BRONCHIAL

ASTHMA

GROUP 4

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Outline
• Definition
• Epidemiology
• Etiology
• Pathogenesis
• Clinical features
• Complications
• Diagnosis
• Management

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Definition
• Asthma is a heterogenous disease, usually characterized by chronic airway
inflammation.
• Defined by symptoms:
• Wheeze
• Shortness of breath
• Chest tightness
• Cough varying over time and intensity
• With variable expiratory airflow limitations

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Epidemiology
• Approximately 300 million people worldwide currently have asthma.
• In Ethiopia, the prevalence of asthma is 8.7%
• For unknown reasons prevalence of asthma has been increasing over the
past 20 years
• More prevalent among children
• Common in males during childhood and vise versa during adulthood

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Phenotypes of asthma
• Allergic asthma: 40-50%
• Non-allergic: triggers often unknown
• Aspirin sensitive asthma: associated with ASA and other NSAIDS
• Severe asthma: difficult to control with high doses of medicine
• Exercise-induced asthma: dry and/or cold air is the trigger

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Allergic vs non-allergic asthma
Allergic asthma Non allergic asthma
Childhood onset Adult onset
Allergic triggers Triggers often unknown
IgE mediated Non IgE mediated
Allergic co-morbidities Non-allergic co-morbidities
Mast cells, basophils, eosinophils involved Neutrophils involved
Responsive to inhaled corticosteroids Not responsive to inhaled corticosteroids

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Etiology
• Development of asthma involves an interplay between risk factors and
exposures

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• Risk factors and exposures lead to airway reactivity to triggers of airway
narrowing

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Pathogenesis
• Asthma is associated with a specific chronic inflammation of the respiratory
mucosa from the trachea to terminal bronchioles with a predominance in the
bronchi (cartilaginous airways)
• It consists of the following three pathophysiologic processes:
1. Bronchial Hyper responsiveness
2. Bronchial Inflammation
3. Endobronchial obstruction

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Bronchial Inflammation
• The inflammatory process is driven by T-helper type 2 cells (Th2-cell) that
manifests in individuals with a genetic predisposition.
• Other principal cells identified in airway inflammation include mast cells,
eosinophils, epithelial cells and macrophages.
• Multiple inflammatory mediators like histamine, PG D2, and leukotriene
are also involved.

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Bronchial Hyper responsiveness
• Airway inflammation in asthma is associated with bronchial hyper
responsiveness.
• Bronchial Hyper responsiveness is the characteristic physiologic
abnormality of asthma and describes the excessive bronchoconstrictor
response to multiple inhaled triggers that would have no effect on normal
airways.
• BHR can be triggered by a variety of factors, including allergens, irritants,
viral infections, exercise, and emotional stress.

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Endobronchial obstruction
• Airflow obstruction can be caused by a variety of changes, including acute
bronchoconstriction, airway edema, chronic mucous plug formation, and
airway remodeling
• Mucus production: In response to inflammation, the airway lining may
produce excess mucus, which can further narrow the airways and cause
obstruction. There will also be goblet cell hyperplasia.
• Bronchospasm: Asthma can cause the smooth muscles in the airway walls
to contract, leading to bronchospasm and obstruction.

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• Airway remodeling or thickening of the basement membrane due to sub
epithelial collagen deposition also contributes to obstruction
• The epithelium is often shed or friable, with reduced attachments to the
airway wall and increased numbers of epithelial cells in the lumen
• Vascular congestion: there is also vasodilation and increased numbers of
blood vessels

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Allergic asthma
• Allergic asthma is a type of asthma that is triggered by exposure to
allergens such as pollen, dust mites, animal dander, and mold.
• IgE-mediated type 1 hypersensitivity to a specific allergen
• Characterized by mast cell degranulation and release of histamine after a
prior phase of sensitization.
• The inflammatory mediators cause the airways to become inflamed,
swollen, and constricted, making it difficult to breathe
• They also increase mucus production, which further obstructs the airways

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Nonallergic asthma
• The exact pathogenesis of non-allergic asthma is not
fully understood, but it is thought to involve a
combination of genetic and environmental factors.
• Some of the possible mechanismsauggested are:
• Dysregulated neutrophil-mediated immune responses
• Defects in resolution of inflammation
• Activation of the IL-17-dependent pathway

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Clinical features
• Wheezing
• Dyspnea
• Chest tightness
•Cough: Persistent, dry cough that worsens at night, with exercise, or on
exposure to triggers/irritants
Some patients, particularly children, may present with a predominant non-
productive cough

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Physical Examination
•Patient might be in respiratory distress
•Tachypnea/tachycardia
•Wheezing: typical-expiratory/ inspiratory
•Hyperinflation
•Barrel chest
•Skin lesions, nasal discharge
•Symptoms may be worse at night and patients typically awake in the early
morning
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Life threatening asthma
•Silent chest-no wheezing or air entry
•Cyanosis/feeble or no respiratory effort
•Pulsus paradoxus, bradycardia, hypotension
• Exhausted, confused or unconscious

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Clinical signs of severe asthma
•Unable to speak in full sentences
•RR>25/min
•PR>110/min
•Peak flow <50% predicted best
•Accessory muscle use

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Complications
 Severe asthma attacks
 Respiratory infections
 Reduced lung function
 Side effects of medication: long-term use of asthma medications can have
side effects, including weight gain, osteoporosis, and cataracts.
 Lung complications: pneumothorax, atelectasis
 Mediastinal and subcutaneous emphysema
 Corpulmonale

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Diagnosis
• Symptoms favoring asthma – Varying
+
• Evidence of variable airflow limitation

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Lung Function Test: Simple spirometry confirms airflow limitation with a
reduced FEV1 and FEV1 /FVC ratio. The FEV1/FVC ratio is normally
more than 0.75-0.80 in adults and more than 0.90 in children
 Reversibility is demonstrated by a >12% and 200-mL increase in
FEV1 after an inhaled short-acting β2 -agonist (SABA; such as
inhaled albuterol 400 μg)
The greater the variation the more likely the diagnosis of asthma can
be
Bronchodilator reversibility maybe absent during severe
exacerbations or viral infections

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Supportive tests
• Chest x-ray: hyperinflation
• Bronchoprovocation (Methacholine challenge test)
• FeNO (Fractioned exhaled Nitric Oxide)
• Biomarkers (Eosinophils, IgE)

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Management
o Can be Pharmacologic or Non-pharmacologic
o Aims of Asthma Therapy:
• Minimal (ideally no) chronic symptoms, including nocturnal
• Minimal (infrequent) exacerbations
• No emergency visits
• Minimal (ideally no) use of a required β2-agonist
• No limitations on activities, including exercise
• Minimal (or no) adverse effects from medicine
o The main drugs for asthma can be divided into bronchodilators, which give rapid
relief of symptoms mainly through relaxation of airway smooth muscle, and
controllers, which inhibit the underlying inflammatory process.

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Bronchodilator Therapies
• There are three classes of bronchodilator in current use:
• β2-adrenergic agonists
• Anticholinergics
• Theophylline
• Of these, β2-agonists are by far the most effective

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β2-adrenergic agonists
• The primary action of β2-agonists is to relax airway smooth-muscle cells
• β2-agonists are usually given by inhalation to reduce side effects
• SABA, such as albuterol and terbutaline, have a duration of action of 3-6
hours. They have a rapid onset of bronchodilatation and are, therefore,
used as needed for symptom relief
• LABA include salmeterol and formoterol, both of which have a duration
of action over 12 hours and are given twice daily by inhalation; and
indacaterol, olodaterol, and vilanterol are given once daily
• LABA should not be given in the absence of ICS therapy as they do not
control the underlying inflammation

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Controllers
• Inhaled Corticosteroids
• Oral Corticosteroids
• Antileukotrienes
• Cromones
• Anti IgE

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Corticosteroids
• ICS are by far the most effective controllers for asthma, and their early use
has revolutionized asthma therapy
• They are the most effective anti-inflammatory agents used in asthma
therapy, reducing inflammatory cell numbers and their activation in the
airways
• ICS are usually given twice daily, but some may be effective once daily in
mildly symptomatic patients
• A course of OCS (usually prednisone or prednisolone 30-45 mg once daily
for 5-10 days) is used to treat acute exacerbations of asthma

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Stepwise approach to asthma therapy according to the severity of
asthma and ability to control symptoms

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• Other treatment modalities include:
• Oxygen given by face mask
• Aminophylline
• Magnesium Sulfate

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Managing exacerbations

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Non-pharmacologic Therapies
• Reduce indoor air pollution by cooking outside or using smokeless stoves
• Avoid allergens that the patient is sensitive to
• Avoidance of tobacco smoke exposure
• Occupational asthma
• Encourage physical activity
• Avoid medications that may worsen asthma
• Remediation of dampness or mold in homes

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References
• Harrison’s Principles of Internal Medicine (20th edition)
• GINA-2020-report

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