Chronic obstructive pulmonary disease, or COPD is characterized by obstruction of airflow due to either inflammation of the airways, or chronic bronchitis, and destruction of the alveolar wall with dilation of the airspaces, or emphysema.
These events are due to inflammation that’s often triggered by inhalation of toxic substances, like tobacco smoke, as well as occupational pollutants like dust and silica.
Most people have elements of both chronic bronchitis and emphysema, so they’re often clumped together under the term COPD.
Alright, now chronic bronchitis is characterized by an inflammatory process that leads to increased mucus production, which obstructs the airways and leads to air trapping behind those mucus plugs.
Chronic bronchitis is clinically defined as having a productive cough for more than 3 months each year for 2 or more consecutive years.
Now, zooming in for a moment, the body maintains a balance between elastases, which destroy elastin in the alveolar wall and respiratory bronchioles, and anti-elastases, which stop elastase from doing just that.
In emphysema an inflammatory response to tobacco smoke tips the balance towards elastases, causing excessive destruction of the alveolar wall.
Without elastin, the elastic recoil that normally maintains the patency of the alveoli and respiratory bronchioles during exhalation is lost, and so these small airways collapse when the person tries to breathe out.
If air can’t get out, it becomes trapped in the alveoli, causing the airspaces to “puff up”.
Also, by destroying the alveolar-pulmonary capillary interface, gas exchange is impaired, resulting in hypoxemia and retention of carbon dioxide or CO2.
But not all cases of COPD are directly related to smoking.
In people under 45 years of age with COPD, it’s important to consider alpha-1 antitrypsin deficiency which is an autosomal dominant disorder.
Alpha-1 antitrypsin is a protein synthesized in the liver and it inhibits neutrophil elastase.
In alpha-1 antitrypsin deficiency the protein isn’t exported out of the liver and is deficient in the lungs, so elastase accumulates, causing damage to the lung parenchyma.
Typically, the onset of symptoms occurs relatively early in smokers versus non-smokers, because smoking just compounds the problem.
Also, because alpha-1 antitrypsin doesn’t leave the liver, it accumulates there and causes liver cirrhosis.
Alright, COPD classically presents with exertional shortness of breath and a chronic productive cough in a long-time smoker, and less commonly, people may report wheezing or chest tightness.
These symptoms can be worsened by a respiratory tract infection, like pneumonia.
A person with COPD is typically sitting up and pursing their lips during expiration. That’s because it helps to prolong expiration which allows them to breathe out as much air as possible.
Because this requires use of accessory breathing muscles like the intercostal muscles of the ribs, these people are expending a lot of energy just to breathe, causing them to lose weight.
Due to air trapping, the anteroposterior diameter of the person’s chest may be increased, making it look like a barrel.
Percussion of the chest may reveal hyperresonance, and auscultation may reveal expiratory wheezes.
Additionally, chronic hypoxemia can cause cyanosis, which is bluish discoloration of the lips or fingertips.
Chronic hypoxemia causes the pulmonary vessels to constrict, called hypoxic vasoconstriction, and that leads to pulmonary hypertension.
Over time, pulmonary hypertension puts a strain on the right heart, and can eventually lead to right heart failure, or cor pulmonale; which manifests as jugular venous distention, peripheral edema, and hepatomegaly due to congestion.
If COPD seems likely, the diagnosis is made using pulmonary function tests, or PFTs.
The most important PFTs are the forced vital capacity, or FVC; which is the maximum amount of air the person can breathe out after a maximum inspiration - and the forced expiratory volume in the first second, or the FEV1; which is the maximum amount of the air the person breathes out in the first second.
In obstructive lung diseases like COPD, both the FEV1 and the FVC are reduced, but the FEV1 is reduced to a greater degree than the FVC, so the ratio of FEV1 to FVC gets reduced.
In COPD, the FEV1 to FVC ratio is less than 70% of what’s normally expected for that person’s age, gender, height, and weight.
If COPD seems likely, an inhaled bronchodilator, like albuterol is given to the person, and then the PFTs are measured again.
Now, unlike asthma, COPD is an irreversible disease, so giving a bronchodilator should not change the person’s PFTs too much.
Reversibility is defined as more than 12% increase in the FEV1 after administering the bronchodilator.
If the FEV1 doesn’t increase by more than 12%, then COPD is the diagnosis, and if it’s more, then it’s likely to be asthma.
In COPD, additional PFT changes include an increase in total lung capacity and residual volume due to air trapping.
Finally, alpha-1 antitrypsin deficiency screening is done if they are less than 45 years of age, have no risk factors for COPD like smoking or occupational dust exposure, have a family history of COPD, or have unexplained liver disease.
Alright, now the long-term treatment for people with stable COPD can be classified into two broad groups: therapies that improve mortality and symptoms, which include smoking cessation, vaccinations, and oxygen - and therapies that only improve symptoms and quality of life, but not mortality, which include bronchodilators and corticosteroids.
Now, the most important thing in COPD is educating the person about the benefits of smoking less or stopping altogether.
Reducing smoking helps improve mortality and symptoms at any stage of the disease.
Also, because infections often trigger COPD exacerbations, people should be given the influenza vaccine annually, and the 23-valent pneumococcal polysaccharide vaccine called PPSV-23; once before the age of 65 and once after.