4_ REAKSI HIPERSENSITIVITAS

7/18/2019 4_ REAKSI HIPERSENSITIVITAS

http://slidepdf.com/reader/full/4-reaksi-hipersensitivitas-56d6712b528e2 1/30

REAKSI HIPERSENSITIVITAS

Y Y



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



(hives)

Allergies

4 types of hypersensitivity reactions



Delayed-type hypersensitivityImmune

complex

disease



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 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)



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……….



Biologic effects of mediators



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



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



Ragweed

Control negative (saline)

Control positve (histamine)

Skin test for allergy



Type I hypersensitivity reaction

12

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



Type I hypersensitivity reaction (continued)13

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



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.



Type II hypersensitivity reaction 17

CAUSES MECHANISM PATHOPHYSIOLOGY CLINICAL

EXAMPLES

Susceptability

to infections

Antigen

Transfusion

reaction

Erythroblastosis

fetalis

Drugs

Autoantibodies

Unknown

Antigeninteracts

with body

cell i.e :

•Erythrocyte

•Leucocyte

•Platelet•Vascular

endothelium

Agranulocytosis

Thrombocytopenia Purpura

Vesicular

purpura

Vasculitis

Erytrhrocyte

hemolysis

Hemolytic

anemia

Reaction of IgG or

IgM antobody withantigen on cell

Activates

complement



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



Type III hypersensitivity reactions (Arthus Reaction) - Ab-Ag Complexes

Critical mediators appear to be C5a-receptor and FcgRIII--probably present on mast cells



Type III hypersensitivity reaction20


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



Diagnosis:

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 memuncak48 jam setelah injeksi antigen

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



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



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 induration lymphocytes,

monocytes,

macrophages intradermal

(tuberculin,

lepromin, etc.)

granuloma 21-28 days hardening macrophages,

epitheloid and giant

cells, fibrosis

persistent antigen or

foreign body

presence

(tuberculosis,

leprosy, etc.)



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



Type IV hypersensitivity reaction

26


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

4_ REAKSI HIPERSENSITIVITAS

Documents

Transcript of 4_ REAKSI HIPERSENSITIVITAS