Difference between revisions of "Diffuse Fibrosing Alveolitis"
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| − | Diffuse Fibrosing Alveolitis/ | + | Diffuse Fibrosing Alveolitis/ Interstitial Pneumonia |
*Diffuse inflammatory process which occurs distal to the terminal bronchioles | *Diffuse inflammatory process which occurs distal to the terminal bronchioles | ||
*Characterised by thickening and fibrosis of the alveolar walls | *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 [[Acute | + | *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 [[Lungs Inflammatory - Pathology#Acute bovine pulmonary emphysema and oedema (ABPEE)|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 | *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 | *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) | *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 | *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 | ||
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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]] | ||
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Revision as of 10:54, 20 August 2010
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