Pathophysiology of COVID-19.


The spike glycoprotein-S which present on coronavirus bind to the angiotensin converting enzyme-2 (ACE-2) receptors cells that help SSRNA to enter the host cell. Where translation occurs and the formation of polyproteins which will cleave by using TMPRSS2 (transmembrane protease serine 2) to make viral components along with SSRNA has the potential to use another enzyme which is RNA-dependent RNA polymerase to replicate the SSRNA.So, both replicated SSRNA and viral components joined to form a virus  (COVID- 19) which signals to release the macrophage upon tissue damage than the other inflammatory mediators(IL-6, IL-10, Tumour necrosis factors, granulocyte colony-stimulating factor, monocyte chemoattractant protein 1, macrophage inflammatory protein 1, is released from the endothelium layer. Which will cause the dilation of blood vessels by contraction of endothelium layer to increase the capillary permeability that causes alveolar edema leads to drowning out a surfactant that responses to increases the surface tension the alveoli will collapse that tends to decrease the gaseous exchange that leads to hypoxemia and increase the work of breathing that causes dyspnea (shortness of breath). 

All inflammatory mediators bring neutrophils from blood to alveoli to destroy the virus by releasing reactive oxygen species (ROS)and protease which damages all cells including (ACE- 1 and 2) and the results sloughing off. Damage cells along with the consolidation of fluid accumulation, protein deposition, and cellular debris alter the gaseous exchange to promote hypoxemia. This causes septic shock the patient becomes hypotensive, decreased total peripheral resistance, blood pressure, and decreased perfusion of their organs. it will also affect the liver to raise levels of AST, ALT, bilirubin, their response on the kidney is to increase the creatinine levels. SARS CoV-2 binds to host cells through the ACE2 receptor, which is expressed by epithelial cells of the lungs, intestine, kidneys, brain, and blood vessels. Which consequently promotes SARS-CoV-2 infection severity.


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