Tuesday, April 14, 2015

Study group discussion: Pathophysiology of liquefactive and coagulative necrosis in hypoxia

Why does hypoxia in the brain cause liquefactive necrosis? And why does hypoxia cause coagulative necrosis in all other tissues?

Let's take it step by step!

What's the basis of coagulative necrosis in hypoxia? How does it appear?

The framework and architecture of the cells is maintained.

The reason is - In hypoxia, there is early reduction of ATP. Hence, there is a switch to anaerobic pathways. Increased lactic acid production causes a decrease in pH which results in the inactivation of even the proteolytic enzymes.

The organelles dissolve to some extent, but as the pH increases, enzymes are inactivated, leaving behind the framework.

So.. Why is there no coagulative necrosis in the brain?

There is no anaerobic metabolism in the brain. Hence, no lactic acid to stop the proteolytic enzymes.

Also, in brain there is no supporting matrix. It is all neurons and supporting cells.
In other words,there are no acellular substances. Whereas in other tissues, there is an acellular supporting matrix.

When hypoxia strikes, everything dies in brain.
Hence, liquefactive. In other tissues, the ECM maintains the structure a little bit.

Cool concept. Made me go woah.

Interesting fact: It has been established that casseous necrosis is not necrosis per say, but it is mass apoptosis of macrophages. Robbins mentions it as necroapoptosis.

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