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BIOL 3324 Human Physiology - 3324_lecture14_1019
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00:02 it sounds like the sound of rock roll. Mhm. All right.
00:07 having a good week so far. bad for two days. Right?
00:11 , what we're gonna do is we're to finish up talking about the
00:14 We're going to jump into the It's a lot more fun when you're
00:19 to Halloween. So, this is starting point. This is where we
00:23 finishing up. And so, we're talking about how the heart pumps the
00:28 through the body, right? We're about flow. And so, we're
00:32 kind of focusing on a little, couple little less details here.
00:36 this picture right here basically shows you cardiac muscle looks like and what this
00:40 intending to show you is that the sides of the heart are not
00:45 right? You have the right side it that way, pretend like I
00:50 circling the right thing. So, rights of the heart, not a
00:53 of muscle there, right? The side of the heart, lots of
00:59 . Now, if you think about , this kind of makes sense because
01:01 rights of the heart is responsible for blood into which system pulmonary and the
01:07 side of the heart is responsible for blood into the systemic. And we
01:12 talked about yet. But you have five liters of blood. And
01:14 you can imagine in terms of if you look at your body or
01:18 my body as an example, how blood do you suppose out of those
01:21 liters are in my pulmonary system About . That sounds good. I like
01:27 , yep less. And then for systemic more a lot more. So
01:33 left side of the heart has to a lot harder than the right side
01:35 the heart, so that the two can work equally to keep blood constantly
01:40 . Right? So that's what we're at here, right? So pulmonary
01:45 is the right side. It has low resistance because there's not a lot
01:49 blood for it to push forward. know, it's not there's no there's
01:52 back pressure is really what we're trying say here. And so there's very
01:56 pressure to overcome. So it doesn't to generate a lot of force.
01:59 the opposite is true for the left . Now this I think is
02:02 right here, right. This shows the arrangement of the heart muscle.
02:07 right. And so if you look that, it has all these twists
02:10 turns to it. Okay. And part of the reason also why you
02:14 the Q. R. S. it kind of goes down and up
02:17 down again is because you're watching the action potential move through that cardiac muscle
02:23 this kind of roundabout way. But what this is trying to show you
02:27 he helped here in the green. gonna be the atrium down here in
02:30 red, those are the ventricles, ? And when the heart beats,
02:33 it does is muscles contract and they in such a way that they ring
02:38 heart kind of like all right. is the question that I almost impossible
02:42 get. No one positively saying I've done it. You wanna hear
02:45 milk a cow or a goat? one to people. All right.
02:50 when you milk a cow or a , you just sit there and yank
02:53 those teats. No, no. do you do you? Uh
02:56 Right. You you basically roll and not gonna be able to do it
02:59 I've never done it. I've just it. And so just like I
03:03 at a Holiday inn. I'm an in everything. Not right, but
03:08 kind of what you're doing. You're ringing and kind of basically forcing the
03:13 in a TT1234 down like that. that's what this is doing. Because
03:17 where we're trying to exit exiting out base and so when we ring we
03:22 down to the ventricles and the ventricles , they pushed up and out and
03:26 do it simultaneously and they're literally ringing blood out of the heart kind of
03:31 . Huh? Yeah, I think kind of cool. All right.
03:36 , next slide, just scratch to . You don't even know anything
03:40 Same thing with this one because it's same side of different pictures. All
03:43 . There was a time. I it was important. I don't think
03:46 so important. You wanna know the of it. We tell you that
03:49 atria ventricles beat up the exact same . Right? So two atria go
03:53 and then two ventricles go together. they're slightly off. That's what it
03:56 says. All right. I'm not to test you on it. Don't
03:59 to know. Skip over it down pictures and micro and molecular stuff.
04:08 . Alright. We already learned about muscle. Everything you need to know
04:11 cardiac muscle, but were afraid to is right here on the slide basically
04:15 the same way skeletal muscle. Some variations. Alright. The small variations
04:20 that the primary source calcium is external the cell. Not internal. All
04:26 . That's that's number one. And then in terms of everything
04:31 it more or less works. The here that we're going to point out
04:34 how do we regulate this? All . So, how do we how
04:38 we change the strength of the Now, obviously, we can point
04:43 the sympathetic and parasympathetic. But I to look at the molecular level and
04:47 basically boils down to that little protein was circling fossil lambent. Alright,
04:52 it is. Okay, pln here . Remember what circa is smooth into
04:57 , particularly calcium pumps. All So, there's circa Foster lambert is
05:02 negative regulator of circa. So, Foster lambert is active, which is
05:07 all the time then what we're doing we're slowing down the rate at which
05:11 pumps. Does that make sense? foster laminate is a break to
05:17 If you fast for late Foster Lam , you're putting the brakes on the
05:23 . That's confusing enough. So you're the inhibitor two wrongs don't make a
05:29 , well, I guess in this they do that, that makes
05:34 This stuff gets wonky when you get the molecular level time out for a
05:39 . He's no longer here. He's the chair, a little old
05:44 Uh, but we had a professor who um, I teach, if
05:48 don't know, I'm responsible for 43 41 03, that's the integration
05:52 If you're a biology major, you to take it to graduate, some
05:55 you might be taking it right but you never see me because ta
05:58 a class, we used to do , a faculty in the university so
06:04 we could chew up their papers and fun of them and stuff because that's
06:07 whole fun about reading papers is chewing other people's work and stuff, saying
06:12 things about them. So, so asked him for a paper said,
06:17 , I need this paper. So gave a paper for the students that
06:19 a fantastic paper. This was an of an inhibitor of an inhibitor that
06:24 a knockout. So it was like , negative, negative, negative.
06:28 basically turn it on, turn it , turn it on, turn it
06:31 again, I was like he comes me after the paper is like,
06:34 what students think of that paper I'm at it was the hardest thing.
06:37 didn't understand the damn paper. Oh , they loved it. It was
06:41 . They worked real hard. So sorry, I told you I'm
06:46 fun today. I'm not a good , probably screwing it up right
06:50 So Foster Landman inhibit circa phosphor relation it was Foster lambert. So basically
06:57 speeds up and slows down how much pumping calcium. If I'm removing calcium
07:02 , what happens to heart rate goes ? And if I leave calcium in
07:07 it's actually leaving calcium lau allows you maintain the length of that contraction for
07:13 . Right? Here's the other Troponin. All right now, when
07:19 talk about your opponent, we just of call it here's proponent, but
07:21 actually three parts to it. There's . I propose Troponin T. And
07:25 see, looking at the name should really clear where those I in antique
07:30 I. T. And C come . C binds calcium I is the
07:35 T binds what's the molecule that we're Troppo Myerson So that just kind of
07:42 you what the three parts are. right. So when this binds to
07:47 in troponin I helps to inhibit Right? But when I fast for
07:52 , what it does is it increases rate at which we're releasing calcium.
07:56 basically increases the heart rate. All . This is going to be downstream
08:00 the beta tron ergic stimulation. So downstream of sympathetic active. This is
08:08 part that gets people all kind of oh this is hard stuff and I
08:12 know, hard scary and stuff. what I want to talk about here
08:15 how do we affect stroke volume? right. So remember we talked about
08:18 output. Cardiac output is equal to two things heart rate and stroke
08:25 So how do we affect stroke In other words? How do we
08:28 the heart to pump more or Right. Because if we know how
08:32 speed up and slow down the Remember that sympathetic parasympathetic. So how
08:36 we adjust stroke volume in there are ways we can affect pre load we
08:41 affect after load or we can add tropics that alter contract phillipe. All
08:47 . And when we look at this have these big long giant walls of
08:50 . If you read the textbook, saw a big giant walls of text
08:53 this rule right here, the frank Law. And if you read that
08:57 you kind of freaked out for a , you were like I don't know
08:59 is complicated and scary and I don't to deal with it. I'm going
09:02 make your life easy. Are you for life? Easy frank Starling Law
09:06 real simple, It says the heart pump what the heart is given.
09:11 right, It's almost like the heart what the heart loves, Right?
09:15 really what it says is, if I send a certain volume of
09:19 to the heart, the heart will respond intrinsically respond to pump that same
09:25 out. So that's a stroke Okay, so if I increase sympathetic
09:32 , which means I increase how much returning back to the heart, then
09:36 heart is going to increase its stroke . Right? In other words,
09:40 we are adjusting when we increase the or the speed of venus return.
09:47 is the pre load. What's going the heart of the pre load,
09:50 that's going to increase the end diastolic . What is in diastolic volume?
09:54 terms of stroke volume, stroke volume the difference between the in diastolic volume
10:00 the systolic volume. Right? So I take in diastolic volume and I
10:06 it. What have I done the volume? I made a bigger
10:11 Remember go back to the to the the wingers diagram is what I'm looking
10:19 . I got Higgs bosons, things in my brain. Sorry, So
10:23 makes sense. Right? If I this then the difference between those two
10:27 got bigger. So the stroke volume bigger, Right? If I reduce
10:33 would happen, stroke volume got Does that make sense? So,
10:39 you remember that frank Starling basically says I give the heart the heart will
10:44 . Now, is there a limit that? Of course. All
10:48 But generally speaking, if I increase amount of flow back to the
10:53 the heart is gonna pump it. I decrease then the heart is going
10:56 decrease its in terms of its That's the easy one. Right?
11:01 simple. Next one after load. another simple one. Again, they
11:07 it nice and complicated for you kind go, oh no, there's so
11:10 big words and stuff. After Is what the heart is working
11:15 All right. So, you can about all that blood in the system
11:19 all that blood in the pulmonary So, systemic circulation or pulmonary
11:23 So when the heart pumps out it's , it's pushing all that blood in
11:28 of it to send it all the back to the other side of the
11:30 . So, that's the after That's the resistance. It's coming up
11:36 . Now, what deals are where do we find resistance from or where
11:39 we where do we get resistance We talked about a couple different
11:44 What are some of the factors? , again, viscosity. Okay,
11:50 viscosity is there but we're not gonna about it so much because it doesn't
11:52 on a regular basis. What's another diameter? All right. This is
11:58 one that we change regularly. So can imagine for example if our arteries
12:04 constricted systemically right? We're gonna come against less volume for all that fluid
12:12 . Right? That makes sense. gonna use volume twice. But remember
12:16 I'm referring to the fluid, the is the space inside the vessels.
12:20 I'm going to have greater resistance. means I have to overcome the
12:24 Right? So if you're standing here an example I'm gonna use him as
12:28 example If he's standing against me. I push up against them there's not
12:32 lot of you know there's not a of resistance. But if he starts
12:34 into me and I push harder to him over I'm gonna have to do
12:38 work. Would you agree? And in essence what the heart is trying
12:41 do with regard to after look if more resistance, the heart has to
12:46 harder to push that same amount of forward. Alright. The thing that
12:50 affecting here is in systolic volume. the first one was E.
12:55 V. The other ones E. . V. Right? So if
12:58 change SV if in other words I increased resistance I'm lowering SV so I'm
13:05 less stroke volume. So to keep same stroke volume. I have to
13:09 harder work to get that SV back to where it was initially so
13:14 Pretty simple. Yeah. Yes. . And we're going to see
13:21 It also does some other things that things up. That makes it
13:25 But it's not it's not horribly It's just like but you just said
13:29 and it's like it's a language So rate of flow versus flow are
13:34 different things and it's all right. are the 22 easy ones. The
13:39 one rumor said, things that affect illit e. All right. These
13:42 the Aina tropic agents. All So anna tropic agents are basically external
13:47 . The other two we just saw were internal to the heart. All
13:51 . So here we're talking about autonomic . Or we're talking about hormones and
13:57 anything that effects or alters contract Itty affects uh the stroke volume.
14:05 right. So, we can be positive or negative in terms of the
14:08 tropes. Now we're going to focus the positive ones because these are the
14:12 common ones. There are negative ones we don't really deal with them.
14:15 are more like drugs that are Whereas these are our typical with how
14:20 body works. All right. So Diana tropes or Aina tropes increased
14:26 If I increase calcium availability, that I'm increasing number of cross bridges
14:31 Which means I'm getting stronger contractions. right. So imagine ergic agonist.
14:35 sympathetic innovation for example. Right? see someone walking by? They're
14:41 Right? And you look at them what does your heart do? It
14:44 pitter pat. Right. Mhm. can feel it right. That would
14:51 an example of a positive china. . Alright, thyroid hormone. What
14:56 does. It increases the number of again ergic receptors available so that you
15:00 positive activity. There's other drugs and in your bodies. But basically what
15:05 does if you increase I'm a trophy increasing stroke volume. Because what you're
15:09 is you're dropping down the E. . V. It's working harder so
15:13 pushing more blood out per stroke. why sp goes up. That makes
15:20 . All right. So this little is kind of the helpful one.
15:23 just sits on every one of these highlighted informed. But if you if
15:27 get past all the very big language the textbook throws at you it becomes
15:33 little bit clear is like oh yeah more I deliver the more I'm allowed
15:37 uh push out. Oh if I'm up against resistance. Oh all
15:41 That means I have to work harder maintain the same stroke volumes. The
15:44 volume goes down when I have Right? If I increased contracted city
15:49 easy mode all I got when I'm contracted the that means I'm lowering the
15:53 . E. S. V. that stroke volume goes up. Not
15:58 . Huh? As scary as it . Not bad. You guys are
16:04 enthusiastic about this. You're gonna blood blood easier. What's blood?
16:12 is two things. It's plasma and cellular elements inside it. And remember
16:16 can always pause me and say time . Can you go back and explain
16:20 to me? That's all right. right. So, it is a
16:24 complex fluid. When you take you'll learn that is It is a
16:29 tissue. It's a weird connective All the connective tissues in your body
16:33 are are kind of hold things But this is one that doesn't The
16:38 is the connective tissue because of its source. All right. It comes
16:42 the Mezzanine and all connective tissue come as in kind. All right.
16:46 , we have the plasma which we the matrix. When you're talking about
16:50 tissues. The environment of the This is a weird matrix because the
16:55 matrix and the cells that are found the matrix are not responsible for the
16:59 . As in other connective tissues. , they just kind of reside
17:03 These are called the formed elements. we call them formed elements rather themselves
17:08 this is a time out. All . Because of all the formed
17:12 Only one class of them are actual . All the rest of them are
17:16 modified cells or parts of cells. right. But you'll hear the term
17:22 red blood cell and red blood cell sites or red blood cells are not
17:28 any longer. They've modified and they're longer functional cells. Okay, so
17:33 just want to make that distinction. when you hear it formed element is
17:36 term we use in colloquial terms. you sell? All right. Here's
17:42 fun little fact. So peripheral sites the red blood cells, lymphocytes?
17:45 blood cells will deal with them. . We don't refer to the platelets
17:50 thrown. Besides, I'm not exactly why. But if you talk to
17:54 who studies the rhombus sides, they really, really, really upset.
17:57 you refer to human thrombin sites as , they call them platelets. They
18:01 they're different. I'm just going to them. All right. So we
18:05 platelets, whatever. All right these things have massive. I put
18:12 in fluid. They'll sink to the of whatever it's in. But the
18:16 is in constant motions. That means formed elements are in constant motion.
18:19 they're equally distributed. Uh it's heterogeneous terms of where you're going to find
18:24 things in fluid. So, if go in and take a sample of
18:27 and put it on it on a and look at the number of cells
18:30 stuff. You can do a sample time and go back in 10 minutes
18:34 take another sample and you'll see it exactly the same. So we say
18:39 basically being well mixed. All Here's a fun little word. Here's
18:45 definition hematocrit, hematocrit refers to the site percentage in humans. It's about
18:52 to 45% of the total volume of . So, if you take 100
18:57 , you should expect to see between 45 mills of red blood cells.
19:01 right. That is what the metacritic . There's also something here called the
19:06 coat that sits right on top. , basically what you've done is you've
19:09 a blood sample, you put it a tube that has an anti coagulating
19:14 . You spin it down. The blood cells are heaviest. So they
19:17 down to the bottom. The next of cells, the white blood cells
19:19 the platelets basically sit in this Buffy and then all the fluid sits up
19:24 top. All right. The Buffy makes up about 1% of the
19:29 Now, here's the thing. If ever come across a tube full of
19:32 blood cells that have been spun you'll see the Buffy coat, but
19:35 not gonna be able to measure that . So, there are some textbooks
19:41 referring to the hematocrit as all of formed elements. But because the Buffy
19:47 is so small, it's almost negligible terms of that. But it always
19:53 to the percentage of Eritrea sites. what it's technically need. You look
19:57 any dictionary or talk to somebody. what they're going to be referring to
20:01 is red blood cell count Or All right. So Depending on our
20:08 in our sex there's going to be volumes. So like I said,
20:13 males are slightly higher because testosterone plays role in erythropoietin production. Females slightly
20:19 partly because of testosterone. All But as long as you're in this
20:24 , sort of you're in good So plasma those are formed elements
20:32 That's the other 55%. It's kind your book says pale white. Other
20:37 , pale white. It's kind of clear. All right. Not quite
20:41 yellow. Kind of like off like put like a drop of dying it
20:47 . Um so that's the other Its job because it's primarily made up
20:52 water is to absorb and distribute That's kind of Neat, right.
20:57 we have water in our bodies. up 90%. About 68% are plasma
21:03 . Then throwing your electrolytes. What your electrolytes? Thank you. sodium
21:09 , potassium electrolytes. Oh, I'm . I just flashed back to
21:17 No one's watching idiocracy. Put it the list. Who's who's keeping
21:21 You know, someone over here? you haven't seen idiocracy, it's on
21:25 list. You watch it tonight. go I think we're moving that
21:32 So electrolytes. It's brandi So that's name of it. I'm sorry.
21:37 dissolved gasses where they dissolved gasses. . Co two. What else?
21:43 . What else? I heard the one, nitrogen next year.
21:47 those all are in the blood. that makes up a percentage and then
21:50 other organics. Which means all the . We don't want to count
21:54 All right. So basically 90% 10%. Everything else. When you
21:58 the word serum, it's basically plasma the clotting factors like fiber engine.
22:04 right. There's other clotting factors, that's the big one. I love
22:07 picture here. Anyone know what this right here. If you look at
22:13 you see that right there, these all proteins. So what is
22:17 It's electrophoresis. But what type of Western. Thank you. Yes.
22:23 . If it's a northern, what it be? Aren't they? Southern
22:28 is DNA. So, we got . Southern Northern Actually I think two
22:33 them are named after people. One just because well, we already have
22:35 Western and southern or something like And it would just be nice if
22:39 was like an Eastern. I don't what you're doing that. But it
22:42 Yeah. Yeah. All right. if you've never seen a western,
22:47 is what it looks like. And it's showing you is it's showing you
22:50 density and that's what this bottom part showing you the density of that protein
22:56 the sample. And so you can here that the plasma proteins there's lots
23:01 different types of plasma proteins are broken into different groups. All right.
23:05 it's kind of showing up here at top. That's what these little dotted
23:08 are. All right. Now, don't have to memorize this. Please
23:11 memorize this. All right. I'm trying to show you what's in a
23:13 protein. As far as plasma the grand majority of plasma proteins are
23:19 . You ever heard of albumin? , if you haven't heard of alchemy
23:22 , your other part of homework while watching idiocracy is go get an egg
23:25 that egg and start playing with the stuff. All right. That's
23:30 Well, high percentage value. All . What's the characteristic of that?
23:35 stuff. Discuss What else is Is it sticky? It's kind of
23:43 . Right? So sticky things like bind the things. That's what albumin
23:47 is in the blood. It can as a non specific transporter. These
23:51 actually fairly small molecules albumin. Um they're small enough that there's there's plenty
23:58 them. And that's what this is of showing you. There's lots and
24:00 of them. All right, then have the globulin. That's what the
24:03 12 beta one beta two gamma represents the different families of globulin. And
24:08 are different types. Alpha globulin are for transporting fats metal ions, they
24:14 as regulators. Generally speaking, we the beta globulin. These also play
24:19 role in transporting things. Some of iron. Let's see if I can
24:23 it here. Here's one transparent is example right there. And then we
24:28 the gamma globulin which you guys some you have been studying or learning about
24:32 your papers. These are your So, here gamma globulin, that's
24:36 body. You can see here they listed here. Here's I G G
24:40 D and E I G A I M 12345. I've got them
24:45 Okay. Right. Just gotta look MaJ M A. D.
24:51 Magic. All right. So, make up about 37%. And
24:56 we're not looking to ask which one of these do. They're just there's
25:00 of different types. And then as single molecule fiber engine Makes up about
25:06 . So, here's your fiber engine there. All right. That's what
25:10 trying to show you this little And then what fibrinogen does. We're
25:15 to see at the end of class plays a huge role in the process
25:18 homeostasis, which is blood clotting. right. So this is an agent
25:22 already in circulation of the plants and . And then there's lots of other
25:26 proteins in here that we're not even into consideration. So, we're really
25:30 we're talking about plants and proteins, talking about these groups of molecules
25:34 what do they do? Well, play multiple roles roles. The key
25:39 that you guys need to understand is they are important in maintaining osmotic
25:43 So, in the blood, in interstitial fluid? Right. So,
25:46 the interstitial fluid you have no plans proteins. Does that make sense?
25:51 would you find the plasma proteins in plasma? Right. That's why they
25:56 that name. If they were the fluid proteins would be called the interstitial
26:00 proteins. So, none in the fluid. We have them in the
26:04 . So, what that does is creates an osmotic gradient which draws water
26:09 the blood and holds water in the . All right. So, that's
26:12 one. Right. So, it to maintain blood volume and blood
26:16 which you can already see. We're of making the transition towards that.
26:21 when we talk about the kidneys were to talk about that even further.
26:25 right. The other thing is that a role in buffering the blood.
26:28 right. So, it alters ph keeps the ph in the range for
26:32 that it needs to be at. , that's one of the two major
26:36 that they play as a group. , individually they have important roles as
26:41 . But we're not looking at the molecules. I mean, we just
26:44 gamma globulin play a role in the system. They're your antibodies alphas and
26:50 . They help transport stuff. what we're gonna do is we're going
26:57 we're moving into what are the Where do they come from? And
27:01 are they? All right. And chart like this can be very,
27:04 confusing. And the good news is don't have to learn everything.
27:08 yeah. All right. And so I want to do is talk about
27:12 process of hematopoietic sis or hemodialysis. those two terms are correct. And
27:17 , this is a continual process of the cells that are found in the
27:22 . There's two distinct processes. Here have one that goes down the myeloid
27:26 , one that goes down the lymphoid . The myeloid line is red blood
27:29 , platelets, Granules, sites and sites. The lymphoid line produces the
27:35 . All right. And so, you look at this this right here
27:38 be your myeloid line. So, going this direction and here's all the
27:43 cells that we just referred to here the lymphoid line. Here's your T
27:47 and B cells. Okay. they all start off as a long
27:52 hematopoietic stem cell. All right. that means they're pluripotent. They can
27:56 anything. All we gotta do is them the right agent. And then
27:59 going to go down the line. this is kind of the stem cell
28:02 stem cells. And then you have short term stem cell which is basically
28:06 , okay, this one we're going keep back here? And we're gonna
28:09 them keep producing the ones that are to differentiate? And that's what the
28:13 term is. The one that differentiates under uh the the the really the
28:19 elements that are given to them. right. And so the colony forming
28:24 see these with those R C F C F U B F U C
28:27 U C F U. Those are specialized cells as they begin going down
28:33 specific track. So up here there's uh there's still potentially ation. They
28:38 go down a whole bunch of different . Like here I can go either
28:43 , I can become a mega carrier or I can become a red blood
28:47 . But the CFO is the colony unit, the one that has become
28:52 specific, they are all dependent upon elements. Now this can get
28:58 really daunting and I try not to difficult questions about this on an
29:03 All right. But I do want point some of these. So,
29:06 the three easy ones. CSF is stimulating factors. So whenever you see
29:11 colony stimulating factor. So the first is GM. So here it
29:16 right there. Gm is a granular monos site meaning I'm going to go
29:20 the pathway that leads to the bazaar the ascena fills and the neutrophils or
29:25 the montecito pathway. So it's basically agent that commits it down this
29:30 As opposed going down that line. guys know any snl Phil basil
29:35 neutral pilar kind of sort of people uh All right. We're going to
29:43 them a little bit later, but granular sites. All right there called
29:46 sites because they have Granules. You look at them, stain them
29:52 a microscope or you stay in there look at them under a microscope.
29:54 can see these big giant dots in . All right there. Named for
29:59 stain that stains them. So cinephiles stained by. Yes. In All
30:09 . I mean, you guys have or seen stain cells like HD human
30:13 esan No, I don't know this yet. Yes. See this is
30:17 danger. We learn more but leave and more out. So you guys
30:21 need to get your hands dirty in lab and go and experience what it's
30:26 to walk home with die on your that don't go away for months.
30:32 awesome. Yeah, it's going to . All right. So that's granule
30:38 site. Monos It it basically takes down this track. Track. The
30:42 site is going to take them down granular sidetrack. Okay? And then
30:47 Montecito track takes things down the Montecito down over here. All right.
30:52 , you can see they're showing you agents that are going to help push
30:57 in particular directions. Interleukin Three and five R two cytokines. Again that
31:02 responsible for specific movements. So like three results in the production of basic
31:08 . So if I'm moving down this , I need I'll three to get
31:12 mature because of Phil Interleukin five in to get an idea of sinful.
31:16 have to have interleukin five. All . So, the key thing in
31:21 in understanding this is just saying if don't have the right signal, I
31:26 produce the right type of cell or need a specific signal to get the
31:30 that I want is really what I'm to get at these two. We're
31:35 to look at a little bit more . All right. So, thrombin
31:38 in T. P. O. a hormone that regulates Trumbull Police.
31:43 it makes it does two different It makes mega Correa sites so you
31:48 see up there here's my mega Correa . That's the big cell. And
31:52 the mega curious sight when throwing a around, it acts on its produce
31:58 . So, there's a little tiny . I'm gonna leave it at
32:01 We're going to come back to it little bit later. I think the
32:04 slide, yes. Is erythropoietin and isis erythropoietin. Is the hormone it
32:10 or stimulates red blood cell production or site production. All right. So
32:17 of this should be particularly heavy or things are named for what they
32:21 Right. Yes. My Mhm. . But but again, you still
32:31 that signal. Right? So, right now we're all producing red blood
32:35 . Right. Listen, this is to keep this one simple.
32:38 there's this kind of baseline production, production. All right. But let's
32:43 um I go to colorado to hang there for two weeks. Now we're
32:49 be oxygen deprived because less oxygen at elevation. Right? So our body
32:55 that oxygen deprivation. So, it uh it's what it really does.
32:59 measuring the oxygen carrying capacity of the and says, huh? In order
33:03 me to carry more oxygen to the or to the body, what I
33:07 is more red blood cells. And it kicks up the metropolitan production that
33:12 in the production of more. Yes. Now, the anna tropic
33:19 there that are specifically acting on the cells to cause the production of calcium
33:24 not production costs, but to increase activity that's going on. All
33:28 But it would be similar in that that sense where it's like there are
33:32 that are circulating in the body is this is what should happen. All
33:36 . We're going to look at your immunology lecture or in our lecture,
33:42 know, is like six minutes of . That's the entirety of our
33:47 And it's both embarrassing and frustrating that how much immunology I get to give
33:51 basically just look at cells go look of the immune system. Um But
33:55 going to point out some of those and I'm going to show you
33:58 okay, can you imagine this In US vs say in the 3rd
34:03 And so you can kind of picture are making changes here. All
34:07 So I'm just making sure I didn't them. So, here's our
34:10 metropolises, red blood cell production. all the things you don't need to
34:14 . You don't need to know all stuff until you get right down to
34:17 . Okay. And you can see is that? That's the hormone.
34:22 , basically starting off through this process basically getting all these different factors to
34:27 us into this into this direction. it's erythropoietin that allows us to differentiate
34:33 a premature Aretha recite. All So, it's called a pro rata
34:39 . All right, so that's the forming units. And so then once
34:43 get to the pro richard blast, cell is still multiplying and dividing.
34:47 as it's multiplying dividing, there's going be signals that are going to cause
34:51 to start changing its structure in Alright? So, it's not just
34:56 getting one cell and I'm just doing these things to one cell. There's
35:00 be a series of divisions. So an amplification and then along the amplification
35:05 . I'm making changes to all those . All right, So how do
35:10 where did this all happen? That's first thing. So primarily in red
35:15 marrow. All right now even you're development biology at Dr stander. You
35:21 if you ever get a chance. you did if you ever get a
35:23 to take development Biology please do. , it is one of the coolest
35:27 will ever take. And the reason it is because like if it's done
35:31 and I'm not saying doctor said he do it right or does do it
35:34 ? I have not taken a But what they do is like for
35:36 first couple classes. Like this is happens on day one. This is
35:39 happens on day two. Is that she did it? Yeah. This
35:42 what happens on day three. This what happens on day four and you
35:46 do this for like the first right. Which is both shocking and
35:52 at the same time. And you how you ever came into existence because
35:55 all the things that could possibly go and then after you get after the
35:58 trimester then it's like yeah, you , and this is what happens in
36:01 next week and this is what happens the next week. And it's kind
36:03 like that. All right. And I want to point out here is
36:07 in development we don't have any red marrow. All right. Your skeleton
36:11 even form until about week. I it's like week six or week
36:17 No. No. Yes. All . If I can't remember it's okay
36:19 you don't remember. So that's how works. Right? So what you
36:24 now is you're basically making red blood and the yolk sac. And then
36:27 is the premature liver and the premature ? So, that's basically the thing
36:31 making all your red blood cells and are going into circulation. And then
36:35 your skeleton forms. And then when born, most of your bones contain
36:39 bone marrow. So, it doesn't where you go. You know,
36:42 long bone and there's gonna be red marrow in it. All right.
36:45 then you hit puberty and then you growing and then your body says,
36:49 know what we don't need all that bone marrow. What we're gonna do
36:51 we're going to swap out that red marrow, we're gonna replace it with
36:56 . So just that's your future. more fat. Yeah. Sorry,
37:03 is fat but it's not it's called marrow. So basically the cells become
37:08 , isn't They can be replaced. can multiply but there are fat cells
37:11 of those cells that are stored up there. And so it's this red
37:14 marrow is now limited. So very specific areas and if you look at
37:19 these are not some very fun areas get to. So, you
37:21 your sternum that's your breastplate, right. And then you're looking at
37:25 heads of your long bones, primarily femur is where you're gonna find a
37:29 bone marrow. So, if you've seen someone who's given red, I
37:32 , you know, bone marrow donations up and shake their hand because they
37:36 through some really brutal surgery to dig some bones that are hard to get
37:41 . So, anyway, so, do we do this? I was
37:45 about oxygen carrying capacity. It's the that's measuring how much oxygen it's getting
37:51 right. It's basically sitting there am I getting enough oxygen, getting
37:54 oxygen? And if it feels like not getting enough oxygen, it is
37:58 one responsible for releasing erythropoietin. And worth repeating is the hormone that circulates
38:04 the blood. And then it goes the bone marrow where the red bone
38:07 is located and it tells the uh really the stem cells to,
38:15 we need to make more red blood . And so that's where that erythropoietin
38:18 in. That's where the rest of process goes. So, you can
38:21 there's multiple steps involved. All And so I'm just pointing out,
38:26 a commitment step. Lots of cell is taking place and this is when
38:30 start producing and accumulating hemoglobin. All . So, you can see up
38:35 this is what's going on. Is poly chromatic and base of Felix,
38:38 starting to accumulate more and more and hemoglobin. And then at a point
38:42 it's mostly hemoglobin were like, we don't have enough space for all
38:45 hemoglobin we want to make. So need to start getting rid of
38:48 And this is where we get rid the nuclei and other organelles. If
38:52 don't have a nucleus or yourself, , if you don't have organelles,
38:56 you really a cell? No. basically what you have, you become
39:00 bag of hemoglobin. All right now can enter into circulation and serve as
39:07 red blood cell as a ridiculous sight still go through the process of maturation
39:12 you can look at blood and if see a high kind of ridiculous
39:15 it's an indicator of high Aretha point activity. All right. So you'll
39:21 a particular sites in a normal blood , but you don't see a lot
39:23 them. But if you do see lot of them, then that's an
39:27 that you're producing a lot of red cells. So this is a red
39:32 cell. This is a section through . That superior view. It looks
39:35 a flattened beret. I guess if don't know the beret as well,
39:39 one of the ladies next to they'll tell you it's that time of
39:43 , isn't it? For Berets? . I'm looking around the room.
39:47 on, No 1's gonna admit it a day. There. You guys
39:51 it was boots and jean weather, you? They know what I'm talking
39:59 . They're not going to admit it the three days in Houston where you
40:03 to wear your boots, your genes your sweater. You know the one
40:05 you bought in the summer? That really, really cute. But you're
40:08 hoping it will be colder for a period, you know? All
40:12 How many red blood cells do we ? We got lots of them about
40:16 times 10 to the ninth. How is that? five billion cells per
40:23 . How many miles do we have average? I said five L.
40:29 take 5000 times that number. And talking to lots of cells.
40:34 So the job of a retro site carbon dioxide transport. That's as simple
40:40 you need to get it primarily But some carbon dioxide which we'll learn
40:44 a little bit later, structurally flat concave So there's the con cavity cavity
40:50 concave disk. And what this does has multi basic, multi purposes,
40:55 ? Large surface area. Alright, , it allows for an easy diffusion
41:00 oxygen across the membrane. I want to picture a completely spherical cell.
41:05 want you take an oxygen molecule and in the middle of that cell,
41:09 means that auction molecules equidistant to the . Right? So it's gonna take
41:14 long time to get to that But if I have a flat disk
41:17 I put that oxygen in the middle that cell. It doesn't take that
41:20 to get to the surface, There is a short distance as well
41:23 long distances. And so I can that short distance to get out of
41:26 cell very, very quickly. that's one reason. Second reason becomes
41:30 , very pliant. Alright, so is a capillary right here.
41:35 capillaries are obviously not very large. about the size of red blood
41:39 All right. And so what this is that these cells can bend and
41:44 and twist really, really easy in capillaries. All right. If you
41:49 vision this think about a basketball, the basketball. Can you bend a
41:55 ? No, it's really hard to in the basketball, but if you
41:57 all the air out of it, you be in the basketball?
42:00 it's been. So, that's the sort of thing around so hard to
42:03 . Flat, sell easy to So it moves very, very easily
42:06 these really, really tight quarters. right, sea surface area diffusion.
42:13 that kind of goes together. And they also like to stack up in
42:16 are called yellows. And so you see here were low basically they're playing
42:20 choo together. Just kind of moved as a group. Just repeating what
42:30 just said. There's a nuclear, no organelles, basically just a bunch
42:35 hemoglobin that's 97% of the content. not gonna ask you percentages back of
42:40 is good enough, right? And to give you a sense of what
42:43 translates into. There's about 280 million of hemoglobin per red blood cell times
42:50 times 10 to 9 red blood cells mill times five 1000 mills. Talking
42:56 lot of hemoglobin in your body. is still not the most numerous protein
43:02 your body collagen is the most numerous . So there's a lot of hemoglobin
43:07 still not the most. All right , Red blood cells use glide collis
43:14 to generate a teepee. They still activity that you're trying to maintain in
43:20 to say that they don't fall They fall apart after about 120
43:23 So you can think four months roughly a lifespan of a red blood
43:27 All right. But you don't want to consume that oxygen. You guys
43:32 living in texas a long time. guys know your Blue bell.
43:36 Blue bell ice cream is right. were willing to live And they used
43:40 have a commercial. We eat what can and we sell the rest.
43:44 ever see that? I mean, like their motto. Have you ever
43:48 to the bluebell factory is not that away. You go up there.
43:53 like a dollar a scoop. They you through and you get to see
43:55 they make it. And then you go and eat your ice cream.
43:59 encourage you to do so, it's good day trip and you can keep
44:04 back and buying more ice cream. of the tour is you go by
44:09 workers a break room and they have big giant wall of freezers that are
44:16 fronted. So you can see all ice cream in it. It's not
44:19 just fake and you'll see the workers there and they can just go grab
44:23 pint, put their name on it sit there and eat it and put
44:25 back and eat it whenever they want . So they live by that
44:28 We make what we can and we what we can. We sell the
44:32 Now imagine a red blood cell with same attitude. Imagine how much oxygen
44:38 get to your tissues. Very little ? So what they've done, red
44:43 cells have been modified so that they use oxygen to foster relations. They
44:48 use glide policies. They don't get get to their oxygen otherwise you'd be
44:54 . Okay. Does molecule looks Have you seen it every year as
45:01 biology student? Started freshman year talking the protein, uh, different levels
45:08 organization. Right, Okay. That's this picture comes from from a freshman
45:14 . All right, hemoglobin is a protein. You can see here is
45:18 pigment, right? That's him, ? It has four globe ins or
45:25 , so there's four chains, There's two alpha chains to beta
45:29 This is an adult in in uh . They use different global chains.
45:34 right. And its job is primarily bind up and carry oxygen. That's
45:40 all it does. But that's the function. All right. So,
45:45 of the oxygen in your body when goes after you breathe it in and
45:49 it from the lungs into the blood arrives and binds up to the
45:54 He seems one in each globe and . Alright. It's basically there's an
45:58 in there that the oxygen binds to it binds and it does so
46:03 And we're going to spend some time respiratory system talking about how and why
46:06 binds this stuff. Now, when binds up the oxygen, we refer
46:11 it as oxy hemoglobin. When the detaches it we call it de oxy
46:17 or the reduced form. All It can bind up to carbon dioxide
46:22 it does so, it's called carb hemoglobin. Which is to distinguish it
46:26 the car boxy hemoglobin when it binds to carbon monoxide. All right.
46:31 you can see you can bind up protons. It can bind up to
46:34 oxide which is visit dilator. It bind up to a whole bunch of
46:37 stuff. All right. But generally , we just focus in on the
46:42 and the carbon dioxide and sometimes the . Now there are some other molecules
46:49 red blood cells that are important, will become more important or more apparent
46:54 you when we look at the respiratory and what hemoglobin is doing there.
46:58 right. We have 23 D. . G. Or die foster obliterate
47:03 it does is it acts on the that says hey you know I know
47:06 attracted to oxygen but I'm gonna tell bad stories about her. So you
47:09 to break up reduce the affinity. didn't like that. I thought that
47:16 funny. Fine. Makes it more and easier to understand. Glutathione basically
47:26 the cell against oxidative damage. Got lot of oxygen there. You might
47:30 to protect against it. Carbonic and . This is an enzyme that allows
47:35 to convert carbon dioxide into bicarbonate. it's a multi step process. But
47:41 this is how we transport carbon dioxide the most part. And then what
47:46 can do is you can reverse bicarbonate return it back to carbon dioxide dependent
47:52 . You can do that actually without enzyme. But the enzyme speeds up
47:55 process. We also have a chlorine bicarbonate exchanger. And what this does
48:01 allows us to take the bicarbonate that making inside the red blood cell pump
48:05 out into the blood so that we make room to make more bicarbonate
48:09 This will make more sense when we at respiration and then we have aqua
48:14 in this particular aqua porn actually serves a carbon dioxide channel. All
48:20 So allows you to move carbon dioxide more quickly into the red blood cell
48:25 out of the red blood cell is , which will play a role in
48:28 apartment questions about chemical. Yeah, we go. Finally slowing me
48:35 I like that. They less. it has more to do with the
48:44 of that particular molecule product. So going to see oxygen is going to
48:49 human globe into buying more oxygen. ? And the presence of carbon dioxide
48:54 a greater loss or, you the release of oxygen. And so
48:58 kind of an additive effect if not . So, it's not so much
49:02 those agents. It's more of what what you're trying to transport oxygen or
49:06 dioxide at any given time. That's good question. But again, we'll
49:10 with that when we get to I think it makes more sense
49:14 Oh, The 6th Minute Immunology Cell . All right, we have Lucas
49:22 . So, the red blood we have one type. Right?
49:24 are three sites. We now have leukocyte, leukocyte or actual cells Eritrea
49:28 are bags of hemoglobin. Alright, we have two different groups of
49:34 We have the granular sites in the sites that tells you in the name
49:37 they have. One has Granules ones not, But there's also some other
49:41 features about the granule cites the granule that help you identify them. Good
49:45 . This is not a histology Not anatomy class. I'm not gonna
49:48 you pictures of these to identify. , this is more for knowledge
49:53 All right. So granule sites have lobed nuclei. A granule sites have
49:58 nuclear. You can see the multi here versus the big fat, single
50:03 looking nucleus. Alright. The granule . So the neutrophils using the fields
50:07 the bazaar fills again, telling you they have Granules that bind up to
50:12 specific dye. That's either basic, or neutral, basically binds both acidic
50:18 neutral. All right, granular sites not hang around for very long periods
50:23 time. They're around for about half day. The a granular sites on
50:27 other hand include the monas sites and . Alright, so many of you
50:31 have been learning about your lymphocytes for most part. Some of you might
50:34 been spending some time up here talking the Granules or the granule sites,
50:38 I'm guessing most of you guys did down here. The model sites.
50:42 you're not familiar, these are the forms of macrophages. Alright, so
50:47 are the big eaters. They just matured to that form Now. These
50:52 slides I stole from my Mp lecture it's fun to look at pictures.
50:56 , so, I'm just kind of these out. So number one are
50:59 neutrophils that we want to look at first granule aside. Alright. It
51:02 up a significant portion of your leukocyte . All right. You can see
51:07 at the nuclei. Do you see it's multi lobed? It looks really
51:11 and weird. Yeah. Alright. what you'd see. Can you see
51:15 red blood cells everywhere? Look at platelets. Yes, sir. Mast
51:21 are a type of Brazzaville and I that very very loosely because um I
51:30 know. I'll be I'll be real because I don't remember all my
51:34 I should but I dont Right. they have all the characteristics of a
51:38 Phil but I don't know if they the same origin. All right.
51:42 I just I don't I don't know origin. All right. So,
51:48 name often used for neutrophils are polymorphic Granules site. So, if you
51:52 that PNG that's what they're referring All right. They're fake acidic.
51:58 they act like macrophages. They basically along and they eat bacteria. First
52:04 of defense. We have lots of . Why? Because we live by
52:08 five second rule. Right. I don't we all I mean it's that's
52:19 going to kill us. And we bacteria living inside us and on us
52:22 around us and near us and So there you go. These play
52:25 important role in your inflammatory response. so what do the Granules have license
52:30 enzymes blow up bacteria peroxide Asus neutralizing and digesting enzymes to help them chew
52:36 stuff. Here's cinephiles. Very very portion looks like population. Their job
52:43 to recognize that in Vegas ties things up in this antigen antibody complex.
52:48 right. One of the fun things do is they attached parasites. When
52:52 talking parasites, I'm talking multicellular parasites worms fill area fun things like
52:58 What they do is they come up say, hey, how you
53:01 And then they release their uh enzymatic that basically punches holes in the sides
53:07 worms and kills off the worms. right. First world like the
53:11 S. We don't have a lot worms. Anyone here know what type
53:14 worms we have floating around the US the most part tapeworm. Yeah,
53:21 so much, but we have What else? Ringworm? Ringworm is
53:25 a fungus. Alright. Fungal All right. So we can throw
53:31 one out. But it's a good . Right. I mean, it's
53:33 of scary. It's like it's a warm. It's not you know,
53:37 one you guys heard of hookworms? huh. All right. Future
53:42 guess what you guys get to You're going to be looking to see
53:46 or not you got worms crawling out your kids. But if you always
53:48 them picking up their butts in the of the night. You want to
53:52 where these hookworms come from deep We like to play out in the
53:59 and if you have cuts and stuff the bottom of your feet, the
54:02 can get into the feet as well the larva and they basically go into
54:07 blood and then they work their way the intestinal system and they hang out
54:11 the large intestine, primarily in the area and then at night and I
54:16 know why they do this. The is that they come up for oxygen
54:19 they don't. But at night you go and inspect a child's rectum and
54:26 see these little things that look like queen. Oh by the way,
54:31 you never take a parasite class, is the best class after development.
54:35 get to find out all the horrible that are trying to kill you in
54:38 world. All right, it's If you ever want to come look
54:42 the book that I have in my , there's stuff in there that will
54:45 your skin curl and you'll be happy you live in the US.
54:49 Here's the thing that's the only major that we have in the US.
54:53 mean tapeworms exist and stuff but they're and far between the primary belt of
54:59 is between the tropic tropic of cancer tropic of capricorn. You know where
55:03 is the tropics? How's that basically belt Around the equator. Alright.
55:10 all the major countries that are found the equator throughout asia. All the
55:15 through africa through south America and wrap way around over and over again.
55:19 is the primary places where we're going find these types of parasites and there's
55:23 , horrible things like your calculus meghan . Oh, it's a nasty,
55:28 little bugger. You got the real worms and stuff like that.
55:31 flukes, all sorts of fun So, you can imagine when you
55:36 living in these parts of the Third countries, Second World. What
55:39 you expect in terms of your S count? It's going to be
55:45 Okay, that's what I'm trying to out here. All right. They
55:50 a small role in allergic reactions. fills all right there. Job store
55:55 . Synthesize the store appears to Alright. Store peppering histamine Aviso.
56:00 . Dilator inflammatory, right? That know this Because when you get all
56:06 and allergies, what do you And I could get stopped up.
56:11 just can't breathe. Everything is all because everything's enslaved. All right.
56:16 stung by a mosquito. Welcome to . Right, inflammation, localized
56:23 That's the histamine. Alright. The dilation allows you the blood vessels to
56:28 , pushes water into the area. creates a positive pressure where the invasion
56:33 taken place, whatever the invasion happens be. Alright, where whether it's
56:38 damage or whether you put a chemical what the mosquitoes infect or injecting in
56:44 . So that's the histamine is And of course the fluid comes from the
56:47 . So, what you want to , we want to make sure it
56:49 coagulate. So, if there's agents their coagulation, that's what the heparin
56:53 for. All right. So histamine attracts other white blood cells.
56:58 Leukocyte is the site of inflammation so you can deal with the issues.
57:02 right. You're gonna learn this when go off to medical school. But
57:05 every disease on the planet is a of inflammation of some sort. All
57:10 , inflammation is a sign of pathology really what it boils down to.
57:15 . And so when you see information your body fighting something that shouldn't be
57:20 . So, that's the easy All right. Plays a role in
57:24 reactions for those. You did the . You probably spend a lot of
57:27 talking about basic feels it's not Very, very small percentage of the
57:33 . Mon besides a little bit the largest of the leukocyte. You
57:37 see there's a big old plain old . I should go back and show
57:41 did you see the Granules, Granules different colors because of the different
57:49 of Granules they are. Alright. here we are. Here's uh here's
57:53 minus side. It's not actually a XL as a model site has to
57:58 mature becomes into the macrophage, macrophage be both residential or it could be
58:03 . So basically um the macrophages that residents or traveling are the ones that
58:09 doing the fact uh chewing things It can also serve as an energon
58:13 cell. Um Since we're not talking immunology, I'm not gonna go through
58:18 all that. Um So basically it alert your immune system to foreign
58:25 Lastly are the lymphocytes, they make another good portion. Most of them
58:29 not in circulation. They're kind of out in different structures. Kind of
58:33 what's going on so that they can do their job. So you can
58:37 of it as a immune defense. . They're basically your army or your
58:41 force in the body. And so you think about a police force because
58:45 easier to think about. We're more with that as a group. Police
58:48 be on the beat or police can out at the police station.
58:52 Or in some neighborhoods, bad you actually have a satellite station.
58:59 ? Have you ever seen those where like a corn the police corner store
59:03 thing? All right. So that's your immune system has basically have a
59:07 of these in circulation. But you have structures that are kind of doing
59:13 and kind of hanging out in tissues for bad things. All right.
59:17 B cells mature in the bone marrow the name be sell their job is
59:22 make antibodies. Alright. So their is to mark foreign substances for
59:28 So when they get stimulated, they and start pumping out tons and tons
59:34 antibiotics. These are plasma cells. they're differentiate T cells on the other
59:39 , they mature in the thymus. the name T. Sell. Their
59:42 is to recognize foreign or compromise So there were the ones that come
59:47 and actually see the uh the thing been marked and they're the ones that
59:54 the job of destroying. Now having that there are many different types of
60:00 cells which we're not going to go . I think I know of five
60:03 types. There's probably another dozen by . All right. And then there
60:07 other types of lymphocytes that are circulating blood. But these are the two
60:11 boys so far. So that was immunology I guess. It went longer
60:17 six minutes. Sorry. And we talk about technology in general. So
60:22 right. The rhombus sides again, whole cells. So here's your progenitor
60:26 . Make a mega carrier site from point. And basically uh All
60:29 So that's the blast. Here's the parasite under the influence of trump
60:33 But this is the other thing that . And does it actually causes the
60:37 start behaving funny. So you can this big old sell its name mega
60:41 site. And then thermal point basically start doing this kind of shimmy thing
60:46 it starts taking parts of its uh membranes and the side of plasma starts
60:51 it outward and then the sheer force blood going by breaks that off.
60:55 that's what you end up with a . So what's inside of platelet is
61:00 some organelles, some side of plasma side exotic elements, right, has
61:06 . So this is what it's trying show you. There's Granules of different
61:09 , there's the alpha Granules, dense Granules. They have different things and
61:13 of them are signaling molecules. Others activating molecules for the process of homeostasis
61:19 they stick around for about 10 days then they removed by macrophages in the
61:25 . So you've got a lot of but they don't hang around for a
61:28 period of time. So like about week. So retro sites how long
61:34 four months roughly? 120 days, days. So a little bit more
61:39 a week here we talked about blood . Yes ma'am. Yeah but what
61:50 doing is you're the mega parasites are enough that they're they're they're still fully
61:55 cells. And what they're doing is making the elements that they then extend
61:59 . So why do you need side solid elements or why do you need
62:02 of skeletons? So you can create . You need to have stuff where
62:05 can have the Granules. So you're have vesicles storing up all these different
62:10 of Granules and stuff. So, essence, of platelet is not a
62:14 , but it's a functional structure because it's actually been made and then the
62:20 you get rid of it is you extend outward and chop off the arm
62:24 Sudo pod, whatever. It's not a suit a pod. But
62:33 no, nothing. Not to the that you're thinking that I think you're
62:39 of in other words, it's not like a cell. I I suspect
62:43 there are metabolic activities to ensure that platelet can stick around for about 10
62:48 . But you can imagine if it such a short life, it's not
62:52 be a lot of metabolic activity. right. All right. So,
62:59 is that relationship between shear stress or force? That's basically the flow of
63:06 fluid and the shear rate, which the velocity gradient. That's really,
63:11 unhelpful. It's basically the thickness and well things move against one another.
63:16 right. So, these are the that affect viscosity. Fibra jin
63:20 Because we talked about viscosity, number of retro sites, vessel
63:26 The bigger the vessel, the less friction. So, you can have
63:31 viscosity, linear velocity, basically the at which things are flowing and temperature
63:36 you increase temperature that is going to viscosity. Um So, I don't
63:46 why I threw that in there. don't think I've ever asked any questions
63:48 disgusting. To be real honest, probably just a remnant. The last
63:53 bit here is homeostasis. I've got minutes to explain the process of how
63:58 blood clots. All right. Four processes. And also, if this
64:03 you out, you might be going the wrong profession. I'm just
64:07 okay, nothing wrong with that. are different types of, if you
64:12 , science, there's different ways you go. But the blood freak
64:15 It might be not the direction you to go. All right.
64:18 human stasis is the prevention of basically, it's your body's band
64:23 All right. So, uh what gonna do is we're gonna make a
64:27 . So, you can think about . I'm scab making there's four steps
64:31 first phase of construction, followed by increasing tissue pressure, followed by the
64:37 plug, followed by coagulation. you can see there's there's multiple steps
64:42 here. And what we're gonna is gonna kind of, walk through
64:46 The vascular spasm is probably the most thing that the body does when it
64:54 to, including blood flow. All . So, what I want you
64:58 imagine is taking a blood vessel and cutting it. All right.
65:04 here's my blood vessel. Here's the . It's been cut, blood is
65:08 escaping out of this. So, I look at it from the
65:11 this is what the blood vessel would like, Right? And I've cut
65:14 , like. So, so, the vascular spasm refers to is what's
65:20 over here on either side, the blood vessel closes, like so
65:24 include the flow of blood kind of . Huh? Now, obviously,
65:29 bigger the vessel, the harder it to do that. But a small
65:32 not too difficult to do. you're basically a including blood flow
65:36 Now, blood would have escaped. you're basically saying no, no,
65:40 . You can't go out. that's the vascular spasm. All
65:43 now, this is going to be by byproducts of the platelet plug
65:49 Other words? So, while this the first step is going to be
65:53 over and over again as the platelets in these areas. All right.
66:02 , that's opposing enough illegal services. right, increasing tissue pressure.
66:08 what you're gonna see is you're going see a decrease in transmittal pressure.
66:11 you remember what transmittal pressure is pressure inside of the tube relative to the
66:20 ? All right. So, if cut that, then what's going to
66:25 is is that let's say I say because basically, including blood flow,
66:31 there's less pressure on the outside, what it says. That doesn't make
66:38 to me right now. And I'm sure why it's not making sense.
66:44 have to think about it for a . So, I don't know why
66:47 not not getting it decreasing trends. pressure results in decrease in blood
66:54 Well, the transmitter pressure is going be the difference, and so,
66:57 I'm dropping the inside, I would that would be increasing the outside.
67:01 I'm not getting it off the So, I'm gonna apologize for
67:05 and just kind of just understand that an increase in tissue pressure. It
67:11 be, but I'm blanking right So, and And this is what
67:15 if you blank. I'm just gonna it worse if I try to
67:19 All right, getting to the platelet . This is where it actually gets
67:23 . There's three steps, and what talking about here is we're jamming in
67:27 platelets to ensure that blood no longer out of the cut. So,
67:33 though we've included the flow, um , I'm sorry, increased issue pressure
67:40 and get it. See, think a second. All right. Including
67:43 flow. The transmittal pressure is gonna greater to help reinforce the inclusion.
67:50 what it's trying to say, is there's a recognition of the damage.
67:53 so, the pressure outside becomes greater help press up against the blood vessels
67:58 prevent the flow from going through. what it's trying to get at third
68:02 here is now we've got the they're aggregating, and there's gonna be
68:06 steps. Adhesion activation. Aggregation, , But, in essence, what
68:10 saying here is that the blood the are looking for something that's different,
68:16 they've never seen inside the blood All right. In other words,
68:21 attracted to elements that are not normally inside a blood vessel. And they
68:29 that they bind to it. And like teenagers with their parents out of
68:35 , they have a house party. right. So, they're attracted.
68:42 like, cool, we're having a and then they invite all their
68:46 That makes sense. Okay, so is kind of where you can kind
68:51 see the adhesion portion. Alright, , what are they adhering to?
68:55 right. Normally you get no but And the reason for that is
69:01 you have the endothelial, basically producing element called prostate cyclone, which is
69:05 a solenoid that basically says, don't to me. This is the old
69:10 living next door that says stay off lawn, right? You don't go
69:15 in the neighbor's yard because they're gonna really, really pissed. So,
69:18 platelets hangout in the blood vessel all time in circulation. But if I
69:25 off part of the or if I through the capillary wall, I'm exposing
69:31 , I'm exposing other elements to those . And what the platelets are going
69:37 do is they're going to recognize that elements like college and should sit back
69:42 little bit. All right. And they start releasing things like Bond will
69:46 factor. This is that activation that going to see the next step.
69:50 . Those are these are the elements cause them to actually bind up to
69:55 collagen or bind up to fiber Nixon laminate these structural proteins that then
70:02 okay, here's different bind to And that's when you're going to get
70:09 . Now activation is basically releasing of dense Granules. So we've got signaling
70:13 . You guys recognize the signaling molecules 1880 p. Do you recognize them
70:18 being signaling molecules? We talked about a little bit earlier a lot earlier
70:24 a neurotransmitter serotonin. What? It's a signaling molecule, neurotransmitter,
70:31 , calcium signaling molecule. All And these are agents that are activators
70:37 other platelets. And so what we now, this is the activation.
70:41 basically each of those cells are now to produce elements. This is like
70:45 getting on tick tock you getting on . Sorry, facebook sucks. Um
70:51 facebook. Help me out here tweeting whatever anything to call every one
71:01 your friends that you've ever met and friends over to your house. That's
71:05 activation. You're sending out the signal get them to all show up and
71:11 they begin to aggregate. That's showing to the party. All right
71:16 you can imagine this will get bigger bigger and bigger and bigger. And
71:18 doesn't it just fill up the whole and just fill up the entire body
71:22 platelets that are activated because the surrounding helium is still releasing the process.
71:29 that say, stay off my And so you're limiting where the activation
71:36 occurring because the elements around them are them from from expanding beyond where the
71:42 of damage is actually taking place. , activated platelets are gonna start binding
71:48 two elements um that are in the already. Here's that molecule fibrinogen,
71:55 , vibrant region is an inactive molecule this point. All right, What
72:00 doing is basically, it kind of when it becomes active. It is
72:03 to serve as a as a network a mesh work and it's going to
72:05 bridges between the platelets. So, is like since we've all been here
72:09 Houston long enough and at least seen hurricane at least in our lives.
72:13 you ever sandbag to hurricane for Start stacking sandbags. And you're basically
72:18 mass between to prevent water from but it doesn't actually stop water
72:22 does it? You have to shoving in between. And so what the
72:26 is, is like the shoving in is basically wrapping up the cells or
72:30 platelets and preventing them from moving And you're creating a mesh work and
72:35 you have acted and admire stand inside platelets that basically start contracting and pulling
72:40 closer and closer together so that there no space in between the individual
72:44 So it actually is forming a plug basically the plug shrinks. And that's
72:49 you're actually getting the plugs. So the second step, right? First
72:56 faster, spasm, Second step, aggregation. Now we gotta get
73:05 I'm watching the time here. I seven minutes. But I have so
73:08 fun with this part. Guys ever scabs, have your picture. Scab
73:13 scabs is fun. Let's face We like picking scabs like little
73:18 You're like, we've all done I can see the disdain the people
73:25 at me like, no, I've never done that. You
73:28 You love it, picking scabs is . Alright, Now notice if I
73:34 blood and I drop it on a , right? If I have a
73:37 nose and it drops on the Is that blood going to collaborate on
73:40 tape? Yes, it will. . But it's there's no collagen on
73:46 table. There's no lamination. Why it coagulate? Because everything we need
73:53 get it to coagulate is already in blood. All right, The coagulation
73:59 is actually two different pathways, We have the intrinsic and we have
74:02 extrinsic pathway then come and meet at common pathway. All right?
74:07 when we look at coagulation, we're asking a question of where what's actually
74:13 this particular pathway. So the intrinsic is basically saying everything is already
74:20 So this is like when the blood in, this table is going to
74:23 because we already have all these elements that just need to be activated.
74:28 I need is some sort of foreign . That foreign surface is enough to
74:33 the coagulation cascade to get it down the common pathway. All right.
74:37 takes long to get that sort of . This is why we like to
74:41 up the scab and blow on right? You're like sitting there going
74:45 basically, you're just watching the intrinsic taking place. Air is not making
74:50 coagulate. It's just fun to blow the common cut, right? Everything
74:54 already there in the blood. That's that happen. The extrinsic pathway,
74:59 the other hand, is when there's damage. And so, what you're
75:01 doing is the tissue itself is actually Factors that cause the coagulation pathway to
75:10 . It's actually very, very Alright, so, this is damage
75:13 occurring outside the blood vessel itself. say, coagulation needs to occur.
75:18 , very short process, takes about seconds versus at 3-6 minutes. And
75:23 bypasses all these steps to get down that common pathway. Now, once
75:29 start, the pathway continues on until clot is actually formed. And which
75:34 you're using is dependent, of on what type of damage you're
75:38 All right? So, either the are telling the blood you need to
75:42 seal uh damage here or the bloods the blood we did. We need
75:47 seal the damage here. That's in what's going on, Right?
75:51 we have different pathways to respond to types of damage. What hemophilia?
76:04 . I don't know which one they're , but I'm gonna take a wild
76:07 . Do you know? Ah All right. So, it's
76:13 All right. So, let's take look. Fine. They're seven.
76:16 , there. All right. Part the extrinsic pathway. All right.
76:19 the thing that sucks about the coagulation . All the factors are named numerically
76:24 roman numerals. They're named in the in which they were discovered. Not
76:27 the order in which they activate each . All right. Yes. It's
76:32 you just kind of All right, . But we're going to focus in
76:36 the important one. We don't care the tens and fives and sevens and
76:39 and the ones in the Yeah. right. Number one in the common
76:44 . This is where we're going to . This is how it works.
76:48 are trying to form a pro thrombin . All right. So, here's
76:52 thurman. And what it has is it can take activated form factor 10
76:57 form factor five. Uh We're going take some calcium and put that all
77:02 . And that's gonna create an activator converts pro thrombin into thrombin. All
77:08 . So, this is our This is program And that's what we're
77:12 to produce what is thrombin thrombin is is multi fold. It basically takes
77:17 , which is already applied a protein in the blood and converts it into
77:21 fibrous fibers. Are the actual fibers can bind up and created a mesh
77:25 . And then what we have is and can also activate factor 13,
77:29 is a cross linker the fiber and that you can make a stable fiber
77:33 molecule. All right, you need little bit of calcium to get that
77:36 happen. So what does thrum and lots and lots of things. It
77:40 the central produce a central factor in of this. So thrombin thrombin thrombin
77:46 is the most important one you have do. So, what does it
77:50 ? It already exists as applied to protein in its inactive form. Gets
77:56 at the first five years. Factory in Acts 13 into
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