Pathogenesis of Severe Acute Asthma: Understanding the Mechanisms and Nursing Priorities

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Severe Acute Asthma; concept map
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Pathogenesis of Acute Severe Asthma
Severe acute asthma reflects a severe exacerbation which doesn’t respond to normal
treatment process by use of bronchodilators and corticosteroids drugs. Basic symptoms
include having a tight chest, shortness of breath, cough which is dry, labored breathing and
excess wheezing. It usually presents itself as a life-threatening condition which often calls for
emergency attention, (Cook & Saglani, 2016).
Asthma inflammation of eosinophils occurs in the early phase and mixes itself with
cellular infiltrate which is composed of eosinophils, lymphocytes cells, neutrophils, and mast
cells. Allergic inflammation often begins with the progression of the predominant helper T 2
lymphocyte which is carried away contrary to a T1 lymphocyte. This allows for allergen
exposure within the genetically susceptible individual.
Specific exposure to allergens with the influence of helper T Cells which often leads to
B-Lymphocyte reflects an elaboration of immunoglobin and antibodies which are specific for
the allergen. Subsequent allergen exposure often leads to cross bridges in the IgE molecules
and leads to activation and releasing an array of mediators. The mediators, in this case, are
the leukotrienes, histamine, C4, D4 and E4 with the host cytokines. These mediators often
lead to bronchial smooth constriction of the muscles, vascular leakage, and cell inflammation.
The process often leads to obstruction of the smooth muscles, airway edema, inflammatory
cells influx and production of intraluminal mucus. The airway inflammation can cause
hyperactivity in the characteristic of asthma. Severe airway obstruction leads to impaired gas
exchange which results in gas exchange and low oxygen levels, (Leatherman, 2015).
Airflow decline in the asthmatic state is caused by a variety of factors and changes in
the air airway; these factors include;
Bronchi constriction
The common symptom of asthma is the airway narrowing which leads to interference
of airflow. In severe acute of asthma, the bronchial smooth contraction which leads to
narrowing of airflow. Bronchi constriction induced by allergens often originates from IgE
dependent mediators released from mast cells which include tryptase, leukotrienes,
histamines, and prostaglandins which have a direct effect on the airway. Drugs can be a
factor in the constriction of the airways, (Puranik, Forno, Bush & Celedon,2017). Aspirin and
other related nonsteroidal drugs have been shown to have an effect on the narrowing of the
bronchioles.
Airway Edema and hyperresponsiveness
When the disease becomes persistent with progressive inflammation, other factors may
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