reaksi hipersensitivitas 2

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    REAKSI HIPERSENSITIVITAS

    YY

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    Hipersensitivity

    Sistem pertahanan thd invasi benda asing(eksogen/endogen)

    Kenyataannya (tidak demikian)

    OK Pada saat yg sama malah merupakan

    KEMATIAN

    KERUSAKAN JARINGAN

    OK RESPON IMUN ITU SENDIRI

    (Ibarat Pedang Bermata Dua)

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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

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    (hives)

    Allergies

    4 types of hypersensitivity reactions

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    Delayed-type hypersensitivityImmunecomplex

    disease

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    Reaksi Hipersensitivitas tipe I

    Reaksi Hipersensitivitas tipe cepat atau anafilaktik

    Diperantarai IgE

    Alergenproduksi IgEberikatan spesifik dengan reseptor di

    permukaan sel mast dan basofil tersensitisasi

    Kontak berikutnya sederetan reaksi biokimiadegranulasi 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

    histaminebronchoconstriction, 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

    PAFplatelet 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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    Type I hypersensitivity reaction

    13

    Capillary dilation

    Pressure ofexudate

    Release of

    chemical

    mediators :

    Histamine

    SRS-A

    Kinins

    Prostaglandins

    Increased

    BloodVolume

    Increased

    Capillary

    permebiality

    Exudation of

    Cell, fluid protein

    Nerve

    irritation

    Constriction

    of smooth

    muscle

    Antigen

    Ingestants

    Food

    Drugs

    Pollens

    Dusts

    Molds

    Injectants

    DrugsStings

    Vaccines

    Serum

    Allergen

    interacts

    with

    IgE on mast cell

    CAUSES MECHANISM PATHOPHYSIOLOGY

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    Type I hypersensitivity reaction (continued)14

    Respiratory tract

    1. 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

    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 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 IgGdgn antigen yang juga merupakan bagian integral membran

    sel atau telah terserap atau menyatu menjadi membran.

    Mengaktifkan sistem komplemen dan sel yang terlibat

    dihancurkan.

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    Type II hypersensitivity reaction 18

    CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL

    EXAMPLES

    Susceptability

    to infections

    Antigen

    Transfusion

    reaction

    Erythroblastosis

    fetalis

    Drugs

    Autoantibodies

    Unknown

    Antigeninteracts

    with body

    cell i.e :

    Erythrocyte

    Leucocyte

    PlateletVascular

    endothelium

    Agranulocytosis

    Thrombocytopenia Purpura

    Vesicular

    purpura

    Vasculitis

    Erytrhrocyte

    hemolysis

    Hemolytic

    anemia

    Reaction of IgG or

    IgM antobody withantigen 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 kecilaktivasi

    kaskade komplemenpelepasan 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 reaction21

    CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL

    EXAMPLES

    Tissue

    destruction

    Inflammation

    Antigen and

    antibody form

    an immune

    complex

    Antigen

    Autoantibodies

    Drugs

    Serum

    ChemicalsForeign antigen

    Bacteria

    Virus

    Glomerulo-

    nephritis

    Vasculitis

    Arthus reaction

    Rheumatoid

    diseases

    Serum sickness

    Deposits on vessel walls

    or 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

    tipeseluler atau tipe lambat (delayed type hypersensitivity)

    > 12 jam

    Contoh klasik: reaksi tuberkulin (Mantoux) yang memuncak48 jam setelah injeksi antigen

    Contoh lain: dermatitis kontak, penyakit autoimun dan infeksiseperti tuberkulosis, lepra, granulomatosa, toksoplasmosis,dll

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    Biological effects of Eosinophil

    mediators

    Late stage of an allergic response includes therecruitment of eosinophils and Th2 cells contrast with

    a DTH (type IV) response which includes infiltration ofmacrophages and Th1 cells

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    Table 3 - Delayed hypersensitivity reactions

    Type Reaction timeClinical

    appearanceHistology 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 monositkerusakan

    Diagnosis:- Mantoux test danpatch test

    Terapi:- Kortikosteroid dan agen imunosupresif

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    Type IV hypersensitivity reaction

    27

    CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL

    EXAMPLES

    Release of :

    Lymphokines

    Migration inhibition

    factorInterferon

    Killer cells

    Transfer factor

    Injury and

    destruction oftarget organ

    Antigen

    Tuberculin

    Poison IvyChemical

    Fungi

    Transplanted

    organs

    Virus

    Contact

    dermatitis

    Graft vs host

    reactions

    Viral infection

    Autoallergic

    disease

    Sensitized

    Lymphocytereacts with

    antigen

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