UPDATED ... how people die from the coronavirus? The exact pathophysiology PART 2, MORE DETAILS
UPDATE: I HAVE UPLOADED THE DIAGNOSTICS PART
COVID-19 Diagnostics
COVID-19 Diagnostics
UPDATE: HOW OUR WORLD WILL BE IMPACTED AFTER THE PANDEMIC IS OVER?
https://curiosnerd.blogspot.com/2020/07/how-our-world-will-be-impacted-after.html?m=1
I am very glad that you decided to watch the second part of the mechanism of death in people who get infected with the coronavirus. In the previous article, I mentioned some mechanisms. However, we now know more about this virus and its other mechanisms with additional details that are available now. Check the first article from here: https://curiosnerd.blogspot.com/2020/03/how-people-die-from-corona-virus.html
1- Well, as we know the coronavirus is transmitted by air droplets. Let's say someone sneezes in front of you and you inhale the viral particles that came out from his mouth. The viral will travel directly to your respiratory system infecting the lining epithelial cells of your bronchi, bronchiole, and, most important, alveoli. It enters the cells through a protein on its surface that binds on a receptor on our alveolar type 2 cells called ACE 2.
2- Inside the cell, the virus begins to utilize the cell machinery to synthesize its proteins using our cells. It literally transforms the cell into a viral protein factory. Hundreds and maybe thousands of viral proteins are synthesized and assembled, then they rupture and the new viral particles infect new cells and so on...
3- The ruptured cells, as they die, begin to release proteins called damage-associated molecular patterns and cytokines. They start to activate the macrophage (immune cell) that sits in the alveoli.
4- The activated macrophages begin to secrete inflammatory cytokines that start a state of acute inflammation inside the lung. To be specific, they release, IL1, 6, 8, TNF alpha, IFN gamma
IL1, 6, TNF alpha migrate to the capillaries that line the alveoli. They start to increase the spaces between endothelial cells that line the capillary making to leakier. It also causes vasodilation
The fluid will begin to leak inside the interstitium and the alveoli. This makes it harder to breathe due to the accumulation of fluid. This makes it harder for oxygen to diffuse inside ---> hypoxemia
--> shortness of breath
Also, carbon dioxide will accumulate inside ---> respiratory acidosis
Also, all these cytokines secreted by the macrophage will increase the expression of a very important molecule on the endothelial lining of blood vessels called VCAM. This protein acts like a magnet; it attracts neutrophils circulating in the blood and causes them to migrate to the site of injury (inside the alveoli)
5- Neutrophils migrate to the site of injury and are also activated by the previous cytokines secreted by the macrophage. They begin to secrete proteases and reactive oxygen species to damage the invading pathogen, but, unfortunately, they also damage the lung alveoli lining. So neutrophils are double-edged weapons. They kill the virus but it comes with a price which is the damage of the tissue itself as well. The will repeat the cycle above leading to more inflammation, damage, and fluid accumulation.
7- Result: damage of type 1 alveolar cells as a result of this whole inflammation. These cells are responsible for gas exchange; this will contribute to more hypoxemia. Also, type 2 alveolar cells are damaged; they are responsible for making the alveoli open. If these cells die ---> alveoli will collapse. This also contributes to more hypoxemia!
8- Additionally, the cytokines secreted by the macrophage will stimulate the formation of microthrombi. It is believed that they increase the pro-coagulant proteins activate and inhibit and anti-coagulant protein activity. This will result in an unbalance that leads to the formation of microthrombi inside the lung leading to pulmonary embolism. This will contribute to more hypoxemia and lung damage!
9- The damaged epithelial cells and surrounding normal cells sense inflammation and begin to
synthesize 2 very important substances called leukotrienes and prostaglandins.
Leukotrienes will act on smooth muscles that line or bronchioles making them to constrict. This will make it harder for the air to move inside the alveoli to be exchanged!
Prostaglandins will contribute to the sensation of pain. They also will increase the vasodilation of blood capillaries leading to more fluid leakage, inflammatory cells migration, and, thus, inflammation.
10- All of these cytokines mentioned above can be secreted into the system circulation. They will have a very bad effect which is the activation of pro-coagulant substances and inhibition of anti-coagulant substances. This will lead to the formation of microthrombi in the whole body in most of the small blood vessels. This is known as Disseminated intravascular coagulation (a very bad complication)!
11- So as we see, it started with viral pneumonia --> progressed to Acute respiratory distress syndrome (the severe inflammation) ---> pulmonary embolism --> progress to multi-organ failure as a result of the DIC
A very bad virus. We hope that all of this will go away!
I hope you enjoyed the article.
UPDATE: I HAVE UPLOADED THE DIAGNOSTICS PART
COVID-19 Diagnostics
I am very glad that you decided to watch the second part of the mechanism of death in people who get infected with the coronavirus. In the previous article, I mentioned some mechanisms. However, we now know more about this virus and its other mechanisms with additional details that are available now. Check the first article from here: https://curiosnerd.blogspot.com/2020/03/how-people-die-from-corona-virus.html
1- Well, as we know the coronavirus is transmitted by air droplets. Let's say someone sneezes in front of you and you inhale the viral particles that came out from his mouth. The viral will travel directly to your respiratory system infecting the lining epithelial cells of your bronchi, bronchiole, and, most important, alveoli. It enters the cells through a protein on its surface that binds on a receptor on our alveolar type 2 cells called ACE 2.
2- Inside the cell, the virus begins to utilize the cell machinery to synthesize its proteins using our cells. It literally transforms the cell into a viral protein factory. Hundreds and maybe thousands of viral proteins are synthesized and assembled, then they rupture and the new viral particles infect new cells and so on...
3- The ruptured cells, as they die, begin to release proteins called damage-associated molecular patterns and cytokines. They start to activate the macrophage (immune cell) that sits in the alveoli.
4- The activated macrophages begin to secrete inflammatory cytokines that start a state of acute inflammation inside the lung. To be specific, they release, IL1, 6, 8, TNF alpha, IFN gamma
IL1, 6, TNF alpha migrate to the capillaries that line the alveoli. They start to increase the spaces between endothelial cells that line the capillary making to leakier. It also causes vasodilation
The fluid will begin to leak inside the interstitium and the alveoli. This makes it harder to breathe due to the accumulation of fluid. This makes it harder for oxygen to diffuse inside ---> hypoxemia
--> shortness of breath
Also, carbon dioxide will accumulate inside ---> respiratory acidosis
Also, all these cytokines secreted by the macrophage will increase the expression of a very important molecule on the endothelial lining of blood vessels called VCAM. This protein acts like a magnet; it attracts neutrophils circulating in the blood and causes them to migrate to the site of injury (inside the alveoli)5- Neutrophils migrate to the site of injury and are also activated by the previous cytokines secreted by the macrophage. They begin to secrete proteases and reactive oxygen species to damage the invading pathogen, but, unfortunately, they also damage the lung alveoli lining. So neutrophils are double-edged weapons. They kill the virus but it comes with a price which is the damage of the tissue itself as well. The will repeat the cycle above leading to more inflammation, damage, and fluid accumulation.7- Result: damage of type 1 alveolar cells as a result of this whole inflammation. These cells are responsible for gas exchange; this will contribute to more hypoxemia. Also, type 2 alveolar cells are damaged; they are responsible for making the alveoli open. If these cells die ---> alveoli will collapse. This also contributes to more hypoxemia!
8- Additionally, the cytokines secreted by the macrophage will stimulate the formation of microthrombi. It is believed that they increase the pro-coagulant proteins activate and inhibit and anti-coagulant protein activity. This will result in an unbalance that leads to the formation of microthrombi inside the lung leading to pulmonary embolism. This will contribute to more hypoxemia and lung damage!
9- The damaged epithelial cells and surrounding normal cells sense inflammation and begin to
synthesize 2 very important substances called leukotrienes and prostaglandins.
Leukotrienes will act on smooth muscles that line or bronchioles making them to constrict. This will make it harder for the air to move inside the alveoli to be exchanged!
Prostaglandins will contribute to the sensation of pain. They also will increase the vasodilation of blood capillaries leading to more fluid leakage, inflammatory cells migration, and, thus, inflammation.
10- All of these cytokines mentioned above can be secreted into the system circulation. They will have a very bad effect which is the activation of pro-coagulant substances and inhibition of anti-coagulant substances. This will lead to the formation of microthrombi in the whole body in most of the small blood vessels. This is known as Disseminated intravascular coagulation (a very bad complication)!
11- So as we see, it started with viral pneumonia --> progressed to Acute respiratory distress syndrome (the severe inflammation) ---> pulmonary embolism --> progress to multi-organ failure as a result of the DIC
A very bad virus. We hope that all of this will go away!
I hope you enjoyed the article.
UPDATE: I HAVE UPLOADED THE DIAGNOSTICS PART
COVID-19 Diagnostics
This is really good work and should be shared reddit, Facebook, Instagram..Any chance we can make this info into memes? Not to take away from your work. But the attention span of Americans is about 5 seconds. So we're stretching it if we have to make 5 memes because the first 3 took that time and they're moving on 😉
ReplyDeleteSeriously though think about it and thank you.
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