Farmer's lung pathophysiology: Difference between revisions

	Farmer's lung Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Farmer's lung from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Chest X Ray
CT
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Farmer's lung pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Farmer's lung pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Farmer's lung pathophysiology
CDC on Farmer's lung pathophysiology
Farmer's lung pathophysiology in the news
Blogs on Farmer's lung pathophysiology
Directions to Hospitals Treating Farmer's lung
Risk calculators and risk factors for Farmer's lung pathophysiology

VisualWikitext

Latest revision as of 15:38, 29 July 2020

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

References

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

[pmid21286564-1] Dales RE, Munt PW (October 1982). "Farmer's Lung Disease". Can Fam Physician. 28: 1817–20. PMC 2306727. PMID 21286564.

[pmid212865642-2] Dales RE, Munt PW (October 1982). "Farmer's Lung Disease". Can Fam Physician. 28: 1817–20. PMC 2306727. PMID 21286564.

[1]

[2]

@@ Line 5: / Line 5: @@
 == Overview ==
-The exact pathogenesis of [disease name] is not fully understood.
+The [[pathogenesis]] of the Farmer's lung disease is [[Type III hypersensitivity|type 3 or type 4 hypersensitivity reaction.]]
-OR
-It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
-OR
-[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
-OR
-Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
-OR
-[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
-OR
-The progression to [disease name] usually involves the [molecular pathway].
-OR
-The pathophysiology of [disease/malignancy] depends on the histological subtype.
 == Pathophysiology ==
-=== Physiology ===
+=== Pathogenesis: ===
-The normal physiology of [name of process] can be understood as follows:
+[[Hypersensitivity]] reaction because of the many immunologic phenomenon present and [[antibodies]] of organism invasion into tissues.
-=== Pathogenesis ===
+===== Acute- =====
-* The exact pathogenesis of [disease name] is not completely understood.
+*[[Type III hypersensitivity|Type 3 hypersensitivity]]
+* 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>
-OR
+===== Chronic- =====
-* It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
+*[[Type IV hypersensitivity|Type 4 hypersensitivity]]
-* [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
+*[[Mononuclear cells|mononuclear cell]] inflammation and [[granuloma]].
-* Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
-* [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
-* The progression to [disease name] usually involves the [molecular pathway].
-* The pathophysiology of [disease/malignancy] depends on the histological subtype.
+===== 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 />
 == Genetics ==
-[Disease name] is transmitted in [mode of genetic transmission] pattern.
+There are no established [[Genetics|genetic]] predispositions.
-OR
+== Associated Conditions ==
+There are no associated conditions.
-Genes involved in the pathogenesis of [disease name] include:
+== Gross Pathology ==
-* [Gene1]
-* [Gene2]
-* [Gene3]
-OR
+===== Acute phase- =====
-The development of [disease name] is the result of multiple genetic mutations such as:
+* Pulmonary [[alveolar wall]] and [[Interstitial|interstitia]]<nowiki/>l accumulation of [[Neutrophil|neutrophils]], [[mononuclear cells]] and [[edema]].
+* Obstructive [[bronchiolitis]] and [[Inflammation|capillary inflammation]] is present.
-* [Mutation 1]
+===== Late phase- =====
-* [Mutation 2]
-* [Mutation 3]
-== Associated Conditions ==
+*[[mononuclear cell]] predominant
-Conditions associated with [disease name] include:
+* presence of [[Granuloma|noncaseating granuloma]]
-* [Condition 1]
-* [Condition 2]
-* [Condition 3]
-== Gross Pathology ==
-On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 == Microscopic Pathology ==
-On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
+<br />
 == References ==
-[[Special:Categories|Category]]:
-* (name of the
-Please help WikiDoc by adding content here.  It's easy!  Click  [[Help:How_to_Edit_a_Page|here]]  to learn about editing.
-==References==
 {{Reflist|2}}