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Chronic Obstructive Pulmonary Disease

COPD is defined as the presence of airflow obstruction due to chronic bronchitis or emphysema. It may include a reversible component and some patients with asthma may go on to develop irreversible airflow obstruction and be included in chronic obstructive pulmonary disease, emphysema, bronchitis, emfasema, empasema

Chronic bronchitis is defined as chronic productive cough for three months in each of two successive years when other causes of chronic cough are excluded. That includes gastroesophageal reflux disease, asthma or something like that. Emphysema is defined as abnormal permanent enlargement of air spaces distal to the terminal bronchioles. This is an airways disease, this is an alveolar disease. So that is the anatomic distinction between chronic obstructive pulmonary disease, emphysema, bronchitis, emfasema, empasema

The risk factors for COPD. Smoking is the most common risk factor. Passive smoking in a few patients, ambient air pollution has been implicated. We talked about hyperresponsive airways such as asthma. Gender and race, there is poor data to support these as risk

I wanted to discuss the relationship of smoking, FEV-1 or lung function and age. This graph essentially summarizes that relationship. On the y-axis you have FEV-1 lung function and age on the x-axis. It is well-known from multiple studies that FEV-1 in everyone declines from generally about age 20-25 throughout the rest of their life. In smokers, that rate of decline is much more rapid than in the normal

Most of the data I showed you on the slide comes from the Lung Health study which looked at smoking cessation and COPD. What they looked at is smoking intervention versus ipratropium four times a day. Ipratropium is Atrovent versus a third group which had

The bottom line here is that smoking cessation should be encouraged at any age to enable those patients to resume the normal rate of less rather than the accelerated loss if they continue to smoke.

These are some of the things that we use to enhance smoking cessation. We have known for a long time that behavioral approaches are probably one of the best things that we can use to get people to stop smoking. First of all, the doctor has to tell them to quit smoking

Who you should screen if you suspect alpha1_antitrypsin deficiency? These presentations should raise your suspicions and prompt investigation. COPD in a never smoker. Very important that they were a never smoker, not a little smoker. Bronchiectasis without risk factors. Chronic sputum production without evidence of frequent infections or things that would predispose to bronchiectasis. Premature onset of emphysema. We talked about the early age. Predominance of basilar emphysema on chest x-ray. That is the

For patients with mild to moderate disease, we usually start with a selective beta-2 agonist mainly because it has a rapid onset of action. It relieves the patient’s shortness of breath and that is why they came to see you in the first place. The problem is that if they are using it fairly frequently and this is what you need to ask them, it has more side effects than ipratropium or Atrovent and that may be an indication to add additional therapy. If you had the ipratropium or the atrovent, they can use the beta-2 agonist as needed and that may be sufficient to keep them under pretty good control. If their symptoms are uncontrolled or they complain of a lot of nighttime symptoms – they wake up, they have lots of cough, etc – you may want to add theophylline in a slow release tablet either twice a day or at bedtime or you can use salmeterol which is the long acting beta agonist, 2 puffs twice a day. Either will help control

This is a list of the beta agonists. These are the specific beta-2 selective agonists on the top here. Below the line, these are the nonselective so we will have much more cardiac effects than you probably want in this age group. I just want to call your attention here to the equivalent metered dose inhaler puffs which will give you this same dose that you would be giving by nebulization. So you would have to use 27 puffs of the metered dose inhaler albuterol in order to get an equivalent dose or 2.5 mg of albuterol that you would

Talk about anticholinergics. Ipratropium bromide or atrovent is the only one approved. The dose in stable COPD patients is 0.5 mg. In this range, the duration is 6 to 8 hours. This was in a large study in stable COPD patients. Oxytroprium is available in Europe. It is not available in this country. Teotroprium is a longer acting anti-cholinergic. It is a twice a 

The side effects of anticholinergics, especially inhaled anti-cholinergics, are low due to the low systemic absorption from the lungs. It reduces mucociliary clearance but it has no effect on unstimulating mucus so it is not going to change how much mucus production your chronic bronchitis patient produces on a daily basis. It may have a bitter taste. Some patients who have sprayed it into their eyes exacerbate their glaucoma problems. Paradoxic bronchoconstriction is a problem with the anti-cholinergics. Any time you spray a

Anti-inflammatory therapy, mainly the steroids is what I am talking about. Routine anti-inflammatory therapy is not indicated in most

In COPD, a minority of stable COPD patients will improve their FEV-1 given steroids. In numbers of studies that have been done, regardless of what you set as your threshold for improvement in FEV-1, be it 15%, 20%, 30%, whatever you select, in that patient group when studied steroids versus placebo, only about 10% of the patients will improve their FEV-1 to the threshold that you have

Antibiotics. These three symptoms are the cardinal signs for using antibiotics in a patient with COPD. Increased shortness of breath,

As I said earlier, Hemophilus influenza is a common bacteria associated with exacerbations of COPD. Moraxella catarrhalis and Strep pneumonia are also common pathogens. These are antibiotics which are effective. Mycoplasma and chlamydia may also be pathogens

Let’s move on to theophylline. Theophylline has significant benefits listed here. The problem is it has significant risks – narrow therapeutic window, lots of GI problems and variable metabolism interaction with other medications. If you are going to use

Mucoactive agents, I will tell you there aren’t any that really work very well except for alpha-dornase. This is the DNAase that we use in cystic fibrosis patients. It works very well in those patients. They had to stop the study in the chronic bronchitis patients because there was an increased mortality that was unexplained. So we do not use it in our chronic bronchitis patients. Acetylcysteine has been

I wanted to call your attention to we are going to move in exacerbations briefly here but I wanted to call your attention to this trial. The Support Trial was an NIH funded study on the outcomes of exacerbations of COPD and a number of other things. All the data about PA catheters increasing mortality in patients comes from this study. A very important study. Basically they looked at these patients with

Continuous nebulization has not been established as safe. It is probably effective but has not been established as safe. You have to be very aware, especially with continuous nebulization that beta agonists in large doses, especially inhaled, will drop potassium levels

We talked about ipratropium, we talked about the dose. Again, ipratropium is very effective but two puffs every three hours in

I’m going to move on to combination therapy. You’ve heard about the new inhaler with atrovent and albuterol in it. It has been shown to have some synergistic effect when used in stable COPD patients but in exacerbations, in numerous studies, there is no greater

I’ll quickly talk about corticosteroids for exacerbations. Is the patient likely to benefit and what is the appropriate dose. In stable COPD, the lower the FEV-1 the greater the likelihood of response to steroids. So the patients with the worst disease are probably going to be more likely to respond to steroids. There is very little data available on acute exacerbations. These are the only four studies looking at steroid doses in exacerbations of COPD.

On the next slide, these are the recommendations. For mild exacerbations, not requiring hospitalization defined as this, oral prednisone with a rapid taper is probably beneficial. These are outpatients. So if you have an exacerbation, prednisone will probably work to stave off hospitalization. In patients who need to be hospitalized with moderate to severe exacerbations, defined by these parameters, a short

The last couple of slides I’m going to talk about the surgical options for COPD. Lung volume reduction surgery which everyone is talking about is resection of discrete emphysematous regions of the lung, performed via thoracotomy or thoracoscopy and done either

I’m going to finish up with lung transplantation. In your handout you have the criteria for transplantation. Transplantation is an option for patients with COPD under the age of 65. It is very effective in these patients. We have very good survival data on these patients out a