Natural Health Nexis
This nhn Emphysema Guide includes information about Emphysema that is written primarily to help Emphysema Patients better understand their condition and the range of Emphysema treatment options that are currently available:
When irritants, such as tobacco smoke or dusts, are inhaled into the lungs they come into contact with the alveoli, causing oxidative damage that triggers an inflammatory response. It is postulated that Cytokines released in association with the inflammation may then be involved in reducing the elasticity of the alveolar walls (Septa), eventually leading to rupture. Despite decades of study, the specific details of causality and pathophysiology currently remain unclear.
Long-term continued exposure to irritants thus leads to accumulation of damage to the alveolar walls so that large cavities, known as Bullae, are formed. Since these Bullae present a lower total surface area for gaseous exchange than the many smaller alveolar spaces in a healthy lung, the ability of the lungs to exchange O2 and CO2 is considerably diminished.
Additionally, since the disease compromises the elasticity of the alveolar septa, inspired air becomes trapped during exhalation, so that the tidal volume of the lungs is decreased.
The resulting inability to absorb enough O2 and release enough CO2 means that the Emphysema patient may not finish breathing out before they feel the need to breathe in. This leads to Breathlessness, which becomes especially apparent with increased activity or exercise.
In late-stage Emphysema patients, the effect of decreased O2 levels and increased CO2 levels often leads to other medical issues including headaches, fatigue, weight loss, muscle wasting, osteoporosis, depression, and heart failure.
In rare cases, a genetic condition called Alpha-1 AntiTrypsin Deficiency may play an additional role in causing COPD. Alpha-1 AntiTrypsin (A1AT) is a natural protein made in the liver, and a statistical link has been drawn between people who produce low levels of A1AT and increased occurrence of Emphysema. It seems that the combination of reduced levels of A1AT and exposure to smoke or other lung irritants can cause aggressively worsening COPD symptoms, and it is estimated that A1AT Deficiency is involved in only ~2% of all Emphysema cases.
Most A1AT Deficient people do not develop Emphysema symptoms. However, it is clear that Smokers with A1AT Deficiency are exposed to a considerable risk of developing Emphysema in the lower pulmonary lobes.
According to the VCU Dept. of Pathology, the combination of Smoking and Severe A1AT Deficiency frequently leads to development of Panacinar (Panlobular) Emphysema, which, affects all portions of the Acini (respiratory bronchioles, alveolar ducts & sacs, alveoli) in the lower lobes of the lungs. Such Panacinar Emphysema can affect patients at a relatively young age, and in such cases, mild Emphysema may often aggressively develop into severe Emphysema over a period of only a few weeks.
In comparison, long-term smokers without A1AT Deficiency usually take a period of many years to contract Centrilobular (Centriacinar) Emphysema, which consists of dilatation of the central structures of the Acinus (respiratory bronchioles & alveolar ducts) affecting the upper lobes of the lungs. In the early stages of this disease, the peripheral portions of the Acinus remain unaffected. However, in the later stages septal damage and dilatation of airspaces may extend to the rest of the Acinus, creating an appearance similar to Panacinar Emphysema, but with areas of patchy dilatation typical of Centrilobular Emphysema.
See also COPD Pathophysiology.
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