Used unUsed un--frequentlyfrequently
Parkinson diseaseParkinson disease
►► A progressive A progressive neurodegenerative neurodegenerative disorder associated disorder associated with loss of with loss of dopaminergicdopaminergicnigrostriatalnigrostriatal neurons.neurons.
►► Distinctive features:Distinctive features:�� Resting tremor, rigidity, Resting tremor, rigidity, bradikinetiabradikinetia, and , and postural instability postural instability
Principle therapyPrinciple therapy
►► Increasing the synthesis Increasing the synthesis and release of dopamine and release of dopamine (L(L--dopa+karbidopadopa+karbidopa, , amantadinamantadin))
To facilitate action of dopaminergic To suppress action of cholinergic
Anti cholinergicAmantadine
L-dopa+karbidopa
Dopamine agonists drugsMAO B inhibitors
Protocol of therapyProtocol of therapy
LL--dovadova ((levodopalevodopa))
►► Dopamine precursor Dopamine precursor ��inactive forminactive form
►► Activated by Activated by decarboxilasedecarboxilase enzyme;enzyme;�� Brain Brain
�� Lever & kidneys Lever & kidneys �� can can not pass through BBB not pass through BBB �� bioavailability bioavailability countered by countered by karbidopa/benserazidekarbidopa/benserazide..
►► On/off phenomenon On/off phenomenon (+) after 3(+) after 3--5 years 5 years application application ��mechanism ??? mechanism ??? Desensitization of Desensitization of dopamine receptordopamine receptor
►► Not a first line therapy Not a first line therapy