S1E33 Restrictive Pulmonary Diseases

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If you haven't checked out the YouTube channel yet, please do. It's cram the pants on YouTube and it has some great visuals to go along with these presentations. Let's get started on restrictive pulmonary diseases. I'm going to say this out right. Probably not the highest yield of all the topics you can study in poem, but there's a few things that you may get questions on. So we'll break it down, of course, the most important things that you need to know and just some of the tricks to ways, tricks to remember these. I'm going to focus more on sarcoidosis in a deopathic pulmonary fibrosis. Those are the two more important and then we'll go over towards the end, the pneumoconiosis. So let's start with sarcoidosis. This is an idiopathic multi-system inflammatory disease and it manifests as what's called non-caseating granulomal. It's most commonly found in the lungs and the interthoracic lymph nodes. Now as far as the pathopts, all about the T cells. So the T cells play a central role. You have this exaggerated T cell response. It leads to the successive cellular immune reaction and because of this, you have inflammation and granuloma formation. So T cells get out of control. You have this immune system that's gone into overdrive. Inflammation, granulomas form throughout the body leading to the clinical manifestations. We'll see. Now risk factors, there's two things that you need to know because this is what's going to be on your vignette. This is who they're going to give you on the vignette. So risk factors, African-American, three to four times more common and then females. There's a slight female predominance. So in the vignette, they're going to give you an African-American female. That's the question you'll get on sarcoidosis, almost 100%. So you look for that in the vignette to kind of differentiate from other conditions, which we'll go over later, whether demographics are going to be a little bit different. So sarcoidosis, remember African-American females, likely who you'll see, in the vignette and in real life too. Now clinical manifestations, bear in mind, this is a systemic disease. It can affect anywhere in the body. So there's a lot of possible clinical manifestations. We could go on and on forever, but let's focus on the common ones and the unique ones because that's the ones that the boards are going to test you on. Now first before we talk about what you'll see in clinical manifestations, be aware many patients about half the patient population is going to be a symptomatic. The disease is only going to be detected on an incidental chest x-ray, prior to the development of symptoms. That's about half the time this is just going to be an incidental finding on chest x-ray. Now if they do have symptoms, half of them are going to be pulmonary complaints. The main things we're looking for is a non-productive cough, dyspneon exertion chest pain. All that's very non-specific, but those are the most common complaints you'll see in sarcoidosis. Now these are the unique ones that you should look out for in the vignette. So the first thing looking into your dermatologic finding, so erythema no-dosum. It's those painful nodules that are most common on the anterior surface of the lower extremities. It's a non-specific finding because it can be found in strep infection. It can be caused from medications, ulcerative collitis. So non-specific, but the key to erythema no-dosum when we're talking about sarcoidosis is a combination of erythema no-dosum, polyarthrilogis and fever and bilateral lymphatonopathy. If you see that, that's known as loftgren syndrome and it is very specific to sarcoidosis. So specific that you don't even need a biopsy to diagnose. So again, loftgren syndrome is a combination of erythema no-dosum, polyarthrilogis, migratory polyarthrilogis, combined with fever and then bilateral, high-larloofatonopathy, which you'll see on chest x-ray. Loftgren syndrome, remember that if you see that right away, you should be thinking sarcoidosis. Another specific finding in derm is something known as lupus perneo. So it's the most specific physical exam finding in sarcoidosis by itself and it's pathonomonic for sarcoidosis. It's these indorated plaques that kind of have this vialacious discoloration. It's mainly found on the face, so the nose, cheeks, lips, sometimes the ears too. And it's more common in the African-American patients with sarcoidosis. So lupus perneo very specific as well. And then on your x-ray, so lymphatonopathy, you may see bilateral, high-larloofatonopathy. So it's this bilateral enlargement of the lymph nodes of the pulmonary high-larloofatonopathy. It's a classic finding in sarcoidosis that you'll see on chest x-ray. And then finally, not as important, but just remember that sarcoidosis is one of your causes of restrictive cardiomyopathy. So it's one of the infiltrated diseases that can cause restrictive cardiomyopathy. It's because of the granuloma deposition of the myocardium. So remember that as well. Now diagnosis, there's no specific or definitive, I'm sorry, there's no definitive diagnostic test for sarcoidosis. You're looking for a combination of a few things. You're looking to make sure they have the clinic, the classical clinical manifestations. You're looking on x-ray to make sure they have those classic findings. They're excluding other diseases like tuberculosis, which can present in a similar way. And then on biopsy, you're looking for a detection of a non-caseating granuloma. So let's generally, what you're looking for to make the diagnosis, don't memorize that. It's not important for the exam, but I just want you to be aware of how the diagnosis is made when you're actually treating patients. All right. So let's actually go down the different tools we use to diagnose. First, chest x-ray. Bialateral high-larloofatonopathy. Half of effective patients with sarcoidosis are going to have bilateral high-larloofatonopathy. So that's one of your first expressions of sarcoidosis. It's the big fluffy stuff. I'd like to have a visual here, but I don't, but it's the big fluffy stuff at the center of the chest x-ray. It's in a large one of those lymph nodes and pulmonary high-larloofatonopathy. On x-ray, you look for this big fluffy stuff right in the center of the chest x-ray. So very classic finding in sarcoidosis. Now labs, you have to know this one. Increased ACE level. So your serum and your tentsinconverting enzyme. The ACE level is going to be elevated in about 75% of sarcoidosis patients that are untreated. So what you should know is that you're definitely going to see this on a vignette. They're definitely going to mention increased ACE levels, but know that it's not really a great diagnostic test. There's a lot of false negatives. But again, it's going to be on your vignette. Just know that in real life, it's not the best test, but you will see this in a lot of your patients. Now pulmonary function testing. Remember, these are all restricted diseases. So you're going to see your restrictive pattern. So your pulmonary, your PFTs, your pulmonary function test will reveal a restrictive pattern. So your FEV1, FEC ratio is either going to be normal or increased. So remember patients with restrictive disease. There's no trouble getting air out. It comes right out. It's just having trouble getting air in. So you always think about just putting a big strap or rubber band over your chest. So you breathe in and then it's hard to breathe in because you have all that resistance from that rubber band, which is really the scar tissue and the fibiotic changes that these patients have with restrictive diseases. So hard to breathe in, but then remember that big rubber band. As soon as you breathe out, it's pushing it right out. So it comes right out easily. And that's why they have this restrictive pattern. So normal or increased FEV1, FEC ratio, you'll see on these patients. The way that I used to remember that because sometimes I forget what is obstructive, what is restrictive, how does it change the ratio. So the R and restrictive disease, it stands for raise the ratio or remain the same. So remember restrictive FEV1, FEC ratio. Restrictive is either going to R raise the ratio or R remain the same. And then obstructive, I always remember, oppress the ratio. It keeps it down because obstructive diseases keep it down. So O, oppress the ratio, R, raise or remain the same. So remember that for your FEV1, FEC ratio. Now biopsy, this is big. So you can biopsy anywhere there's an accessible lesion. You don't have to go all the way into their lungs into the intratherasic lymph nodes. You can get it anywhere. If there's a cutaneous lesion, if there's a palpable lymph node. And then what you're looking for on biopsy, the characteristic feature of sarcoidosis is a non-caciating granuloma. That's what you're looking for on biopsy. Again, it can be biopsy anywhere that there is an accessible lesion. Treatment is very easy. Treatment is just steroids. So oral corticosteroids, first line, that's all you need to know for treatments. Don't waste any time with anything else. Not every patient's going to need treatment, because a good number of patients with sarcoidosis will have a spontaneous remission, or they may have a benign clinical course not requiring treatment. But if they ask you for treatment, 100% steroids. All right. So there's a few things you need to know with sarcoidosis. Let's give you a way to remember that. So remember, we said those ACE levels were super high. So ACE levels super high. ACE levels L super S high H. So that stands for A African American. Remember three to four times more common. The C stands for cough, dry cough, pulmonary findings are the most common. The E stands for erythema no dosum. The L stands for lupus perneal. Remember your most specific finding. S stands for steroids, first line treatment for patients that need it. And then the H in high stands for high large lymphatonopathy bilateral. So remember ACE levels super high. African American cough, erythema no dosum, lupus perneal steroids and high large lymphatonopathy. Okay. So that's sarcoidosis. Let's move on to idiopathic pulmonary fibrosis. So this is a rare form of fibiotic disease with no known etiology. That's what idiopathic obviously stands for. You're going to have progressive scarring of the lungs over the period of several years. This isn't going to be something that's going to come on quickly. It's an insidious onset. And while there's no specific cause known, there are a couple of important risk factors, which you'll see are quite different than sarcoidosis. So an idiopathic pulmonary fibrosis risk factors cigarette smoking. Majority of patients with pulmonary fibrosis are going to have a history of cigarette smoking. Males. So it's actually more common in males than females. This is the opposite of sarcoidosis, which will help in your vignettes, which remember was more common in females. And then finally you're going to see this in older patients, generally over 60. It's most commonly seen in the sixth and seventh decades of life. It's rare to see idiopathic pulmonary fibrosis in patients less than 50. Okay. Now the clinical manifestations on pulmonary fibrosis, I'm just going to start calling it that rather than idiopathic pulmonary fibrosis every single time. There's really nothing specific, which means anytime there's nothing very specific, you're probably not going to get an exam question. But the clinical manifestations are going to be dyspnea. It's going to be generally on exertion, non-productive cough. Again, remember in city of soonset. So generally over the span of a few months, maybe a year. And then physical exam. Bibasilar crackles. So they may be absent early on in the disease, but that is something you will likely hear in these patients. Remember, bibasilar just means that the basis of both lungs. So biceps, bilateral basilar, base of the lungs. So crackles at the base of both lungs. And then clubbing. Because remember, clubbing other fingers, anytime you have a chronic hypoxemic state, clubbing of the fingers is something that is definitely a possibility. So all of those really nothing specific to idiopathic pulmonary fibrosis. And then diagnosis. A few things. So remember pulmonary function test. Of course, this is a restrictive pattern. So normal or increased FEV1, FEC ratio. Restrictive R remains the same or raises the ratio. Chestics rate. Not very specific. Again, you're going to have these increased particular markings. Which is great. But you can see that in any interstitial lung disease and in heart failure. So not specific. Chest CT is where you're going to have a little bit more specificity as far as diagnosing. And really all patients with pulmonary fibrosis or suspected pulmonary fibrosis need a CT. Much more sensitive and specific than a chest x-ray. And it's really essential in the diagnostic workup. So there's three findings you're going to see on CT that are characteristic of pulmonary fibrosis. The first one is something known as honeycombing. So honeycombing is this peripheral basal or predominant opacities to put that in a way that we kind of understand it. It's really just these cysts that are spread throughout the lung field. They're all different sizes. Generally pretty small, about three to 10 millimeters. And they're clustered together. So you have these little cysts that look like holes on CT. And when you have all of these cysts that are clustered together, they just look like a honeycomb. If you look at a honeycomb, it's just these little holes all next to each other. So that's what honeycombing is on a CT. And you can see this in medopathic pulmonary fibrosis. Something else you may see on CT is something known as traction bronchiectasis, bronchiolectasis. Just due to the damage of the bronchioles, you have these distorted abnormally dilated bronchioles. And then finally, something else known as bilateral ground glass opacities. So when you look at the CT or even a chest x-ray, you have this hazy increased lung opacity. Just due to all the scarring and fibrosis that are overlaying the lungs. It can be seen in other interstitial lung diseases, sarcoidosis, etc. But it's generally more prominent in pulmonary fibrosis. So again, ground glass opacities, just this hazyness you'll see over the lung fields because of all the fibiotic changes and scarring over the lungs. Now biopsy, what you're going to see is alternating areas of normal lung, fibrosis, and honeycombing. So you have, you look at the biopsy and then you see these fibiotic changes with varying levels of severity. So different ages, varying ages, next to normal lung, next to honeycombing. So that's the hallmark findings. You have alternating areas of normal lung, fibiotic changes, and honeycombing. That's biopsy. And then treatment. So there's no cure for idiopathic pulmonary fibrosis outside of a lung transplant. And most of the measures you're going to take are going to be supportive. So some of your supportive measures, smoking cessation, is an obvious one. And then supplemental oxygen. All patients with pulmonary fibrosis are eventually going to require oxygen. Initially, it's just going to be with exertion, but eventually they're going to progress to a point where they're all going to be on it continuously. You of course, want to make sure that these patients get all their routine vaccinations. They're pneumonia vaccine. They're influenza because this is a bad interstitial lung disease. If they get these pulmonary infections, it can be pretty severe for them. Now medications, these are the only medications you need to know. They're not going to ask you supportive measures. It's just hard to ask a question about should they stop smoking, obviously they should. These are probably the only two that you should know. So there's a lot of drugs that have been tried in idiopathic pulmonary fibrosis that have shown no clear benefit. You might see anti-coagulants, phosphodiesterase inhibitors. None of these really showed any real benefit. The only ones that have shown some benefit. The only ones that you need to know are two known as nittatinib and perphenidone. They're anti-fabrotic agents. They are by no means a cure, but they slow disease progression. It's really the best thing we have right now outside of a lung transplant. Remember, if they ask you a medication, it's either going to be nittatinib or perphenidone. Those are your anti-fabrotic agents that slow disease progression. And then your definitive treatment, which of course is a lung transplant. So going over all that, you're going to realize there's a lot of stuff in pulmonary fibrosis that's just very non-specific. So it's unlikely you're going to get a question on it. The presentation's not specific. Most of the imaging findings are generally non-specific. It's not much in the way of treatment outside of those two I went over. So I wouldn't waste too much time on that. All right. So let's finish up with our pneumoconiosis. These are also known as occupational or environmental lung diseases. So they're a group of interstitial lung diseases, which are caused by inhalation of dust, minerals, exposed, and patients that are commonly exposed are ones that have exposure in the workplace. So these are pretty low yield. I'm going to focus on the risk factors for each one because that's the question you're likely going to get. A description of their job and then they're going to ask you what job or they're going to tell you the job they work in. Like they're going to say they work in the textile industry and then you just need to know that that's that's bisonosis. So that's likely what they'll give you. So we'll focus on the the risk factors, the workplaces they're at. And then I'll go over a couple other things that I think are important. As far as treatment, there's really nothing specific for these. You just, they're not going to test you on. It's generally subordinate of our steroids. Those are really the main treatment options for these conditions. So I have a couple tricks. My first trick for memorizing these is that the diseases, some of these diseases are going to have pulmonary nodules with a pred election for a certain part of the lung. So either the upper or lower lobes. And the easy way to remember this is that the lobe, the nodule is found in. So the upper or lower lobe is the opposite of the height that the person does their work in. So let me explain this, give you an example. So if they work in roofing, roofing and addicts, they repair insulation, high up in addicts, like an asbestosis, that's up high. So the nodule will be found opposite. So nodules generally found in the lower lobes. If they do work on the ground or deep in the ground, like a coal miner, coal miner, nodules are generally found up high in the upper lobes. And that works with all of these. I'll go over the few that the, because not every condition is going to have a specific lung zone that it's found in, but the ones that do actually work. So this works out really well. So an easy way to remember. All right, let's start with co-workers pneumoconiosis. So this is obviously caused from inhalation of cold dust particles. So that there's nothing really to memorize there. It makes sense. Now patients with co-workers pneumoconiosis work deep down in the coal mines. So what do you think their nodules will be found? Just like I just said, the opposite. So nodules and co-workers pneumoconiosis generally found primarily in the upper lobes. They're these small nodular capacities, generally less than a one centimeter in diameter, and most commonly found in the upper lobes. Now one of the things I'll mention, I don't think it's super important, but there's something known as capline syndrome. And all capline syndrome is a combination of co-workers pneumoconiosis and rheumatoid arthritis. One of those things not super high yield, but maybe your preceptor will ask you it and you'll sound very smart if you know it. So capline syndrome co-workers pneumoconiosis combined with rheumatoid arthritis. All right, let's move on to bisonosis or bisonosis. I don't know how you want to pronounce that. But the only thing that I remember for this is bisonosis is at risk for people who work in the textile industry, which is where cotton fabrics are made. So they have this cotton mill dust exposure. So people that work in the textile industry, I don't know if you knew this, I didn't know this, but the textile industry is just people who work with like yarn and making cotton into yarn and things like that. So bisonosis cotton mill dust exposure from people that work in the textile industry. That's all you need to know for that one. All right, as bestosis, inhalation of asbestos fibers, which leads to diffuse pulmonary fibrosis, who we're going to see this in, people who renovate old buildings, insulation like up in addicts, shipyards is another one, and then installation of roofing tiles or shingles. And the US asbestos has been limited since the 1970s. The only place you can use this in the US asbestos is in breakpads and gaskets and cars, roofing products and fireproof clothing. But the key is that if it's an old building that you're renovating and you're up in the attic, you're in the insulation and this building was built in the 1950s, they can still have exposure. So know that in real life and for the vignette, if they say something about an old building. Now chest x ring, these patients work up with roofing tiles, shingles, they work in insulation and buildings and in addicts. Those are all up high. So where are we going to find their pulmonary findings? It's going to be down low. So these aren't so much nodules, but they're plural plaques and they're commonly in the lower lobes. So patients with asbestos will have plaques on the parietal plura generally in the lower lung zones. Remember, opposite of where they're working. And then another thing you need to know about chest x-ray, there's something known as a shaggy heart sign. All it is is this indistinct heart border. So the interstitial and plural involvement caused this hazy another ground glass appearance to the chest x-ray and it blurs the diaphragm and the heart border. And that's why they call it the shaggy heart sign. And then finally, these patients obviously have an increased risk of bronchogenic heart sonoma, particularly in your smokers, because there's a synergistic effect with smoking and people with asbestos. So people who smoke and have asbestos exposure, super high risk of bronchogenic heart sonoma, I think it increases your risk by like 8.7 folds. So really high risk for that. All right, a couple more and then we'll wrap it up. So next one is known as berylliosis. This is chronic beryllium disease. It's a granulomatous disease caused by exposure to beryllium. Beryllium just so you know, it's lighter than aluminum six times stronger than steel. And for that reason, we kind of see it used in certain work, you know, workplaces. So aerospace, the aeronautics industry is a big one. Electronics people, people who manufacture electronics computers. We also see using the defense industry dental appliances, but the two you need to know, the two they'll test you on is the aeronautics industry air aerospace and electronics. So know those two for berylliosis. Okay, so silicosis our last one. This is inhalation of silicone dioxide risk factors any job that they mention breaking up silica can silica containing rock or anything they mention rock stone moving the earth digging up the earth think of silicaosis. So people who work with granite, quartz, sandblasting, which we know is just broken up rock, masonry work slate again. If you remember, if it mentions a rock, right away think of silicaosis. Chest x ray. So two things you need to know on chest x ray that may come up. Now these patients, they work with stones and rocks and minerals where you find stones and rocks and minerals up in the sky. No, it's found in the ground down low. So we're going to find their nodules, the opposite, upper lobes. So nodules primarily found in the upper lobes and silicaosis. And then the other one they should know something known as eggshell calcifications. It's this thin layer of calcification around the high-lar lymph nodes. They look like eggshells on chest x ray. It's not only seen in silicaosis. You can see on co-workers pneumoconiosis, long standing sarcoidosis, but it's commonly seen in silicaosis. It's normally the one they'll mention it in. So be aware of that as well. That's it for silicaosis. So just know the patient and the vignette are going to is going to work with rocks, quartz, granite, sandblasting, and then on x ray, look for upper lobe nodules and eggshell calcifications. All right. So that's really all I think you need to know. Don't waste your time digging any deeper than this. There's just it's just not high yield enough to waste your time any further than that. I have a little story to help you memorize the things you need to know in those pneumoconiosis. I like stories for memorization. I think it helps. You kind of create this visual in your head and you can remember for the exam. So hopefully this will help you. It did for me. So I'm going to give you a little story and it'll help you remember the key things you need to know. So here we go. Sylvia was tough as a rock, but this tough exterior would shatter like an egg shell every day. She'd be grudgingly had to go to work. So Sylvia S.I.L stands for silicaosis. She was tough as a rock. That rock because remember silicaosis risk factors occupation exposure to rocks granite slates and blasting, but her tough exterior would shatter like an egg shell every day. She had to go to work. Remember egg shell and silicaosis. Those are your calcifications in the hyalur lymph nodes. So again, Sylvia Silicaosis was tough as a rock. That's your risk exposure, but this tough exterior would shatter like an egg shell egg shell calcifications every day. Sylvia longed for the day. She could say buy to the textile factory she worked at. So she longed for the day. She could say buy. That's buy synosis buy and then textile factory because remember buy synosis increased risk for textile industry workers. Okay, her dream was to one day build space shuttles. So each night when she got home from work, she would bury her head in books about aerospace and electronics. So every day she get home from work, she would bury B.E.R.Y. Berylyosis. Her head in books about aerospace and electronics. Remember Berylyosis increased risk for individuals working in aerospace and electronics. Okay, last sentence. For now, this was just a dream and she would have to do her best to get through the long days at the broken down poorly insulated old building she worked at. So for now, this was just a dream. She would have to do her best as an as best doses to get through the long days at the broken down poorly insulated old building she worked at. Remember as best doses commonly found in insulation repair renovation old buildings. So I'm going to read it one more time. She'd be grudgingly how to go to work. Sylvia long for the day she could say buy to the textile factory she worked at. Her dream was to one day build space shuttles. So hopefully you're taking the exam and then all of a sudden you see something that mentions maybe somebody that works in aerospace and you're like, "Are you very, very, very burly-oated?" She buried her head. I hope that helps and I hope that'll create some visual in your head so you can remember. And if you need a little bit better of a visual there on my YouTube page, I have some visuals combined with the story plus you can actually see the words which can sometimes help. All right, so that's it. Let's do five quick questions and we'll wrap it up. Question one, 45-year-old African-American female presents the office today for a persistent, non-productive cough she's had for the last five months. On exam, you note, "violacious plaques on her nose and cheeks." Bilateral high-large lymphatonopathy is visualized on chest x-ray. First line medication for the likely diagnosis in this patient is going to be oral corticosteroid. So this is obviously sarcoidosis. Lupus perneal was described by those violations findings on the face. Bilateral high-large lymphatonopathy on the chest x-ray and then remember in the vignette, it was an African-American female. All signs point to a sarcoidosis which oral corticosteroids are your first line if you do knee treatment. Question two, a 66-year-old male presents the office with the history of a non-productive cough. It works for a construction company that restores and renovates old buildings. On chest x-ray, bilateral pleural plaques are noted in the lower lobes. What diagnosis should be suspected in this patient? So that of course is going to be asbestosis. Plural plaques in the lower lobes works in the construction business, repairing old buildings, which remember is one of the risk factors for asbestos. And then of course those pleural plaques in the lower lobes because remember it's the opposite of the work they're doing the height. Question three, patient with sarcoidosis presents with erythema noidosum, bilateral high-large lymphatonopathy, and polyarthoralges with fever. The syndrome is known as, remember that is known as Lothran syndrome in sarcoidosis. Question four, a patient with co-workers pneumoconiosis would likely have nodules in which part of the lungs. So remember co-workers pneumoconiosis, they're working deep down, so they're going to have nodules in the upper lobes of the lungs. And then question five, last one, what medications are used in patients with idiopathic pulmonary fibrosis to slow progression of disease? These are the only medications you need to know for idiopathic pulmonary fibrosis and it's going to be parapheredone and it's adenib. Alright, so that was it. I hope that was helpful. That is your restrictive pulmonary diseases and that is following the NCCB blueprint, the ones that they want you to know. Please let me know in the comments if it was helpful. Please check out the YouTube page if you haven't yet. And thank you as always for all the really nice comments you have been leaving. Good luck on your pants, your pantryurus, and good luck in PA school.