Farmer's lung pathophysiology: Difference between revisions
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== Overview == | == Overview == | ||
The pathogenesis of the Farmer's lung disease is type 3 or type 4 hypersensitivity reaction. | The [[pathogenesis]] of the Farmer's lung disease is [[Type III hypersensitivity|type 3 or type 4 hypersensitivity reaction.]] | ||
== Pathophysiology == | == Pathophysiology == | ||
=== Pathogenesis: === | === Pathogenesis: === | ||
Hypersensitivity reaction because of the many immunologic | [[Hypersensitivity]] reaction because of the many immunologic phenomenon present and [[antibodies]] of organism invasion into tissues. | ||
===== Acute- ===== | ===== Acute- ===== | ||
* Type 3 hypersensitivity | *[[Type III 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 [[Complement|complements]] and attract [[Neutrophil|neutrophils]], causing [[inflammation]] by release of their [[Toxic|toxic enzymes]] and [[Radical (chemistry)|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- ===== | ||
* Type 4 hypersensitivity | *[[Type IV hypersensitivity|Type 4 hypersensitivity]] | ||
* mononuclear cell inflammation and granuloma. | *[[Mononuclear cells|mononuclear cell]] inflammation and [[granuloma]]. | ||
===== Unifying hypothesis- ===== | ===== Unifying hypothesis- ===== | ||
Sensitized [[Macrophage|pulmonary alveolar macrophages]] activated by antigen attract [[Neutrophil|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 /> | |||
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== Genetics == | == Genetics == | ||
There are no established genetic predispositions. | There are no established [[Genetics|genetic]] predispositions. | ||
== Associated Conditions == | == Associated Conditions == | ||
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===== Acute phase- ===== | ===== Acute phase- ===== | ||
* Pulmonary alveolar wall and | * Pulmonary [[alveolar wall]] and [[Interstitial|interstitia]]<nowiki/>l accumulation of [[Neutrophil|neutrophils]], [[mononuclear cells]] and [[edema]]. | ||
* | * Obstructive [[bronchiolitis]] and [[Inflammation|capillary inflammation]] is present. | ||
===== Late phase- ===== | ===== Late phase- ===== | ||
* mononuclear cell predominant | *[[mononuclear cell]] predominant | ||
* presence of noncaseating granuloma | * presence of [[Granuloma|noncaseating granuloma]] | ||
== Microscopic Pathology == | == Microscopic Pathology == | ||
Latest revision as of 15:38, 29 July 2020
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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 phenomenon 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-
Sensitized 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