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An approach to histopathological reporting of  the pulmonary parenchymal biopsies:

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.

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E-book - History of  Medicine with special reference to India

Introduction of Pathology

An outline of Diagnostic Techniques available in Pathology

Cellular Injury

Diagram showing Structural Changes in Reversible and Irreversible Cell Injury

Autolysis

Heterolysis

Necrosis

Coagulation (Coagulative) necrosis

Caseative (Caseous) necrosis

Liquefaction necrosis

Fat necrosis

Fibrinoid necrosis

Apoptosis

Gangrene

Pathologic Calcification

Hyaline Change

Atrophy

Hypertrophy

Hyperplasia

Metaplasia

Aplasia

Hypoplasia

Circulatory Anatomy, Physiology and RegulationNormal Fluid Balance

Edema

Diagram showing Capillary System and Mechanisms  of Edema Formation

Morphology of Edema

Hemostasis and Thrombosis

Embolism

Fat Embolism

Air Embolism

Decompression Sickness

Amniotic Fluid Embolism  

Cellular Accumulations

Accumulation of Glycogen, complex lipids and carbohydrates

Pigments

Melanin

Pigments derived from Hemoproteins

Hemosiderin and Hemosiderosis

Primary Hemochromatosis

Hematin


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