Research Paper on Asthma Condition and Pathophysiology

Disease and Definition

Asthma is a chronic inflammatory disorder that causes airway constriction and causes recurring symptoms of airflow limitation. However, the obstruction of the airway is normally triggered by reversible chemical changes in the body and attacks can easily be reversed by using inhalers. The principal caustic factors for asthma conditions include genetic factors and environmental aspects such as allergens and pollutants that also trigger attacks, making it rather easy to predict and avoid them.

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Etiology

According to Cohn, Elias, and Chupp, the causes of asthma are not clear but certain factors such as allergies may increase the likelihood of it developing (790). Breathing certain allergens or irritants may expose one to the asthmatic condition for example; pollens, dust tobacco smoke, cold air or weeds. When these allergens are breathed, they cause constriction of the surrounding muscles of the windpipe and inflammation of the lungs, therefore, causing the difficulties in breathing.

The other factor is the lifestyle of an individual for example smoking, stress, or overexertion on the body. All the triggers start bodily chemicals to react and initiate inflammation of bronchial tissues. Genetic risk factors are some of the most common predictors of susceptibility to asthma. For example, an identical twin has a 25% chance of developing the condition if their twin has it too. However, some genetic causes of asthma have been found to result in the condition only after environmental exposures come into play.

Types of Asthma

Asthma is a condition that causes slight or severe disability in 19.4 million individuals as of 2004 and kills every 1 in 100,000 people in America. A further 7% of the United States populace, 5% in the United Kingdom, and 14-15% in countries like Canada, Australia, and New Zealand live with asthma. A total of 358 million people had asthma in 2015 and 397,100 deaths were caused by the disease, with a majority of them occurring in the developing world (U.S Department and Human Services).

Asthma without allergies occurs in some individuals whereby bronchial inflammation is not triggered by allergens but an upper respiratory infection either cold or flu which sets it off. another is the Aspirin Exacerbated Respiratory Disease (AERD) which causes some individuals to experience asthmatic attacks after taking aspirin. Individuals may have nasal polyps, rhinitis, sneezing and a runny nose.

Exercise-induced asthma is induced by physical exertion on the body that leads to coughing, difficulties in breathing and chest tightness that relieves when exertion is stopped. It exhibits similar characteristics with the cough variant type of asthma that is characterized by a dry hacking cough. Finally, occupational asthma occurs when something on the job sparks an asthma attack may be irritants like smoke or chlorine.

General Signs and Symptoms

The signs and symptoms of asthma differ from individual to individual. The severity of asthmatic attacks is also not uniform. While some people may experience mild blockage of the bronchial tract, in others the inflammation is severe enough to risk suffocation. Some signs and symptoms of asthma include:

• Individuals experience shortness of breath.
• Chest pain
• Trouble sleeping caused by shortness of breath, coughing or wheezing
• A persistent whistling or wheezing sound during exhalation
• Coughing or wheezing attacks that are worsened by a respiratory virus.

Diagnosis

A wide range of irritants and allergens causes asthmatic infections. The fact that its signs and symptoms are not permanent but exhibit periodically under the "right" conditions makes it harder to diagnose. Robinson proposes a diagnosis after detecting a history of breathing difficulty exhibiting in patients at particular moments or after exposure to particular allergens, air pollutants, infections, or exercise (59). Physicians then use a spirometer to check the vital capacity of a patient to help in prescribing some intervention to the trigger. The testing involves a physical exam that includes the doctor asking the patient questions about the signs and symptoms and conditions under which they manifest.

Other tests include the methacholine challenge in which increasing concentrations of suspected irritants or allergens are inhaled by the patient to detect the levels at which an asthmatic attack is likely (Brightling 1700). In the measurement of lung function capabilities, pulmonary function tests are administered to find out how much air moves in and out the lungs as the individual breath. These tests may include Spirometry and Peak flow among others.

Pathophysiology

Irritation of the bronchial tubes is the physiological disorder that leads to asthma. As the key airway into the respiratory system, inflammation of the bronchial tubes involves the interaction of numerous types of cells and several linkages within the respiratory system. In a full-blown mode, the abnormality leads to the distinctive pathophysiology observed in people suffering from the disease. According to the National Asthma Education and Prevention Program, there are several strains of asthma (2). They are classified according to the environmental factors that cause the inflammation of the bronchial tissue. Allergic asthma occurs when an allergy sets off an asthma blaze and is caused by the breathed allergens named in the causes. Food sensitivities also play a role in other individuals. For example, there exists a strong link between casein, the protein in milk and cheese, and the triggering of asthmatic attacks.

To begin with are Lymphocytes cells which have two subpopulations; T helper 1cells (Th1) and T helper 2 (Th2). The two sub-populations have separate mediator characteristics and they affect the proper functioning of the airway in different ways. While animals display a discrete characteristic of allergic inflammation brought by lymphocyte infections, human infected with asthma display a turn towards the Th2-cytokine profile (National Asthma Education and Prevention Program 16). According to Cohn, Elias, Jack, and Chupp, the overt production of Th2 cytokines has a direct relationship to the production of excess IgE that brings eosinophils, the chemical agents directly responsible for the occurrence of irritation in the air tract (2004). Conversely, the inhalation of disease-causing antigens stimulates the mast and Th2 in the windpipe, leading to the reduction in regulatory T cells, a subgroup of lymphocytes whose function is to hinder Th2 cells.

Secondly, the stimulation of mucosal cells leads to the release of agents that are responsible for causing constriction in the bronchial tissue. According to Boyce, the agents are histamine, prostaglandin, and cysteinyl-leukotrienes (26). The accumulation of many mast cells in the soft tissues in the respiratory tract is directly linked to irritability in the airway and may also lead to the release of cytokines that contribute to the alteration of the airway and cause inflammation limited contact with allergens notwithstanding.

Another important consideration in the pathophysiology of asthma is the presence of eosinophils cells. These cells carry irritant enzymes and contain an assortment of inflammation-causing cytokines. The severity of an asthmatic condition often depends on the amount of buildup of eosinophilic cells that occurs in the respiratory tract. People with acute asthma infection exhibit increased the buildup of neutrophils in the windpipe and accumulation in the sputum. Although their pathophysiological role in causing asthma has not been proved conclusively, the diagnosis is especially significant during asthmatic attacks, and a person smokes.

Dendritic cells are the main medium of interaction between antigen-presenting cells and allergens from the windpipe. They also transmit an infection to the lymph nodes, enabling the contact with disease-causing cells. Eventually, dendritic cells accelerate the secretion of Th2 cells from naive T cells (Kuipers and Lambrecht 706). Macrophages exist in large numbers along the air tract. They are stimulated by IgE receptors to discharge irritants and cytokines that intensify the response of airway tissues to the inflammation caused by cytokine production (Kuipers & Lambrecht 705).

Chemokines are another type of mediator cells that are quite significant in the conversion of normal cells to inflammation. Cytokines determine asthma severity by directing and modifying the irritating response to the agents that cause it. Ultimately, the agent Cysteinyl-leukotrienes that, like many other asthmatic allergens, comes from mast cells, is responsible for the constriction of the windpipe during asthmatic attacks. Immunoglobulin E, a significant chemical for the outbreak of many allergy-based disorders, activates the allergic asthma attacks.

General Treatment

Asthma treatment depends on what has caused it. For example, if it is exertion on the body, one should stop doing the activities that so much exerts pressure on the body. If it is the lifestyle the individual should stop for example to smoke. In severity there some inhalers that relieve one's pain and at least reduce the inflammation.

This figure shows a normal airway and during the asthma symptoms.

Works Cited

Brightling, Christopher E. Bradding, Peter. Symon, Fiona A. Holgate, Stephen T. Wardlaw Andrew J. & Pavord, Ian D. "Mast-cell infiltration of airway smooth muscle in asthma." New England Journal of Medicine, vol. 346, no. 22, 2002, pp.1699-1705.

U.S Department and Human Services. "Guidelines for the Diagnosis and Management of Asthma. Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma." 2007. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK7223/Boyce, Joshua. "Mast cells. Beyond IgE." Journal of Allergy and Clinical Immunology, vol. 111, no. 1, 2003, pp. 24-32.

National Asthma Education and Prevention Program, Third Expert Panel on the Diagnosis and Management of Asthma. "Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma." Bethesda (MD): National Heart, Lung, and Blood Institute (US); 2007 Aug. Section 2, Definition, Pathophysiology and Pathogenesis of Asthma, and Natural History of Asthma.

Cohn, Lauren. Elias, Jack A. Chupp, Geoffrey L. "Asthma: mechanisms of disease persistence and progression." Annual Review of Immunology, vol. 22, 2004, pp. 789-815.

Robinson, Douglas S. The role of the mast cell in asthma: induction of airway hyperresponsiveness by interaction with smooth muscle? Journal of Allergy and Clinical Immunology, vol. 114, no. 1, 2004, pp. 58-65.

Kuipers, Harmjan. Lambrecht, Bart N. "The interplay of dendritic cells, Th2 cells and regulatory T cells in asthma." Current Opinions on Immunology, vol. 16, no. 6, 2004, pp. 702-708.