Farmer's lung pathophysiology: Difference between revisions

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Revision as of 01:06, 28 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 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.

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.

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

@@ 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 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 phnomenon present and antibodies of organism invasion into tissues.
-=== Pathogenesis ===
+===== Acute- =====
-* The exact pathogenesis of [disease name] is not completely understood.
+* 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.
-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 4 hypersensitivity
-* [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
+* 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- =====
+Sensitised pulmonary alveolar macrophages activated by antigen attract neutrophils and also modulate T cell activity leading to appearance of mononuclear cells and granuloma.
+<br />
 == Genetics ==
-[Disease name] is transmitted in [mode of genetic transmission] pattern.
+There are no established 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 accumulation of neutrophils, mononuclear cells and edema.
+* obstructive bronchiolitis and 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 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}}