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FACULTY OF MEDICINE MALANG ISLAMIC UNIVERSITY. The MTCT-Plus Initiative2 Applying the tuberculin skin test Courtesy of Dr. Marc Steben.

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Presentasi berjudul: "FACULTY OF MEDICINE MALANG ISLAMIC UNIVERSITY. The MTCT-Plus Initiative2 Applying the tuberculin skin test Courtesy of Dr. Marc Steben."— Transcript presentasi:

1 FACULTY OF MEDICINE MALANG ISLAMIC UNIVERSITY

2 The MTCT-Plus Initiative2 Applying the tuberculin skin test Courtesy of Dr. Marc Steben

3 The MTCT-Plus Initiative3 Applying the tuberculin skin test

4 The MTCT-Plus Initiative4 Applying the tuberculin skin test Courtesy of Dr. Marc Steben

5 The MTCT-Plus Initiative5 Reading the tuberculin skin test  Read 2-3 days after placing the test  Feel for induration  Color change without induration is not included in the measurement  Use a ruler or calipers  Have someone else check if unsure  Always document the exact size (mm) – not just “positive” or “negative”

6 The MTCT-Plus Initiative6 Reading the tuberculin skin test Courtesy of Dr. Marc Steben

7 The MTCT-Plus Initiative7 Reading the tuberculin skin test

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12 YY

13  Hipersensitivitas adalah suatu reaksi yang tidak diharapkan dari respon imun tubuh.  Coombs dan Gell membagi menjadi 4 tipe (mekanisme dan waktu):  Rx. Hipersensitivitas tipe I  Rx. Hipersensitivitas tipe II  Rx. Hipersensitivitas tipe III  Rx. Hipersensitivitas tipe IV

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15 (hives) Allergies 4 types of hypersensitivity reactions

16 Delayed-type hypersensitivity Immune complex disease

17 Reaksi Hipersensitivitas tipe I  Reaksi Hipersensitivitas tipe cepat atau anafilaktik  Diperantarai IgE  Alergen  produksi IgE  berikatan spesifik dengan reseptor di permukaan sel mast dan basofil  tersensitisasi  Kontak berikutnya  sederetan reaksi biokimia  degranulasi dan pelepasan mediator2 (histamin, leukotrien dan sitokin)  reaksi alergi  menit setelah terpapar antigen, kadang keterlambatan (10-12 jam)  Dapat melibatkan kulit (urtikaria dan eksema), mata (konjungtivitis), nasofaring (rinitis), jaringan bronkopulmoner (asma), dan GI tract (gastroenteritis)

18  Contoh: reaksi anafilaksis terhadap bisa hewan, hay fever, urtikaria akibat makanan, dermatitis atopik, rhinitis alergika, konjungtivitis, asma, dll  Gejala : ketidaknyamanan ringan sampai kematian  Berat ringan gejala dipengaruhi :  antibodi IgE  jumlah alergen  faktor-faktor lain yang dapat meningkatkan respon (infeksi virus dan polutan) Reaksi Hipersensitivitas tipe I……….

19 Biologic effects of mediators

20 Table 1. Pharmacologic Mediators of Immediate Hypersensitivity MEDIATOR Preformed mediators in granules histamine bronchoconstriction, mucus secretion, vasodilatation, vascular permeability tryptaseproteolysis kininogenase kinins and vasodilatation, vascular permeability, edema ECF-A (tetrapeptides) attract eosinophil and neutrophils Newly formed mediators leukotriene B 4 basophil attractant leukotriene C 4, D 4 same as histamine but 1000x more potent prostaglandins D 2 edema and pain PAF platelet aggregation and heparin release: microthrombi

21 Tes diagnostik  Skin test (prick dan intradermal)  Kadar total IgE dan IgE spesifik terhadap alergen yang dicurigai (ELISA)  IgE tinggi pada kondisi atopik Terapi:  Antihistamin, adrenalin, bronkodilator, kortikosteroid, menghindari paparan alergen dan immunoterapi

22 Ragweed Control negative (saline) Control positve (histamine) Skin test for allergy

23 Type I hypersensitivity reaction 23 Capillary dilation Pressure of exudate Release of chemical mediators : Histamine SRS-A Kinins Prostaglandins Increased Blood Volume Increased Capillary permebiality Exudation of Cell, fluid protein Nerve irritation Constriction of smooth muscle Antigen Ingestants Food Drugs Pollens Dusts Molds Injectants Drugs Stings Vaccines Serum Allergen interacts with IgE on mast cell CAUSESMECHANISMPATHOPHYSIOLOGY

24 Type I hypersensitivity reaction (continued) 24 Respiratory tract 1.Upper “sinus headache” itching of eyes tearing, sneezing, watery nasal discharge, itching of nose, throat irritation 2.Lungs wheezing, dyspnea, dry cough, tightness in chest MANIFESTATIONS CLINICAL EXAMPLES Gastrointestinal Glossitis, cardiospasm Nausea, vomitting Irritable bowel Diarrhea, pruritus ani Skin Urticaria, pruritus, Angioedema, weeping erthematosus vesico-papular lessions Respiratory tract 1.Upper “sinus headache” itching of eyes tearing, sneezing, watery nasal discharge, itching of nose, throat irritation 2.Lungs wheezing, dyspnea, dry cough, tightness in chest Conjunctivitis Asthma Food allergies Atopic dermatitis Urticaria Allergic rhinitis

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26 Reaksi Hipersensitivitas tipe II  Reaksi hipersensitivitas sitotoksik  Waktu reaksi : menit - jam  Contoh: reaksi transfusi, drug-induced hemolytic anemia, granulositopenia, dan trombositopenia  Diperantarai IgM atau IgG dan komplemen  Fagosit dan sel K punya peran  Interaksi antigen-antibodi pd permukaan sel, IgM atau IgG dgn antigen yang juga merupakan bagian integral membran sel atau telah terserap atau menyatu menjadi membran.  Mengaktifkan sistem komplemen dan sel yang terlibat dihancurkan.  Terapi: anti-inflamasi dan agen immunosupresif

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28 Type II hypersensitivity reaction 28 CAUSESMECHANISM PATHOPHYSIOLOGY CLINICAL EXAMPLES Susceptability to infections Antigen Transfusion reaction Erythroblastosis fetalis Drugs Autoantibodies Unknown Antigen interacts with body cell i.e : Erythrocyte Leucocyte Platelet Vascular endothelium Agranulocytosis Thrombocytopenia Purpura Vesicular purpura Vasculitis Erytrhrocyte hemolysis Hemolytic anemia Reaction of IgG or IgM antobody with antigen on cell Activates complement

29 Reaksi Hipersensitivitas tipe III  Reaksi hipersensitivitas kompleks imun / reaksi Arthus  3-10 jam setelah terpapar antigen  Diperantarai kompleks imun (antigen-antibodi)  Antigen eksogen (bakteri, virus, atau parasit)/endogen (SLE)  Contoh: serum sickness,SLE,rx Arthus,lupus nephritis,RA,dll  Terbentuk kompleks antigen-antibodi (toksik terhadap jaringan di tempat mereka diendapkan seperti ginjal / paru- paru)  infiltrasi dinding pembuluh darah kecil  aktivasi kaskade komplemen  pelepasan bahan aktif secara biologis, termasuk faktor-faktor yang menarik sel-sel fagosit yang akan menfagositosis kompleks tersebut

30 Type III hypersensitivity reactions (Arthus Reaction) - Ab-Ag Complexes Critical mediators appear to be C5a-receptor and FcgRIII--probably present on mast cells

31 Type III hypersensitivity reaction 31 CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL EXAMPLES Tissue destruction Inflammation Antigen and antibody form an immune complex Antigen Autoantibodies Drugs Serum Chemicals Foreign antigen Bacteria Virus Glomerulo- nephritis Vasculitis Arthus reaction Rheumatoid diseases Serum sickness Deposits on vessel walls or basement membrane

32 Diagnosis:  Biopsi jaringan (endapan Ig dan komplemen)  Kompleks imun pada darah dan penurunan jumlah komplemen Terapi:  Anti-inflamasi

33 Reaksi Hipersensitivitas Tipe IV  tipe seluler atau tipe lambat ( delayed type hypersensitivity)  > 12 jam  Contoh klasik: reaksi tuberkulin (Mantoux) yang memuncak 48 jam setelah injeksi antigen  Contoh lain: dermatitis kontak, penyakit autoimun dan infeksi seperti tuberkulosis, lepra, granulomatosa, toksoplasmosis, dll

34 Biological effects of Eosinophil mediators Late stage of an allergic response includes the recruitment of eosinophils and Th2 cells contrast with a DTH (type IV) response which includes infiltration of macrophages and Th1 cells

35 Table 3 - Delayed hypersensitivity reactions TypeReaction time Clinical appearance HistologyAntigen and site contact48-72 hreczema lymphocytes, followed by macrophages; edema of epidermis epidermal ( organic chemicals, poison ivy, heavy metals, etc. ) tuberculin48-72 hrlocal induration lymphocytes, monocytes, macrophages intradermal (tuberculin, lepromin, etc. ) granuloma21-28 dayshardening macrophages, epitheloid and giant cells, fibrosis persistent antigen or foreign body presence (tuberculosis, leprosy, etc. )

36  Mekanisme perusakan melibatkan limfosit T dan monosit dan/atau makrofag  Sel t sitotoksik (Tc) menyebabkan kerusakan langsung sedangkan sel T helper (TH1) mensekresi sitokin  aktivasi Tc, makrofag serta monosit  kerusakan Diagnosis: - Mantoux test dan patch test Terapi: - Kortikosteroid dan agen imunosupresif

37 Type IV hypersensitivity reaction 37 CAUSESMECHANISM PATHOPHYSIOLOGY CLINICAL EXAMPLES Release of : Lymphokines Migration inhibition factor Interferon Killer cells Transfer factor Injury and destruction of target organ Antigen Tuberculin Poison Ivy Chemical Fungi Transplanted organs Virus Contact dermatitis Graft vs host reactions Viral infection Autoallergic disease Sensitized Lymphocyte reacts with antigen

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