Bronchial asthma is a disease characterized by attacks of breathlessness caused by failures in the bronchial patency. Asthma may be of an acute or a chronic character, and the major distinction between these two types of disease is the severity and longitude of an aggravated condition. It is commonly considered that the terms “acute” and “chronic” refer to diametrically opposite phenomena. The former usually refers to a rapid onset of the disease and a brief duration, and the latter implies an enduring aggravated condition with the slow progress of recovery.
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At the same time, the terms “acute” and “chronic” are deeply interrelated – acute asthma exacerbation (AAE) may occur during the progression of chronic asthma, while the first acute asthma attack may result in the development of the chronic syndrome if untreated (U.S. National Library of Medicine, 2016). Overall, there are both similarities and differences between the two introduced diseases. And the purpose of the given paper is the review of their distinctions and similarities in such aspects as pathogenesis, interactions with the genetic factor of disease development, as well as diagnosis and treatment methods.
Bronchospasm and Status Asthmaticus
Bronchospasm is the general manifestation of asthma. The term refers to the reaction of the organism to the lack of carbon dioxide in the blood. During a spasm, the breathing failure occurs, and the content of the gas in the blood increases, while the number of oxygen decreases (Huether & McCance, 2008). As soon as the gas content is balanced, the attack ceases. The primary pathogenic distinction of AAE from the chronic condition is its close association with asthmatic status. Asthmatic status can be developed as a result of an enduring and unmanageable asthmatic attack and followed by bronchioles edema and accumulation of mucus in airways, increasing suffocation combined with hypoxia (Agarwal & Kache, n.d.). In its turn, hypoxia leads to a drastic decrease in the content of oxygen in the blood or particular body organs and tissues. During this process, the vital body organs are exposed to some irreversible transformations (Huether & McCance, 2008). Therefore, status asthmaticus requires immediate intensive intervention measures because a high risk of a fatal outcome is present.
Inflammation plays a significant role in the development of the disease. Its nature is very complex as it is based on several processes mediated by various cells and factors; their interaction causes inflammation and consequent airway remodeling (Huether & McCance, 2008). Humoral and cell-mediated immune reactions and functions affect asthma-related inflammation as well. Plasmatic cells developed out of the B-lymphocytes produce specific antibodies in humoral immune reactions while T-lymphocytes are involved in the cell-mediated immune reactions (Popescu, 2016). T-cells also control the functions of B-lymphocytes and participate in inflammatory processes, causing cytotoxic activity. For example, actively involved in asthma’s pathogenesis Th2-helpers generate cytokines IL-4, IL-5, IL-9, IL-13, and IL-16 (Huether & McCance, 2008). It is observed that Th2-cytokines are responsible for the development of bronchial hyperresponsiveness (Huether & McCance, 2008). The central cytokine in the allergic response is IL-4 – it directs the differentiation of T-cells into Th2-helpers and causes B cells to isotope switching to IgE synthesis (Popescu, 2016).
According to Ciepiela, Ostafin, and Demkow (2015), the increased number of neutrophils in the acute inflammatory reactions indicates the difference between acute and chronic (allergy-induced) asthma models. An increased number of neutrophils is observed in the bronchoalveolar lavage fluid of the patients suffering from acute asthmatic attacks. As the researchers continue, this type of intense inflammation is resistant to high-dose parenteral corticosteroids that usually is not seen in chronic asthma (Ciepeila et al., 2015)
Genetic Factors and Suggested Treatment
Asthma development is closely related to genetic and ecological influences. However, while environmental factors can be managed, the genetic ones are mostly not manageable. For instance, atopic disease and bronchial hypersensitivity are the two major prerequisites for asthma development, and both of the conditions are inheritable. The predisposition to atopy, as well as the production of IgE-antibodies and bronchial hypersensitivity, constitutes the genetic basis of bronchial asthma (Ober & Yao, 2011). The major predisposition genes are contained in chromosomes 5, and 11 and the cluster of IL-4 genes plays a particular role in it (Ober & Yao, 2011). Each of the genetic factors increases the risk of both chronic and acute asthma progression even if environmental factors do not impact a person much.
In case a patient is predisposed to frequent inflammatory diseases in the area of the airway, the diagnosis of asthma should be based on the sputum, biochemical, or urinal analysis. For instance, the evaluation of sputum microflora helps to reveal the level of a patient’s sensitivity to antibiotics (Institute for Clinical Systems Improvement [ICSI], 2012). Along with laboratory tests, AAE can be diagnosed via blood gas assessment because the level of carbon dioxide is elevated.
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When speaking of asthma treatment, five major types of drugs can be implemented depending on the severity and acuteness of the condition. For instance, beta-agonists relieve symptoms; INN-based medicines and glucocorticosteroids have and anti-inflammatory effect and help to stabilize the condition; and corticosteroids are used to treat the chronic and acute forms of asthma (ICSI, 2012). However, corticosteroids can be ineffective in severe acute forms of the disease due to specific inflammatory processes mentioned above.
Nowadays, sublingual immunotherapy aimed to develop resistance towards allergens provoking inflammation is considered one of the most progressive methods. It is especially effective in the case of the genetic predisposition to atopy and asthma. Long-term therapy includes the identification of allergens and the injection of their solutions into the organism. When the doses increase, the patient develops tolerance towards their influence. The early start of the therapy can lead to better outcomes, and it thus can be recommended for children.
Agarwal, S., & Kache, S. (n.d.). Status asthmaticus. Web.
Ciepiela, O., Ostafin, M., & Demkow, U. (2015). Neutrophils in asthma—A review. Respiratory Physiology & Neurobiology, 20913-16. Web.
Huether, S. E., & McCance, K. L. (2008). Understanding pathophysiology. St. Louis, MO: Mosby/Elsevier.
Institute for Clinical Systems Improvement. (2012). Health care guideline: Diagnosis and management of asthma. Web.
Ober, C., & Yao, T.-C. (2011). The genetics of asthma and allergic disease: A 21st century perspective. Immunological Reviews, 242(1), 10–30. Web.
Popescu, A. (2016). Assessment of inflammation markers in asthma. Acta Medica Transilvanica, 21(1), 59-61.
U.S. National Library of Medicine. (2016). Acute vs. Chronic Conditions. Web.