Asthma. Pathologic basis of disease - Research Paper Example

? ASTHMA Institute Asthma Asthma is a chronic inflammatory disease of air passage. Asthma causes recurring episodes of breathlessness, chest tightness, wheezing and cough. The episodes mostly occur at night or early in the morning. Due to the inflammation of the airways, the airways become more prone to constriction on stimulus. The constriction of the airways on stimulus limits the airflow to lungs and due to scarcity of air these symptoms occur. The patient suffering from asthma experience attacks of dyspnea, coughing and wheezing. Dyspnea is the shortness of breath or air hunger. The bronchospasm is the major cause of dyspnea. Asthma can be divided into different groups on the basis of severity of attacks that are mild intermittent, mild, moderate and severe persistent asthma. But typically the asthma is classified into extrincsic asthma and intrinsic asthma. Extrinsic asthma is set off by type 1 hypersensitivity reaction caused by an extrinsic antigen. Intrinsic asthma is initiated by various mechanisms including pulmonary infections caused by viruses especially, cold, stress, exercise and inhaled irritants. Some categories classify asthma in accordance to the agent that causes the constriction of air passages for example seasonal asthma, exercise asthma, occupational asthma, drug induced asthma and asthmatus bronchitis. The genetic susceptibility to type 1 hypersensitivity, chronic inflammation and bronchial hypersensitivity are the major factors that cause asthma. Our immune system contains Type 2 helper T cells (Th2) which is type of CD4+ helper T cell secretes interleukins. The interleukins then promote allergic inflammations and stimulate B cells to produce IgE and different antibodies. Type 1 helper T cells (Th1) are also a type of CD4+ helper T cell which secretes interferon-? (gamma) and intereukin-2. The interferon-? (gamma) and interleukin-2 activates the macrophages and cytotoxic T cells which kills the viruses and other invading organisms. These two types of helper T cells form an immunoregulatory loop that is the cytokines from type 1 helper T cells inhibit type 2 helper T cells and cytokines from type 2 helper T cells inhibit type 1 helper T cells. These two types of helper T cells respond to different immunogenic stimuli and try to destroy them. Any imbalance in the regulatory loop of these two types of helper T cells makes it easier for the viruses and agents to attack the bronchopulmonary tree and cause inflammation which leads to asthma. In patient suffering from hypersensitivity as occur in asthma, when an antigen is presented to the skin, a wheal and flare reaction occurs. This wheal and flare reaction is clear example of hypersensitivity type 1. In air passages when the allergen reaches the epithelial lining it stimulates the induction of type 2 helper T cells (Th2). The type 2 helper T cells secrete various cytokines such as interleukin 4 (IL-4) and interleukin 5 (IL-5). The interleukin 4 (IL-4) then triggers the production of immunoglobulin IgE by the B cells and promotes the growth of mast cells. The interleukin 5 promotes the growth and activation of eosinophills. The reaction mediated by IgE to the allergens elicit an acute response and late phase reaction. The acute response to the allergens consist of bronchoconstriction, edema, mucous secretion and in rare cases the decrease of blood pressure. The acute response occurs by this mechanism; the contact of antigens to the mast cells stimulates the secretion of mediators which mediate the reaction. In the case of air passage diseases when the allergens reach the mucosal surface, the reaction of allergens first occurs with the mucosal mast cells. In this reaction mediators are secreted which opens the tight junction in between the mucosal cells and improve the entrance of the antigens to the submucosal mast cells. This reaction causes the broncoconstriction, edema and mucous secretion which is acute response. Vagal stimulation in lungs also called bronchoconstriction. Mast cells secrete IL-5 which initiates the influx of neutrophils, monocyte and eosinophills. These cells cause the late phase reaction which starts after 4 to 8 hours. The late phase reaction may continue for 1 day or more. Atopic asthma is the most common type of asthma. Atopic asthma usually begins in childhood. In atopic asthma the environmental antigens enhance the disease such as dusts, pollens and animal dander. Patients suffering from atopic asthma have positive family history of atopy. Atopy is the genetic predisposition to type 1 hypersensitivity. Sometimes eczema, allergic rhinitis and utricaria occur before the asthmatic attacks. Eczema is a skin disease which includes rashes, weeping and peeling of skin. Utricaria is reddish swelling of skin also called hives. The genes in which the hypersensitivity type 1 occurs are those genes which perform some of our immune functions. The hypersensitivity type 1 may occurs in the genes that are involved in antigen presentation, T-cell activation, cytokines production, regulation and functions of various cytokines. Nonatopic asthma is that type of asthma which is caused by respiratory tract infections. Viruses are more effective in causing nonatopic asthma than bacteria for example rhinoviruses, parainfluenza virus. In nonatopic asthmatic patient the serum immunoglobulin IgE level is normal. In patient suffering from nonatopic asthma the skin test for determining hypersensitivity is generally negative. Other air pollutants such as sulfur dioxide, ozone and nitrogen dioxide cause air passages inflammation and their hyperreactivity when inhaled. Drug induced asthma is the kind of asthma which is caused by the hyper reactivity to some drugs. Aspirin is a drug which is usually given after heart attacks to decrease the viscosity of blood so that the blood tendency to clot is reduced. Some patients are extremely sensitive to aspirin. If a small amount of aspirin is administered to aspirin sensitive patient, the patient experience severe asthmatic attack and utricaria as well. This is called aspirin sensitive asthma. In aspirin sensitive asthmatic patient it is possible that the aspirin inhibits the cylclooxygenase pathway of arachidonic acid metabolism without interrupting lipooxygenase pathway. As a result the bronchoconstrictor leukotrienes are released which cause asthma. Occupational asthma is another type of asthma which is triggered by fumes, organic dusts, chemical dusts, gases and other chemicals. After many times exposure to these chemicals and dusts, small amount of these chemicals are capable of stimulating asthma causing bronchoconstriction and hyperreactivity. Asthma is a pathological condition which can be treated by medical therapy as well as physical exercises and education. A research carried out by Weisgerber and his colleagues presented the fact that asthmatic children who were placed on different levels of exercise obtained benefits from performing exercises and there was an improvement in their living with a decreased severity of symptoms accompanied by reduced number of attacks. The aim of physical activity in the treatment of asthma is directed towards increasing the efficiency and working of the cardiovascular as well as the respiratory system. It is also aimed towards providing better breathing training to the patients and decreases the severity of the attacks of breathlessness. Proper physical activity programs will hence enhance the living standards of the patient and improve their performances. The level of the activity is chosen according to the age and severity of asthma that the patient has. The younger patients are more often kept on moderate exercise patterns as compared to the older age groups. The duration is also varied for the physical activity according to similar strategies. Exercises include regular cycling, walking or swimming. The patients can also be encouraged to carry out regular activities in home like cleaning or other household chores. These activities serve to be very beneficial for the patients. The patient with mild asthma needs only bronchodialators inhaler occasionally example albuterol. If the patient requires this therapy more than two times a week and if the nocturnal symptoms appear more than two times a month then the patient is treated with leukotriene receptor antagonist eg montelukast. Nowadays theophylline is given to that patient in whom the symptoms are not controlled in spite of treatment with anti-inflammatory inhaled agent regularly. If the asthmatic symptoms occur repeatedly then inhaled corticosteroids should be used to treat the patient. Some people do not want to use corticosteroids due to the corticosteroid toxicity and this state is known as steroid phobia. To prevent the issue of steroid phobia the patient is given cromolyn by inhalation or leukotriene receptor antagonists orally. Both the treatments are less effective than corticosteroid therapy but still they are used. In chronic severe asthma the patient is treated by anti IgE antibody. ReferencesTop of Form Kumar, V., Abbas, A. K., Fausto, N., Robbins, S. L., & Cotran, R. S. (2005). Robbins and Cotran pathologic basis of disease. Philadelphia: Elsevier Saunders.Bottom of ForTop of Form Katzung, B. G. (2006). Basic & clinical pharmacology. New York: McGraw-Hill Medical. Top of Form Lenz, T. L. (2008). Lifestyle modifications in pharmacotherapy. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Bottom of Form Top of FormWeisgerber, M., Meurer, J., Berger, S., Webber, K., Danduran, M., & Flores, G. (December 01, 2008). Moderate and vigorous exercise programs in children with asthma: Safety, parental satisfaction, and asthma outcomes. Pediatric Pulmonology, 43, 12, 1175-1182. Bottom of Form Bottom of Form Read More