reaksi hipersensitivitas

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REAKSI HIPERSENSITIVITAS YY

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Page 1: REAKSI HIPERSENSITIVITAS

REAKSI HIPERSENSITIVITASYY

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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 time Clinical 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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