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Emphysema: Pathogenesis A

by Carlo Raj, MD
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    00:01 We talked about the pathogenesis. The subtyping of emphysema becomes very important for us.

    00:06 This will then tell us as to where the damage is taking place and what the exact cause is, and this becomes really crucial for us to then identify other parts of the body that are also affected. What the heck am I talking about? For example, if the centrilobular and then you call this the proximal acinar. The reason we call this centrilobular is because the entire lung is not affected. I paused at the term “entire” because the term that you use clinically for the entire structure to be involved is “pan”. So, this is not panacinar emphysema, it is centrilobular a.k.a. proximal acinar emphysema. Now, when I say proximal, please understand, I don’t mean definition of proximal. I do not mean as proximal as being the bronchi and the trachea. That makes no sense. By proximal, I mean that this is going to be proximal to the actual alveolus maybe referring to the dilation or destruction of the? Let’s take a look, respiratory bronchiole. Are you picturing this? Next, epidemiology, commonly encountered in what type of patients? Well, , you want to put two patients together here and these would be coal workers and smokers. So, what is occurring and how do you keep this straight? What do you mean? Because if it is strictly smoking and you were to then induce, and we’ll go through the pathogenesis further, but if you were to then induce, the recruitment of your neutrophil causing damage to parenchyma.

    01:43 Then you know that you’re resulting in some type of emphysema and this is called centrilobular, right? Okay, that's obstructive lung disease and that’s where we are right now, but then if you shift over to our second differential here which is your coal workers' pneumoconiosis, that’s nothing to do with obstructive, does it? In fact, it comes under what? It comes under your restrictive. But, may I ask you something? In real life, clinically speaking, many of your coal workers who are working in mines, extremely young, very much influenced and may not have access, unfortunately, to proper education. Now we have to be stereotypical here, so please bear with me. Many of your coal workers are going to be smokers, let’s be smart about this. And if they’re smokers, do you think that they might be suffering from emphysema? Absolutely.

    02:32 So, what do you want to keep in mind is from henceforth, yes, we are going through pathology in a black and white manner, but then you also have to apply it in real-life scenarios and this is one of them.

    02:48 Continue discussion of pathogenesis. So, what about these smokers? Well, , imagine now that you are introducing tons, about tons of antigens into the lungs. Well, all these antigens are being introduced to the lungs. And so therefore, what’s going to happen? They are going to recruit an acute inflammatory cell and these would be your neutrophils.

    03:09 And what about these neutrophils? Well, , it has certain enzymes in them so that it can combat these antigens, but if you have such recruitment and access of your neutrophils and you’re releasing your elastase, or the other name for this is a proteolytic enzyme know, as your proteinase, then understand that now, you’re overwhelming the entire system. What entire system am I referring to? The lungs right now. And so, therefore the elastase that you’re then now releasing, stop there and I need you to tell me about what normally neutralizes the elastase once the job of neutrophil has been completed? It’s a anti-protienase, isn’t it? This is your alpha-1 antitrypsin. Now be careful here, all that I’m doing is laying down the normal function of an alpha-1 antitrypsin.

    04:04 What is it? It’s a proteinase inhibitor. So, if you’re a proteinase inhibitor then what does that mean to you? It means that you are existing to neutralize your proteolytic enzyme known as elastase. But now, if you have these elastase in abundance guess what? You completely overwhelm the system and you start causing damage to the adjacent lung parenchyma. What does this mean? Does this mean that every single elastase is causing damage to the entire lung? No, more commonly you’ll have these areas that are highly concentrated with neutrophils, that is highly concentrated with elastase, therefore, usually in the upper lungs in which it causes damage to the parenchyma, upper lungs only. So, if it’s only one portion of the lung that’s being damaged, how could you possibly call this pan? You cannot.

    04:59 And so therefore, what is the topic at this point? Our specific sub-type of emphysema is? Good, this is our centrilobular, proximal type of emphysema.

    05:12 Let’s continue. The loss of tissue is what happens here and when you lose these elastic tissue now I need to make sure that you understand the concepts so that you understand what’s going on with your pathology. So, here you have an airway, shall we say a tube, okay? And this tube has to remain open obviously. When you inhale has to expand so that you increase that flow so that you fill up that alveoli. Sure, okay. Then upon expiration, what happens? Well, your pleural pressure is then going to become positive and the alveoli is going to become positive pressure, it’s squeezing out the air into the airway, isn’t it? Okay. Now, at first, upon expiration or exhalation, think of your loop spirometry. The top half of the loop in which at first, air is coming out really fast, great. So, that’s going to keep the airway open, but as expiration continues, well, there isn’t as much air in your alveoli. Please tell me, at first, what’s maintaining the patency of the alveoli? That obviously is surfactant, right? But then, what about the airway? It’s not surfactant of the airway, that makes no sense. It’s the elastic tissue, right? So, elastic tissue literally keeps the airway open just enough so you get air in and get air out but then as air decreases can you ever afford for your airway to collapse? That makes no sense. So therefore, the elastic tissue will keep it just open, will keep it open just enough. Don’t collapse, okay? So, you’re keeping it open, you have to. But what happens in emphysema? That elastic tissue, how appropriate, elastic tissue is being damaged by what’s the name of this enzyme that’s being released by neutrophil? Oh elastase, yeah that’s right.

    07:03 So the elastase, guess what causes damage to the elastic tissue, gone is elastic tissue.

    07:09 Now, air is coming out. What kind of disease is emphysema? Obstructive. Obstructive meaning what? Difficulty with air getting in or getting air out? Good, having difficulty getting air out so now as air is moving out it’s getting less, there’s no elastic tissue.

    07:28 What happens to airway? Gone. Airway’s gone, collapsed. Welcome to emphysema. Welcome to specifically what I’m telling you here what’s called as your well centrilobular type of emphysema. Loss of elastic tissue, why? Where excess recruitment of neutrophils.

    07:45 What happens? Increase elastase. What happens? Damaged elastic tissue, I collapsed my airway.

    07:51 Everything we just talked about.

    07:52 Now, what happens here as air is trying to get out then it’s an obstructive issue it gets trapped in there. Its lost all ability to properly handle that type of air travelling through here. Okay, now, let me tell you something else. I guess, at some point in time, you as a clinician, what might you want to do based on everything that I just talked about here? What might you want to do, as a clinician, to prevent this collapse from occurring in a patient that you know has emphysema because you saw that their FEV1/FVC ratio was drastically decreased? Maybe on a chest X-ray you find that they’re barrel chest, so on and so forth. What would you recommend a simple, non-medical type of issue that you could tell the patient to do? What the heck did you try to tell your patient to do? That’s not very nice. Yes it is. You have introduced a resistor. What did I just do? Try it at home, it’s pretty fun. It makes your lips feel really good, So, it’s vibration. In other words, you pursed your lips. When you purse your lips, what have you done? You’ve introduced a resistor, haven’t you? Are you with me? Seriously, you’ve introduced a resistor in a series.

    09:02 Close your eyes, think series, not parallel. You’ve learned in physio that in a series when you add a resistor what happens to the pressure proximally? Increases. Your lips, that’s the resistor that you’ve added, purse them. What will happen proximally? Increased pressure. Yup, so when you increase that pressure what have you done? You’ve allowed for the airways to stay open because guess what happened to this respiratory apparatus? It’s like a bag. It’s just floating in the air, really thin, okay? Really thin, and all it wants to do is just collapse when there’s no air in there. How do you keep this open? You purse your lips, you add a resistor, increase the pressure and you keep it open, are we good? I don’t think I could be any more dramatic, you purse your lips so that you increase that pressure. Who cares about the pressure distally, outside the mouth who cares it’s irrelevant. So, will you take the information that you learned in physio every single time you give it a clinical tag, you’re in fantastic shape.

    10:01 Okay, let’s move on. Loss of respiratory bronchiole mostly where? In the upper and middle lobe. Think about this as being smoke rising. So, when you’re a smoker remember this has nothing, I repeat, has nothing to do with alpha-1 antitrypsin deficiency, is that clear? Perfectly normal amounts of alpha-1 antitrypsin. This is a patient that is smoking and so, therefore, introducing a lot of antigens. And so, therefore, recruiting neutrophils and hence, elastase. Having fun yet? Let’s continue.


    About the Lecture

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


    Included Quiz Questions

    1. Centrilobular emphysema is associated with the destruction of all parts of the acinus
    2. Cigarette smoking is an important risk factor
    3. Release of proteolytic enzymes destroys the alveoli
    4. Loss of tissue causes loss of radial traction upon expiration and subsequent air trapping
    5. Loss of air bronchioles usually in the upper and middle lobe
    1. Septal loss
    2. Dilatation of the acinus
    3. Decreased recoil
    4. Rupture of the acinus
    5. Compression of the affected acinus
    1. Neutrophils
    2. Lymphocytes
    3. Macrophages
    4. Clara type 1 pneumocytes
    5. Clara type 2 pneumocytes
    1. Alpha 1 antitrypsin
    2. Protease
    3. Surfactant
    4. Mucopolysaccharides
    5. Enolase
    1. Purse the lips and breath out
    2. Breathing into a plastic bag
    3. Coughing up sputum to expectorate the mucus
    4. Opening the windows to breathe in fresh air
    5. Sleeping with 3 pillows under the head
    1. It provides resistance, allowing an increase in pressure at the alveoli to prevent the collapse of it
    2. It provides more oxygen to the lung
    3. It helps maintain the respiratory drive
    4. It prevents the progression of the disease
    5. It helps exchange of gases in the alveoli

    Author of lecture Emphysema: Pathogenesis A

     Carlo Raj, MD

    Carlo Raj, MD


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