IMUNOLOGI DASAR

PENYAKIT ALERGI

OLEH :

Dr. BIMA WISNU N. SpTHT. MKes.

Kasubdep THT. Dep MATA THT & KULKEL
RS Tk II AK GANI PALEMBANG.
Allergy is .............
AN
OVERREACTION
OF THE IMMUNE SYSTEM

..........TRIGGERED BY AN
ALLERGEN
THE TYPE OF ALLERGEN
1. House dust
mite
2. House dust
3. Human dander
4. Fungi
5. Animal dander
6. Cockroach
 Allergy Can Affect Different
People in Different Ways

Nasal Symptoms Rhinitis

Itchy Eyes
Eye Symptoms
Asthma
Lung Symptoms Rash & Itching

Skin Symptoms Stomach Pains & Diarrhoea

Digestive Symptoms
PHYSICAL EXAMINATION

Allergic salute
Allergic crease
Mannerism
Mouth open/facies
adenoid
Height arched-palate
 MANY Organs MAY AFFECT
ALLERGIC DISEASE
NOSE
ALLERGIC RHINITIS
EXTERNAL EAR
ATOPIC DERMATITIS
ALLERGIC CONTACT DERMATITIS
MIDLE EAR
OTITIS MEDIA WITH EFFUSION
LARYNGOPHARYNX
ACUTE SEVERE LARYNGOPHARYNGITIS
CHRONIC LARYNGOPHARYNGITIS
 THE NATURAL COURSE OF ATOPIC DISEASE IN
CHILDHOOD

figure
RISK OF DEVELOPING ALLERGY BASED ON
FAMILY HISTORY
THE IMMUNOPATHOLOGICAL MARCH
(the immunological induction and expression of allergy)

Tertiary
Secondary

Tissue
Primary Chronic Hyper-
Maternal responsive- Chronic
Inflammation
Allergen ness Symptomatolog
y (e.g.Status
Exposure (Allergic
Asthmatics/
Rhinitis,
Boosting Subclinical Asthma, COPD)
Th2 Repeated Responses Atopic
Memory (MPI)
Postnatal Immune
Exposure (MPI) dermatitis)
Th1
Exposure Deviation Memory
Intrauteri Tissue
ne Th2- Deletion Reversion
Remodeling
skewed Anergy
to Th1

Unresponsiveness

Holt et al, 1998

Priming
RISK FACTORS IN ATOPIC DISEASES : POTENTIAL MEANS OF PREVENTION

Allergens in food, Smoke, damp buildings, Urban living,

inhalants western lifestyle, Socioeconomic factors

Other infections (e.g. BCG)

RSV
Older siblings

Genes, Sensitization

boys
Inflammation
Primary
Secondary
Hyperreactivity

Symptoms

Tertiary
Damage
 REAKSI HIPERSENSIFITAS

Reaksi type I (Anafilaksis dengan AB Ig E )

Reaksi type II (Sitolitik atau sitotoksik dengan AB
Ig M/Ig G)
Reaksi type III (Reaksi imun komplek dengan AB
Ig M /Ig G)
Reaksi type IV (cell-mediated immunity atau
reaksi tipe lambat)
8
KARAKTERISTIK REAKSI TYPE I

Syok anafilaktik
Rhinitis alergika
Urtikaria
Asma bronkiale

9
PERJALANAN REAKSI TIPE I

Stadium I : Sensitisasi

Stadium II : Aktifasi

Stadium III : Efektor

10
Guntur, 1999
11
13
Mast cell activation and physiological effects of mast-
cell derived mediators

14
 MEDIATOR REAKSI TIPE I

HISTAMIN
SEROTONIN
HEPARIN
ECF-A dan NCF - A

SRS - A (LTC4, LTD4, LTE4), & LTB4

PROSTAGLANDIN
BRADIKININ
SITOKIN (IL 1, TNF , IL-6, IL-8)

15
(Kuby, 2000)
 Mediator Release from Mast
Cells
Allergen

2+
Ca

2+
MEMBRANE- Ca
DERIVED
MEDIATORS

PROSTAGLANDINS
LEUKOTRIENES

HISTAMINE
CHEMOTACTIC FACTORS
PLATELET ACTIVATING FACTOR

PREFORMED
MEDIATORS
 Allergic Mediators Released
from Mast Cells
OTHER
SEROTONIN
(VIA PLATELETS) ALLERGIC SYMPTOMS
LEUKOTRIENES
RUNNY, OR BLOCKED NOSE
PROSTAGLANDINS
SNEEZING
HISTAMINE RED, ITCHY, WATERY EYES
(The major Allergic
mediator released
from ITCHY THROAT / EARS
the Mast Cell)
RASH
 THE DEFINITON OF
ALLERGIC RHINITIS
RECENT DEFINITION
The inflammation of the mucous
of the nose which mediated by
IgE/type 1 hypersensitivity,
following allergen exposure; and
causes symptoms: nasal
congestion or obstruction, itching,
sneezing, watering/rhinorhoea
and of the nose.
 BASIC CONCEPT
RECENTLY
The domination
of TH 2 function
compare to TH 1

OLD
The hypo function of T
cell suppressor compare
to T cell helper.
 THE CHANGES IN THE
NOSE MUCOSA

Sensitization stage
Activation stage
Effector stage:
Rapid phase reaction
Late phase reaction
Hyperresponsive
condition
D. Patogenesis Rinitis Alergi

Sumber : Kay (2001)

 ASMA = INFLAMASI KRONIS SALURAN NAPAS

Melepas
BANYAK SEL : MEDIATOR
SEL MAST Histamin
EOSINOFIL PDG 2, LTc 4
NETROFIL OBSTRUKSI
EPITHELIAL LIMFOSIT TNF, PAF, DIFUS
SHEDDING EPITEL Eo chemo F. SALURAN
GM-CSF
NAFAS

PENINGKATAN MEKANISME BATUK, WHEEZING, SESAK

NEURAL
SEMBUH
SEMBUH
BHR TERHADAP
BERBAGAI STIMULI SPONTAN TERAPI
 ASTHMA INFLAMMATORY PROCESS

ALLERGEN EXPOSURE

INFLAMMATORY MEDIATORS RELEASE

ARACHIDONIC ACID
CHEMOTACTIC PAF HISTAMINE CYCLOXYGENASE LIPOXYGENASE
FACTORS

PROSTAGLANDIN LEUKOTRIENES

BRONCHO INCREASED DECREASED CHEMO INCREASED

CONSTRICTION MUCUS MUCUS TAXIS VASCULAR
SECRETION CLEARANCE PERMEABILITY

SYMPTOMS
SYMPTOMSOF
OFASTHMA
ASTHMA
 PATHOGENESIS OF ASTHMA
antigen
Nave T-lymphocyte
IL-12 [-]
Th-O
Th-O

dendritic cell Th-2 response

[-]
IL-4 IL-9 IL-3, IL-5
IL-12 [+] IL-13 IL-4
IL-3
GM-CSF

Th-1
Th-1response
response Ig E Mast Cell Basophils Eosinophil
IFN, lymphotoxin, IL-2

Mediators of inflammation

Cell
Cellmediated
mediatedimmunity
immunity Histamine,
Histamine,prostaglandins,
prostaglandins,
And
And Leukotrienes,
Leukotrienes,enzymes
enzymes
Neutrophilic
Neutrophilicinflammation
inflammation

Bronchial
Bronchial Hyperresponsiveness
Hyperresponsiveness
Asthma
AsthmaSymptoms
Symptoms Airway
Airway Obstruction
Obstruction
C. Eosinofil dan Reaksi Inflamasi Alergi

Sumber : Rotherberg (1988).

 Therapeutic considerations of AR management
Allergen avoidance
indicated when ARIA WHO 2001
possible

Pharmacotherapy Immunotherapy
Safe
Effective
Easy administration
Costs Effective
Specialist prescription
May alter the natural
course of the disease

Patient education
always indicated

Optional therapy:
Other medications and/or surgery for complications
or
Treatment combination of both approaches