Asthma: Definition, Etiology, Pathogenesis, Signs and Symptoms, Interventions, and Nursing Implications

Running head: ASTHMA 1
Health Variations
Name
Institutional Affiliation

ASTHMA 2
Question 1
a) Definition and etiology
Asthma is a chronic airway disease characterized by airway hypersensitivity, reversible
airflow obstruction and variable airflow obstruction. Generally, the pathogenesis of asthma
involves genetic and environmental factors. Genetic factors include atopy, a positive family
history of asthma and polygenic intolerance. Others include gender and ethnicity (Ferreira, et al.,
2017). Environmental factors that can predispose one to asthma include outdoor pollutants like
pollen, smoke and exhaust fumes. Dietary factors can also contribute to the progression of
asthma. Dietary deficiency of vitamin C and foods rich in antioxidants have been shown to
enhance progression of asthma. Indoor pollutants comprise of house dust, ciggerate smoking and
smoke from firewood (Lambrecht & Hammad, 2015). Drugs like Non-steroidal anti-
inflammatory (NSAIDS) like aspirin and oral contraceptives also predisposes one to developing
asthma. Jackson Smith may have had a history of asthma in the family, which was triggered by
an allergen (Kumar, Abbas, & Aster, 2015). Both genetic and environmental factors play a role
in asthma predisposing and allowing for progression of asthma. The hall mark of the disease is
airway inflammation, bronchoconstriction, bronchial smooth muscle and mucous glands
hypertrophy (Wagner, 2014).
b) pathogenesis
Genetic predisposition to type 1 hypersensitivity reaction (atopy) has been attributed to
be the major etiologic evidence of asthma (Craft et al, 2015). After being exposed to an
offending stimuli, inflammation ensues. Major inflammatory cells are eosinophils and
neutrophils. In atopic asthma, TH2 production is excessive. It stimulates production of IL-4

ASTHMA 3
which then stimulates production of IgE. IgE production is also produced by B cells which is
activated by IL-13. IL-13 also stimulates mucous production. IL-5 activates eosinophils (Craft et
al, 2015). When IgE coats mast cells on exposure to allergen, degranulation occurs and an early
and late wave of reaction occurs (Magge, Pascanu, & Salerno, 2017). Early wave is
predominantly characterized by bronchoconstriction, increased production of mucus and variable
vasodilation. Constriction of bronchial smooth muscles is triggered by direct stimulation of vagal
receptors. The late phase has inflammation which leads to activation of eosinophils, neutrophils
and T cells. Inflammatory reaction is amplified by continues chemotaxis and activation of
eosinophils due to chemokines released by TH2 cells (Kumar, Abbas & Aster, 2013). Repeated
exposure to allergen causes hypertrophy of bronchial smooth muscles and mucus glands.
Signs and symptoms
Jackson Smith presents with Acute Severe Asthma (ASA). ASA is an acute
excercubation of asthma that does not respond to standard treatment with bronchodilators or
corticosteroids, (Kumar, Abbas & Aster, 2013). Severe dyspnea that Jackson presented with is
due to airway hyperactivity to an allergen. The bronchial smooth muscles undergo inflammation
and increased mucus production that limit amount of air entry and outflow. Airway remodeling
is also a contributing factor. Due to repeated exposure to allergen, the smooth muscles and
mucous glands undergo hypertrophy (therefore narrowing). This makes the patient have and
increased respiratory effort due to buildup of carbon dioxide (Aitken, Marshall & Chaboyer,
2015). Carbon dioxide (CO2) sensitizes the respiratory center to increase respiratory rate (as
Jackson Smith’s) so that excess CO2 can be expelled. As a result, saturation at room air was to be
low, as it was 90% in Smith’s case.