Chronic Bronchitis: Pathogenesis

by Carlo Raj, MD

My Notes
  • Required.
Save Cancel
    Learning Material 2
    • PDF
      Slides ObstructiveLungDisease ChronicBronchitis RespiratoryPathology.pdf
    • PDF
      Download Lecture Overview
    Report mistake

    00:01 Now, the pathogenesis becomes important for us. It’s hyperplasia of mucous glands in the bronchi. Think about where you are. Okay. Next, before we move on, well, give me a couple of ways in which the alveoli might collapse. The alveoli may collapse, well, a common method. Let’s say that you are post-surgically resting in a bed in a hospital.

    00:27 And as you rest there and you’re non-ambulatory and at some point of time, maybe you start developing a fever. Now this is rather problematic and should therefore, clue you in that your patient is on the verge of most likely developing what's known as resorption atelectasis. What does that mean to you? Resorption atelectasis, while you lay there, non-ambulatory, not moving, postoperatively, in a bed for a long periods of time, you might start developing mucous plugs in the bronchi. If that occurs, then what then happens with the alveoli distally? Called resorption atelectasis. Guess what? The same kind of issue that also take place here amongst others. So therefore, if the alveoli perish, tell me about your patient.

    01:12 Are they pink puffer or are they blue? They’re blue, they’re cyanotic early.

    01:16 Let’s continue. Greater than 50% thickness, is hyperplasia of the mucosal glands. Greater than 50% thickness of mucous glands layer to thickness of wall between the epithelium and cartilage. Stop there. Take a look at the ratio here. We are actually looking at a ratio, this ratio that we’ll then call Reid index is the following: greater than 50% thickness of mucous glands layer / to thickness of the wall between, think about the epithelium please, and the cartilage. So, when there’s a greater than 50% thickness in mucosal glands, guess what you’re doing? Oh, my goodness, I’m occupying the space that’s in the bronchi. That’s a problem, ladies and gentlemen. This is chronic bronchitis, ladies and gentleman. Hyperplasia of mucous, well guess what? That is going to be productive cough, ladies and gentlemen. For how long? 3 months consequently over 2 years sequentially.

    02:14 Next. What else may happen? In the upper airways, which normally has what kind of cells? Good.

    02:22 Ciliated columnar cells, may then undergo squamous metaplasia. Divide this into two different portions so that you understand the two different pathogenesis that are taking place concomitantly. You have hyperplasia of the mucous glands in the bronchi. That’s huge. Reid index is what you’re looking for there with the ratio of the thickness mucous gland and between the epithelium and the cartilage. And then number 2, the squamous metaplasia of upper airways.

    02:50 What else may happen here? Well, goblet cell metaplasia and peribronchiolar inflammation.

    02:56 So once you start undergoing the process of more of your goblet cells and around the bronchiole you have inflammation, what’s going to happen? The bronchioles are a lot smaller than the bronchi, right? Just like arteries, well, arterioles are much smaller than arteries.

    03:17 So, arterioles – arteries, bronchioles – bronchi. Okay.

    03:21 So, if the bronchiole is quite tiny to begin with and then you undergo peribronchiolar inflammation, what’s this called when you obliterate bronchiolitis? Okay. So, some may call it obliterans brohiolitis or obliterans bronchioles or bronchiolitis obliterans. It’s seen in later stages of chronic bronchitis due to fibrosis. Stop there.

    03:49 So, if it’s fibrosis, what does that mean to you? Extremely generic. What does that mean? Fibrosis up and down our body. Many causes. Whenever there’s fibrosis, you know that it’s chronic type of issue in which there is enough damaging lesion, whether repair process ended up depositing tons of fibrosis. What does fibrosis mean to you? It means contraction. In this case, here the fibrosis has taken place around the bronchioles. So, what’s happened to bronchioles? Go on. Where did you go? Oh, obliterated. Why? Because of the fibrosis. Are you with me? So, we’ve looked at a few different issues with pathogenesis here up in the upper airways along with the bronchi and such, you might add squamous cell metaplasia along with what we’ve talked about with Reid index with increased mucosal glands. As you get further distally into the bronchioles, goblet cell metaplasia is what you’re looking for and with increased destruction or fibrosis, please understand, you have complete obliteration of the bronchiole. Understand, however, we’re going to revisit bronchiolitis obliterans in other pulmonary pathologies that may result in fibrosis deposition. And during that time, I’ll refer to back to what we looked at here.

    05:05 Clinical presentation. Significant V/Q mismatching. Such a thing may or may not be the case with emphysema. It was minimal V/Q mismatching in emphysema, wasn’t it? What happened possibly with that hypoxemia in emphysema? Is it possible that you may or may not have hypercapnia? Yes. In emphysema, I showed you specifically in that topic where we looked at the oxygen dissociation curve versus your carbon dioxide dissociation curve. If you missed that discussion, please go back and review that particular topic.

    05:39 Now, with chronic bronchitis, because of inflammation taking place and mucous production in the bronchi, there’s really no chance of you having regional type of compensation. It is going to be cyanosis, immediately. Retention of carbon dioxide, immediately. There is none of this with or without. There will be significant V/Q mismatching, wheezing, crackles upon auscultation.

    06:03 Shunt, wait, stop. Shunt, stop. Why? Because I need you to understand the significance.

    06:12 Don’t just read stuff, listen, conceptualize. So with shunt taking place here in chronic bronchitis, how does that occur? I just gave you two examples in which that alveoli may perish.

    06:23 Two. One was, I told you about postoperatively where patient lays in the bed for long periods of time, therefore accumulating mucus plugs and fever, and infection. What then happens to the alveoli distally? Gone. What do we call that? Resorption atelectasis. Is that common? Yes, we’ll talk about that later. If this is chronic bronchitis, can we say that it’s pretty much the same pathogenesis? Maybe they’re smoking, there’s irritation, there’s goblet cell metaplasia, increased mucous production in the bronchi. What happens to the alveoli? Gone. What is that? A shunt or dead space? Good. It’s a shunt and gone is the alveoli. Good. Therefore, shunt results in early onset of hypercapneic, stop there. Such a instance, because I’m being really deliberate here, because you need to be quick about differentiating between emphysema and chronic bronchitis. You don’t have all day. In asthma as well. Asthma, remember, many of times, you can reverse it. Okay. Now, early onset of hypercapnea, hypoxemia is going to be present in any type of COPD.

    07:32 That doesn’t tell you much, but the early cyanosis and the early hypercapnea, absolutely.

    07:37 What does that mean? I’ll give you an ABG, arterial blood gas, where your carbon dioxide is what? Good, above 40. What’s your pH? Good. Acidic. What does that mean? Less than 7.35. Do you understand how important this statement is? It’s probably the most important in terms of for you to be able to diagnose your patient quickly.

    07:57 Resulting in cyanosis, quickly, polycythemia. Why? If there’s hypoxic chronically, who’s going to respond? The kidney. What’s the kidney going to do? Oh, yes, I forget about that sucker. Who is this that I’m referring to? Erythropoietin, EPO. So, here comes my erythropoietin and what kind of polycythemia is this to be technical? Good, secondary polycythemia.

    08:24 We call these patients blue bloaters.

    08:27 Late onset of dyspnea with chronic complications of, this says, pulmonary arterial hypertension (PAH). What kind? What do you mean what kind? Primary or secondary? Good, secondary pulmonary arterial hypertension. We’ll talk about this later, don’t you worry. And we have secondary right-sided heart failure. Are we clear about the abbreviations? Okay? PAH – pulmonary arterial hypertension, secondary type. Those of you who are ahead of me, you know exactly why. If not, that’s okay, just digest what I’m giving you. And then secondary right-sided heart failure. Why? Lungs are offering more resistance, right ventricular hypertrophy, may eventually result in cor pulmonale. That is not good.

    About the Lecture

    The lecture Chronic Bronchitis: Pathogenesis by Carlo Raj, MD is from the course Obstructive Lung Disease.

    Included Quiz Questions

    1. Thickened airways and mucus plugs
    2. Dilated alveoli with thinning of septa
    3. Cavity with increased hilar shadows
    4. Increased space in the pleural region
    5. Increased hilar shadowing
    1. Ratio of more than 50% thickness of mucus glands layer to the thickness between epithelium and cartilage
    2. Less than 50% thickness of mucus glands to the thickness between epithelium and cartilage
    3. Ratio of more than 50% thickness of mucus glands including the subepithelium and cartilage
    4. Ratio of more than 50% thickness of only stroma to the thickness between epithelium and bone
    5. Ratio of the glands with more than 50% thickness of mucus glands to the thickness including epithelium and bone
    1. Squamous and goblet cell metaplasia
    2. Columnar and goblet cell metaplasia
    3. Tubal metaplasia and squamous metaplasia
    4. Clear cell metaplasia and goblet cell metaplasia
    5. Columnar and squamous metaplasia
    1. Secondary polycythemia
    2. Primary polycythemia
    3. Polycythemia rubra Vera
    4. Secondary myelofibrosis
    5. Primary myelofibrosis
    1. Alveoli
    2. Lobar bronchi
    3. Segmental bronchi
    4. Bronchioles
    5. Primary bronchi
    1. Fibrosis
    2. Mucus
    3. Inflammation
    4. Edema
    5. Bronchial secretions
    1. Due to increased erythropoietin levels causing secondary polycythemia
    2. Due to a decrease in erythropoietin causing secondary polycythemia
    3. Due to an increase in erythropoietin levels caused by primary polycythemia
    4. Due to decrease in erythropoietin levels caused by primary polycythemia
    5. Due increased of angiotensin levels, causing secondary polycythemia
    1. Early onset hypercapnic hypoxemia
    2. Late onset hypercapnic hypoxemia
    3. Early onset hypoxemia
    4. Late onset hypoxemia
    5. Early onset hypoxia
    1. Alveolar shunts
    2. Alveolar mucus
    3. Alveolar collapse
    4. Bronchial inflammation
    5. Bronchial edema
    1. Pulmonary arterial hypertension
    2. Rupture of lung
    3. Pneumothorax
    4. Collapse of lung
    5. Left heart failure

    Author of lecture Chronic Bronchitis: Pathogenesis

     Carlo Raj, MD

    Carlo Raj, MD

    Customer reviews

    3,0 of 5 stars
    5 Stars
    4 Stars
    3 Stars
    2 Stars
    1  Star

    2 customer reviews without text

    2 user review without text