Asthma:
Asthma is a common lung condition that involves periodic episodes severe but
reversible bronchial obstruction in adults and children with hypersensitive and
hyperresponsive airways (VanMeter and Hubert, 2014). It is characterised by
hyperresponsiveness and bronchospasm. Frequent acute asthma attacks may lead
to the damage of lung tissue and the development of chronic asthma. Asthma often
affects children of school-going age with a significant rise in episodes requiring
hospitalization in children has occurred during the past 20 years, and approximately
4 million children under the age of 18 reported having at least one asthma attack
within a 12-month period (VanMeter and Hubert, 2014).
Asthma can be classified in many ways such as acute or chronic, or mild and intermittent to severe
and persistent. Asthma can be categorised into extrinsic asthma and intrinsic asthma based on
their triggers; however, the pathophysiology of asthma remains the same.
1. Extrinsic Asthma: This occurs when an acute episode is triggered due to an inhaled antigen.
This is commonly associated with dust, pet hair, allergic rhinitis (hay fever) and allergic
dermatitis (eczema). Usually there is a familial history of allergic conditions, and the onset of
this asthma is usually in childhood.
2. Intrinsic Asthma: This occurs when stimuli target hyper-responsive tissues in the airway and
initiate the acute attack. Stimuli can include respiratory infection, exercise, cigarette smoke,
perfumes, smog and air pollution, stress, exposure to cold/damp conditions and some drugs
such as aspirin. The onset of intrinsic asthma occurs in adulthood however, many patients
will have a combination of both extrinsic and intrinsic triggers.
What happens in our bodies during and asthma attack?
An asthma attack targets the smooth muscle of the lower airway, the bronchi, and bronchioles to be
exact. The bronchi and bronchioles respond to these attacks with three changes; 1) inflammation of
the mucosa with oedema, 2) contraction of smooth muscle, and 3) increased mucus secretion.
During the first phase of an acute attack (usually within minutes), the antigen reacts with T-Helper 2
cells which trigger a response from plasma cells. These plasma cells release immunoglobulin E (IgE)
on the previously sensitised mast cells in the respiratory mucosa. The mast cells then release
chemicals such as, histamine, prostaglandins, kinins and other chemical mediators. *This is known
as a type 1 hypersensitivity reaction* The release of these chemicals result in inflammation,
oedema, increased mucus secretion and smooth muscle contraction (bronchospasm). This results in
a narrowing of the airway and the onset of symptoms.
The second stage of an acute attack will occur for hours after the initial exacerbation. Due to the
release of inflammatory mediators lead to a recruitment of more white blood cells into the
bloodstream such as eosinophils and leukocytes. This process continues the bronchospasm, oedema,
and increased muscle secretion. The precise mechanism of how this occurs in patients with intrinsic
asthma has not yet been determined. Research suggests that chronic T lymphocyte activation that is
possibly occurs due to an internal antigen is the cause. The tissues are hyper-responsive, and an
underlying chronic inflammation or imbalance un autonomic innervation to the tissues is also
suspected (VanMeter and Hubert, 2014).
