Chronic Obstructive Pulmonary Disorder (COPD)

Definitions Old and New

• Originally, COPD was defined as a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema.
• The new definition from the Global Initiative for Chronic Obstructive Lung Diseases (somehow the acronym is GOLD…pretty convenient, dropping a few letters there, don’t you think?) is:
  • A disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
  • This definition de-emphasizes the disease processes focused on in the first definition (emphysema and chronic bronchitis).
    • This is because both diseases are commonly seen together with components of both affecting a single patient. Sometimes airway hyperreactivity (asthma) can also be seen).
• Of course, even though they are almost always seen together. However, we will look at each problem separately…
  • Chronic bronchitis is defined as a chronic productive cough for 3 months in each of 3 successive years when other causes of chronic cough have been excluded.
    • The last part of that definition is important. Lots of other things can cause chronic cough like smouldering TB or a benign irritating tumor. These all must be ruled out before a diagnosis of chronic bronchitis can be made.
    • Also, some gunner from a couple years ago made a stink during this lecture because he had read that you only needed a chronic productive cough for two years not three. Time is not specific. It’s a long-standing cough and that’s about all you need to worry about.
  • Emphysema has a more concrete, pathological definition. There’s none of this year ambiguity we had with chronic bronchitis. It is an abnormal, permanent enlargement of airspaces distal to the terminal bronchioles.

Epidemiology and Risk Factors

• For a long time COPD “got no respect”. However, it is a very significant problem
• Somewhere between 10 and 25 million people have chronic bronchitis.
• Around 1.65 million have emphysema.
• There has been a 42% increase in the numbers of people with COPD since 1982.
• COPD is the 4^th leading cause of death in 1991 and 2002.

• The number one risk factor for COPD is smoking (definitely active smoking, but “passive” or second-hand smoke is probably also a risk factor).
  • So for all you smokers out there, please stop…please?
• Air pollution seems to predispose individuals to COPD.
  • COPD can be reproduced in animals by exposing them to air pollutants found in large cities.
  • Living in urban centers (with high air pollution) seems to increase risk.
• Hyperresponsive airways are found in patients that have responses to environmental triggers that normally would not cause problems (cold air is an example).
  • If you have hyperresponsive airways and you smoke you have an even greater risk of developing COPD.
• Genetic factors are also thought to play a role. One gene has been isolated so far.
  • Alpha 1-antitrypsin deficiency will lead to COPD.
    • It alters the balance between proteases and protease inhibitors in the lungs
    • Proteases are triggered by inflammation of airways and alpha 1-antitrypsin turns these proteases off before they damage the lung tissue itself.
  • While genes may play a role, only 1% of COPD patients have a protease inhibitor deficiency so there are other significant factors like those mentioned above.
  • A patient with early onset of COPD (in their 40’s perhaps) or with a family history of COPD may indicate a genetic mutation.

Clinical Features of COPD

• As mentioned above, most people with COPD are smokers.
  • On average, these smokers have at least a 20 pack year history (1 pack per day for 20 years or 2 packs/day for 10 years, etc).
• COPD usually presents in the 5^th decade of life with a productive cough or acute chest illness.
  • Often, the presentation is a cough that is worst in the morning.
  • Many smokers downplay this symptom, saying it is just “smoker’s cough.”
• By the 6^th or 7^th decade, dyspnea upon exertion is present and this is a less easily ignored symptom that will bring patients to the doctor.

A Comparison of Chronic Bronchitis and Emphysema Patients

• Keep in mind that patients will typically present with some symptoms from both diseases. It’s a spectrum and this will show you the opposite ends.

• Tom Petty (a pulmonologist, not the singer) described emphysemics as “pink puffers” because of their lack of cyanosis and their difficulty breathing.
• “Blue bloaters” are chronic bronchitics because they are cyanotic and overweight.

• Above is a picture of two patients. The one on the left has chronic bronchitis; the one on the right has emphysema. And for some reason they’re showing a little skin. Maybe they’re getting ready for a three legged man race?
• Thinking back to our case study, the man is predominantly emphysemic.
• On a CXR other differences can be seen.
  • Emphysemic patients will show evidence of hyperinflation, bullous changes like a narrowing of the heart, and in general just a smaller heart.
  • Chronic bronchitic patients show increased markings at the base of the heart and a larger heart in general.
• Pulmonary function test (PFT) results also differ.
  • Emphysemics will have mildly decreased air flows, relatively high PaO2 and low PaCO2 (until late in the course of the disease), and a decrease in diffusing capacity.
    • Decreased diffusing capacity refers to a loss of capillary beds and alveoli within the lung, making it harder to absorb oxygen.
  • Chronic bronchitics will have moderate to severe air flow decreases, low PaO2 and high PaCO2, and normal diffusing capacity.
    • Bronchitics retain CO2, decreasing the amount of oxygen that can get in and contributing to their early cyanotic appearance.
    • Ventilation – Perfusion mismatch causes cyanosis. Both have mismatch from various problems, not just diffusing capacity. Chronic bronchitics just have more mismatch.

Therapies for COPD

• Stop smoking!
  • It’s better to stop before COPD begins, but even after diagnosis, quitting can slow the progression of the disease.
• Limit damage from new lung infections.
  • Remember that inflammation will lead to further lung destruction, particularly in those with hyperreactive airways.
  • Treat acute cases of bronchitis aggressively with antibiotics.
    • There’s some controversy here because a lot of bronchitis is viral, so Dr. Marin compromised and said that once you’re sure that the infection is bacterial, treat it very aggressively.
• The major problem of COPD is airway obstruction (shocking, I know), so maybe we should try to treat that?
  • Mucolytic agents haven’t been very useful so far. There is a search for new drugs at the moment, but breaking up the mucus that builds up in these patients would decrease obstruction.
  • Bronchodilators, particularly β2 agonists, anticholinergics, and theophylline are all used.
    • Theophylline is used less than the first two for reasons that will be discussed in the asthma drugs lecture.
  • Anti-inflammatory agents are also good for acute problems, but are not recommended for long-term use.
• Treat hypoxemia with supplemental oxygen.

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