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Video transcript

the pathophysiology of emphysema which just means the disease process behind it how do we get from a normal lung to having a vizima I would say in a nutshell it's the destruction of elastin which is this protein in the lungs that gives it that nice elastic quality elastin and elasticity so elastin kind of looks like a coil I think of it as a coil and actually if you look at the protein itself it looks kind of coiled like that and we take a coil and you stretch it like that with force and then you let it go what happens it immediately snaps back into the original shape and size right because it's elastic the elastin in the lungs allows it to do just that so the top for breath the alveoli which are these air sacs at the end of the airway it looked puffed up and full of air like this and this is just like are stretched out coil and because the walls are full of elastin when you exhale which is just relaxing the air comes out by itself and the area kind of goes back to its original shape and size kind of like that so there's not that much air left in here but like I said in emphysema all the elastin is getting destroyed so we have fewer of these nice walls and whatever is left is no longer elastic so the top of a breath it might look like this do you see how all the partitions and stuff are gone but what's worse is when you've let go not that much changes it's like a spring without the elastic quality is just a wire so when you let it go just going to sit there and all that air in here is further obstructed because the airway here actually collapses so it collapses because without the elastin to hold it open the pressure in the chest cavity that acts on the airway collapses it that's why we say in emphysema you have obstructive lung disease because the air is obstructed back there so in a normal healthy functioning lung the elastin is actually normally being broken down all the time so elastin is broken down by elastase which is a protease inhibitor and by that which is made something that breaks down protein so the job of the last days is to cleave the elastin so that new tissue will have room to grow and who's going to keep track of days is something we call alpha 1-antitrypsin it's something that made that's made in the liver and again I'm gonna use red because the inhibit in elastase so if it inhibits the thing that inhibits elastin then the relationship here is going to be alpha 1-antitrypsin allows there to be more elastin it's kind of like in the ocean if you have shrimp here at the bottom of a food chain it's eaten by a small fish it's eaten by let's say Nemo so red Nemo eats fish and then behind it there's a big fish you shouldn't call that Nemo so just a big fish I see a shark eats this small fish so in this food chain the relationship if the food chain is this simple then the big fish or the shark allows you to be more shrimp by eating up all the small shirt small fish it's kind of like that where they last in the last days and alpha 1-antitrypsin in our whole problem here with emphysema is too much elastase too much elastase leads to emphysema now in terms of too much elastics there are too many ways to have that too much anytime you see ace here a se that's usually a protease inhibitor so it destroys a certain kind of protein number one here we have inflammation at anytime there's inflammation in the body it's kind of like a war is breaking out and all these soldiers are being recruited and one main one is called a neutrophil it's a type of white blood cell that's always in the blood and when there's inflammation it goes there and more importantly for us right now it's the mother of elastase literally the mother because it makes it last days so whenever there's too much neutrophils in the area it's going to go nuts making elastase inflammation is usually in response to an invading foreign thing right it could be bacterial or just any kind of particles and in here especially in the lungs the big culprit is going to be smoking it's even though you see the smoke rising from cigarettes looks like just air but it's actually made of millions of billions of tiny little particles that gets inhaled into the lung so this inflammation all all the time what I drew there actually looks more like a big cigar but you get the point is that any time you're putting extra irritants into the area the inflammation is going to go rampant and our last days two shoots up so number two the second reason is something that rises from the body itself which is something called anti alpha 1-antitrypsin deficiency we don't have this in the lungs this is the equivalent of taking out that big fish in the food chain so the small fish is going to go up without the big fish eating it and the shrimp poor shrimp they're all going to be gone now every one antitrypsin is made in the liver and is coated by a gene and this problem this diffusion see here is really due to defect in the gene because the gene has a problem here and when it's made in the liver the antitrypsin becomes miss folded and they can't leave it doesn't fit through the channel for the normal and d'etre person to leave so this actually causes liver disease but in terms of the lungs again we have too much elastase because it's go it's unchecked and again with the elastics going nuts here our last is going to go down you have emphysema