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Ppt penggunaan antibiotik yang bijaksana

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  • Data dari Amrin study: 55-80% penggunaan AM di suatu RS di Sby adalah tanpa indikasi, sedangkan untuk profilaksis13-55% juga tanpa indikasi
  • Let’s review the basic science of resistance briefly. How does resistance develop? It is genetic. Resistance genes certainly occur naturally. (The definition of an antibiotic is a naturally produced substance which and antimicrobial activity). There are three basic mechanisms by which resistance genes work: 1. They encode for enzymes that degrade the antibiotic, 2. They encode for changes in the site of action, or 3. They encode for molecular mechanisms to prevent entry or speed exit of the antibiotic from the cell
  • Bacteria have been around for 3.5 billion years longer than we have. They’ve gotten good at genetic engineering and they can do it with a generation time of 20 minutes under optimum circumstances.. Bacteria can alter their genetic material in many more ways than higher animals. Unlike higher animals, bacteria posses both chromosomal and plasmid DNA. Resistance can be acquired by: Chromosomal Mutation with vertical transmission to progeny Horizontal Transfer of Resistance Genes by plasmids, integrons, bacteriophages and scavenging into either plasmid or chromosomal DNA. Resistance genes often travel in cassettes on integrons or in clusters on plasmids, so selection driven by the presence of a single antibiotic can simultaneously select for resistance to multiple antibiotic classes. Horizontal gene transfer occurs not just intra-species, but inter-species as well.
  • Many more poorer prescription can be found, e.g. including enzymes, loperamide, combination of antimicrobials in compound.
  • An antibiotic is a substance or compound that that kills or inhibits the growth of bacteria. They are broadly classified based on lab behavior as bactericidal (kill bacteria directly) or bacteriostatic (prevent cell division). Also categorized by target-specificity: Narrow-spectrum antibiotics target specific bacteria such as Gram-positive or Gram-negative bacteria, while broad-spectrum antibiotics affect a wider range of bacteria.
  • This diagram shows the various targets of antibiotics on the structure and functions carried out by bacteria. The beta-lactams group of antibiotics, which I will talk more about shortly, has an effect on the construction of cell walls by many different types of bacteria.
  • Ampicillin is a type of beta-lactam antibiotic that has been used extensively to treat bacterial infections since 1961. It is considered part of the aminopenicillin family and belongs to the B-lactam group of antibiotics because of its characteristic B-lactam ring that consists of 3 carbon atoms and 1 nitrogren atom. (Show Slide 4) Ampicillin is a broad-range antibiotic so it can penetrate both Gram-positive and Gram-negative bacteria. The penicillin derivative acts as a competitive inhibitor of the enzyme transpeptidase, found on the inner surface of the cell surface membrane and which is essential for bacterial cell wall synthesis. It inhibits the third and final stage of cell wall synthesis, which ultimately leads to cell lysis. Ampicillin can also act as a bactericidal in the presence of E. Coli bacteria. However, as I mentioned before, beta-lactam drugs such as ampicillin have been popular for decades for the treatment of bacterial infection, hence certain bacteria have been able to develop counter-measures to nullify the antibiotics effectiveness. This evolutionary process is known as a buildup of drug resistance. There are several different underlying molecular mechanisms to antibiotic resistance, and I will explain the mechanism specific to ampicillin.
  • Ampicillin resistance is achieved by the cleavage of the beta-lactam ring by the beta-lactamase enzyme.
  • The enzyme is coded for by the plasmid-linked bla gene which hydrolyzes ampicillin by cleaving the beta-lactam ring. This can be witnessed when a plasmid that has been inserted into a bacterium is first coupled with the bla gene and then the bacterium is placed in a culture medium containing ampicillin – causing ampicillin levels to be continually depleted.
  • So now the most important question, is how the ampicillin-beta lactamase mechanism can be useful to us as a synthetic biology technique? It is often used as a selective agent to confirm the uptake of genes by bacteria (eg. plasmids). As we heard in a previous presentation, bacterial transformation results in the integration of the same of foreign DNA from the media surrounding the bacteria to produce chemically competent cells. If the exogenous DNA is tagged with an antibiotic resistance gene eg beta-lactamase and then grown in a medium containing ampicillin, only the bacteria that had successfully taken up the desired DNA become ampicillin resistant and do not become lysed by the ampicillin. This is then quite an accurate way to confirm whether or not successful bacterial transformation has occurred.
  • Kanamycin is a chemical compound which targets the 30s ribosomal subunit in prokaryotes, binding in such a way as to cause a frameshift in every translation. This has a "bacteriostatic" effect: the bacterium is unable to produce any proteins correctly, leading to a halt in growth and eventually cell death.
  • Over-use of kanamycin has led to many wild bacteria possessing resistance, which is encoded in plasmids. As a result of this (as well as a lot of side effects in humans), kanamycin is widely used for genetic purposes rather than medicinal purposes, especially in transgenic plants. Resistance is often to a family of related antibiotics, and comes in three variaties: antibiotic-degrading enzymes, reduced membrane permeability, or proteins protecting the 30s subunit.
  • Chloroamphenicol is also bacterio static; it halts bacterial growth by inhibiting the enzyme peptidyl transferase, a protein that assists in the binding of tRNA to the 50s ribosomal subunit in prokaryotes. Three methods of resistance exist: reduced membrane permeability, mutation of the 50s subunit, and an enzyme called chloramphenicol  acetyltransferase, which inactivates chloramphenicol by covaltly linking groups. Indeed, there is much similarity in function, use and resistance between kanamycin and Chloroamphenicol.

Transcript

  • 1. REFERATPenggunaan Antibiotik Yang Bijak Dan Benar Pada Anak Oleh: Mahesa Suryanagara Pediatric Infectious and tropical medicine division
  • 2. PENDAHULUAN
  • 3. PENDAHULUAN Penelitian pada Negara berkembang: anak Vietnam  25-50% penggunaan 91% infeksi akut saluran napas atas antibiotik  tidak anakterapi rasional. antibiotik. Penemuan antibiotik 1943 ↓ angkakesakitan dan kematian RESISTENSI akibat infeksi  KUMAN pengunaan berlebih!!! Masalah Global !!! Blondeau J. M. Appropiate antibiotic use
  • 4. Frekuensi penggunaan antibiotika untuk kasus anak di Indonesia (Purnamawati, 2006)
  • 5. Frekuensi penggunaan antibiotika di Puskesmas AFRICA Sudan Sw aziland Cam eroon Ghana Tanzania Zim babw e ASIA Indonesia Nepal Bangladesh L.AMER. & CAR. Eastern Caribean El Salvador Jam aica Guatem ala 0% 10% 20% 30% 40% 50% 60% 70% % of PHC patients receiving antibiotics Source: Quick et al, 1997, Managing Drug Supply 5
  • 6. ResistensiBakteria • Resistensi obat hasil dari paparan obat. • Dapat bersifat genetik  Mengecah akses obat k tempat kerja ○ ↓ Influx ○ ↑ Efflux  Menginaktifasi obat  Perubahan Tempat kerja obat (Change Site of Action)http://www.sciam.com/1998/0398issue/0398levybox2.html
  • 7. Lebih hebat dari yang diperkirakan!! Horizontal Transmission of Resistance Genes among Speciesa.konjugasi:bakteri-bakterib.transduksi: bakteri via virus-bakteric.transformasi:paparan exogen DNA bakteri-bakteri Gene Transfer in the Environment. Levy & Miller, 1989 http://www.sciam.com/1998/0398issue/0398levybox3.html
  • 8. Memutus “Lingkaran setan”
  • 9. Prinsip Dasar Penggunaan AB FenomenaPenerapan Penggunaan PenggunaanAntibiotik Secara Bijak Antibiotik pada dan Benar Pada Anak Pasien Anak
  • 10. Prinsip Penggunaan Antibiotik
  • 11.  Berguna hanya untuk terapi infeksi bakteri... Tidak semua demam karena infeksi Tak semua infeksi karena bakteri  Tidak ada bukti bahwa antibiotik akan mencegah infeksi bakteri sekunder pada pasien dengan infeksi virus!! Nyquist A. C
  • 12.  Tak semua infeksi bakteri membutuhkan antibiotik  Pertimbangkan pilihan lain :  Antiseptik  Tindakan pembedahanNyquist A. C
  • 13.  Pada prinsipnya: pastikan..  Diagnosis klinis pasien  Beratnya kondisi pasien  Lama pasien sakit:  Contoh penggunaan yg salah: dokter di Indonesia amoksisilin untuk anak dengan infeksi virus ISPA (influenza) ↑↑ resistensi S. pneumonia terhadap gol. betalaktamNyquist A. C
  • 14.  Tidak semua diagnosis klinis infeksi harus didukung dengan pemeriksaan biakan dan uji kepekaan  Pewarnaan Gram Informasi pentingKS  Pengambilan spesimen sebelum pemberian AB
  • 15.  Berpikir Etiologi sebelum pemberian AB  Diagnosis Klinis KlinisKS Kemungkinan sumber infeksi Patogen yang paling mungkin Terapi empiris Data universal Data lokal
  • 16.  Infeksi oleh > satu jenis kuman yang sensitif pada antibiotik berbeda..  Eg: perforasi intra-abdomeninfeksi Gram negative, positif & anaerobkombinasi Infeksi mikroba diketahui tidak boleh diobati dengan anti- mikroba tunggal. Eg:TBC Terapi awal pada infeksi berat. Eg:sepsis. Terbukti antibiotik tunggal tidak cukup: endkokarditis bakterialis oleh Sterptococcus viridians.
  • 17. World Health Organization; 1994.
  • 18.  Ingat profile Farmakokinetik / Farmakodinamik (PK/PD)  Absorpsi  Eksresi  Kadar di jaringan  Level puncak, Kosentrasi inhibisi minimum Toksisistas dan “adverse effects” Interaksi obat ke obat Biaya
  • 19. Parameter PK/PD ↑↑ pengetahuan PK/PD dengan efikasi klinis mencegah resistensi Memudahkan dokter mengatur dosis rejimen.
  • 20. Important PK/PDPK/PD Parameter Parameters 8 Antibiotic concentration (ug/ml)-Waktu diatas MIC (T above MIC): waktu yg 6 Drug A dibutuhkan suatu obat untuk Drug A bisa mempertahankan Drug B 4 kosentrasi diatas MIC Drug B (kosentrasi hambat minimal).Makin singkat intervalnya, 2 makin sering pengulangan B B dosisnya (kurva B) 0 A Time Time above MIC
  • 21. Important PK/PDPK/PD Parameter Parameters 2 B B 0-MIC: minimum inhibitory concentration: kosentrasi min.u/berefek pd mikroba-Time>MIC: wkt yg dibutuhkan untuk berada tetap di reseptor dgn kosentrasi obat diatas kosentrasi MIC
  • 22. Important PK/PDPK/PD Parameter ParametersBerdasar afinitas terhadapReseptornya pada mikroorganisme: 2 B B 0
  • 23. •AB Tergantung kadar (concentration dependent) : harustercapai kadar obat tinggi sekali dalam darahsuntikanbolus •Eg: aminoglikosida tidak lagi dosis kecil tiap 8 jam dosis besar (5- 7 mg/kg BB) sekali per hari. (gambar kurva PK/PD A)•AB tergantung waktu (time dependent): kadar tidak perlutinggi sekali infus kontinu selama beberapa jam. (gambarkurva B)
  • 24. Pemilihan cara pemberian  Oral vs parenteral  Pandangan Tradisinal  “serius = parenteral”  Kurangnya antibitik “broad spectrum” dengan bioavailabilitas terpercaya  Obat Oral Terkini  Kadar serum > tinggi dan konstan  u/ infeksi tertentu  Sebaiknya parenteral
  • 25. Kelebihan Pengobatan Oral  Eliminasi risiko komplikasi terkait jalur intravena  Mempersingkat lama rawat inap  Menghemat kerja dan waktu perawat  Menghemat pengeluaran
  • 26. Biaya Pengobatan  Bukan hanya “obatnya”  Pertimbangkan :  Biaya pemberian obat  Lab  Lama rawat inap  Level monitoring  Kepatuhan pasien
  • 27.  Lama pengobatan tergantung dari jenis infeksi dan jenis antibiotik yang dipakai. Infeksi saluran napas atas oleh S. Pyogenes penisilin V atau roksitromisin selama 10 hari.  Communitiy-acquired pneumonia terapi benzyl penisilin atau klaritromisin selama 7 hari.  Osteomielitis akut pada anakminimum 4 minggu.12
  • 28.  Deeskalasi  Infeksi berat (misalnya sepsis), terapi antibiotik harus segera dimulai tanpa menunggu hasil biakan Kondisi pasien membaik pengurangan jenis antibiotik sesuai dengan hasil biakan.
  • 29. Fenomena Penggunaan Antibiotik Pada Pasien Anak
  • 30. Contoh penggunaan AB yang tidak rasional (1) Tanggal: 21 Maret 2011 Anak perempuan, 2 thn., menderita cacar air. Ia mendapat resep:  Cefspan (cefixime) sir. 2 x 2.5 mL/hari  Zovirax (acyclovir) 3 x 150 mg/hari Pertanyaan:  Apa alasan untuk meresepkan AB untuk suatu infeksi viral?  Dan andaikan pun ada indikasi untuk memberikan AB, mengapa dipilih sefiksim?
  • 31. Contoh penggunaan AB yang tidak rasional (1)Tanggal : 9 Feb. 2012 Seorang anak laki2, 3 tahun dengan diare 5 kali sehari selama 2 hari, tanpa tanda2 dehidrasi, keadaan umum baik. Ia mendapat resep:  Bactrim (cotrimoxazole) sir: 1 sendok teh tiap 12 jam  L-bio (probiotik): 1 sachet tiap 8 jam  Zincare (zinc sulphate): 1 tab tiap 24 jamPertanyaan:  Apakah rasional meresepkan AB untuk anak ini?  Apakah rasional mengombinasikan Bactrim dgn. L-bio?
  • 32. Penerapan Penggunaan Antibiotik Pada Pasien Anak
  • 33. Faktor yang mempengaruhi penggunaan obat Prior Intrinsic Scientific KnowledgeInformation Habits Information Influence Social & of Drug Cultural Factors Industry Treatment Societal Workload & Choices Economic & Staffing Legal Factors Workplace Infra- Authority & structure Relationships Supervision With Peers Workgroup WHO, Dept. Essential Drugs and Medicines Policy 36
  • 34. WHO, Dept. Essential Drugs and Medicines Policy 37
  • 35. WHO, Dept. Essential Drugs and Medicines Policy 38
  • 36. Take Home “Message”1. Jangan resepkan AB untuk demam, batuk, flu, atau diare nonspesifik yang tidak berat dan berbahaya. Tunggu dan amati pasien2. Jangan resepkan antibiotik untuk sakit tenggorok bila tidak disebabkan oleh streptokokus grup A3. Hindarkan penggunaan AB berspektrum luas bila tidak ada indikasi kuat
  • 37. Bila kita perlu meresepkan AB untuk faringitis?Dapat digunakan The scoring system by the American College of Physician and CDC (Ebell MH, Am Fam Physician 2003; 68:938): ○ Demam +1 ○ Tidak ada batuk +1 ○ Limfadenopati servikal +1 ○ Eksudat di tonsil +1 ○ Umur: < 15 tahun +1 Jumlah skor: ….Bila jumlah skor: 0 → tidak perlu AB atau pemeriksaan lanjutan 1-3 → rapid antigen testing (RAT) 4-5 → Terapi empiris + RAT
  • 38. Kesimpulan
  • 39.  Penggunaan antibiotik sering rasional ataupun yang tidakdampak resistensi kuman.. Pemberian antibiotik yang bijak dan benar pada anak:  Awali dengan pemilihan antibiotik secara rasional  Perhatikan pola bakteri setempat (sensitifitas)  farmakokinetik/farmakodinamik  harga. Pengetahuan dokter : farmakokinetik dan farmakodiinamik antibiotik, pola dan agen penyakit setempat, indikasi terapi antibiotik, ketajaman klinis, serta edukasi atasi masalah resistensi antibiotik
  • 40. Pengendalian resistensi kuman (1) Infeksi pada Obathewan/manusia Antibiotika Berbagai faktor Berbagai faktor Human/animal Rational drug Monitor infections use Monitoringpenggunaan suplai obat obat Monitor Pengendalian resistensi kuman resistensi Adapted from Simonsen et al, 2004
  • 41. Pengendalian resistensi kuman (2) Infeksi pada manusia/ hewan Beban penyakit Diagnostik Perilaku peresepHarapan pasien dan kepatuhannya Penggunaan obat rasional Adaptasi dari Simonsen et al, 2004
  • 42. Pengendalian resistensi kuman (3) Obat Antimikroba Regulatory framework Drug procurement lists Drug quality Management of drug supplyPenggunaanobat rasional Adapted from Simonsen et al, 2004
  • 43. Campaign to Prevent Antimicrobial Resistance in Healthcare Settings Resistensi Antimikroba : Strategi pencegahan Patogen yang dituju Antimicrobial-Resistant Pathogen Pathogen Cegah Cegah Transmisi Infeksi Infeksi Resistensi Antimikroba DiagnosisPenggunaan & Terapi Optimal Efektif Penggunaan Antimikroba
  • 44. Campaign to Prevent Antimicrobial Resistance in Healthcare Settings12 langkah MemutusResistensi Antimikroba 12 Break the chain 11 Isolate the pathogen Prevent Transmission 10 Stop treatment when cured 9 Know when to say “no” to vanco 8 Treat infection, not colonization Use Antimicrobials Wisely 7 Treat infection, not contamination 6 Use local data 5 Practice antimicrobial control 4 Access the experts Diagnose & Treat Effectively 3 Target the pathogen 2 Get the catheters out1 Vaccinate Prevent Infections
  • 45. Biol 1220 Synthetic Biology Mahesa
  • 46. the basics Used to kill or inhibit the growth of bacteria Classified as bactericidal or bacteriostatic Kill bacteria directly Prevent cell division Classified by target specificity:Narrow-spectrum vs Broad range Most modified chemically from original compounds found in nature, some isolated and produced from living organisms
  • 47. sites of antiobiotic action
  • 48. ampicillin Belongs to β-lactam group of antibiotics – contain β-lactam ring Broad-spectrum Penicillin derivative that inhibits bacterial cell wall synthesis (peptidoglycan cross-linking) Inactivates transpeptidases on the inner surface of the bacterial cell membrane Bactericidal only to growing E. Coli Widespread use leads to bacterial resistance. HOW?
  • 49. ampicillin resistance Cleavage of β-lactam ring by β- lactamase enzyme
  • 50. ampicillin resistance β-lactamase is encoded by the plasmid- linked bla (TEM-1) gene Hydrolyzes ampicillin Ampicillin levels in culture continually depleted
  • 51. use in synthetic biology To confirm uptake of gene (eg. of plasmids) by bacteria Bacterial Transformation: DNA integrates into bacteria’s chromosome and made chemically competent Exogenous DNA tagged with an antibiotic resistance gene eg. β-lactamase Grown in medium containing ampicillin Ampicillin resistance indicates successful bacterial transformation
  • 52. Kanamycin Targets 30s ribosomal subunit, causing a frameshift in every translation Bacteriostatic: bacterium is unable to produce any proteins correctly, leading to a halt in growth and eventually cell death
  • 53. kanamycinuse/resistance Over-use of kanamycin has led to many wild bacteria possessing resistance plasmids As a result of this (as well as a lot of side effects in humans), kanamycin is widely used for genetic purposes rather than medicinal purposes, especially in transgenic plants Resistance is often to a family of related antibiotics, and can include antibiotic- degrading enzymes or proteins protecting the 30s subunit
  • 54. chloramphenicol Bacteriostatic: functions by halting bacterial growth, which is done by inhibiting the enzyme peptidyl transferase, a protein that assists in the binding of tRNA to the 50s ribosomal subunit Three methods of resistance: reduced membrane permeability, mutation of the 50s subunit, and an enzyme called chloramphenicol acetyltransferase, which inactivates chloramphenicol by covaltly linking groups Easy/cheap to manufacture, but unused in western countries because of possible aplastic anemia as a side effect
  • 55. Antibiotic Classificationaccording to Goodman Narrow Spectrum Active against only one of the four classes of bacteria Broad Spectrum Active against more than one of the classes Boutique Highly specialized use Restricted to ID physicians
  • 56. Narrow Spectrum Active mostly against only one of the classes of bacteria gram positive: glycopeptides, linezolid, daptomycin, telavancin aerobic gram negative: aminoglycosides, aztreonam anaerobes: metronidazole
  • 57. Narrow Spectrum GPC GNR Fastid AnaerVanc ++++ ----- ----- only clostridiaLinezolid ++++ ----- ----- Only gram posDapto/Te ++++ ----- ----- -----lavancinAG ----- ++++ ++ -----Aztreon ----- +++ + -----Metro ----- ----- ----- ++++
  • 58. Broad Spectrum Active against more than one class GPC (incl many MRSA) and anaerobes: clindamycin GPC (not MRSA*) and GNR: cephalosporins, penicillins, sulfonamides, TMP/Sulfa (*include MRSA), FQ GPC (not MRSA*), GNR and anaerobes: ureidopenicillins + BLI, carbapenems, tigecycline (*MRSA), tetracyclines (*MRSA), moxiflox GPC and fastidious: macrolides
  • 59. Penicillins/Carbapenems Strep OSSA GNR Fastid AnaerPen ++++ -- +/-- -- +/--Amp/ ++++ -- + +/-- +/--amoxTicar ++ -- ++ +/-- +Ureid +++ -- +++ +++ ++U+BLI +++ ++++ ++++ +++ ++++Carba ++++ ++++ ++++ ++++ ++++
  • 60. Cephalosporins GPC non GNR FASTID ANAER -MRSACeph 1 ++++ + -- --Ceph 2 ++ ++ + --cefoxitin ++ ++ + +++cefotetanCeph 3 +++ +++ +++ --Ceph 4 +++ ++++ +++ --
  • 61. MAHESAFARMAKOLOGI 2004
  • 62. Antibiotika…. Zat yg dihasilkan organisme Bersifat baktericid dan bakteriostatik Kemoterapi : bahan kimia yang mampu menghambat kehidupan kuman di dalam tubuh Perang peneliti,klinisi versus bakteri
  • 63. nomenklatur Pewarnaan gram : identitas bakteri patogen dari dari tempat infeksi & pewarnaan Kultur : pembiakan dan identifukasi mikroba Kultur positip palsu : bila kultur terkontaminasi Kultur negatip palsu : sampel terinfeksi & media kultur & teknik tidak sesuai KHM : Konsentrasi HAmbat Minimal adalah konsentrasi antibiotik yg d/ mencegah pertumbuhan kultur
  • 64. Resistensi Timbulnya daya tahan kuman terhadap obat Resistensi kuman bisa massal oleh kuman yg resisten Epidemi nosokomial di RS
  • 65. Faktor resistensi Pengobatan yg terlambat Dosis terlalu rendah Kuman adaptasi d/ obat Pemberian A.B tidak tepat sasaran Keadaan fisik penderita t/ mendukung terbentuknya kuman d/ cepat
  • 66. hiperreaksi Hipersensitifitas Toksisitas Super infeksi Efek kumulasi
  • 67. Klasifikasi Antibiotika Penisilin & sefalosporin Tetrasiklin & kloramfenikol Aminoglikosida Antibiotik lain : makrolida, eritromisin
  • 68. PENISILIN & SEFALOSPORIN PENISILIN  BAKTERI GRAM - & GRAM +,STREPTOKOKUS,STAFILOKOKUS,S PIROKETA,KLOSTRIDIA,ANTRAKS,AK TINIMISETES PENISILIN PER OS BAIK,BEBERAPA TIDAK,RUSAK KRN ENSIM & HCl
  • 69. PENISILIN (ß Lactam) DISTRIBUSINYAAD KE OTAK ELIMINASI VIA RENAL INDIKASI: PNEUMONIA,MENINGITIS,OTITIS MEDIA,FARINGITIS,DEMAM REUMATIK,ENDOKARDITIS,GONORE, ANTRAKS,KLOSTRIDIA GAS GANGREN & TETANUS,OSTEOMILITIS,DIPHTERI
  • 70. PENISILIN…. PERTAMAKALI DIISOLASI DARI JAMUR PENICILLIUM TH 1949 OVER PENISILIN RESISTENSI (PEMBENTUKAN PENISILINASE) SIFAT KIMIA : PENISILIN,SEFALOSPORIN,MONOLAKT AM (AZTREONAM) DAN KARBAPENEM (IMIPENEM) CINCIN ß LAKTAM DI PUSAT->PECAH BY ß-LAKTAMASE
  • 71. GOLONGAN PENISILIN PENISILIN G (300.000-6 JUTA UNIT) PROKAIN PENISILIN BENZATIN PENISILIN AMPISILIN AMOKSISILIN OKSASILIN & KLOKSASILIN SEFALOSPORIN
  • 72. PENISILIN…. ASAM KLAVULANAT , PROBENISID MEMPERKUAT KERJA PENISILIN (contoh: AUGMENTIN & TIMENTIN) REAKSI ALERGI: REAKSI PENISILIN BERKISAR DARI RUAM KULIT SAMPAI SYOK ANAFILAKTIK & POTENSIAL MENGANCAM JIWA
  • 73. SEFALOSPORIN MEKANISME SAMA D/ PENISILIN 15 % Px ALERGI PENISILIN JUGA ALERGI SEFALOSPORIN PERTAMA KALI U/ BAKTERI GRAM POSITIP
  • 74. GOLONGAN SEFALOSPORIN GENERASI I GENERASI II GENERASI III GENERASI IV
  • 75. GENERASI I SEFALEKSIN SEFAZOLIN SEFALOTIN SEFRADIN SEFADROKSIL SEFAPRIN
  • 76. GENERASI II SEFAKLOR SEFUROKSIM SEFAMANDOL SEFOKSITIN SEFOTETAN SEFONICID SEFORANID SEFOMETAZOL
  • 77. GENERASI III SEFOTAKSIM SEFTRIAKSON SEFIKSIM SEFTIZOKSIM SEFOPERAZON MOKSALAKTAM SEFZIDIM
  • 78. TETRASIKLIN GOL SPETRUM LUAS PADA BAKTERI GRAM + DAN GRAM - PADA RIKETSIA,AMUBA,MIKOPLASMA, TRAKOMA PER OS BAIK, METABOLIT PADA GIGI & TULANG
  • 79. KLORAMFENIKOL SPEKTUM LUAS JUGA SPESIFIK PADA BAKTERI SALMONELLA TYPOA, HEMOPHILIS INFLUENZA, Boedetella Pertusis Efek SAMPING : KEBUTAAN & ALERGI LARANGAN IBU MENYUSUI
  • 80. GOLONGAN TETRASIKLIN DOKSISIKLIN METASILIN KLORTETRASIKLIN TETRASIKLIN OKSITETRASIKLIN
  • 81. Tetrasiklin Antibiotik spektrum luas Baik pd bakteri gram -/+ Juga pd Riketsia,amuba,trakoma Bila dosis tidak tepat menyebabkan resistensi/kebal Penggunaanya per os Dipengaruhi makanan,logam semacam Al,Mg,Ca dan Fe
  • 82.  Metabolit tetrasiklin ditimbun di tulang &gigi Keracunan obat: mual & muntah Bisa diare dan dehidrasi berat Keracunan gawat pada hati & ginjal Merupakan obat pilihan kolera Juga dapat pada infeksi pernapasan,gonore,akne Dosis 1-2 gram per oral
  • 83. Aminoglikosida Bakteriostatik thd gram – Contoh: Streptomisin Neomisin, kanamisin, Amikasin gentamisin, tobramisin, sisomisin,
  • 84. streptomisin Bentuk injeksi Bakteriostatik Obat pilihan untuk TBC,Lepra Hati2,resistensi sangat cepat Ekskresi melalui ginjal & empedu Keracunan: reaksi alergi sampai syok anafilaksi berat
  • 85. Kanamisin,Neomisin,Amikasin,Gentamisin & Tobramisin Bakterisid pd gram + dan – Penyerapan neomisin & kanamisin per os jelek sdgkan gentamisin & tobramisin baik Sediaan salep Gentamisin banyak diberikan pd luka bakar & luka pd kulit
  • 86. Eritromisin Aktivitas mirip penisilin Kekuatan lebih rendah Sebagai preparat pengganti penisilin Per os baik Keracunan: mual,muntah,superinfeksi dan alergi Spiramisin mirip eritromisin(Ex Spiradan tab & syrup) Azitromicin tab,syrup (Zitromax tab,syrup)
  • 87. Kel Polimiksin Polimiksin A Polimiksin Byang dipakai Polimiksin C Polimiksin D Polimiksin Eyang dipakai Keduanya aktif untuk bakteri gram – Indikasi : infeksi pseudomonas,shigela,disentri & enterobakter Banyak dipakai untuk topikal (salep) saja,sal napas