CORONAVIRUS INFO PROVIDED BY DR. JIM HARRIS – 02/14/2021
HELLO: If you’re busy or in a good mood, don’t read the second article today, or, maybe, ever. Happy Valentine Day.
(J. Harris: This is worth downloading to use as a reference. NEJM sent is out for physicians, but it’s nice and basic.
HOW COVID MAKES YOU SICK (This material will not be included on the final exam–it’ FYI)
J.Harris: Hobart Burton sent me this article and explanation. The article itself is exceedingly complicated. Here’s how Hobart explains it:
“This article, from Oak Ridge Labs…may be one explanation of why your buddies described intubating a C19 patient was like trying to intubate a brick. The virus instigated dysregulating of the Renin-angiotensin system (RAS), as in down regulating the ACE receptors and up regulating the ACE2 receptors, which created a bradykinin storm in the lungs which caused them to fill up with a substance called hyaluronic acid, creating a hydrogel. This stuff can absorb 1000 times its weight in water and cause a jello-like substance in the lungs, preventing oxygen intake and preventing CO2 outflow. Nasty. Of course, this also explains many other symptoms of the virus.” Thank you, Hobart.
J. Harris: The portion of the article that follows describes the clinical aspects of the Covid cases. Most cases are without symptoms and the infected person does not even know he’s sick. This bit of the article is a description of what might happen to some patients, and some or all of the manifestations of this horrible disease:
Clinical aspects of COVID-19
“According to the CDC, the majority of SARS-CoV-2 infections are asymptomatic or mild. Those that proceed to more severe forms present with fever, a non-productive cough that may result in hemoptysis and shortness of breath. Other common symptoms are myalgia, fatigue, sore throat, nausea, vomiting, diarrhea, conjunctivitis, anorexia, and headache (cdc.gov/coronavirus/2019-ncov/hcp/clinical-guidance-management-patients.html). Reports from blood studies include leukopenia, eosinopenia, neutrophilia, elevated liver enzymes, C-reactive protein, and ferritin (Fan et al., 2020; Huang et al., 2020; Goyal et al., 2020). Furthermore, autopsies have reported extensive hyaline membrane formation in the lungs of COVID-19 patients …. Specifically, histological analysis of the lungs of a deceased COVID-19 patient showed organizing hyaline membranes in the early stages of alveolar lesions and prominent hyaline membranes in the exudative phase of diffuse alveolar damage… In a seperate post mortem study of lung tissue from COVID-19 patients, microscopic examination found ‘numerous hyaline membranes without evidence of interstitial organization’ … Furthermore, in another autopsy study of a COVID-19 patient, histological analysis found extensive hyaline membranes, which the authors interpreted as indicative of ARDS …. Finally, a meta-analysis showed that there was a statistically significant 4.6 fold difference [increase] in lung weight of COVID-19 patients versus controls, which they conclude is consistent with the HA-hydrogel formation known to occur in ARDS….
Although much focus has been on the lung due to the need for ventilator support of end-stage disease, COVID-19 also affects the intestine, liver, kidney, heart, brain, and eyes ...Nearly one-fifth of hospitalized patients experience cardiac injury… many of whom have had no history of cardiovascular problems prior to infection. Responses include acute myocardial injury, myocarditis, and arrhythmias …. that may be due to viral infection directly, which is consistent with high expression of the SARS-CoV-2 receptor ACE2 in cardiac tissue… An important extension of the RAS[Renin/Antiotensin System] in controlling cardiac contraction and blood pressure is the potent inotrope apelin (APLN), which acts as an NO-dependent vasodilator when its receptor (APLNR) heterodimerizes with BDKRB1 (Bai et al., 2014). APLN (98 fold), APLNR (3190 fold) and BDKRB1 (2945 fold) are all upregulated in COVID-19 BAL. As with BK and ANG derived peptides, APLN is inactivated by Neprilysin (MME), which is significantly downregulated in the BAL samples from COVID-19 individuals (−16 fold). Therefore, increased APLN-signaling can be added to the imbalanced RAS. (I don’t know what any of this italicized portion means.)
In addition to cardiac dysfunction, neurological involvement in COVID-19 was revealed after an MRI assessment of COVID-19-positive patients with encephalopathy symptoms in France identified enhancement in leptomeningeal spaces and bilateral frontotemporal hypoperfusion … which are consistent with increased vascular permeabilization in the brain. Furthermore, earlier reports from China indicate [a lot of] of dizziness, headache, as well as taste and smell impairment …The most recent reports from the United States and China indicate that 30–50% of COVID-19 patients experience adverse gastrointestinal symptoms …. Direct infection by the virus and damage to the kidney was also observed, specifically in the proximal tubules … These latter two findings are not surprising given the higher expression of ACE2 in these tissues compared to tissues overall …, which would facilitate infection by the virus. Finally, COVID-19 patients also frequently display skin rashes, including ‘covid-toe’ that appear to be related to dysfunction of the underlying vasculature.
This diagram explains it all. What a simple solution. It makes one wish to be a Virologist?
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