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Resources » Articles/Knowledge Sharing » Health »
Asthma-Etiology, Environmental, Genetics, Pathogenesis, Cellular immunity
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Asthma
Etiology
Bronchial asthma is common in young people with a history of colds, recurring, or a family history of asthma. Asthma attacks relate to the consumption of certain foods or the presence of certain allergens agents.
The causes of bronchial asthma and motivate response mainly immunological mechanisms are classified as:
• Extrinsic. Started in children with positive family history for allergies and is associated with type 1 hypersensitivity and other allergic manifestations (IgE), induced by agents allergens such as pollen, wool, dust, etc., Or air pollution, irritating materials, changes weather , aspergillosis, and others. In approximately 50% of children with asthma and a lower percentage of adults, exposure to allergens is partially or substantially responsible for the asthmatic inflammation through reactions of hypersensitivity. The crises are sudden, self-limited and brief in duration. Present with good prognosis, response to immunotherapy and steroids long term inhaled through tiny systemic absorption, so that the effects on the rest of the body are virtually nonexistent.
• Intrinsic or idiopathic. It usually begins at age 35 years, and no personal or family history. It is initiated by immunological stimuli, without raising IgE, represented by microbes, fungi, cough, mental disorders, stress, etc..
• Mixed. Combination of nature often bacterial intrinsic and extrinsic factors.
Environmental
Several environmental risk factors that are associated with asthma, yet few have been replicated consistently or that contain meta-analysis of several studies that highlight a direct association. Some of these environmental factors include:
• Poor air quality, pollution caused by automobile or high levels of ozone tend to be repeatedly associated with increased morbidity and asthma have suggested an association with the first occurrence of asthma in an individual.
• Environmental tobacco smoke, especially maternal smoking is associated with an increased risk of asthma prevalence and morbidity including infections respiartorias.
• Viral infections at an early age, along with exposure to other children in day care may be protective against asthma, although results are controversial and that this protection may appear in the context of a genetic predisposition.
• The use of antibiotics early in life may lead to development of asthma by altering the normal microbial flora of an individual, predispose a modification the immune system.
• The Caesarean section tend to be associated with asthma more frequently than the birth vaginally, apparently for reasons similar to antibiotics, ie a modification of the microbial component and the individual's immune born by cesarean section.
• Psychological stress.
• Viral infections. Several viral infections such as HSV, VSV, CSV, have been correlated with various types of asthma
Genetics
It has involved more than 100 genes with asthma, at least in a genetic study. Although the study is still needed to add a component of genetic replication, for 2005, about 25 genes have been associated with asthma in six or more different populations, including GSTM1, IL-10, IL-4, IL-13, CTLA4, CD14, TNF and ß-2 adrenergic receptor ADRB2.
Many of these genes are related to the immune system or modulate the processes of inflammation. However, despite this list of genes and their possible association with asthma, the results are not entirely consistent among different populations, is, these genes are not associated with asthma in all conditions, but the genetic cause of asthma is a complex interaction of various factors.
Pathogenesis
Although it is known that asthma is a condition caused by inflammation (Latin inflammatio, light, a fire) or chronic persistent airway, the precise components of this inflammation are yet to be elucidated and the causes of this inflammation is uncertain . Many inflammatory cells may be involved and interact with others in some complex way. The activation of these cells and the subsequent production of inflammatory mediators may be more significant than the mere presence of these cells in the
This process of chronic inflammation may lead to structural changes such as fibrosis, thickening or hypertrophy of smooth muscle bronchial hypertrophy of glands and angiogenesis that may lead to irreversible obstruction of the airway.
From an emotional standpoint, but has not clarified its cause, is well established that the patient's emotions take a major role in the development of the disease. On a subconscious level can be further developed asthma in infants who come from troubled homes, thus highlighting that stress is the main trigger. Fundamental to the patient with asthma, a life full of care not only in relation to pathogens triggers but also care about their emotional environment for a smooth life stress.
Cellular immunity
Initial studies in patients dying of status asmaticus revealed marked inflammation of the bronchial tree with studies histological tract affected confirm the presence of inflammatory cells of longstanding.
Use of bronchoalveolar lavage has shown that mast cells play an important role as mediators of the immediate response to the allergen, the airway inflammation and hyperreactivity induced by stress and related foods. Other cells responsible for chronic inflammation causing bronchial hyperreactivity are the macrophages, the eosinophils and T lymphocytes, all of them are activated in asthma, even in asymptomatic patients. A line of T lymphocytes, T H 2 cells are programmed to produce certain cytokines that lead to characteristic eosinophilic inflammation. This programming includes antigen presenting cells such as dendritic cells in the epithelium of the airways. Other mediators of inflammation reactions occur such as vascular congestion, edema, increased mucus production, and so on.
About the epithelium bronchial demonstrates increased expression of major histocompatibility complex type II and other infiltrating cells such as monocytes. The clinical severity of asthma has a close correlation with the severity of the inflammatory response, suggesting a complex interaction between these cells and the mediators they generate, such as IL-3, IL-5 and GM-CSF. For example, alveolar macrophages from asthmatic patients produce twice as much GM-CSF in non-asthmatics. The IL-4 and interferon-gamma are important elements on the biosynthesis of IgE.
Disclaimer: Please consult a medical practitioner before using sensitive information. Neither the site nor the author will be responsible for losses or damages resulting out of the use of this article.
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