Hypersensitivity pneumonitis pathophysiology: Difference between revisions
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== Overview == | ==Overview== | ||
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]]. | |||
==Pathophysiology== | |||
===Acute HP=== | |||
There are noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution. Giant cells are prominent. | |||
===Subacute or intermittent HP=== | |||
The noncaseating granulomas are more well formed. There is bronchiolitis with or without organizing pneumonia. Interstitial fibrosis is present. | |||
== | ===Chronic HP=== | ||
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: | |||
* '''Predominantly peripheral fibrosis:''' in a patchy pattern with architectural distortion and fibroblast foci similar to usual interstitial pneumonia (UIP) | |||
* '''Homogeneous linear fibrosis:''' similar to fibrotic nonspecific interstitial pneumonia (NSIP) | |||
* '''Irregular predominantly peribronchiolar fibrosis''' | |||
=== Immune Response=== | |||
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. | |||
==References== | |||
{{ | {{reflist|2}} | ||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
[[Category:Pulmonology]] | |||
Latest revision as of 16:00, 9 June 2016
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Hypersensitivity pneumonitis Microchapters |
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Differentiating Hypersensitivity pneumonitis from other Diseases |
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Diagnosis |
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Treatment |
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Hypersensitivity pneumonitis pathophysiology On the Web |
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American Roentgen Ray Society Images of Hypersensitivity pneumonitis pathophysiology |
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Directions to Hospitals Treating Hypersensitivity pneumonitis |
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Risk calculators and risk factors for Hypersensitivity pneumonitis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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.
Pathophysiology
Acute HP
There are noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution. Giant cells are prominent.
Subacute or intermittent HP
The noncaseating granulomas are more well formed. There is bronchiolitis with or without organizing pneumonia. Interstitial fibrosis is present.
Chronic HP
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:
- Predominantly peripheral fibrosis: in a patchy pattern with architectural distortion and fibroblast foci similar to usual interstitial pneumonia (UIP)
- Homogeneous linear fibrosis: similar to fibrotic nonspecific interstitial pneumonia (NSIP)
- Irregular predominantly peribronchiolar fibrosis
Immune Response
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.