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    Asma Bronkial CUTE 2018 Dr. Teguh

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    Athari Aditya
    Bronchial asthma is a chronic airway disorder that affects 5-10% of the global population. Symptoms are triggered by factors like viral infections, allergens, tobacco smoke, exercise and stress. The pathophysiology involves an inflammatory reaction in the airways with recruitment of immune cells like mast cells, macrophages, and T lymphocytes. This leads to inflammation, increased mucus production, airway remodeling, and bronchial hyperresponsiveness. The inflammation involves type 2 T-helper cells and cytokines that activate B cells to produce IgE. Persistent inflammation causes structural changes in the airways. Allergic rhinitis and bronchial asthma often co-exist as part of a united airway disease.

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    Asma Bronkial CUTE 2018 Dr. Teguh

    Uploaded by

    Athari Aditya
    40 views50 pages
    Bronchial asthma is a chronic airway disorder that affects 5-10% of the global population. Symptoms are triggered by factors like viral infections, allergens, tobacco smoke, exercise and stress. The pathophysiology involves an inflammatory reaction in the airways with recruitment of immune cells like mast cells, macrophages, and T lymphocytes. This leads to inflammation, increased mucus production, airway remodeling, and bronchial hyperresponsiveness. The inflammation involves type 2 T-helper cells and cytokines that activate B cells to produce IgE. Persistent inflammation causes structural changes in the airways. Allergic rhinitis and bronchial asthma often co-exist as part of a united airway disease.

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    Bronchial asthma is a chronic airway disorder that affects 5-10% of the global population. Symptoms are triggered by factors like viral infections, allergens, tobacco smoke, exercise and stress. The pathophysiology involves an inflammatory reaction in the airways with recruitment of immune cells like mast cells, macrophages, and T lymphocytes. This leads to inflammation, increased mucus production, airway remodeling, and bronchial hyperresponsiveness. The inflammation involves type 2 T-helper cells and cytokines that activate B cells to produce IgE. Persistent inflammation causes structural changes in the airways. Allergic rhinitis and bronchial asthma often co-exist as part of a united airway disease.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    40 views50 pages

    Asma Bronkial CUTE 2018 Dr. Teguh

    Uploaded by

    Athari Aditya
    Bronchial asthma is a chronic airway disorder that affects 5-10% of the global population. Symptoms are triggered by factors like viral infections, allergens, tobacco smoke, exercise and stress. The pathophysiology involves an inflammatory reaction in the airways with recruitment of immune cells like mast cells, macrophages, and T lymphocytes. This leads to inflammation, increased mucus production, airway remodeling, and bronchial hyperresponsiveness. The inflammation involves type 2 T-helper cells and cytokines that activate B cells to produce IgE. Persistent inflammation causes structural changes in the airways. Allergic rhinitis and bronchial asthma often co-exist as part of a united airway disease.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
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    Asma Bronkial

    Patofisiologi
    Teguh Harjono K
    ANGGOTA PAPDI DEPOK
    RS . SENTRA MEDIKA
    Introduction

    • Bronchial asthma is a serious global health problem. 5% to 10%


    of persons of all ages suffer from this chronic airway disorder.

    • Symptoms may be triggered or worsened by factors such as


    viral infections, allergens, tobacco smoke, exercise and stress
    Epidemiology
    Prevalensi Asma Bronkial menurut pendapatan per kapita
    Hygiene hypothesis
    • The "hygiene hypothesis" postulates that an imbalance in the
    regulation of these TH cell types in early life leads to a long-term
    domination of the cells involved in allergic responses over those
    involved in fighting infection. The suggestion is that for a child being
    exposed to microbes early in life, taking fewer antibiotics, living in a
    large family, and growing up in the country stimulate the TH1 response
    and reduce the odds of developing asthma.[7]
    Hiper reatifitas tipe 1
    Pathophysio
    logy of
    asthma
    Pathophysiology of allergic
    asthma
    Patofisiologi inflamasi pada Asma
    Inflamtion Cell

    • Asthma is a complex
    syndrome
    characterized by a
    state of airways
    hyperresponsiveness
    (AH) and caused by a
    multi-cellular
    inflammatory reaction
    that leads to airway
    obstruction.
    • Recruitment and activation of mast cells, macrophages, antigen-
    presenting dendritic cells, neutrophils, eosinophils, and T lymphocytes
    result in an inflammatory and cellular infiltration of the airways.
    • Type 2 T-helper cells (Th2) have a major role in the activation of the
    immune cascade that leads to the release of many mediators such as
    interleukins (IL)-3, IL-4, IL-5, IL-13, and granulocyte macrophage
    colony stimulating factor (GM-CSF).
    • Some mediators such as IL-4 activate B lymphocytes to produce
    immunoglobulin E (IgE), and others (for example, IL-3, IL-5, and GM-
    CSF) are related to the eosinophilic airway inflammation.
    • Severe asthma may present various inflammatory phenotypes, such
    as persistent eosinophilic bronchitis, neutrophilic infiltration of the
    airway, and a pauci-granulocytopenic type of inflammation.

    • Such persistent inflammatory process results in airway remodeling


    with deposition of extracellular proteins, smooth muscle hypertrophy,
    and increased goblet cell production.
    • Airway epithelium becomes fragile and thin, and the epithelial
    basement membranes thicken with increased mucus production and
    endothelial leakage leading to mucosal edema.
    • Mediator-induced abnormalities in the parasympathetic and
    nonadrenergic noncholinergic nervous systems may also lead to
    increased bronchial hyperresponsiveness.
    Asthma Bronchial
    Bronchial Asthma and Allergic Rhinitis

    • Recent data has shown that involvement of the upper airways by


    similar inflammatory reaction is present in almost all asthmatic
    patients, irrespective of the presence of symptoms of rhinosinusitis
    • Studies have shown that stimulation of the nose by an irritant instilled
    in the nose leads to eosinophilic infiltration in the lungs a few hours
    later. Such coexistence of inflammation in both upper and lower
    airways led to the suggestion of new terminology called united airway
    disease.
    • In clinical practice, failure of recognition and treatment of
    concomitant rhinosinusitis may affect asthma control.
    Allergic Rhinitis
    and Bronchial
    Asthma
    Pencentus serangan asma ;
    Asthma Bronchial :

    • Asthma is thought to be caused by a combination


    of genetic and environmental factors. Environmental factors include
    exposure to air pollution and allergens. Other potential triggers
    include medications such as aspirin and beta blockers.[
    Patofisiologi Asma dan PPOK
    Terima Kasih
    Pathophysiology Asthma Bronchial
    Pathophysiology Asthma and COP

    AHR = airway hyper responsiveness

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