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Patofisiologi COPD dan Asma

The pathogenesis of COPD involves irritation, infection, and allergens causing chronic inflammation in the lungs. This results in damage to lung tissue over time, including loss of elasticity of the lungs. The inflammatory response narrows the airways and causes mucus hypersecretion, leading to impaired gas exchange and reduced airflow. Repeated damage and scarring can cause emphysema and bronchitis, obstructing airflow and further worsening lung function. Allergic asthma involves similar inflammatory processes driven by IgE antibodies and eosinophils in response to allergens. Non-allergic asthma may involve autonomic nervous system imbalance and beta-adrenergic blockade impairing bronchodilation.

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35 views3 pages

Patofisiologi COPD dan Asma

The pathogenesis of COPD involves irritation, infection, and allergens causing chronic inflammation in the lungs. This results in damage to lung tissue over time, including loss of elasticity of the lungs. The inflammatory response narrows the airways and causes mucus hypersecretion, leading to impaired gas exchange and reduced airflow. Repeated damage and scarring can cause emphysema and bronchitis, obstructing airflow and further worsening lung function. Allergic asthma involves similar inflammatory processes driven by IgE antibodies and eosinophils in response to allergens. Non-allergic asthma may involve autonomic nervous system imbalance and beta-adrenergic blockade impairing bronchodilation.

Uploaded by

Dellavia Enta
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOC, PDF, TXT or read online on Scribd

PATHOFISIOLOGI COPD

IRITAN INFEKSI ALLERGEN

Ggn elastisitas oleh Iritasi broncial Mukosa Obst


Alpha-1- antitrypsin bronchial midbronch
sensitif ial

Abnormal jl nfs dan Bronchial inflamasi


kerusakan alveoli dan
atau bronchioles IgE
Delatasi
Hyperthropi & hypersekresi terminal
cell goblet & Bronchial bronchi
Elastic recoil  mucous gland

broncial
hyperactyvity Kerusakan
Menurunnya Penyempitan
ddg
&Congesti jl nfs kecil
pertukaran gas broncial

Hyper
Residual sekresi
Hyper skresi Scar tissu
volume  Jaringan fibrotik mucosa
dan
bronchospas
me
Obstructive
emphysema chronic Simple Delatasi
brochitis chronic permanen
bronchitis Asthma
Bronchial

Obstructive chronic bronchitis Bronc


Chronic asthmatic hiecta
& emphysema bronchitis sis

Created by diputra Page 1


PATOFISIOLOGI

Astma Allergi

Ag

IL-12 IL-4
Limfosit-
Th- Th-2
CELL MHC II B Proliferasi
0
APC
IL-1 IL-2 (-) IL-5 Cell
IL-10 Plasma
(-) Th-
IFN Gama 1 IFN Gama
TNF β NK. Cell
Ab
IL-2 Ig-E

Cell sudah memiliki Ig-E dg afinitas lemah Berikatan

Ikatan Ig-E Mastoit dalam jar


Pada Paparan Rentan & Basofil dalam
permukaan II sirkulasi
mastoit dan
basofil

Degranul
Influk C++ cAMP  asi Cell Mediator
dilepas
(ECF-A),
(NCF)

ASTMA Bronchospasme
BRONCHIAL

Created by diputra Page 2


Non Allergi
Teori blockade andrergig beta

Stress
 aktifitas
infeksi

Gggn Saraf otonom


(sympatis)

Hyperaktif adrenergic alfa Blockade adrenergic beta

 Adenyl cyclase
 broncho constriksi
 hypersekresi
 edem kelenjar
mukosa
Ggn ATP dalam cel

Sesak nafas

3,5 cAMP terhambat

 Ggn fgs delatasi otot polos


 Ggn fgs menghambat
mediator (mastoid/basofil)
 Ggn fgs menghambat
sekresi kelenjar mukos

Created by diputra Page 3

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