Difference between revisions of "Diffuse Fibrosing Alveolitis"
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m (Text replace - "Category:To Do - Blood" to "Category:To Do - BloodCategory:To Do - Clinical") |
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[[Category:Allergic Respiratory Diseases]][[Category:To Do - Blood]][[Category:To Do - Clinical]] | [[Category:Allergic Respiratory Diseases]][[Category:To Do - Blood]][[Category:To Do - Clinical]] | ||
+ | [[Category:Type III Hypersensitivity Diseases]] | ||
+ | [[Category:Bronchi and Bronchioles - Pathology]] | ||
+ | [[Category:Respiratory System - Inflammatory Pathology]] |
Revision as of 16:00, 19 February 2011
Diffuse Fibrosing Alveolitis/ Interstitial Pneumonia
- Diffuse inflammatory process which occurs distal to the terminal bronchioles
- Characterised by thickening and fibrosis of the alveolar walls
- The precise underlying aetiology of this condition is obscure and it is likely to represent the end stage of a variety of initial insults including EAA and fog fever
- Progression from an acute exudative phase through a proliferative phase (proliferation of type II pneumocytes) to a final irreversible stage of fibrosis is the hallmark of DFA
- The rate of the ensuing fibrosis is heavily dependant on the intensity of the inflammation associated with it
- Underlying pathogenesis of the fibrosis is complex and involves a relative increase of type I collagen fibres (dense, high tensile strength) over type III fibres (reticulin)
- Stimulation of fibroblast proliferation and collagen deposition are thought to be induced by macrophage derived cytokines, e.g. IL-1, TGFalpha and TGFbeta, GM-CSF