A Chronic Inflammatory Disease Asthma
Asthma is a chronic inflammatory disease of the airways which occurs in genetically predisposed individuals. Asthma is a reactive airway disease. This common disease has an epidemic progression in western countries (Wenzel, 2003). Environmental factors are likely to be the cause of the progression of this disease. Asthma can be triggered by various stimuli and can result in either a bacterial or viral infection.
Asthma occurs when inflammation constricts the airways when the lungs are reacting to physical activities, respiratory infections, allergens, irritants or stress. Asthma may be acute or chronic. According to Medical Health Research the lungs may narrow or become blocked, resulting in an impeded breathing (Hamid, 2007). Asthma creates difficulty breathing with symptoms including coughing, wheezing, chest stiffness or shortness of breath. Patients with asthma usually have exacerbation due to non-compliance, respiratory distress and airway obstruction (Barrios, 2006). Patients also have remissions that were caused by stress, pollen and other allergens (Duncan, 2017). Asthma can affect the trachea, bronchi, and bronchioles. Two airway cell types are critical for asthma pathogenesis: epithelial cells and smooth muscle cells (Barrios, 2006). Airway epithelial cells are the first line of defense against inhaled pathogens and particles, these cells initiate airway inflammation and produce mucus, an important contributor to airway obstruction (Barrios, 2006). The other main cause of airway obstruction is contraction of airway smooth muscle (Barrios, 2006).
During inhalation air passes through the trachea and enters the right and left main stem bronchi and then enters the bronchioles. The trachea, bronchi and bronchioles stay partly open because they are supported by hyaline cartilage imbedded in their smooth muscles (Kaufman, 2011). The terminal bronchioles do not contain cartilage so they can constrict and collapse under certain conditions (Kaufman, 2011). The terminal bronchioles divide into lobules. These lobules consist of alveolar ducts and sacs that allow gas exchange. Asthma typically effects the mucosal lining of the bronchi and bronchioles (Schreck, 2006). This lining consists of three layers; the epithelial layer, the basement membrane and the lamina propria. In the epithelial layer goblet and claricells produce mucous that prevents irritants from entering the lungs (Kaufman, 2011). When irritants enter the bronchioles their immediate reaction is to stick to the mucous then cilia push up towards the pharynx for expectoration.
During asthma exacerbation a trigger causes mast cells and T lymphocytes in the lamina propria to release inflammatory substances such as histamines (Wenzel, 2003). When these inflammatory substances attach to receptor cites on the bronchial lining the mucosa becomes inflamed and swollen. Eosinophils macrophages and neutrophils make their way to the inflamed area, these cells increase mucous production, slow cilia movement and damage the epithelial layer. When epithelial lining is damaged the mucosa overreacts to triggers which cause bronchoconstriction (Wenzel, 2003).
If pollen or another allergens trigger exacerbation, inflammatory substances cause plasma cells in the lamina propria to release large amounts of immunoglobulin E (IgE) (Barrios, 2006). This antibodies effects the lungs in four ways, it increases vascular permeability causing airway inflammation, damages the mucosal epithelium causing airway hyper reactivity, stimulates neuro reflexes resulting in Broncho constriction and causes cells to produce more mucous that is viscous and can form plugs (Schreck, 2006). Whether an exacerbation is caused by an allergen or another trigger airflow obstruction, they both cause airflow obstruction. During an exacerbation a person can inhale partial air through the inflamed airways to reach the alveoli however on exhalation the intrathoracic pressure rises completely closing off the airway. This cause some alveoli to hyper-inflate while other alveoli fill with mucous and collapse (Schreck, 2006). Since some alveoli have either hyper-inflated or collapsed less gas is exchanged across the alveolar capillary membrane.
Patients with Asthma will have signs and symptoms listed below. Symptoms are what the patient perceives to be feeling (Kacmarek, 2017).
- Chest tightness, pain
- Shortness of breath
- Rapid breathing
- Chest pressure
Due to the variance of signs and symptoms of patients. Properly diagnosing Asthma can be difficult. A proper detailed patient’s history must be obtained as well as lung functions tests. The two most common are spirometry and the methacholine challenge (Duncan, 2017). Spirometry is a simple breathing test that measures lung volumes and air flow. Spirometry is the preferred method for diagnosis because it gives clear identification of airflow obstruction (Duncan, 2017). Spirometry can differentiate between a restrictive or obstructive lung diseases. Spirometry measure the forced vital capacity (FVC) and the forced expiratory volume in the first second (FEV1) (Duncan, 2017). This test is conducted by asking the patient to perform a forced expiration after a maximum inspiration and the highest of the three measurements is recorded. The ration of FEV to FVC provides a useful measurement of airway obstruction (Kacmarek, 2017). Ratios below 70% suggest airway obstruction and the lower the ratio the more severe the obstruction (Kacmarek, 2017). Poor spirometry technique and coaching can result in an inaccurate diagnosis and inappropriate treatment. Another spirometry test is the Peak expiratory flow measurement (PEF). This type of test measures the maximum flow of air achievable from a forced expiration that is started from the positon of maximum lung inflation. This test requires the patient to stand and take the deepest inhalation possible and then blow out as hard as possible while lips are sealed around the mouthpiece. Both spirometry test are related to a person’s age, gender, height and ethnicity (Schreck, 2006).
The methacholine test evaluates how reactive and responsive your lungs are to things in the environment. During this test, patients will be asked to inhale doses of methacholine, a drug that can cause narrowing of the airways (Kacmarek, 2017). A breathing test will be repeated after each dose of methacholine to measure the degree of narrowing or constriction of the airways (Kacmarek, 2017). The test begins with a very small dose of methacholine and increasing the doses until either you experience 20 percent drop in breathing ability, or you reach a maximum dose with no change in your lung function (Kacmarek, 2017). The test is considered positive if the patient experiences a 20 percent or more decrease from the baseline in breathing (Kacmarek, 2017).
According to the Centers for Disease Control and Prevention (CDC), 1 in 13 people have asthma. More than 26 million Americans have asthma. This is 8.3 percent of adults and 8.3 percent of children. It affects 5% of the United States population and accounts for 2 million emergency department visits, 470 000 hospitalizations, and 4500 deaths annually. Although Asthma had already been recognized in many cultures such as Chinese’s, Hebrews, Greeks, and Romans, asthma was first described by the ancient Greek physician Hippocrates and derived from the Greek word “asthmaino which means “panting or gasping (Hamid, 2007). Since the ancient times, there has been a considerable amount of advances that have been made in understanding the genetics, epidemiology and pathophysiology of asthma (Hamid, 2007). The Georg Ebbers Papyrus, found in Egypt in the 1870s, contains prescriptions that were written in hieroglyphics for over 700 asthma remedies (Hamid, 2007). Herbal treatments were amongst the most common. Ancient Egyptians would heat up herbs on a brick, and inhale the fumes through a reed.
Current therapies include a variety of therapeutic interventions that include several routes of administration. The main methods of treatment include short acting inhaled beta 2 adrenergic agonists; inhaled oxygen; and systemic: intravenous fluids and intramuscular or oral corticosteroids (Vignola, 2003). Systemic corticosteroids are recommended for moderate to severe exacerbations or patients with inadequate response to beta 2 agonists (Vignola, 2003). Inhalation corticosteroids are not recommended for acute asthma exacerbation because of its limited systemic availability (Vignola, 2003). The oral route of administration is as effective as the intravenous route (Vignola, 2003).
There is no cure for asthma at this time, treatment is the only option available.
Barrios, R. J., Kheradmand, F., Batts, L., & Corry, D. B. (2006). Asthma: Pathology and Pathophysiology. Archives Of Pathology & Laboratory Medicine, 130(4), 447-451.
Duncan, D. (2017). Respiratory Care : Assessment and Management. Keswick: M&K Publishing.
Hamid, Q., & Tulic, M. K. (2007). New insights into the pathophysiology of the small airways in asthma. Annals Of Thoracic Medicine, 2(1), 28-33.
Kaufman, G. (2011). Asthma: pathophysiology, diagnosis and management. Nursing Standard, 26(5), 48-56.
(Vignola, 2003) (Wenzel, 2003)fundamentals of respiratory care (11th ed.). St. Louis, Mo.: Elsevier/Mosby.
Schreck, D. M. (2006). Asthma pathophysiology and evidence-based treatment of severe exacerbations. American Journal Of Health-System Pharmacy, 63(10), S5-S13. doi:10.2146/ajhp060127
Vignola, A. M. (2003). Effects of Inhaled Corticosteroids, Leukotriene Receptor Antagonists, or Both, Plus Long-Acting ??[sub 2]-Agonists on Asthma Pathophysiology: a Review of the Evidence. Drugs, 63(21), 35-51.
Wenzel, S. (2003). Severe Asthma: Epidemiology, Pathophysiology and Treatment. Mount Sinai Journal Of Medicine, 70(3), 185.