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113 ANAK
$14 MILYARD
KELUHAN:
NAPAS PENDEK+WH
LIFE-THREATING
ECES: HEALTH: ASTHMA, ALLERGIES, AND OTHER RESPIRATORY DISORDERS, 23/12/2002
ODONNELL:
- INCREASE CASE
- ONE HAS EVER BEEN ABLE TO
SAY WHAT CAUSES ASTHMA
-POLLUTAN IS A CAUSE IS A
VERY SIGNIFICANT STATEMENT
NORMAN H. EDELMAN:
OZON ASSOCIATED WITH ASTHMA
BRITISH SCIENTIST:
DAVID KING:
SMOKE GUN
POLLUTANT
CAUSE
POLLUTANT
DEVELOPMENT OF
ASTHMA
ASTHMA
GLOBAL
WARNING
ECES: HEALTH: ASTHMA, ALLERGIES, AND OTHER RESPIRATORY DISORDERS, 23/12/2002
U.K.:
1. 17 ANAK
(INCRESE 6X THAN
25 YR AGO
2. 5 JUTA
3. 18.000 BARU
DIAGNOSED/WEEK
4. 1.500 DEATH/YR
PREVALENSI ASMA
(ERJ, 2002)
SELURUH NDIVIDU, 2 12%
PADA PENDERITA RHINITIS ALERGIKA
10 40 %
PENDERITA BRONKIAL
HIPEREAKTIVITI, 3,5 28 %
RENDAH U.K., U.S., AUSTRALIA, NEW
ZELAN, IRLANDIA
TINGGI DI MEDITERIAN COUNTRIES,
ICELAND, EROPA TIMUR DAN INDIA
GENETIK
EVIRONMENTAL
POLLUTAN
FOOD PEOPLE EAT
GAYA HIDUP
OCCUPATIONAL
EXPOSURE:
BIOLOGICAL &
MINERAL DUST
HYGIENE
INFECTION
EATING HABIT
RURAL
URBAN
ENVIROMENTS
IKLIM
(PADA ANAK)
POLUSI UDARA
Dr. Marian Frieri, can contribute to
asthma inflamation ozon biang keladi
utama
Dr. Jonatan Patz, Johns Hopkins
Blooberg School of Public Health an
important conclution
AGENT
HOST
ENVIRONMENT
AGENT
(ALERGEN)
INFEKSI
NONINFEKSI
HOST:
GENETIK
VIRUS
NONIN
FEKSI
KUMAN
LINGKUNGAN:
POLUTAN
IRITAN
INFLAMASI
HYPERRESPO
NSIVENESS
SESAK
HIPOTESA INFLAMASI
ALERGEN
O3
PAM
SEL MAST
EPITIL
CHEMOTATIC MEDIATOR
LTD4 , PAF, NCF
NETROFIL
O2
RADIKAL
ENZYM
TXA2
NERVE
SEKRESI
MENINGKAT
KESEMBABAN
MUKOSA
PENYEMPITAN
S.N
KELUHAN ASMA
SPASME OTOT
POLOS S.N
INFLAMASI
ACTH
IL-1
ECF
INFLAMASI
CORTISOL
KRONIS
RANGSANGAN
TNF
LT
TX
KININ
MEDIATOR
INFLAMASI
AKUT
PATOFISIOLOGI ASMA
-EXAGERATED
CONSTRICTION
-INCREASE
SMOOT MUSCLE
MASS
ACUTE
INNFLAMATION:
SMOTH
MUSCLE
DYSFUC
TION
-INCREASE
RELEASE OF
MEDIATOR
AIRWAY
INFLMATION
AIRWAY
REMODELLING
- CELLULAR ROLIFERATION
>SMOOTH MUSCLE-CELL
>MUCOUS GLAND
-INCREASE MATRIX PROTEIN DEPOSITION
-BASEMEMBRANE THICKENING
-ANGIOGENESIS
-INFLAMATORY
CELLS
ACTIVATION
-INFLAMATORY
MEDIATOR
RELEASE
CHRONIC
INFLAMATION:
-INCREASE
INFLAMATORY
NUMBER
-EPITHELIAL
DAMAGE
ACUTE
INFLAM
ATION
BRONCHOCONSTRI
CTION
CHRONIC
INFLAMA
TION
AIRWAY
REMODELLING
-INCREASE
INFLAMATORY
CELL NUMBER
-CELLULER
PROLIFERATION
INCREASE
-EPITHELIAL
DAMAGE
-EXTRACELLULAR
MATRIX
MUCOSAL OEDEM
AIRWAY
SECRESION
AIRWAY
NARROWING
SYMTO
MES
BRONCHIAL
HYPERREACTIVITY
REDUCED AIRWAY
REVERSIBILITY
EXACER
BATION
EPITHELIAL DISRUPTION
ELASTIC FIBRE
FRAGMENTATION
INCREASE VASCULARITY
EXTRACELLULAR MATRIX
GLYCOPROTEIN
SUB-BASEMEMBRANE
THICKENING
SUB-EPITHELIAL
FIBROSIS
DEPOSISI CLAGEN I,
COLAGEN II DAN
FIBRONECTIN
PROLIFERATION INDUCED BY
INFLAMATORY MEDIATOR
NERVE
CYTOKINES
GROWTH FACTOR
MYOFIBROBLAST
SMOOTH
MUSCLE
DYSFUNC
TION
AIRWAY
INFLAMATI
ON
CS
LABA
RONCHOCONSTICTI
ON
INFLAMATORY CELL
INFILTRATION ACTIVITY
BRONCHOHYPERRE
ACTIVITY
MUCOSA OEDEMA
HYPERPLASY
INFLAMATORY
MEDIATOR RELEASE
CELLULAR
PROLIFERATION
EPITHELIAL DAMAGE
BASEMEMBRANE
TICKENING