Pathophysiology of COPD

[Music] all right engineers in this video we're going to talk about copd or chronic obstructive pulmonary disorder so let's go ahead and get started all right so let's go ahead and get started on copd so there's two conditions with copd chronic bronchitis and emphysema okay so that's the two important ones that we're going to talk about here sometimes people will consider chronic asthma as a part of the copds but again we're going to keep it separate for itself okay so the main ones that we usually classically associate with is chronic bronchitis and this one is going to be classically seen with uh you know that that mucous production that productive cough that's one of the hallmark signs of chronic bronchitis we usually can diagnose this based off clinical diagnosis so how much sputum they're producing how often how long that kind of stuff and the other condition that we're going to talk about is emphysema emphysema is usually described as being structural changes and we'll talk about why okay now what are the causes of copd so we're going to go over the pathophysiology we're not going to go into an insane amount of detail but we're going to try to hit the most you know the most important stuff so what are the main risk factors associated with copd well the one that i want you to remember that is the biggest one the most important one causes like 90 to 95 percent of the copd cases is smoking so let's draw a little sig here look at that nice little sig little uh pleat there then here this guy's burning it right now at the end and then here we're going to have some smoke coming out of it all right again don't smoke not promoting that all right smoking it is the number one cause the number one cause of copd we'll talk about how what is this actual reaction that causes copd but again this is the most common one don't forget that one other ones that are less common but still important to mention is going to be environmental exposure so what do i mean so certain things where you're exposed to a lot of dust you know maybe silica and another one is even just air pollutants okay so air pollutants from exhaust from different types of things within the atmosphere another big one is actually going to be a genetic condition and this one is called alpha one anti-trypsin deficiency we're going to put a down arrow here so alpha 1 anti-trypsin deficiency now this one is the kind of the least common but it can happen it's an autosomal dominant disorder one of the things with this one is that usually you have to have like a family history of copd some underlying unknown reason why there's liver disease and also they usually have to be less than about 45 to 50 years old in order for you to take into consideration alpha-1 anti-trypsin deficiency but again the most common smoking now how does this all play into it how does these risk factors are these things that we believe to be the cause lead to chronic bronchitis emphysema one other point i want to make sure that you realize here is that copd is not always clear-cut it's not always the sense that you only have chronic bronchitis or you only have emphysema one of the big things that we need to understand is these things often coexist that is an important point to remember now let's go over chronic bronchitis first we'll go over the pathophysiology we'll talk about some of the things that can develop from that and then we'll go over emphysema first things first chronic bronchitis i want you to think mucous buildup okay so we have these mucous glands they're actually located if you guys remember a little bit about your anatomy we have a mucosa lining which is their epithelial tissue maybe some lamina propria and then outside of that you have a submucosa which is kind of a loose connective tissue and you're going to have these submucosal glands they're naturally producing mucus okay they naturally produce mucus to humidify the airways to trap up certain types of pathogens and help to be able to keep the airway moist and and and humidified okay but in situations with chronic bronchitis the problem is is that the mucus production increases significantly okay and it's the result of usually these irritants smoking dust exposure and what happens is this mucous plugging causes the narrowing of the airway you can obviously see that because obstructive disorder is you're narrowing the airway so one of the big things here is that we have to remember there's going to be hypertrophy and hyperplasia of these mucinous glands and it's because of the airways coming into contact with all these irritants the smoke the dust the silica the pollutants and it's causing this agitation of the mucosa and the way that our actual body deals with that is we stimulate these mucous glands to produce more mucus to coat that area so because of that one of the classic things that we'll see here is hypertrophy and hypertrophy is just an increase in the size of the mucinous glands they're going to get bigger the second thing is that you're going to make more of them so that's called hyperplasia and these are the classic signs for these mucous glands okay now because we also have other cells that are important for the mucous production there is a couple of them scattered along the airway we have these special cells and they're called goblet cells goblet cells are also responsible for producing that mucus and it's more of that again that alkaline mucus which helps to be able to coat the airway helps to moisten the air humidify the air helps to be able to filter out any pathogens right that is important so because of this these different risk factors there's going to be hypertrophy hyperplasia of the mucous glands as well as for the goblet cells so again you're going to have mucus glands and goblet cells okay so that's important so there's going to be a lot of mucus production the next thing that happens is unfortunately smoking especially there's so much irritation in this area that it can actually cause destruction of the cilia so there can be ciliary shortening and they're also going to have less motility so because of that what's going to happen now because of that you're going to have so much mucus just accumulating in the airways and this mucus is going to be really really hard to get out so because of that you're going to have what's called ciliary dysfunction so there's going to be some ciliary dysfunction and again the ciliary dysfunction is because the cilia are getting shorter they're becoming less motile and they're not able to beat that mucus up because that's one of the functions of the cilia they help to beat mucus up that we can spit it out or swallow it right but because there's so much mucus and the cilia aren't properly working what's gonna happen that mucus is just gonna sit there in the airways and plug up the airways and cause obstruction to the airways narrowing of the airways that is the problem with this one now imagine take for a second and imagine here i plug up this airway here right here's going to be a mucous plug so here's a mucus plug here let's say here's a mucus plug here what's going to happen think about this both ways here our airways are responsible for bringing oxygen into the actual alveoli right so o2 is supposed to be able to make it down into the alveoli but because of this mucous plug very little of the oxygen is going to make it down a lot of it won't make it it might have to divert to other areas where there's more uh patent airways so one of the big things here is that there's not going to be a lot of oxygen getting in the opposite is that we want to breathe co2 out so because of that what's going to happen now the co2 that we're trying to breathe out is going to get stuck or trapped so one of the big things with this that you'll notice with chronic bronchitis is that we can't get air as much air in oxygen wise and we can't get a lot of the air out but more of it more specifically getting air out that is the big thing so one of the big big things that you're going to see in patients who have this chronic bronchitis is they have what's called air trapping okay and this air trapping just is basically again think about it as you're trying to exhale as you try to exhale your actual bronchials get a little bit smaller when you exhale you have elastin to kind of keep them open but in general they get a little bit smaller so if you already have this mucous plug there narrowing the airway and then you're exhaling and that actual airway gets even smaller are you going to be able to get that air out no so a lot of that air starts sitting down in these airways and a lot of it builds up and especially co2 so you get very little oxygen in and you get very little co2 out and this causes that classic air trapping now going off of that air trapping effect think about it again you have low oxygen coming in because of that mucous plug here we'll draw that mucous plug again here's this mucous plug okay because of this mucociliary dysfunction increase hyperplasia hypertrophy of the mucinous glands the goblet cells and dysfunction of the cilia causes that mucus buildup causes air trapping on top of that less oxygen is going to be making it into the airway because of that mucous plug but more significantly is you're going to have more co2 building up because again remember co2 exchanges here right but because of this mucous plug occluding the airway especially especially during expiration because as we expire the airways get a little bit smaller it's going to cause so much co2 to build up now this is two things the co2 is going to start building up in the blood okay and less oxygen is going to make it down into the airway and perfuse into the tissue this is a vq mismatch right this can lead to hypoxemia and another one which is really bad here hypercapnia and hypoxemia is the low partial pressure of oxygen and hypercapnia is the high partial pressure of co2 so this is one of the big common findings that we're going to see in patients with chronic bronchitis okay so again hypertrophy hyperplasia of the goblet cells the mucus glands because of these irritants they make more mucus to compensate for the irritation the mucus starts obstructing the airways on top of that especially with due to smoking and again those air pollutants as well the cilia are becoming become shorter and they're going to become less efficient and being able to beat the mucus so now you have an increase in mucus and you can't even get the mucus out that builds up and causes mucus plugs these mucous plugs lead to less air coming in but specifically more of the actual issue is going to be there's less air getting out particularly co2 because of that you're going to have a buildup of co2 particularly and this is called hypercapnia but also you're not going to be able to get as much oxygen into the lungs because of that actual obstruction and that's going to cause hypoxemia another thing that we have to think about with chronic bronchitis and i want you to think naturally here if you remember from our pneumonia video we talked about how chronic bronchitis or copd puts people at risk of developing infections lung infections especially because of the mucus plugging if you guys remember there were two bacteria that are commonly seen in patients who have copd that can actually cause this increased risk of demonia so there's going to be an increased risk of pneumonia and again this was because of two types of bacteria one is called hemophilus influenza we're going to put h flu and the other one is called merexella cataralus okay these are the ones that are going to increase the risk of that pneumonia and again when we talk about this this could be usually your strep pneumonia or it could be a low bar so here would be a um this right here could be a low bar pneumonia where it's actually forming what's called a consolidation and then this one over here on the left side could be a bronchopneumonia where there's actually diffuse scattering particularly at the bases of the lungs so that's going to be an increased risk of pneumonia okay because that mucus is building up and it because that mucus building up it's going to lead to that h flu and that marxial catarralis just basically feeding in that area which can then again lead to an infection so these are the big things that i want you guys to see especially with chronic bronchitis okay so again to recap it hypertrophy hyperplasia of the mucous glands and the goblet cells that causes mucus buildup ciliary dysfunction because the smoking and the pollutants destroy the cilia and lead to either a decreased number in the cilia as well shortening the cilia and less motility leads to mucus buildup that mucous buildup can form plugs the plugs can lead to air trapping okay which is a classic sign again because of the mucous plugs you can have less oxygen coming in leading to hypoxemia less co2 being blown out causing hypercapnia and another complication that can develop because of chronic bronchitis is you increase the risk of developing pneumonia especially with chronic bronchitis because of the mucus buildup and particularly h-flu and morexotic caloralis are the etiological bacteria responsible for that okay so that's chronic bronchitis we're going to talk about another complication that is extremely common and it's a bad bad diagnostic sign in in patients who have chronic bronchitis and we'll get to that when we get to this part here okay let's go to emphysema for a second and then again we'll talk about the complications that can develop from these two the biggest one with emphysema again i want you to remember that this is a structural issue and then for chronic bronchitis i want you to remember that this is a mucus issue with emphysema what happens is these situations here the smoking the pollutants or another one that will talk about alpha one anti-trypsin deficiency all lead to this condition how let's go with the first two here the smoking and the pollutants so let's say here i have some pollutants okay let's say that it's from the smoke from cigarette smoke or maybe it's from the silica the dust what it will generally do is we have certain types of cells in this area right and they're resident macrophages these are called alveolar macrophages and what they'll do is they'll undergo phagocytosis of this actual these pollutants are particles now when it undergoes phagocytosis of these particles the next step is it's going to go ahead and start actually releasing particular particular cytokines so now look it'll undergo the phagocytosis of the particle once it's activated it's going to start releasing a bunch of different cytokines these cytokines are going to activate some particular nice little acute cells to this area and these are called neutrophils so there's going to be a lot of neutrophils there'll also be some more macrophages that can come to the area but one of the main culprits in this is going to be your neutrophils okay so these cytokines are going to activate these guys now when these cytokines activate these guys it's going to basically say okay there's a lot of inflammation in this area from this smoke or dust or silica or pollutants what the neutrophil and the macrophage are going to start doing is they're going to start releasing particular proteases so they're going to start releasing these specific enzymes and the enzymes that they're going to release are going to be called proteases so they'll release proteases they can release other enzymes as well but these are going to be the big ones but the main protease that i want you to remember that it'll actually start releasing here is called elastase now you can already imagine what that does elastase means it breaks down elastin which is a connective tissue right so because of that you see this pink stuff here this elastin has multiple functions okay so let's recap really quickly what is elastin4 like it's important to understand sometimes in anatomy physiology comes in handy when it comes to talking about pathophysiology obviously right so one of the big things for elastin is it helps to increase the recoil of the lungs what does what i mean by that you know whenever we're inspiring it requires respiratory muscles the diaphragm the intercostals and so because of that that's going to expend energy but that's a whole part of the inspiration it's an active process expiration normally should be a passive process so whenever our lungs are actually reached their full capacity of inhalation the elastic tissue is designed to draw the lungs back to their normal size but if you lose that elastic recoil then what's your lungs going to do they're going to expand really easily but they're not going to be able to recoil and push a lot of the air out what does that cause that air trapping right so that's one big thing here it also keeps airways open at the same time so think about this if you're exhaling right remember i told you when you exhale your actual your respiratory airways get a little bit smaller right if you had elastic tissue it actually keeps those airways open they have an opposite force it's called the bernoulli principle so the bernoulli principle says that in the airway there's going to be low pressure because of high velocity airflow so you need elastic tissue to pull in the opposite direction to keep that airway open but if you lose the elastic tissue you lose that opposing force and so then what happens the pressure inside of the actual airway is so low the airway will collapse and again that contributes to the air trapping and we'll talk about this here but again that's the significance here so if you give them if you actually have a lot of this uh constant exposure from the smoke the pollutants these irritants or you have alpha one antitrypsin deficiency it's going to cause increased macrophage phagocytosis increased inflammatory cytokines increased number of macrophages and but particularly neutrophils to come to the area and release a ton of proteases the proteases the specific one is elastase but it does have collagenases the elastase is going to do what it's going to start breaking down this elastic tissue this nice pink tissue here and again imagine what that's going to do it's not good i can tell you that right so you're going to lose your ability for your lungs to recoil that's going to lead to an increase in compliance but air trapping and you're not going to be able to keep the airways open so they're going to collapse and that's going to again contribute to the air trapping so let's talk about how that happens okay oh but before we do that one last thing here i mean i talked about these pollutants right how does alpha-1 anti-trypsin deficiency come into this i want to make sure i mention this let's draw the good old liver my favorite organ this guy here is so cool and what he does is he releases a specific protein into the blood right and this protein is called alpha one anti-trypsin alpha-1 anti-trypsin is an anti-protein okay so because of that its job is to inhibit the action of these elastases so if you have your liver producing this at constant amounts what it's going to do is it's going to try to be able to break down this actual elastase and prevent it from being able to cause this damage to the elastic tissue can you imagine that if you had an autosomal dominant disorder so auto somal dominant disorder and again that means that you actually have two defective copies and what happens is your liver isn't able to produce this alpha-1 anti-trypsin or if it does it produces in a very little amount what's going to happen your inhibition of the elastases is going to be overcome and you're going to have a lot of elastases and they're going to start producing damage so you can see why alpha one antitrypsin deficiency can be a cause here for emphysema now going back to that thing i was talking about with the bernoulli principle let me put that down in this diagram so this is the bernoulli principle and what the bernoulli principle says is that when you get air coming out of the lungs okay air leaves and a high velocity okay so it's going to leave in a high velocity manner so when air is leaving in a high velocity manner what happens is the airway inside of there should be a low pressure so because of that high velocity means you're going to have low pressure in the airway think about this if there's low pressure and there's higher pressure out here what's going to happen the airway would collapse but guess what we got that beautiful elastic fibers and what the elastic fibers do is is they create an outward force and this outward force is going to help to be able to keep the actual airways open even despite the fact that air is moving at a high velocity and causing a low pressure in the airways imagine imagine for a second though you lose this elastic tissue then what this pressure it's going to be low are you going to be able to resist the collapsing pressure no so because of that what would be the result think about it so imagine this for a second imagine you lose this elastic ability to keep the actual airway open because again the low pressure according to bernoulli's principle what will happen is whenever you try to exhale you're not going to have that actual elastic fibers to keep it patent so now when you exhale the airways are going to collapse and because of that what's going to happen to that air it's just going to sit here in this actual asynus and then over time as that air starts to collect guess what happens oh man you start losing the surface area and it starts getting really really expanded and because of that not just because of the loss of the elastic tissue in the small airways but you also lose a lot of the elastic tissue in the alveoli area so it starts actually breaking down the alveolar septa and because of that you just get a small surface area it destroys the surface area okay so that's one shot what i really want you to remember because of emphysema you lose the elastic tissue here in the actual small airways because of that whenever you exhale they aren't able to keep the airway open it collapses when it collapses air is trapped and it's not able to be left from the lungs because of that over time that air starts actually causing kind of dilation and expansion of the actual small airways are the asynus another thing is the elastases start breaking down the alveolar tissue which form the septa and so now instead of having little alveoli to increase the surface area you just have one big ballooned out area of an asynus and that's a problem especially depending upon what kind it is and we'll talk about those because they can cause pneumothorax all right all right so i just wanted to make sure that i mentioned that now the next thing that can happen here is think about it if that airway collapses what's going to happen are you going to be able to blow co2 out no so because of that think about it the co2 that you're trying to exhale is going to start building up because it's going to be so narrow and the same way think about oxygen when that oxygen is going to be able to come in because again here's what i want you to remember it's there's the big thing with the oxygen is with chronic bronchitis that mucus is still going to be there during inhalation you're able to bring air in with emphysema but it's just not as much okay hypoxemia and hypercapnia are way more common in chronic bronchitis hypoxemia and hypercapnia for emphysema is usually a later event okay a lot of the problems with the copd is with expiration because of again when we expire those airways get a little bit more narrow especially if there's mucus blocking it or if you lose the elastic tissue so that should make sense but again there is going to be a little bit of oxygen not as much getting into the airway so what's that going to lead to if you think about it that's going to lead to again hypoxemia and as well as hypercapnia but again what i want you to realize is that it's very mild okay and this is usually going to develop later stages so after someone's had chronic emphysema for a long period of time they're going to develop hypoxia to the point where it actually is severe and it can lead to a very very dangerous complication right side heart failure we'll talk about that okay so again we understand the collapsing of the airways we understand one of the big complications that can develop within the later stages of emphysema more common in chronic bronchitis the next thing i want to make sure that we mention is the morphology so remember i told you that with that actual um that asynus over time it becomes kind of dilated and because of the air trapping and on top of that the elastic tissue is being destroyed it's losing the alveolar septa and because that you just develop these big balloons in the actual lungs there's three types of emphysema that we generally see so again this one is called sentry asana emphysema okay now here's what i want you to remember again going off of that uh that little diagram i had here this one here remember as the airway gets narrow right and over time as the elastic tissue starts actually becoming destroyed it leads to these big dilated pockets of air with decreased surface area they can occur in different parts of the airways if these pockets are these dilated pockets of air forming the proximal airways it's called sentry asana emphysema if these pockets of airways these dilated pockets of airways develop in the distal airways okay like norton more the distal airways that can form another type and that is called pan async or emphysema pan asana emphysema and the one that's really really bad and we really got to watch out for is when it affects the distal alveoli and the distal alveoli usually are forming near the actual pleural tissue okay so near the actual visceral and parietal pleura area so because of that this is the one that you got to be careful of because it can actually form little blebs that can rupture and form spontaneous pneumothorax okay so this one has two names i'm going to write this simple one it's called distal asana emphysema but they also call it paraceptal emphysema this is the one that i want you to remember because specifically this can form one of the complications that can develop from this one is you can develop a pneumothorax usually a secondary spontaneous pneumothorax and that can lead to atylactasis compression at lactase is where the lung can collapse now i'm going to highlight again just to be specific where these uh actual these little dilated airways or expanded airways would occur for distal again remember near the pleura okay so this green here that i'm highlighting this is where it will generally occur so you'll form these different types of little blebs little diluted airways near the distal alveoli that's usually in the periphery of the lungs okay pan aciner usually affects the lower lobes of the lungs sentry astoner usually since it affects the proximal airways affects the upper lobes of the lungs okay so it's not too hard right again century astoner proximal airways upper part of the lungs pan acinar distal airways again that should be the lower part of the lungs and then distal astiner is it effects near the actual alveolar they also call it periceptal emphysema and again it affects the distal alveoli and that's going to be usually near the pleura and again these can actually form little blebs that can rupture into the actual pleural space and that air in the pleural space is called a pneumothorax we call it spontaneous pneumothorax but it's secondary because they have an underlying lung disease okay all right so that's the big things that i wanted to make sure that we mentioned here with the emphysema now remember i told you that there was a big complication that can develop with uh emphysema and chronic bronchitis and it was related to this hypoxemia in this hypercapnia and again i can't stress this enough hypoxemia and hypercapnia are way more common in chronic bronchitis it can happen in emphysema but it is usually in the late stages okay how does this work well if you guys remember a little bit about your physiology what happens is over time you have this uh hypoxemia if you remember kind of a small little diagram here of a small little diagram let's say here we have an alveoli and then here we have a blood vessel if you guys remember we said that whenever there is low ventilation low ventilation low v right based off that vq ratio which is equal to 0.8 okay and again this was what we learned in physiology okay we say that a vq is equal to 0.8 if you decrease the ventilation to the alveoli what do you need to do to the denominator to actually make it to at least equal 0.8 well if you decrease the top number it's going to make the small the overall number smaller so we have to make the profusion also smaller so we as a result we have to decrease the perfusion so that we can bring the uh overall number back up to 0.8 so because of that whenever you have low ventilation to a specific point of the airway it is going to decrease the perfusion and you can remember because they called that hypoxemic vasoconstriction it's a normal autoregulatory mechanism of the lungs so with hypoxemia it's going to result i'm sorry with this situation of low ventilation it's going to lead to hypoxemic vasoconstriction now that's fine if it's only just a small part of the airway but imagine if this is affecting multiple parts of the actual lung so imagine that there's actually multiple of these guys multiple these alveoli within the lungs that are having so much vasoconstriction eventually these pulmonary vessels are going to develop a really really high pressure okay so because of that imagine it like this imagine this kind of diagram imagine here there's one arterial and this arterial branches out into multiple different little terminal arterials and these guys are going to the alveoli i'll draw a little alveoli here a little alveoli here a little alveoli there imagine this one had low ventilation what do you do you constrict it right so now this area here as a result will constrict if there was low ventilation send it to the other areas but what if this alveoli is also having low ventilation then i'm going to constrict that one too what if this alveoli is also having low ventilation i'm going to constrict that one where is this blood going to go it's just going to go backwards and build up what's that going to do to the pressure in this area it's going to increase it and it's going to cause what's called pulmonary hypertension because you're having so much widespread vasoconstriction that this is causing the blood pressure to rise so high in the pulmonary arteries so this hypoxic vasoconstriction over time can lead to pulmonary hypertension and the htn now think about it like this if the pressure in the pulmonary arteries are high then the ventricle the right ventricle is going to have to increase its workload it's going to have to pump and pump and pump against high pressure so they can push the same card i'm sorry the same stroke volume out because of that it's going to put so much workload on the right side of the heart that eventually there can lead to what's called right ventricular hypertrophy but then unfortunately over time failure and this is what we refer to as core pulmonal it's a complication that can develop because of chronic obstructive pulmonary diseases and how would you know that if somebody has right or ventricular failure or right side heart failure remember the fluid backs up into the superior and inferior vena cava so what will they have an increased jugular venous pressure they'll have apatomegaly splenomegaly maybe they'll have peripheral edema all of these things are going to be common signs of someone having right ventricular heart failure so again that is something that we want to take into consideration as a very serious complication of chronic obstructive pulmonary disorders again you will see this more specifically with chronic bronchitis or the later stages of emphysema okay and again ruling out right ventricular heart failure obviously you have to you know check their bmp levels it's called the brain natritic peptide it's made by the ventricles you could do an echo to see if there's a decreased ejection fraction and if you really want to you can check what's called a swan's gonz catheter it's a right ventricular catheterization and you do you check the pulmonary capillary wedge pressure and you look to see if it's greater than 18 millimeters of mercury those are usually ways that we can see if a person has right sided heart failure okay but again the gold standard would be the swansen's catheter all right so that's what we would have to know out of all of these for our chronic bronchitis and of emphysema pathophysiology [Music] you

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Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, COPD, Chronic Obstructive Pulmonary Disease, chronic bronchitis, pulmonary medicine, emphysema, copd pathophysiology, copd management, Lung, lungs, spirometry, Pathophysiology, COPD symptoms

Id: ipi1RphFqDU

Length: 37min 44sec (2264 seconds)

Published: Wed Nov 18 2020