Farmer's lung pathophysiology: Difference between revisions

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* 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- =====
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===== 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

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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 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


References

  1. Dales RE, Munt PW (October 1982). "Farmer's Lung Disease". Can Fam Physician. 28: 1817–20. PMC 2306727. PMID 21286564.
  2. Dales RE, Munt PW (October 1982). "Farmer's Lung Disease". Can Fam Physician. 28: 1817–20. PMC 2306727. PMID 21286564.