Difference between revisions of "Adult bronchiolitis pathophysiology"

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==Overview==
 
==Overview==
The pathogenesis of adult bronchiolitis is to be the result of inflammation and immunological responses that cause cellular injury and damage. Eventually, respiratory compromise results, which may be irreversible and fatal. Associated conditions include asthma and primary immunodeficiencies. The gross pathology of bronchiolitis includes bronchiolar and airway destruction. Microscopically, fibroblasts and lymphocytes are noted.
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The pathogenesis of adult bronchiolitis is to be the result of [[inflammation]] and immunological responses that cause cellular injury and damage. Eventually, respiratory compromise results, which may be irreversible and fatal. Associated conditions include [[asthma]] and [[Primary immunodeficiency|primary immunodeficiencies]]. The gross pathology of bronchiolitis includes bronchiolar and airway destruction. Microscopically, [[Fibroblast|fibroblasts]] and [[Lymphocyte|lymphocytes]] are noted.
  
 
==Pathophysiology==
 
==Pathophysiology==
 
===Pathogenesis===
 
===Pathogenesis===
*The bronchioles are the terminal conducting airways that lack in cartilage and glands.<ref name="pmid15776367">{{cite journal |vauthors=McNamara PS, Flanagan BF, Hart CA, Smyth RL |title=Production of chemokines in the lungs of infants with severe respiratory syncytial virus bronchiolitis |journal=J. Infect. Dis. |volume=191 |issue=8 |pages=1225–32 |date=April 2005 |pmid=15776367 |doi=10.1086/428855 |url=}}</ref><ref name="pmid16493150">{{cite journal |vauthors=Visscher DW, Myers JL |title=Bronchiolitis: the pathologist's perspective |journal=Proc Am Thorac Soc |volume=3 |issue=1 |pages=41–7 |date= 2006 |pmid=16493150 |doi=10.1513/pats.200512-124JH |url=}}</ref><ref name="pmid16088569">{{cite journal |vauthors=Couture C, Colby TV |title=Histopathology of bronchiolar disorders |journal=Semin Respir Crit Care Med |volume=24 |issue=5 |pages=489–98 |date=October 2003 |pmid=16088569 |doi=10.1055/s-2004-815600 |url=}}</ref>
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*The bronchioles are the terminal conducting airways that lack in [[cartilage]] and [[Gland|glands]].<ref name="pmid15776367">{{cite journal |vauthors=McNamara PS, Flanagan BF, Hart CA, Smyth RL |title=Production of chemokines in the lungs of infants with severe respiratory syncytial virus bronchiolitis |journal=J. Infect. Dis. |volume=191 |issue=8 |pages=1225–32 |date=April 2005 |pmid=15776367 |doi=10.1086/428855 |url=}}</ref><ref name="pmid16493150">{{cite journal |vauthors=Visscher DW, Myers JL |title=Bronchiolitis: the pathologist's perspective |journal=Proc Am Thorac Soc |volume=3 |issue=1 |pages=41–7 |date= 2006 |pmid=16493150 |doi=10.1513/pats.200512-124JH |url=}}</ref><ref name="pmid16088569">{{cite journal |vauthors=Couture C, Colby TV |title=Histopathology of bronchiolar disorders |journal=Semin Respir Crit Care Med |volume=24 |issue=5 |pages=489–98 |date=October 2003 |pmid=16088569 |doi=10.1055/s-2004-815600 |url=}}</ref>
*The bronchioles are of 2mm in diameter.
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*The [[Bronchiole|bronchioles]] are of 2mm in diameter.
*The area of gas exchange known as the acinus is made up of three parts, the respiratory bronchile, the alveolar duct and the alveolus.
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*The area of gas exchange known as the [[acinus]] is made up of three parts, the respiratory [[bronchiole]], the [[alveolar duct]] and the [[alveolus]].
*The respiratory bronchiole contains Clara cells and neuroendocrine cells, which produce somatostatin and serotonin.  
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*The respiratory bronchiole contains Clara cells and neuroendocrine cells, which produce [[somatostatin]] and [[serotonin]].  
*When an assault towards the bronchioles happens whether infectious or irritant in origin, an inflammatory process will begin followed by an immunological response which results in bronchiolitis.
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*When an assault towards the [[Bronchiole|bronchioles]] happens whether infectious or irritant in origin, an inflammatory process will begin followed by an immunological response which results in bronchiolitis.
**Immediately following exposure cellular destruction begins with the release of proteolytic enzymes and IgE in a type I hypersensitivity reaction.
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**Immediately following exposure cellular destruction begins with the release of proteolytic enzymes and [[Immunoglobulin E|IgE]] in a [[type I hypersensitivity]] reaction.
 
**The initial inflammatory reaction leads to:
 
**The initial inflammatory reaction leads to:
 
***Increased mucus secretion  
 
***Increased mucus secretion  
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***Increased airway resistance
 
***Increased airway resistance
 
**Within 18 - 24 hours the effects of an irritant or infection begin to appear.
 
**Within 18 - 24 hours the effects of an irritant or infection begin to appear.
**The infected epithelial cells lining the bronchioles begin to release chemokines and cytokines, this augments the immune response leads to the production of interferon and interleukins 4, 8 and 9.
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**The infected [[epithelial cells]] lining the bronchioles begin to release [[Chemokine|chemokines]] and [[Cytokine|cytokines]], this augments the immune response leads to the production of [[interferon]] and [[Interleukin|interleukins]] 4, 8 and 9.
 
**The immune response leads to:
 
**The immune response leads to:
 
***Bronchial obstruction
 
***Bronchial obstruction
 
***Ventilation-perfusion mismatch
 
***Ventilation-perfusion mismatch
***Dyspnea
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***[[Dyspnea]]
***Necrosis of respiratory epithelium
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***[[Necrosis]] of respiratory epithelium
***Atelectasis
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***[[Atelectasis]]
 
****Due to destruction of cilia
 
****Due to destruction of cilia
 
***Lymphocytic filtration
 
***Lymphocytic filtration
****Leads to submucosal edema
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****Leads to submucosal [[edema]]
 
***Hyperinflation
 
***Hyperinflation
**Repair is eventually started with the establishment of granulation tissue in place of the damage cells
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**Repair is eventually started with the establishment of [[granulation tissue]] in place of the damage cells
**May result in permanent fibrosis, which may be submucosal or peribronchiolar and therefore, obliterates the bronchiolar lumen.
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**May result in permanent [[fibrosis]], which may be submucosal or peribronchiolar and therefore, obliterates the bronchiolar lumen.
 
**May also result in complete resolution
 
**May also result in complete resolution
 
==Genetics==
 
==Genetics==
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==Associated Conditions==
 
==Associated Conditions==
*Asthma
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*[[Asthma]]
*Primary immunodeficiencies
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*[[Primary immunodeficiency|Primary immunodeficiencies]]
 
**Such as severe combined immunodeficiency
 
**Such as severe combined immunodeficiency
 
*Immunodeficient states
 
*Immunodeficient states
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*Congenital bronchopulmonary dysplasia
 
*Congenital bronchopulmonary dysplasia
 
*Pre-exisiting cardiovascular or pulmonary lung disease
 
*Pre-exisiting cardiovascular or pulmonary lung disease
*Rheumatoid arthritis
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*[[Rheumatoid arthritis]]
*Heart/lung/kidney transplant
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*Heart/lung/kidney [[Organ transplant|transplant]]
  
 
==Gross Pathology==
 
==Gross Pathology==
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==Microscopic Pathology==
 
==Microscopic Pathology==
*On microscopic histopathological analysis, fibroblasts, macrophages, and lymphocytes and plasma cells are characteristic findings of adult bronchiolitis.
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*On microscopic histopathological analysis, [[Fibroblast|fibroblasts]], [[Macrophage|macrophages]], and [[Lymphocyte|lymphocytes]] and [[Plasma cell|plasma cells]] are characteristic findings of adult bronchiolitis.
[[Image:bronc.gif|thumb|center|500px|Source:commons.wikimedia.org, shows a terminal bronchiole completely occupied by macrophages and tobacco pigments. By Yale Rosen from USA - Respiratory bronchiolitisUploaded by CFCF, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=31127983 ]]
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[[Image:bronc.gif|thumb|center|500px|Source:commons.wikimedia.org, shows a terminal bronchiole completely occupied by macrophages and tobacco pigments. By Yale Rosen from USA - Respiratory bronchiolitisUploaded by CFCF, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=31127983]]
  
 
==References==
 
==References==

Latest revision as of 19:12, 3 March 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

Overview

The pathogenesis of adult bronchiolitis is to be the result of inflammation and immunological responses that cause cellular injury and damage. Eventually, respiratory compromise results, which may be irreversible and fatal. Associated conditions include asthma and primary immunodeficiencies. The gross pathology of bronchiolitis includes bronchiolar and airway destruction. Microscopically, fibroblasts and lymphocytes are noted.

Pathophysiology

Pathogenesis

  • The bronchioles are the terminal conducting airways that lack in cartilage and glands.[1][2][3]
  • The bronchioles are of 2mm in diameter.
  • The area of gas exchange known as the acinus is made up of three parts, the respiratory bronchiole, the alveolar duct and the alveolus.
  • The respiratory bronchiole contains Clara cells and neuroendocrine cells, which produce somatostatin and serotonin.
  • When an assault towards the bronchioles happens whether infectious or irritant in origin, an inflammatory process will begin followed by an immunological response which results in bronchiolitis.
    • Immediately following exposure cellular destruction begins with the release of proteolytic enzymes and IgE in a type I hypersensitivity reaction.
    • The initial inflammatory reaction leads to:
      • Increased mucus secretion
        • Due to goblet proliferation
      • Bronchial constriction
      • Alveolar cell death
      • Mucosal debris
      • Increased airway resistance
    • Within 18 - 24 hours the effects of an irritant or infection begin to appear.
    • The infected epithelial cells lining the bronchioles begin to release chemokines and cytokines, this augments the immune response leads to the production of interferon and interleukins 4, 8 and 9.
    • The immune response leads to:
      • Bronchial obstruction
      • Ventilation-perfusion mismatch
      • Dyspnea
      • Necrosis of respiratory epithelium
      • Atelectasis
        • Due to destruction of cilia
      • Lymphocytic filtration
        • Leads to submucosal edema
      • Hyperinflation
    • Repair is eventually started with the establishment of granulation tissue in place of the damage cells
    • May result in permanent fibrosis, which may be submucosal or peribronchiolar and therefore, obliterates the bronchiolar lumen.
    • May also result in complete resolution

Genetics

  • Genetic susceptibility is thought to play a large role in the pathogenesis of infantile bronchiolitis and will not be discussed here.
  • However, age-related genetics may be implicated in the development of bronchiolitis in the elderly.

Associated Conditions

Gross Pathology

  • On gross pathology, (thickened bronchial walls) increased reticular markings, fibrous tissue proliferation, and airway destruction are characteristic findings of adult bronchiolitis.

Microscopic Pathology

Source:commons.wikimedia.org, shows a terminal bronchiole completely occupied by macrophages and tobacco pigments. By Yale Rosen from USA - Respiratory bronchiolitisUploaded by CFCF, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=31127983

References

  1. McNamara PS, Flanagan BF, Hart CA, Smyth RL (April 2005). "Production of chemokines in the lungs of infants with severe respiratory syncytial virus bronchiolitis". J. Infect. Dis. 191 (8): 1225–32. doi:10.1086/428855. PMID 15776367.
  2. Visscher DW, Myers JL (2006). "Bronchiolitis: the pathologist's perspective". Proc Am Thorac Soc. 3 (1): 41–7. doi:10.1513/pats.200512-124JH. PMID 16493150.
  3. Couture C, Colby TV (October 2003). "Histopathology of bronchiolar disorders". Semin Respir Crit Care Med. 24 (5): 489–98. doi:10.1055/s-2004-815600. PMID 16088569.

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