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Asthma is a syndrome characterized by airflow obstruction

that varies markedly, both spontaneously and with treatment
Asthmatics harbor a special type of inflammation in the
airways that makes them more responsive than
nonasthmatics to a wide range of triggers, leading to
excessive narrowing with consequent reduced airflow and
symptomatic wheezing and dyspnea
Narrowing of the airways is usually reversible, but in some
patients with chronic asthma there may be an element of
irreversible airflow obstruction

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Prevalence
Asthma is one of the most common
chronic diseases globally and currently
affects ~300 million people
~1012% of adults and 15% of children
affected by the disease
Asthma can present at any age with a
peak age of 3 years
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 In childhood- M:F is 2:1, in adults it is 1:1
Children "grow out of their asthma"
Adults with asthma, including those with
onset during adulthood rarely become
permanently asymptomatic
The severity of asthma does not vary
significantly within a given patient

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Etiology
Asthma is a heterogeneous disease with
interplay between genetic and
environmental factors

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 Genetic predisposition suggested by-
familial association of asthma and a high
degree of concordance for asthma in
identical twins
The severity of asthma is also genetically
determined
Environmental factors-in early life
determine which atopic individuals
become asthmatic
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 Atopy is the major risk factor for asthma
Patients with asthma commonly suffer from
other atopic diseases, particularly allergic
rhinitis, over 80% of asthmatic patients, and
atopic dermatitis (eczema)
Allergens that lead to sensitization are usually
proteins that have protease activity
Commonest allergens are derived from house
dust mites, cat and dog fur, cockroaches, grass
and tree pollens, and rodents

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 Intrinsic Asthma or nonatopic asthma-
~10% have negative skin test to common
inhalant allergens and normal serum
concentrations of IgE
Usual adult onset

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Pathogenesis
Asthma is associated with a specific chronic
inflammation of the mucosa of the lower
airways
The airway mucosa is infiltrated with activated
eosinophils and T lymphocytes, and there is
activation of mucosal mast cells
The degree of inflammation is poorly related to
disease severity and may be found in atopic
patients without asthma symptoms

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 A characteristic finding is thickening of the
basement membrane due to subepithelial
collagen deposition
These pathologic changes are found in all
airways but do not extend to the lung
parenchyma

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Clinical features
Wheezing, dyspnea, and coughing which
are variable, both spontaneously and with
therapy
Symptoms may be worse at night
Typical physical signs are inspiratory, and
to a great extent expiratory, rhonchi
throughout the chest
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 Diagnosis- is confirmed by lung function test
Simple spirometry confirms airflow limitation with
a reduced FEV1, FEV1/FVC ratio, and PEF
Reversibility is demonstrated by a >12% or 200
mL increase in FEV1 15 min after an inhaled
short-acting beta 2-agonist or, in some patients,
by a 2- to 4-week trial of oral glucocorticoids
methacholine or histamine challenge rarely
needed to confirm airway hyperresponsiveness

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Treatment

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 Treatment
Two groups of drugs are used
Bronchodilators
beta 2-adrenergic agonists,
anticholinergics, and
theophylline
Controllers
Glucocorticoids
Antileukotriens
Cromones
antiIGE
Immunotherapy

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Management of chronic asthma
Avoid triggers
Pharmacotherapy stepwise therapy
Patient education
Goals
Reduce impairment
Reduce risk
no cure but symptoms can be controlled

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 Asthma severity is determined by
considering the following factors
Reported symptoms over the previous two to four
weeks
Current level of lung function (FEV1 and
FEV1/FVC values)
Number of exacerbations requiring oral
glucocorticoids per year

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Adjusting therapy
Assessment of control is used to adjust
treatment in asthmatics
Symptoms over the past 2 to 4 weeks is
used to decide whether to step up or step
down treatment

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Management of acute severe asthma
The best strategy for management of
acute exacerbations of asthma is early
recognition and intervention, before
attacks become severe and potentially life
threatening
Treatment starts with assessment of
severity of attack
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 High flow oxygen therapy to keep oxygen
saturation >90%
High dose inhaled short acting beta
agonists are the main stay of therapy
(nebulized or via metered dose inhaler)
Add inhaled anticholinergics if no
adequate response

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 Start systemic glucocorticoids if there is
not an immediate and marked response to
the inhaled short-acting beta agonists
Slow infusion of aminophylline may be
effective in patients not responding to high
dose bronchodilators
Make frequent (every one to two hours)
objective assessments of the response to
therapy until definite, sustained
improvement is documented
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 For patients with respiratory failure, it is
necessary to intubate and institute
ventilation
Consider antibiotics if signs of pneumonia

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Refractory asthma
A small proportion of patients (~5% of
asthmatics) are difficult to control despite
maximal inhaled therapy
Some of these patients will require maintenance
treatment with oral corticosteroids
The most common reason for poor control of
asthma is noncompliance with medication

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