Hey peeps, calling all medfags, physiofags and other healthcare faggots.
New data is suggesting that ACE inhibs and ARBs COULD be a potential treatment for COVID-19 since SARS-CoV-2 enters type II pneumocytes via the ACE2 protein (which was seen previously with SARS back in the early 2000's). Since ARBs and and ACE inhibitors are used for people with T2DM and hypertension (ACE2 is highly expressed in these pops), how would these affect the RAS in normal individuals that would otherwise have no comorbidity if tested positive for SARS-CoV-2?
Follow up, if type-II pneumocytes are destroyed in the process once infected by the virus, would that not affect surfactant production and cause atelectasis? Other sources are saying the accumulation of inflammatory mediators (consolidation) resulting in pneumonia is main cause.
Just wondering what your thoughts are on the pathophysiology of SARS-CoV-2.
New data is suggesting that ACE inhibs and ARBs COULD be a potential treatment for COVID-19 since SARS-CoV-2 enters type II pneumocytes via the ACE2 protein (which was seen previously with SARS back in the early 2000's). Since ARBs and and ACE inhibitors are used for people with T2DM and hypertension (ACE2 is highly expressed in these pops), how would these affect the RAS in normal individuals that would otherwise have no comorbidity if tested positive for SARS-CoV-2?
Follow up, if type-II pneumocytes are destroyed in the process once infected by the virus, would that not affect surfactant production and cause atelectasis? Other sources are saying the accumulation of inflammatory mediators (consolidation) resulting in pneumonia is main cause.
Just wondering what your thoughts are on the pathophysiology of SARS-CoV-2.
