Bax_Cadarn

Bax_Cadarn t1_jatgzop wrote

You seem to misunderstand what a mutation means. A mutation is a random change in a gene. That happens millions of times in millions of cells in our body. Many of those mutations cause the cell to die, some don't change anything, some may make it get better at something, like not dying - putting it on the path to cancer.

If cell#74729194 mutates and becomes cancerous, it divides, divides and divides. If chemo poisons it and all its descendants, You should be cancer-free.

In reality, the more a cell's DNA is altered, the less stable it becomes, which makes every next generation of cancer different from the previous ones. That in turn makes it so all the cells are different, which can cause say 70% of the cells to respond to chemo while the rest won't.

The other problem You touched upon is what is considered a remission - yes, if we don't find a trace of it, we will consider it a remission - but we can't deconstruct a human to check every cell if there aren't 3 metastatic ones in that person's brain, one in the little left toe, and some next to where the tumor was. Best we can do is find a new small tumor, or some activity suggesting a metastasis, which can look similar to say an infection (and inflammation).

It is complicated, I think the first 2 paragraphs show what You wanted, and the rest is more corrections. Hopefully they are clear.

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Bax_Cadarn t1_j9fbmpq wrote

Close but not precisely. Think of it like a road system. Whdn You drive off a highway going north, You don't use the same way to go south. You need to drive to a smaller road to later rejoin increasingly larger roads until You enter the main flow from another side.

In ither words arteries branch off into increasingly smaller vessels up to the capillaries, then those collect into bigger and bigger veins

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Bax_Cadarn t1_j97cf64 wrote

I'm studying for a big exam and basically every disease, restrictive or obturative, lowers DLCO lol. (Barring alveolar hemorrhage). Not just COPD or smoking-related diseases like DIP.

By identifying cells from BF or EBUS or biopsies, You mean like looking for macrofages loaded with soot?

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Bax_Cadarn t1_j9630xk wrote

I can't say that was ever discussed during patophysiology.

One case which I can speak about is malaria. There, it is due to Plasmodium's life cycle. It takes 3 days for them to mature in a cell. So day 1 they enter the cells, they 4 they burst the cells open, which releases all its crap simultaneously from many cells. Day 7 it's hatching time again etcetc.

I reckon there's also 1 with 4 day life cycle.

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Bax_Cadarn t1_j8udy5w wrote

I would like a neurologist/immunologist to correct me if I'm wrong but. Isn't the biggest reason is that while differenciating leukocytes reacting with brain's molecules aren't destroyed the same way ones reacting with other irgans are? So basically they see a foreign material and attack it?

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Bax_Cadarn t1_ixmqkic wrote

I don't know what makes poorly differenciated glial cells any special but yes, gliala cells makes myelin sheath, as well as supporting cns tissues, and differenciation is the process of a cell turning from a basic, undifferenciated cell into one with a very specific function.

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