Asthma: Its Causes and Treatment - Research Paper Example

Asthma: Its Causes and Treatment Introduction Asthma is a disorder of the lungs that is receiving increasing attention by pulmonary researchers and clinicians as its incidence has risen to epidemic proportions worldwide. Currently, it is estimated that 300 million people are suffering from this chronic disease, which often begins in childhood. Epidemiological studies have shown that the incidence of asthma in the US is among the highest in the world. The incidence of asthma is much greater (up to 20%) in the US, UK, Australia, New Zealand, and the Republic of Ireland. The global incidence is lowest (2-3%) in Eastern Europe, India and Ethiopia. In the US childhood incidence had increases fro 3% to 9% since 1980. Among different ethnic groups in the US, Puerto Ricans have the highest incidence of asthma. African Americans also have a high incidence of this disease. Irish Americans and Hawaiians also have a high incidence of asthma. The lowest incidence is found in the Mexican population. Although the incidence of pediatric asthma is higher in males than in females, the occurrence of this disease is much higher in adult females, who are twice as likely to die of this disease as males. Moreover, the incidence of asthma is higher in lower socioeconomic groups who reside in urban centers. Disease Symptoms There are two primary forms of this disease: acute and chronic. The acute form of the disease is characterized by the occurrence of in worsening symptoms and unstable bronchial function. The chronic form of the disease is a stable, non-progressing condition (Adam 10). Many patients with asthma vary over time between the two disease states. Asthma can be distinguished from several other major forms of lung disease by means of differential diagnosis. Unlike emphysema which affects the structure and function of the alveoli, the primary site of gaseous exchange in the lung, asthma affects the airways or conductance passage that transport air between the lung tissue and the external opening of the body. Likewise, COPD is an irreversible deterioration of the primary lung tissue; in contrast at the inflammatory manifestations of asthma are reversible (Adam 20-23). Asthma is a chronic pulmonary disorder characterized by inflammation of the major airways of the lungs and has a complex etiology. The recurring inflammatory episodes result in hyper-responsiveness of airway vessels that causes tissue swelling with many physiological consequences (Adam 44). These episodes cause symptoms of wheezing, tightness of the chest, coughing and restricted airflow that result in breathlessness. The primary symptoms of asthma are wheezing, chronic cough, difficulty breathing, tightness of the chest, all of which occur on a recurrent basis. In addition, asthmatic episodes may typically vary according to the time of day (worse at night) and the season. These clinical manifestations of the disorder can usually be controlled or moderated with the appropriate medications, but reliable control may be difficult to achieve, resulting in persistent chronic symptoms and the risk of sudden death from airway obstruction (Saunders 85). Tachycardia, or rapid heart rate may occur as a compensatory mechanism during an asthma attack to increase airflow through inflamed and obstructed airways. Over-inflation of the chest, lungsounds (rhonchous) and a paradoxical pulse which is weaker at inhalation and stronger at exhalation may also be observed in patient examination (Saunders 89). In some children, the occurrence of asthma is limited to exercise-associated symptoms (Adam 63). Therefore, exercise testing of PEF values may be important for children suspected of having exercise-induced bronchoconstriction. Another specialized form of asthma is called occupational asthma. This is associated with exposure to lung irritants in the workplace. Causes The occurrence of asthma is linked to allergies that comprise the primary cause of lung inflammation associated with dysregulated immune responses to allergens (Jaber 231). Some of the more common allergens associated with asthma are dust mites, house pets, molds, pollen and cockroaches (Jaber 232). In addition, chemical irritants can trigger inflammatory responses that may contribute to the development of asthma. These include cigarette smoke, air pollutants, and chemicals inhaled in occupational settings. Indoor air pollutants in the form of aromatic volatile organic compounds may serve as triggers of asthmatic reactions in sensitive patients. These include soaps, shampoos, cosmetic and creams as well as paints (Jaber 233). Infections can also play a role in asthmatic conditions; these usually involve viral infections of the lungs. Epidemiological studies suggest that upper respiratory disease infections early in life may exert a protective effect against the development of asthma. In contrast, primary lung infections such as pneumonia or bronchiolitis in young children may predispose to the later development of this disease (Jaber 240). Maternal cigarette smoking during pregnancy has been cited as an important contributing factor to the development of childhood asthma (Jaber 244). More recently cited causes include childhood obesity, high exposure to pollutants and environmental toxins from a very early age and delivery by C section, all of which are correlated with a higher incidence of pediatric asthma (Jaber 248). In patients with asthma, stress may serve as a trigger for asthmatic episodes due to its effects on the immune system function (Jaber 251). The extensive use of antibiotics in young children is believed by some to contribute to the development of pediatric asthma due to its effects on the composition of the microbial flora of the gut, which affects the development of the immune system early in life. This theory is called the “Hygiene Hypothesis”. This hypothesis suggests that the increased incidence of asthma in developed nations is the results of increased hygiene which limits the development of an effective immune system early in life (Jaber 257). Asthma may also involve a genetic component. At least 100 genes have been linked to the disease in genetic screening studies. Approximately 25% of these may actually comprise candidate genes conferring a predisposition to the development of this disease (Maddox 477). Many of these genes encode proteins that play a role in the development of the immune system and in the regulation of immune system responses (Maddox 478). Different forms of the disease may involve different genes. For example, a single nucleotide polymorphism on the long arm of chromosome 17 is linked to the development pediatric asthma (Maddox 485). Most importantly, genes associated with asthma operate in the context of associated environmental factors that together determine whether or not an individual will develop this disease. Researchers have identified a single nucleotide polymorphism (SNP) in the CD14 gene that poses a predisposing risk factor for the development of pediatric asthma when combined with bacterial endotoxins (Jaber 269). Genetic studies have indicated that the most important risk factor for the development of asthma is family history of atopic allergies which has been found to increase the risk for developing asthma by three to four-fold (Maddox 289). Pathophysiology The first important theory on the origins of asthma was proposed by Andor Szentivanyi in 1968, and is called the Beta-2 Adrenergic Theory of Asthma. The theory proposed hat the primary cause of asthma is a block of the beta-2 receptors in the bronchial tissue smooth muscle cells. This blockade prevents the muscle tissue from relaxing, thereby facilitating the hyperconstriction of airway vessels following their activation (Maddox 272). Many years later, Szentivanyi showed that IgE antibodies, which are over-produced during immune responses to airway allergens or irritants, block the beta-2 receptor molecules, providing concrete evidence for his theory (Maddox 273). The hyperreactiveaiway responses observed in patients with asthma are associated with over-production of mucous and extreme tightening of the smooth muscle tissue surrounding the airway vessels (Maddox 281). Swelling and edema associated with hypersensitive immune responses further contribute to the restriction of airflow to the lungs, which is the primary symptom of this disease (Maddox 282). In patients with asthma, Type I hypersensitivity immune responses occur following exposure to trigger allergens or irritants present in the air. This produces a muscle spasm in the bronchi which is followed by bronchial inflammation which is associated with the excessive production of mucous, which further restricts airflow to the lungs (Jaber 250). This initial event may be followed some hours later with a repeated response associated with bronchoconstriction and airway obstruction by mucous. The function of the bronchial tissues is controlled by the parasympathetic branch of the nervous system (Jaber 252). Exposure to allergans or irritants in the air act as a stimulus that triggers depolartization of nerve endings in the bronchial tissue that send a message to the vagal center of the brain. Tjhis then triggers the release of acetyl choline in the efferent nerve ending in the bronchi. Acetylcholine triggers the formation of inositol 1,4,5-trisphosphate, a second messenger that triggers muscle contraction which reslts in the constriction of the bronchial vessels( Maddox 287). The allergic component of the airway response is the result of the activation of antigen presenting cells (APCs) by allergens present in the airflow. APCs then trigger immune system responses to the allergen in the form of T-helper cells that further orchestrate immune system responses to the inhaled allergen (Jaber 255). The T-helper cells of non-allergic individuals will not respond to ther presence of this type of stimulus. The activated T-helper -2 lymphocytes in patients with asthma trigger the activation of humoral immune system components which are associated with the production of antibodies directed against the allergen. The humoral response induces the production of mucous and the growth of mucous producing cells that further contribute to the hyper-reactive inflammatory responses associated with chronic forms of this disease (Jaber 257). The asthmatic response of the body associated with inflammation and airway obstruction may have evolved as a protective mechanism by the immune system to block the lungs from the damaging effects of lung irritants and poisons (Adkinson 407). In this context, asthma is viewed as part of an evolutionary defense mechanism that becomes overactive in responses to allergens in sensitive individuals. Diagnosis The clinical assessment of patients with asthma involves a number of tests of lung function. Asthma is often seen in multiple members of the same family; family history is an important diagnostic tool (Saunders 66). One of the most important primary tests involves the measurement of lung function using an instrument called a spirometer (Saunders 76). This measures the peak expiratory flow (PEF) or the rate of airflow during expiration. This assessment provides information on the severity of airway restriction as a diagnostic confirmation of disease and also as part of an assessment of disease severity. In pulmonary expiratory flow increases by 20% or greater following the administration of a bronchodilator, this is consistent with a diagnosis of asthma (Saunders 78). Asthma is generally classified according to the severity of the disease (Adkinson 410). Disease severity is determined by PEF values as indicators of the degree of airway restriction, associated symptoms, and variability in lung function. The major classifications of asthma include: Intermittent, Mild Persistent, Moderate persistent and Severe Persistent. Asthma is also classified according to the degree to which the major clinical manifestations of this disorder can be controlled with therapeutic intervention (Adkinson 411). The levels of disease management are classified as: controlled, partly controlled or uncontrolled. Controlled asthma refers to the complete and effective management of all symptoms of this disease by medication such that asthmatic episodes occur only two times per week or less that may or may not require medication (Adkinson 412). There are no limitations on activity and no worsening of symptoms at night. Lung function tests are normal and no exacerbation of disease symptoms occurs. Partly controlled asthma refers to clinical management that is associated with breakthrough symptoms occurring more than twice per week that require medication, the occurrence of exercise limitations and some degree of worsening of symptoms at night (Adkinson 413). Recorded lung function is 80% or better. The exacerbation of disease symptoms may occur at intervals of a minimum of one year. Uncontrolled asthma refers to the most severe form of the disease in terms of treatment unresponsiveness (Adkinson 417). In this category, patients experience breakthrough symptoms that require medication three or more times per week and experience limitations on activity and the worsening of symptoms at night on a recurrent basis. Variable levels of lung function below 80% and the exacerbation of symptoms occur despite therapeutic intervention. Severe forms of asthma that do not respond to therapeutic intervention are called status asthmaticus, and may cause death (Adkinson 420). Treatments There are a number of medications that have been used effectively to control asthma. Inhaled glucocorticosteroids are the primary form of disease management for most patients with asthma (Adam 168). Their use is consistently associated with decreased occurrence of primary symptoms as well as decreased occurrence of disease exacerbation over time. Long-term improvements of lung function are associated with decreased mortality rates and improved quality of life in patients with this disease (Adam 170). The primary effect of this class of drugs is the reduction of airway inflammation due to their immunosuppressive effects. This control of airway hyperresponsiveness that characterizes the primary clinical manifestation of this pulmonary disease has an overall beneficial effect on lung function. There are many side effects, however, associated with the long-term use of these drugs, including increased appetite, fat redistribution in the body, weight gain and dysregulation of glucose metabolism (Saunders 282). These side effects are less problematic with the targeted use of glucocorticoids in the form of inhalants in which systemic exposure to these drugs is markedly reduced. However, risk for the development of osteoporosis is increased by the use of glucocorticoid inhalants and may require prophylactic treatment (Saunders 285) Another group of drugs with consistently positive therapeutic benefits in the treatment of asthma are Beta-2 adrenergic agonists (Adam 207). Side effects may occur with the use of short-acting beta-2 adrenergic receptor agonists such as albuterol. At high doses, this may involve elevated heart rate or blood pressure (Adam 208). A newer form of the drug, levalbuterol, has fewer side effects of this type (Saunders 290). The prolonged use of agents of this type may also weaken their anti-inflammatory effects due to desensitization. Long-acting bronchodilators achieve effects that may persist for as long as 12 hours and can be used twice daily (Adam 179). These beta-2 adrenergic agonists have the same mechanism of action as the short acting variety but have longer chemical side chains which potentiates the duration of their effect. Their use has been controversial as worsening of symptoms and even deaths have reported following their use (Saunders 289). The results of a major clinical study published in 2006 indicated that significantly increased (up to 4-fold) patient hospitalizations and death rate were associated with the use of long-term beta-2 agonists (Saunders 292). The study indicated that although bronchodilation was achieved using this type of drug, there was an increased risk of exacerbated inflammatory responses associated with patient demise. In 2008, the US banned the use of these drugs in children (Saunders 295). Another class of drugs used in the treatment of asthma are leukotriene modifiers (Adam 180). These drugs exert both anti-inflammatory and anti –spasmodic effects in the lung. They may be used in conjunction with inhaled steroids and do not produce side effects (Adam 182). Preventive therapeutic approaches that may reduce the frequency of asthma attacks involve the use of mast cell stabilizers that prevent the initiation of inflammatory responses to allergen or irritant triggers of asthma (Adam 190). They cannot be used to treat an on-going attack, but their regular use has decreased the frequency of such occurrences in many patients with asthma. Patients with severe, uncontrolled asthma sometimes respond to a monoclonal antibody therapeutic directed against IgE antibodies overproduced in asthma attacks, called Omalizumab (Saunders 300). Non-medical approaches include trigger avoidance strategies, where possible, to prevent the initiation of an asthmatic attack (Adam 187). In addition, dietary supplements such as vitamin C (1500 mg per day) may exert a protective effect, as low levels of vitamin C intake have been shown to be associated with pulmonary dysfunction. Clinical research studies have shown that vitamin C reduces the frequency and severity of asthmatic attacks in many patients (Saunders 305). Approximately 50% of children diagnosed with asthma will eventually recover from this disease in the 10 year period following diagnosis (Adam 200). Some studies have suggested that early intervention with glucocorticoid therapy may prevent long-term damage from bronchial remodeling associated with this disease (Adam 205). Efforts to control environmental exposure to potential allergens that may trigger the development of asthma have had mixed results; simply reducing exposure to potential allergens does not definitively reduce the risk for the development of pediatric asthma (Adam 309).. Patient Interview A woman of age 22, whom I will “Julia” has suffered from asthma since the age of 5 years. She agreed to be interviewed for the purpose of this paper, to give readers a better understanding of what it is like to live with this chronic lung disorder. The interviewer is designated “I”; Julie is designated “J”. I: How long have you had asthma? J: I was diagnosed with asthma when I was 5 years old. I had been sick that winter with lots of colds and congestion. After the infections cleared up, I noticed that I as out of breath a lot and would wake up at night coughing. It was a little bit terrifying, because sometimes I felt like I could not breathe. My mother took me to the doctor. He examined my breathing with a stethoscope. An X-ray was taken of my lungs, but it revealed nothing. The doctor prescribed an inhalant, to see if that would help. The next time I felt out of breath, I breathed in to the inhalant and suddenly I felt as though I could breathe again. The doctor said I had asthma. I: How did you feel about the diagnosis? J: I was scared. I had never heard the word before. I was afraid I would stop breathing and that I would die. I still remember how I felt that day. In many ways, that day changed my life. I: How? J: Well, I felt different from other kids, because I had a “disease”. I was constantly reminded of this because I had to take medicine every day. I didn’t like breathing the inhalant as it made my throat dry and smelled funny. But I felt better afterward, so I knew I had to take it. In the beginning, it affected my friendships. I was embarrassed to show my inhalant or take it in front of the other kids, so sometimes I wouldn’t take it at school, even if I felt an attack coming on. I was also afraid to play games like jump rope at recess for fear of bringing on an attack. Exercise and running around often made me wheeze, so for awhile I was afraid to play games outside with the other children. I was lonely and afraid. I: Did things ever get better for you? J: Yes, in an unexpected way! When I was 7, I had a bad case of tonsillitis and while recovering, I had a bad asthma attack. I couldn’t breathe at all. My mom called an ambulance and I was rushed to the hospital. They put an oxygen mask on me which helped right away. I was so relieved to be able to breathe again! I stayed in the hospital for two days. My classmates were told about what happened and everyone sent me cards and get well wishes. When I finally went back to school, everyone applauded when I came in the room. Suddenly, I felt special- I realized that even though I had an illness, everyone still cared about me and accepted me. The experience changed my whole attitude. I no longer hid my illness. I saw that my friends cared about me and wanted me to be well. I appreciated my life so much more after that incident. I became a whole person again! I: How is your life now? J: Well, over the years I’ve had my ups and downs. Asthma is a chronic disease and often lasts for your whole life. I’ve gotten much healthier as I’ve gotten older, but I still have occasional attacks- when I catch colds or when I’m overtired and stressed. These days I only take medication during and after an attack, so I’m not on long-term meds as I was when I was a child. I tend to avoid outdoor exercise in the winter, because it often still brings on an attack. I exercise at the gym and that works out ok for me. I also volunteer at a local pediatric clinic where I often meet with kids recently diagnosed with asthma. When I tell them my story, they often give me a hug. I know it helps them to realize that they’re not alone in this. There are so many people with asthma. We need to help each other. I: Why do you think that there are so many people with asthma? J: I really don’t know. I’ve heard that it has a lot to do with city living and air pollution. Also, smoking is really bad. In my case, I was allergic to milk from birth and had bad eczema. The doctor said that children with eczema are more likely to develop asthma. I’m still very allergic to certain foods and also to pet hair. All these things are predisposing factors. Even though we can’t control our allergies or genes, I think it’s important to make sure that children are not exposed to environmental substances that can trigger this disease. I: Is there anything else that you’d like to say about this? J: I welcome the opportunity to share my experiences. It is important that people with asthma realize that although they have a serious disease that requires careful monitoring, it is not a death sentence. You can live a normal, productive life with asthma, if you take good care of yourself and try to avoid things that trigger attacks as much as possible. Many people get better as they grow older and there are lots of good medicines today to prevent attacks and treat them quickly if they occur. Each case is different, you need to understand your own condition and do the best to keep yourself healthy. You can live a normal happy life even if asthma is part of it. Works Cited Adam Lane, D.J. . The Asthma Sourcebook: Everything You Need to Know New York: Contemporary Books, 1995. Adkinson, N.F., Bochner, B.S., Busse, W.W., Holgate, S.T., Lemanske, R.F., and Simons, F.E.R. ."Chapter 42 - Epidemiology of Asthma and Allergic Diseases - Risk factors for Asthma." Middletons Allergy Principles & Practice. New York: Elsevier, 2008. Jaber, R. “Respiratory and Allergic diseases: From Upper Respiratory Tract Infections to Asthma.” Prim Care. June 2002 ; vol.29, no.2: 231–61. Print. Maddox ,L., and Schwartz, .A. (2002). "The Pathophysiology of Asthma".  Annu. Rev. Med. 2002 vol. 53: 477–98. Print. Saunders , J. "Asthma".  Mason: Murray & Nadels Textbook of Respiratory Medicine, 4th Edition. Eds. Homer A. Boushey Jr. M.D., David B. Corry M.D., John V. Fahy M.D., Esteban G. Burchard M.D., Prescott G. Woodruff M.D., et al. New York: Elsevier, 2005. Read More