Pathophysiology of Asthma and Clinical Manifestations: A Case Study

Running head: HSNS 264 1
Title of the Paper
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Introduction
Asthma is a chronic immune-mediated disease that affects the lung airways.
Inflammation and obstruction of the airways characterize asthma. The main symptoms of asthma
include wheezing, chest tightness, coughing, increased breathing rate, and shortness of breath.
The incidence of asthma is more prevalent in children: it is the leading cause of chronic illnesses
in pediatrics. Asthma triggers include various etiologic and pathophysiologic factors, which
includes pollen grains, spores, dust, cold air viruses, and genetics. Asthmatic attacks occur at
varied occasions within days, weeks or months. The prevalence of asthma in Australia is
estimated to about one in every nine people, which is equivalent to about 2 million people.
Asthma is more prevalent in young males below 15 years; however, it is common in females
above 15 years. Besides, asthmatic attacks are more predominant in Indigenous Australians when
compared to non-Indigenous Australians. The disease is a source of both financial and social
burden in Australia’s economy. Approximately 451 children below 15 years in every 100,000 are
hospitalized due to asthmatic attacks (Asthma Australia, 2018). More also, 400 deaths reported
annually for the past decade. Asthmatic patients and families report poor quality of life as 34%
state that the disease interferes with their daily activities while another 21% requested time off
from work and school (Asthma Australia, 2018). This essay discusses the case of Zachy who has
a running nose, prolonged expiration, expiration wheeze, and a running nose. Zachy’s clinical
manifestations correlate with the pathophysiology of asthma.
Discussion
Pathophysiology of Asthma
Asthma pathophysiology is critical in the diagnosis and treatment practices. The
pathophysiology of asthma involves complex categories: bronchiolar inflammation, airway

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obstruction, and bronchial hyperresponsiveness (Mims, 2015). Asthma affects the trachea,
bronchioles, and bronchi. Inflammation may occur despite the absence of common signs and
symptoms. Cytokines and chemokines cause airway inflammation. Cytokines are produced by
various cells such as the mast cells and lymphocytes. T-helper lymphocytes produce cytokines
that trigger intense inflammation in allergic asthma incidents (Mitchelle & O’Byrne, 2017).
Chemokines recruit pro-inflammatory lymphocytes such as neutrophils, which have a distinct
role in the pathogenesis of asthma.
Bronchoconstriction arises due to muscle damage, edema, excessive mucus, and
bronchospasms. Bronchospasms are the sharp contraction of the bronchial smooth muscles,
which cause narrowing of the airways (Alfieri et al., 2014). Besides, edema that arises from
microvascular leakage contributes to the narrowness of the airways. More also, the dilation and
leakage from the airways capillaries cause edema that, in turn, hinders mucus clearance from the
lungs. Asthma expands the mucus-secreting glands, which increases the number of mucus-
secreting cells. Increased mucus secretions result in plugs that block the airways.
The airway epithelium is a target of infectious and environmental factors, which cause
injury through the influx of pro-inflammatory cells. Epithelium peeling due to injury causes
extreme airway impairment. The loss of the epithelium layer allows the penetration of allergens,
causing airway hyperresponsiveness. The extent of hyperresponsiveness is dependent on a
patient’s immunity and inflammation (Fraser et al., 2017). However, bronchodilator therapy is
ineffective in treating hyperresponsiveness; instead, anti-inflammatory medications are essential.
Asthma results in the loss of enzymes, which degrade inflammatory mediators. This is
due to subsequent reflexive neural effects relating to the exposure of sensory nerves. In the case
of improper treatment measures, asthma may result in airway remodeling. Airway remodeling