Sistem limfatik farmasi
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  • 1. Lymphatic/Immune System
  • 2. Lymphatic/Immune System:Major Role:The main role of the immunesystem is to destroy and removeinvading microbes and virusesfrom the body. The lymphaticsystem also removes fat andexcess fluids from the blood. Major Organs:Lymph, lymph nodes and vessels,white blood cells, T- and B- cells.
  • 3. SIRKULASI LIMFATIK• cairan & protein yg berlebihan yg disaring melalui kapiler sistemikyang berada di ruang interstitial akan di angkut oleh pembuluh limfe dalam bentuk cairan limfe(cairan limfe)• Untuk kemudian dikembalikan ke sirkulasi sistemik melalui pembuluh2 pengumpul yg letaknya dekat dengan vena yg bersangkutan
  • 4. Pembuluh limfe• Membawa cairan limfe melalui ductus thoracicus dan ductus lymphaticus dexter ke dalam sistem vena subclavia (sirkulasi limfe)• Limfe : cairan jaringan yang mengandung faktor pembekuan darah, protein, lemak dan limfosit.
  • 5. SISTEM LIMFOIDLimfosit terdapat di seluruh tubuh, dancenderung terpusat dalam jaringan limfoidYang termasuk Jaringan limfoid : kelenjarlimfe, limpa, timus, jaringan limfoid ygberhubungan dengan permukaan mukosa,& sumsum tulang
  • 6. Kelenjar limfePaling banyakMerupakan nodul nodul jaringan limfoid ygdiselubungi kapsul dan terdapat pada tiapbagian tubuh
  • 7. LimpaMassa besar yg tdd limfosit & makrofag ygdirangkai dalam aliran darahSinusoidnya dipenuhi oleh darah dandiantaranya terdapat nodulus jaringanlimfoid
  • 8. Timus• Jaringan limfoid yg terletak dalam rongga dada anterior & bagian atas jantung dan pembuluh2 darah besar
  • 9. Edema• Akumulasi cairan di bagian interstisial, yang menyebabkan pembengkakan jaringan• Penyebabnya adalah:• hal hal yang menyebabkan keluarnya cairan dari pembuluh darah:1. Peningkatan tekanan darah, permeabilitas kapiler2. Katup vena yang inkompeten, penyumbatan pembuluh darah3. hypoproteinemia, protein plasma berkurang shg
  • 10. Edema• Kegagalan cairan interstitital diangkut oleh pembuluh limfe, akibat• Penyumbatan (pengangkatan) pembuluh limfe e.g elephantiasis, post mastektomi ec Ca mammae
  • 11. Defence Mechanisms  non-specific ; inflamasi  specific
  • 12. InflammationThe body’s response to injury
  • 13. Inflammation Signs and SymptomsAnatomical: Redness, swelling, heat, pain, poor function.Histological: Leukocytes accumulate in inflamed tissues.
  • 14. Inflammation Degrees of severityAcute: Short duration (hours, days) Possible neutrophil influxChronic: Long duration (weeks, months) Immune system recruited (lymphocytes)
  • 15. Inflammation Underlying MechanismsBlood vessels: changes in diameter and permeability.Leukocytes: chemotactic emigration.Both regulated by the production and release of inflammatory mediators.
  • 16. Inflammation Inflammatory Mediators Derived from plasma proteins: • e.g. products released during clotting. Derived from cells: • e.g. histamine, cytokines. Only released/act locally. (hormonal-like specificity)
  • 17. Inflammatory Response Tissue Pathogen damage Chemical mediators Increased released Chemotaxis vascular permeability Increased numbers of Fibrin mesh white blood cells isolates injury site at injury site Pathogens contained & destroyed
  • 18. Chemical defences1. Complement• group of about 20 serum proteins• when combined with foreign substances a “complement cascade” is activated• complement proteins rupture bacterial membranes2. Interferon• stimulate body cells to resist viral infection• inhibits viral replication
  • 19. The Immune System•Specific: via receptor ligand interactions• Acquired: via “education” oflymphocytes Memory: via survival oflymphocytes•Systemic: via emigration oflymphocytes.
  • 20. The Immune SystemSpecificity is driven by receptor-ligand typeinteractions.Two main pathways:1. Humoral pathway (involves B lymphocytes).2. Cell mediated pathway (uses T lymphocytes)
  • 21. Humoral PathwayANTIBODIES: proteins secretedby activated B lymphocytes, thatbind to antigens(immunoglobulins).ANTIGENS: any chemical whichelicits an immune response(usually foreign).
  • 22. B-lymphocytesProduce antibodies against foreign proteins5 main classes1. IgG - most abundant2. IgM - first circulating Ig released3. IgE - involved in inflammatory responses4. IgA - body secretions5. IgD - surface receptor
  • 23. Antigenic Determinants Different antigenicdeterminants Antigen
  • 24. Humoral Response
  • 25. Humoral ResponseConsequences of immune complexformation.1. Neutralisation of toxic antigens.2. Activation of leukocytes.3. Formation of inflammatory mediators.4. Destruction of bacteria.
  • 26. Cell Mediated ResponseAntigen-receptor interactions occur on thecell surface.Two types of interaction: Antigen presenting cells (APC) and Helper T cells. Cytotoxic T cells and abnormal cells.
  • 27. Cell Mediated Response APCAntigen Helper T cell MHCII MHCII-antigen T-cell complex receptor Cytokines Released MHC = Major-Histocompatibility-Complex molecule.
  • 28. Cell Mediated Response Infected Cell CytotoxicVirus T cell MHCI MHCI-antigen T-cell complex receptor Infected cell Killed
  • 29. Cytotoxic T-cell Response Cell lysis initiatedVirus infected cell Time Killer T cell
  • 30. “Education” by Clonal Selection ATTACK Memory cells
  • 31. Reaksi Alergi= Hipersensitivitas merupakankeadaan cedera tubuh akibatinteraksi antara antigen dan antibodiReaksi Alergi ada 4 tipe yaitu :1. Reaksi tipe I (anafilaktik),diperantarai oleh antibodi IgE yangterikat pada permukaan sel mast.
  • 32. 2. Reaksi tipe II (Sitotoksik),diperantarai oleh antibodi IgG atauIgM yg bereaksi dengan antigenpada permukaan sel target– ADCC (antibody dependent, cell- mediated cytotoxic)
  • 33. 3. Reaksi tipe III (Kompleks imun),diperantarai melalui pembentukankompleks-kompleks antigen antibodi,sebagian besar dengan antibodi Ig GReaksi tipe IV (diperantarai sel),diperantarai oleh limfosit T ygmengalami sensitisasi dematitis kontak alergi
  • 34. SINDROM IMUNODEFISIENSIKeadaan dimana jaringan limfoidtidak dapat bereaksi secara normalthd berbagai antigenPrimer (genetik), cth:agammaglobulinemia terkait-X(defisiensi sel B),Sekunder, cth: keganasan, AIDS
  • 35. AIDSBentuk spektrum imunologis & klinis ygpaling ekstrim dari infeksi HIVHIV ditransmisikan melalui kontakseksual, darah atau produk darah ygterinfeksi, & cairan tubuh tertentu, sertamelalui perinatalHIV menginfeksi sel molekul CD4 (limfositT4), monosit, makrofag, dendrit,Langerhans dan mikroglia
  • 36. Setelah virus memasuki sel RNA nyaditranskripsi menjadi DNA. DNA yg barusaling bergabung masuk sel target danmembtk provirus. Provirus inimenghasilkan protein virus baru ygmerupakan pabrik bagi virus yg baru.Sel target normal akan membelah danmemperbanyak diri, pd keadaan iniprovirus menyebarkan anak-anaknya
  • 37. TERIMA KASIH