Pulmonary Disorders and COVID-19: Difference between revisions
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==== Pathogenesis ==== | ==== Pathogenesis ==== | ||
As data on COVID-19 has been incomplete and evolving, the pathogenesis of pulmonary embolism has not yet been completely understood. Various contributors | As data on COVID-19 has been incomplete and evolving, the pathogenesis of pulmonary embolism has not yet been completely understood. Various contributors to the pathogenesis of pulmonary embolism in these patients are listed as | ||
* Endothelial | * Endothelial cells dysfunction: It has been proposed that endothelial cells contribute towards the initiation and propagation of ARDS by changing the vascular barrier permeability, increasing the chance of procoagulative state that leads to endotheliitis and infiltration of inflammatory cells in the pulmonary vasculature.<ref name="Teuwen Geldhof Pasut Carmeliet p. ">{{cite journal | last=Teuwen | first=Laure-Anne | last2=Geldhof | first2=Vincent | last3=Pasut | first3=Alessandra | last4=Carmeliet | first4=Peter | title=COVID-19: the vasculature unleashed | journal=Nature Reviews Immunology | publisher=Springer Science and Business Media LLC | date=2020-05-21 | issn=1474-1733 | doi=10.1038/s41577-020-0343-0 | page=}}</ref> It has been proposed that COVID-19 can directly affect endothelial cells leading to widespread endotheliitis. SARS-CoV-2 also binds to the ACE2 receptors which alter the activity of ACE2. Reduced ACE2 activity leads to activation of kallikrein-bradykinin pathway, which increases the vascular permeability. The activated neutrophils migrate towards the pulmonary endothelial cells and produce cytotoxic mediators including reactive oxygen species. <ref name="Teuwen Geldhof Pasut Carmeliet p. ">{{cite journal | last=Teuwen | first=Laure-Anne | last2=Geldhof | first2=Vincent | last3=Pasut | first3=Alessandra | last4=Carmeliet | first4=Peter | title=COVID-19: the vasculature unleashed | journal=Nature Reviews Immunology | publisher=Springer Science and Business Media LLC | date=2020-05-21 | issn=1474-1733 | doi=10.1038/s41577-020-0343-0 | page=}}</ref> | ||
===Hypoxemia=== | ===Hypoxemia=== | ||
Revision as of 06:45, 19 June 2020
To go to the COVID-19 project topics list, click here.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2]
Overview
Covid-19 infection is associated with pulmonary complications such as acute respiratory distress syndrome, pneumonia, pulmonary embolism, hypoxemia, superinfection, respiratory failure, and increased mortality in patients with an underlying pulmonary disease such as chronic obstructive pulmonary disease (COPD).
Complications
Acute respiratory distress syndrome
Pneumonia
Pulmonary embolism
In May 2020, various autopsies studies revealed pulmonary embolism to be the common cause of death in these patients. These patients in their mid-70s had preexisting medical conditions such as cardiac diseases, hypertension, diabetes and obesity.These studies highlight the role of hypercoagulability as main contributor towards the fatality in these patients. Various studies have described Virchow's triad to be the main component of the hypercoagulable state in these patients.
Pathogenesis
As data on COVID-19 has been incomplete and evolving, the pathogenesis of pulmonary embolism has not yet been completely understood. Various contributors to the pathogenesis of pulmonary embolism in these patients are listed as
- Endothelial cells dysfunction: It has been proposed that endothelial cells contribute towards the initiation and propagation of ARDS by changing the vascular barrier permeability, increasing the chance of procoagulative state that leads to endotheliitis and infiltration of inflammatory cells in the pulmonary vasculature.[1] It has been proposed that COVID-19 can directly affect endothelial cells leading to widespread endotheliitis. SARS-CoV-2 also binds to the ACE2 receptors which alter the activity of ACE2. Reduced ACE2 activity leads to activation of kallikrein-bradykinin pathway, which increases the vascular permeability. The activated neutrophils migrate towards the pulmonary endothelial cells and produce cytotoxic mediators including reactive oxygen species. [1]
Hypoxemia
Superinfection
Respiratory failure
Increased mortality in COPD patients
- According to a study conducted in China, having an underlying comorbidity such as chronic obstructive pulmonary disease (COPD) conferred a mortality hazard ratio of 2.681, even after adjusting for smoking status.