4_ REAKSI HIPERSENSITIVITAS (1)
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REAKSI HIPERSENSITIVITAS
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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
4 types of hypersensitivity reactions
(hives)
Allergies
Immu Delayed-type ne compl
hypersensitivity
Reaksi Hipersensitivitas tipe I
Reaksi Hipersensitivitas tipe cepat atau anafilaktik Diperantarai IgE Alergenproduksi 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 15-30 menit setelah terpapar antigen, kadang keterlambatan (10-12 jam) Dapat melibatkan kulit (urtikaria dan eksema), mata (konjungtivitis), nasofaring (rinitis), jaringan
Reaksi Hipersensitivitas tipe I.
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)
Biologic effects of mediators
Table 1. Pharmacologic Mediators of Immediate Hypersensitivity MEDIATOR Preformed mediators in granules histamine bronchoconstriction, mucus secretion, vasodilatation, vascular permeability proteolysis kinins and vasodilatation, vascular permeability, edema attract eosinophil and neutrophils basophil attractant same as histamine but 1000x more potent edema and pain platelet aggregation and heparin release: microthrombi
tryptase kininogenase ECF-A (tetrapeptides) Newly formed mediators leukotriene B4 leukotriene C4, D4 prostaglandins D2 PAF
Tes diagnostikSkin 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
Skin test for allergyRagweed Control negative (saline) Control positve (histamine)
CAUSESAntigen Ingestants Food Drugs Pollens Dusts Molds Injectants Drugs Stings Vaccines Serum
MECHANISM
PATHOPHYSIOLOGYIncreased Blood Volume
Capillary dilation Release of Allergen chemical interacts mediators : Exudation of Increased with Histamine Cell, fluid protein Capillary IgE on mast cell SRS-A permebiality Kinins Prostaglandins Pressure of exudate Nerve irritation Constrict ion of smooth muscle
12
MANIFESTATIONS Respiratory tract Respiratory tract 1. Upper sinus headache 1. Upper sinus headache itching of eyes itching of eyes tearing, sneezing, tearing, sneezing, watery nasal discharge, watery nasal discharge, itching of nose, itching of nose, throat irritation throat irritation 2. Lungs wheezing, dyspnea, 2. dry cough, tightness in chest Lungs wheezing, dyspnea,Gastrointestinal Glossitis, cardiospasm Nausea, vomitting Irritable bowel Diarrhea, pruritus ani
CLINICAL EXAMPLES
Allergic rhinitis
Conjunctivitis
dry cough, tightness in chest
Asthma
Food allergies
Atopic dermatitis Skin Urticaria, pruritus, Angioedema, weeping erthematosus vesico-papular lessions UrticariaType I hypersensitivity reaction (continued)13
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
CAUSES Antigen Transfusion reaction Erythroblastosis fetalis Drugs Autoantibodies Unknown
MECHANISM
PATHOPHYSIOLOGY
CLINICAL EXAMPLES Hemoly tic anemia Susceptabi lity to infections Purpu ra Vesicul ar purpura
Antigen interacts with body cell i.e : Erythroc yte Leucocyt e Platelet Vascular endotheli um
Reaction of IgG or IgM antobody with antigen on cell Activates complement
Erytrhroc yte hemolysi s Agranulocytosis
Thrombocytopenia Vasculiti s
Type II hypersensitivity reaction17
Reaksi Hipersensitivitas tipe III
Reaksi hipersensitivitas kompleks imun / reaksi Arthus 3-10 jam setelah terpapar antigen Diperantarai kompleks imun (antigenantibodi) 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
Type III hypersensitivity reactions (Arthus Reaction) - Ab-Ag Complexes
Critical mediators appear to be C5a-receptor and FcgRIII-probably present on mast cells
CAUSESMECHANISMAntigen
PATHOPHYSIOLOGY CLINICAL EXAMPLESGlomerulonephritis Vasculitis Arthus reaction Rheumatoi d diseases Serum sickness
Antigen and Deposits on vessel walls Autoantibodies Tissue antibody form basement membranedestructio Drugs or an immune Serum n complex Chemicals Inflammat Foreign antigen ion Bacteria Virus
Type III hypersensitivity reaction20
Diagnos is:Biopsi
jaringan (endapan Ig dan komplemen) Kompleks imun pada darah dan penurunan jumlah komplemen
Terapi:Anti-inflamasi
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
Late stage of an allergic response includes the recruitment of eosinophils and Th2 cells contrast with
Biological effects of Eosinophil mediators
a DTH (type IV) response which includes infiltration of macrophages and Th1 cells
Table 3 - Delayed hypersensitivity reactions Type Reaction time Clinical appearance 48-72 hr eczema Histology Antigen and site epidermal ( organic chemicals, poison ivy, heavy metals, etc.)
contact
lymphocytes, followed by macrophages; edema of epidermis
tuberculin
48-72 hr
local induration lymphocytes, monocytes, macrophages hardening macrophages, epitheloid and giant cells, fibrosis
intradermal (tuberculin, lepromin, etc.) persistent antigen or foreign body presence (tuberculosis, leprosy, etc.)
granuloma
21-28 days
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
CAUSES
MECHANISM
PATHOPHYSIOLOGY
CLINICAL EXAMPLES Contact dermatiti s Graft vs host reactions Viral infection Autoallerg ic disease
Antigen Tuberculi n Poison Ivy Chemical Fungi Transplan ted organs Virus Sensitized Lymphocy te reacts with antigen
Release of : Lymphokines Migration inhibition factor Interferon Killer cells Transfer factor
Injury and destructio n of target organ
Type IV hypersensitivity reaction26