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Ill Defined Centrilobular Nodules and Subpleural Nodules
The infiltration of lymphocytes, histiocytes and plasma cells along the lymphatics of the lungs, can sometimes result in ill defined nodules that may be centrilobular or subpleural in location
Ashley Davidoff MD TheCommonVein.net
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 Infiltration of Lymphocytes Plasma Cells and Histiocystes into the walls of the Bronchioles and Small Airways
Artistic rendering shows a normal bronchiole (a) with early infiltration into the wall of the airway, (b) withprogressive infiltration with luminal compromise (c) evolving into obliteration (d). This would result in centrilobular nodules radiologically. Subsequently there is necrosis and a thin walled cyst remains
Ashley Davidoff MD TheCommonVein.net  139264.lungs

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 Small Airway Fibrosis and Luminal Narrowing or Obstruction 
The diagram shows fibrotic changes around and within the small airways including the terminal bronchiole, respiratory bronchiole and the alveolar duct.  In this instance the increase density from the fibrotic tissue would result in ground glass changes in the parenchyma and solid centrilobular nodules.  Obstruction of the small airways  would result in air trapping.
Ashley Davidoff MD TheCommonVein.net lungs-0778

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 Small Airway Fibrosis
The diagram shows fibrotic changes around the small airways including the terminal bronchiole, respiratory bronchiole and the alveolar duct.  In this instance the increase density from the fibrotic tissue would result in ground glass changes in the parenchyma and ground glass centrilobular nodules.  Since the airways are patent there would be no air trapping.
Ashley Davidoff MD TheCommonVein.net lungs-0777

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 Acute Eosinophillic Pneumonia
Alveolar and Interalveolar Interstitial Infiltration with Eosinophils and Inflammatory Exudate – Ground Glass Changes
The ground glass changes are a combination of the cellular and exudative inflammatory response in the small airways, alveoli, interalveolar septa and interstitium, and thickened alveolar septum
The diagram shows the abnormal secondary lobule (a) The involved components include the small airways(b) alveoli and interalveolar interstitium (c) and the thickened interlobular septum (d) surrounding the secondary lobule due to an inflammatory process, cellular infiltrate and congestion of the venules and lymphatics in the septum.  An anatomic specimen of a secondary lobule from a patient with thickened interlobular septa and interstitial thickening is shown in image e, and is overlaid in red (f) . A magnified view of an axial  CT of the lungs in a patient with acute eosinophillic pneumonia shows thickened interlobular septa and centrilobular nodules (g) The inflammatory changes in the aforementioned structures result in an overall increase in density of the lung manifesting as ground glass changes (g) and overlaid in red (h) 
Ashley Davidoff MD The CommonVein.net  lungs-0762

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 Acute Eosinophillic Pneumonia
Interlobular Septal Infiltration with Eosinophils and Inflammatory Exudate – Thickening of the Interlobular Septa – Crazy Paving Kerley B lines
The diagram shows the thickened septum surrounding the secondary lobule due to an inflammatory process, cellular infiltrate and congestion of the venules and lymphatics in the septum (a) .  An anatomic specimen of a secondary lobule from a patient with thickened interlobular septa is shown in c and overlaid in d.  CT of the lungs in a patient with acute eosinophillic pneumonia shows thickened interlobular septa and centrilobular nodules and the thickened septa are overlaid in red (e).
Ashley Davidoff MD The CommonVein.net 
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 Acute Eosinophillic Pneumonia
Small Airways Infiltration with Eosinophils and Inflammatory Exudate – Centrilobular Nodules
The diagram shows the small airways of the lung including the respiratory bronchiole, alveolar ducts and alveolar sacs in coronal (a) and in cross section (b) and correlated with an anatomic specimen of a secondary lobule that contains a thickened interlobular septum .  The respiratory bronchiole is overlaid in maroon (d), next to the arteriole.  Images e and f are magnified views of a CT of the lungs in a patient with acute eosinophillic pneumonia and the centrilobular nodules reflecting small airway disease are highlighted in f.
Ashley Davidoff MD The CommonVein.net lungs-0760b

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 A collage shows the normal small airway(a) alveoli (b) and secondary lobule (c) and the changes in the airways in acute eosinophillic pneumonia.  There is filling of the the small airways(d) alveoli (e) are filled with inflammatory changes in the interalveolar septa (e) and thickening of the interlobular septa (f) The CT findings include consolidation at the lung bases (g)with thickening of the interlobular septa, centrilobular nodules,  and ground glass opacity (g)
Ashley Davidoff TheCommonVein.net lungs-0757b

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 A collage shows the normal small airway(a) alveoli (b) and normal CT 9c) and small airways infiltrated with eosinophils, (d) the alveoli infiltrated with eosinophils(e) and the radiological findings with aiirbronchograms within a consolidation (f) and thickening of the interlobular septa, centrilobular nodules and ground glass opacity (g)
Ashley Davidoff TheCommonVein.net lungs-0757

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 The collage provides a perspective of disease of the small airways and the alveoli that results in ground glass appearance on Xray. A process that increases the density of the lungs to a net “gray” regional density will result in a ground glass opacity whether it is inflammation of the walls ((second column) fluid within the lumen of the small air ways and alveoli (3rd column) or whether it is fibrosis in the walls of the small airways or alveolar septa (last column alveoli. The net result on CT is a ground glass opacity (bottom row). In fibrosis there are secondary changes which include bronchiolectasis in this case, but other associated changes may include reticulations or centrilobular nodules
Ashley Davidoff MD TheCommonVein.net lungs-0733

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 Image a shows a normal bronchiole.  Smoking excites the Langerhans cell which in turn  induces attracts  early cellular interstitial infiltrates of surrounding the bronchiole (b) including  lymphocytes, macrophages, eosinophils, plasma cells, and fibroblasts.  The cellular infiltrate progresses in a peribronchial pattern with mass effect on the bronchiole which becomes narrowed (c) and eventually disappears, a nodules of varying size manifest in the bronchiole pathway, sometimes round but often spiculated as the inflammatory reaction extends into the interstitium  (d) The wall of the bronchiole breaks down and the cellular infiltrate may undergo necrosis resulting in thick walled cavities, sometimes round in shape (e)  and sometimes with bizarre shapes (f) Eventually the inflammation recedes and a thin walled cyst remains (g ,h) 
Ashley Davidoff MD TheCommonVein.net

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 MORPHOLOGY OF THE STRUCTURAL CHANGES
“S” of SARCOIDOSIS
The granulomas start as micronodules in close association with the lymphatics (1) spread in the intralobular septa and centrilobular bronchioles ((2) cluster and conglomerate to form macro nodules (4,5) sometimes manifesting as the galaxy sign (6). As they cluster and conglomerate they can cause conglomerate masses along the pathway (7) most commonly centrally as the lymphatics become confluent in the hila (7)
The lymphovascular bundles may be accompanied by nodularity (8) or just by thickening (9).
The lymph nodes in the mediastinum become significantly enlarged and fleshy (10). They often calcify (12) sometimes on the calcify on the rim of the node (eggshell calcification (11)
Sarcoidosis is a nodular granulomatous disease which predominated in the upper lobes and has its epicenter in the lymphoid tissue of the lungs.
The ?S? drawn on the thoracic cage outlines the lymphatic distribution of the lungs, starting in the pleura involving the lymphatic system in the pleura, interlobular septa, bronchovascular bundles and lymph nodes.
The granulomas start out as micronodules and there is a tendency for these to coalesce, sometimes forming large granulomatous masses
When the disease affects the interlobular septa, it causes thickening and nodularity in the septa of the secondary lobule.
When it involves the lymphatics in the pleura or fissures it causes nodularity and thickening.
When it involves the lymphatics around the terminal bronchioles it results in centrilobular micronodules, and when it involves the larger airways it causes thickening and nodularity
Lymph nodes in the hila are characteristically large and flesh like (sarcoid = meat) The Pawnbrokers sign (aka Garland sign or the 1,2,3 sign) describes the enlarged right paratracheal node with bilateral hilar adenopathy.
Parenchymal nodules and micronodules sometimes coalesce to form a central confluent mass with surrounding micronodules, described as the galaxy sign.
Ashley Davidoff MD TheCommonVein.net 132082-S06L