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A 78-year-old woman comes to the emergency department in mild respiratory distress. She has a past medical history of chronic bronchitis, type 2 diabetes, hypertension and hyperlipidemia. She has smoked 1 pack per day for the past 60 years. She is admitted to the hospital for an acute COPD exacerbation and started on supplemental oxygen, IV and inhaled corticosteroids, inhaled B2 agonists, anticholinergics and antibiotics. The patient responds appropriately to treatment is and ready for discharge on day 4 of hospitalization. In addition to smoking cessation, which of the following is proven to improve survival in patients with COPD?
Content Reviewers:Rishi Desai, MD, MPH
Contributors:Tanner Marshall, MS
Bronchitis means inflammation of the bronchial tubes in the lung, and it’s said to be chronic when it causes a productive cough—which means produces mucus—for at least 3 months each year for 2 or more years.
These two are different in that chronic bronchitis is defined by clinical features, like a productive cough, whereas emphysema is defined by structural changes—specifically enlargement of the air spaces.
That being said, they often coexist, probably because they share the same major risk factor — smoking.
Other risk factors for chronic bronchitis include exposure to air pollutants like sulfur and nitrogen dioxide, exposure to dust and silica, as well as genetic factors like having a family history of chronic bronchitis.
With COPD, the airways become obstructed, and the lungs don’t empty properly, and that leaves air trapped inside the lungs.
For that reason, the maximum amount of air people with COPD can breath out in a single breath, known as the FVC, or forced vital capacity, is lower.
This reduction is especially noticeable in the first second of air breathed out in a single breath, called FEV1—forced expiratory volume (in one second), which typically is reduced even more than the FVC.
A useful metric therefore is the FEV1 to FVC ratio, which, since the FEV1 goes down even more than FVC, causes the FEV1 to FVC ratio to go down as well.
Alright so say normally your FVC is 5 L, and your FEV1 is 4 L, your FEV1 to FVC ratio would end up being 80%.
Now, someone with COPD’s FVC might be 4 L instead, which is lower than normal, but the volume of air that he or she can expire in the first second is only 2 L, so not only are both these values lower, but their ratio is lower as well—and this is a hallmark of COPD.
All that had to do with air breathed out right? Conversely, for air going in, the TLC, or total lung capacity, which is the maximum volume of air that can be taken in or inspired into the lungs, is actually often often higher because of the air trapping.
Alright, so chronic bronchitis is a type of COPD that’s diagnosed based on clinical symptoms, specifically coughing up a lot of mucus. But why does this happen?
Well, first off, in the lungs, the walls of normal airways have a couple layers to think about.
Lining the lumen of the airways you’ve got the epithelium, composed of ciliated pseudostratified columnar epithelial cells, which are named that because these epithelial cells have hair-like projections called cilia, their nuclei don’t align so it looks like they’re more than one layer even though they’re not, hence, pseudostratified, and because the cells are mostly tall and narrow - or columnar in shape.
This layer also contains the occasional Goblet cell which makes some of the mucus that lines the airway.
Going deeper past that layer you’ve got the basement membrane and loose connective tissue, called the lamina propria—which together with the epithelium makes up the mucosa.
Beyond the mucosa, there is smooth muscle followed by more connective tissue, and together, these two layers make up the submucosa and this is where the bronchial mucinous glands live.
These are the glands that secrete the majority of the mucus into the lumen of the bronchi, helping to catch and filter out particles and pathogens.
Alright so people who smoke expose their airways to all sorts of irritants and chemicals. Whatever the irritants are, their effect is to stimulate hypertrophy and hyperplasia of the mucinous glands in the main bronchi, as well as the goblet cells in the smaller airways - the bronchioles, which increases mucus production in both locations.