| 00:01 | All right, y'all, let's see we can do here. Um |
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| 00:05 | we're continuing with the uh heart, last little bit about the heart, |
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| 00:09 | we're going straight into blood and blood , is pretty straightforward. I |
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| 00:14 | So if I talk fast, maybe get out of here quick. I |
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| 00:18 | , I don't know. Uh First we wanna do is we wanna talk |
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| 00:21 | uh just the contraction of the, uh cardiac muscle and what regulates |
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| 00:26 | So, does this all look familiar you? Does this look like something |
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| 00:28 | seen before? Yes. No, kind of, did that look kind |
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| 00:34 | familiar? So this is just like muscle. The only difference here is |
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| 00:38 | have a Dyad instead of a This is not the uh the terminal |
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| 00:43 | , it's just sarcoplasmic curriculum. Second I'd point out here is calcium doesn't |
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| 00:49 | come from the sarcoplasmic curriculum. It comes from the outside of the cell |
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| 00:53 | well. And so you can see have pump systems that are pumping calcium |
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| 00:57 | of the cell as well as into sarcoplasmic reticulum. But otherwise the contraction |
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| 01:01 | the same. I did want to something out here just because I like |
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| 01:05 | give you guys a little bit of nudge or a heads. Uh, |
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| 01:08 | mean, like a step ahead of else across the country, you |
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| 01:11 | and give you much more harder But, um, I'm gonna point |
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| 01:15 | uh some regulators. So, what we have here is if I |
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| 01:20 | to increase the rate of relaxation, I'm gonna do is I'm gonna phosphor |
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| 01:24 | inhibitors, right? So there there are things that slow down |
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| 01:29 | any system you have, we, don't really talk about them all, |
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| 01:32 | that much but any system you you have regulators both positive and |
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| 01:35 | And so in this case, we're about inhibitors and we have one |
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| 01:39 | it's called phosphor labin. And if look here on the map, there |
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| 01:42 | phosphor labin notice that it's associated with sarcoplasmic reticulum. It's associated with |
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| 01:47 | it is an inhibitor of circa. , if I am, um if |
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| 01:51 | inhibiting circa, that means I'm not uh the calcium away from the |
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| 01:57 | So that means there's more calcium If there's more calcium available, I'm |
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| 02:02 | a contraction, right? So basically heart slows down because of that sustained |
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| 02:07 | , you get the contraction lasting And so if I phosphor that what |
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| 02:11 | doing is I'm phosphorylation, the So I'm inhibiting the inhibitor. Does |
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| 02:17 | make sense? So there's a lot double negatives here. So if I |
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| 02:22 | phosphor lain, I'm no longer inhibiting . So what do I do is |
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| 02:26 | increase the rate at which I go into relaxation. So that would be |
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| 02:30 | example. Another one is troponin. we talked about uh troponin. We |
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| 02:35 | really go in a lot of detail the three sub units, but there |
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| 02:38 | three sub units. One binds up , right? One binds up tropy |
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| 02:44 | the other one is the hinge portion that hinge portion is uh there to |
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| 02:50 | of inhibit, that's why it's called eye that inhibits the contraction. So |
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| 02:53 | I phosphor that it's going to increase the rate at which I release the |
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| 02:59 | , which when I release the what did that do? Brings the |
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| 03:02 | back into place? So basically, causing relaxation to occur. So the |
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| 03:08 | here is that there are ways that inhibit this process and I'm just showing |
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| 03:12 | two of these ways right here. I want to do is I want |
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| 03:16 | deal with stroke volume. All we've talked about it in a |
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| 03:19 | very brief way. We said cardiac is equal to what I mean. |
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| 03:26 | gotta remember stuff, week to Yeah, I'm gonna help you |
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| 03:30 | Cardiac output is equal to heart rate . There you go. All |
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| 03:36 | which is not art. All And so the question here is what |
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| 03:39 | the things that actually affect stroke what increases or decreases the amount of |
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| 03:44 | my heart is pumping and there are different ways that we can look at |
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| 03:47 | . All right. First, we're to ask what's coming to the |
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| 03:50 | right? What are the things that the blood, turning to the |
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| 03:53 | Secondly, what are those things that the contractility of the heart? And |
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| 03:58 | third thing is what is the after ? What is preventing blood from leaving |
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| 04:03 | heart? So that's afterload. So gonna look at preload. How do |
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| 04:06 | regulate or what is the afterload? is resisting uh that movement? And |
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| 04:13 | there's a lot of words on these . Good news. You don't have |
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| 04:17 | read all the words. I'm gonna give it to you in a |
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| 04:19 | All right, preload. This is the blood is doing coming back to |
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| 04:24 | heart. All right. So if have veins and they have blood in |
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| 04:28 | , if I want more blood to to the heart, what do I |
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| 04:30 | to the veins? What do you ? Do I dilate them or constrict |
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| 04:35 | if I want more blood to return the heart? So think of |
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| 04:38 | we haven't talked about veins, what do. But if I have just |
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| 04:41 | of a tube, if I if I have fluid in a tube |
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| 04:44 | I want to get the fluid out the tube, what do I |
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| 04:48 | I, I squeeze it right. what would happen is that blood has |
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| 04:52 | go in the direction that, that only allowed to go. All |
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| 04:55 | And so it pushes towards the So now the heart just received a |
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| 04:59 | bunch of blood. All right, is Venus return. Ok. So |
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| 05:04 | heart goes, what do I do all this? Now, the good |
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| 05:08 | is there were two scientists who are the heart and trying to figure out |
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| 05:14 | does the heart work and what they was, hey, the heart actually |
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| 05:19 | care of itself. It doesn't need sort of external signal or anything to |
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| 05:24 | with the extra fluid that comes to . And ba basically what that graph |
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| 05:28 | showing you, there is basically their and really what it is is they |
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| 05:32 | up with this rule, they call the Frank Starling law. So Frank |
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| 05:34 | Starling were the two guys. All . And this is the gist of |
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| 05:37 | Frank Starling law, the blood what the blood receives. I'll say |
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| 05:45 | again, the blood pumps, what receives. So if I give it |
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| 05:47 | blood, the pump, the heart that blood, if I give it |
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| 05:53 | blood, the heart pumps less So there's this natural relationship. So |
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| 06:00 | you can remember that you're good to . So if I increase the amount |
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| 06:04 | blood by squeezing the Venus side of system, and more blood returns back |
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| 06:10 | the heart that doesn't cause problems. increases how much the heart will |
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| 06:16 | So, increasing blood flow, increases volume, decreasing blood flow from the |
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| 06:24 | side, decreases stroke volume. All , that's the relationship. And really |
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| 06:30 | , what you're dealing with here is end volume. Because if you |
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| 06:34 | we said, hey, stroke volume here is equal to two things. |
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| 06:37 | difference between two things. Do you what those two things were? End |
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| 06:43 | volume and end diastolic volume. And at the end of diastole, what |
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| 06:49 | I doing? That's my, that's much I've ejected out. And so |
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| 06:53 | that blood has to go all the back around and it's pushing and filling |
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| 06:58 | right before. So what you're looking here is you're increasing the amount of |
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| 07:02 | showing up in the atria and then just gonna flow on in and that's |
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| 07:06 | we're dealing with there. Ok. remember the hard thing to remember is |
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| 07:10 | whole thing is connected. So if pushing stuff out stuff has to come |
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| 07:13 | . All right. So Frank Very simple. The blood pumps, |
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| 07:17 | you give it kind of nice even there's a lot of words up there |
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| 07:22 | the back side, we have the . All right, the afterload is |
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| 07:26 | back pressure. Ok? You know back pressure is? Give you an |
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| 07:32 | . Simple one. You're filling up balloon if you don't pinch off the |
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| 07:39 | , what's the air gonna wanna it's gonna wanna come back, |
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| 07:43 | Because the elastic walls of the balloon creating a pressure inward and that air |
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| 07:48 | just trying to find the quickest way of that, that space. We're |
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| 07:52 | have to learn about that pressure here little bit when we start talking about |
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| 07:55 | lungs. All right. So every you push fluid into the aorta or |
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| 08:03 | fluid into the pulmonary arteries, those are stretching and then they're creating a |
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| 08:11 | . Now, what that pressure is gonna do is it's gonna drive the |
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| 08:14 | forward, but it's just looking for way to flow. And so when |
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| 08:19 | heart pumps, right, it's pushing out of the ventricles, it's going |
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| 08:24 | feel that pressure, it's a back . So the greater that pressure, |
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| 08:29 | less blood is going to be able leave the heart. Does that make |
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| 08:33 | ? Right. Do you remember that example? I gave a little while |
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| 08:37 | about trying to fill up the smart with kid with students, right? |
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| 08:41 | more people you put in the smart , the less it's gonna be likely |
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| 08:44 | you're gonna get the next person right? Because there's a back pressure |
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| 08:49 | that's the same thing that's going on when we talk about high blood pressure |
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| 08:53 | making the heart work harder. This what you're trying to overcome is a |
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| 08:57 | pressure. Put another way you have five liters of blood in your |
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| 09:02 | In circulation, the heart is only about 70 mils of that a portion |
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| 09:07 | it probably about 1/5 is in pulmonary . So in systemic circulation, you |
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| 09:14 | about four liters of blood that the is actually pushing forward 70 out of |
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| 09:18 | heart, plus the the rest of blood that goes throughout all your |
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| 09:22 | That is creating a back pressure that have to overcome Now, and helping |
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| 09:29 | this value, this amount of back is more or less constant. So |
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| 09:33 | , that's just part of the pumping , right? Ok. I've got |
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| 09:36 | push all this blood forward. But you have issues, that's what we're |
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| 09:41 | about. That's what the high blood is. That's why it's so problematic |
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| 09:45 | it makes your heart work too hard that can cause problems right. |
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| 09:51 | if the A load goes up, that's gonna do is that's gonna result |
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| 09:55 | an increased ESV. Now, why ? Why in systolic volume? |
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| 10:00 | when the heart contracts, we call , what's the other word for |
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| 10:06 | Systole? And the in systolic volume the amount of blood left inside the |
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| 10:13 | at the end of systole ESV. ? So if I have greater back |
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| 10:21 | , less blood leaves a heart that or increases ESV. All right, |
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| 10:27 | I increase ESV, again, the , right, it's the difference between |
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| 10:33 | NTO and the in systolic volume. if ESV goes up and EDV stays |
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| 10:38 | same, same number minus a bigger is a smaller number. So stroke |
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| 10:45 | is affected so far. Does that of make sense? Kind of sort |
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| 10:52 | my goodness. He's using big words abbreviations and I am confused. All |
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| 10:58 | . Yes, sort of. Look at the third thing inotropic agents |
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| 11:05 | excuse me, not, not, inotropic, inotropic inotropic agents. These |
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| 11:09 | those external factors, those extrinsic factors can affect the, the activity of |
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| 11:15 | heart. So when I see someone , my heart beats faster. |
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| 11:20 | all right, that's autonomic innovation. that affect stroke volume? Yes, |
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| 11:26 | does. All right. Uh different can affect stroke volume. We're gonna |
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| 11:31 | about those hormones a little bit Um after contraction, what we're gonna |
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| 11:37 | here is um or we're not after , but we're gonna alter contraction. |
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| 11:41 | , um when I exercise and run heart beats harder, right? And |
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| 11:46 | I eject more at the same So these are things that have an |
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| 11:52 | on the ability of the heart to the amount of blood that it's gonna |
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| 11:55 | both positive and negatively. So if a positive inotrope, what we're doing |
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| 11:59 | we're increasing the availability of calcium. means I'm gonna get harder pumps, |
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| 12:04 | gonna get faster pumps. All but it's the that stronger pump. |
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| 12:08 | do you think a stronger pump can an afterload? Like a constant |
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| 12:13 | What do you think? Yeah, should. Does that make sense? |
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| 12:17 | mean, you got, I just like the expression of a couple of |
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| 12:20 | like what now? Right. So I, if I have resistance and |
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| 12:24 | am pushing harder against that resistance, that resistance gonna more likely to move |
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| 12:29 | if I Yeah, so that's, what we're saying here. All |
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| 12:32 | So that's number one. Um So got some examples up there. So |
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| 12:36 | you know, adrenaline nor norepinephrine. , sympathetic innervation is an example. |
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| 12:41 | hormone increases the availability of beta one . And so that's gonna increase the |
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| 12:48 | the activity of the sympathetic side. are certain drugs you can take that |
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| 12:53 | do that as well. And then negative inotrope, not iono trope um |
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| 12:58 | the negative inotrope is gonna decrease calcium . So you get softer heartbeats, |
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| 13:04 | hard ones. All right. Those overcome after load, but they change |
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| 13:09 | contract, the the contract ail of heart. In other words, it |
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| 13:12 | down the heart and P and pumps heart pumps less. So you can |
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| 13:17 | here that we have things that can it outside of the two systems on |
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| 13:23 | side. So, preload deals with Venus return, ok? So blood |
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| 13:32 | to heart, Venus return, afterload with arterial pressure. So blood leaving |
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| 13:39 | heart, right. Frank Starling says does what pumps what you give it |
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| 13:48 | . And then knowing ESV and E , what am I altering? So |
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| 13:54 | I'm dealing with preload, I'm altering . When I'm dealing with afterload, |
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| 13:58 | dealing with ESV. Right? And can just play with the math SV |
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| 14:03 | EDV minus ESV. That's not right? And just say what happens |
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| 14:08 | I increase or decrease this and you see how it affects stroke volume. |
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| 14:11 | lastly, I have external factors that body uses external to the heart that |
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| 14:17 | affect the contractility of the heart, can affect stroke volume. All |
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| 14:24 | A simple one. If you drink six monster drinks, what's that gonna |
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| 14:27 | to your heart? Hummingbird, OK. There you go. All |
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| 14:34 | . If we're comfortable with that, hope we are. That was gonna |
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| 14:37 | the last thing we were talking about week. Let's go through blood. |
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| 14:40 | right, blood is a connective It's a specialized connective tissue. It's |
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| 14:44 | weird one. It's the only connective tissue. Um It is a |
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| 14:49 | of three things. All right, have what are called the formed |
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| 14:53 | The formed elements we use formed element of cells because we're dealing with mostly |
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| 14:58 | . But some of the things that would call cells are altered cells and |
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| 15:03 | they're not entirely cells anymore. So we call them the elements. |
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| 15:07 | also a matrix in there and a is simply a bunch of, of |
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| 15:12 | and other materials that form uh an in a connective tissue. So plasma |
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| 15:18 | the matrix of the blood plasma consists all these different types of, of |
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| 15:23 | which we're gonna kind of go looking . Um generally speaking, in connective |
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| 15:29 | , connective tissues, the cells in matrix are responsible for making the |
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| 15:34 | But that's not what happens in connective or in, in the, in |
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| 15:38 | blood. Uh it's called blood because its, I mean, blood is |
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| 15:41 | connective tissue because of its embryological I'm not gonna ask you that. |
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| 15:45 | just so if you ever said, , I don't understand why it's a |
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| 15:47 | tissue. That's why it's just its . All right. Now, if |
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| 15:52 | leave blood and take out the coagulating , what will happen is is that |
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| 15:57 | will see the formed elements, the stuff will basically float out of solution |
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| 16:02 | they'll like land at the bottom of container, right? So you'll see |
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| 16:06 | blood cells and other things kind of themselves out just by virtue of |
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| 16:10 | of their size and mass. All . And so this doesn't happen in |
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| 16:16 | body because blood is in constant So if you were to take some |
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| 16:21 | of solution, let's just make it simple one. If you take Kool |
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| 16:24 | and dump it into a glass, Kool Aid crystals will float to the |
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| 16:28 | , won't they? Some of them suspend or dissolve, but most of |
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| 16:31 | will just float to the bottom. how do you prevent that from |
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| 16:34 | Shake, shake, shake, shake and they will stay in suspension |
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| 16:38 | the time. All right. And part of the reason our blood is |
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| 16:42 | while it's heterogeneous in this or it's in the sense that we have equal |
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| 16:47 | stuff. The reason for that homogeneity um is because you're in constant motion |
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| 16:52 | constant circulation. So nothing's ever allowed really settle. When we look at |
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| 16:59 | , we can separate it out into parts. We have what is called |
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| 17:03 | hematocrit. The hematocrit is the packed volume. So typically, uh |
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| 17:09 | what we're saying, when we say is we are really referring to the |
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| 17:13 | of erythrocytes, right, the amount red blood cells. So this will |
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| 17:17 | between 42 and 45% sometimes incorrectly, more commonly than needs to be is |
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| 17:25 | will refer to the pack cell meaning the Buffy coat as well. |
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| 17:30 | Buffy coat would be part two. Buffy coat are your leukocytes and your |
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| 17:35 | , it makes up a very small about 1%. So if you were |
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| 17:39 | take a blood sample centrifuged out, can actually cause all those heavy things |
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| 17:44 | kind of press on down. And , rather than waiting for it to |
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| 17:48 | out, you can push them And so you'd see the red, |
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| 17:50 | red blood cells, which are the than the white blood cells in that |
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| 17:53 | coat and then the plasma would remain on top. The hematic crit normally |
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| 17:58 | refers to red blood cells, but they include the Buffy coat. All |
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| 18:06 | , on the test. If I it on there, if it says |
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| 18:09 | presume red blood cells, because that's correct definition. OK. Now, |
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| 18:19 | hematocrit is to be uh change depending your age and your sex. I |
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| 18:22 | point this out here because it's just example of how men and women are |
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| 18:27 | . Men have a slightly higher And the reason for that is testosterone |
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| 18:31 | an important role in uh erythropoietin which is what is responsible for producing |
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| 18:38 | uh red blood cells. It's the that is responsible for that plasma. |
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| 18:44 | the other hand, is mostly it's water plus other stuff. So |
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| 18:48 | about 90% water. Here's the list other stuff. Um If you take |
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| 18:54 | the uh uh take out fibrinogen and clotting factors, you can call plasma |
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| 19:00 | . So basically, now it won't , it is now capable for transfer |
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| 19:05 | whatnot. And what I wanna do just kind of show you the different |
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| 19:07 | of plasma proteins. I'm just gonna the question. If you don't know |
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| 19:11 | answer, that's fine. Do you know what this is right up |
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| 19:15 | What that looks like? What that western blood? OK. Good. |
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| 19:19 | just wanted to see if anyone here some if you haven't done lab work |
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| 19:23 | you're looking at western blocks, that's . I'm not, it's not |
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| 19:27 | not everyone's gonna be in the But you know, this is just |
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| 19:30 | example of what a Western block looks if you've never done that. And |
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| 19:34 | , if, what you would want do with something like this is if |
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| 19:36 | could do a 3D gel, you actually run it out and it would |
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| 19:39 | out into not only in that one but also the other dimension. So |
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| 19:43 | could see these different groups. And what plasma proteins are just simply proteins |
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| 19:48 | are found in the plasma, they're in a couple of different areas, |
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| 19:51 | primarily the liver, but there's some places where you can see them being |
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| 19:55 | . Um The reason that they're significant not so much about what types that |
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| 20:01 | gonna find there. All right, are important, but for our purposes |
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| 20:06 | , those that is less important. I want to point out is the |
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| 20:10 | we're concerned about them. Why we is that the presence of the proteins |
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| 20:15 | in the plasma establishes an osmotic gradient to the interstitial space. OK. |
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| 20:23 | when you put water into the water is drawn towards the presence of |
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| 20:28 | plasma proteins because there's no plasma proteins in the interstitial space, water doesn't |
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| 20:33 | to float out and away from the . It wants to stay where the |
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| 20:36 | actually is located inside the capillaries and , the veins and the arteries. |
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| 20:41 | . That's why it's really kind of for us. All right. Um |
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| 20:47 | it draws water fluid to there. , the other thing plasma proteins do |
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| 20:52 | bringing fluid into that space. What gonna do is it's gonna help you |
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| 20:56 | regulate and maintain blood pressure and blood . All right. And you'll see |
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| 21:01 | this is important because we're gonna bring up over and over and over |
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| 21:04 | Not only in this unit, but the next unit we start talking about |
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| 21:07 | renal system and how we regulate All. All right. Now, |
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| 21:11 | some common proteins. Um, Have you ever heard of the Al |
|
| 21:16 | ? No. All right. Um you go home, get an |
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| 21:19 | crack it open and just like play it for a little bit, play |
|
| 21:23 | the wa the clear stuff that is albumin and water. All right. |
|
| 21:28 | really, really gross. All But it's a sticky protein, |
|
| 21:31 | If you play, it's really, sticky. It's actually egg eggs we |
|
| 21:35 | use as the example, but it's the struck or it's not the, |
|
| 21:38 | , the food that has most And I think if I remember |
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| 21:42 | it's like turkey does. II, can't remember exactly but someone's gonna google |
|
| 21:47 | real quick. Say which food has most albumen by volume or something, |
|
| 21:52 | know, whatever. All right. anyway, why, why we care |
|
| 21:56 | it. And so here this is albumin right here uh on the |
|
| 21:59 | it basically is capable of binding lots things in a very non-specific way. |
|
| 22:04 | it kind of serves as a uh carrier in the blood. Uh You've |
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| 22:09 | of the globulins before? Have I'm sure you had, I |
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| 22:12 | maybe not ha you may not have of the alpha or the betas, |
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| 22:15 | you've definitely heard of the gamma right? Those are your antibodies. |
|
| 22:20 | . So your blood is filled with and you can just kind of go |
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| 22:23 | here and go. OK. here's the alpha of the betas and |
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| 22:25 | gammas, they're kind of marked up . So they're all over the |
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| 22:28 | All right. Um alpha and beta uh globulins look what they transport lipids |
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| 22:34 | ions. So again, it's another of transporter and then the other protein |
|
| 22:39 | want to point out to you is and fibrinogen is important because of the |
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| 22:43 | we're gonna talk about at the very of class, which is how you |
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| 22:46 | about clotting the blood. All So, fibrinogen is a plasma |
|
| 22:50 | it's already in circulation. So if cut yourself, this stuff is already |
|
| 22:55 | , ready to create the human band to hold your blood in your |
|
| 23:00 | OK? That's part of its All right. So that process is |
|
| 23:05 | to as hemostasis when we get we'll, we'll talk about that. |
|
| 23:10 | it's less important to know what each these individual things do and kind of |
|
| 23:13 | like, oh yeah, there's, these proteins that play an important role |
|
| 23:18 | maintaining um a osmotic pressure, but have other real roles individ uh independently |
|
| 23:25 | individually. Right? That's kind of key thing. And what I wanna |
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| 23:29 | is I want to talk about how we make these formed elements? All |
|
| 23:33 | . Now, generically, the term use when we say we're gonna make |
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| 23:38 | cells is we call the process hemostasis not hemostasis, hematopoiesis. All |
|
| 23:44 | you might even see hemopoiesis. All . And that's what this little big |
|
| 23:47 | this little chart, this little big . All right, here's the |
|
| 23:54 | Do not memorize the stairs, please not memorize the hormones involved. All |
|
| 24:04 | , there was a time I thought might be important. I have sense |
|
| 24:07 | matured. OK? And it's not important. The idea here though is |
|
| 24:12 | want you to show that there is relationship that all the, all the |
|
| 24:15 | cells in your body are derived from same stem cell line. All |
|
| 24:21 | that's what we're kind of seeing OK. We have these long term |
|
| 24:25 | hematopoietic stem cells, they become short . So basically what we're saying is |
|
| 24:29 | have this, this pluripotent cell or cell that kind of sits there and |
|
| 24:34 | a pool and then that pool divides . And then from there we get |
|
| 24:38 | . So we always have a stem group. We always have another group |
|
| 24:41 | which the other ones are derived and always preserve our stem cell line. |
|
| 24:45 | what this is. But then what do is we then go into these |
|
| 24:49 | colonies and we're gonna be driven down of two lines. And so down |
|
| 24:53 | , what you're looking at that is lymphoid line and then all the rest |
|
| 24:57 | this stuff that's the myeloid line. right. So you're going down and |
|
| 25:02 | myeloid like cells, which include the blood cells, includes the platelets or |
|
| 25:07 | thrombocytes and includes the mega carys plus couple of the other types of, |
|
| 25:13 | um granulocytes. When we're talking about lymphoid line, we're talking about uh |
|
| 25:19 | group of white blood cells that are like the T cells and the B |
|
| 25:24 | , right? So they are, are unique from the other uh group |
|
| 25:27 | white blood cells, the granulocytes. right. So I just wanted to |
|
| 25:32 | of show you that and then I this big long thing that's not really |
|
| 25:36 | . Like I said, don't memorize of these things. But what you |
|
| 25:39 | see is once I move down a , I'm committed to a specific |
|
| 25:43 | right? And then once I, the thing that allows me to commit |
|
| 25:47 | a specific hormone or signaling molecule that , all right, when I receive |
|
| 25:53 | , that is going to cause me change or differentiate enough in order to |
|
| 25:57 | forced down this particular track. So I become uh a colony forming unit |
|
| 26:04 | the basophils, I can't switch and oh no, no, no, |
|
| 26:07 | . We need more granular or we more neutrophils. So never mind, |
|
| 26:11 | gonna become a neutrophil. Now, you make a certain step, you're |
|
| 26:14 | stuck on that track. And I to say it was like uh when |
|
| 26:18 | declared your major in college, but can change your major any time at |
|
| 26:21 | point. Right back in the it was like, oh, I'm |
|
| 26:25 | down this track if I wanna graduate time, this is what I need |
|
| 26:28 | do. And so you get Yeah. Mhm Did you? So |
|
| 26:43 | when they choose. So for we'll use this one. So you |
|
| 26:46 | see here this, this uh colony unit will allow me to become pretty |
|
| 26:50 | anything, right? So, depending which uh hormones are available, it's |
|
| 26:55 | drive me down a particular track. here this is called granulocyte monocyte calling |
|
| 27:01 | factor. This is why I didn't you to memorize it because there's also |
|
| 27:04 | . But when these things are available I three, then that's gonna force |
|
| 27:08 | down this path. So you'll either a neutrophil or you become a mac |
|
| 27:13 | , then you don't have a right? Oh Well, what if |
|
| 27:16 | go down this line, well, gonna be another type of granular site |
|
| 27:20 | factors. Probably G CS F. then what you do is, |
|
| 27:23 | when IL five or LL three is , it's gonna drive you down this |
|
| 27:27 | track kind of going off the It's OK. Go into never. |
|
| 27:36 | , it is. Literally, I've my major. I'm now stuck a |
|
| 27:40 | major. I can never change Yeah. Yeah. Once you've made |
|
| 27:47 | step forward, you're now committed. , what I wanna do is I |
|
| 27:51 | show you that commitment through erythrocytes. think this one is the easy one |
|
| 27:57 | look at. Not so much to memorize all the different stages because |
|
| 28:01 | are a lot of stages, but shows how this works. All |
|
| 28:04 | And so you can see here, know, here's that short term um |
|
| 28:09 | cell line that goes into the myeloid and you can see that, that |
|
| 28:14 | can identify multiple stages along the That's really what I'm trying to show |
|
| 28:18 | this particular picture. All right. these stages are important because what they |
|
| 28:22 | is they're, they're showing those key that cause it to change into something |
|
| 28:27 | . All right. Now, where this actually take place? Well, |
|
| 28:32 | you're a kid, well, this takes place in red, red |
|
| 28:35 | All right. But in utero, don't have bones really to have red |
|
| 28:40 | . So you don't do that So have the spleen. It usually is |
|
| 28:43 | the important one liver. But prior that, it's gonna be yolk |
|
| 28:47 | So, before you have your the yoke is responsible for making red |
|
| 28:50 | cells. All right. So you making them very early on if, |
|
| 28:55 | that's kind of the take home All right. And then when you're |
|
| 28:58 | kid, most of your bones have bone marrow. So you can go |
|
| 29:02 | you know, any bone basically crack open. There's gonna be red bone |
|
| 29:05 | . Please don't do that to They don't like that. It's not |
|
| 29:09 | . All right. And then as start exiting out of puberty and you |
|
| 29:13 | becoming an adult, your red marrow starting to be replaced by yellow marrow |
|
| 29:18 | most of the bones. So really long bones in particular is where you're |
|
| 29:21 | see, you know, like if cracked open a femur, you'd see |
|
| 29:24 | red marrow there. But in an , you crack it open, you'll |
|
| 29:27 | yellow marrow, red marrow now become in some very specific locations, primarily |
|
| 29:33 | these flat bones like in the hips at the ends of the long |
|
| 29:37 | So that what we call the And these are not easy to get |
|
| 29:41 | . So, you know, when see someone donating marrow, like an |
|
| 29:45 | donating marrow, for somebody understand that are going to go through some really |
|
| 29:50 | surgery to get access to that So you should just give them a |
|
| 29:53 | old thumbs up and then go buy a card and maybe a, a |
|
| 29:57 | , you know, one of the cookies. All right. Now, |
|
| 30:01 | process of erythropoiesis is gonna be regulated the kidney. And the reason we |
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| 30:05 | the kidney or my presumption is why body chose the kidney is that all |
|
| 30:10 | needs to pass through the kidney to cleansed of the waste that it's going |
|
| 30:14 | . All right. So it just like this would be an easy structure |
|
| 30:18 | your blood has to go through All right. And so what the |
|
| 30:22 | is doing is it's responding to the carrying capacity of the blood. |
|
| 30:27 | this is a uh a long winded way of saying it's monitoring how much |
|
| 30:33 | it's receiving and how much oxygen it's is gonna be dependent upon how much |
|
| 30:38 | blood cells actually circulating in the blood . So, if you start losing |
|
| 30:43 | blood cells, there's not the same of oxygen being carried by the |
|
| 30:48 | So the kidney is oxygen starved and should be the signal that says, |
|
| 30:52 | , I need more red blood So it releases a hormone called erythropoietin |
|
| 30:57 | then goes to the bones and to bone marrow, red bone marrow and |
|
| 31:00 | , hey, start making more red cells. And so this is that |
|
| 31:04 | that you're seeing behind you. That's is called erythropoiesis. All right. |
|
| 31:09 | that's the simplified version of this. what happens is, is a red |
|
| 31:14 | cell goes through this process of extruding portions of its, of its cellular |
|
| 31:22 | and replaces it with protein that it's . And the protein it makes is |
|
| 31:27 | . So it just makes tons and of hemoglobin. And as it's |
|
| 31:30 | it, it starts getting rid of nucleus, it gets rid of the |
|
| 31:33 | uh uh the organelles, all the it doesn't need and it changes its |
|
| 31:38 | . So you can imagine this is cell that is basically like a round |
|
| 31:42 | . And what you do is just deflating the basketball. And now you |
|
| 31:44 | a thing that looks like a All right. And if you don't |
|
| 31:47 | what a beret is, well, see a picture here in just a |
|
| 31:50 | . All right. So that's what these things represent. And in |
|
| 31:56 | if your body is truly desperate, will actually release reticulocytes out into the |
|
| 32:01 | , which hasn't completed the whole maturation , they can still carry oxygen, |
|
| 32:05 | they're not as efficient as the full blood cell, full erythrocyte. And |
|
| 32:11 | there are ways that you can look say, oh, you're going through |
|
| 32:15 | erythro erythropoiesis because your reticulocyte count is high, you know, anyway, |
|
| 32:21 | that's, that's what, what all is basically saying is you're getting rid |
|
| 32:24 | all this material along the way. that you're basically creating a cell that |
|
| 32:30 | a bag of hemoglobin. So this what this is. Um So in |
|
| 32:35 | of the number of cells you you have about five times in the |
|
| 32:37 | uh cells per mil of blood. if you want to figure out how |
|
| 32:41 | you actually have, you can just , OK, a men are around |
|
| 32:45 | liters, women are around 4.5 That's again based on average height, |
|
| 32:49 | going to be different. If you're tall woman, you're going to have |
|
| 32:52 | red blood cells and if you're a woman, but same thing with men |
|
| 32:55 | so on and so forth. But you want to calculate it out, |
|
| 32:57 | use the number 55 liters. So five yeah, five liters. So |
|
| 33:02 | mills times that number gives you an of how many red blood cells you |
|
| 33:06 | . Still not the most numerous number cells in the body for anything. |
|
| 33:11 | right. Now, its primary purpose to transport oxygen and I have it |
|
| 33:16 | in parentheses, carbon dioxide as We'll see what that is a little |
|
| 33:20 | later when we talk about the respiratory . All right, you can see |
|
| 33:25 | how, when I say it's it's like a beret. You can |
|
| 33:28 | it's a biconcave disc. So it like we've taken a round cell and |
|
| 33:32 | flattened it in the middle, And what this does is, it |
|
| 33:37 | the inside of the cell near the , right? The more pancake like |
|
| 33:41 | have the less distance you have to if you're an oxygen molecule, right |
|
| 33:46 | leave or enter into the cell. this is one of the benefits that |
|
| 33:49 | does, it increases surface area through that diffusion can take place. |
|
| 33:55 | it's not any different in terms of area from our round cell because you |
|
| 34:00 | , a cell is a cell is cell. If it's round or |
|
| 34:03 | think again, think about a basketball completely deflate it. Have I changed |
|
| 34:07 | surface area of the basketball? but what I've done now is I've |
|
| 34:11 | a larger surface area to which contact take place. Right? So as |
|
| 34:16 | running along the sides, uh through blood vessel, I now have this |
|
| 34:20 | surface area where the exchange can occur it's running through. Um They tend |
|
| 34:27 | stack up. So you can see here, this is a capillary. |
|
| 34:30 | very capillaries are very small. They're about the size of a red blood |
|
| 34:34 | and you can see what they've done they've stacked up like a stack of |
|
| 34:38 | , like a bunch of Pringles. what they're doing is they're just rolling |
|
| 34:41 | in the capillary. And so that's they move. And because of their |
|
| 34:48 | their shape, you can bend they're very pliant. And so |
|
| 34:52 | as you can see here are small they like to twist and turn a |
|
| 34:55 | . And it allows for these cells bend and twist in these capillaries |
|
| 35:00 | as you're traveling along delivering oxygen. through the process erythropoiesis, we have |
|
| 35:11 | a cell that is a nucleus. right, it has no organelles. |
|
| 35:16 | replaced all of its cytosol with a or filled its cytosol with a whole |
|
| 35:20 | of hemoglobin. So I like to it a bag, a bag of |
|
| 35:24 | . Uh You have about 280 times to the six molecules of hemoglobin per |
|
| 35:29 | multiply that by five times 10 to nine cells times 5000 liters. And |
|
| 35:34 | still not the most abundant protein in body. It seems like it |
|
| 35:39 | All right, they do not generate TP via oxidative phosphorylation. They use |
|
| 35:47 | and this makes 100% sense if you about it. Do you guys like |
|
| 35:50 | ice cream? Yes. Well, an exception to the rule everywhere. |
|
| 35:58 | OK. They used to have a actually, this used to be their |
|
| 36:03 | . We, we eat what we and we sell the rest. Have |
|
| 36:07 | ever, have you ever seen a commercial? In fact, if you |
|
| 36:10 | to the Blue Bell Factory, I you to do. So. It's |
|
| 36:12 | there in Brenham. They have an cream shop associated with the factory. |
|
| 36:17 | can go in, it's a dollar scoop and they have flavors there that |
|
| 36:20 | do not put out to the general . But if you do the |
|
| 36:23 | one of the things they do is can go up there into the break |
|
| 36:26 | . They, you, you it's a glass room. And so |
|
| 36:29 | like animals at the zoo right in break room and they have freezers of |
|
| 36:35 | cream. And what they do is can take out an ice cream and |
|
| 36:37 | put their name on it and then set it into the employee ice |
|
| 36:41 | So they can have as much ice as they want whenever they want, |
|
| 36:44 | much or whenever. Right. they eat what they can, they |
|
| 36:48 | sell the rest. All right. , if that sounds like a dream |
|
| 36:52 | for you, I encourage you to into it because, mm, ice |
|
| 36:56 | . All right. It is But you know, who cares? |
|
| 37:04 | if, let's think, keep that mind. If I did oxidated |
|
| 37:09 | they make a TP, what would to all the oxygen I'm carrying. |
|
| 37:15 | would use it all, wouldn't and I'd make a whole bunch of |
|
| 37:16 | TP. I would burn through the thing that I'm trying to carry. |
|
| 37:21 | that was kind of the joke of commercials. It had like a new |
|
| 37:24 | and he'd drive up and he'd go the delivery spot and they open up |
|
| 37:27 | back and there was no ice cream there. He'd eaten it all on |
|
| 37:29 | way to the delivery space. I . So, that was what would |
|
| 37:33 | , what would happen. So they are capable of doing glycolysis. So |
|
| 37:39 | still have to make a TP. still things that the red blood cells |
|
| 37:41 | doing that are energy dependent, but will not use oxy phosphorylation. All |
|
| 37:48 | . Now, they survive in circulation about 100 and 20 days. All |
|
| 37:52 | . So about every four months you replacing, you know, a red |
|
| 37:57 | cell that was just newly made. , that's a roughly a rough |
|
| 38:03 | Now, here's a molecule that you've learned about a long time ago. |
|
| 38:07 | old hemoglobin. If you've seen the 1000 times. All right. It |
|
| 38:11 | a protein that has a pigment associated it. All right. This is |
|
| 38:16 | heme. All right. So there's parts to it. We have 1234 |
|
| 38:23 | of globin. All right. And associated with each other. And then |
|
| 38:27 | each of those globin, we have heme. It's the heme that binds |
|
| 38:31 | the oxygen, which type of globin present is gonna be depend upon which |
|
| 38:35 | of life you're in. And so , for example, you can see |
|
| 38:38 | here we have an alpha and the chain, I think uh uh |
|
| 38:42 | new or newly born, you newborns are like they have a gamma |
|
| 38:46 | a delta chain. I'm, I can't remember exactly but it's definitely |
|
| 38:49 | alpha and beta and they're actually able hold on to oxygen much more efficiently |
|
| 38:56 | that they don't run out of oxygen whatever reason. Right. But when |
|
| 39:02 | think about blood, most of the that you are inhaling in and entering |
|
| 39:08 | your bloodstream is going into the red cell. Some of it will dissolve |
|
| 39:14 | the fluid into the plasma and sit just kind of like carbon dioxide in |
|
| 39:18 | soda. All right. Except it be forming bubbles. That would be |
|
| 39:22 | , right? But you will have and carbon dioxide and nitrogen dissolved in |
|
| 39:29 | blood, dissolved in your tissues. when we're talking about carrying oxygen around |
|
| 39:33 | body, the most efficient way to it is to bind it up to |
|
| 39:35 | hemoglobin and then use the red blood which have all the hemoglobin carried |
|
| 39:40 | So, if you need oxygen, , here you go. There's a |
|
| 39:43 | of it for you right now. right. That's the idea. |
|
| 39:46 | So hemoglobin is not in the it's in the red blood cell, |
|
| 39:54 | ? Not in the plasma in the element. So, in the lungs |
|
| 40:02 | we're gonna, again, when we about um respiration, we're gonna go |
|
| 40:07 | a lot more detail about this. right. So when you're in the |
|
| 40:11 | , you have more oxygen, oxygen driven into the red blood cell driven |
|
| 40:16 | to hemoglobin. And what we form something called uh oxyhemoglobin. All |
|
| 40:21 | So it's binding up to the Iron has the affinity towards that. |
|
| 40:25 | then as you move to the there's less oxygen in the blood. |
|
| 40:28 | oxygen is uh driven off the off the iron. And so now |
|
| 40:35 | we do is refer to that as oxyhemoglobin. Amazing how those words |
|
| 40:40 | right? And then oxygen or hemoglobin can actually bind other gaseous molecules |
|
| 40:46 | they have special names for those as . Uh The one that we're most |
|
| 40:49 | in is the one that binds up carbon dioxide, carbon dioxide actually binds |
|
| 40:53 | to the globin chain, not up the heme. All right. And |
|
| 40:57 | it does, it causes a small in the shape of the molecule. |
|
| 41:01 | when we do that, we're going call it carb amina hemoglobin, we |
|
| 41:06 | want to call it carboxyhemoglobin. That's happens when you bind carbon monoxide to |
|
| 41:11 | . And that's going to bind to heme portion and carbon monoxide binds irreversibly |
|
| 41:17 | the heme. So oxygen is no available to bind or the oxygen binding |
|
| 41:22 | is no longer available. So you to get rid of that, destroy |
|
| 41:25 | molecule in order for that to Ok. But some other things, |
|
| 41:30 | are imported. We're gonna get that carbonic acid. This is gonna be |
|
| 41:33 | reaction we're gonna look at, it's of the most important reactions in the |
|
| 41:36 | . It just appears over and over over again shortly. So today we're |
|
| 41:40 | gonna talk about it but just know coming up um nitric oxide. So |
|
| 41:44 | gas and then there's some other ones always a fun on hydrogen sulfide. |
|
| 41:51 | like rotten eggs. All right. , I'm going to mention these now |
|
| 41:57 | they're going to become, again, important when we talk about ventilation. |
|
| 42:02 | these are other R BC molecule and proteins that are important. So, |
|
| 42:08 | dye or you might see in some , b phospho glycerine. All |
|
| 42:13 | What this does is it binds up hemoglobin and reduces its affinity towards |
|
| 42:19 | So, oxygen we're gonna see has a changing affinity based on how many |
|
| 42:25 | binds to the hemoglobin. One of ways that we can kick or reduce |
|
| 42:30 | affinity is when tissues release uh the or the 23 DPG and basically tell |
|
| 42:38 | red blood cells, hey, start the oxygen. And so it will |
|
| 42:43 | that affinity. And so oxygen floats and out and into the tissues. |
|
| 42:48 | protects against oxidative damage. Can't imagine the oxygen is coming from to cause |
|
| 42:54 | . But it's there one person got . Thank you. Uh Carbonic anhydrase |
|
| 43:00 | gonna play an important role in uh carbon dioxide into bicarbonate. And it's |
|
| 43:06 | bicarbonate that we're gonna actually transport carbon as um it's so it's, it |
|
| 43:11 | an important role in this reversible which will deal with. If you're |
|
| 43:16 | this inside the red blood cell, making bicarbonate in the red blood |
|
| 43:20 | you want to get rid of that . So you need an exchanger. |
|
| 43:23 | we have a chlorine or a chloride uh transporter. It's basically, it's |
|
| 43:30 | exchanger. And so this is what what, what is known as the |
|
| 43:34 | shift. And lastly, we want , this is a carbon dioxide channel |
|
| 43:40 | though it's an aquaporin with the family it's in. So what it |
|
| 43:43 | it allows carbon dioxide to come into red blood cells quickly so that we |
|
| 43:47 | then convert it into bicarbonate so that can then uh move carbon dioxide easier |
|
| 43:54 | this dissolved form. So take home here, erythrocytes, their primary |
|
| 44:03 | Uh what's the primary job of an oxy oxygen transport? OK. There |
|
| 44:09 | means by which we, that we this, OK. We bind to |
|
| 44:16 | and he specifically, OK. All , we're gonna deal with the |
|
| 44:21 | Later. The other formed elements are cells with the exception of one. |
|
| 44:28 | right. And so what we're talking here and this, this is an |
|
| 44:31 | part of the talk for me because was trained in a immunology lab. |
|
| 44:37 | didn't do immunology work. But excuse me, half the lab worked |
|
| 44:42 | immunocyte. So cells, the lymphoid and then, then my half of |
|
| 44:47 | lab worked on uh reproductive stuff. the cell that we've discovered happened to |
|
| 44:53 | an immunocyte that had this gene that worked on. All right. And |
|
| 44:57 | every seminar I ever had to go was an immune seminar. You |
|
| 45:02 | So, because it was departmental, go to your departmental seminars and stuff |
|
| 45:05 | that and I'm about to run through cells and if my boss heard me |
|
| 45:11 | way I was teaching this stuff to , he would disown me because it's |
|
| 45:15 | this is all you need to know end. All right. So first |
|
| 45:18 | , two groups of leukocytes, these the white blood cells, two |
|
| 45:22 | one are called the granulocytes. One's the A granulocytes. Why do you |
|
| 45:26 | them granulocytes? What do they have ? A granular sites are called a |
|
| 45:31 | sites because they don't good. All . Just making sure you guys understand |
|
| 45:36 | language. All right. The key about the granular sites, two things |
|
| 45:41 | distinguish them is one of the presence the Granules. Number two are these |
|
| 45:46 | looking nuclei, what we call multilobed . It looks like someone took AAA |
|
| 45:52 | animal and deflated portions of it. . You can kind of see examples |
|
| 45:58 | the cartoons, but we're gonna see in more real life. But look |
|
| 46:00 | that. I mean, they they're awful looking. All right. |
|
| 46:03 | , the three types of granular sites the neutrophils, asins and the |
|
| 46:07 | They are named based upon the stain stains them. That's where they got |
|
| 46:13 | name. OK. So have you taken a class where you looked at |
|
| 46:19 | ? Right? And one of the common stains on a slide is what |
|
| 46:22 | call H and E, have you of that? H and E staining |
|
| 46:27 | person on that anyone else? H and E is hematoxylin and |
|
| 46:34 | All right. So Eoin, we're see here is a stain that stains |
|
| 46:39 | that are acidic. All right. , these hang out in the blood |
|
| 46:45 | very, very short periods of So they're called on and they don't |
|
| 46:49 | a lot of time in the The other two types are the A |
|
| 46:53 | . And so these have these single , they don't have any Granules. |
|
| 46:57 | they don't have these weird looking They're really easy to identify. These |
|
| 47:00 | the monocytes and lymphocytes. And these things are distinguishable from each other because |
|
| 47:04 | matters. All right, really obvious see them. So I am not |
|
| 47:09 | make you identify them. I'm gonna or less ask you, what do |
|
| 47:11 | do? All right. For my MP class, they have to identify |
|
| 47:15 | bad boys. All right. But not the hardest thing, but you |
|
| 47:19 | have to learn if you're, when, when you're so again, |
|
| 47:23 | school, dental school. All All right. You will do a |
|
| 47:27 | through the histology course. You will a histology course. You will have |
|
| 47:30 | learn what tissues look like under the . And some of these things you're |
|
| 47:34 | like, I have no idea. look all the same to me. |
|
| 47:37 | right. This is one of those where you do a blood smear and |
|
| 47:39 | like, ok, what cells do have here? And that's what you're |
|
| 47:42 | at up here is a blood All right. So the most common |
|
| 47:46 | of granular site is the neutrophil. right, makes up about 50 to |
|
| 47:50 | of all the leukocytes that are in in blood at any given moment, |
|
| 47:54 | lobe nuclei. So you can see multi lobe nuclei, their Granules are |
|
| 47:59 | small. So that's one of the features from them when you're looking at |
|
| 48:04 | . Um the nucleus is referred to a poly morpho nucleus. That's the |
|
| 48:11 | word for just saying funky looking poly morpho different shaped nuclei. All |
|
| 48:18 | And so sometimes you'll hear pngs polymorph PM PM NGS. Those are polymorphonuclear |
|
| 48:25 | . So that's the neutrophil. All . Now, this is an easy |
|
| 48:29 | . Neutrophils are fag acidic. All . So that's the thing you circle |
|
| 48:34 | there. These are a fag acidic or fag acidic if you like like |
|
| 48:39 | pronounce it that way. All What does a peg acidic cell |
|
| 48:43 | It eats stuff. All right. that shouldn't be there, cellular |
|
| 48:48 | foreign substances. That is its primary . It is the first line of |
|
| 48:53 | against bacterial invasion. All right. Granules that you have primarily lysosomal perox |
|
| 49:02 | . So they're peroxidase. So their is to break things down and anything |
|
| 49:06 | could damage cells, we're gonna destroy stuff and, and reduce it. |
|
| 49:11 | , this is part of your inflammatory whenever you see inflammation, one of |
|
| 49:15 | first things that arrives is a Ok? You skin your knee, |
|
| 49:21 | will be there very, very All right, you want to go |
|
| 49:25 | something cool. Go to youtube type neutrophil attacks bacteria and it's basically a |
|
| 49:32 | and you get to watch a bacteria this and you get to watch a |
|
| 49:35 | chasing it around. They are hunters they kill things. It's awesome. |
|
| 49:40 | group eosinophils. All right, eosinophils stained by an acidic stain. All |
|
| 49:46 | . Again, you can see the is all funky. Their job is |
|
| 49:51 | lot more interesting. We don't have lot of ascent ils in western uh |
|
| 49:56 | . All right, because we don't have parasite problems here. Every now |
|
| 49:59 | then you'll have a kid who uh, you know, like, |
|
| 50:02 | , hook worms or something like But you don't really have the problems |
|
| 50:07 | parasites that you see in the third . And so in the third |
|
| 50:10 | you're gonna see high as in ail . These are cool. What they |
|
| 50:13 | is they come wandering up to a worm, some sort of parasite |
|
| 50:17 | , hey, how you doing? then it opens up and release a |
|
| 50:20 | bunch of chemicals that basically punch holes the worms and other fun things. |
|
| 50:24 | right, that's their job. They play a role in allergic reactions in |
|
| 50:28 | cases. All right. Not but, but sometimes, all |
|
| 50:33 | they also look for and uh fatties are called antibody antigen complexes. |
|
| 50:39 | an antigen is anything that your body as being foreign. And so one |
|
| 50:44 | the ways that we do this is have antibodies that can recognize very specific |
|
| 50:49 | and they create larger structures and it's larger structure that these cells are |
|
| 50:54 | They're like, oh, I see portion of the antibody, that part |
|
| 50:57 | the antibody is bound to the thing shouldn't be here. So me grabbing |
|
| 51:00 | portion of the antibody allows me to in the thing that shouldn't be here |
|
| 51:03 | I can destroy it. Third type the basil. Anyone here struggling with |
|
| 51:11 | right now, struggling with allergies. . You got the, the oak |
|
| 51:18 | and the ragweed and all the other stuff that's going along right now. |
|
| 51:22 | wake up every morning, you got ounces of mucus in your throat and |
|
| 51:25 | like, right, you walk out us all day and you're sniffling. |
|
| 51:30 | do you take to do that? do you, what do you |
|
| 51:32 | You take the antihistamine? All So the reason you're feeling all this |
|
| 51:37 | . Why, why you have this because these cells become very, very |
|
| 51:42 | in the presence of these foreign pollens stuff that are getting in your |
|
| 51:45 | And what they do is they release , which is an inflammatory and what |
|
| 51:50 | does, it opens up the blood so that blood goes into those areas |
|
| 51:54 | basically creates a pressure to trap that material. All right, you get |
|
| 52:00 | and you get the uh in inflammation because the blood might be leaking out |
|
| 52:05 | capillaries, you don't want it to up. So you also put an |
|
| 52:08 | in there. That's heparin. So is the uh is the inflammatory and |
|
| 52:14 | um uh Bazo Dilator, the Heparin the coagulant and when you get all |
|
| 52:19 | up and you don't feel comfortable, because of all that swelling. And |
|
| 52:23 | you take your antihistamines and it doesn't the signal, it just prevents it |
|
| 52:28 | happening. All right. In other , you're still releasing the histamine, |
|
| 52:31 | just not working and then it'll, ever notice you get that nasty rebound |
|
| 52:36 | . Yeah, that's the rebound is all those things are still there. |
|
| 52:40 | right now, um Their job allergic reactions, what we're doing is |
|
| 52:49 | trying to track uh or attract other blood cells, the neutrophils and other |
|
| 52:54 | into an area where infection might be place. So you're creating that inflammation |
|
| 52:58 | draw things, trap things and draw in the monocytes. You already know |
|
| 53:07 | another name. A monocyte is the form of the macrophage. All |
|
| 53:12 | So, basically, you've gone through mutation process or not mutation, but |
|
| 53:15 | differentiation process you're now creating a The macrophage now does a job just |
|
| 53:21 | the neutrophil does. It's more of surveillance molecule. It basically can sit |
|
| 53:25 | a tissue. So, for in your skin, you have Langerhans |
|
| 53:30 | , Langerhans cells are a type of . You have macrophages in the nervous |
|
| 53:35 | . Um They can be found moving tissue to tissue. This would be |
|
| 53:40 | a uh wandering macrophage. So if in a tissue and doesn't move |
|
| 53:45 | it's a resident macrophage. So they be kind of in all these different |
|
| 53:49 | . And what they're doing is they're surveilling. It's like the cop sitting |
|
| 53:52 | in his car waiting for you to speeding by, right? And that's |
|
| 53:57 | you can kind of think of your system as is literally, it's, |
|
| 54:00 | , it's police officers on patrol and they get active, they're gonna alert |
|
| 54:06 | else and kind of get things All right. So it's the macrophage |
|
| 54:11 | doing all this work. It basically also as an antigen presenting cell. |
|
| 54:15 | don't talk about immunology in this An antigen presenting cell is every cell |
|
| 54:19 | your body can present an antigen. this is a very specific type that |
|
| 54:23 | the immune system as part of the system. And what it does is |
|
| 54:27 | it consumes something, it takes all parts that it consumed, it basically |
|
| 54:31 | it up and then it says, , do you, do you immune |
|
| 54:34 | ? Do you recognize any of these ? Is there, is there anything |
|
| 54:36 | that we need to go after and the rest uh the adaptive system? |
|
| 54:41 | so, um when you guys were uh dealing with the COVID issue, |
|
| 54:48 | , what were we doing is we introducing with the new vaccines, we're |
|
| 54:52 | small pieces parts that would hopefully show inside cells and be presented as antigen |
|
| 54:57 | alert our adaptive systems. That that's the principle or high in that |
|
| 55:01 | of vaccine. Last little group are lymphocytes. These are the lymphoid |
|
| 55:10 | uh 20 to 40%. You can here in our picture, I wasn't |
|
| 55:14 | pointing things out here. So let just go back here. So basophil |
|
| 55:18 | the big blues, the uh the we already pointed out that would be |
|
| 55:22 | ascent ofhis monocytes are big. Notice nucleus is is rather large. And |
|
| 55:27 | when you look at the lymphocyte or cell is rather large, when you |
|
| 55:30 | at the lymphocyte, this the nucleus fairly large, cytoplasm, fairly small |
|
| 55:36 | not a lot of Granules. All . So anyway, these are the |
|
| 55:41 | when we think of immune defense, is what we um these are the |
|
| 55:44 | we think about for the most part cells are the cells that produce |
|
| 55:50 | So they sit in like your lymph and other lymphoid like tissues and they're |
|
| 55:55 | as things pass through. And when are presented to them, what they |
|
| 55:59 | is they differentiate into a different type cell called a plasma cell. And |
|
| 56:02 | plasma cell takes and starts producing antibodies the specific antigen that was presented to |
|
| 56:09 | . And so what you do is basically start up with very few of |
|
| 56:12 | particular type of antibody. And you that out where you make tons of |
|
| 56:15 | and they just start producing tons and and tons of that antibody. And |
|
| 56:20 | the antibody is able to bind up the antigen and then other immune cells |
|
| 56:23 | come along and remove the antibody antigen . The T cell is um and |
|
| 56:31 | cells are formed in the uh hence the name B cell, that's |
|
| 56:35 | they, that's where they originate. do T cells, but they, |
|
| 56:38 | B cell matures in the bone T . On the other hand, while |
|
| 56:42 | made in bones, they're transported to thymus and it's in the thymus that |
|
| 56:46 | go through a unique type of maturing . And what you end up |
|
| 56:50 | There's, there's about, I think the last count, I think there's |
|
| 56:53 | 20 different types of T cells. you're probably most familiar with the the |
|
| 56:57 | helper and the T side of toxic , the th or the TC, |
|
| 57:01 | what they do is they're in circulation they come across a foreign agent. |
|
| 57:06 | what they do is they bind that material, foreign agent and then |
|
| 57:11 | they serve as the Aler of the response. And so what they do |
|
| 57:16 | t helper cells activate T side of cells. T side of toxic cells |
|
| 57:20 | multiply create hundreds and hundreds of So it's basically like creating an army |
|
| 57:25 | the same type of, of, soldier to go specifically after that one |
|
| 57:30 | of antigen. And that's how they of work. All right now, |
|
| 57:36 | I said, there are more than two, but those are like the |
|
| 57:38 | big boys um when it comes to lymphoid light. So white blood |
|
| 57:46 | just what do they do? What's type, what do they do? |
|
| 57:49 | , what distinguishes it? What does do? I'm not gonna ask |
|
| 57:52 | here's a, here's a blood tell me what you're looking at because |
|
| 57:57 | would struggle 55 minute struggle. I'm gonna do that to you. So |
|
| 58:04 | CS one type of formed element. it a cell or? No? |
|
| 58:10 | , not a cell because it doesn't a nucleus incapable of multiplying has no |
|
| 58:14 | . It's a bag of hemoglobin, , survives surrounding 20 day white blood |
|
| 58:18 | . Are they cells? Yes, have nuclei. They are able of |
|
| 58:22 | , so on and so forth, we have this one, the |
|
| 58:25 | all right, we call them platelets other organism. You might see the |
|
| 58:29 | thrombocytes. People who work on platelets really, really upset when you call |
|
| 58:32 | thrombocytes. So, um, but giving you both names just so, |
|
| 58:35 | know that they're congruent terms. All . So what we do is we're |
|
| 58:39 | go through, um, and we're produce a cell called a megakaryocyte. |
|
| 58:46 | right. And the hormone that drives production of this is called thrombopoietin. |
|
| 58:52 | , what happens is, is you megakaryocyte and platelets are production of a |
|
| 58:59 | , it's really not a production but basically, you're tearing off portions |
|
| 59:02 | the mega cary simply by sheer So as blood goes by the mega |
|
| 59:08 | sends out an extension of itself and the force of the blood going by |
|
| 59:13 | that portion off and then you end with a little tiny cellular structure. |
|
| 59:17 | it's not truly a cell, it's a pinched off portion of the cell |
|
| 59:22 | contains a whole bunch of elements in and has a cell membrane. And |
|
| 59:28 | what causes that to happen is the of the thrombopoietin. All right. |
|
| 59:33 | first, thrombopoietin allows you to make mega carys. And the second thing |
|
| 59:38 | it does, it starts making it that little poochy dance so that you |
|
| 59:42 | tear off pieces of the platelets. , there's two types of Granules, |
|
| 59:49 | Granules. You may have heard of Willebrand factor. Have you heard of |
|
| 59:53 | ? No. All right, we'll to that a bit. We have |
|
| 59:56 | dense core Granules. So these are signaling molecules. These are probably, |
|
| 60:01 | are molecules that play a role in clots. That's probably the easiest way |
|
| 60:06 | think about that. The job that platelet plays is in hemostasis. They're |
|
| 60:11 | circulation for roughly about 10 days. compare and contrast red blood cells for |
|
| 60:18 | , these 10 days. So you're a lot of these all the time |
|
| 60:23 | breaking them down and replacing them over over and over again. Blood has |
|
| 60:32 | to it. Basically, it's the of sheer stress versus uh the sheer |
|
| 60:37 | . So in essence, it's, a thickness question. All right, |
|
| 60:41 | are different factors that can affect If I have more red blood |
|
| 60:47 | what's gonna happen? It increases it becomes thicker, right? There's |
|
| 60:53 | a lot of elbow room fibrinogen, is that plasma protein. If I |
|
| 60:58 | more of that, if I have little tiny molecules in my fluid, |
|
| 61:01 | get thicker, right. The radius a vessel matters. All right, |
|
| 61:09 | will decrease viscosity in small vessels. right. But as I get to |
|
| 61:16 | larger vessel, then I'm not gonna affect viscosity. It just flows, |
|
| 61:21 | just moves just fine. All But when I get those small |
|
| 61:25 | I don't have red blood cells that into each other. What are the |
|
| 61:28 | blood blood blood cells bumping into Yeah, they're, they just have |
|
| 61:34 | wall, they basically line up so just kind of move through. All |
|
| 61:40 | . If I increase uh linear I'm gonna increase viscosity. So that's |
|
| 61:43 | pressure flow thing. And then also increases viscosity. So, um I'm |
|
| 61:50 | sure why, but your book explains like, look colder temperatures, you'd |
|
| 61:55 | things to thicken up at the colder gets. But that's not what actually |
|
| 61:58 | . It's the opposite. It's the that does that. So this last |
|
| 62:02 | bit the last 20 minutes here and probably won't even be 20 minutes. |
|
| 62:05 | see how long it takes. We're deal with this question of hemostasis. |
|
| 62:10 | right. So, the easiest way think about hemostasis is that hemostasis is |
|
| 62:14 | body's way of making bandaids. All . It's to cl the flow of |
|
| 62:19 | from the body. Is your blood ? Yes. So we don't want |
|
| 62:23 | to leave the body. No, , that's right. All right. |
|
| 62:28 | we're resting the flow of blood. right, we call it making a |
|
| 62:33 | , right? There's prevention of So, any of these things are |
|
| 62:39 | and there's four basic steps to All right. First is gonna be |
|
| 62:44 | followed by an increase in tissue which you could probably say is, |
|
| 62:49 | associated with that. The next step be the formation of the platelet |
|
| 62:53 | followed by the formation of the Right. So there's, there's two |
|
| 62:58 | occurring at the end that basically occlude flow. Our starting point here is |
|
| 63:04 | vascular spasm. All right. What doing here. So you can see |
|
| 63:08 | , we've taken a knife and we're a blood vessel. All right. |
|
| 63:11 | you can see down here that the vessel has been torn. All |
|
| 63:15 | That's what we're trying to show Now, I want you to picture |
|
| 63:19 | the picture I don't think does a job because you're looking at it from |
|
| 63:21 | e but in essence, what you've is you've split the blood vessel like |
|
| 63:25 | , so where does the blood wanna up and out? Right? So |
|
| 63:29 | gonna happen is, is that we're see vasoconstriction on either side of the |
|
| 63:35 | ? All right. So I'm gonna this way. Do you see how |
|
| 63:37 | we can go through? Right. have a normal blood vessel. I've |
|
| 63:41 | it. So what's gonna happen is gonna get vasoconstriction. Can you |
|
| 63:45 | Can you see through my hands All right. So you can imagine |
|
| 63:49 | on the opposite side of that I'm actually occluding the flow of |
|
| 63:53 | Now, I may not be doing good job of occluding the flow of |
|
| 63:55 | , but I'm doing a better job not doing anything at all. So |
|
| 63:59 | the first step. All right. gonna slow the blood flow through that |
|
| 64:04 | . All right, by collapsing the , it just squeezes it closed. |
|
| 64:08 | then what that's also gonna do is it's going to start causing the chemicals |
|
| 64:16 | the surrounding area to start being to attract the platelets and to cause |
|
| 64:22 | clot to start being formed. So is the first step. It's basically |
|
| 64:26 | , hey, damages occurred here at point, come and arrive at this |
|
| 64:31 | and start addressing this issue. That's that second part is there. So |
|
| 64:40 | talked about the different types of pressures a vessel. One of those is |
|
| 64:43 | transmural pressure, right? Transmural Remember is the pressure difference between the |
|
| 64:49 | and the outside of the vessels across wall. All right. So when |
|
| 64:56 | have no flo fluid flowing in a vessel, that means the pressure inside |
|
| 65:00 | dropped. So what has happened to transmural pressure is increased? All |
|
| 65:07 | And so now that pressure is being on the outside, that greater |
|
| 65:11 | So it helps to occlude the flow blood. All right. Now, |
|
| 65:18 | you can't visualize that, think about you cut yourself, right? What |
|
| 65:22 | you do apply pressure guys when you yourself shaving, what do you |
|
| 65:30 | Press on it, get that little of toilet paper, press real |
|
| 65:33 | Maybe I'll stop. All right. the same thing. The transmural pressure |
|
| 65:38 | this simply through the simple laws of , right? I dropped the pressure |
|
| 65:43 | the inside of the blood vessel. basically an increase in transmural pressure. |
|
| 65:47 | reinforces the spasm. Next step, plug. All right, platelets are |
|
| 65:59 | to arrive at the site of They're attracted to it. All |
|
| 66:04 | Now, the reason they're attracted to is because the chemicals that are being |
|
| 66:07 | by the damaged tissue. All And they actually start sending a signal |
|
| 66:13 | . Now, I know you guys get out out all that much, |
|
| 66:15 | I'm gonna just give you a scenario and tell me if this sounds |
|
| 66:18 | All right, you find out, about high school. All right, |
|
| 66:22 | would be less common now. But about high school. You have a |
|
| 66:27 | whose parents have gone out of All right. And so that friend |
|
| 66:32 | you over and a couple of his friends or her friends over to come |
|
| 66:36 | out? Ok. So what have done is we've attracted in teenagers and |
|
| 66:43 | are teenagers gonna do? They're gonna on their phones and they're gonna start |
|
| 66:50 | all their friends. Hey, and so's parents are out of |
|
| 66:53 | Why don't you come hang out and those people are gonna start texting their |
|
| 66:59 | and those friends are gonna start texting friends and so on and so on |
|
| 67:02 | so on. Have you ever been a party like that? And what |
|
| 67:07 | the response? Get out more? right. Now, if you've paid |
|
| 67:15 | attention to movies over time, about five or seven years, a new |
|
| 67:19 | comes out about a block party type where a party of control movie, |
|
| 67:23 | is a standard fare to attract to it's an attractive proposition, parties can |
|
| 67:30 | out of control like that. Right . You can imagine that if a |
|
| 67:36 | like that got out of control, would cause great distress to the surrounding |
|
| 67:41 | . Would you agree? Yeah. there are not only chemicals that are |
|
| 67:47 | the platelets, there are also chemicals are preventing platelets from showing up. |
|
| 67:53 | . So there are three steps that part of these two things that we |
|
| 67:58 | described. All right. So platelets gonna show up and start aggregating. |
|
| 68:03 | right, and start adhering to the and then what they're gonna do is |
|
| 68:08 | become activated and they start activating other to come in. And so that's |
|
| 68:12 | you get that aggregation from. But the same time, the surrounding tissue |
|
| 68:16 | going to be the old man sitting door saying stay off my lawn if |
|
| 68:21 | have any neighbors like that. Stay, I'm, I'm I'm that |
|
| 68:24 | . Stay off my lawn. I don't care. But if you |
|
| 68:28 | a block party on my street, let you know, you better invite |
|
| 68:32 | . All right. So three adhesion. That's the first step. |
|
| 68:36 | platelets bind to themselves and bind to things now are platelets always in |
|
| 68:45 | What do you think? Yes or . Are they part of the formed |
|
| 68:50 | ? Yeah. So they're always in . OK. Something is happening to |
|
| 68:56 | them to bind to themselves and to things. Something must be different. |
|
| 69:03 | right, that's number one, you activation, the binding, the, |
|
| 69:08 | changes that are occurring in the platelets going to cause greater change inside that |
|
| 69:14 | so that they can then do their function of creating the clot. And |
|
| 69:18 | third is you're gonna start getting the . Those are the platelets sending out |
|
| 69:23 | signal saying, hey, platelet over , come check this out. We're |
|
| 69:27 | a party. OK. Those are steps. The reason they don't normally |
|
| 69:34 | is because the endothelium of the capillaries the blood vessels produce prostacyclin. All |
|
| 69:41 | . So this is trying to show what's going on. Look, the |
|
| 69:45 | are sitting there going look, I'm , but normally the tissue around here |
|
| 69:50 | releasing prostacyclin saying, stay away, off my lawn. All right. |
|
| 69:57 | something's changed what has changed in the . It's broken. You have endothelium |
|
| 70:05 | when you tear the endothelium underlying, is connective tissue, connective tissue is |
|
| 70:09 | made up of collagen and other large . When something is different, that |
|
| 70:16 | the thing that causes a platelet to activated. Now, to help you |
|
| 70:20 | this, think about this. Have ever gotten a bloody no nose or |
|
| 70:23 | like that and drip blood on the . Did that blood coagulate on the |
|
| 70:32 | ? Think about it for a I mean, usually you'll probably clean |
|
| 70:35 | up really quickly. But if you it sit there, does it |
|
| 70:43 | She's saying? Yes, Sammy. think? Yes, you wanna |
|
| 70:47 | Think. No. Yeah, you're . No. All right. Sounds |
|
| 70:53 | someone needs to go home and punch little brother and find out what happens |
|
| 70:57 | in the nose. Let a couple at the ground and apologize and then |
|
| 71:01 | clean them up. And what you'll is the blood drops if you leave |
|
| 71:07 | , be will coagulate independent of So what that tells you is everything |
|
| 71:15 | need to know about blood, that to form a clot, every anything |
|
| 71:19 | everything you need to form a clot already there in the blood. |
|
| 71:22 | That's number one, the thing that causing the blood to coagulate on the |
|
| 71:26 | like on a table or on a is the same thing that is causing |
|
| 71:31 | to coagulate inside a nose or in torn uh thing. It's a foreign |
|
| 71:38 | , something it's not seen before. the endothelium is something it's seeing and |
|
| 71:43 | sending a signal. Stay away, away, stay away. But when |
|
| 71:46 | tear away that endothelium, I now collagen, the collagen is what is |
|
| 71:52 | . And so the platelets bind up it and when the platelets bind up |
|
| 71:55 | it. That's when you're going to it. Now, the molecule that |
|
| 71:59 | a role, this is Von Willebrand . It is what it's gonna |
|
| 72:05 | I suppose, collagen, other act molecules as well. So now you're |
|
| 72:11 | activation. All right, calcium plays important role. So we're going to |
|
| 72:15 | releasing those, those molecules that I are signaling molecules. A TP ad |
|
| 72:19 | serotonin calcium. These are all signaling . What they're doing is they are |
|
| 72:25 | the nearby platelets and themselves. And what you're also doing is you're releasing |
|
| 72:30 | fibers that are reinforcing the activation process causing the clot to get bigger and |
|
| 72:36 | . And then the surrounding tissues are , no, no, no, |
|
| 72:40 | stay where you are. And that's the clot stays small is because the |
|
| 72:45 | tissues prevent them from happening. You're see changes that take place inside the |
|
| 72:51 | , they're gonna start squeezing themselves. right, they're gonna start making themselves |
|
| 72:55 | and what they're trying to do is trying to fill up that space. |
|
| 72:58 | it becomes a dam. Um You're , like I said here, um |
|
| 73:05 | changes in receptors and they're gonna seal brake. So they have actinomycin within |
|
| 73:09 | . And so they're gonna tighten themselves and flatten themselves out. And |
|
| 73:14 | what you're gonna do is you're gonna using a series of plasma proteins, |
|
| 73:18 | proteins that are part of what is the coagulation cascade now, here's the |
|
| 73:23 | out, right. If you look this, you're gonna see a bunch |
|
| 73:26 | Roman numerals. You see all those Roman numerals and like the 10, |
|
| 73:30 | seven, the five, the the 12, these are not named |
|
| 73:36 | the order in which they activate each , they're named in the order in |
|
| 73:41 | they were discovered. All right. the good news, we don't have |
|
| 73:46 | know the actual cascades. All what we need to know is |
|
| 73:52 | what's happening. And I'm going to out the important ones that you need |
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| 73:55 | know. All right, and what can see here is we have two |
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| 73:58 | top and we have one in the , right? So on the two |
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| 74:02 | , the two on top one is the intrinsic path pathway. One's called |
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| 74:05 | extrinsic pathway. And then they converge form what is called the common |
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| 74:11 | Now, why both of these I couldn't tell you. All |
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| 74:14 | But what this tells you is that is a process that says in the |
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| 74:19 | is everything we need to form the event. So it's all there. |
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| 74:24 | that's what the intrinsic pathway is. showing you these are the things that |
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| 74:28 | to be activated in order for us get coagulation independent of anything else, |
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| 74:33 | will just happen if we activate this process, the extrinsic on the |
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| 74:39 | hand, is a faster pathway and it does is it gets activated when |
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| 74:43 | tissue damage. And now the tissues are external to the blood are |
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| 74:47 | hey, damage has occurred. So you see the difference here in the |
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| 74:52 | that's inside the blood? I don't a signal other than the activation. |
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| 74:56 | like a a foreign surface, But an extrinsic pathway saying, |
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| 75:01 | hey, hey, hey, damage occurred right here. You need to |
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| 75:04 | this one's gonna be faster than the . All right. So intrinsic, |
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| 75:12 | right, injuries taking place on the , just a micro tear or something |
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| 75:16 | that. I don't need the tissue to say, hey, damage is |
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| 75:20 | place. What will happen is some of foreign surface will activate factor 12 |
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| 75:25 | then through a series of cascades, you'll do is you'll ultimately activate factor |
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| 75:31 | . All right. So the key here is the, the bottom is |
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| 75:35 | be factor 10. All right. takes a little bit of time for |
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| 75:40 | to happen. It takes somewhere between and six minutes. Are we friends |
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| 75:44 | this class? Can we talk about things? Yeah, we are. |
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| 75:50 | many you guys like to pick your ? You know, like you have |
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| 75:53 | little tiny scab and you pick at ? Yeah. OK. And then |
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| 75:56 | breaks, then what do you, do you have, you have the |
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| 75:58 | blood and what do you do with ? Do you do that? |
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| 76:04 | just, just us two, You do. No, no. |
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| 76:08 | . Yeah. Yeah, I'm looking here, you got that big old |
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| 76:13 | on your face, like, maybe. No, man, you're |
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| 76:16 | out on some fun. I it's like, yeah, you, |
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| 76:21 | blowing on the sc, see, know, you, you dig a |
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| 76:25 | bit deeper and all of a sudden like, yeah, you know, |
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| 76:26 | do do that, huh? You , I scraped my knuckle against the |
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| 76:30 | . I got the scab. Yeah. Oh, yeah. You |
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| 76:35 | the itch and then you scratch at . Yeah. Ok. Yeah. |
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| 76:38 | right. Now, notice what happens , right? And I'm, I'm |
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| 76:42 | that particular thing out is because you the little bubble of blood, |
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| 76:45 | The little little droplet of blood. what do you do is it takes |
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| 76:49 | 3 to 6 minutes for it to , right? So, this would |
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| 76:52 | an example of the intrinsic pathway. not like there's damage that's happened |
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| 76:57 | There's already just an open vessel and just like, oop, I'm just |
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| 77:00 | let the blood come out and it's take a little bit of time. |
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| 77:03 | extrinsic pathway. On the other is very, very quick. It |
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| 77:06 | incredibly quickly. All right. And what we're doing is we're, we're |
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| 77:11 | on some sort of tissue damage and it's the tissue itself that's sending out |
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| 77:15 | signal. It's saying, hey, has occurred here and that activates the |
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| 77:20 | . And again, it's gonna be these factors. Factor seven, ultimately |
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| 77:25 | factor 10. So notice each of have their own little pathway. One's |
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| 77:31 | , one sh uh ones uh uh and why we have two of |
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| 77:37 | they probably developed independently of each other the body just preserved them. |
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| 77:43 | what will happen is when you activate 10, there's a whole bunch of |
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| 77:45 | things. There's gonna be this common and these will stay, you'll keep |
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| 77:50 | pathways going until that clot is actually . All right. And what you're |
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| 77:56 | do is you're gonna create an you're basically gonna activate more and more |
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| 78:00 | . Now, the common pathway, are where you do need the |
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| 78:03 | Now, there are some plasma So each one of those t tho |
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| 78:07 | factors, right? Those uh TF , so on and so forth. |
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| 78:12 | they are uh or the factory 10 whatnot. They are plasma proteins, |
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| 78:17 | there already. And so all they're for is that signal to get the |
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| 78:22 | running reactivated. So there's a couple others, we have a uh a |
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| 78:26 | protein called prothrombin. And we already about uh fibrinogen being present. And |
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| 78:31 | these are just molecules that are but they're not active yet. What |
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| 78:34 | need to do is we need to them. And so the first thing |
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| 78:38 | gonna do is we're gonna take factor and we're gonna take prothrombin So this |
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| 78:43 | that platinum protein and that factor five we bring them together and now we |
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| 78:48 | the prothrombin activator and what it does it's going to take this activator. |
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| 78:53 | it's all this stuff together and it's take prothrombin and it's going to turn |
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| 78:57 | into thrombin. Now, I'm just tell you a hint. Now thrombin |
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| 79:01 | everything. All right. And then the prothrombin does is after it activates |
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| 79:07 | . Thrombin goes and says, here's that other plasma protein fibrinogen. |
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| 79:12 | I'm gonna convert it into its active fibrin. And then what fibrin is |
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| 79:16 | do is fibrin is then gonna be linked with other fibrin molecules and it's |
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| 79:20 | create this mesh work that basically holds platelets in place. And so it's |
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| 79:25 | helps establish the clot. Yeah, , there's so much more story here |
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| 79:32 | I already run out of time. was getting excited to tell you all |
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| 79:35 | this. We're gonna stop on this here. I'm, no, |
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| 79:39 | no, no. I wanna tell what the Raman does. I said |
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| 79:41 | does everything. And if we walk of here without knowing that, then |
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| 79:44 | gonna all fade from your brain and gonna have to start all over |
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| 79:47 | OK. So here's what it This is a protease. All |
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| 79:50 | it activates downstream factors. So what it activate? It converts fiber ingen |
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| 79:55 | fibrin? It also activates this last to help create that strong network. |
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| 80:01 | throm is key in forming the All right. What does thrombin do |
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| 80:06 | the top side? Well, on top side, it is the activator |
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| 80:10 | both of these systems, it activates . You kit thrombin, it activates |
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| 80:16 | activator. And so you make more more. So you get this massive |
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| 80:20 | , it activates the pathway through the pathway. It activates the pathway over |
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| 80:26 | , activating factor five to get our . It is a key key |
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| 80:34 | All right. So that molecule becomes , really important. The other thing |
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| 80:41 | it's gonna do is that it's activating . And what's it telling the platelets |
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| 80:45 | do? Keep sending out the social . And then what is it doing |
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| 80:51 | to the, in, in the cells? Tell those platelets to get |
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| 80:55 | my lawn? Do you see it's all sorts of things? This is |
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| 81:01 | it's the key factor. Now, over by a minute. I |
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| 81:05 | but I had to finish up with Raman. When we come back. |
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| 81:09 | talk about how we |
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