PERBEDAAN FAKTOR RISIKO KEJADIAN STROKE ISKEMIK DAN STROKE …
Dr.fifi OBAT STROKE Edit
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8/12/2019 Dr.fifi OBAT STROKE Edit
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Fathiyah Safithri
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Tujuan terapi pd Stroke Iskemik akut :
Meminimalisir volume jaringan otak yginfark (irreversibel)
Tx REPERFUSITx NEUROPROTEKSI
Mencegah komplikasiMencegah kecacatanMencegah STROKE ULANG
EUSI 2003
STROKE ISKEMIK
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STROKE ISKEMIK
REPERFUSI= memperbaiki aliran darah ke daerah
iskemi NEUROPROTEKSI
= melindungi sel dari kerusakan akibat
iskemi
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OBAT UTK REPERFUSI
1. Menghambat aggregasi platelet (stl 48 jfase akut, preventif sekunder )
Antitrombotik / antiplatelet2. Menghancurkan trombus (Reperfusi dini,onset < 3 jam)
Trombolitik
3. Mencegah bekerjanya faktor2 koagulan (pdatrial fibrillasi, resiko emboli >>, antiplatelettdk efektif cegah stroke ulang meski tdkada risk emboli )
Antikoagulan
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Recommendations for Pharmacotherapy ofIschemic Stroke
diambil dari Pharmacotheraphy-Pathophysiologic Dipiro-2005
Stl 7hr fase akut
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ANTITROMBOTIK
= Menghambat aggregasi platelet &pembent trombus
a.Menghambat sintesa TXA2 :aspirin
b.Antagonis reseptor ADP (adenosindiphosphate) :ticlopidine,clopidogrel
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ASPIRIN
Mek kerja : Menghambat enzCOX1 perub AA menjPGH2 produksi TXA2 &PGI2
Relatif selektif thd COX-1(hamb thd COX1>200x dibandCOX2) pd dosis kecil cendbekerja pd COX1
Supresi agregasi plateletselama 7-10 hr (=ms hidupplatelet). COX1 diasetilasi o/aspirin sec irreversibel & tdkdpt diresintesa oleh platelet oktdk punya nuklei
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ASPIRIN (lanj)Cepat diabsorbsi di GITSebag alami first pass di
hepar menj salisilatDistribusi luas
Hemostasis kembali normal
stl 36 jam (Sutul releaseplatelet baru)
Efektifitas dlm memortalitas IMA hampir samadg Streptokinase
ES : iritasi GIT, me resikoperdrhan otak,bronkokonstriksi
Penggunaan:a. unstable angina
b. non-Q-wave myocard infark
c. mencegah re-infark pd MI, stroke
d. mencegah rekkuren TIA & meresiko stroke pd pasien TIAe. me resiko arterial trombosis pdkateterisasi koroner, balloonangioplasti, bedah vaskuler
Pemakaian pd sindr koroner akut :loading dose 325 aspirin chewable,selama MRS 160-325mg/hr,maintenance 80mg/hr
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TICLOPIDINE, CLOPIDOGREL
Mek kerja :blok ADP yg release olehplatelet yg teraktivasihamb rekruitment & aktivasiplatelet lbh lanj platelet yg
tdk teraktivasi, tdk terj perubkonformasi R/GPIIb/IIIahamb ikatan fibrinogen dgR/GP IIb/IIIaMempengaruhi ikatan vwF (yg
direlease kollagen p.d) thdR/GP1b hamb adhesi &agregasi plateletHambatan thd agregasibersifat irreversibel
Peak effect 2j, efek inhibisi thdplatelet stl hr ke 4, steady statestl hari ke 14-21prodrug metab di hepar
drug aktif
Penggunaan :Preventif rekurrren trombosis pdstroke&TIA (affikasi>aspirin)Unstable angina. Loading dose
2x250 slm 3 hrTdk dipakai pd kasus yg perlu efek
antitrombotik segera ES : purpura, bleeding GIT (
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DIPYRIDAMOLE
Mekanisme kerja :Hamb enz PDE me
cAMP Vasodilatorkoroner
Hamb sintesa TXA2,potensiasi efek PGI2 dlmme adhesi platelet
efek antiplatelet
Penggunaan : Kombinasi dg aspirin :
me resiko stroke 16-37% Kombinasi dg warfarin
hamb embolisasi pdkatub jant buatan
Blok uptake adenosin pdRBC me kdradenosin di plasma
me efek vasodilator& antiplatelet
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Goal : Stop bleeding (fibrin-clot formation)Components : clotting-coagulation factors
Process : secondary hemostatic plug formation(fibrin-clot formation)
FASE KOAGULASI
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Mekanisme Kerja Antikoagulan
HeparinEnoxaparin
Warfarin
Berikatan dgn AT III me aksi ATIIIAT III hambat protease fak. pembekuan(fak. IIa, Xa, IXa) hambat prosespembekuan darahCegah reduksi vit. K teroksidasi
(Antikoagulan oral) aktivasi fak.koagulasi (II, VII, IX, X, prot C &prot S) di hepar terganggu
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WARFARINMek kerja : hamb enz vit- Kepoxide reductase me prodvit K yg aktif (reducedhydroquinone), yg diperlukansbg cofaktor proses -
karboksilasi u/ aktivasi faktkoagulan yg dependen vit K(fakt II, VII, IX, X, prot C dan SEfek antikoagulan timbul stlproses karboksilasi tdk terjadi
Efek antitrombotik tampak stlTx hr ke-5Paling efektif mencegah strokepd pt atrial fibrillasiLong half life, slow onsetES : bleedingKI : ibu hamil (teratogenik)
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Faktor pasienEffikasi me : pe BB,
usia > 80th, akut illness,ggn fs hepar, gagal jantung, gagal ginjal,peminum alkohol]Effikasi me : pe BB,diare & vomit, usia< 40th,
Faktor yg mempengaruhi EffikasiWarfarin
Interaksi Obatme ikatan prot :aspirin,fenilbutazon, CPZ, sulfinpirazonHamb metab warfarin :simetidin,eritromisin, Na valproatme metab warfarin: fenitoin,barbiturat, karbamazepinme sintesa fakt II, VII, IX, X :fenitoin, salisilatme absorbsi vit K : AB broadspektrum, laxative
me resiko ulkus peptik: NSAID,SteroidTrombolitik : tPA, StreptokinaseAntiplatelet drug : Aspirin, NSAID
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HEPARIN
ES : bleeding (tx dg protamin sulfat), trombositopeni (ok Ab antiplatelet), rx allergi
Short half life, rapid onset
Effikasi dimonitor dg PPT, dosis dititrasi s.d target PPT 2xkontrol N
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HEPARIN
never been proved to positively affect strokeoutcome, and it significantly increases the risk ofintracerebral hemorrhage.
Efektif hanya utk trombosis vena dalam
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TROMBOLITIK
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Skema Mekanisme Kerja TrombolitikPlasminogen
Proaktivatordarah
Hambatan
Aktivatordarah
t-PA, urokinase
Antiaktivator
Asam aminokaproat
Streptokinase
FibrinogenPenghancuran Fibrin Hasil pembelahan fibrin
Aktivasi berbagairangsangan
+
+
+
+
Plasmin
Trombin
-
-
+
AktivatorProaktivator
Anistreplase
+
fibrinogen
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Mekanisme Kerja Trombolitik
Streptokinase(dr Streptokokkus)
Urokinase(dr sel ginjal mns)
Alteplase /Recombinant Tissueplasminogenactivator (rt-PA)
Bergabung dgn plasminogen & membentukkompleks aktivator kompleks aktivatormengkatalisa perub plasminogen menjadiplasmin hidrolisa fibrin plug, fibrinogen &fakt V & VII clot hancur Sec langsung mengubah plasminogenmenjadi plasmin dg memotong ikatanarginin-valin pd plasminogen sec langs merusak fibrin & fibrinogen
Aktivitas enz tgt ada/tdknya fibrin. Sec cepatmengaktivasi plasminogen yg terikat pdfibrin. Kurang mempengaruhi plasminogenyg bebas ES bleeding sistemik
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Penggunaan klinis Trombolitik
Streptokinase
Urokinase
Tissueplasminogenactivator (t-PA)
Tx dini emboli paru akut & IMA 3-4 jamsetelah timbul gx (intracranial bleedingrisk
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OBAT UNTUK NEUROPROTEKSI
PIRACETAM (Noothropil)PENTOKSIFILIN
CITICOLIN
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BLOCKAGE OF KEY PATHWAYS IN THE ISCHEMICCASCADE BY AVAILABLE NEUROPROTECTIVE AGENTS
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PIRACETAM
acts on the CNS and has been described as anootropic;to protect the cerebral cortex against hypoxia.
to inhibit platelet aggregation and reduce bloodviscosity at high dosesdid not influence the outcome if given within 12hours of the onset of acute ischaemic stroke. Thedata did not support routine use of piracetam inacute ischaemic strokeES : Anxietas, Irritabilitas,Headache, Agitasi,Tremor,NervousnessIndikasi : Stroke, ischemia and symptoms, adjunctto intensive speech therapy in improving aphasiafollowing stroke
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PENTOKSIFILIN
xanthine derivative used in the treatment of peripheralvascular diseaseoften classified as a vasodilator, its primary actionseems to be a reduction in blood viscosity, probably byeffects on erythrocyte deformability and plateletadhesion and aggregation
increase blood flow to ischaemic tissues and improvetissue oxygenation in patients with peripheral vasculardisease and to increase oxygen tension in the cerebralcortex and in the cerebrospinal fluidinhibits production of the cytokine, tumour necrosisfactor alpha (TNF),
Meningkatkan fungsi neurotransmitter Ach melaluireseptor muscarinik cholinergic yang mencakup prosesmemori.Aktivasi metabolik peredaran darah otak meningkatkankecepatan metabolik serebral oksigen dan glukosaregional menormalkan aliran darah ke daerah iskemik,dengan sekunder menurunkan rasio laktat/piruvat.
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SITIKOLIN
derivative of choline and cytidine that is involved inthe biosynthesis of lecithin. It is claimed toincrease blood flow and oxygen consumption inthe brain
meningkatkan norepinephrine and dopamine diCNS pada kondisi aneuroprotective andischemicmenurunkan volume lesi iskemikrestore the activity of mitochondrial ATPase andmembrane Na+/K+ATPase, untuk menghambataktivasi phospholipases, dan mempercepatreabsorbsi cerebral edema.Menghambat terjadinya apoptosis yang
berhubungan dengan terjadinya cerebral iskemik,neurodegeneration
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STROKE PERDARAHAN
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-Aminocaproic acid (EACA),(Tranexamic acid)
Antifibrinolitik dg blok tempat ikatan fibrinpd plasminogen hamb aktivasiplasminogen menj plasmin
ES : trombosis intravasc(ok hamb aktivasiplasminogen), hipotensi, miopati, diare.
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