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FACULTY OF MEDICINE MALANG ISLAMIC UNIVERSITY. SKIN TEST. Applying the tuberculin skin test. Courtesy of Dr. Marc Steben. Applying the tuberculin skin test. Applying the tuberculin skin test. Courtesy of Dr. Marc Steben. Reading the tuberculin skin test.

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faculty of medicine malang islamic university
FACULTY OF MEDICINE

MALANG ISLAMIC UNIVERSITY

SKIN TEST

applying the tuberculin skin test
Applying the tuberculin skin test

Courtesy of Dr. Marc Steben

The MTCT-Plus Initiative

applying the tuberculin skin test1
Applying the tuberculin skin test

The MTCT-Plus Initiative

applying the tuberculin skin test2
Applying the tuberculin skin test

Courtesy of Dr. Marc Steben

The MTCT-Plus Initiative

reading the tuberculin skin test
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”

The MTCT-Plus Initiative

reading the tuberculin skin test1
Reading the tuberculin skin test

Courtesy of Dr. Marc Steben

The MTCT-Plus Initiative

reading the tuberculin skin test2
Reading the tuberculin skin test

The MTCT-Plus Initiative

slide13
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
slide16

Immune complex disease

Delayed-type hypersensitivity

reaksi hipersensitivitas tipe i
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 i1
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)
tes diagnostik
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
slide22

Skin test for allergy

Ragweed

Control negative (saline)

Control positve (histamine)

type i hypersensitivity reaction
Type I hypersensitivity reaction

Capillary dilation

CAUSES

MECHANISM

PATHOPHYSIOLOGY

Antigen

Ingestants

Food

Drugs

Pollens

Dusts

Molds

Injectants

Drugs

Stings

Vaccines

Serum

Increased

Blood

Volume

Release of

chemical

mediators :

Histamine

SRS-A

Kinins

Prostaglandins

Allergen

interacts

with

IgE on mast cell

Exudation of

Cell, fluid protein

Increased

Capillary

permebiality

Pressure of

exudate

Nerve

irritation

Constriction

of smooth

muscle

23

type i hypersensitivity reaction continued
Type I hypersensitivity reaction (continued)

CLINICAL EXAMPLES

MANIFESTATIONS

  • Respiratory tract
  • Upper “sinus headache”
  • itching of eyes
  • tearing, sneezing,
  • watery nasal discharge,
  • itching of nose,
  • throat irritation
  • Lungs wheezing, dyspnea,
  • dry cough, tightness in chest
  • Respiratory tract
  • Upper “sinus headache”
  • itching of eyes
  • tearing, sneezing,
  • watery nasal discharge,
  • itching of nose,
  • throat irritation
  • Lungs wheezing, dyspnea,
  • dry cough, tightness in chest

Allergic rhinitis

Conjunctivitis

Asthma

Gastrointestinal

Glossitis, cardiospasm

Nausea, vomitting

Irritable bowel

Diarrhea, pruritus ani

Food allergies

Atopic dermatitis

Urticaria

Skin

Urticaria, pruritus,

Angioedema, weeping erthematosus vesico-papular lessions

24

reaksi hipersensitivitas tipe ii
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
type ii hypersensitivity reaction
Type II hypersensitivity reaction

Erytrhrocyte

hemolysis

Susceptability to infections

  • Antigen interacts with body cell i.e :
  • Erythrocyte
  • Leucocyte
  • Platelet
  • Vascular endothelium

Agranulocytosis

Thrombocytopenia

Vasculitis

PATHOPHYSIOLOGY

CAUSES

MECHANISM

CLINICAL

EXAMPLES

Antigen

Transfusion

reaction

Erythroblastosis

fetalis

Drugs

Autoantibodies

Unknown

Reaction of IgG or

IgM antobody with

antigen on cell

Activates complement

Hemolytic anemia

Purpura

Vesicular

purpura

28

reaksi hipersensitivitas tipe iii
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
slide30

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 reaction
Type III hypersensitivity reaction

PATHOPHYSIOLOGY

CAUSES

MECHANISM

CLINICAL

EXAMPLES

Antigen

Autoantibodies

Drugs

Serum

Chemicals

Foreign antigen

Bacteria

Virus

Glomerulo-nephritis

Antigen and

antibody form

an immune

complex

Tissue destruction

Deposits on vessel walls

or basement membrane

Vasculitis

Inflammation

Arthus reaction

Rheumatoid diseases

Serum sickness

31

diagnosis
Diagnosis:
  • Biopsi jaringan (endapan Ig dan komplemen)
  • Kompleks imun pada darah dan penurunan jumlah komplemen

Terapi:

  • Anti-inflamasi
reaksi hipersensitivitas tipe iv
Reaksi Hipersensitivitas Tipe IV
  • tipeseluler 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 eosinophil mediators
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

slide36
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
Type IV hypersensitivity reaction

PATHOPHYSIOLOGY

CAUSES

MECHANISM

CLINICAL

EXAMPLES

Antigen

Tuberculin

Poison Ivy

Chemical

Fungi

Transplanted organs

Virus

Release of :

Lymphokines

Migration inhibition

factor

Interferon

Killer cells

Transfer factor

Contact dermatitis

Graft vs host reactions

Viral infection

Autoallergic disease

Sensitized

Lymphocyte reacts with antigen

Injury and destruction of target organ

37