Hypersensitivity pneumonitis: Difference between revisions
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= Hypersensitivity | {{Infobox medical condition | ||
| name = Hypersensitivity pneumonitis | |||
| image = | |||
| caption = | |||
| synonyms = Extrinsic allergic alveolitis | |||
| specialty = [[Pulmonology]] | |||
| symptoms = [[Cough]], [[dyspnea]], [[fever]], [[fatigue]] | |||
| complications = [[Pulmonary fibrosis]], [[respiratory failure]] | |||
| onset = Hours to years after exposure | |||
| duration = Variable | |||
| causes = Inhalation of organic dusts | |||
| risks = Occupational exposure, [[farming]], [[bird keeping]] | |||
| diagnosis = [[Clinical history]], [[imaging]], [[lung biopsy]] | |||
| treatment = Avoidance of antigen, [[corticosteroids]] | |||
| prognosis = Variable, depends on chronicity and management | |||
}} | |||
[[ | '''Hypersensitivity pneumonitis''' (HP), also known as '''extrinsic allergic alveolitis''', is an inflammatory syndrome affecting the [[lungs]], caused by the inhalation of a variety of organic dusts. It is characterized by an immune-mediated response that leads to inflammation of the [[alveoli]], the small air sacs in the lungs. | ||
== | ==Etiology== | ||
Hypersensitivity pneumonitis is caused by repeated inhalation of organic antigens. These antigens are typically found in occupational or environmental settings. Common sources include: | |||
* [[Bird droppings]] and feathers (e.g., in bird fancier's lung) | |||
* Moldy hay (e.g., in farmer's lung) | |||
* Contaminated humidifiers or air conditioners | |||
* [[Mold]] spores from [[compost]] | |||
==Pathophysiology== | |||
The pathophysiology of hypersensitivity pneumonitis involves a complex immune response. Upon inhalation of the antigen, the body mounts an immune response that involves both humoral and cell-mediated immunity. Key features include: | |||
* Formation of [[immune complexes]] | |||
* Activation of [[T cells]] | |||
* Release of [[cytokines]] | |||
* Recruitment of [[macrophages]] and [[neutrophils]] | |||
This immune response leads to inflammation and damage to the alveoli, resulting in impaired gas exchange. | |||
==Clinical Presentation== | |||
The clinical presentation of hypersensitivity pneumonitis can vary depending on the duration and intensity of exposure. It is typically classified into three forms: | |||
===Acute=== | |||
=== Acute | * Symptoms appear 4-8 hours after exposure | ||
* [[Fever]], [[chills]], [[cough]], [[dyspnea]] | |||
* [[Malaise]] and [[myalgia]] | |||
=== Subacute | ===Subacute=== | ||
* Gradual onset of symptoms | |||
* Chronic cough and dyspnea | |||
* Fatigue and weight loss | |||
=== Chronic | ===Chronic=== | ||
* Progressive dyspnea | |||
* [[Clubbing (medicine)|Clubbing]] of fingers | |||
* [[Pulmonary fibrosis]] | |||
== Diagnosis == | ==Diagnosis== | ||
Diagnosis of hypersensitivity pneumonitis | Diagnosis of hypersensitivity pneumonitis is based on a combination of clinical history, imaging, and sometimes lung biopsy. | ||
== | ===History=== | ||
* Detailed occupational and environmental exposure history | |||
* | * Identification of potential antigens | ||
[[ | ===Imaging=== | ||
* [[Chest X-ray]]: May show diffuse infiltrates | |||
* [[High-resolution computed tomography]] (HRCT): Ground-glass opacities, nodules, and fibrosis | |||
== | ===Lung Biopsy=== | ||
* May be required in uncertain cases | |||
* Shows interstitial inflammation, granulomas | |||
== | ==Management== | ||
The primary treatment for hypersensitivity pneumonitis is avoidance of the offending antigen. Additional treatments include: | |||
* | * [[Corticosteroids]] to reduce inflammation | ||
* | * [[Immunosuppressive therapy]] in severe cases | ||
== | ==Prognosis== | ||
The prognosis of hypersensitivity pneumonitis varies. Acute forms may resolve completely with antigen avoidance, while chronic forms can lead to irreversible lung damage and [[pulmonary fibrosis]]. | |||
==Prevention== | |||
Preventive measures include: | |||
* Identification and control of environmental sources of antigens | |||
* Use of protective equipment in occupational settings | |||
==See also== | |||
* [[Interstitial lung disease]] | |||
* [[Occupational lung disease]] | |||
{{ | {{Pulmonary diseases}} | ||
[[Category:Pulmonary diseases]] | |||
[[Category:Occupational diseases]] | |||
[[Category:Immune system disorders]] | |||
Revision as of 21:29, 1 January 2025
| Hypersensitivity pneumonitis | |
|---|---|
| Synonyms | Extrinsic allergic alveolitis |
| Pronounce | N/A |
| Specialty | Pulmonology |
| Symptoms | Cough, dyspnea, fever, fatigue |
| Complications | Pulmonary fibrosis, respiratory failure |
| Onset | Hours to years after exposure |
| Duration | Variable |
| Types | N/A |
| Causes | Inhalation of organic dusts |
| Risks | Occupational exposure, farming, bird keeping |
| Diagnosis | Clinical history, imaging, lung biopsy |
| Differential diagnosis | N/A |
| Prevention | N/A |
| Treatment | Avoidance of antigen, corticosteroids |
| Medication | N/A |
| Prognosis | Variable, depends on chronicity and management |
| Frequency | N/A |
| Deaths | N/A |
Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is an inflammatory syndrome affecting the lungs, caused by the inhalation of a variety of organic dusts. It is characterized by an immune-mediated response that leads to inflammation of the alveoli, the small air sacs in the lungs.
Etiology
Hypersensitivity pneumonitis is caused by repeated inhalation of organic antigens. These antigens are typically found in occupational or environmental settings. Common sources include:
- Bird droppings and feathers (e.g., in bird fancier's lung)
- Moldy hay (e.g., in farmer's lung)
- Contaminated humidifiers or air conditioners
- Mold spores from compost
Pathophysiology
The pathophysiology of hypersensitivity pneumonitis involves a complex immune response. Upon inhalation of the antigen, the body mounts an immune response that involves both humoral and cell-mediated immunity. Key features include:
- Formation of immune complexes
- Activation of T cells
- Release of cytokines
- Recruitment of macrophages and neutrophils
This immune response leads to inflammation and damage to the alveoli, resulting in impaired gas exchange.
Clinical Presentation
The clinical presentation of hypersensitivity pneumonitis can vary depending on the duration and intensity of exposure. It is typically classified into three forms:
Acute
Subacute
- Gradual onset of symptoms
- Chronic cough and dyspnea
- Fatigue and weight loss
Chronic
- Progressive dyspnea
- Clubbing of fingers
- Pulmonary fibrosis
Diagnosis
Diagnosis of hypersensitivity pneumonitis is based on a combination of clinical history, imaging, and sometimes lung biopsy.
History
- Detailed occupational and environmental exposure history
- Identification of potential antigens
Imaging
- Chest X-ray: May show diffuse infiltrates
- High-resolution computed tomography (HRCT): Ground-glass opacities, nodules, and fibrosis
Lung Biopsy
- May be required in uncertain cases
- Shows interstitial inflammation, granulomas
Management
The primary treatment for hypersensitivity pneumonitis is avoidance of the offending antigen. Additional treatments include:
- Corticosteroids to reduce inflammation
- Immunosuppressive therapy in severe cases
Prognosis
The prognosis of hypersensitivity pneumonitis varies. Acute forms may resolve completely with antigen avoidance, while chronic forms can lead to irreversible lung damage and pulmonary fibrosis.
Prevention
Preventive measures include:
- Identification and control of environmental sources of antigens
- Use of protective equipment in occupational settings
See also
| Pulmonary diseases | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|
This pulmonary disease related article is a stub.
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