Tracheitis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
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* Viral pathogens include Influenza, Parainfluenza, Respiratory Syncitial Virus, Adenovirus and Echoviruses. | * Viral pathogens include Influenza, Parainfluenza, Respiratory Syncitial Virus, Adenovirus and Echoviruses. | ||
* Viruses cause desquamation of the pseudostratified columnar epithelium. | * Viruses cause desquamation of the pseudostratified columnar epithelium. | ||
* The epithelium regenerates into stratified non keratinized epithelium through metaplasia. | * The epithelium regenerates into stratified non keratinized epithelium through metaplasia.<ref name="pmid18039138">{{cite journal |vauthors=Taubenberger JK, Morens DM |title=The pathology of influenza virus infections |journal=Annu Rev Pathol |volume=3 |issue= |pages=499–522 |date=2008 |pmid=18039138 |pmc=2504709 |doi=10.1146/annurev.pathmechdis.3.121806.154316 |url=}}</ref> | ||
* As host defenses become weak, bacterial invasion becomes more likely. | * As host defenses become weak, bacterial invasion becomes more likely. | ||
* Bacterial pathogens include [[Staphylococcus Aureus]], [[Hemophilus Influenza]], [[Moraxella Catarrhalis]], [[Klebsiella Pneumonia]] | * Bacterial pathogens include [[Staphylococcus Aureus]], [[Hemophilus Influenza]], [[Moraxella Catarrhalis]], [[Klebsiella Pneumonia]] | ||
Revision as of 15:03, 27 June 2020
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Overview
The exact pathogenesis of [disease name] is not fully understood.
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
Trachea connects larynx with the bronchi and conducts air to the lungs. It is made of C shaped rings of cartilage. Muscles and fibers connect the tracheal rings together. This structural strength enables the trachea to withstand the variations in air pressure during each breathing cycle. The mucus membrane of trachea is lined by pseudostratified ciliated columnar epithelium. The goblet cells in the epithelium secrete mucus which captures inhaled pathogens. The cilia propagate the movement of the mucus towards the larynx and pharynx. It is either swallowed or expectorated as phlegm out of the body. Bronchial Associated Lymphoid tissue further augments the defensive system by providing humoral and cellular immunity. As tracheal inflammation occurs the mucosal edema signficantly constricts the tracheal lumen. This increases the airflow due to Venturi effect. The decrease in luminal diameter generates negative pressure which increases the propensity for airway collapse. This causes turbulent airflow which can be heard as a stridor. Children have a narrower subglottic region compared to adults. Tracheal inflammation further reduces the luminal diameter which causes difficulty in breathing. Therefore patients with tracheitis present with tachypnea, tachycardia, respiratory fatigue and stridor.
Pathogenesis
- The tracheal mucosa serves as a protective barrier to all inhaled pathogens
- Tracheitis means inflammation of the trachea. The larynx and bronchi can also be involved in the inflammatory process, causing laryngotracheobronchitis.
- Viruses enter the body through inhalation and damage the mucosal lining of the trachea.
- Viral pathogens include Influenza, Parainfluenza, Respiratory Syncitial Virus, Adenovirus and Echoviruses.
- Viruses cause desquamation of the pseudostratified columnar epithelium.
- The epithelium regenerates into stratified non keratinized epithelium through metaplasia.[1]
- As host defenses become weak, bacterial invasion becomes more likely.
- Bacterial pathogens include Staphylococcus Aureus, Hemophilus Influenza, Moraxella Catarrhalis, Klebsiella Pneumonia
- They infiltrate the epithelial lining causing mucosal edema, mucopurulent exudation and necrosis of the tracheal wall.
- A systemic inflammatory response develops due to cytokine release, causing septic shock.
With impaired defenses, bacterial invasion becomes more likely.
- Bacteria cause a secondary infection characterized by marked inflammation of the trachea. Thick exudates develop resulting in the formation of pseudomembranes which can acutely obstruct the trachea.
Genetics
There is no known genetic cause.
Associated Conditions
There are no known associated conditions.
Gross Pathology
On gross pathology, mucosal edema, ulceration, and exudates with thick membranes are characteristic findings of tracheitis.
Microscopic Pathology
On microscopic histopathological analysis, microabscesses and mononuclear inflammatory cells in the tracheal wall are characteristic findings of tracheitis.
References
- ↑ Taubenberger JK, Morens DM (2008). "The pathology of influenza virus infections". Annu Rev Pathol. 3: 499–522. doi:10.1146/annurev.pathmechdis.3.121806.154316. PMC 2504709. PMID 18039138.