Pathophysiologically, uh, bronchiectasis is characterized by, uh, three major events. The first is the loss of cilia on the surface of the bronchial tubes, uh, which are normally the, uh, mucociliary elevator, uh, for the lung. Uh, and the second is proliferation of mucous glands, so that you make more mucus, and without the cilia, you have more difficulty, uh, moving it out of the lung. And finally, There is dilation of the bronchus. All three of these events lead to increased mucus production, uh, decreased efficiency of removing mucus, and retention of these, uh, secretions in the lung. Uh, all of the, uh, microbes that are associated with bronchiectasis. Uh, thrive in that environment. Uh, so, again, a bug like Pseudomonas, uh, Mycobacterium avium, uh, or Aspergillus, uh, that is the environment that creates the attraction, uh, for these, uh, organisms. Now, the inflammatory process itself is kind of interesting. Uh, initially, there, there may be a stimulus from, say, uh, pseudomonas, uh, such that neutrophils, uh, come in, uh, as a response, uh, to this particular pathogen. But after a while, uh, the endobronchial inflammation becomes a self-perpetuating process. So, neutrophils, uh, uh, enter the area, uh, from the blood. Uh, where, where there is inflammation. And one of the things that they do is they release proteolytic enzymes. Those proteolytic enzymes have, have kind of a yin and a yang in the sense that they do help kill microbes, but they are also non-specifically toxic and perhaps more to the point, uh, they recruit more neutrophils. So you get a cycle where you get neutrophils moving into the area of inflammation. Um, they, uh, release their proteolytic enzymes that recruit more neutrophils, who in turn, uh, release new, uh, proteolytic enzymes and recruit more neutrophils, uh, which goes on and on without a specific stimulus, uh, for the process. Uh, it is a self-perpetuating, uh, process, which is sometimes called a, uh, uh, a vicious cycle or vicious vortex. Now, uh, when you have an acute infection, uh, like pneumonia or a chronic infection like, uh, Mac, uh, then that process may be accelerated or exacerbated. But with or without a specific stimulus, it, uh, it goes on and on. Now, the things that we have done traditionally for bronchiectasis like uh airway clearance and antibiotic therapy, kind of nip at the margins of the inflammatory process. They don't directly impact that, uh, that endobronchial inflammation. They, they may lessen it. Uh, but again, it isn't, uh, uh, doesn't have a direct impact on, uh, that self-perpetuating, uh, inflammatory process. Now, uh, it is perhaps counterintuitive, but steroids, either inhaled or, uh, uh, systemic, Uh, have a detrimental effect on this process. So for instance, inhaled cortical steroids seem to predispose patients to mycobacterial infections. Uh, and the steroids, uh, seem to have uh an immune suppressive effect on the organisms in the, uh, uh, in the tracheobronchial tree. So neither uh inhaled steroid or systemic steroid is uh indicated for patients with bronchiectasis under uh usual circumstances.
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