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Investigated Disease Process Asthma is a chronic disease of the lungs, it affects between 7% and 10% of all children and 7% to 9% of all adults worldwide (Britannica, n.d.). It is also estimated tha... t worldwide asthma causes 250,000 deaths per year, and that by 2025 more than 100 million people will be diagnosed with this disease, with the majority of them being children. Asthma is extremely prevalent throughout the world but with proper management of triggers, symptoms, and exacerbations individuals effected with the disease can live a full productive life. The key in preventing negative outcomes of the disease process is in the prevention of asthma exacerbations. Asthma is not only a disease that causes inflammation of the bronchi but over time can cause the bronchi to mutate and become less compliant in gas exchange within the lungs (Kudo, Ishigatsubo, and Aoki, 2013). Pathophysiology The majority of acute asthma exacerbations are a result being exposed to an irritant such as dust, mites and cockroaches, airborne pollution and particulates, animal dander, mold, fungi, and other allergens. Asthma typically starts in children who are exposed to these various elements and become sensitized to these allergens. Asthma is an immune response that is stimulated by an individual’s T helper type 2 (Th2) cells proliferating and produce an allergic inflammatory response within the body and more specifically the lungs as this is the tissue that the irritants come in contact with. This triggering or allergic sensitization is caused by dendritic cells up Asthma 3 taking the allergen and producing antigenic molecules that then are transmitted to the Th2 cells. Asthma is a localized disease process that effects the lungs only, but in particular the upper airway also known as the conducting zone of the lungs and more specific the lower half of the conducting zone. The specific areas of the conducting zone of the lungs effected by asthma consists of the bronchial tree, bronchus trachea, and the bronchioles (Kudo, Ishigatsubo, and Aoki, 2013). The disease process of asthma is typically concentrated in the bronchial tree of the lungs, this is the area that helps create the pathway between the outside air to the alveolar sacs that make gas exchange possible. The bronchi are composed of elastic fibers and smooth muscle tissue, during an acute asthma exacerbation the smooth muscle tissue contracts and acts in the manner of a one-way valve, that is air can get through but then becomes trapped in the alveolar sacs and below the bronchi. Naturally the smooth muscle tissue in the bronchi will expand and contract to allow air to flow through the bronchi and is regulated appropriately, however during an asthma exacerbation the relaxation of the smooth muscle tissue is interrupted due to immunological and inflammatory disturbances (Sinyor & Perez, 2019). Asthma exacerbations consist of two phases known as the early phase and late phase. During the early phase of an asthma exacerbation a person is exposed to the causative factor and their immune system release IgE antibodies throughout the body. Once the IgE antibodies are in circulation within the body they attach themselves to the basophils and mast cells. The mast cells then degrade due to the release cytokines. This degrading or de-granulating of the mast cells causes histamine, leukotrienes, and prostaglandins to be released which cause the smooth muscle of the bronchi to constrict. Lymphocytes that are also released during the inflation Asthma 4 process also cause the sustained inflammation of the bronchi which causes the narrowing of the bronchi. Specifically, Th2 lymphocytes produce interleukins 4, 5, and 13 combined with GMCSF are responsible for the sustained inflammation within the bronchi. Interleukins 3 and 5 are also released to help sustain the eosinophil and basophil response which further advances the inflammatory process. Interleukin 13 also causes the bronchi remold and causes hyperplasia and fibrosis of the tissues. This initial phase progresses into the late phase. The late phase of an asthma exacerbation is characterized by the basophils, neutrophils, helper and memory T-cells, and eosinophils flooding the lungs and results in bronchoconstriction and further inflammation. This obstruction in the airway causes a patient to have an increased work of breathing also. By understanding what phase of and acute exacerbation a patient is in will guide treatment (Sinyor & Perez 2019). Other key features of asthma include hyperresponsiveness of the airway to various stimuli that if exposed to a non-asthmatic would cause no effects. Patients who suffer from asthma frequently have more smooth muscle mass in their lungs when compared to no asthmatics, this is due to increase in histamine released by the immune system during the mediation between the body and the irritant. During an acute exacerbation of asthma, the body will also have an increased vagal tone and release of free calcium throughout the body which also helps to further progress the construction of the smooth muscle tissue (Sinyor & Perez 2019). The immune system is also responsible for releasing granular white blood cells during an asthma exacerbation. These WBCs cause the body to produce mucous and other exudate, which clog the bronchiolar trees. The release of myofibroblasts by disease progression also cause collagen to be produced that then cause an increase in the mass of the epithelium leading to Asthma 5 further narrowing and remodeling of the airway. This remodeling is caused by the epithelial cells converting themselves into mesenchymal stem cells that become smooth muscle. The interaction of eosinophils with mast cells can also cause airway remodeling due to the release of TGF-B and cytokines. If the patient’s asthma is not well managed this continued immune response will cause incremental harm to the patient over time and lead to lungs that are not compliant with gas exchange (Sinyor & Perez, 2019). A factor attributing to asthma exacerbations is that in individuals effected by the disease their epithelium cells are damaged and can no longer function as a barrier to outside factors that react and cause allergic immune responses within the lungs. This ineffective barrier allows for the allergen to enter the airway tissue. Other mediators that have recently been discovered to have a role in an exacerbation of asthma include T helper cells 17 and 9 (Th17 and Th9). These helper cells produce interleukin 17A, 17F, and 22 which further enhance airway inflammation. Interleukin 17A also aids smooth muscle in contractility (Kudo, Ishigatsubo, and Aoki, 2013). Standard of Practice The standard of care for patients diagnosed with asthma were last revised in 2007. T [Show More]

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