Pathophysiology Of Asthma

1645 Words 7 Pages
Asthma is characterized by the pathological changes in the submucosal glands, the increase of smooth muscle composition and hardening of the lamina reticularis; due to the recurrent inflammation and overproduction of mucus in the airways (Holgate & Sly, 2014). The inflammatory response is highly associated with the clinical symptoms of wheezing, coughing, short of breath and chest tightness (Cosio, Rosado & Rossi, 2012). The objectives of this essay is to discuss the pathophysiology of asthma, outline the current acute asthma management in Australia and then lastly discuss the Nurses role in Sara’s scenario with the use of a management plan.

Background

Asthma is triggered by common risk factors such as:

• Environmental exposures (e.g. tobacco
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The immunologic antibody IgE attaches itself to the trigger, therefore a reaction signals the eosinophils, neutrophils and T lymphocytes in the circulation to the airways (Holgate & Sly, 2014). In conjunction, the alveolar macrophages and mast cells, are mediators that trigger an allergic response to environmental triggers, which live in the alveoli (Holgate & Sly, 2014). The immunologic antibody IgE attaches to the trigger and signals the mast cells to attach to the IgE, where histamine mediators are released from the mast cells, resulting in an allergic reaction. The inflammation to the site, due to the histamine, causes the vasodilation of blood and the influx of immune cells (eosinophils, neutrophils and T lymphocytes) that trigger the resident cells (goblet cells) to increase the production of thick mucus and swelling of the muscular layer. Therefore, partially or fully occluding the respiratory bronchial lumen resulting in air not being exhaled. These are mechanisms to stop the irritation and rubbing of the airways, but consequently, impacts on the individuals’ ability to breathe as it …show more content…
Hyperplasia is defined as the increase of body cells due to the rapid cellular proliferation (Mosby, p. 647). Evidently, the increase in smooth muscle cells can result in a decreased lumen. Recent studies have not shown evidence on how this process occurs, but studies have hypothesized that it may be due to the constant bronchospasm and bronchoconstriction of the smooth muscle layer in the respiratory tract (Holgate & Sly, 2014). In conjunction with the hyperplasia in the respiratory tract, there is a thickening of the lamina reticularis, which lies under the respiratory epithelium and is commonly found in the large conducting airways (Lugogo MD, Que MD, Gilstrap MD, & Kraft MD, 2016). Pathologically, the thickening of the lamina reticularis is due to the accumulation of collagen fibers, leading to the fibrosis (scarring) of the subepithial tissue of the lower airways. The accumulation occurs secondary to cell injury of the membrane as growth factors and collagen fibers accumulate. Therefore, elasticity of the bronchi and alveoli becomes decreased; leading to subsequent air trapping, hyperinflation and reduced functional activity of the lungs (Lugogo MD, Que MD, Gilstrap MD, & Kraft MD,

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