Farmer's lung pathophysiology: Difference between revisions
Jump to navigation
Jump to search
(→References: pathophysiology) |
(→Acute-: references) |
||
Line 15: | Line 15: | ||
* Type 3 hypersensitivity | * Type 3 hypersensitivity | ||
* When moldy hay antigens complex with antibodies, to bind complements and attract neutrophils, causing inflammation by release of their toxic enzymes and radicals. | * When moldy hay antigens complex with antibodies, to bind complements and attract neutrophils, causing inflammation by release of their toxic enzymes and radicals.<ref name="pmid21286564">{{cite journal |vauthors=Dales RE, Munt PW |title=Farmer's Lung Disease |journal=Can Fam Physician |volume=28 |issue= |pages=1817–20 |date=October 1982 |pmid=21286564 |pmc=2306727 |doi= |url=}}</ref> | ||
===== Chronic- ===== | ===== Chronic- ===== | ||
Line 23: | Line 23: | ||
===== Unifying hypothesis- ===== | ===== Unifying hypothesis- ===== | ||
Sensitised pulmonary alveolar macrophages activated by antigen attract neutrophils and also modulate T cell activity leading to appearance of mononuclear cells and granuloma. | Sensitised pulmonary alveolar macrophages activated by antigen attract neutrophils and also modulate T cell activity leading to appearance of mononuclear cells and granuloma.<ref name="pmid212865642">{{cite journal |vauthors=Dales RE, Munt PW |title=Farmer's Lung Disease |journal=Can Fam Physician |volume=28 |issue= |pages=1817–20 |date=October 1982 |pmid=21286564 |pmc=2306727 |doi= |url=}}</ref><br /> | ||
<br /> | |||
== Genetics == | == Genetics == | ||
There are no established genetic predispositions. | There are no established genetic predispositions. |
Revision as of 01:09, 28 July 2020
Farmer's lung Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Farmer's lung pathophysiology On the Web |
American Roentgen Ray Society Images of Farmer's lung pathophysiology |
Risk calculators and risk factors for Farmer's lung pathophysiology |
Overview
The pathogenesis of the Farmer's lung disease is type 3 or type 4 hypersensitivity reaction.
Pathophysiology
Pathogenesis:
Hypersensitivity reaction because of the many immunologic phnomenon present and antibodies of organism invasion into tissues.
Acute-
- Type 3 hypersensitivity
- When moldy hay antigens complex with antibodies, to bind complements and attract neutrophils, causing inflammation by release of their toxic enzymes and radicals.[1]
Chronic-
- Type 4 hypersensitivity
- mononuclear cell inflammation and granuloma.
Unifying hypothesis-
Sensitised pulmonary alveolar macrophages activated by antigen attract neutrophils and also modulate T cell activity leading to appearance of mononuclear cells and granuloma.[2]
Genetics
There are no established genetic predispositions.
Associated Conditions
There are no associated conditions.
Gross Pathology
Acute phase-
- Pulmonary alveolar wall and interstitial accumulation of neutrophils, mononuclear cells and edema.
- obstructive bronchiolitis and capillary inflammation is present.
Late phase-
- mononuclear cell predominant
- presence of noncaseating granuloma
Microscopic Pathology