Download SKIN TEST

FACULTY OF MEDICINE
MALANG ISLAMIC UNIVERSITY
SKIN TEST
Applying the tuberculin skin
test
Courtesy of Dr. Marc Steben
2
The MTCT-Plus Initiative
Applying the tuberculin skin
test
3
The MTCT-Plus Initiative
Applying the tuberculin skin
test
Courtesy of Dr. Marc Steben
4
The MTCT-Plus Initiative
Reading the tuberculin skin test
 Read 2-3 days after placing the test
 Feel for induration
 Color change without induration is not
included in the measurement
 Use a ruler or calipers
 Have someone else check if unsure
 Always document the exact size (mm) – not
just “positive” or “negative”
5
The MTCT-Plus Initiative
Reading the tuberculin skin
test
Courtesy of Dr. Marc Steben
6
The MTCT-Plus Initiative
Reading the tuberculin skin test
7
The MTCT-Plus Initiative
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REAKSI HIPERSENSITIVITAS
 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
Immune
complex
disease
Delayed-type hypersensitivity
Reaksi Hipersensitivitas tipe I
 Reaksi Hipersensitivitas tipe cepat atau anafilaktik
 Diperantarai IgE
 Alergenproduksi 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)
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
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
Skin test for allergy
Ragweed
Control negative (saline)
Control positve (histamine)
CAUSES
Antigen
Ingestants
Food
Drugs
Pollens
Dusts
Molds
Injectants
Drugs
Stings
Vaccines
Serum
MECHANISM
Allergen
interacts
with
IgE on mast cell
PATHOPHYSIOLOGY
Release of
chemical
mediators :
Histamine
SRS-A
Kinins
Prostaglandins
Capillary dilation
Increased
Capillary
permebiality
Increased
Blood
Volume
Exudation of
Cell, fluid protein
Pressure of
exudate
Nerve
irritation
Constriction
of smooth
muscle
Type I hypersensitivity reaction
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MANIFESTATIONS
Respiratorytract
tract
Respiratory
1.1. Upper
headache”
Upper“sinus
“sinus
headache”
itching
itchingofofeyes
eyes
tearing,
tearing,sneezing,
sneezing,
watery nasal discharge,
watery nasal discharge,
itching of nose,
itching
of nose,
throat
irritation
throatwheezing,
irritation dyspnea,
2. Lungs
2. dry
Lungs
wheezing,
cough,
tightness dyspnea,
in chest
dry cough, tightness in chest
Gastrointestinal
Glossitis, cardiospasm
Nausea, vomitting
Irritable bowel
Diarrhea, pruritus ani
Skin
Urticaria, pruritus,
Angioedema, weeping erthematosus vesico-papular lessions
CLINICAL EXAMPLES
Allergic rhinitis
Conjunctivitis
Asthma
Food allergies
Atopic dermatitis
Urticaria
Type I hypersensitivity reaction (continued)
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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.
CAUSES
Antigen
Transfusion
reaction
Erythroblastosis
fetalis
Drugs
Autoantibodies
Unknown
PATHOPHYSIOLOGY
MECHANISM
Antigen
interacts
with body
cell i.e :
• Erythrocyte
• Leucocyte
• Platelet
• Vascular
endothelium
Reaction of IgG or
IgM antobody with
antigen on cell
Activates
complement
Erytrhrocyte
hemolysis
Agranulocytosis
Thrombocytopenia
Vasculitis
CLINICAL
EXAMPLES
Hemolytic
anemia
Susceptability
to infections
Purpura
Vesicular
purpura
Type II hypersensitivity reaction
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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 / paruparu) infiltrasi dinding pembuluh darah kecil  aktivasi
kaskade komplemen pelepasan bahan aktif secara
Type III hypersensitivity reactions (Arthus Reaction) - Ab-Ag Complexes
Critical mediators appear to be C5a-receptor and FcgRIII--probably present on mast cells
CAUSES
MECHANISM
PATHOPHYSIOLOGY
Antigen
Autoantibodies
Drugs
Serum
Chemicals
Foreign antigen
Bacteria
Virus
Antigen and
antibody form
an immune
complex
Deposits on vessel walls
or basement membrane
Tissue
destruction
Inflammation
CLINICAL
EXAMPLES
Glomerulonephritis
Vasculitis
Arthus reaction
Rheumatoid
diseases
Serum sickness
Type III hypersensitivity reaction
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 Biopsi jaringan (endapan Ig dan komplemen)
 Kompleks imun pada darah dan penurunan
Diagnosis:
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
Biological effects of
Late
stage of an allergicmediators
response includes the
Eosinophil
recruitment of eosinophils and Th2 cells contrast with
a DTH (type IV) response which includes infiltration of
macrophages and Th1 cells
Table 3 - Delayed hypersensitivity reactions
Type
contact
tuberculin
granuloma
Reaction time
48-72 hr
48-72 hr
21-28 days
Clinical
appearance
Histology
Antigen and site
eczema
lymphocytes,
followed by
macrophages;
edema of epidermis
epidermal ( organic
chemicals, poison
ivy, heavy metals,
etc.)
local induration
lymphocytes,
monocytes,
macrophages
intradermal
(tuberculin,
lepromin, etc.)
macrophages,
epitheloid and giant
cells, fibrosis
persistent antigen or
foreign body
presence
(tuberculosis,
leprosy, etc.)
hardening
 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
CAUSES
MECHANISM
Antigen
Tuberculin
Poison Ivy
Chemical
Fungi
Transplanted
organs
Virus
Sensitized
Lymphocyte
reacts with
antigen
PATHOPHYSIOLOGY
Release of :
Lymphokines
Migration inhibition
factor
Interferon
Killer cells
Transfer factor
Injury and
destruction of
target organ
CLINICAL
EXAMPLES
Contact
dermatitis
Graft vs host
reactions
Viral infection
Autoallergic
disease
Type IV hypersensitivity reaction
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