Asthma
Asthma
Asthma is a medical condition which causes inflammation and narrowing of the air ways. It causes wheezing that recur, shortness of breath, coughing which occurs early in the morning, or at night, and chest tightness. This condition affects all ages and often starts during childhood.
Pathophysiological Mechanisms of Chronic Asthma and Acute Asthma Exacerbation
Asthma is characterized by recurrent limitation of airflow due to a variety of changes in the airways. These changes include; airway hyper-responsiveness, edema, airway remodeling, and broncho-constriction. Broncho-constriction is the major physiological process that leads to clinical symptoms, and results in interference with the air flow. Broncho-constriction simply means narrowing of the bronchi. In acute exacerbations of asthma, broncho-constriction occurs very quickly and narrowing the airways and it is stimulated through exposure to various stimuli, which include irritants or allergens. Mast cells release IgE dependent mediators, for example; tryptase, prostaglandins, histamine, and leukotrienes. These molecules are responsible for allergen induced acute broncho-constriction. In some patients, aspirin and other anti-inflammatory drugs, which are nonsteroidal, can, also cause acute broncho-constriction. In some patients; exercise, irritant, and cold air are other stimuli for acute air flow obstruction. Also, stress may be the contributing factor to asthma exacerbation.
As the disease persists and inflammation progresses, airflow is further limited by other factors, which include; mucus hypersecretion, edema, inflammation, formation of mucus plugs, which are inspissated, and also structural changes such as hyperplasia of the smooth muscle, and hypertrophy, which may not respond to the usual treatment. Airway hyper responsiveness is an exaggerated response by the broncho-constrictor to a wide variety of stimuli. This is the major feature of asthma. Anti-inflammatory treatment can improve control of asthma as they can reduce hyperresponsiveness. In some asthmatic patients, permanent structural changes can occur in the airway, and can lead to a progressive lung function that cannot be reversed or prevented by the current therapy. It involves the activation of many structural cells, which result in permanent changes, in the airway, increasing airflow responsiveness and obstruction and makes the patient respond less to therapy. The structural changes which occur can include sub-epithelial fibrosis, thickening of the sub-basement membrane, blood vessel dilation and proliferation, and mucus gland hypersecretion and hyperplasia. The process of repair and regulation is likely to be the cause of the persistent nature of the disease and its limitation to response to therapy.
Inflammation plays a big role in the development of asthma. Inflammation occurs when there is interaction of cell of many types and multiple mediators with the air ways, which results in pathophysiological characteristics of the disease. The features include; airflow limitations, bronchial inflammation, that result in persistent cough, shortness of breath, and wheezing. These interactive events occur in unknown processes that lead to bronchial asthma.
Inflammatory cells are exhibited in asthma. Lymphocytes subtypes T helper 1 cells and T helper 2 cells have distinct inflammatory mediator profiles and have effects on the functioning of the airway. The variation in the number of the T lymphocytes gives information about inflammation reaction. A long with other airway cells, T lymphocytes can determine the development of remodeling, and the degree of remodeling. Mucosal mast cells activation releases mediators of broncho-constriction, which include; cysteinyl-leukotrienes, histamine, and prostaglandin D2. During acute exacerbations, and in the presence of smoking, an asthmatic person has an increase in the number of neutrophil in the sputum and the air ways. Dendritic cells are cells which act as key antigen presenting cells, and interact with allergens in the airway surface, and regulatory cells in the lymph region to stimulate the ultimate production of Th2 cells from the desensitized T cells. Allergens can activate macrophages using the low-affinity IgE receptors to release mediators of inflammation, and the response amplifying cytokines. The airway smooth muscles cell activation, proliferation, hypertrophy, and contraction can lead to airway dysfunction of asthma. Epithelial cells of the airway lining are critically being involved critically in asthma. Production of inflammatory mediators, activation, and recruitment of inflammatory cells or even respiratory viruses infection, can cause epithelial cells produce more mediators of inflammation to destroy the epithelial itself.
Implication of Inflammation for Therapy
Inflammatory processes have been used to develop therapies which are targeted at interrupting the processes of inflammation. This is based on the recent scientific research and developments, some of which have yielded good results, for example, development of anti-IgE monoclonal antibody therapy and leukotriene modifiers. The studies also indicate that subtypes of asthma exist; these phenotypes require a different approach of treatment. Novel therapies targeted at the chemokines, cytokines, and the inflammatory cells are being investigated, for instanceTh2 inflammatory pathway inhibiting drugs, may have a wide spectrum of effects, for example, the airway.
Reference
Kathryn L., (2010), Pathophysiology, The basis for Disease in Adults and Children. Retrieved from,http://books.google.co.ke/books?id=cChAPgAACAAJ&dq=inauthor:%22Kathryn+L.+Mccance,+Ph.d.%22&hl=en&sa=X&ei=bsvbUPWbOpCJhQel1oDwBQ&ved=0CDoQ6AEwAA On December 27, 2012.
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