1 / 26

FARMAKOLOGI OBAT GI TRACT

FARMAKOLOGI OBAT GI TRACT. d rh. Dian Vidiastuti PKH UB 2012. UPPER GIT. Acid Production. 2,5 l / hari pH < 1 Diproduksi pleh sel parietal lambung Mucus production : Produced by mucus-secreting cells Also produce bicarbonate, which becomes

masato
Download Presentation

FARMAKOLOGI OBAT GI TRACT

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. FARMAKOLOGIOBAT GI TRACT drh. Dian Vidiastuti PKH UB 2012

  2. UPPER GIT

  3. Acid Production • 2,5 l / hari • pH < 1 • Diproduksi pleh sel parietal lambung Mucus production: • Produced by mucus-secreting cells • Also produce bicarbonate, which becomes trapped in the mucus layer => pH gradientacross the mucus layer (can becomdestroyed by alcohol)

  4. H. pylori Ulcus peptic

  5. ANTACID • Menetralkan asam lambung  peningkatan pH  menurunkan aktivitas pepsin kurangi nyeri • OA : tergantung kelarutan & kec netralisasi asam • Antacid : Sistemik & Non sistemik • ES : pemakaian jangka panjang  Sindroma susu alkali, nefrolith, osteoporosis, neurotoksisitas, diare, asupan Na naik • IO : me – abs tetrasiklin, sulfonamid, digoksin, Chlorpromazin

  6. NaHCO3  kelarutan tinggi, antacid sitemik NaHCO3 + HCl  NaCl + H2O + CO2 * ES : abs dlm usus halus  retensi Na & oedema  urin alkalis  alkalosis metabolik  Nefrolithiasis 2. Aluminum hydroxide : Al(OH)3 * Adsorbsi pepsin  inaktivasi * Kerja lambat * ES : konstipasi

  7. 3. Magnesium hydroxide : Mg(OH3) * tdk larut dlm air  DOA lama * Efek katartik  diare 4. Magnesium Trisiklat : Mg2Si3O8H2O * OA lambat * abs : usus  Kombinasi dg simetikon (antifoaming)

  8. PENGHAMBAT SEKRESI HCl

  9. PELINDUNG MUKOSA • SUKRALFAT * tdk diabs scr sistemik  mengalami polimerisasi pd pH 4  terikat pd jar nekrotik ulkus * ES : mengandung Al  hati2 gagal ginjal * IO : warfarin, tetrasiklin, digoksin, ciprofloxacin, norfloxacin  perhatikan interval pemberian

  10. INHIBITOR POMPA PROTON • Penghambat sekresi as lambung lbh kuat • Bekerja di proses terakhir produksi as lambung • Posologi : Omeprazol, Lansoprazol, Esomeprazol • F’dinamik : butuh suasana asam, stlh abs  difusi ke sel parietal lambung  sulfonamid tetrasiklik

  11. Btk aktif berikatan dg gugus sulfihidril enzim, H+/K+ATP ase (pompa proton)  enzim dihambat scr ireversibel, shg sekresi asam hanya tjd stlh sintesis enzim baru • ES : mual, nyeri perut, konstipasi, flatulence, diare

  12. ANTAGONIS RESEPTOR H2 • FAMOTIDIN * F’dinamik : hambat sekresi as lambung 3x lbh poten drpd ranitidin * F’kinetik : kadar puncak stlh 2 jam PO, ekskresi di ginjal, metabolit aktif Famotidin- S-oksida * IO : tdk mengganggu oksidasi diazepam, Teofilin, warfarin di hepar

  13. 2. RANITIDIN & SIMETIDIN * Memblok histamin pd sel parietal * Me – nyeri ulkus * Abs sistemik, termasuk SSP, metabolisme di hepar * Simetidin punya efek antiandrogen, hambat cytochrom P450 * IO : antasid & metoklopramid me – bioavailabilitas simetidin, abs ketokonazol, warfarin, teofilin, kafein ber – bersamaan pemberian simetidin

  14. LOWER GIT

  15. STIMULAN MOTILITAS  Yg dipengaruhi : Res dopamin, 5HT (5 HidroksiTriptamin) • METOCHLOPRAMID * Antagonis dopamin  blok res dopamin sentral pd CTZ  efek antiemetik * Hambat pelepasan ACh akibat aktivasi 5HT4 * IO : Hindari pemberian bersama digoksin 2. DOMPERIDON * Antagonis dopamin * mengurangi refluks empedu dr duodenum ke lambung

  16. 3. ONDANSETRON * Antagonis serotonin selektif (5HT4) * Sering diberikan utk profilaksis pasien post kemoterapi 4. CISAPRID * khusus digunakan pd gangguan refluks oesoph * Biotransformasi di hepar, abs di usus

  17. ANTI DIARE • Sbg tx simtomatis diare akut ringan-sedang • meningkatkan konduktansi Kalium  ACh turun • Sebagian obat bersifat analgesik maupun adsorben

  18. LOPERAMID * opioid efek lokal  hambat peristaltik * drug of choice anti diare * memulihkan sel yg mengalami hipersekresi cairan • SENYAWA OPIOID * Posologi :(morfin, kodein, papaverin) * pengaruhi res µ * Efek sistemik

  19. 3. CARBO ADSORBEN * arang aktif  adsorbsi zat2 yg molekulnya besar (alkaloid, toksin) 4. KAOLIN * mrp Al silikat * indikasi : Kolitis ulceratif 5. ATTAPULGIT * serbuk tanah lempung * Mg-Al silikat

  20. LAKSATIF • Konstipasi  kesulitan defekasi Causa : - feses keras - kelumpuhan otot polos - gangguan refleks defekasi • Obstipasi  kesulitan defekasi krn obstruksi (CA colon)

  21. Mekanisme Kerja Laksatif • Memiliki sifat hidrofilik  massa, konsistensi & transit feses bertambah • Bekerja pd mukosa colon menurunkan absorbsi NaCl & air • Meningkatkan motilitas usus krn menurunnya abs garam & air

  22. JENIS-JENIS LAKSATIF • Melunakkan feses, perstaltik - • Parafin cair, olive oil

More Related