Chronic Obstructive Pulmonary Disease (COPD)

COPD is a chronic, slowly progressing disease characterised by a persistant limitation to airflow that varies very little. COPD is used to describe a spectrum of diseases that includes:

1. Chronic Bronchitis
2. Emphysema
3. Chronic Asthma that has stopped responding to treatment
4. Small Airways Disease.

COPD is classified according to its severity:

1. Mild COPD

   A clinical diagnosis is given where there is a productive cough on most days for three consecutive months in two successive years. This can be labelled Simple Bronchitis, and is characterised by excessive secretion of bronchial mucus with little airflow obstruction (Tortora, 2000).

   The single most important cause of COPD is cigarette smoking. Active smoking causes mucus hypersecretion and a decline in lung function (Barnes, 2001). Air pollution, occupational exposure to dust, fumes and solvents, and repeated chest infections have also been implicated. Inhaled irritants lead to chronic inflammation of the lung lining which stimulates the mucus glands to enlarge and multiply. Therefore more mucus is produced, which serves to narrow the airways and inhibit ciliary function (Tortora, 2000).

   Clinical features of mild COPD include a smoker’s cough and mild dyspnoea with no other abnormal signs. Early COPD is detectable only by carrying out a lung function test using a spirometer (Bellamy & Brooker, 2000).

2. Moderate COPD

   Follows the same pathway as mild COPD, and can be called Chronic Bronchitis (Bellamy & Brooker, 2000). It is characterised by excessive secretion of bronchial mucus with some airflow obstruction (Tortora, 2000).

   In moderate COPD the cilia are destroyed trapping the mucus, which may become infected therefore preventing oxygen from diffusing into the blood (Halpin, 2001). The infected mucus may attract an immune response, which unfortunately aids in the destruction of the walls of the alveoli.

   Clinical features of moderate COPD include a productive cough, thickened sputum, and dyspnoea on exertion with some abnormal signs. Examination of the chest may show it to be slightly hyperinflated i.e. the diameter of the chest is slightly enlarged, and wheezing noises may be heard (Halpin, 2001).

3. Severe COPD

   Again is a progression of mild and moderate COPD, and can be called Emphysema. It is characterised by excessive secretion of mucus, severe airflow obstruction and widespread destruction of the alveolar walls (Barnes, 2001).

   Repeated chest infections cause a battleground effect in the alveoli. The leukocytes involved in the immune response die and as the excessive mucus is blocking access to the blood stream they remain in the alveoli. As the leukocytes die they release an enzyme that destroys the alveolar walls producing abnormally large airspaces. These abnormal airspaces remain filled with air during expiration and so reduce the lung capacity. They also have a reduced surface area available for oxygen diffusion (Halpin, 2001).

   Clinical features of severe COPD include a productive cough, thickened and purulent sputum, and breathlessness on any activity. Findings upon examination of the patient with severe COPD may include: hyperinflation of the chest (causing it to look barrel shaped), wheezing and peripheral oedema (Halpin, 2001).

   Traditionally patients with severe COPD are divided into two categories:

   • Blue Bloaters – Cannot get enough oxygen into their system (hypoxaemia) and cannot get carbon dioxide out (hypercapnia). This places a strain on their heart and they develop peripheral oedema (Halpin, 2001). The ‘blue’ derives from the cyanosed appearance of these patients, while ‘bloater’ comes from the large body build.
   • Pink Puffers – suffer from extreme dyspnoea (breathlessness) and so increase their ventilation. This helps them to maintain their normal carbon dioxide and oxygen levels, however it is very exhausting. The ‘pink’ is derived from the reddish appearance of the patient due to the exertion of breathing. While the ‘puffer’ refers to the breathlessness and panting respiration.

References

Barnes, P.J. (2001) Managing Chronic Obstructive Pulmonary Disease. London. Science Press.

Bellamy,D. & Brooker, R. (2000) Chronic Obstructive Pulmonary Disease In Primary Care. London. Class Publishing.

Halpin, D.M.G. (2001) COPD. London. Mosby.

Tortora, G.J. & Grabowski, S.R. (2000) Principles Of Anatomy And Physiology (9th Edⁿ). New York. John Wiley & Sons Inc.

It all boils down to a choice, the choice between vigorous smoking or vigorous fucking. "What choice", I hear you yelling, "I do both!" For a while you do, sure. But then COPD sets in. And you find that you made your choice long ago - vigorous smoking is suddenly your only remaining alternative. Because you now have COPD - Chronic Obstructive Pulmonary Disease.

This is how it works:

Cigarette smoke attracts inflammatory cells into the lungs, from the surrounding body. These cells start releasing an enzyme, ELASTASE, which evolution has devilishly designed to break down Elastine, the nice structural material of lung tissue. But don't despair -- evolution also gave us an ELASTASE inhibitor, AAT (alpha-1 antitrypsin). So the lungs should be safe from the effects of the evil ELASTASE, protected as they are by AAT, right? Well, yes -- sort of. Normally, yes, of course. But if you smoke a lot, then the number of inflammatory cells that smoke attracts -- each of them releasing its own dose of evil ELASTASE, remember -- gets unmanageably large. And so the total amount of ELASTASE becomes far too large for the available AAT to handle.

A different kind of SOB

The result is that uninhibited evil ELASTASE starts breaking down your nice Elastine and thus dangerously weakens your lung tissue. In combination with mechanical stresses from coughing (never heard of "smoker's cough"?), the walls between the individual alveoli break down and larger cavities form. The total surface area of these larger cavities is much smaller than that of the original alveoli. Because of the reduced contact area between the air in the lungs and the blood stream, the blood can no longer take up as much oxygen as it needs, leading to a terrible SOB. Unfortunately, in medical parlance SOB doesn't mean Son Of a Bitch. Rather, it is short for Shortness Of Breath. If it gets short enough, it will kill you. Until then, it makes all ordinary physical activity difficult or impossible - preventing you from running, climbing stairs sprightly, fucking vigorously. The sum total of this particular misfortune is called Emphysema.

Package deal

Emphysema seldom comes alone. It usually comes packaged with Chronic Bronchitis. To you Chronic Bronchitis means that the walls of the small air pipes (bronchi) in your lungs are constantly inflamed. The inner lining of the pipes starts producing mucus, so much of it that the airways become partly clogged and narrowish. OK, but there are small waiving hairs, cilia, which wave unwanted stuff away from the airways! And Macrophages, which eat toxins and all kinds of pulmonary trash! Past tense please - there ONCE WERE cilia and macrofages. These have long since been inactivated by the toxins from all that cigarette smoke and / or pot that you inhaled with such pleasure.

So here you are, presented with a nice package of COPD, combining emphysema and chronic bronchitis. You can't do anything about it. There is no way to recover what is lost. And the degradation continues unyieldingly, whether you stop smoking or not. Of course, if you stop, then the rate of degradation decreases.

Not getting the message

COPD is not an odd freakish little disease that leaves most people alone. It's in fact the fourth commonest cause of death in the Western world. Only it has not been correctly diagnosed, until fairly recently. Lung cancer, undeservedly, took all the headlines. But COPD is much, much, much more common. True, not all smokers get it, some seem to have genetic protection against COPD. But uncomfortably many don't get it -- the message -- so they get COPD.

In my case I made my choice in the nick of time. I still have 75% left of my lung function, so I can yet moderately vigorously practice this other thing, the thing you are able to do when you are not vigorously smoking. And for some curious reason my red blood cells and their haemoglobin have grown much more efficient since I quit smoking, so the sum total of my bad lungs and my good blood amounts to the equivalent of 87% lung capacity.

Reference:

General COPD information: http://www.lung.ca/copd/

British site with COPD statistics: http://www.priory.com/cmol/copd.htm

Boeringer (pharmaceutical company with COPD relief drugs): http://www.airwavesonline.com/

A COPD patient informs: http://www.copdadvocate.com