REAKSI HIPERSENSITIVITAS

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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