reaksi hipersensitivitas
DESCRIPTION
antigen-antibodyTRANSCRIPT
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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 IRx. Hipersensitivitas tipe IIRx. Hipersensitivitas tipe IIIRx. Hipersensitivitas tipe IV
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(hives)
Allergies
4 types of hypersensitivity reactions
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Delayed-type hypersensitivityImmune complex disease
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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 bronkopulmoner (asma), dan GI tract (gastroenteritis)
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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……….
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Biologic effects of mediators
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Table 1. Pharmacologic Mediators of Immediate Hypersensitivity
MEDIATOR
Preformed mediators in granules
histamine bronchoconstriction, mucus secretion, vasodilatation, vascular permeability
tryptase proteolysis
kininogenase kinins and vasodilatation, vascular permeability, edema
ECF-A(tetrapeptides)
attract eosinophil and neutrophils
Newly formed mediators
leukotriene B4 basophil attractant
leukotriene C4, D4 same as histamine but 1000x more potent
prostaglandins D2 edema and pain
PAF platelet aggregation and heparin release: microthrombi
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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
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Ragweed
Control negative (saline)
Control positve (histamine)
Skin test for allergy
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12
Capillary dilation
Pressure of exudate
Release of chemical mediators :HistamineSRS-AKininsProstaglandins
IncreasedBloodVolume
Increased Capillary permebiality
Exudation ofCell, fluid protein
Nerve irritation
Constrictionof smoothmuscle
AntigenIngestants
FoodDrugs
PollensDustsMolds
InjectantsDrugsStings
VaccinesSerum
Allergen interacts withIgE on mast cell
CAUSES MECHANISM PATHOPHYSIOLOGY
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Type I hypersensitivity reaction (continued)13
Respiratory tract1. Upper “sinus headache”
itching of eyestearing, sneezing,watery nasal discharge,itching of nose,throat irritation
2. Lungs wheezing, dyspnea, dry cough, tightness in chest
MANIFESTATIONS CLINICAL EXAMPLES
GastrointestinalGlossitis, cardiospasmNausea, vomittingIrritable bowelDiarrhea, pruritus ani
SkinUrticaria, pruritus,Angioedema, weeping erthematosus vesico-papular lessions
Respiratory tract1. Upper “sinus headache”
itching of eyestearing, 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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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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Type II hypersensitivity reaction17
CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL EXAMPLES
Susceptability to infections
Antigen
Transfusionreaction
Erythroblastosisfetalis
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 orIgM antobody with antigen on cell
Activates complement
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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
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Type III hypersensitivity reactions (Arthus Reaction) - Ab-Ag Complexes
Critical mediators appear to be C5a-receptor and FcgRIII--probably present on mast cells
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Type III hypersensitivity reaction20
CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL EXAMPLES
Tissue destruction
Inflammation
Antigen and antibody forman immunecomplex
Antigen
Autoantibodies Drugs SerumChemicals Foreign antigenBacteria Virus
Glomerulo-nephritis
Vasculitis
Arthus reaction
Rheumatoid diseases
Serum sickness
Deposits on vessel wallsor basement membrane
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Diagnosis:
Biopsi jaringan (endapan Ig dan komplemen)Kompleks imun pada darah dan penurunan
jumlah komplemen
Terapi:Anti-inflamasi
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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
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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
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Table 3 - Delayed hypersensitivity reactions
Type Reaction timeClinical appearance
Histology Antigen and site
contact 48-72 hr eczema
lymphocytes, followed by macrophages; edema of epidermis
epidermal ( organic chemicals, poison ivy, heavy metals, etc.)
tuberculin 48-72 hr local indurationlymphocytes, monocytes, macrophages
intradermal (tuberculin, lepromin, etc.)
granuloma 21-28 days hardeningmacrophages, epitheloid and giant cells, fibrosis
persistent antigen or foreign body presence (tuberculosis, leprosy, etc.)
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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
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Type IV hypersensitivity reaction
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CAUSES MECHANISM PATHOPHYSIOLOGY CLINICALEXAMPLES
Release of :Lymphokines Migration inhibition factorInterferonKiller cellsTransfer factor
Injury and destruction of target organ
Antigen
TuberculinPoison IvyChemicalFungiTransplanted
organsVirus
Contact dermatitis
Graft vs host reactions
Viral infectionAutoallergic disease
SensitizedLymphocyte reacts with antigen
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