01/04/2021
Pathophysiology of COVID -19
Corona viruses are Large, enveloped, single stranded RNA viruses,
It has a diameter of 60nm to 140nm and distinctive spikes, ranging from 9nm to 12nm, giving the virion the appearance of solar corona.
Bats are thought to be a natural reservoir for Sars-Cov2, but it has been suggested that humans become infected via an intermediate hostsuch as pangolin.
EARLY INFECTION
Target cells are nasal, bronchial epithelial cells and pneumocytes.
The spike protein binds to ACE 2 receptor.
The transmembrane serine protease type 2(TMPRSS2), present in the host cell promotes viral uptake by cleaving ACE 2 and activatingSARS-COV2 protein, which mediates COV entry into the cells.
ACE 2 and TMPRSS2 are expressed in alveolar epithelial type 2 cells.
It causes profound lymphopenia, impairs lymphopoiesis and increase lymphocytes apoptosis.
LATER STAGES
Viral replication accelerates, epithelial -endothelial barrier integrity is compromised.
SARS-COV2 infects pulmonary capillary endothelial cells, accentuating the inflammatory response and triggering an influx of monocytes and neutrophils.
Interstitial mononuclear infiltrates and edema develops and appear as ground glass opacities on CT imaging.
Endothelial barrier disruption, dysfunctional alveolar capillary oxygen transmission and impaired oxygen diffusion capacity are the characteristics feature of Covid 19.
SEVERE COVID 19
Fulminant activation of coagulation and consumption of clotting factors occur.
It leads to high incidence of thrombotic complications such as dvt, pulmonary embolism, limb ischemia, ischemic stroke, MI in critically ill patients.
The development of viral sepsis can lead to multi organ failure.