I) In the bronchioles:

- Peribronchial or peribronchiolar inflammation:

   Non-specific:  Reactive lymphoid follicles as in follicular bronchiectasis  or follicular bronchiolitis  ;  Granulomatous .

- Obliterative changes in bronchioles with fibrous scarring, as in bronchiolitis obliterans:

- Organizing granulation tissue in bronchiolar lumina, as in cryptogenic organizing pneumonia (also known as bronchiolitis obliterans organizing pneumonia or BOOP).

II) In the alveoli and interstitium:

- Architecture:

-Destruction of alveolar walls without fibrosis in emphysema ;

-Destruction of alveolar walls with interstitial and intra-alveolar fibrosis, alveolar collapse, and bronchiolization in advanced interstitial lung disease;

-Alveolar walls:

- Interstitial inflammatory infiltration ;

- Focal acute inflammation with central necrosis and scattered giant cells in fungal pneumonias;

- Heavy lymphocytic infiltrate, as in lymphoid interstitial pneumonia (LIP), extrinsic allergic alveolitis, monomorphic and atypical lymphoid infiltrate, as in malignant lymphoma;

- Non-necrotizing well formed granulomas in sarcoidosis ;

- Non-necrotizing poorly formed granulomas in extrinsic allergic alveolitis;

- Necrotizing granulomas in mycobacterial and  fungal infection ;

- Palisaded granulomas in Wegener’s granulomatosis and rheumatoid nodules ;

- Interstitial fibrosis;

-  Asbestos bodies;

-  Amyloid;

- Smooth muscle cells in lymphangioleiomyomatosis ;

- Lymphatic infiltration by tumour cells as in extra-pulmonary primary adenocarcinoma (lymphangitis carcinomatosa), lymphoma, Kaposi's sarcoma , epithelioid hemangioendothelioma ;

- Calcification- metastatic in the elastic of alveolar walls, dystrophic in areas of long-standing fibrosis;

- Calcified bodies (Schaumann bodies) in areas of hyaline fibrosis in sarcoidosis;

- Hemosiderin deposition in areas of hemorrhage;

- Alveolar lining cells:

- Hyaline membranes in diffuse acute alveolar damage;

- Proliferation of type II pneumocytes in the reparative phase of hyaline membrane disease;

- Multinucleate giant cells:

      -giant cell interstitial pneumonia (hard metal disease);

      -giant cell pneumonia ( measles infection in children, occasionally respiratory syncytial virus infection  or parainfluenza B);

      -viral inclusions, such as cytomegalovirus  or measles;

      - cytoplasmic hyaline in type II pneumocytes, first identified in asbestosis but also seen in other conditions;

       -atypical cells: seen with some cytotoxic drugs such as busulfan or bleomycin;

      -bronchiolisation of distal air spaces in advanced diffuse pulmonary fibrosis;

      -squamous metaplasia as a result of chronic inflammation ;

      -tumour cells lining alveoli in bronchioloalveolar carcinoma, which may be mucus secreting or non-mucus secreting.

- Alveolar lumina:

-Inflammatory cells:

        -polymorphs in bacterial pneumonias ;

        -eosinophils in eosinophilic pneumonia ;

        -histiocytes/macrophages - foamy in obstructive pneumonitis or lipid pneumonia  , containing fine lipofuscin pigment in desquamated interstitial pneumonia, ‘blue bodies’ associated with lysosomal accumulation in such conditions as DIP ;

         -multinucleate foreign body giant cells, often associated with cholesterol crystal clefts, in obstructive pneumonitis or pulmonary alveolar proteinosis  ;

-Granular eosinophilic debris, often with cholesterol crystals, in pulmonary alveolar proteinosis,

- Granular and foamy lightly eosinophilic material in pneumocystis pneumonia ;

- Hemorrhage or accumulation of haemosiderin- laden macrophages in hemorrhagic diathesis, pulmonary capillaritis, idiopathic pulmonary hemosiderosis, pulmonary venous hypertension;

- Intra-alveolar irregular laminated calcospherites in pulmonary microlithiasia;

- Organizing exudates (Masson bodies -Masson's Tumour) in organizing pneumonia;

III) In the blood vessels:

- Vasculitis:

-Eosinophil infiltration with granuloma formation in Churg-Strauss syndrome;

-Extravascular granulomas and areas of necrosis in Wegener’s granulomatosis;

-Granulomas in vessel walls in sarcoidosis , necrotizing sarcoidal granulomatosis, and reaction to talc particles in drug addicts;

- Capillaritis with alveolar hemorrhage in Wegener’s granulomatosis, microscopic polyarteritis and hypersensitivity vasculitis;

- Infiltration of vessel walls by atypical lymphoid cells in angiocentric lymphoma (lymphomatoid granulomatosis);

- Pulmonary hypertension and thromboembolic disease:

- Muscular arteries - medial hypertrophy in hypoxic pulmonary hypertension, pulmonary venous hypertension and plexogenic pulmonary arteriopathy; subintimal longitudinal muscle fibres in hypoxic pulmonary hypertension;

- Intimal thickening-eccentric in thromboembolic pulmonary hypertension, associated with organizing thrombus or other embolic material, concentric in plexogenic pulmonary arteriopathy ; dilatation lesions, plexiform lesions and fibrinoid necrosis in plexogenic pulmonary arteriopathy;

- Muscularization of arterioles in hypoxic pulmonary hypertension ;

- Veins:

- Obliteration by connective tissue in pulmonary veno-occlusive disease;

- Thickening of the media with arteriolization in pulmonary venous  hypertension;

- Replacement of the vein wall by a network of capillaries with abnormal capillaries in alveolar walls in pulmonary capillary hemangiomatosis.

Custom Search