Hypersensitivity pneumonitis Microchapters |
Differentiating Hypersensitivity pneumonitis from other Diseases |
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Hypersensitivity pneumonitis pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Hypersensitivity pneumonitis involves inhalation of organic dusts which act as an antigen. This leads to an exaggerated immune response, which is called hypersensitivity reactions. In hypersensitivity pneumonitis, its either Type III hypersensitivity or type IV hypersensitivity.
There are noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution. Giant cells are prominent.
The noncaseating granulomas are more well formed. There is bronchiolitis with or without organizing pneumonia. Interstitial fibrosis is present.
There is chronic interstitial inflammation and alveolar destruction (honeycombing). There is dense fibrosis. The pathologic findings of chronic HP that are often associated with a poorer prognosis include the following 3 patterns of fibrosis:
Exposure results in the development of circulating immunoglobulin G antibodies that are specific for the offending antigen. This antibody that forms is called the precipitating antibody, and it reacts with the specific putative antigen to form a precipitant. Initially the disease process was thought to be immunecomplex-mediated. However, subsequent studies have demonstrated that cell-mediated immunity is more important.
In the acute phase, there is a local increase in neutrophils in the alveoli and small airways. This is followed by an influx of mononuclear cells which release proteolytic enzymes, prostaglandins, and leukotrienes.