Symptoms and genetic aspects of Bronchitis and Emphysema
A simple cough mustn't be ignored. If this cough transforms into a persistent productive cough with an excessive airway mucus secretion we can think that it is bronchitis. if the process becomes chronic and the cough and sputum persists for minimum three or six months during one or two years with very short periods in which the cough disappears, the diagnosis is sure. All this symptoms leads to the diagnosis of Bronchitis, a disease of the lungs from the COPD category. In Bronchitis the large and small airways can be obstructed and it becomes very difficult to move air in and out of the lungs.
Another aspect is the deficiency of alpha-1-antitrypsin. This deficiency is caused by the loss of elastin which is a structural protein. All this leads to Emphysema. Because elastin is involved in the maintenance of the strength of the alveolar walls, in Emphysema there will be a permanent destruction of the alveoli.
There is a form of Emphysema influenced by a long period of smoking called "Smoker's Emphysema". It develops usually in older patients. Another type of Emphysema is the one with a hereditary transmission. In this case there is a deficiency of alpha-i-antitrypsin (AAT), but just one to three percent of all cases of Emphysema are due to AAT deficiency. This happens because in the lungs, at cells level there is an imbalance between elastin and AAT. The reaction between this two proteins is mediate by an enzyme called elastase. When there is a genetic deficiency of AAT the elastin degradation occurs unchecked. This phenomenon is worsen if the patients with genetic deficiency of AAT smoke and the symptoms appears early middle age. The deficiency of ATT is detected by blood tests made in specialized laboratories.
Regarding Smoker's Emphysema and the hereditary one studies showed that in the lungs cells the mechanism is the same. One of the tobacco smoking effects is the elastese-AAT imbalance. The explanation is that smoking stimulates excessively release of elastase. There was also confirmed the theory that the inhaled smoke stimulates the migration in the lungs of the elastase producing cells. Another aspect of smoking is the effect of the oxidants from the cigarette smoke. The antioxidants inactivate a significant portion of the elastase inhibitors and as a consequence it is upsetted the elastase-antielastase balance. But there are also other factors in addition to smoking effects that influences the development of Emphysema. Nowadays the effect of these other factors is not very clear. There was estimated that only twenty percent of smokers develop Emphysema.
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