e [Music] hi everyone and welcome to another season of free Friday live streams in the run up to our annual virtual conference radi opedia 2025 my name is bar pooi and I am a radiologist practicing in London in the United Kingdom my subsp specialty areas of Interest are breast and muscular scutal Imaging it's my great pleasure to be one of the conveners for radi opedia 2025 along with Lee alali and Joe mullu the three of us together with a huge backstage team are putting together our sixth virtual conference and I know it's said every year but this one really will be the best one yet you can register for the whole conference or purchase yourself an all access pass which gets you the conference and a heap of other content from our library the registration page is ready so go and check out the full lineup and your registration options don't forget that anyone in one of the 125 low and middle income countries listed on our website can claim free access for the whole conference we do that because it's our driving philosophy to to be able to provide education for the whole world regardless of ability to pay over the next few months we'll tell you all about what we have in planned for radi opedia 2025 but suffice to say that you'll be spoiled for Choice with new lectures workshops case sets and Anatomy teaching as well as panel discussions from our expert speakers one really important message for now we had just opened our abstract submission for the r posters the deadline for this is the 9th of March 2025 and just like in previous years selected R posters will be shown at the conference and will receive a DOI as well as a certificate please make sure you put some time aside to get those abstract in that you can be part of our conference right let's get to the lecture this first live stream is done by none other than your favorite thoracic radiologist Dr morand shimoi she's from Melbourne in Australia and her talk is on diffuse nodular lung diseases and I guarantee that no matter what level of radiology you're practicing at you will find a pearl to take away from Miranda's lecture take it away [Music] Miranda hello and welcome to this discussion of diffuse nodular lung disease by which I mean a profusion of Micron modularity typically 2 to 3 mm in size and widely distributed my name is Miranda sham noich thank you very much for joining me iology in diffuse nodular lung disease is differentiated by appreciating idiosyncratic nodule distribution nodule patterns are determined by the transit of materials through the lung in the everyday function of this organ this is the secondary pulmonary Lobel 1 to 2 and 1/2 cm in size makes up the entire volume of the lung perena and in the center of this the terminal branches of the pulmonary arteries and the terminal Airways which bring air in to sacks of Alvi called Asin which make up the volume of the secondary pulmonary lobu and are interwoven between the capillary bed which drains into veins and venules in the inter lobular scepter taking blood back to the left heart multiple materials pass through the secondary pulmonary lul you start with air comes in through the center of the lobu fills the Asin goes back out the way it came in and disease that relates to the terminal Airways manifests as nodularity in the center of the secondary pulmonary loviel because the Airways can't make it out to the exterior parts of the lobu blood comes in through the center through the terminal branches of the pulmonary arteries and diffuses through the capillary bed fills the volume of the lobule and then drains into those venules and veins and back to the media stum disease that relates to the capillary bed will be diffusely uniformly distributed across the volume of the lob lymph drains from from the lung perena along two distinct lymphatic beds the bronchovascular lymphatics and the septal lymphatics disease that relates to the pulmonary lymphatics will present with nodularity along the bronchovascular bundles and along the SEPTA which are anatomically continuous with the fishes and the plura so when we differentiate between disease that relates to these three materials we ask one underpinning question in interpreting the radiology and that is is the plura involved and the answer to this question is no sometimes or very yes let's see how that works disease relating to the Airways will manifest in the center of that secondary pulm lobu as we've seen the Airways don't make it out to the edges of the lob so the plura is not involved this is the central lobular pattern of disease disease that relates to the capillary bed has a uniform distribution and the plura is sometimes involved because disease that maps to the capillary bed will occasionally land at the scepter land at the fishes and land at the plura but the degree of nodularity associated with these structures is not out ofing with the degree of nodularity Elsewhere in the lung Del disease relating to the pulmonary lymphatics will Very Yes involve the plura because one of those two lymphatic beds runs in the scepter in the fishes in the plura and there will be a disproportionate involvement of the plura so we're going to see nodularity that predisposes to the fishes and plura as a recognizable manifestation of the paral lymphatic nodul disease distribution in clinical practice we see images like this so three separate patients with three different disease etiologies showing these nodule patterns and all with high Fusion 2 mm size nodules that are widely distributed in the centry lobular pattern we've got black lines along the fishes so we've got sparing of this pericial lung we've got sparing of the lung periphery with black lines out at the peripheral plura in the uniform distribution of disease we've got nodules along the fishes but the number of nodules the nodule count per unit area associated with the fishes is in keeping with the nodule count in other areas of involved lung in the paril lymphatic disease distribution very yes the plur is involved here's a portion of the oblique Fisher in the right lung and there's nodu nodule nodu nodule nodu nodule this is involvement of the septo lymphatics passing into the fishes and it is out of keeping with the degree of nodularity Elsewhere in the lung and also here nicely seen involvement of that bronchovascular lymphatic bed with studying of these bronchovascular structures so let's talk about the calob nodule disease pattern the most common manifestation of this that we see every day is the tree in Bud pattern and the most common cause for this first 2 third and 17th in your differential diagnosis is infection this relates to Airways commonly associated with aspiration as foreign material is introduced down that bronchial tree and seats and causes infection let's look at three different patients who all have risk factors for aspiration and see how these nodule patterns interrelate this is a patient who's ventilated and in the superior segment of the right lower lobe they've got extensive tree Bud nodularity we'll just look at one little example here with cluster of three little 2mm nodules and they surround a little Central branching opacity that is the tree in the tree and Bud and that is an opacified terminal Airway it's not a vessel it's an airway way let's keep looking at the rest of this case because the patient has very high extent disease and a beautiful demonstration of this tree and Bud pattern with these little clustered micro nodules and the little branching opacities Associated not notice also the distribution of nodularity here because we've got a wedge shaped distribution of spared segments and Subs segments here and involved segments adjacent because material is introduced down the bronchial treat and it's distributed in that wedge shaped anatomical segmental recognizable pattern of involvement so extensive TR bud in an infectious bronchiolitis associated with ventilation see that the large Airways are also involved so we've got thickening of these segmental Airways we've got extensive mucus secretions within large Airway changes go hand inand with small Airways disease and we're always looking for that when we're interpreting these nodule patterns here is a patient with a very disted esophagus when we scroll down we've got this laparoscopic gastric banding device increased pressure across the band results in chronic distension of the esophagus retention of fluid retention of debris and a predisposition to recurrent aspiration in the right upper lobe a few clustered hazy nodules that are this tree in Bud opacity are the little buds within it and scrolling down there's much greater extent of disease with much more confluent opacities but notice that all of this disease is nodular it's hazy with a central consolidative focus and peripheral ground glass opacity and where you see these discrete nodules you can appreciate that they are still centry lobular in distribution here this nodule is associated with the adjacent bronchovascular bundle and here another beautiful example of these clustered confluent nodules there's peripheral ground glass opacity and they're associated with these branching bronchovascular structures so this is the buds part of tree and bud there's not a lot of tree happening in this patient with quite extensive and bilateral in fact aspiration pneumonia this patient had a squamous cell carcinoma of the Flor of mouth with segmental mandibulectomy and reconstruction and that altered oral biomechanics results in a high risk of recurrent aspiration and that's what they have in the superior segment of the right lower lobe again we've got a few scattered fosa of Tre and butt opacity with a few nodules associated with these branching opacities but in this case the dominant abnormality is of that large Airways disease so gross bronchial wall thickening bronchial dilation mucous impaction bronchiectasis and again just those few scattered fosi of train B opacity so this is the tree without a lot of the buds so three patients with a wide presentation of aspiration iated Airways centered infection infectious bronchitis aspiration pneumonia and large Airways Associated complications with bronch acasis now a phrase that everybody loves to use is infective inflammatory change and it's a good term but it's also important to be cognizant of the reason that you're using terminology so what do we mean when we say inflammatory what what are the disease entities that is running through our minds that may be a possibility in the patients that we're examining let's look at a couple of different disease etiologies that are non-infectious inflamat cses of centry lobular nodularity so here a patient with high profusion wide extent centrilobular ground glass nodularity is the plura involved no look at that beautiful black line along the peripheral plura look at the way that that peripheral lung is spared in fact the disease is so gross in distribution that the fure which is here is obscured and we're not getting a nice feral sparing but just look at this right mid Zone here and just dwell for a moment on this beautiful black lace work that is cobbled between all of this nodular ground glass opacity because this is the interlobular septer and those partial septations of the intralobular scepter that are spared in the centry lobular distribution of mic ular disease so this is part of that beautiful centry lobular distribution and what else does this patient have they have these scattered Lucent polygonal structures which are secondary pulmonary lobules sometimes several abing one another that are involved in air trapping and if we did expir Imaging on this patient we would exaggerate the difference between that dense ground glass lung and the Lucent air trapped lobules and this is of course the typical appearances of hypersensitivity ptis so old terminology Subacute hypersensitivity intis and updated terminology from this paper the clinical practice guideline published in the blue journal in 2020 of nonfibrotic hypersensitivity in neumonitis why have we updated the terminology where what are we trying to align with this is in recognition of the fact that the terminology of Subacute versus chronic is arbitrary there's this chronological cut off of 3 months that uh tips you into chronic hypersensitive adontis but it doesn't acknowledge the the disease process that's occurring in the background because we know that patients who can have very long-term exposure to these inhaled organic antigens may not necessarily go on to develop fibrosis and fibrosis doesn't necessarily begin at 3 months so separating out the terminology away from these arbitary cut offs and more closely aligning with the histopathology which indicates either the presence or absence of fibrosis gives us a cleaner more accurate radiological set of terms this is a table with a lot of words what I want you to take away from it is that non-fibrotic hypersensitivity neumonitis requires the satisfaction of two criteria so we have ground glass paral infiltrate as a penal manifestation of this process and we need to also satisfy the criteria of evidence for Airways involvement and the two features radiologically that indicate Airways involvement are the centry lobular distribution of nodules and or air trapping and the previous case we've seen both of those features a beautiful appearance of typical non-fibrotic hypersensitivity pneumonitis in this case the Distribution on the coronal and axial images is diffuse and that is all of the Hallmarks of the typical appearance otherwise we see other features which we'll have a look at in this case of more confluent ground glass opacity consolidation and even cysts let's have a look here the ground glass opacity is still recogniz ly distributed in that c centry lobular pattern is the plur involved no we've got beautiful black lung out at the prery of the hemithorax and we do have these nice black bands along the fishes to show that centry lobular distribution and as we come down we've got this more confluent Geographic ground glass opacity here beautiful uh few adjacent secondary pulmonary lobules that are loosened that's the air trapping so tick a lot of boxes and another case of non-fibrotic hypersensitivity pontis the alternative differential diagnosis that people often use in the same sentence for ground glass Cent lulin ularity is respiratory bronchiolitis which is the working diagnosis in this case let's have a look at what we see so this is an active smoker we've got scattered centrilobular lucencies which is low volume mild Cent lobular empyema we do also see mild ular wall thickening so there isn't bronchitis present active in this case typical in active smoking and then on the background of that are innumerable faint small centr lobular ground glass nodules we see that by just appreciating the number of round structures on each slice and seeing that these exceed the number of normal vascular markings that you would expect in this lung I'll just scroll up and down because those moving images show it better the profusion of these faint centry lobular ground glass opacity so this is respiratory bronchitis histopathologically what we see is an accumulation of intraalveolar pigmented macrofagos radiologically it's this ground glass opacity small Cent lobular nodules and what we see in these cases is that the ground glass opacity can in fact evolve to become airspace destruction and empyema so the ground glass of respiratory bronch itis May in fact be a precursor and part of the mechanical evolution of empyema how do we differentiate between these two diseases the most helpful clinical practice point is the profusion of nodularity so let's look at that HP case on the left hand side you can see that extensive distribution that high profusion of nodularity compared to the lower profusion more interspersed intermittent nodularity as well as the superimpose empyema in the respiratory bronchitis and that nodule count that degree of profusion can actually be quite helpful and most non-fibrotic hypersensitivity neumonitis really will have that huge volume nodularity with respiratory bronchitis being uh much more subtle invisible on the 5mm slices degree of change we all grew up being taught that smoking had this paradoxical protective effect uh of against hypersensitivity in human itis but the reality is that we see plenty of HP in smokers so the most useful practice point that I find is this profusion of nodularity so the central lobular pattern of nodules we're thinking infectious change 1 2 third and 17th in the differential diagnosis we're thinking inflammatory causes hypersensitivity pneumonitis respiratory bronchitis the uniform distribution of nodules is most commonly referred to as the so-called random pattern of nodularity this is a term to which I strongly OB object because the use of the term random indicates that this is arbitrary that there's no meaning behind it is completely inexplicable and that's just not the case much better term is uniform nodule distribution because that indicates what we're actually seeing it's describing the pattern that we appr iate on radiology and it's acknowledging the anatomical explanation behind the disease production which is mapping back to the capillary bed which is uniformly distributed through the lung let's have a look at a couple of cases we've got a patient here who has millery tuberculosis and they've got a hyperfusion of 2 mm soft tissue density nodules is the plur involved sometimes a few scattered nodules that are out in the lung periphery that are landing touching that plura and along the fishes again a few occasional nodules contacting the fishes and plura let's just scroll further through this case and we can see that the nodule count again per unit area of nodules along the fishes is in keeping with a degree of nodularity Elsewhere in the lung so this is a uniform distribution millery tuberculosis another patient same diagnosis millery TB and again a lower profusion of nodules that same distribution where we've got the occasional involvement of the plura is the plura involved sometimes here here here here not out of keeping with the degree of nodularity Elsewhere in the lung smaller nodules that are therefore appearing more loosen than in the previous case and of lower density but that same uniform distribution so two cases of millery tuberculosis and just a single image from a patient with millery metastasis to illustrate the point occasional involvement of the peripheral plura not out of keeping with the degree of nodularity Elsewhere in the lung so of course the cancers that come to mind when we're thinking about millery metastases are those hypervascular cancers thyroid melanoma renal cell carcinoma but not to forget breast and pancreas which can also be not uncommonly associated with this millery pattern of disease production so uniform pattern Micron modularity millery infection millery metastases the paril lymphatic nodule distribution is recognized by nodules nestling in along those bronchovascular structures in association with the bronchovascular lymphatic bed and the septal lymphatic bed in a septol plural distribution septol plural it's not a common word in fact when I looked this up I found that it's almost not a word but I use it because it reminds us that the interlobular septer are anatomically continuous with the fishes and the plura and that is the driver behind the plural predominant component of the paril lymphatic nodule distribution the Hallmark disease for a paral lymphatic distribution is that of sarcoidosis and let's have a look is the plur involved Very Yes nodu nodule nodule nodu nodule nodule nodule extensive involvement of that peripheral plura let's keep coming down and just admire the degree of nodularity along the superior aspect of that right oblique fissure nodule nodule nodule nodule nodule nodule all Landing along as we scroll down we also notice the other feature of sarcoidosis which is of course that mid and upper Zone predominance and the way that the nodules fade out towards the lung bases let's have a look on the coronal images and we've got extensive nodularity Landing along that that fisher with this disproportionate involvement of the fishes and of the peripheral plura classic appearance of pulmonary sarcoidosis another case of pyoid similar extent disease similar profusion of nodularity just to show an illustration of the bronchovascular predominant manifestation of perilymphatic nodularity so down here in the superior segment of the left lower lobe there's absolutely stunning beating along this bundle as it comes back towards theum and up in the right upper lobe this beautiful association with these bronchovascular bundles and extensive beating along these bronchovascular structures beautifully seen so bronchovascular and fishal and plural distribution in paral lymphatic nodularity now the disease that people mention in the same breath with sidossis when differentiating between different etiologies of nodular lung disease is silicosis another example of paral lymphatic disease distribution so here is a stonemason we're starting down at the lung bases and we've got nodules scattered out along the periphery of the lungs so is the plura involved very yes we're already seeing that relationship with the peripheral plura let's keep coming up because again this is a mid and upper Zone distribution disease where we've got relative sparing of the lung bases and the action happened much higher up and as we come up there's greater profusion of nodularity there's more and more nodules Landing along the periphery of the lung and Landing along that fissure look at the Distortion of the fure associated with that nodularity and as we keep coming all the way up these nodules which are peripheral and peribronchovascular are associated with this reticulation in a perilobular distribution at the center of the lung Apes it's more so on the right it's bilateral and it's really in that center part of the apex of the lung this is a very characteristic and typical appearance of reticulation and early fibrosis in silicosis when pyoid does fibrosis and Architectural Distortion by and large it tends to start out in the mid zones with the where the bronchovascular bundles start to curve they create these C- shapes which don't get in normal linear branching of undisturbed lung perena but in silicosis this center of the Apes fibrosis with reticulation is very typical and something to note and something to file away now we can't leave the paral lymphatic disease distribution without talking about lymphangitis carcinomatosis here is a patient with a cavitating cancer in the right Apex and on the lung Windows the lungs are filled with Micron modularity it's high profusion and straight away we appreciate just how studded and beaded and irregular and nodular that oblique Fisher is in the left lung just watch that as we come down this is hyperfusion nodularity very yes the plur is involved and just wait till I show you the sagittal in this case which show it even more impressively this oblique Fisher with this irregular stuttered beaded appearance nodu nodu nodu nodu nodule and in the background this Lacy network of the interlobular scepter which are demarcated by this beaded nodular thickening so interlobular sepal thickening commonly overcalled as lymphangitis carcinomatosis in the setting of lung cancer because the concepts are closely related and once we see that thickening we want to talk about lymphangitis but the most common cause for intralobular sepal thickening in the setting of lung malignancy is bulky hila disease that causes extrinsic compression of pulmonary veins and a segmental Venus congestion with this beaded appearance the diagnosis is unequivocal this is clear classic lymphangitis carcinomatosis so in paral lymphatic diffused nodular disease we're thinking about cyclosis we're thinking about silicosis we're thinking about lymphangitis so that's the framework we're doing well now I want to add another layer across these groups are you ready here is a patient with high extent centry lobular ground glass nodularity this High profusion innumerable faint ground glass nodules is the plura involved no we've got a beautiful thick black line around the periphery of the lung sparing that immediate sub plural lung we've got demarcation of the fishes this is Central lobular distribution they also have a few more confluent nodules scattered between this patient is 35 years old they've got no history of exposures they've got significant respiratory impairment and they've got this main pulmonary artery this is ghostly enlarged remembering that the upper limit of normal rule of thumb for the main pulmonary artery is 30 mm it's 27 in Women 29 in men I would accept higher let say 33 in elderly people with no risk factors but this patient has documented respiratory Decline and acute pulmonary hypertention and what they have is excipient lung disease this is somebody with a history of intravenous drug use and injection of crushed oral medication and excipient lung disease is a result of the EM embolization of insoluble binders that are present Within These medications and when they embolize throughout the lungs we get a mechanical and inflammatory occlusion of the pulmonary vascular bed this results in acute often profound pulmonary hypertension and in some cases chronic pulmonary hypertension this is an important differential because the significant barriers to disclosing this drug use in patient s may require the radiologist to be the first person to Think Through the possibilities and it's a reminder that in the center of the secondary pulmonary lobu There lives the terminal Airway but there also lives the terminal branches of the pulmonary artery so C centry lobular nodules and look at the media stum look at the size of the main pulmonary artery and think about how the patient is presenting here is another patient also in her 30s grossly enlarged main pulmonary artery and chronic pulmonary hypertension and in the lungs she has this appearance is the plura involved no she's got widespread patchy IL defined ground glass nodularity not the punctate fine nodularity that we've seen in other cases in the excipient lung disease and in the hypersensitivity pontis but this more thumb prints of ground glass this is the typical radiological appearance of pulmonary capillary hemangiomatosis PCH is a proliferative disorder it may in fact be a low-grade neoplastic process histopathologically there are diffuse angiomatous lesions which themselves are proliferating capillaries and it's a disorder that exists often alongside pulmonary venocclusive disease pvod which is a patchy fibbr seclusion of pulmonary veins they may in fact be along the spectrum of the same disease and this patient went on to lung transplant the explant showed both PCH and pvod this is the typical appearance radiologically of pulmonary capillary hemangiomatosis again think about the pulmonary artery look at the medium look at the size of the pulmonary artery in patients presenting with either acute or chronic disease PCH and pvod are important entities to appreciate because the classic firstline medical management for patients with idiopathic pulmonary hypertension results in a precip decline in these patients because of the different physiology that's driving the pulmonary hypertension I want to go back to thinking about the pulmonary lymphatics and I want to Think Through the bronchovascular lymphatic bed heading Upstream out from the medeor stum and back to where the lymph begins to drain from the lung parena and appreciate for a moment that where the lymphatic bed joins the bronchovascular bundle is of course the center of the secondary pulmonary lobu so let's pause for a minute and reflect that Cent lobular nodules are an anatomical subset of paral lymphatic nodularity so that means that we when we have patients like this stonemason opper Zone architectural Distortion confluent opacities Progressive massive fibrosis which is in fact the end stage of the perilobular reticulation that we saw in the other the case when we assess the nodular component of this patient's disease and we see that it in fact it has a centry lobular distribution that's not a problem at all are we worried about that no because Cent lobular nodules are an anatomical subset of the paril lymphatic nodule distribution so respirable crystalline silicone is inhaled in occupational exposed workers and reaches and penetrates the lung parena so of course there is a second driver of why this disease should manifest at centry lobula but also the rest of this process involves engulfment of silica particles by pulmonary macres which is a terminal event for the maccrage which may then be engulfed by another maccrage and continue the cycle and silica then Aggregates in silicotic nodules which undergo attempted lymphatic clearance so that is the explanation why we have a peribronchovascular and a septal plural distribution of nodularity in these patients and why as you see even on these lung windows we will have mediastinal and hyon noal involvement seen in this case as coarse calcification so an explanation behind the manifestation of central lobular nodules in silicosis this is another patient with silicosis 35 years old a stonemason and they have a profusion of scattered nodules is the blur involved no this is a centry lobular pattern some soft tissue density nodules but a large contribution of ground glass density nodules and a widespread coronal distribution with some sparing at the bases so how do we know that this is silicosis and do we need to think about hypersensitive intis a clue in this case is that cause calcification of the medial and Hy lymph nodes so a reminder to check the media stum for not just the pulmonary artery and the size of it but the status of the nodes to flag whether or not we might be dealing with a lymphatic compartment disease this patient has so-called accelerated silicosis and the appearance of accelerated silicosis is Central lobular nodularity with a significant ground glass component simple nodular chronic silicosis that we're familiar from Days of Y is associated with occupational exposures in excess of 10 years that's a really long latency period accelerated silicosis happens much faster has a much more aggressive course can come on in as little as 4 years after commencement of exposure and is associated with working with artificial stone engineered Stone engineered stone is a much more toxic compound so thinking about Natural Stone thinking about marble has a respirable crystalline silica content of 3% something like Granite is up at 30% but when you take the toxic silica compound out of natural stone and you concentrate it together and you bind it with resin and you put it in your kitchen you have a respirable crystalline silica content of greater than 90% this is a public health crisis that is much further reaching than asp veos it occurs in younger patients it has a much higher penetrance with up to 1 in four occupationally exposed workers diagnosable with silicosis and a course that in can involve lung function decline death requirement for lung transplant and really requires a public health response over the last 6 months Australia has banned the production use and trade in engineered Stone in multiple jurisdictions and I'm looking forward to seeing that extending more broadly nationally and internationally accelerated silicosis with Central lobular ground glass nodularity one more case of a patient with Central lobular ground glass nodules and again a patient with accelerated silicosis young short duration of exposure and on this slice here not a lot to differentiate from hypersensitivity intis but when you get right up to the center of the Apes just like we saw in that first case of silicosis we start to see that perilobular reticulation which is the clue that this is what we're dealing with check the Apes check for that Central apical perilobular distribution reticulation because when hypersensitive intis starts to fibros then we're talking about that three density appearance we're talking about quite diffuse distribution of reticulation and um fibrosis that is much more wide spread in its distribution throughout the lung whereas accelerated silicosis gives itself away with this Central apical distribution perilobular fibrosis notice also the enlarged lymph nodes even on these lung windows with Central fatty lucency but large short axis diameter and another clue that we're dealing with a lymphatic compartment disease so in the central lular pattern the is spared infection is 1 second third and 17th on your differential diagnosis we've got inflammatory etiologies of hypers sensitivity numers nonfibrotic the new terminology respiratory bronchitis low profusion scen inactive smokers we've got vascular causes arterial causes check the medyum check the size of the main pulmonary artery think about excipient lung disease think about pulmonary capillary hum angiomatosis and we've got lymphatic compartment disease manifesting as pure Cent lobular nodularity In the case of accelerated silicosis with ground glass opacity nodules in uniform disease distribution the plur is sometimes involved we've got millery infection millery metastases a common pattern that people are comfortable with we've got paral lymphatic disease distribution with centr lobular nodules peribronchovascular nodules septol plural disease almost not a word we've got sosis we've got silicosis and we've got lymphangitis carcinomatosis not to be overcalled in the setting of smooth interlobular sepal thickening but looking for that beaded thickening with nodules studying the fishes and the interlobular sceptor so we've got three disease patterns we've got three distinct sets of etiologies and we've got three interrelated anatomical explanations for the radiological manifestations thank you very much for your time what a fantastic way to start our new season of Friday live streams and now we all know what to expect from Miranda and that's just pure gold if you enjoyed that you won't want to miss Miranda again at radi opedia 2025 where she will be presenting a case set on lung nodule CT as well as co-hosting a chest Imaging workshop with Sally aasa so that's all we have for now don't forget to check out the conference registration page and really importantly don't forget to get your abstracts in for the r posters we really want as many of you to be involved in the conference as possible I'll see you again for another Friday live stream bye for now [Music] e [Music] [Music]