Chronic Obstructive Pulmonary Disease, COPD (COAD)

Chronic Obstructive Airways Disease, COAD, changed its name to Chronic Obstructive Pulmonary Disease, COPD, not for reasons of obscurity or exclusivity, but to reflect the way bronchial abnormalities are completely integrated with abnormalities in the surrounding lung parenchyma.

The pathology is related to stiffening and reduction in the elasticity of the lung from destruction or change in the cellular components of the basic pulmonary unit, including the alveaolus and neighbouring tissues. The best way to destroy the fine anatomy of the basic pulmonary unit remains smoking, but continuing escalation of urban ozone and particulate pollution is also popular with some politicians.

Processes, like infection or chemical damage will change the biochemistry of micelles and molecular film physics in alveoli. This may result in cellular destruction or the inward migration of other cells. Additional cellular messengers may be produced, either by cells already present but also by cells like macrophages or "T" cells that have migrated in.

Although initially fairly rigid, the bronchial walls may be destroyed by infection or stretched by changes in the lung and thus be unsupported, when they should stay open in forceful expiration.

The alveolar bronchiolus may lose its flexibility and control of its lumen may no longer be possible.

All of this results in affected airways being wider in inspiration and partially obstructed during expiration.

The alveoli may be partially or completely destroyed by infection and chemical damage so that they do not resist distension by the retained gasses, the condition known as emphysema. Ask any smoker. The diaphragm gets lower and flatter as the end-respiratory volume of the lung increases and this loss of diaphragm efficiency means that the accessory respiratory muscles do more work. Just watch that long-time smoker's shoulders rise with each breath.

The air-spaces in the diseased lung can become very large, since there is no mechanism for air drainage, other than "collateral air drift" through pores between adjacent basic pulmonary units beyond the terminal bronchiole. Inefficient drainage, with the potential lumen of the bronchiole impaired, can produce visible large spaces, Bullae.

Not only does the abnormal lung retain gases that should be breathed-out, but the diseased structure may inhibit gaseous diffusion across the alveolar walls. Low oxygen tension can affect the lung locally, particularly surfactant. A general lowering of oxygen tension may affect control of circulation within the lung or may affect cardiac efficiency. After all, the job of the lungs is to put blood only in the place where carbon dioxide may be exchanged for oxygen. The normal control of circulation in pulmonary disease with altered ventilation / perfusion ratios may affect the expression of various pathologies, pulmonary oedema, for example.

Chronic changes may reduce the sensitivity of the neurological control of respiration. This is especially in those cases where the acidity of retained carbon dioxide no longer stimulates respiration. These people, dependent on the respiratory drive from hypoxia, can be rendered much worse by the administration of oxygen. These "blue bloaters", often in an acute lung infection, if not already with a high flow and impending cardiac failure, retain fluid stiffening their already diseased lungs reducing diffusion of gases and rendering their respiratory mechanism even less efficient.