Cram The Pance - S1E26 Chronic Obstructive Pulmonary Disease (COPD)

Episode Date: June 10, 2021

Chronic Obstructive Pulmonary Disease (Emphysema, Chronic Bronchitis) review for your Pance, Panre and Eor’s.►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so really quick, thank you to everybody for the likes, the comments, the new subscriptions. I always say it, but I really do appreciate it. So I want to tell you every time, even if it's annoying. And please check out my YouTube channel if you haven't yet. It's crammed the pants on YouTube. So let's get started with COPD, chronic obstructive pulmonary disease. This is a progressive pulmonary disease, and this is the key. It's not fully reversible.

Because remember, in asthma, they may have similar symptoms, but asthma in many cases is completely reversible. COPD is generally not reversible, and it's a progressive. progressive disease. It's characterized by a combination of small airway disease, parankhamal destruction, and the structural changes that we see in COPD, like narrowing of airway, destruction of alveoli, lead to airflow limitation, mucociliary dysfunction, which we'll see in chronic bronchitis, lead to a number of clinical manifestations. And there's two forms of COPD, it's emphysema and chronic bronchitis. Now, just for the sake of accuracy, there is technically a third subset. It's

chronic obstructive asthma, but only if they have this type in it and they have this irreversible airway obstruction. It's pretty rare and they don't ask you to know it for the for the pants blueprints. We're not going to go over that. It's not important. It's not how you'll focus on emphysema and chronic bronchitis. So COPD affects more than 5% of the population, has a high morbidity, high mortality rate. It's actually the fourth leading cause of death in the US. So should know this really well so you can treat your patients and make sure you prevent a lot of these things help them feel better. Okay. So let's start with emphysema. Emphysema, one of the two that we're going to go over. Emphasima is all about the

alveoli and the destruction. That's the main thing you need to know here for the actual, the patho and everything that's going on. So it's a permanent destruction of the alveoli, which leads to these enlargement of the terminal air spaces. So the damage to both the alveolar walls and the capillary surface of the alveoli result in this loss of surface area available for oxygen exchange. So the same way with microvilli in the small intestine you have all these microvilli so you have this extra surface area for absorption of nutrients it's the same thing with alveoli you have tons of alveoli all of these uh the walls of the avioli so you have this increased surface area and as these start to pop and break down and you know they they they're destroyed you have less area available for oxygen

exchange and that's the main problem we have with these patients and in addition to that as you have this alveoli destruction the damage that's done of the avioli as well as the lung parankuma leads to a loss of elastic recoil. And you have airway collapse, which leads to one of the main clinical manifestations in these patients. They have difficulty getting air out. So they have difficulty with expiration. They're going to have this long exhalation per slips to try to get it out. And the reason why this happens is if you think about a balloon, you blow up a balloon with air, you let go, and all the air just comes out.

It has recoil. It has that spring that pushes all the air out. Well, these patients, because of the breakdown of the avioli and everything else, they lose that elastic recoil. So when they take in a breath, they actually have to put in some effort to push the air out. It's not just an easy process like with you and me when we exhale. There's really nothing to it. It's more of like blowing air into like a paper bag. There's no recoil to push it back out.

So these patients have trouble with expiration. And because of this, they actually have retained CO2 because they can't push all of the air out of the lungs. Okay, now as far as these heologies, there's really just two that you need to know. The big one is smoking. Smoking by far most common cause of both chronic bronchitis and emphysema. It's your number one cause. It's also possible to get it from airway pollution and things like that that will see more commonly in third world countries. But here in the U.S., especially smoking is your number one cause.

But in emphysema, there's actually a second one that you need to be familiar with. And this is a genetic cause. It's known as Alpha-1 antitripsin deficiency. So don't go too deep into this, but no, if you see a vignette that presents a patient with emphysema or they describe emphysema to you, but it's a young patient, they're a non-smoker. Right away, you should be thinking you have alpha-1, alpha-1 antitrips and deficiency. So really, emphysema, no, smoking, and alpha-1 antitrips and deficiency, and you should be good. That's really all you need to know. Now, there's a couple different types that you should know.

Really, there's three subtypes, but there's only two that you should be familiar with. and that's central lobular emphysema and panacinar emphysema. I'm going to keep this brief because there's really only a couple of things that you need to know. These aren't really high yield, but there's a couple things that you should know about both. So central lobular. These are both of these terms are just ways to describe the area that's involved involved in the area of the distal terminal bronchials. But what you need to know about both of these types is that central lobular, Central lobar, if you see this, this is most commonly seen in smokers.

So the way that I used to remember that, Central Lobar, that starts with the C, so I think cigarettes. Okay, so Central Lobar, that's going to be cigarette smokers, most commonly seen in smokers. The other one, Panacinar, this is most commonly seen in patients with Alpha 1 antitripsin deficiency. And this is the question I got on my clinical medicine exam, I remember. And the easy way to remember this, or at least to me it's easy. I created this visual. So you have panacinar. Panasinar starts with a PAN, pan.

So what I think of is I think of a pan cooking a steak. And that pan in the steak in the pan, you're pouring A1 steak sauce over it because it's delicious and why not? So, and then you remember A1 steak sauce, alpha 1 antitripsin, A1, alpha 1 antitripsin deficiency. So panacinr, as soon as you think that, think of a steak in a pan, pouring A1, one steak sauce on it and then you'll remember panisina are is most commonly seen in alpha

one antitrips and deficiency hopefully that helps you it's a good little visual all right so now let's go on to history and exam what are we going to see what are we going to hear in these patients so first they're going to have dyspnea it's pretty common sense they're going to have trouble breathing and initially it's going to be remember this is a progressive disease so initially it's just going to be with exertion but as it progresses these patients are going to have dyspnea at rest eventually they're going to have trouble even speaking full sentences and remember as well they're going to have that prolonged expiration they're having trouble getting air out and a way that they compensate this is another thing you'll see on exam and another thing you may see in the vignette

is that they're going to have what's called what's known as pursed lip breathing purse lip breathing so this is a way that they compensate and they prevent the airway collapse so they they they purse their lips together and they push air out and what they do when they do this they actually increase the air pressure in the avioli and this increased pressure and this increased pressure actually keeps the aviola from collapsing, at least temporarily, and it helps them, helps make expiration easier for them. So they're going to have dyspnea, purse lip breathing. All right, now let's talk about some other things that you're going to see. First, these patients are not going to be cyanotic. They're not going to appear blue. They're not going to have blue lips.

They're not going to have any of the changes we'll see with cyanosis and hypoxia, like clubbing in the fingers. They're going to be non-cyonotic. So why is that? No hypoxemia in these patients. Well, patients with emphysema have matched VQ defects. So they have a problem with oxygenation in the lungs, but the body compensates for this. So what it does is the body recognizes this decrease oxygen, and it responds by decreasing cardiac outputs. You have less blood, and then it increases the respiratory rate. So they hyperventilate, and you have less blood coming. This compensatory mechanism results in limited blood flow through these lungs that are still getting fairly well oxygen, So they have less blood, but enough oxygen, that the blood is able to become oxygenated and they don't become hypoxic.

But like any compensatory mechanism in the body, there's going to be consequences. And the consequence here is because of the low cardiac output. These patients are going to have muscle wasting weight loss. They may appear thin and emaciated. I believe the term is cachectic. I may be saying that wrong, but cachectic is like this muscle wasting. So emphysema patients are normally going to appear hematiotic. thin and kind of wasting away.

And that's the, they're also known as pink puffers. And the reason they're known as pink puffers is one again, like I said, they're going to appear pink. They're not going to be blue. They're not going to be hypoxic. So pink, like normal, no hypoxia or no bluing of the, the mucus membranes. And then puffers, because like I said before, they do purse lip breathing.

So sometimes they're known as pink puffers and then chronic bronchitis are known as blue bloaters, which I'll go over soon. But again, so non-cyonotic, they're going to appear pink. and no hypoxia. And just as like a little note here, so this is an easy way to remember this for the exam, pink puffers, blue bloaters, but in real life, emphysema chronic bronchitis

can pretty commonly coexist. So it's not always that cut and dry. It will be for the exam, but in real life, not so much, but so just so you know that. All right, so another thing you're gonna see on exam is that they're gonna have this increased AP diameter. It's known as a barrel chest. And it's just due to chronic overinflation

of the lungs because they have all this retained air. They're retaining all this air, air trapping due to the elastic recoil. They develop this barrel chest. So they may have an increased AP diameter. So remember when you're doing your OSCEs and you're checking AP diameter, well, if they describe it's over a certain amount, you should be thinking of isema. And then let's go over what you're actually going to hear on auscultation. So what are your esculatory findings that you'll hear in emphysema?

So the key to emphysema, and this is different than chronic bronchitis, is that you're going to have absent or decreased breath sounds, and you're going to have hyper resonance to percussion. Remember, hyper resonance is kind of like when you're puffing out your cheek and you're tapping on it. You're going to hear that like, dung, dunk, dunk. It's going to be hyper resonant. And that's because they have these hyperinflated lungs. So just like when you puff out your cheek and it's full of air,

it's the same thing that's going on because they're retaining all of that air. So hyperresidence to percussion and then also decrease breath sounds because it's all full of air. So same thing with like a pneumothorax. You have decreased breath sounds because it's all that air that's out. So remember, the way that I used to remember that was emphysema. You should remember that E stands for empty. Their lungs are empty. And that's why you have like hyperpercussion, I'm sorry, hyperresonance and decreased breath sounds.

It's just full of air. It's like empty. Whereas I'll go over later in chronic bronchitis. It's full of mucus. You're going to have all these other things going on. So remember, sculptory findings, absent decreased breath sounds, hyper resonance of percussion. And again, remember the non-sionotic appearance. Okay.

So that's going to be your physical exam findings and different clinical manifestations for these patients. And let's actually go on to diagnosing these patients and diagnosing COPD in general. So the gold standard test, the best test for COPD, whether it's emphyseum or chronic bronchitis, is going to be your pulmonary function test. So that's your best way to diagnose. It's with your PFTs. So what are you going to see in pulmonary function testing? So you do a pulmonary function test. Patient breathes in, blows out, makes some measurements,

and what measurements matter in the diagnosis of COPD. So in emphysema, it's two measurements you're looking at. FEV1, which is your forced expiratory volume, which is the amount of air you can quickly exhale in one second. and then your FVC, which is the total number of air you can exhale after maximal inhalation, so all the air that you can get out, your forced vital capacity. So you measure both of those. You divide your FV1 by your FVC ratio, and whatever percentage you get makes the actual

diagnosis. So if you divide your FV1 by FVC ratio, generally the lungs can hold about 6 liters of air, so, you know, depending on what the measurements are. If you get a number that's less than 70, you've made the diagnosis of COPD. Now, keep in mind, patients with asthma are also going to have a decreased FV-1 and FEC ratio. So the way that you differentiate is you can use an inhaled broncholidilator. So you can use like an albuterol. So you do your FV-1-F-E-C ratio.

Then you do a broncholidilator challenge. You give them a broncholidilator inhalation. and then if you see a dramatic improvement, like a drop by like, or an increase by like 50%, something crazy, you know it's asthma. It's gotten much better. Now, if you see like a little mild increase, they went from like maybe 60 to 70 or 70 to 80. That could still very well be COPD. So you're looking for a dramatic change with the bronchodilator to indicate asthma rather than COPD. Because COPD, remember, this is a permanent destruction.

the changes aren't really going to improve that dramatically with the bronchodilator like asthma will. So that's a way that you differentiate. Now, the FEV-1 and the FEC ratio are going to be the same an emphysema as they are in chronic bronchitis. They're both going to be decreased less than 70%. So the way that you differentiate between the two is by using something known as DLCO. So this is going to be a test that is going to measure the diffusing capacity of the lungs for carbon myoxy. carbon monoxide. So in emphysema, there's aviolar destruction, decreases the gas exchange surface, and then this is going to lead to decrease diffusing capacity of the lungs. And that's why we see,

and that's why it's going to be decreased in emphysema. So DLCO is another test that you'll do to differentiate. In emphysema, it'll be low. Your diffusing capacity will be low. It's going to be normal and chronic bronchitis. So that's a key to differentiate between those two. Now, chest x-ray, there's a couple things that usually look for an patient with emphysema. And it's, It's a flattened diaphragm and something known as B. B also be aware that chest x-ray is not really sensitive for COPD. Really only about half the patients with COPD are going to have any findings of the disease present on chest x-ray. So it's a good initial test, but it's certainly not enough to diagnose.

So let's go over those two findings. So flattened diaphragm you're going to see on chest x-ray. And a normal patient diaphragm is obviously going to have some curvature, but in particular, patients with COPD, the diaphragms weakened. And this is from the chronic airflow limitation. It taxes the respiratory muscles, put strain, and eventually breaks down the muscles in the diaphragm. And it just becomes flat. You just have flattening of the diaphragm. And inability to generate tension with respiration, this all causes a further decline in these patient's symptoms. But flattened diaphragm is one key finding you'll see on chest x-ray.

And then something else known as Bollet. So Bollet are these areas in the lungs that form. They're over a centimeter. They're one plus centimeter diameter air-filled space that form due to emphysemitis destruction of the lung parincoma. So when you have these alveoli that are damaged, when they do, they develop these large pockets of air. So initially you had this space that had all of these little grape-like alveoli filling this area. But now just imagine they all popped. And in that space, you just have this big pocket of air left. So you can actually visualize that on chest x-ray, really better on C-ray.

really better on CT, but you can see it on X-ray as well. And they're just these bubbles of air that you'll see, and they're known as Boulay, and they indicate emphysema. So C-T is another test that you can do it as better, it's greater sensitivity and specificity than a chest X-ray, of course. You're going to look for a lot of the same things, though, Bollay, flatten, hemidiofram. CT is just going to have better image quality.

And it can also, an important thing with CT, it can differentiate between your central lobular and your pan-lobular. So different types of the emphysema that we see. So that's one thing that you can do with a CAT scan that you can't do with x-ray. All right. So that's emphysema. I'm going to go over treatment at the end because the treatment's the same for emphysema and chronic bronchitis.

So chronic bronchitis, there's actually a definition that you need to know for this. So chronic bronchitis is going to be a chronic productive cough for at least three months a year for two consecutive years. So for two consecutive years, each year they had at least three months of a chronic. productive cough. And also you need to make sure you exclude other causes of chronic cough like bronchiasis and things like that. So three plus months a year for two consecutive years of a chronic productive cough. So that is chronic bronchitis. Now what is chronic bronchitis? What is it cause from? So the main thing you need to think of with chronic bronchitis. So emphysemo is all about the alibi. Chronic bronchitis is all about mucus. Mucous and inflammation. So it's an overproduction

and hypersecretion of mucus by goblet cells in response to chronic inflammation. This inflammation, of course, is mostly caused by cigarette smoke, other toxins. Smoking, of course, is the main one. So your bronchial mucus membranes, particularly during acute exacerbation, can become edematose, hyperemic, and it leads to airflow impediment. And this, in addition to the mucus buildup and other debris in the airway can all cause chronic obstruction that we see in these patients with chronic bronchitis. So etiologies, I'm sure you guessed it, smoking. That's going to be the main one by far smoking. It can be caused by exposure to other toxins,

like I said before, air pollution, et cetera, but overall smoking, most common cause, no genetic cause that you need to know of here for chronic bronchitis. So history and exam, obviously dyspnea, just like we saw an emphysema. But then the key here is that they're going to have this chronic productive cough. So they're going to have sputum production, all this mucus coming up with this cough and that's the key difference in the actual history of the patient. Now as far as your sculptory findings, remember emphysemo is all about being empty. This is where full or full of mucus or full of other things. So crying bronchitis patients are going to hear a bunch of different things. They're going to hear crackles, wheezing, ronkai. Again, remember, they're full of mucus.

So you're going to have all of these different findings. Like I said, crackles, wheezing because of all of that mucus, all of that inflammation in the bronchials. Now, key here remember we said emphysema they were non-cyonotic bronchitis patients they're going to be cyanotic so why what's the difference here so in chronic bronchitis um they have this poor ventilation and they're having difficulty air getting through these congested and inflamed bronchiales which leads to alveolar hypoxia so they're not getting enough oxygen in their lungs in the avioli so the body just like in emphysema tries to compensate for this the way it compensates and chronicitya bronchitis is by decreasing the ventilation and increasing cardiac output, the opposite of what we saw in emphysema.

But this, unfortunately, creates a really bad VQ mismatch. So you have all a large volume of blood being sent to this poorly ventilated lung, and these patients are going to become extremely hypoxic. If this goes on long enough, which it will, of course, because this is progressive, these patients are going to develop hypercapnia and respiratory acidosis. When this happens, another thing happens now. So now they're hypercapnia, respiratory acidosis. This is going to cause the pulmonary vasculature to vasoconstrict. So all this hypoxia is going to cause vasociniction in the pulmonary vasculature. So now we have a new problem. Now we have pulmonary hypertension. And what happens with pulmonary hypertension? Leads the right-sided heart failure. The right-sides having trouble pushing into the pulmonary vasculature. So now we have

right-sided heart failure. So patients with chronic bronchitis are are going to have right-sided heart failure in addition to everything else. And that's why they're known as blue bloaters. So the blue bloters, one, blue stands for the cyanosis that you're going to see. They're going to have blue lips, blue gums, fingernails. They're going to be cyanotic. So that's why they're known as blue. They're known as bloaters because, remember, again, we have right-sided heart failure in these

patients. So they're going to be, they're going to have edema, they're going to have JVD, they're going to have peripheral edema. everything that we talked about in right heart failure, they're going to have, unfortunately, because the heart is now failing because it's pushing against those vasoconstricted vessels in the pulmonary vasculature. So blue bloaters, blue, they're cyanotic bloaters

because of the edema from the right-sided heart failure. So that's how they're going to appear. They're going to be big. They're going to appear like obese. They're just full of fluid opposite of the emphysema patients. Remember that we're skinny and wasting away. So that's their presentation. So now as far as a diagnosis, it's going to be similar to what we did in emphysema.

You're going to do your pulmonary function test. Again, this is your gold standard. You're going to see the same thing. You're going to see decreased FEV-1, decreased FEV-1, FEC ratio. Remember that number you need to know is less than 70%. But the key to differentiating here is their DLCO is going to be normal. There's no aviolari disease in chronic bronchitis. so the diffusing capacity of the lungs is unaffected.

So normal DLCO, that's going to be your key to not only diagnosing in real life, but on the vignette. If they say they have decreased FV1, decrease FEC ratio, it's 60%, remember less than 70, non-responsive to broncholator, DLCO is normal. And that's going to be your answer there because you're going to need to know, is this emphysema or is a chronic bronchitis. So DLCO, normal, normal diffusing capacity of the lungs. Now, the rest of the diagnostic findings, I'm not going to go over, you know, and really in depth, but they're all going to be related to right-sided heart failure, which you should be familiar with. So on chest x-ray, you're going to see an enlarged heart, especially that right border.

The EKG is going to show right atrial enlargement, right-axis deviation. Their H&H, their hemoglobin hematocrit are also going to be increased due to chronic hypoxia. So everything that you see in right-sided heart failure, they're going to see this isn't really specific. so I'm not going to go crazy. I mean, that's really all there is to it. So it's really just you do your pulmonary function test, normal DLCO, and then all of those other findings are all related to the right-sided heart failure in patients with chronic bronchitis.

All right, so let's move on to treatment. Again, treatment's going to be the same for emphysema as it is for chronic bronchitis. Before we get into the actual meds, I just want to go over a few interventions that you need to address in all patients with COPD. Be aware that no treatments outside of a lung transplant have actually been shown to greatly improve lung function. All the meds that we're going to go over, they make the patients feel better,

but they don't improve mortality. The only two things in COPD patients that have been shown to improve mortality is oxygen therapy and a patient who needs it, which I'll go over those numbers that you need to know, and smoking cessation. Smoking cessation is huge.

Everything else, all the meds, all the other interventions, just make them feel better. So first, smoking cessation. It's the single most important therapeutic intervention for COPD if they ask you what is the best treatment for a patient with COPD and they have all these meds on there albuterol everything and they have smoking cessation it's smoking cessation it's the number one thing the number one therapeutic intervention decreased

mortality second thing is supplemental O2 so oxygen now it's not every patient only if the patient has an O2 saturation less than or equal to 88 percent so that's going to be like from your pulse ox on your finger less than 88 percent or a PAO2, which is your partial pressure of oxygen, which you measure from arterial blood gas, less than or equal to 55. So only patients getting oxygen that show mortality benefit is going to be patients with an 02 sat less than an 88%, less than or equal to 88% or 02, or equal to 55 millimeters of mercury. If not, you give them oxygen, it's not going to improve the mortality benefit. Why would you do that? So oxygen can improve mortality, but only if you have those things.

met. Now, you may have heard you don't want to over oxygenate COPD patients that it can be harmful. And that's true. So let's go over why. So with COPD patients, you really only want to oxygenate them to get their O2 SAT as high as 92%. You're shooting between 88 and 92%. Why not higher? Why don't you want to get them to like a normal sat of like 98? Well, the reason is, let's go over that. So in a normal patient, you have chemoreceptors in your body. These chemoreceptors monitor carbon dioxide levels. And as it builds up in the body, it tells your body to start breathing. Breathe off that CO2. So that's the reason why when you hold your breath, you're building up all of the CO2, you go crazy and you have to breathe. Something's telling you start breathing. You need to. And it's because these chemoreceptors are sensing that increase of carbon dioxide.

They're telling your brain, breathe, get that carbon dioxide out. Well, in a COPD, deep, patient, like we went over, they have these chronically elevated levels of carbon dioxide all the time. And due to this, the level of carbon dioxide in the blood, it's no longer the trigger to tell them to breathe. The body's gotten used to that. So it's no longer, your body no longer responds to that. It's become accustomed to that. So now what your body does is instead of responding to carbon dioxide, it actually responds to the level of oxygen or the lack thereof. So it's actually your respiratory drive is actually in COPDU patients based on hypoxia. So let's, let's, of oxygen in the patients. And the idea is, is that these patients, if you give them really high

levels of oxygen, you get them up to like 98%. Well, their body is going to say, we're at 98%. We're only responding to the oxygen drive now. So there's no need to keep breathing the way we have. Respirationers are going to start to slow down. It's going to blunt their hypoxic drive. And it can lead to an acidosis because they're going to breathe much slower than they should to get off the carbon dioxide. So that's why you don't want to over. oxygenate these patients. You don't want to go higher than 92% because if you oxygenate them too high, their body's not going to respond to that hypoxic drive and they're going to wind up leading to an acidosis. So it's a long answer, but I think it's important for you to know. And then also know that

there are some studies showing maybe it's not 100% true that with high flow oxygen, it may overcome some of this, but that's kind of like not really proven yet. Overall, you should know for your exams not to over-oxygenate these patients. over 92%. Okay. So those are the two things that improve your mortality. Also be aware these patients absolutely need their annual influenza vaccines, their pneumococcal vaccinations. You don't want them to get these pulmonary infections, obviously can lead to really bad exacerbations and potentially it can be fatal. All right, let's move on to your meds. So medical management. So the way you decide for medication for patients with COPD is based upon this grading system known as gold scores. Gold scores are

classified they're even further classified into an ABC or degrading system these levels are based on fvv1 results number of exacerbations hospitalizations blah blah blah don't waste your time do not memorize this I was never asked it and if your professor asks you it's just being cruel there's really no need they're confusing and it's just not something that you need to know do not waste your time I'm going to list them just so we can kind of classify the meds that go into each category Do not waste your time memorizing these. All right, so let's go into the meds. I'm trying to make this as easy as I can because it can be a little bit overwhelming all the different categories of meds that you need to know.

But I'm keeping it really basic, really focused to make this pretty simple. So you have your minimally symptomatic patient, group A, is the gold classification. So this is as minimal as it gets, this patient is not very symptomatic. What are you going to give them? You're going to give them a sabah. So that's your short acting beta agonis. albuterol, level buterol. Now, Sabas, they're used in your minimally

symptomatic patients in your group A, your first patients, but they're also used across the board. So every category I list, just know you're always giving them a sabba, but now you're adding additional things. So group A, minimally symptomatic sabas, your albuterol, short-acting beta agonis, albederol. That's it.

That's your group A. That's all you need to know. Now, let's move on to group B. More symptomatic, but they have a low risk of exacerbation. So a little bit more symptoms, group B, still low risk of exacerbation. Obviously, you're going to give them your sabas, your up uterol, but now you're adding either a laba or a llama. You have a choice. You can use either one.

This one isn't telling you one or the other. So labas is going to be your long-acting beta agonis, and then llama is your long-acting muscarinic antagonist. The llama, the one you'll most hear, I'm going to use the abbreviations. It's just too long to keep saying. Lama, the one you'll most likely hear about is teotropium. which is Spareva. I'm sure we've all heard of sporeva. So teotropium is your llama. And then your labas are going to be your cell meterole, formetrol. And there's a slight preference for llamas. They have reduced exacerbation rate compared to lavas. But anyways, so group B,

sabas, and then you're adding either a lava or a llama. That's it. Now group C, minimally symptomatic, but high risk of exacerbation. So this is why this is this is this, this classification system is so confusing. So group B was a little more symptomatic. Group C is minimally symptomatic, but they have a high risk of exacerbation. That's what bumps it to the next group. So anyways, group C, we're now moving to the next level. Of course, you're Saba, so your albuterol, but now you don't have a choice anymore. You don't choose between a Laba or a Lama. You're giving them a Lama. So they're going to get their Spareva, their teotropium. Plus or minus an inhaled glucocorticoid. It's not really recommended for all these. Really focus for your group C, Saba, and

llama no choice here you have to use a llama teotropium now group deep this is your worst class this is your they're more symptomatic and they have a high risk of exacerbation this is your worst class so group d now you're going to not give them a lava or a llama you're giving them both you're going to give them a lava and a llama or you have an option you can give them a lot if you give them a lava you have to combine it with inhaled corticosteroids so that's going to be fluticicin with salmeterol which is adver HFA, Budescine, Formetrol, which is simbacourt. So group D, more symptomatic, high risk of exacerbation, laba plus a llama, or if you're going to give them a lava, which, remember, is the less effective.

You have to combine it with an inhaled cortic steroid like in your adver or your sympathar or your Cibacore. All right, so let's go over that again. So group A through D, group A minimally symptomatic, saba, albuterol. Group B, a little bit more symptomatic. You're going to give them a saba again, of course. a laba or a llama you have a choice here group c sabba again of course and now you don't have a choice anymore it's a llama teotropium and then group d your worst one of all sabah of course and then either a lama

combined with a laba or a lava within an uh inhal corticosteroid like your bodesonide and your form at all okay so i try to make that as straightforward as i can it's you know it's one of those things that's a little bit difficult especially through a podcast but that's it it's not really that bad when you kind of go over it a few times. The only other thing that I wanted to go over is patients with acute exacerbations. You don't give everybody antibiotics. You'll kind of hear that antibiotics for acute exacerbations, but you don't give it to everybody. You want to avoid that.

It's really only reserved for moderate or severe exacerbations. And you decide how severe their exacerbation is because how, I mean, how can you really know? The patient comes in with COPD. A lot of times it seems like severe all the time. So you decide this by seeing as their disc may increase, they have increased sputum volume, increased sputum purulence to indicate if this is an acute exacerbation. You need two out of the three.

So really, it's getting a good clinical history from the patient, them telling you this is bringing up more sputum than I normally do. My shortness of breath is worse than it normally is because a lot of times they'll be coming into the ER. You don't know these patients. Okay, anyways. So that's acute exacerbations. What are you going to do for an acute exacerbation, moderate or severe?

You'll give them antibiotics. Generally, the class you're going to hear about is it going to be macrolides, azithromycin in particular, because your macrolides, like azithromycin, actually have, in addition to the bacteriostatic and bactericidal effect, they actually have an anti-inflammatory effect in the lungs. It's not just the lungs. It's actually the GI tract, a few different areas. It's actually a really great class of meds. But generally, you'll see macrolides being used as itchromycin, fluoroquinolone. I'm sorry, fluoroquinolones can also be used. a couple different classes, but macrolides you'll see being used most commonly.

Actually, is itromycin can be used prophylactically at low doses in some patients. Then the other things you'll see being used, either PO or IV medications, all depending on their severity level. Bronco-dilators, of course, your albuterol, your Ipertropium, which combined is like as a breathing treatment. You combine both of those to do a breathing treatment for these patients. But generally, for your acute exacerbations, you'll be looking at those antibiotics. Macrolides is going to be the big ones.

One other miscellaneous thing I wanted to go over before we do five questions on this is if you ever see multifocal atrial tachycardia and they ask you what common condition is associated with multifocal atrial tachycardia severe COPD. Remember that. I'm telling you that because I always ask that if you ever see multifocal atrial tachycardia and they ask you what is this associated with severe COPD. That's just a little miscellaneous thing that I wanted to mention. All right. So that's it. Let's just do five quick questions and then we will wrap it up. So one, what is the most common cause overall of both chronic bronchitis and emphysema? You should definitely know this one. That is going to be smoking. Question two, define chronic bronchitis. Of course, I'm talking about the definition, the clinical manifestations, the time, you know, kind of guiding you there because the question's kind of broad.

So define chronic chronic bronchitis. That's going to be a productive cough for at least. least three months a year for two consecutive years. So chronic bronchitis, productive cough for at least three months a year for two consecutive years. Question three. Panicenar or diffuse scenery involvement. So never mind. Panicinar. I don't want to make that confusing. So Panicinar involvement is seen in which type of emphysema. Panicinar is seen in which type of emphysema. That's going to be alpha-1 antitripsin deficiency. Remember? pan with a stake in it, you're pouring your A1 sauce, Alpha 1 antitrips and deficiency, panacinar. It's going to be the type you'll see that in.

Question four, oxygen therapy in a patient with COPD should only be initiated if their O2 SAT and their PAO2 are at what levels. So when would you initiate oxygen in a patient with COPD at what O2 SAT levels and what PAO2 levels? So that's going to be an oxygen saturation less than or equal to 88 percent, and a PAO2 two of less than or equal to 55 millimeters of mercury. All right. Last question. Patient with Group D, COPD.

They have high risk of exacerbation, high symptom burden, the worst, most severe patient of COPD. What type of medical management should this patient receive? So remember Group D, this is the most severe patient. What are you going to give them as far as medical management? So again, remember Saba, everybody gets a Saba. And then either a Lama or a Laba. combo or a lava combined with an inhaled corticosteroid like the budescine with formetorol.

Okay, so that is question number five, and that is COPD. I think that's some good high-yield stuff that you should definitely get your questions right. I've covered most of the bases there and the things that you need to know. So thank you so much for listening. Thank you for the support, like the comments, everything else. And good luck on your pants, your pannery, your EORs, and good luck in PA school.