good afternoon everyone um my name is n cangar um I'm joined here today by Dr Robert Sue who's the U professor of rad radiology at UCLA as well as the inter as well as The Residency program director for the Radiology residency at UCLA as well as a director of Interventional Radiology there uh this is an interactive session so there are embedded questions that you're going to see and we're going to be asking for you to actually use the audience response system as we go through these questions that will lead up to specific areas that uh Dr Sue will be highlighting so please make sure when we get there to all vote so without further Ado uh Rob right great all right thank you all for coming uh thank you ner all right so all right okay so when looking at a high resolution CT it's really important to keep the pathology based terms clear and distinct uh compared to the pattern-based terms so the pathology based terms are really what's reflected on pathology so these are going to be entities like uip nsip lip AIP organizing pneumonia uh desaive interstitial pneumonia respiratory bronchitis interstitial lung disease and langran cell histiocytosis and lymphangiomyomatosis the pattern-based terms on the other hand are basically are kind of a bird's eye or airplane view of what's happening at the pathology level or what we're seeing inct is just a reflection of what's happening on the pathology so these terms are going to be a little bit vague but for lack of better these are kind of descriptive findings such as reticulations nodules cysts and there may be some terms like heterogeneous attenuations so that there's alteration in the uh lung parena and you'll see terms and we'll go over this Mosaic attenuation airspace attenuation or consolidation and this can be in the form of heavy ground glass or just ground glass and true airspace consolidation where you can't see the underlying lung structures so the patterns that we're going to discuss this afternoon are simply reticulations nodules cysts and airospace disease and some of the common entities uh that display these sort of radiographic patterns so under reticulations you have mostly the interstitial lung diseases UI NSP chronic hypersensitivity pneumonitis the nodules uh pattern or nodular pattern and we'll go through a number of these patterns but clinical entities would be sarcoidosis metastases more of the airway born things like Subacute hypersensitive pneumonitis Cy as we kind of mentioned those two entities and airspace are prom dominant airspace disease in the form of organizing pneumonia and dip so our first case uh is a 77y old man uh with a three-year history of progressive dision exertion the cases are intentionally kept brief so we can get through more so you're going to see a few axial images and a coral there and then I'll go back through them so what is the most likely diagnosis here is this nsip asbestosis idiopathic pulmonary fibrosis or chronic hypersensitivity pneumonitis please vote great 94 so you guys uh you guys all have this down I would just uh session's over yeah you know I I think just although only 1% selected it just to recognize that asbestosis could have very similar features I mean what are we seeing here the predominant features we saw here is a reticular pattern with that is more lower lung field peripheral predominance with reticulations honeycomb changes uh traction bronchiectases and bronchiolectasis and uh minimal amount of ground glass asbestosis would not be inappropriate here if there were other features of as asbestos related lung disease like plural plaques rounded auses and a clear history um so that's the only other answer that could make sense with the appropriate additional findings okay so obviously we're in the first ort of gamut which is reticulations and again we talked about me briefly mentioned uip nsip chronic HP and the clinical entities that this may rep represent uh ipf collagen vascular disease drug toxicity or maybe in some cases asbestosis or diseases that might give you reticulations so when dealing with reticulations it's important to look at the dis differentiating features and so you'd like to know what the distribution of those those reticulations are is it upper versus lower Central versus peripheral segmental versus diffuse is it the pattern that you're seeing a heterogeneous pattern is there more homogeneous pattern when you compare right and left sides do they kind of overlay or mirror one another or are they very different you also want to look for honeycombing sub plural sparing ground glass attenuation and there may be some other Clues on the film that give you uh maybe some idea or maybe a cue as to what the patient might have in terms of ancillary findings so with asbestosis or asbestos exposure you might look for plural plaques you might see arthropathy or dilated esophagus in some of the connected tissue diseases as well as subcutaneous calcifications in the setting of amiodarone toxicity there may be a hyperdense liver or thyroid and certainly uh history is hugely important to help narrow the differential diagnosis for the or at least figure out what the pattern may be representing so as you all know uh uip pathologically is characterized by temporal and spatial heterogeneity and it's the characteristic or most distinctive feature here is the fibrogenic fosite now the CT features the most common things that you'll see are going to be peripheral reticulation with a basil or predominance and honeycombing if you see it and you see it in generally 60 to 70% of the cases there is Le not too much consolidation but again lower lung predominance right so here's just a example of a a classic case of uip and this sort of classic presentation uh or what we call um consistent with uip pattern is seen in about 50% of patients um so here we see from top to bottom you can see that the disease is predominantly sub plural predominantly B Las is characterized by lines reticulations and certainly there's a huge degree of honeycombing and honeycombing if there's nothing else that you take away from this session is that honeycombing is characterized by again these sort of thick walled polygonal hexagonal structures but within the actual area or the center of that is air density not gray gray lung but really black air density that's similar to the air that's for instance within the trachea or the larger broni and that's really the true definition of radiographic honeycombing so here we see just some uh additional images and again these are true honeycomb cysts again very thick sort of inter and intralobular SEPTA irregular and within the center of that area is clear air density not more gray density of lung and here we see the his pathology that goes along it again the thickened uh SEPTA we see the fibrogenic fosi and the honeycombing and again the gross specimen that that the the uh CT images reflect uh here's kind of the natural progression of what we see in ipf uip uh and again this is over two years so it's a sort of a slow but stepwise deterioration over time you see areas of course ground glass and reticulation ultimately becoming Honeycombs and with increasing architectural Distortion and traction bronchiectasis and bronchiolectasis so uh in 2009 song looked at or com uh tried to compare those patients with connective tissue or collagen vascular disease uip versus those with idiopathic pulm fibrosis they F they looked at 100 patients and found that the ones with uip with collagen vascular disease largely were younger women and non-smokers and was associated with better survival they had less fibrogenic fosi less honeycombing and honeycombing spaces but had more germinal centers and inflammation and they coined the term atypical uip without honeycombing the German Al Center score was the best discriminative factor of distinguishing these two diseases and age total lung capacity and honeycombing were independent sort of prognostic factors for improved survival so so here we just have a couple cases all are path proven uip and here we see a uh person with a dilated esophagus and again this is what I mean by looking at these ancillary findings for Clues but you see again a basil or predominant disease reticulation and honeycombing and with a dilated esophagus this was diagnosed as Scleroderma on your right on the top we see another patient with uip but notice again you see the dilated esophagus but not quite the honeycombing and you see a lot more ground glass in this case and so again not your classic uip pattern and the degree of ground glass may make you think it's something altogether different than uip but again this turned out to be Scleroderma lung disease with uip on the bottom uh we see uh more ground glass attenuation and you see that there's a lot more ground glass uh than the reticulation that we see here and again it is a sub plural predominant disease and uh not much honeycombing as you can see and on the soft tissue Windows look what you see a little paracardial affusion and you see soft tissue calcifications so this is a patient with dermatomyositis with lung disease again path prooven uip so the uip that we see with collagen vascular disease may be somewhat different or often is very different than the uip that we see with ipf so let's look at some uh of these sort of more unusual features of uip ipf so sometimes you'll see a ground glass predominance as you see in this top image here again uh the ground glass is a lot more than the reticulation or outweighs of articulation there may be asymmetric involvement on this bottom image you see that the left lung is more considerably involved in the right and it's not so symmetric you might see areas of focal a trapping which again is not uncommon but unusual for uip ipf you may see areas of pulmonary oifc and so I don't know if it projects very well but you see little hyperdense nodules within the densest areas of fibrosis on the bottom image and these correspond to areas of pulmonary osificante in 90% or more depending on which series you look at those patients with ipf uip have what we call Med small to medium siiz lymph nodes and so these are diameters short axis of 1 to 2 cm and again it's a reactive phenomenon and in about 10 to 15% of patients uh with ipf you have an accelerated deterioration or exacerbation so here's a case that had just pretty much reticulations uh on the initial or Baseline CT but during the exacerbation you can see an extreme amount of ground glass that has come about uh involving all loes and almost all portions of the lung this was a case of sort of AIP on top of the uip that happened um here we see sometimes when you're dealing with patients with very diffuse lung disease common disease are sometimes very difficult to tease out and in this situation the only C as to the diagnosis here is the if the sort of uh astute observation of small symmetric plural diffusions that you can see and this was a case of somebody with idiopathic pulm fibrosis with a congestive heart failure exacerbation represented by the plural diffusions and small paracardial diffusion uh these patients as you all know are susceptible to infection here on the top image we see a necrotizing pneumonia with a bronco plural fistula and a numo thorax air fluid level in within the destroyed lung on the other side in the left Apex you see a motoma uh you see a more classic kind of Consolidated pneumonia in this bottom patient in the right middle lobe and in the left lower lobe and as you all know these patients are uh susceptible to lung cancer and here's the same patient a more Superior image you see a spiculated nodule in the left upper lobe as well as one in the left Flor lobe this was a case of synchronous lung cancer in somebody with pulmonary fibrosis and certainly um you you can have air leaks or Barrel trauma and so here you've got numo mediastinum uh and you have some left numo thorax that you see in this case down below that brings us to our next case so This Is A 42-year-old uh with a one-year history of progressive dnia with mild exertion as well as a chronic cough I just like the bigness of these images right like so many talks you see little images so what do you guys think what is the most likely diagnosis here is this nsip asbestosis ipf or chronic HP please vote outstanding so uh 2third of you got this right um and that onethird I think is is not entirely wrong but what we're seeing here on Imaging was a reticular pattern with a considerable amount of ground glass attenuation the ground glass attenuation and the reticulations although more lower lung field were actually very peribronchovascular along the Bronco vascular bundles or the axial inum as we call it with actually some areas of sub plural sparing there was also some degree of traction bronch acasis as well as bronchial wall thickening um so chronic hypersensitivity pneumonitis would more often give you a reticular features with areas of U Mosaic attenuation and air trapping and uh the Rob will go over in a bit um but uh but really this was most consistent with nsip okay so we're still in the gamut of articulations and so we'll talk a little bit about uh nsip so unlike uip the pathologic features can be divided into cellular and fibrotic nsip and again unlike NS uip we're going to see a temporally and spatially homogeneous disease with a lot more inflammation without this characteristic fibrogenic fosi there's architectural not too much architectural Distortion and certainly almost almost no honeycombing what we see on CT is predominantly ground glass and mixed with reticulation of variable uh severity and um it in many cases uh will spare the subp plural uh periphery or the very edge of the lung in about six um 66% of cases and so this is what I'm so here we see again we see a more axial disease meaning the center of the lung is involved or the center of the lobe uh and see a lot of ground glass and the ground glass outweighs the degree of articulation here right so what we're seeing is more of this sort of dense gray uh lung uh and what you can see is by sub plural sparing we mean that the the the entity comes up to the sub plural lung but just has a ribbon of where the lung is not involved and with NSP this is probably the most characteristic finding that we see and we see it in about 60 6 65% depending on what study you look at uh of of the time it's predominantly a lower lung disease and as the fibrosis progresses you'll see more architectural Distortion you'll see more traction bronchiectasis now here's a a different case and here we can again see the ground glass at mixed with the reticulation favoring the lung bases and posterior periphery but note again that we see kind of that characteristic sub plural sparing and so so if you see this it's very good for nsip um if you look at a cellular nsip case it's often very steroid responsive because of the INF uh intense inflammation associated with this entity and you can see that after cortical steroids all that ground glass has pretty much resolved I mean there's still some areas and then there are some more reticulations in coarse pattern which is the underlying maybe fibrosis that has already uh ensued so if you compare this to uh uip they're kind of two ends of the Spectrum in terms of looking uh NSP tends to be more soft homogeneous it's a little patchier and again we have that characteristic sub plural sparing but on the opposite end of the spectrum we have ipf uip which is course it's lot of irregular lines reticulation and there's honeycombing right and rather than the sub plural sparing the disease comes all the way to the lung Edge and so here we can see some nice characteristic images again ground glass it mixed with reticulation subpal sparing in sip again here we see reticulation basil or predominance suboral involvement and the characteristic honeycombing that we've come to expect with a uip pattern um now just a a a note about chronic hypens sensitivity pneumonitis um this is characterized by what we call very heterogeneous lung onct and so we've got areas of ground glass attenuation reticulation uh and then we have these areas of hyperlucent lung or black lung that look to be sort of groups or uh isolated secondary pulmonary lobules that are hyperexpanded and ultimately if you do expiratory imaging these May or you wouldn't be surprised if they trap a high degree of air so this uh at TLC when you see the ground glass reticulation and mixed with air trapping this is what we call the head cheese sign this can be uh segmental the pattern can be segmental there may be Airway thickening because it is an airway process you certainly will see reticulation there may be a basil or predominance in about a third of cases um but the extreme lung bases may still be spared and as you know um there may be some Subacute findings depending on the chronic antigen exposure and most of the time we don't know what antigen has caused this process so here we see just a different case again we can see quite a bit of ground glass associated with this add mixed with areas of fibrosis and what to uh what turns out to be lobular sparing or mosaic attenuation due to uh air trapping so our next case is a 45 5-year-old uh African-American male with a 3-month history of cough disa and intermittent fevers so what is the most likely diagnosis here is this Subacute HP stage two sarcoidosis silicosis or a milary TB please vote great uh you guys are you guys are right on this is indeed stage two sarcoidosis what we saw here was a completely different pattern a micron nodular pattern of nodules less than 1 cmet that are too numerous to count moreover these nodules were really preferentially lining areas that involve the lymphatic such as the plura the fissures as well as the axial interum or the bronchovascular bundles on the uh axial views we saw that the distribution was slightly more preferential to the mid to upper lung zones and if you paid some more attention to the nodes you did indeed appreciate that there were even though these were lung Windows some degree of mediastinal and Hyer adenopathy so this indeed was uh stage two sorid all right so as you can may have guessed we're heading into a different gamut of nodules or a nodular pattern now when differentiating nodular pattern of disease it's really important to understand the structure of the secondary pul lobu and by that here we have a unit uh the secondary pulmonary lobule it ranges in size anywhere from 1 and 1 half to 2 and2 cm and you see that here's the plura you see interlobular SEPTA and within the inter lular SEPTA you have the uh sepal vein and each secondary plary lobu is subtended by a lobular bronchial and an arterial and that has a little bronchial artery and also U there are lymphatics that run all along this as well as within the SEPTA and along the uh Co the plura as well and so here we see on CT just kind of what that secondary line lob pul Lobel would look like so when um when dealing with this nodular pattern it's trying to you're you're trying to figure out what the nodules relationship to the secondary pul lobal structures are and that gives you maybe some insight as to what the distribution pattern overall is of where these nodules are caused by or where they're locating and so what really you want to look at are the relationship of these nodules to the fissures the plura the and make the observation are these nodules clustered or they kind of just diffuse and random and we'll go over so if you're dealing with a small subcentimeter nodule or pattern or a lot of them first question you want to ask yourself are these nodules on these lymphatic plural surfaces are they on the fissures are they on the the plura are they on the septo or on the peribronchovascular lymphatics next question you want to ask yourself are these nodules clustered or they sort of isolated and you see one at a time and when you decide on localization these are the patterns of distribution so you think of paral lymphatic patterns of nodules random patterns of nodules Central lobular meaning it's the center of the secondary prary lobu or is it more of a small Airways pattern so let's break this open a little bit if we see most of these nodules congregating in areas that contain lymphatics in plura the fissures the SEPTA uh and the plura as well as the peribronchovascular lymphatics if we see that we're really dealing with a he lympo hematogenous process this could be isolated just or isolated to just a paril lymphatic process sarcoidosis silicosis lymphogenic carcinomatosis or it may be that it's a random pattern meaning that for instance Mets and milary infection are seeding those lymphatic structures but they're also going elsewhere within the lung if we don't see this sort of lymphatic uh pattern then we're really dealing with kind of an inhalational process so the the the uh agent is coming in through the Airways it could be more generalized in a central lobular pattern meaning it's hitting all sorts of Airways at one time as in the case of smoking related lung disease hypersensitive pneumonitis or it may just be isolated to the Airways and kind of clustered in focal and the cases of cellular bronchitis and pan Bron ulitis now if we add the clustering meaning that these nodules are clustered on surfaces uh if they are clustered and we dealing with the paral lymphatic process you're really talking about sarcoidosis for the most part and if you uh see them clustered but not in a ly paral lymphatic way um and none of those surfaces are involved you're really talking about a small Airways process so uh in addition to the distribution localization sometimes the morphology of the nodul is important the density how dense is it is it small dense or soft tissue as opposed to more ground glass what are the edges like are they sharp IL defined and what's the morphology are they branching or what we call tree and Bud so let's look at the paral lymphatic pattern and up here you see a diagram again we see the secondary palmary lobule the subtending lobular bronchus uh and the artery and first of all you notice that these nodules are small and very dense with sharp margins next you know that look they're involving all these lymphatic structures that we talked about the SEPTA the plura the peribronchovascular lymphatics now some would say that you need at least 10% of the nodules going on those surfaces to call it that these surfaces are involved others would say greater than 90 and again you see that they're clustering to the lymphatics and so really again this is characteristic of paral lymphatic disease sarcoidosis silicosis and to some degree lymphangitic cancer so here again we see some cases uh different case we see again look at where all these sort of welldefined soft tissue nodules are they're on the fissures they're on the plura and they're on the SEPTA and along the peribronchovascular lymphatics here you see the specimen of loosely formed granuloma and interstitial thickening which is characteristic of sarcoidosis here we see in a different patient again you see nodules but you see that the nodules are again on the SEPTA you see them on the plural surfaces the fissures and along the peribronchovascular lymphatics so this is a paril lymphatic process first and foremost you think of sarcoidosis here we just have another image again look at the the fissures just beaded with nodules right you see sepal thickening nodularity plura and again some beating of the peribronchovascular lymphatics now here we see a case where you got larger irregular nodules but that really shouldn't dissuade you from thinking that it may be cetosis because look at where these nodules are again along the fissures along the SEPTA right and along the peribronchovascular septo lymphatics and so again this is another case of sarcoidosis now with sarcoidosis so sometimes you'll get architectural Distortion meaning that the lay of the land is not quite what it should be and areas are of lung look to be stretched others sort of distorted and cicatrized and that's because this is a chronic inflammatory process you may see um this what we call peribronchovascular beating and so when we look at the bronchus the bronchioles and the broni as well as the arteries they look like they have little nodules are studying along the surface as that fibrosis is sets in with the chronic inflammation you may see sort of this angulated bronchovascular because of the Distortion in fibrosis associated with it if you were to look at this patient in maybe three sort of divided them into thirds in a chronal situation or plane you can see that characteristic of sarcoid the uh apico posterior segments are the first and most severely involved and it's a middle third disease here see that in two different cases and as you all know uh these areas of fibrosis are going to gravitate to the mid and upper lung and again um coronal sagittal reformats as well as chest x-ray really help you in cases of diffuse disease to see where the the concentration or predominant portion of the disease is uh and here in some cases you might see honeycombing even in cases of sarcoidosis uh rare presentations or features of sarcoidosis you may see ground glass attenuation or even airspace attenuation as is in this case of alve sarcoid you might see sepal thickening as you can see here now a lot of times if you see a lot of sepal thickening rather than lung infiltration itself you might want to think of a cardiac or cardiac involvement of the sarid with heart failure and on some occasion you can have what we call Bullis sarcoidosis and so this is due to error obstruction and cyst formation as you can see in this case and on rare occasions you may see plural affusions but again that may be in the context of more cardiac sarcoidosis with heart failure all right moving on uh 28-year-old male presenting uh with a six we history of fevers night sweats nonproductive cough and 25lb weight loss I think every year we say that we want music but we never we forget to do it so what is the most likely diagnosis here Subacute HP stage two sarcoid again silicosis or milary TB please vote great the majority of you got this indeed right this is milary TB if you just go back Rob um we did see nodules there were too numerous to count they were they were clearly involving areas lined by lymphatics we clearly saw fissures were involved uh the plural was involved but there were also nodules that were not not involving those areas nodules that were kind of randomly dispersed without predeliction to the paril lymphatic structures and that's what we call random and certainly in this case it would be a hematogenous infection that would work hematogenous Mets would be a possibility here uh certainly usually there would be variation in the sizes as Rob will point out occasionally papillary thyroid cancer can give you very very small Millet seed nodules not dissimilar but often there too there is some very ability and not necessarily uh these Millet seed nodules as we see here with humanogen spread of of tuberculosis all right so now we're kind of talking about random nodules and moving away from paril lymphatic and so here again you can see nodules fairly well defined well marginated and carry a little bit of soft tissue density or at least more than just simple ground glass now again when you ask this question are they involving the lymphatic surfaces yeah you have a few on the plura you might have a few on the SEPTA you might have a few along the peribronchovascular lymphatics but then you have other nodules that hey I don't know they're just kind of floating in space within that secondary pul lobu and so when you see this sort of kind of uh distribution involving the paral lymphatic surface a bit more and you can't place some of these nodules this is what we describe as a random pattern when you're dealing with Rand random pattern really you're only dealing with sort of this lympo hematogenous spread of malignancy or infection so again clustering not so much clustering like we saw with the paral lymphatic uh diseases with all the nodules on the lymphatic surfaces or structures so this is what random looks like you can certainly see nodules on the plura you can even see some nodules lined up along a Septa but other nodules are just kind of thrown out there and what you have is a fairly homogeneous profusion like if you move your eyes from the lateral part of the the lung to the medial part you kind of see an evenness to these this distribution of nodules so uh with random distribution they're fairly uniform they're not clustered uh they may be low or low predominant because if they came in via the bloodstream it's going to go where the blood flow is the most they're solid density with sharply defined margins now some of these nodules may share similar size depending on the gradient so for instance if they're all getting to the lower lung by blood flow sometimes the earliest metastases may be all very similar in size and larger down in the lower lung than in the upper lung there may be a feeding vessel sign owing to the fact that they're U vascular born they may cavitate and if it's uh They may involve lymphatics as they sort of uh take up residence in that area so uh when you're dealing dealing with metastases uh we're dealing with renal testicular thyroid and melanoma with milary infections we're talking about tuberculosis but other fungal infections like coxy hiso and even pyus and sometimes occasionally viral infections again you see that again the lymphatic surfaces are certainly involved but you see a lot of other nodules that seem to just be floating within the lung Paran itself and uh here again in another case we see some infusions but look at all these nodules I mean like when you look from the medial lung to the lateral lung or top to bottom it looks all fairly homogeneous but the nodules are all over fairly equal throughout the lung now just a few words about lymphangitic cancer again this is a paral lymphatic process it's characterized by smooth or regular or sometimes even nodular sepal thickening and it's a much more linear disease or a reticular disease than a nodular disease per se there may be some uh frequently there's axial involvement generally there's no architectural Distortion because cancer in itself doesn't necessarily scar unless it's been treated uh there may be adenopathy in about 30% of cases maybe plural affusion and the entities that we're talking about the adnoc carcinomas the unknown primary but certainly lung breast colon and pancreas and again comparing contrast what we saw with the other for instance the paral lymphatic sarcoid here it's a much more septile disease it's more linear yes we see some nodules but that's really not too much of the feature and for the most part you see preservation of the uh architecture and the secondary pulmonary lobules are not very distorted and here we just see another case of lymphangitic cancer again a lot more lines or sepal thickening there's a few nodules here and there but again it's a more linear disease and on the soft tissue Windows you can see media stal and bilateral higher adenopathy in this case so our next case is a 23-year-old female non-smoker with a three-month history of increasing Disney on dry cough I think these are a little bit harder to see that's why we have it magnified here just to get a better sense of things so what is the most likely diagnosis here is this RB is this Subacute HP is this pacus jovic pneumonia or is this pulmonary coido micosis please vote great uh it looks like the the top two choices are the ones that are most correct what we see here are again nodules that are two numerous to count and nodules if you look carefully they did not have a uh Peril lymphatic distribution they were actually not involving areas lined by lymphatics they were not involving the fissures the plura and the morphology of these nodules is very poorly defined or ground glass and they're rather diffuse uh there is no clustering is rather diffus so this takes us into that inhalational category and that more diffuse involvement uh that we call a pure centrolobular pattern and of the two choices uh the reason why Subacute hypersensitive pneumonitis first and foremost is uh is is probably more correct here is because in that little brief oneliner we did say a nonsmoker certainly RB that occasionally tends to be a little bit more patchy uh would be expected in a smoker whereas Subacute HP would be in a non-smoker as in this case okay so um here we have the secondary puline lobu and when we call Central lobular we're talking about something within the center of that secondary pom lobu and the core often these things gravitate or surround the core structure which again consists of a arterial a bronchial lymphatics and a bronchial artery now sometimes you'll see if you know what the cause or how the nodule or the pattern got there we really think it's an airway process we may use the term rather than centrolobular but call it Bronco Centric or bronchocentric if we think that it's more hematogenous uh as in the case of maybe Mets then we will call it angiocentric and so forth so um Central ular nodules can be solid but more often they're going to be this sort of ground glass generally they're going to be bigger maybe 5 millim or larger fluffier looking they may be branching and they may be tree and Bud which are these sort of uh kind of jacks or they look like Jacks and again if you impose or superimpose the secondary lobular structures you see all these nodules are in the center or cluster to the center of that secondary primary lobule so let's look at this on the diagram that we've been looking at and here we see again a fluffier less dense nodule generally bigger in size less density ill marginated or fluffy right you see that none of the paral lymphatic structures that we've been talking about are involved by these nodules the fissures are spared the sep are spared the par bronchovascular structures are spared so there is no paril lymphatic or lymphatic structure involvement there's no clustering fairly homogeneous within the secondary pulmonary lobu and for that matter within the lung itself so there's no clustering no uh lymphatic structure involvement brings us into this centrolobular pattern or inhalational pattern uh more diffuse things like cigarette smoke causing rbl or antigen exposure to organic agents most commonly in the form of Subacute hyper Sensi netis HP can be uh acute Subacute chronic depending on the length of time and exposure uh acute tends to be more ground glass attenuation or even airspace attenuation as the granul is form you might start seeing centrolobular poorly defined nodules Subacute is much more of the nodular pattern that we see there may be also air trapping at this point as you can see here which are these areas of uh pranom will loosens your blacker lung and then certainly in The Chronic phases I've already shown you you're going to see the fibrosis here again we see a more involved case of Subacute hypersensitive pneumonitis look at these nodules they're ground glass they're bigger they're in the center of the lobules such that you almost see kind of a separation from clusters of nodules because there that's the outer part of each of those lobules right and uh with regards to respiratory bronchitis interstitial lung disease again this also has a very similar if not almost identical Central lobular pattern favoring the upper loes there may be also some Airway thickening this is seen exclusively in smokers and basically it's a smoker with a symptomatic uh who becomes symptomatic with shortness of breath and cough maybe a mixture of pfts and this is what this disease is is basically an over proliferation and infiltration of the pranama and around the Airways with this uh pigmented macras is rather the alular macras some people feel or most people feel that this is on a spectrum of disease our respiratory bronchitis being the least sort of U severe going all the way to dip here we see again you can see that there's just a diffuse uh ground glass pattern none of the lymphatic surfaces are involved there's no uh clustering and so this is an inhalational process the two things that should come to mind are Subacute hyper sensity pneumonitis and RB so case six is a 63-year-old Japanese female with a three-month history of chronic cough weight loss and subjective fevers so what is the most likely diagnosis here based on uh the brief clinical history and the radiographic features is this myobacterium avum intercellular intercellular or complex is it pulmonary TB with Associated endobronchial involvement metastatic bronchogenic cancer or pulmonary coido micosis we have to always bring that up we're in California please vote okay there there is a little bit of a spread here and um I I let's just quickly go over this uh what we saw here were a number of features there were macroon nodules uh that were cavitating and they were thick walled cavi there and then there were also adjacent micronodules that had a patchy distribution that were clearly centrolobular they were not involving areas lined by lymphatics and they had a y-shaped or trean Bud morphology that constellation here really makes TB with endobronchial spread more likely now the Endo bronchial or cellular infiltrates can be a feature of uh Mac but with Mac you'd often expect more localized disease uh more uh bronchiectasis the macron nodules here is really what points to this perhaps being TB with endobronchial involvement causing those micronodules that are tree and Bud um and patchy in distribution okay so uh we're kind of moving on to small Airways disease and the small Airways are those without cartilage these are generally 2 mm or less and they represent bronchial or in some cases very small bronchi and so the bronchials that we're talking about are the membranous terminal and respiratory bronchials and this has sort of changed over the years with better CTS and we can probably resolve these bronchials even maybe 1 cimeter from the plural Edge so the direct signs of small airway disease are going to be the things that involve the air small Airways and so again we talked about ground glass nodules we see branching nodules we see what we call tree and Bud or the sort of Jack sort of shape nodules and we may uh as the process becomes more chronic we may even see bronchiolectasis or dilation of those very peripheral small Airways and so these are all forms of um sort of direct signs of Airway involvement now if we go back to our diagram we see that again unlike the uh centrolobular pattern of nodules we see that again these nodules still are going to be airs spaced or maybe ground glass or maybe car but maybe overall carry slightly more density they are clustered but not necessarily on a lymphatic surface but within the secondary lobu itself and so here again we don't have any par lymphatic or lymphatic structure involvement they're clustered not very dissimilar to the more ground glass centrolobular pattern that I showed you just before this so when we see this clustered pattern of central opular nodules we we're really focusing on the small Airways Pro process and this is generally going to be a cellular bronchitis of which most commonly is going to be an infection or pan bronchiolitis so here again we see again notice that we see the clustered nodules here isolated to the center of the secondary pul lobu you don't see any uh sort of nodules on the lymphatic surfaces or structures and you see that it's kind of patchy it's not all the way throughout the lung it's sort of isolated to this area that area other areas and what's uh maybe helpful if you see it is that maybe the airwaves that are subtending that area are maybe thickened as well indicating or indicative of an airwave process here we see just a little bit more involvement we see again the sort of uh little denser nodules some are kind of ground glass little fluffy some have a tree and Bud look to it we see that uh again not the lung is not homogeneously sort of involved with these nodules and none of the lymphatic structures are we also see more centrally that the Airways are quite thick again suggestive that this may be an airway process which indeed it is and we also see a little hyperinflation which may indicate air trapping so pan bronchiolitis is seen in Asians mostly Japanese it's a diffused pattern or cellular bronchitis uh they can get colonized with pomonis it's accompanied by pantis with hrct we see small centrolobular nodules in a tree and Bud fashion often and again as the disease progresses we see more large Airway involvement in the later phases we may see cyst bulle and air trapping here we see two cases of pan bronchitis again you see first and foremost you see dilated Airways with thickening and then you see small clustered nodules trein Bud again within the lung or in the center or uh Central portions of the secondary pulmonary lobules but none on the lymphatic surfaces and again it's a patchy disease not like an inhalational process where it's much more homogenius uh so there are some indirect signs of small Airways disease and you may come across the term Mosaic attenuation and Mosaic attenuation is when you see hyperlucent and hypol suent lung or gray lung sort of juxtaposed to one against one another and they're in a geometric fashion corresponding to uh either isolated or clusters of secondary PM lobules so here we see gray lung and black lung simply and again it's a very geographic pattern and you can kind of Imagine that these areas correspond to clusters of those secondary pulmonary lobules now when we see this pattern on inspiratory CT we ascribe the term uh Mosaic attenuation now uh the other thing that you want to take note is that the dark areas often are devoid of vasculature or small uh or they're attenuated or smaller in caliber and that's because these areas are generally going to be air perhaps air trapping or obliterated and they're shunting blood to the more gray areas of lung now on expiration when this pattern becomes much more pronounced meaning that the gray and The Black Lung become much more obvious and you can see a more obvious gradient on expiration that's what we call Air trapping okay so uh if you see uh Mosaic attenuation these are the three things that you think of it's an obliterative small Airways process obliterative vascular process or maybe you just have an infiltrative process in the lung that fortuitously is giving you this pattern okay and I'll show you again you want to analyze it a little further and if those areas of very black lung have very small or sparse vessels then you can kind of take this process out for the most part and really comes down to one of these two things and the way that you differentiate between obstructive small Airways versus an obliterative vascular process is you guest it to do the expiratory Imaging so what does normal expiration look like and here we have a patient on inspiration and expiration and so as the patient expires the lung becomes grayer and it becomes grayer with a dependent gradient meaning that as you go to the more dependent area it becomes grayer because of blood flow and you may have small areas of air trapping but notice that again it's not really very profound certainly not any more than about 25% of a lobe or even on that one cut and certainly not a lot of air trapping in the non-dependent lung so on top you have a normal inspiration and expiration and down below you have inspiration and expiration in a different patient now first of all you notice on the image on the lower left you can see that wow there's this crazy Mosaic attenuation right now when we look at the gray lung and The Black Lung and compare notice that the black part of the lung has almost no vasculature right when you see this this is really called Mosaic hypo profusion and what you're thinking here is not of an infiltrative process but first and foremost obliterative small Airways disease or a obliterative vascular process now notice on the expiration right it almost looks the same if not the black areas look even more pronounced the gradient between the black and the gry lung is preserved and even accentuated and so in this case this is due to air trapping now here's another case here we've got on top we see again Mosaic lung attenuation on inspiration but notice how The Black Lung almost has no vasculature or what the vessels that we see are very attenuated and so really focusing on this these two processes when you do the expiration that gradient becomes really pronounced so rather than thinking of vascular causes you steer yourself to a small Airways or air trapping process now look at this case here we have uh a patient with large sort of central um thrombo emoli and you can see that again there's Mosaic limia or mosaic attenuation with gray and black lung the the dark lung the vessels are again attenuated and smaller but now let's do the expiration so on top we have the PE the person with the patient with thromboembolic disease we have the inspiration and expiration and notice that these black areas become grayer right because they're not holding on to air or not air trapping and so the hypo profused lung because the clot won't let blood profused that lung becomes grayer and can expel air and becomes grayer and the more hyper profused lung also becomes grayer and so that difference between those two areas or that gradient does not become more accentuated okay unlike the case we have below so let's think about it in a sort of cartoon sense so we'll take the case of air trapping so here we got again um black lung gry lung right so this is on inspiration and then what do we do we have them expire what happens well the areas that trap air stay black or become blacker and the areas that are gray because they're not trapping air and can force the air out become grayer so that gradient between the two becomes accentuated now let's look at this case of No Air trapping as in the case of chronic in the PE case so again we have a little bit of a gradient to begin with with because we've got black lung because it can't get profused because the PE is in the way or the emilii are in the way we have gry lung that is hyper profused or shunted too now on expiration well there's no obstruction here from the airway so both can expire air the the hyper profused area becomes grayer the under profused area becomes grayer too the gradient really doesn't become accentuated all right all right uh case 7 is a 29-year-old African-American um male with a 2year history of progressive Disney on cough moving on to a different pattern here sorry okay uh what is the most likely diagnosis is this lymphangiomyomatosis or lamb or is this pyus gerovich langerhan cell histiocytosis or granulomatosis or lymphocytic interstitial pneumonitis please vote all right so slight majority I got this right I think the key here this is a cystic lung disease they're clear defined cyst they're walls that are appreciable um moreover the intervening lung that separates these cysts was not normal the unaffected lung actually had slight nodularity and irregularity and that's really one thing that as Rob will talk about will help distinguish a disease like langerhan cell histiocytosis where the intervening lung is often nodular because the disease often starts off with nodules that cavitate and then form cyst versus lamb where the intervening lung is almost pristine so uh really if you think about those two as being the primary uh processes in a differential here um you can clearly see that the unaffected lung here I mean this is a very Advanced case as actually ended up going for heart lung transplantation because he actually had uh a group five pulmonary hypertension from the Langer hands um but nonetheless the intervening lung was very abnormal here there was really no normal lung okay so now we've moved on to the category of cyst and as uh n mentioned the two foremost diseases are langran cell and pangio myomatosis but there are other cystic diseases that we'll talk about about so cysts are round paranam uceny usually thin wall typically containing air but sometimes they can contain fluid or even soft tissue cavities develop within sort of nodules or areas of consolidation so when you're dealing with predominantly a cystic pattern then again there are some questions you like to sort of ask yourself first of all is there a perceptible wall to these cysts yes or no and what is the relationship of this cyst to the uh Central ular core structure that we talked about is it does it look like the core structures or like the arterial the bronchial are going through the center of the cyst or does it look like they're sort of embedded and sort of plastered against the wall of the cyst uh as n mentioned you also want to see or look for nodules yes or no and is there an upper lower lung predominance of these cysts if if anything so these are kind of the questions that You' like to ask and when you're dealing with cystic lung disease these are probably the most com well probably the first four most common central ular empyema by far Langer anell and pangul myomatosis lymphatic intertial pneumonia and the Bert hog dubet I know we kind of always talk about it but we don't see it that often so let's look at the case of um Central ular empyema so first of all here we see kind of in a mid mid cut here we see we see these little holes in the lung throughout and the first question you ask yourself is is there a perceptible wall I think you can pretty much see that although you see the cyst you don't really see a wall around them that's very obvious and when you ask your next question is there what's the relationship with the core and again you look at some of these and it looks like the uh Central lular core structures are going right through the center and I have some better images of this but look at this looks like that structure is going right through the middle of the cyst and that's because the these cysts are clustering around it there's obviously no nodules and it's favoring the upper lung talking about Central lular empyema so this is what I meant about this core structure going right through what it looks to be going through the center of that cyst and again that's because the lung destruction is occurring all around the core structure uh affecting the respiratory bronchial in the center of the secondary pul lobu so let's look at uh for instance compare and contrast with lamb okay so here again we see Cy right dark little air air containing clai but the difference when you compare that to empyema is that all of these cysts have a little bit of a wall right 1 to 2 mm and if you look closely the core structure looks like you don't most of these cysts don't have anything seeming like they're running through the middle of it and if you look at the for structures they look like they're embedded or plastered within the wall itself certainly no nodules and again it's a and I don't show you all the images but I guarantee that this is a more diffused process this is lymphangiomyomatosis so as you know this occurs in women of childbearing age uh in 30% of these cases you can have re renal angom myomas and what this represents is an abnormal proliferation of smooth muscle affecting the peribronchovascular structure if it's affecting the airway causes obstruction and cyst formation if it's affecting the lymphatics you get kyus plural diffusions in uh almost 3/4 in as much as 3/4 of those patients again here you can see the the gross specimen that kind of goes along with the CT um you can see that the cysts are going to be numerous they're thin walled and in between those cysts unlike lingrell you have fairly normal inter in lung you may see nodules but that's so exceedingly rare that you you almost never see that and because it's a cystic lung disease uh in 30 to 40% of these cases the presenting sign may be a numo thorax and here we see just a number of different patients uh with uh lamb of varing severity and you can see that again look at that the cyst and the core structure looks like it's embedded in the wall you don't see any of these cyst have something going through the center of them and they all have a thin perceptible wall normal intervening lung no really uh zonal predilection for these cysts but fairly diffuse and this is these are cases of lamb so uh tuber sclerosis can also give you cystic pulmonary disease that's identical to lamb uh with the exception of the kyus plural diffusions the Triad as you all know associations or other sort of um ectodermal issues angiomyolipomas cardiac rabdom myomas retinal fomas osteomas and subungal for uh fibromas and again when you look at the lung disease pattern it looks identical to to lamb all right so moving on to the the next entity we're going to talk about a little bit about Langer hand cell and again you ask your question you see the cyst so you ask your question do I see walls on these cysts and I think everybody can certainly see walls on these cysts right and then you look at the core structure and the relationship to the cysts and again you don't see anything really going through the heart of the cyst or the center of the cyst right looks like the core structures are all again plastered or embedded in the wall of the cyst and here I don't show you too many nodules but this entity certainly has a much more um predominance of nodules than uh certainly lamb so um this is goes through stages starts with a bronos cent or centrolobular nodule that nodule grows and cavitates then becoming what we call these thin wall bizarre cysts these cysts May coales and you get areas of pseudo osma and fibro Bullis disorganization and destruction and intervening fibrosis in the early stages of disease you won't have fibrosis but later on there is there generally is a sparing of the extreme lung bases as well as the tips of the right middle lobe and lingula and again here we can see just how many nodules these are all small little nodules and you can start seeing down on below some of these nodules starting to cavitate and become cysts and as the disease progresses you can see again more fibr Bullis changes more extensive cyst look at the intervening lung is just highly abnormal and then you get sort of this fibr Bullis disorganization in the most ofe cases okay uh um moving on to cystic lip you see again cysts maybe not so numerous with a perceptible wall uh with regards to the association with the core structure you can may see some cyst with things going through the center as I'll show you or embedded in the wall there may or may not be any nodules and localization is usually just kind of scattered cyst as opposed to the more diffuse proliferation of cyst as we've seen so in um at least jao looked at the radiographic features of lip found that ground glass attenuation was the most common uh or and that was tied with centrolobular nodules in almost all of their or in all of their cases they sometimes see par lymphatic nodules in a high number of cases because this is kind of a lymphocytic or and here again you see more lymphatic based nodules in another case and maybe some septile thickening indicating a lymphatic or lymphatic process and here we see the kind of cyst that we're talking about in about almost 70% of cases again you see a wall uh that's perceptible and in some of these cases you can see that kind of the structures are against the wall and here you can see the core structure kind of in the center with number of cyst sort of clustering around it and so with lip cyst or the cystic variant these cyst generally tend to be 3 cm or less sometimes there this multiloculated or lobulated uh or multiseptated cyst and generally you can count them uh they're not so many and numerous as in the other cases of cystic lung disease that I've showed you and collectively they may only have 10% or less lung involvement of these cysts case8 is a 53-year-old female with a one-month history of persistent non-productive cough disia with exertion and some weight loss so what is the most likely diagnosis here is this maai acute interstitial pneumonia metastatic bronchogenic carcinoma or organizing pneumonia please vote great um so we've moved on here to the last category which is airspace disease and as we see here we saw airspace disease that was mostly Bronco Centric as well as peripheral we had uh areas of patchy airspace disease along with bronal wall thickening um there was also um some areas that you could vaguely say there was uh maybe a reverse Halo sign or ATL sign that was um it's only found in about 20% or so of patients with organized pneumonia um but uh clearly um this is an airspace disease and as Rob will talk about here uh clinical history is really important when you're dealing with airspace disease because the differential is often very broad okay so again uh these are some of the other entities that we see that's predominantly characterized by airspace disease uh acute and chronic EIC pneumonia acute interstitial pneumonia and diffuse alv damage and pulm alv prosis so with organizing pneumonia the pathology is patchy organizing pneumonia with intraluminal fibrosis involving the bronchioles and airs spaces and there's often these sort of endoluminal granulation tissue PPS or mome bodies and there may be some interstitial infiltrates or inflammation associated with this as well um this sort of honeycombing architectural Distortion associated with fibrosis is uh not very common with organizing pneumonia the CT features are predominantly consolidation with the lower lung predominance sometimes there may be uh ground glass opacities and the distribution again within the lobe itself is going to be sub plural and sort of per Bronco vascular so it's a combination uh other less common features you might see bronchial dilation you may see a non-al linear or reticular pattern there may be more uh obvious nodules uh and masses in 15% of cases and overall as you know fibrosis is fairly uncommon and and certainly honeycombing is not a feature of this disease so here we see some of the common things here we see a consolidation airspace attenuation we see that after treatment there's a little residual ground glass that ultimately probably will resolve and here we see more extensive ground glass in a different patient we see the bronchial dilation in the areas of heavy involvement and even a little peribronchial thickening which is not unusual in this bottom case we see more reticular pattern yes there's ground glass but you see a lot of lines here and this is what we call kind of the non sepal reticular opacities in this pattern here you can see that the ground glass or the sort of thickening is confined to the edges of the secondary pulan Lobel and this is what we refer to as a perilobular pattern and this is seen at least in one Article 5 7% of the cases of organizing pneumonia here and again if you think back to that diagram I showed you with all the secondary prom lobules you can see almost make them all out here the only difference of the SEPTA being rather than the SEPTA being thick it's more kind of consolidation outlining the edges there um there may be as I said more obvious nodules and sort of mass-like consolidations in 15% of patients again it's a sub plural peribronchovascular kind of combination and rarely and uncommonly you may get to this point where there is actually fibrosis caused by this uh this entity this is what n was referring to as the reverse Halo sign that you see in almost 20% of patients so what you have is basically an area of dense consolidation and within the center of that consolidation you see ground glass attenuation and so this is supposedly like an atle which is an aisle in the ocean right and here just a different case of radiation induced organizing pneumonia again you see that very dense Leading Edge and within the inside of that Leading Edge you see ground glass attenuation um moving on to a little dip uh again this is characterized by ground glass opacity that you see here uh it often favors the lower lob sub plural lung can be patchy uh or diffuse as I've shown you in 10% of cases you may see small little Cy here and that's due to air flow obstruction and um they also may just represent fortu a or intercurrent empyema as well and again with this entity uh you really don't see too often honeycombing now with any airospace disease you want to uh try to differentiate them the the sort of the feat teachers and tease them out again looking at the distribution whether or not there's architectural Distortion accompanying lymphadenopathy you if you have it is this an acute or chronic process whether it's clinically or radiographically has there been a history of treatment response uh what's the patients's occupation immune status are they on any new medications or drugs that are associated with lung disease and ultimately you may just have to get biopsy results here are just some other uh airspace entities here we see a peripheral lung involvement favoring the upper loes this is a chronic eosinophilic pneumonia here we see again more of a um kind of ground glass in the right lung more dense airspace consolidation in the other lung and this is a case of uh um U the pneumonic form of Bronco alvear cell carcinoma here we see uh these cases are what we call crazy Paving and you may uh run into this term and what we mean by by crazy Paving is that you see ground glass attenuation and within that area of ground glass you see the sort of this linear pattern of sepal intralobular septal thickening as well as intralobular septal thickening resembling sort of pave or okay so here again you see that everywhere you see ground glass you see the inter and intralobular SEPTA being thick crazy Paving has been associated with primary alular prosis but can be seen in a number of things and certainly is not pathum monic for just Pap but certainly you can see it in pyus infection mucinous U BAC or adnoc carcinom and citu that's the pneumonic form even hydrostatic pul edema pulm Hemorrhage and lipoid pneumonia so um these are kind of the categories that we talked about reticulations nodules cysts and airspace disease some of the common entities uh again when you're dealing with a nodular pattern you want and you're dealing with multiple or numerous subcentimeter nodules first question you want to ask yourself is are they involving the lymphatic structures uh if that's the case then you're really dealing with a lympo hematogenous process whether it's paral lymphatic or random if not uh you may be dealing with a more inhalational process then the next question you want to ask yourself is is there any clustering of these nodules uh if they are involving lymphatic structures and clustering you're really talking about paril lymphatic processes primarily sarcoidosis and if you're dealing with a more inhalational category uh then you're dealing with small Airways disease and remember the morphology of the nodules as well so here I just put side by side all of the uh nodular diseases so again these are the patterns across the top the plural or lymphatic structures paral lymphatic random yes they involve those Central lular small Airways no the clustering as we talked about before paral lymphatic and small Airways not so with the random and centrolobular and the morphology of the nodules paral lymphatic solid sharp random solid sharp centrolobular as we get to more inhalational or Airway processes these nodules become more IL defined right or even branching in tree and Bud the cystic lung diseases that we talked about empyema lambs lch and lip again you want to ask yourself is there a perceptible wall and uh again empyema no but the other three entities yes as you've seen what's the relationship with the centrolobular core is if it looks like it's going right through the center of some of these cysts that means that the cysts are surrounding that core fairly evenly uh and that's what you see with centrolobular empyema if it's eccentric you're probably dealing with one of these two entities and if you have kind of both and these nodule or these cysts are much more finite you may be dealing with as is shown here lip uh presence of nodules again the only two diseases that have nodules as I've shown you are lch and lip and localization empyema as you know is in the upper lung lamb sort of diffuse with no zonal predilection lch sparing the bases right middle lobe and lingula tips and L IP usually again a finite number of cysts less than representing less than 10% of lung involvement and they're kind of randomly scattered Aerospace disease again I think history is first and foremost the most important and so that brings us to kind of ride out with a bunch of quiz questions all right so just no history here you guys are experts uh what is the most likely diagnosis here uh is this YP nsip metastatic CA or organizing pneumonia outstanding uh clearly uh everybody most everyone got it right the degree of honeycombing that's present here you would not expect to see honeycomb changes with nsip the disease would actually have a rim of sub plural sparing that we don't see here the disease here goes all the way out to the plural surfaces it's very reticular very coarse very minimal ground glass so uh uip uh as most of you got is the right answer all right the next case go ahead and vote great uh so here we had uh back to a micron nodular pattern two two numerous nodules two numerous to count clearly the nodules look like they are involving the Peril lymphatic structures moreover they are clustering along those areas as Rob talked about so if you look along the fissures the plural surfaces and the axial interum it looks like it's being riddled by micronodules so it is a very uh Peril lymphatic disease moreover it is these nodules are clustering in areas lined by lymphatics so uh the best answer here would be uh sarcoidosis all right next case so on your left is inspiration on your right expiration same patient fantastic um so there is quite a bit of ground glass but is as Rob talked about earlier there is this Mosaic attenuation that gets uh exemplified during exploratory scans so you have these areas of lobular air trapping that is really pathic of hyper uh with Hyper sensitivity pontis in this case case of Subacute HP so let me just give you so these are uh the image on your uh far left is one patient and the image in the middle and the magnified image are from the same patient but a different patient please vote ahead and vote please vote oh yeah there you go all right a little bit of work to do here um so what we're seeing here are uh CIS they're lucencies but without clearly defined walls if you really try to draw an outline around these lucencies as it's very difficult you don't see that thin 1 to 2 mm wall uh moreover if you look carefully in some of the magnified views you see that the central lobular core the cyst surrounds that Central lobular core and that is pathum monic for smoking related Central lobular empyema um langerhan cell histiocytosis or granulomatosis you would actually have a perceptible wall and the central lobular core is eccentric or pushed against the wall and that is not not not the case here so this is Central lular empyema how about this go ahead and vote all right so a majority got this uh right this is uh clearly uh Langer hands what you're seeing here are clearly defined cysts with perceptible walls we're seeing a two axial Cuts mostly mid and upper lung zones and what we see is that the intervening lung is is slightly abnormal uh there uh there are some slight nodularity to the intervening lung outside of the cyst moreover uh the central lular core structures look like they're eccentric or pushed up against the wall here um so this would be most consistent with langerhan cell histiocytosis all right the next case please go ahead and vote all from the same patient all right great 2/3 got this right what we're seeing here are um somewhat IL defined nodular opacities that do not have a predeliction for the paril lymphatic structures moreover they're clustering and in some areas they do especially on the uh on the sagittal and coronal views have a tree and Bud morphology this is consistent with a cellular bronchitis and infectious bronchitis and clearly the differential is pretty broad would include things such as aspiration microbacterium avium infection TB with Endor bronchial spread particularly if you have a fosi like a large cavity as well as uh atypical fungal infection such as coxy so this is an infectious bronchitis how about this case think about the wall of the CIS great so here here um in some ways this is not too dissimilar from that Central lobular empyema Rob pointed out with two distinctions number one there is a perceptible wall you can actually draw a nice outline whereas with the central lul empyema was just kind of poorly defined lucencies secondly the central lobular core here unlike Central lobular empyema is not in the center the cyst is not surrounded but rather it's eccentric or pushed up against the wall and then what kind of differentiates this from Langer hands is the intervening lung here is pretty pristine there is no involvement or abnormality of the intervening lung not involved with cysts and then the last case is this so go ahead and vote ah great great way to end the day there you go 97% so this is clearly uh organizing pneumonia you see areas airspace opacities that are somewhat paty involving the uh per Bronco vascular t as well as periphery with Associated Broncho wall thickening all right thank you very much give yourselves a hand I think you're the highest correct answer percentage of all the audiences n and I the privilege to teach have a good evening