| 00:07 | Alright. 3rd Calibration. 3rd What were your thoughts? Good |
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| 00:17 | Bad paper. It was a decent . Okay. So I heard a |
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| 00:26 | for good paper. So tell me was good about it? What was |
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| 00:33 | about it was mediocre about it? to follow. Okay. Was it |
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| 00:44 | A. Maybe I heard. Real Confident in that one. All |
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| 00:59 | . Did it, was it easy understand? Did you understand what they |
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| 01:02 | trying to trying to tell you? they were did they follow the conventions |
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| 01:08 | the paper or of the instructions? . Did they demonstrate what their topic |
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| 01:14 | ? Very early on? Established in abstract. Established in the introduction. |
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| 01:21 | they prove it? You know what mean? To prove it? You're |
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| 01:28 | , I don't know. I mean guys seem real nervous about this, |
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| 01:33 | ? And again the point is is they making claims and then being able |
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| 01:40 | demonstrate that through their writing, presenting for that. So for example, |
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| 01:45 | I was trying to prove that the are gonna win the world Series, |
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| 01:50 | make that claim. I'd have to well let's look at their competition. |
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| 01:55 | example. Let's look at the A. Dodgers. I saw you |
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| 01:59 | your thumb down Children. Yeah. , he did. But no, |
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| 02:10 | say. All right. Let's take look at the record. The record |
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| 02:13 | the the Astros is 106 and something something. I don't know 60 |
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| 02:18 | So is that an indicator of astro . What do you think? Someone |
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| 02:25 | doesn't care about baseball? What do think? I don't know. |
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| 02:35 | fair enough. How about they completely their division series? How many losses |
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| 02:46 | they have? Well zero the playoff lost? San Diego? Dude Padres |
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| 02:56 | great Padres. Great Padres are We'll see. My point. Is |
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| 03:01 | that all we gotta do is we got appointed to see what you're doing |
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| 03:04 | now is he's actually he's creating argument ? And so I'm not creating strong |
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| 03:09 | one because I don't follow baseball, know, So I don't have strong |
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| 03:13 | for it. But the idea is are they making a case for their |
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| 03:18 | if they're making a claim? Is evidence there to prove their claim? |
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| 03:22 | what do you think we're talking about ? Yeah, that's not what we're |
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| 03:35 | about right now. We're talking about . What we're talking specifically about the |
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| 03:39 | . You guys just read All Remember this is not about grades were |
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| 03:44 | . So you went through, you through the first time. How was |
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| 03:47 | score the first time? Bad. ? I'm too harsh. Come |
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| 03:56 | Get real. I'm too harsh. harsh. Come over to your house |
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| 04:00 | beat you up and kick your Alright. So how do you think |
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| 04:04 | too harsh? What did you What did you think was good about |
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| 04:07 | paper? You thought it was? type of paper did you think it |
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| 04:10 | make your case? Like what? , keep going. Alright. You |
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| 04:27 | it? But then what was your the first time going through? Okay |
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| 04:34 | 20 not good because I mean you're not good and and other people are |
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| 04:38 | gonna be very very different. All . So I mean were you like |
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| 04:41 | , way off in your scores like the 20%ile? Was your score like |
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| 04:44 | of off in the 60th%ile or you the 80th%ile and that made you feel |
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| 04:49 | ? Okay, so so not entirely point with what I was saying. |
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| 04:55 | anyone here like her, anyone like Yeah 11 person is willing to admit |
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| 05:00 | to people 345. Okay. And when you went back the second |
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| 05:05 | what happened, did you did you to guess your way into what my |
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| 05:09 | were? Or did you kind of at it more with a with a |
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| 05:13 | eye and say am I looking for that are R. O. I |
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| 05:19 | know better or worse than what I in other words, Am I judging |
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| 05:24 | not because I feel bad for the or I want them to do well |
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| 05:27 | I judging it for what they presented that's really the hardest thing to do |
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| 05:32 | I mean I'm gonna just tell you my perspective when I read other, |
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| 05:35 | I read you guys works and stuff that, I'm rooting for you? |
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| 05:38 | right, When I get personal statement this is where I do most of |
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| 05:41 | reading, right? I get personal for all you guys playing school. |
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| 05:44 | like, come on, let this let this one be the good |
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| 05:48 | You know? So I said that this one be the good one. |
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| 05:50 | it's like because what we're trying to is we're trying to communicate clearly. |
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| 05:57 | that's the goal here. It's not the grade. And I know you |
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| 06:00 | are still stuck on, it's about grade. It's not about the |
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| 06:02 | Are they accomplishing what they're what they've out to do? And the rubric |
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| 06:07 | what they're set out to do. are you meeting those particular standards? |
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| 06:11 | , let's take a look. Let's what dr Wayne thought. Let's see |
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| 06:15 | he was harsh. Is that the ? Harsh? Alright, So, |
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| 06:20 | just gonna go down for the A four or three or three and |
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| 06:24 | three. So, did they meet standards? Yeah. Okay. Doesn't |
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| 06:30 | like I was harsh. Introduction. or 4 and four. Okay, |
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| 06:38 | 344333332 mm. In text citations. the text references are really excited using |
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| 06:48 | correct format as laid out in the . So, they screwed up something |
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| 06:53 | citations. Probably didn't use the proper . All right, general. So |
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| 07:00 | conforms to the instructions on formatting four , tables figures. I can't remember |
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| 07:04 | they had won game 333333 and So this was a three. It's |
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| 07:15 | functional good paper. It's appropriate. is what I expected junior to |
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| 07:20 | All right. So, it wasn't bad paper. I wasn't harsh. |
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| 07:23 | was a good paper. So score basically uh right. Right. Smack |
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| 07:28 | the mean, can't read my own , 77 points out of 110, |
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| 07:32 | think is why I say here, comes out to about 77.3. It's |
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| 07:37 | a bad paper. So, the isn't that It's that I'm I'm like |
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| 07:43 | things. I thought this was a paper was in a great paper, |
|
| 07:48 | ? Not everything can be the great , You know, the hardest thing |
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| 07:53 | science because you got a bunch of . That's what I'm gonna use. |
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| 08:01 | right. Everyone wants to prove, their bona fides. And so when |
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| 08:05 | right, they're gonna just slimy. critics mean evil nasty people who go |
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| 08:11 | to the ego and they stab And that's gonna happen to you |
|
| 08:16 | All right? You're gonna get five and you're gonna see one of your |
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| 08:20 | . It's gonna stand out as a thumb to the other four reviews that |
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| 08:23 | gonna get and you're gonna focus heavily that one review. And you're gonna |
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| 08:28 | ? Why did this person hate my ? They're jerks. All right. |
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| 08:34 | people just great harshly. All But don't worry about that. Look |
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| 08:37 | the other four. right? And am I meeting the standard? If |
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| 08:42 | meeting the standard, you're in good . All right. Not everything is |
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| 08:46 | be perfect. In fact, I I don't write perfect stuff, |
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| 08:51 | In fact, every time I write guys an email back, I promise |
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| 08:54 | I have to make at least six in that one sentence email. All |
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| 08:59 | . Because I got fat fingers and hit like three keys at the same |
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| 09:02 | . It's awful, right, tenses sorts of things. So, |
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| 09:09 | with this. So ultimately, did come back and hit a score that |
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| 09:12 | were happy with? I keep looking again real. But let's look at |
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| 09:16 | rest. You guys ultimately How many got it right the first time. |
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| 09:23 | 45. Okay, good. You guys calibrated you guys are |
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| 09:30 | right? Alright. And that's the you should be the rest of you |
|
| 09:33 | . You're gonna go in there, go in open minded for every |
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| 09:37 | Even the one that pisces you off first time. Take that step |
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| 09:41 | Go back into the second paper and , this is a new paper because |
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| 09:45 | promise you the first time you read bad paper, you're gonna be mad |
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| 09:48 | you're gonna want to take it out everybody else. You know, you're |
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| 09:51 | probably if you have a pet you're kick You're gonna kick the pet. |
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| 09:54 | right? But what we're trying to here is to make sure. So |
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| 10:00 | of you have emailed me and said a second. I don't understand why |
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| 10:02 | got these scores or blah blah Look, you guys are ultimately determine |
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| 10:06 | other's grades. But I get to whether or not you grade it |
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| 10:13 | right? That's what the calibration was us to make sure we're all on |
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| 10:16 | same page and now we know what what the same page looks like. |
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| 10:21 | , so when you guys grade each and there will be some of you |
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| 10:25 | here. Actually probably not in here you guys are actually showing up for |
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| 10:28 | of the people who don't show You're gonna look at the assignment. |
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| 10:30 | crap. I gotta do write my and you're gonna click on you're gonna |
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| 10:33 | here's my score. You're gonna just number and you're gonna go straight down |
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| 10:37 | list. All right. So if receive that that review, how would |
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| 10:41 | feel about that that make you happy ? Will that make you happy |
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| 10:46 | No. So that's gonna make you one. Number two. It's not |
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| 10:50 | be fair because you actually worked right? You read all five of |
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| 10:53 | reviews, five of those papers and like come on. Right. So |
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| 10:58 | job is to make sure everyone's doing reviews and I can do that because |
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| 11:02 | can simply look at all five reviews determine whether or not you're way off |
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| 11:05 | then I can look at all five your reviews and see how far off |
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| 11:08 | are and all the other reviews. so I get to adjust your grade |
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| 11:12 | , 95% of you, 98% of . Let's go 99% of you. |
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| 11:16 | do everything right if you grade the honestly and if you're and I'm looking |
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| 11:22 | you, Gabby, you know, if you grade the papers and you're |
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| 11:26 | easy grader relative to other people, you're consistently grading the same way and |
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| 11:30 | using the same sort of judgment. paper I can't subjectively say that you're |
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| 11:36 | right? Because your opinion, in opinion, we're not gonna come come |
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| 11:41 | an agreement mark. Are we going come to agreement which the better team |
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| 11:45 | okay? Yeah. Because you're never to accept the fact that the Astros |
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| 11:50 | have whooped the Dodgers. They would whipped the Dodgers would have would have |
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| 11:56 | I can say that because I'm in top of the front of the |
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| 11:59 | We would we would never know because not playing the game right? But |
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| 12:06 | can have differing opinions, right? we have to look at it using |
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| 12:10 | same lens. Alright. And it's fair for me to make an opinion |
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| 12:14 | I'm not a big baseball follower. Dodgers had a deeper bullpen but offense |
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| 12:22 | better for the Astros. Yeah. right. now having said all |
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| 12:30 | We have a paper due monday you done with the paper yet one person |
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| 12:40 | got a week of just sitting on butt. That's awesome, awesome. |
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| 12:45 | rest of you guys. Do you that? Just think you could be |
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| 12:48 | your butt doing nothing for a All you gotta do is get it |
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| 12:51 | , turn it in, turn it will actually tell you what your uh |
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| 12:56 | similarity score is. If you're not with that you can go and make |
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| 12:59 | , you can keep doing that. the last paper you turned in before |
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| 13:02 | actual deadline for the paper will be accepted. So whatever the last one |
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| 13:06 | , that's the one that counts. so if you want to start turning |
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| 13:09 | in right now And start affecting the scores you can think up to the |
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| 13:15 | three you have to wait 24 But first three our first three are |
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| 13:19 | . It's kind of like cocaine I . I don't know. It's trying |
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| 13:25 | come with some silly drug reference. So we got that going on. |
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| 13:31 | Anything else? You guys nervous? questions? I know you have a |
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| 13:36 | we'll get to. Yeah it Well so let's say you're an easy |
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| 13:46 | and you come across a paper that's crap and you give them an |
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| 13:49 | And everyone else because it says it's crap. What do you think is |
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| 13:52 | happen? I'll fix your score. that? Yeah. That's that's in |
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| 13:58 | what it is. It's basically saying now again there's some subjectivity to |
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| 14:02 | Right? So I know I've had graders in my class before and you'll |
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| 14:07 | like four scores that will all be together. This is this is gonna |
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| 14:09 | true. Everyone's gonna get if you all five of your reviews which my |
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| 14:14 | is you will if you turn into you have five reviews to do. |
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| 14:16 | you don't do those reviews just go and just start taking points off each |
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| 14:19 | the for each of the reviews that miss. All right? You can |
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| 14:23 | a zero on a paper even if turn on paper and if you don't |
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| 14:25 | your reviews. Okay. Those two are tied together. Some people don't |
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| 14:30 | that on this last assignment. I'm it clear right now. The two |
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| 14:34 | are attached to one another. If don't know the instructions, go back |
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| 14:38 | read them. Don't be like my who was ready to murder last night |
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| 14:41 | missing several assignments. I didn't read instructions Professor for God's sakes. Follow |
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| 14:49 | directions anyway. Sorry. Um So two things are tied together. All |
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| 14:59 | ? You will get four. I you'll get five reviews. If you |
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| 15:02 | get five you get four reviews. okay. That's just a function of |
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| 15:06 | algorithm and dividing this number of people the number of reviews. But what |
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| 15:11 | happen is you'll probably get if you all five reviews for the reviews will |
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| 15:15 | clustered, one will be an it may be an outlier on the |
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| 15:18 | end, it might be an outlier the front end but that's just very |
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| 15:22 | typical of what happens just which is we have five reviews and basically it's |
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| 15:27 | average of all five reviews will determine final grade on the paper and presuming |
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| 15:31 | did your reviews, that's gonna be grade for the paper. But if |
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| 15:35 | don't do your views and I'm gonna points off based on the number of |
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| 15:37 | you don't do. So now your was that yeah, average of the |
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| 15:44 | . Right and remember how many versions this paper do we have? |
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| 15:51 | So can you have a perfect The first go round. Right, |
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| 15:55 | want to see perfect scores. I be honest if it's a really good |
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| 15:59 | , say it's a really good paper I don't wanna see perfect scores because |
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| 16:03 | that person won't know know how to improvements for the 2nd 1. So |
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| 16:07 | know try to see where you can them make improvement. So calibration number |
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| 16:14 | is right in the middle good Not perfect. Okay. Okay. |
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| 16:27 | first I think it's like three or days. I found that if I |
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| 16:31 | you guys too much time, everyone to the last minute anyway so it's |
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| 16:35 | easier to get it up at the end and everyone just do it and |
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| 16:38 | you have plenty of time to do second one around and everyone knows how |
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| 16:41 | read all their individual reviews. You figure it out, you go to |
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| 16:44 | grade, click the grade and then can actually see you can cycle through |
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| 16:49 | . But again it's not it's not to cycle through them. Right? |
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| 16:52 | it a little tiny arrows? shows you bad design and what they |
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| 16:57 | with it, wow. All This where we left off. |
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| 17:13 | this is just an introduction of the slides. First slide when we talked |
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| 17:19 | that uh When we talk about the and the heart pumping, the heart |
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| 17:24 | a wave, right? It's a wave in the aorta. We have |
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| 17:29 | and diastolic pressure which systolic represent maximum . Very good. Alright. Over |
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| 17:37 | distance as you move away from both those values drop right as a |
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| 17:42 | of search within our resistance and eventually end up with a nice smooth um |
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| 17:50 | of blood. So the question is in order to get the blood back |
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| 17:55 | the heart right? Then the atria the right side has to be the |
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| 18:02 | point of pressure, right? Because gonna flow from an area of highest |
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| 18:06 | to the area's lowest pressure, So you have to imagine then that |
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| 18:12 | basically going high to low, my are not my lowest point alright, |
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| 18:17 | pressure inside my feet that are still blood forward but there's also other types |
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| 18:23 | pressures. So for example when the beats, what it's gonna do, |
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| 18:26 | gonna squeeze and then squeezing, it creates pressure on the atria right? |
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| 18:31 | creates back pressure onto the vena cava so on. And so you end |
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| 18:35 | with these other sorts of pressure Now first year I thought this actually |
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| 18:40 | to memorize this stuff. You need memorize these particular peaks and stuff like |
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| 18:43 | . But what this is just trying show you is what that pressure actually |
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| 18:47 | like in the jugular vein. And you can see it goes up and |
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| 18:51 | you can see the pressure dropping but goes up again and it kind of |
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| 18:55 | that and that's a function of the that the hardest creating as a function |
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| 18:59 | its own beating backwards. Alright so it's a back pressure. Alright? |
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| 19:08 | in doing that by increasing the pressure the jugular veins which is the vein |
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| 19:11 | gonna mp into the vena cava. that gonna do if I increase the |
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| 19:15 | there? What happens to the rate flow into the into the vena |
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| 19:22 | It increases, right? So what doing is I'm I'm basically starting over |
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| 19:27 | pressure that looks like this, A slope. It's pretty pretty shallow |
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| 19:32 | . And what I'm doing is doing . So that drives blood quicker back |
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| 19:38 | the atrium. Which is why the fills up so quickly, right? |
|
| 19:42 | it's like pushing and think of yourself a bathtub if I push the water |
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| 19:46 | from where I am, is that gonna come rushing back faster at |
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| 19:50 | Yeah. So that's what it's doing just a function of just the regular |
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| 19:57 | . We also have what is called respiratory pump. Alright. Not very |
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| 20:01 | . You see this being demonstrated while lying on your back and actually it's |
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| 20:05 | easier to see that when you're lying your back. All right. But |
|
| 20:08 | you're not familiar with the anatomy just that you understand there's a muscle that |
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| 20:11 | after thoracic cavity to the abdominal cavity the diaphragm, right? When you |
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| 20:16 | in, what you do is you're your thoracic cage. We're gonna talk |
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| 20:20 | about that in a couple of right? And that what you do |
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| 20:23 | you're expanding the thoracic cage so the goes outward and the diaphragm pushes downwards |
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| 20:29 | that the thoracic volume increases its volume what happens according to Boyle's law with |
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| 20:37 | decreases. Alright. So now what done is I've created a a tilt |
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| 20:43 | towards the abdomen from the abdominal cavity the thoracic cavity what you're doing is |
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| 20:48 | dropping the thoracic pressure. So you're increasing the slope. So blood flows |
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| 20:54 | the thoracic area as a function of just breathing in. It's actually sucking |
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| 21:00 | up towards the thoracic region. similarly if your diaphragm is being pushed |
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| 21:06 | into the abdomen, what's happening to pressure in the abdominal region? It's |
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| 21:12 | . So I'm tipping the thoracic region . But I'm tipping the abdominal region |
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| 21:19 | . So every time I breathe in creating abdominal pressure and decreasing thoracic |
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| 21:24 | So the flow of blood is being towards the thoracic region faster. And |
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| 21:29 | when I exhale I make my thoracic smaller diaphragm goes up. What happens |
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| 21:36 | the pressure in the abdomen? It what happens to the pressure in the |
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| 21:41 | cage and increases so it pushes the into the heart and then it pulls |
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| 21:46 | from the lower limbs up into the . So what have I done that |
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| 21:50 | created a bellows or a pump just a function of breathing, pull it |
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| 21:55 | the legs, move it to the , breathe in push it from the |
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| 21:59 | into the thoracic cage, breathe push from the thoracic cage pulled back |
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| 22:03 | from the lower limbs. So you what I'm doing is not just the |
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| 22:08 | doing all the work your muscles as function of breathing are doing the |
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| 22:14 | Alright that's what all that says? we have the skeletal muscle pump. |
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| 22:18 | you noticed that you can't sit still a chair. That's not because you |
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| 22:22 | a. D. D. Although might be able to associate some |
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| 22:26 | But you know that you wiggle a . You move around a lot |
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| 22:29 | You kind of feel that uncomfortableness in lower limbs. Alright. Well what |
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| 22:34 | doing is basically you're contracting muscles to blood. So most of your veins |
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| 22:40 | Which is how we're returning blood back the heart are found deep within skeletal |
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| 22:47 | . Alright. And if you can , all right. I I know |
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| 22:52 | going to talk about this in a of lectures when we talk about the |
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| 22:54 | vessels. So not this lecture, the next lecture uh within veins you |
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| 22:59 | these valves and it forces blood to in one direction. Alright. But |
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| 23:03 | for a moment you didn't have these . Alright. And so here you |
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| 23:06 | standing in this is showing you where heart is and this this this is |
|
| 23:10 | the vasculature volume, the venus volume the heart. And so just like |
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| 23:16 | any sort of cylinder, the pressure here at the bottom is going to |
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| 23:20 | much much greater than the pressure up at the top? Because that volume |
|
| 23:24 | fluid is pushing down and being pulled gravity. Right. And so fluid |
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| 23:28 | gonna have a tendency to pull in lowest point. But where does the |
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| 23:33 | want to go? Let's go up the heart. So remember the pressure |
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| 23:39 | this point in the venus system is very low. Right? Remember that |
|
| 23:44 | we we looked at where it showed here is the pressure over here in |
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| 23:47 | aorta and it was dropping down the and elastic arteries and it went down |
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| 23:50 | the resistance arteries and then it finally down to the capillaries where it's smoothed |
|
| 23:54 | . And then you're now over here the small veins and then you're into |
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| 23:57 | venous return and then finally you're back here in the atrium. You remember |
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| 24:01 | picture and it was just like kind a sigmoid curve. I'd have to |
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| 24:06 | flip him back there about 30 slides find it. So you can imagine |
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| 24:09 | slope down here on the venus return very, very low. It's like |
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| 24:14 | 15 millimeters down to like zero millimeters mercury. So that that return is |
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| 24:19 | , very slow. And with gravity on all that fluid, it just |
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| 24:23 | to stay down on the feet. . So part of that is arrested |
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| 24:28 | a function of the valve that breaks that that wall alright? Or breaks |
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| 24:33 | that column. But skeletal muscle does same thing. Skeletal muscle also breaks |
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| 24:40 | the column by squeezing in particular so that you end up with these |
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| 24:45 | columns or of blood in in you know, these regions. So |
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| 24:51 | just trying to say look between the and the calf. So you can |
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| 24:53 | in the space. So instead of a column, that is what do |
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| 24:56 | think? 4.5 ft? four It's called four ft. So instead |
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| 25:01 | a calming four ft tall, it's 8" tall. So the pressure at |
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| 25:06 | bottom here is much much smaller than pressure of the volume there. And |
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| 25:12 | of course you're resetting. So the here is almost nothing relative to the |
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| 25:18 | there. And then if I'm squeezing tube, that's one way. If |
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| 25:24 | squeeze here, what's the blood gonna to do? Think of a tube |
|
| 25:28 | toothpaste? All right. How many you have that horrible habit of screaming |
|
| 25:32 | from the middle. Alright. Just make sure when you have a |
|
| 25:37 | they do the same thing. All . Cause they're doing it from the |
|
| 25:40 | , they're gonna be really upset with . But if you squeeze in the |
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| 25:42 | where the toothpaste gonna go, something out, some goes back. But |
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| 25:48 | I put a valve in there where squeezing which way they're going to |
|
| 25:52 | Only the way that the valve allows . So, your skeletal muscles in |
|
| 25:57 | legs and in your limbs in general doing that. They are used as |
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| 26:02 | pump to push blood to create that to help drive it back to the |
|
| 26:08 | , to oppose the activity of gravity to return blood to where it needs |
|
| 26:12 | go, kind of cool. So not just a function of your heart |
|
| 26:17 | that gets the blood back to where goes. You have all these mechanisms |
|
| 26:21 | create these very, very short term gradients that help push blood back to |
|
| 26:27 | heart, even though they're not technically of the system. Okay, this |
|
| 26:38 | kind of cool. A lot of here. Alright, so your skill |
|
| 26:43 | your cardiac muscle, this is your . You can see we kind of |
|
| 26:46 | through it now. What I want show you here is that if you |
|
| 26:49 | a slice through the heart, you see that the two sides of the |
|
| 26:53 | are differ in terms of their thickness density. All right. So, |
|
| 26:59 | some real simple logic, if I a big thick muscle, is that |
|
| 27:02 | stronger or weaker than a thin Stronger. Okay, good. |
|
| 27:05 | we're all on the same page, kind of understand this concept. |
|
| 27:08 | you can see right here, we the left and the right. Look |
|
| 27:10 | the right, right over on this , right, has a thin |
|
| 27:14 | left, has a thick wall. right. And so we're looking primary |
|
| 27:18 | the ventricle. So why would this ? Well, the blood from the |
|
| 27:23 | side of the heart goes into which ? Left side? Oh yeah, |
|
| 27:28 | sorry, I should have said right . I'm on the wrong side. |
|
| 27:32 | she's right, I'm wrong. Blood the right hand side goes into which |
|
| 27:36 | , pulmonary and the left goes into . Alright, looking at me and |
|
| 27:42 | me as an example how big is pulmonary system from here to where |
|
| 27:48 | I like that right about there. and so my systemic is everything |
|
| 27:53 | Right? So you can imagine the of blood that's being moved into both |
|
| 27:58 | is the exact same. But I more blood in the systemic system that |
|
| 28:02 | have that is resisting the blood coming right? So my left side of |
|
| 28:08 | heart has to work a lot harder inject blood into the systemic system than |
|
| 28:12 | right side of the heart has to to eject that same volume of blood |
|
| 28:16 | the pulmonary system. And that muscle that it's like sitting there lifting weights |
|
| 28:22 | all you're doing is you're sitting there curls all day long with your right |
|
| 28:25 | side and that muscle is gonna be whereas your left hand side is gonna |
|
| 28:29 | a little weak thing. Alright that's going on there. There's a high |
|
| 28:33 | of resistance in the systemic side. that heart muscle has to work harder |
|
| 28:39 | get that same volume of blood The other thing that's really kind of |
|
| 28:43 | . So I told you um I it was thursday about my friend had |
|
| 28:47 | upside down BCG right? So his . C. G. Was a |
|
| 28:51 | P. And then the Q. up and then the r. Went |
|
| 28:56 | and then the s came back up then he had a normal t. |
|
| 29:00 | how did this happen? You I didn't even know he says because |
|
| 29:04 | development his heart muscle didn't arrange the way. This is what your heart |
|
| 29:10 | looks like. All right. And can see it has this kind of |
|
| 29:14 | orientation. The green represents the muscle the atria. The red represents the |
|
| 29:18 | around the ventricles. So when your beats, yes it is propelling blood |
|
| 29:22 | the atria to the ventricles and the outward. But it's doing it like |
|
| 29:26 | wring a towel, it's going so if you've ever milked a goat |
|
| 29:32 | a cow how do you squeeze the out of the teat? Do you |
|
| 29:37 | pull straight down? That's gonna really the goat or the cow? |
|
| 29:42 | What do you do? Right. basically push it out in a sequence |
|
| 29:52 | the spiral representation this muscle does the thing. It pushes it downward and |
|
| 29:58 | it pushes it upward in in that of way. So when that signal |
|
| 30:03 | down through the septum and up through muscles on the outside, what it's |
|
| 30:06 | is it's causing the muscle itself to of ring that blood downward and back |
|
| 30:12 | out through the ventricles out through the of the of the simulator valves. |
|
| 30:18 | now in his case his muscles are flopped in the ventricles. So they |
|
| 30:22 | arrange this way they arranged backwards. what does the E. C. |
|
| 30:26 | . Represent the electrical activity of the . And so when the CG reads |
|
| 30:32 | it's reading the muscles were going backwards of forwards and that's why you got |
|
| 30:37 | really weird funky QRS way for Which is kind of cool. So |
|
| 30:42 | was a developmental thing. All Don't need to know anything on this |
|
| 30:48 | . Basically. What the slide basically says is that the two sides work |
|
| 30:53 | . But if you look really really they're not actually 100% in sync. |
|
| 30:57 | I never asked any questions about Alright so this is the other thing |
|
| 31:02 | trying to show you is how it its contractions. So the right side |
|
| 31:06 | the heart when it's contracting is acting like a bellows. So squeezing back |
|
| 31:11 | forth like this. Whereas when you're at the right side of the ventricle |
|
| 31:16 | it's more like a tube where it's from all sides. Alright. And |
|
| 31:20 | even though it still has that ring because of the size of the muscle |
|
| 31:24 | how it's arranged. It has kind a different sort of appearance. That's |
|
| 31:29 | early what all this stuff is talking . Yeah I think it actually matches |
|
| 31:39 | . Yeah. All right skeletal muscle muscle. Are they different? Yes |
|
| 31:50 | have different names. They have their alright but how they work is very |
|
| 31:55 | similar. The the primary difference here we saw the action potential in the |
|
| 32:00 | I'll muscle is more like that plateau like a table, right? And |
|
| 32:04 | said in this particular case yes calcium involved in both. But what we |
|
| 32:08 | here is the action potential that's being . The function of that sodium and |
|
| 32:12 | potassium later. And the calcium coming . And the calcium that's coming in |
|
| 32:17 | acting on the troponin in the same that it wouldn't skeletal muscle. Pulling |
|
| 32:21 | triple my son out of the way allowing the contraction to take place. |
|
| 32:25 | right now we have some regulators. . And the way that we regulate |
|
| 32:29 | regulators threw phosphor relation. So if go back and look at the picture |
|
| 32:32 | the first one is gonna be fossil . Let's see if I can find |
|
| 32:35 | . There it is. It's trying show you. So here's circa what |
|
| 32:38 | circa sorry, smooth muscle or not smooth smooth into plaza in |
|
| 32:46 | Um calcium channel. So what we're is to get calcium out. We're |
|
| 32:50 | be pumping calcium using circle to get into the circle plasma particular. |
|
| 32:55 | so um our molecule fossil Lamborn is molecule that inhibits the activity of circuits |
|
| 33:02 | break on circa. So when you fossil lamin around it slows down the |
|
| 33:07 | at which circuit pumps. So that allow circuit of pumps calcium. It |
|
| 33:11 | calcium out in the cytoplasm. But we phosphor elated, what we're doing |
|
| 33:16 | we're hitting we're inhibiting the break so putting a brake on the break. |
|
| 33:19 | two negatives make a positive. So doesn't once you phosphor relate basically circuit |
|
| 33:24 | at a normal rate. The other is Troponin has three sub units. |
|
| 33:29 | talked about those three subunits briefly saying there are three subunits. One binds |
|
| 33:33 | calcium. Can you guess which The one with the C. |
|
| 33:36 | That's real hard. What do you that binds to troubled mind? |
|
| 33:41 | it's all not that hard. I was the one that's binding to |
|
| 33:46 | acting. All right. So when phosphor relate the trope trope excuse |
|
| 33:53 | The troponin C component. What that's do is it's going to increase the |
|
| 33:57 | at which we release calcium when we calcium were no longer being pulled away |
|
| 34:01 | said we're now in a position where covering and protecting the acting. So |
|
| 34:05 | that's going to increase the rate at we are returning back to rest. |
|
| 34:12 | So both of these allow us to more relaxed quicker. So when there |
|
| 34:18 | no phosphor relation, the return back rest is um is shorter. Are |
|
| 34:26 | is is longer it takes longer to back to rest when phosphor relation is |
|
| 34:30 | . We're increasing the rate at which remove calcium or make that acting binding |
|
| 34:36 | available. So we returned to rest lot quicker. All right. Oh |
|
| 34:45 | we go. Alright back to the cardiac output is equal to. |
|
| 34:52 | ma'am. We need to go Um Yeah. All right. |
|
| 35:02 | I think in terms of All take all regulators out of the |
|
| 35:05 | Alright, so to come back to . What are the two things that |
|
| 35:09 | going to do? We want to rid of calcium? Right. |
|
| 35:12 | So whenever we get a contraction to back into relaxation, remove calcium. |
|
| 35:17 | calcium, no contraction. Right. , if I want to stay in |
|
| 35:21 | contracted state longer, I want to calcium more available. Right? |
|
| 35:26 | by by having fossil lamb in their Landman block circa circa pumps calcium. |
|
| 35:34 | , when fossil Lamborn is present. works slower. That help when I |
|
| 35:40 | for late Foster lam binh, I inhibiting the activity of Foster lemon. |
|
| 35:47 | circle works faster or at its normal . So calcium leaves faster when we're |
|
| 35:53 | with Troponin, troponin basically releases calcium a at a specific rate. But |
|
| 35:59 | I lost four late troponin, what gonna do is it's gonna release calcium |
|
| 36:04 | . And so that's gonna allow me get rid of the calcium so that |
|
| 36:07 | go back to my original position of . Help. Okay, Alright, |
|
| 36:15 | cardiac output said it had a formula output is equal to and heart |
|
| 36:23 | stroke volume and heart rate. All . So, if I want to |
|
| 36:27 | cardiac output, I can affect stroke or I can affect heart rate. |
|
| 36:31 | gonna deal with stroke volume right Alright, how do I affect stroke |
|
| 36:35 | . Alright, so, there are basic ways I can do this. |
|
| 36:40 | can affect pre load. I can affect after load, or I can |
|
| 36:46 | chemicals apply themselves to the heart that going to alter its contract illit |
|
| 36:51 | All right, So, that's how going to look at this. We're |
|
| 36:53 | to pre load first after load and you're gonna go there's a lot of |
|
| 36:57 | in there, that things make All right. So, we're using |
|
| 37:01 | words than we need to understand and I'm gonna try to keep it |
|
| 37:05 | for you and I need to go right direction. Alright, so, |
|
| 37:09 | can see there's a lot of words . See up there frank Starling, |
|
| 37:12 | you read frank Starling, was it to you? Was there a lot |
|
| 37:15 | blah, blah, blah. another head say yes, Okay, |
|
| 37:19 | Starling is really, really simple And Starling were to cardiologist and they |
|
| 37:23 | looking at how the heart works. what they described as essentially this the |
|
| 37:28 | of blood you give to the heart the amount of blood that the heart |
|
| 37:30 | pump. That's pretty simple. So, if I increase the amount |
|
| 37:35 | blood coming to the heart, the pumps more blood. If I take |
|
| 37:40 | blood, you know, in other , I don't return as much blood |
|
| 37:43 | the heart and the heart pumps All right. This is an intrinsic |
|
| 37:48 | of the heart. So the heart what you give it? All |
|
| 37:52 | So what we're really affecting when we're how the heart pumps is, we're |
|
| 37:57 | not what the heart is doing. affecting what is coming to the |
|
| 38:02 | Alright. So how do I How do I increase how much blood |
|
| 38:06 | coming to the heart? What do think I can do exactly? I |
|
| 38:12 | hear what she said. Well, resistance will be on the front |
|
| 38:16 | on the back end. I want increase resistance. In other words, |
|
| 38:20 | I wanna do is I want to want to go through a contraction. |
|
| 38:24 | ? So here I've got a it has a certain amount of blood |
|
| 38:27 | the tube. All right. So I want to get more blood out |
|
| 38:32 | the tube faster than what am I do, squeeze it? So when |
|
| 38:37 | have venus contraction, what that's gonna that squeezes the tube. That pushes |
|
| 38:42 | to the heart. All that blood up in the atria frank. Starling |
|
| 38:46 | the heart looks all that blood and I need to get this out of |
|
| 38:49 | heart. So it sends it to ventricles and the ventricles then contracts and |
|
| 38:53 | that blood outward. Alright? So I increase pre load I'm going to |
|
| 39:00 | the contract style activity of the I'm gonna increase SV now. |
|
| 39:04 | What I'm doing is I'm dealing with diastolic volume. Right? So what's |
|
| 39:08 | diastolic volume says it in the right? The max volume I get |
|
| 39:16 | rest. Right? So remember the contracts diagnostically we're here refers to the |
|
| 39:23 | . And so what happens is when contract and send all that blood into |
|
| 39:28 | ventricle before it contracts it still and that that volume that's inside the ventricle |
|
| 39:35 | the end diastolic volume. So, I'm doing is I'm increasing E. |
|
| 39:41 | . V. Okay. Here's the SV is equal to E D V |
|
| 39:50 | E. S P E S In systolic volume. Alright, So |
|
| 39:56 | I increase cTV and I keep PSV same, what's happened to SV? |
|
| 40:05 | increases. Right. Just making up number E D V is 100 E |
|
| 40:10 | V. Is 10. What's the ? So, SV would be |
|
| 40:14 | Okay. If I take a tv give it 50 more. So, |
|
| 40:17 | 100 and 50 mg SV stays the . So 100 15 minus 10 equals |
|
| 40:23 | stroke volume has increased decreased same. by how much? 50. |
|
| 40:30 | truly 40 because SV is what we're how much is SV increased? |
|
| 40:35 | So do you see no, you're . 50. You get the gold |
|
| 40:40 | I get the minus f minus. right. So that's what we're dealing |
|
| 40:44 | you increase E. G b you're increase SV Because we're not talking about |
|
| 40:49 | right now. All right. I that's alphabet soup, but in diastolic |
|
| 40:53 | takes more time to say. All . Because frank. Starling observed |
|
| 40:59 | and Starling observed the heart pumps what pumps. Alright? You give |
|
| 41:03 | It does. Alright, so increase return. How do I increase venous |
|
| 41:08 | ? We have talked about that yet activity, we'll get to it. |
|
| 41:13 | will yield an increase in stroke So that's one way that we affected |
|
| 41:17 | in diastolic volume secondly, after after load is something you already understand |
|
| 41:23 | well. Alright? We we refer it as another term. We talk |
|
| 41:28 | blood pressure. If I have raised pressure, what am I doing? |
|
| 41:33 | increasing resistance to the blood being pumped of the heart. So, if |
|
| 41:38 | have greater after load, right? my arteries are saying don't give me |
|
| 41:42 | blood and my heart saying, but have to pump what I have to |
|
| 41:47 | , then what does the heart have do? It has to work |
|
| 41:52 | Right? So now what I'm doing I am increasing my E. |
|
| 41:58 | V. Right? Because the resistance you can't let out as much as |
|
| 42:02 | as you want to let out. still letting some out. But I'm |
|
| 42:05 | have more left over in the Alright? The SV is just the |
|
| 42:09 | left over the heart. So, I increase the SV and I'm not |
|
| 42:12 | about the E. D. At all. That stays constant |
|
| 42:15 | D. V minus E. And SV is increasing decreasing stroke |
|
| 42:20 | All right that makes sense. If if I'm being resisted against and I'm |
|
| 42:28 | increasing the amount of work I'm doing amount of stuff that's the amount of |
|
| 42:33 | that I'm accomplishing is less. So this case I'm moving blood volume so |
|
| 42:38 | I'm not able to move as much volume that means I have more left |
|
| 42:41 | on this side. So after load the end systolic volume and it results |
|
| 42:48 | an increase of that in systolic All right now for all of us |
|
| 42:53 | is pretty pretty constant. PsV stays or less constant. It's once you |
|
| 42:58 | developing pathologies like high blood pressure where see after load having a great |
|
| 43:03 | And so much of the medicines that do is there to reduce um the |
|
| 43:09 | load right? Because what we're concerned is not how much blood is leaving |
|
| 43:15 | heart but how much work the heart doing and if the heart works too |
|
| 43:18 | what's it gonna want to do? wants to rest too Just once it |
|
| 43:28 | . Doesn't really do much else after seizes up and dies. Alright I'm |
|
| 43:35 | tropic agents in a tropic refer to things that are going to change the |
|
| 43:41 | of calcium. Alright. Positive. know tropes increased calcium ability. Negative |
|
| 43:46 | decreased calcium availability so you can go read through all this stuff But if |
|
| 43:51 | increasing calcium availability? What's that? that gonna do to the activity of |
|
| 43:56 | heart? It's gonna increase the rate which it beats and it's gonna increase |
|
| 44:04 | strength. Alright. So examples again agonists. Alright. Anything that's going |
|
| 44:11 | make the heart beat harder? So think about it. Think about |
|
| 44:16 | adrenaline does. What does adrenaline due your heart faster and harder? |
|
| 44:23 | I mean you're saying that? All . That's extra calcium. So that's |
|
| 44:29 | a positive item trump does stronger increases the available of calcium. Plus |
|
| 44:35 | the number of cross bridges. So negative tropes do the opposite. So |
|
| 44:40 | have natural ones. Those things in bodies like what is listed here. |
|
| 44:45 | then there are things that are external are referred to as many trips as |
|
| 44:49 | . Alright. Which you'll get the of you are going to farm |
|
| 44:52 | get to learn the whole big All right. So this is just |
|
| 44:57 | example. So what we're doing is changing the force of contraction. So |
|
| 45:04 | do we change stroke volume? In pre load affecting pre load effects |
|
| 45:10 | D. V. After load effects . S. V. Right. |
|
| 45:17 | here what we're gonna do is we uh basically you're gonna increase stroke volume |
|
| 45:24 | decreasing SV basically those hard contractions causes blood to leave. All right in |
|
| 45:31 | response. So if I have more leaving the heart heart faster, what |
|
| 45:35 | that going to do to the V. What do you think I |
|
| 45:41 | more blood leaving the heart? What's to happen to the blood returning to |
|
| 45:45 | heart? It's going to increase as . So think about think about what |
|
| 45:52 | right when you are exercising right? hearts beating harder. More blood is |
|
| 45:56 | back to the heart. Hearts beating . It's basically a system that has |
|
| 46:00 | stay in constant motion. So what gonna do is you're gonna see that |
|
| 46:05 | come back on the on the back . That kind of makes sense. |
|
| 46:13 | right. Ready to do the easy . Ready to move away from the |
|
| 46:20 | stuff. All right. It's really that hard. Alright. What's |
|
| 46:27 | It's a fluid consisting of a whole of stuff. The fluid portion is |
|
| 46:33 | plasma has within it. A bunch molecules will get to what the most |
|
| 46:37 | ones are. Just minutes. So it's a fluid matrix is what |
|
| 46:41 | refer to it as. So it's plus stuff has specialized blood cells which |
|
| 46:46 | not entirely blood cells. These are called the formed elements because as we |
|
| 46:50 | see in just a moment of parasites the platelets is a term that we |
|
| 46:55 | in humans, other species we call but you'll see them every now and |
|
| 46:59 | elsewhere as homicide. But these two are not actually cells anymore. They |
|
| 47:06 | from cells but they're not cells any . Only sells here, the |
|
| 47:11 | So if you're not familiar with these sites, these are red blood |
|
| 47:14 | leukocyte or white blood cells. Platelets sometimes referred to as homicides. |
|
| 47:19 | if I just take all these things put them in a in a, |
|
| 47:23 | don't know a vial, let's just it that way. These formed elements |
|
| 47:28 | very, very heavy. So what they going to do? They're gonna |
|
| 47:31 | . Right. And so the cardiovascular ensures a constant motion and a constant |
|
| 47:39 | of this fluid informed elements. So these things are equally distributed. |
|
| 47:43 | so they're in constant distribution. The hematocrit is a term we use |
|
| 47:53 | refer to the packed cell volume. specifically, it refers to the percentage |
|
| 47:59 | sites I have seen in some textbooks in some places that they also include |
|
| 48:04 | Buffy coat because Buffy coats are really small and why not just include |
|
| 48:10 | . But for your purposes. And the exam, when you see |
|
| 48:13 | it's the original site percentage which comes between 42 and 45%. The Buffy |
|
| 48:19 | is represents the rest of the formed . So that the sites is that |
|
| 48:25 | cell volume and that Buffy coat is final 1%. So that's why most |
|
| 48:31 | kind of consider both together because like doesn't matter that 1% doesn't really change |
|
| 48:36 | Now. What you see here in hematocrit, It's gonna be dependent upon |
|
| 48:41 | whole bunch of factors primarily aging your . So, males typically have a |
|
| 48:46 | dramatic red and that's because testosterone is promoter of erythropoietin production, which is |
|
| 48:52 | for making red blood cells. And females have a slightly lower one about |
|
| 48:57 | , but they're close enough. Um what is plasma? Um I'm just |
|
| 49:04 | to show you here. It's kind clear ish, kind of It's really |
|
| 49:06 | clear. It's it's it's opaque kind of yellowish in nature. Um |
|
| 49:11 | makes about 55%. It's because it's made up of water about 90%. |
|
| 49:16 | does a really good job of distributing heat. Um with regard to |
|
| 49:20 | else is in there, about 68% plasma proteins. We'll look at some |
|
| 49:25 | the general ones in just a plus a whole bunch of other |
|
| 49:28 | And these are things we kind of about. So electrolytes, we don't |
|
| 49:31 | don't really count them in that We just know that their electrolytes |
|
| 49:35 | You're dissolved gasses that includes oxygen and dioxide and nitrogen. All those things |
|
| 49:40 | you find in your atmosphere in those concentrations roughly are going to be found |
|
| 49:46 | the plasma as well. But when talk about the lungs and what they |
|
| 49:50 | , that's not the fluid we're really or the gasses, we're talking |
|
| 49:54 | It's gonna be gasses that are being through the urethra sights. For the |
|
| 49:57 | part there's other organic molecules that aren't part of the plasma proteins. So |
|
| 50:02 | signaling molecule, any hormone and they're there as well. But because |
|
| 50:07 | not made in the liver and they're part of the plasma protein cohort, |
|
| 50:10 | just kind of ignore them. There percentage is so small. The term |
|
| 50:15 | , when you hear serum it is without fibrinogen, which is one of |
|
| 50:19 | plasma proteins and the other clotting factors are included in uh those plasma |
|
| 50:25 | Alright, so that's what serum ultimately very, very similar. What we're |
|
| 50:32 | at here is a western block. guys know what Western blot is. |
|
| 50:36 | people. Four people nodding your Alright. And really what they're trying |
|
| 50:39 | show you where these different plasma proteins located and so why we're interested in |
|
| 50:45 | plasma proteins is because of the effect they have on osmolarity and the effect |
|
| 50:50 | the movement of water through the interstitial back to the plaza and back and |
|
| 50:56 | again. Alright, so they're responsible creating an osmotic gradient. Alright, |
|
| 51:01 | those platinum proteins are too big to their way into the interstitial fluid. |
|
| 51:04 | only found in the plasma, hence name. And so they attract water |
|
| 51:09 | into the blood because of that osmotic . Alright, this is when we |
|
| 51:16 | concerned about blood pressure and blood Part of it has to do with |
|
| 51:21 | presence of these plasma proteins. So have to know of their existence and |
|
| 51:23 | going to see their effect Over the of the next couple of lectures, |
|
| 51:28 | of the most common ones albumin. guys heard albumin before? It's a |
|
| 51:32 | itsy bitsy teeny tiny protein. Um you go crack open an egg, |
|
| 51:36 | that clear stuff, not the The clear stuff is is is a |
|
| 51:40 | high concentration of albumin. It's actually the highest concentration, but it's one |
|
| 51:45 | where you can actually see it and it. You can see albumin is |
|
| 51:48 | of sticky. Right? Does a good job of binding things in a |
|
| 51:52 | , very non um specific manner That up almost 60 the globulin. Have |
|
| 51:59 | heard of globulin before? You've heard one in particular? Those are the |
|
| 52:04 | globulin. Gamma globulin. Those are antibodies. All right, so they're |
|
| 52:09 | but you'll have alpha globulin, beta . You have to have an alpha |
|
| 52:12 | a beta. So, these are transporters, they transport all sorts of |
|
| 52:16 | . Primary lipids and other ions primarily . For the most part they can |
|
| 52:21 | as regulators. And if you look the picture in here anything with an |
|
| 52:26 | , Right, Those are like the globulin. Let me see if I |
|
| 52:29 | find there's I g a gamma globulin there's a beta globulin for you. |
|
| 52:34 | right. You can see where the czar look look at that big old |
|
| 52:38 | . Right then we have fibrinogen. we'll get to that here at the |
|
| 52:42 | of class fibrinogen plays the main major role in homeostasis. That's blood |
|
| 52:47 | And you can see fibrinogen there it . Right, it's this peak that |
|
| 52:56 | trying to represent this red line. , so that's fibrinogen and then there's |
|
| 53:00 | proteins in there and you can kind go through there. It is |
|
| 53:04 | you can go through and kind of you know, oh what's this? |
|
| 53:09 | that? They're all sorts of fun in there. So there's a whole |
|
| 53:12 | of proteins is really what it boils to and they have varying roles in |
|
| 53:16 | plasma, primarily carriers but also play major role in clotting pronounce that word |
|
| 53:24 | me please. Oh I like that sis poetess is it's a fun word |
|
| 53:33 | say. So mad opposes. It could be you'll see uh him oppose |
|
| 53:39 | . So they they take out the and just called Hema polices refers to |
|
| 53:44 | production of these formed elements. So all originate from the same um origin |
|
| 53:50 | if you look at this you can here's my red blood cell um right |
|
| 53:53 | , that's the um mega carrier These are your lymphocytes all through here |
|
| 54:01 | the way down. And so you see they all start off as a |
|
| 54:05 | or from a progenitor. And so you need in order to get this |
|
| 54:10 | happen and to get these things as can see marked here in red? |
|
| 54:14 | are specific molecules that kind of direct particular uh pluripotent cell down a specific |
|
| 54:22 | . So what happens is you go this pluripotent cell, that can be |
|
| 54:27 | type of hematopoietic cell, which then of goes, okay, do I |
|
| 54:30 | down the lymphoid line or do I down the myeloid line? And then |
|
| 54:33 | I go down one of those lines what which way are you directing |
|
| 54:37 | So once you go down a particular you can't go back alright, you've |
|
| 54:42 | differentiated too far to uh go backwards really what it is. All |
|
| 54:47 | And so that's what this is just to tell you, is that there's |
|
| 54:50 | pathway of differentiation that's going to be upon the type of side of kind |
|
| 54:55 | type of signaling molecules that are available drive in a particular direction. |
|
| 55:00 | And so this is just kind of big list. Honestly, you |
|
| 55:04 | I'm not sure, I may ask question on this, but really this |
|
| 55:08 | what it boils down to the tells you what it is. So |
|
| 55:10 | is a granule site monta site, , colony stimulating factor. It basically |
|
| 55:16 | you down the Nile Lloyd line so you either produce a granule side arm |
|
| 55:20 | a site and that's what all these are right here? Right? And |
|
| 55:23 | this pushes you down specifically. Am going to become a granule site or |
|
| 55:27 | I becoming a mon a site? , So it's G CSF or |
|
| 55:31 | S. M CSF. Um Don't about the inner Lukens throw is gonna |
|
| 55:38 | you from this sort of stem Either down to the mega carrier site |
|
| 55:42 | if I have or it is going push me towards the red blood |
|
| 55:48 | So, the big picture here is I want to make a specific type |
|
| 55:52 | cell, I have to have specific that tell me what to do. |
|
| 55:58 | right. And so what I want show you here is the oasis. |
|
| 56:02 | right. We all need red blood . We agree with that. |
|
| 56:06 | Okay. So this is gonna occur the red bone marrow. All right |
|
| 56:10 | you don't always have red bone marrow utero. You have no red bone |
|
| 56:15 | . And so all your red blood are gonna be made primarily first initially |
|
| 56:18 | the yolk sac and then when you your liver and your spleen form very |
|
| 56:22 | on, that's when it takes over then eventually the bones form. And |
|
| 56:25 | when you have you you populate the um um cavities of the bones and |
|
| 56:31 | ends of the bones with this red . And so during most of childhood |
|
| 56:35 | have a whole bunch of red bone but then we get old and we |
|
| 56:38 | up that red those those spaces with is called yellow marrow, which lack |
|
| 56:41 | a better term is really just kind fat. All right now, it's |
|
| 56:45 | fat, but it's like fat and you can actually revert yellow marrow back |
|
| 56:49 | red marrow in dire needs. But essence, your red bone marrow is |
|
| 56:54 | to be found in some very, hard to reach places. So, |
|
| 56:58 | are not like when you talk about long bone, we're talking about the |
|
| 57:02 | head of the femur, for not easy to get to. You |
|
| 57:05 | to actually go digging through a whole of muscle and actually dig through the |
|
| 57:09 | koksal, which is your hip to to the head of the femur. |
|
| 57:13 | , not a fun place to go this stuff. Now, the way |
|
| 57:17 | decide how much red blood cell we're is dependent upon how much oxygen the |
|
| 57:22 | receives. So, our kidney is oxygen sensor. All right now, |
|
| 57:27 | your tissues are dependent upon the oxygen delivered to it. But only the |
|
| 57:31 | is the one that responds to the received. So, if it's not |
|
| 57:34 | enough oxygen and says, wait, , wait, wait, Where's my |
|
| 57:37 | ? Well, apparently, I don't enough red blood cells carrying enough |
|
| 57:41 | So, I'm going to tell the bone marrow to make more red blood |
|
| 57:46 | . That may not even be the , but that's how it determines |
|
| 57:49 | Yeah corn kidney. No, because still censoring, you're still monitoring is |
|
| 57:56 | kidney getting the oxygen needs? no, this is. So, |
|
| 58:04 | we're talking here, we're really talking big picture stuff. So, if |
|
| 58:07 | put you underwater and hold you underwater two minutes, your kidneys not going |
|
| 58:10 | my oxygen? I mean, it , but your brain is really kind |
|
| 58:14 | doing more of the where's my oxygen than your kidney is. Alright, |
|
| 58:18 | , we're talking about a long term , a long term hormonal response |
|
| 58:22 | Not minutes, minute. Yeah, , I think, and we may |
|
| 58:33 | it to another on another slide. so, yes, so, the |
|
| 58:37 | here is this is more representative of oxygen carrying capacity of the blood. |
|
| 58:42 | , the number of red blood cells how well the blood carries oxygen. |
|
| 58:48 | it represents the number of red blood . Because your red blood cells are |
|
| 58:52 | cell that carries oxygen. So, you don't, if your kidneys aren't |
|
| 58:56 | enough oxygen, it's got to be fault of the number of red blood |
|
| 58:59 | I have. Right. And using your example, if I go |
|
| 59:04 | a high altitude, which we know a higher altitude, the oxygen in |
|
| 59:08 | atmosphere is a lot lower kidney doesn't , oh, I'm sorry, I'm |
|
| 59:12 | colorado I'm at 10,000 ft. It's less auction around. It just |
|
| 59:16 | wait a second. Apparently, I have enough red blood cells. |
|
| 59:19 | what I'm gonna do is I'm going make more red blood cells so that |
|
| 59:24 | auction carrying capacity can increase. now there are a lot of steps |
|
| 59:32 | , you see here is that stem and you can see. So, |
|
| 59:35 | I want to point out here is is the step that requires us to |
|
| 59:40 | from that noncommittal step to the committed of producing the red blood cell. |
|
| 59:46 | , The original site. And what's here is that what we're gonna |
|
| 59:49 | We're modifying a cell from a functional that can divide to a cell that |
|
| 59:55 | is basically a bag of hemoglobin. right, so, you can see |
|
| 59:59 | what it says. Look, I'm go through a series of divisions |
|
| 60:02 | So I'm gonna still get a series divisions. But what I'm gonna start |
|
| 60:06 | is my machinery says, I need start making hemoglobin. And so it |
|
| 60:10 | making tons and tons of this protein it starts filling up the cytoplasm of |
|
| 60:14 | cell. And to the point where like, I don't want my other |
|
| 60:18 | , All I want is hemoglobin. so we extrude all our organelles, |
|
| 60:23 | extrude the nucleus. And at this , we're just basically a container full |
|
| 60:29 | hemoglobin. And there's still some steps need to take place. But what |
|
| 60:34 | do is we get to this immature called a particular site. And that |
|
| 60:38 | site can enter into the uh circulation serve as a red blood cell while |
|
| 60:45 | still goes through that last few steps organelles removal. And so once you |
|
| 60:50 | an original site, you're now using , very basic cellular activity to maintain |
|
| 60:58 | function. And that cell function is circulate and hold on oxygen. You |
|
| 61:04 | still do a little bit of glycol . But that's about it right. |
|
| 61:09 | not much else going on inside the . So massive, massive modification in |
|
| 61:15 | to the erythropoietin. Alright, erythropoietin produced by which structure starts with a |
|
| 61:24 | kidney kidney is monitoring how much oxygen need. It's the one that's sending |
|
| 61:29 | signal to the red marrow, it's a to make that signal. |
|
| 61:35 | how many retro sites do you You have about five times 10 cells |
|
| 61:39 | mill of blood. Adult males are 5.5 liters. Females are about 4.5 |
|
| 61:45 | of blood. So, if you to do the math to figure out |
|
| 61:47 | many red blood cells are in circulation now, that kind of gives you |
|
| 61:51 | sense. And again, that's an . If you're smaller, you're gonna |
|
| 61:54 | fewer. If you're taller, you're have more or bigger. All |
|
| 61:57 | So, when we think of a sites, think transport of oxygen as |
|
| 62:02 | as the transport of carbon dioxide. is their function very flat. You |
|
| 62:06 | see here there by concave and the this shape allows them to uh navigate |
|
| 62:13 | the intricate structures of the capillaries. themselves are very very small. They're |
|
| 62:19 | as almost as big as the red cells themselves. And typically what will |
|
| 62:23 | is that you'll get a stack of blood cells that kind of jam up |
|
| 62:27 | , create this this kind of like of red blood cells, it's called |
|
| 62:33 | . And they kind of move together you can kind of see that in |
|
| 62:36 | picture. Alright now this shape does couple of things. It allows them |
|
| 62:41 | move very very easily in these blood . So think about a basketball basketball |
|
| 62:46 | round. Right think of it being at the proper P. S. |
|
| 62:49 | can you bend the basketball in No, so it would be very |
|
| 62:53 | difficult to go through a very very capillary that has a sharp turn. |
|
| 62:58 | if I deflate the basketball, remove the air from it. Could have |
|
| 63:01 | the basketball now. So that's kind what we've done here, It's the |
|
| 63:04 | volume inside. It's just now I a flexible structure. Second thing is |
|
| 63:10 | it also increases or decreases the distance the center of the cell to the |
|
| 63:15 | . So if I'm completely filled up hemoglobin, the rate at which oxygen |
|
| 63:20 | move in and out of the cell very very quick because the distance between |
|
| 63:24 | hemoglobin is and where the outside of cell is is very very short. |
|
| 63:29 | , so it's advantageous to the cell have this particular shape. So a |
|
| 63:36 | no, basically no organelles, about of 7% of its contents hemoglobin. |
|
| 63:42 | have about 280 times 10 to the million or 10 to 6 million. |
|
| 63:46 | to 10 to the six molecules per . Again, if you want to |
|
| 63:50 | the math, you can go back multiplying too much hemoglobin. You |
|
| 63:56 | you do make a teepee uses glycol . Why you guys like blue bell |
|
| 64:02 | cream? Do you remember the We eat what we can and we |
|
| 64:07 | the rest. Do you remember that that used to be their big ad |
|
| 64:12 | they had a listeria. In which I don't know what happened. I |
|
| 64:15 | there the week that they had the listeria problem. I was still eating |
|
| 64:18 | cream. I could care less. know, they'll kill me or it |
|
| 64:22 | either way I die happy. Anyway, so that used to be |
|
| 64:27 | , add it would be like this driver and says alright son, you |
|
| 64:30 | have whatever you want. And then finally gets to the destination, he's |
|
| 64:33 | all the ice cream in the right? And actually if you go |
|
| 64:36 | the factory and you should, if never been, it's not too far |
|
| 64:40 | Brenham. It's a weekend trip, can eat ice cream, they right |
|
| 64:44 | there. But they have you they you go by during the tour, |
|
| 64:47 | get to see the break room and whole wall of the break room is |
|
| 64:51 | and you basically, they have all points that all the workers have and |
|
| 64:55 | put their names on the pint and just sit there and that's their ice |
|
| 64:58 | . And then when they run out they go get another point and they |
|
| 65:00 | their name on it and that's there's a bad job if you don't mind |
|
| 65:06 | cream. All right. So, idea why do I tell this |
|
| 65:10 | Because it's the same thing. You not want yourselves to consume the oxygen |
|
| 65:14 | you're carrying. Otherwise your kidney is be really, really upset. And |
|
| 65:19 | the rest your body is gonna be as a function. And they stick |
|
| 65:22 | for about 100 and 20 days. about 100 and 20 days, they've |
|
| 65:25 | beat up enough that they're just kind basically barely being held together. And |
|
| 65:28 | when they arrive in the spleen. spleen is like this horse shows roller |
|
| 65:33 | for these places basically bust up the and causing the rupture and then you |
|
| 65:38 | recycle the hemoglobin and or really the the iron and you break everything |
|
| 65:43 | So the spleen is where we recycle . So here's a molecule you guys |
|
| 65:49 | seen ever since you've been freshmen. remember that first time you talked about |
|
| 65:54 | structure and show you a picture of . Yeah. So what do we |
|
| 66:02 | here? It's just a pigment. iron here in the center is capable |
|
| 66:06 | binding of oxygen. So there's two . We have 1234 globe and molecules |
|
| 66:12 | two pairs of different types of globe . All right in the center of |
|
| 66:16 | of you. That's where the heat . That's what the oxygen is |
|
| 66:19 | So each hemoglobin combined. How many 4? Which makes it really simple |
|
| 66:26 | if you find one you're 20% 25% to 50% saturated, 3, 75% |
|
| 66:32 | , 400% saturated. See how easy math is. I love things like |
|
| 66:37 | thing is hemoglobin. Doesn't just buy oxygen. Alright so one of the |
|
| 66:42 | so that option will bind the iron when it does it binds and we |
|
| 66:46 | that molecule now oxy hemoglobin. when you remove the oxygen, the |
|
| 66:51 | hemoglobin and then like I said you other things. So carbon dioxide can |
|
| 66:56 | to the globe and portion and when does so we refer to as carb |
|
| 66:59 | hemoglobin. Alright not carb oxy that's what you get when you bind |
|
| 67:05 | to the irreversible carbon monoxide. you can bind up two protons when |
|
| 67:11 | happens. And so this is a that hemoglobin can actually serve as a |
|
| 67:15 | to the blood. It binds up free protons combined. Up to nitric |
|
| 67:20 | serves as a vase, a dilator all this is to the hemoglobin. |
|
| 67:24 | molecules cyanide. Uh So fox side hydrogen sulfide. These are other things |
|
| 67:31 | can serve as a carrier for. , but we're gonna be really primarily |
|
| 67:36 | in the carbon dioxide, the protons well as the oxygen. There are |
|
| 67:42 | molecules that you need to be aware . The 1st 123 D faster Glycerin |
|
| 67:48 | a molecule released by cells that basically , hey give me your oxygen. |
|
| 67:53 | so what it does is that that fossil glycerin causes hemoglobin to say I'm |
|
| 67:59 | longer interested in binding up to the . So the oxygen is released and |
|
| 68:03 | that comes from the red blood Glutathione just helps against protect against oxidative |
|
| 68:09 | . Where we're gonna get oxidative damage . Not a trick question from the |
|
| 68:16 | . And it's carrying right? So um carbonic anhydrous, we're gonna learn |
|
| 68:22 | whole bunch about it helps to convert dioxide into bicarbonate. If you don't |
|
| 68:26 | that molecule right there should have a sign on top that bicarbonate is going |
|
| 68:30 | be like your best friend for the couple of weeks. Alright. Um |
|
| 68:34 | is really really important for carbon dioxide . We're gonna have a proton exchange |
|
| 68:41 | proton a chlorine by carbon exchanger. allows us to move these two uh |
|
| 68:46 | ions back and forth very very quickly the red blood cells wall. And |
|
| 68:50 | we have aqua porn's which can serve a carbon dioxide channel, which allows |
|
| 68:54 | to move carbon dioxide in and out the cell very very quickly in the |
|
| 68:57 | blood cell. It's interesting. That's aqua porn, isn't it? |
|
| 69:04 | All right. This is basic, , basic, basic basic immunology. |
|
| 69:13 | not even immunology. You need to your Lucas sites. All right. |
|
| 69:16 | what they do. Alright, we two basic types of Granules are two |
|
| 69:20 | types of sites and a granule Granule sites have Granules. Granules sites |
|
| 69:27 | . So basically, if you stain , you're going to see that those |
|
| 69:31 | staying with a di specific type of and that's where their name came |
|
| 69:36 | So, there's three types of granule , neutrophils get cinephiles and besa |
|
| 69:40 | All right. They don't really exist that long in the blood. They |
|
| 69:44 | of hang out there for a little , but then they arrive in their |
|
| 69:47 | and that's where they kind of hang . The a granule sites are the |
|
| 69:50 | that you primarily see in circulation. key feature between these, if you |
|
| 69:56 | at the granule sights, you're gonna that their nuclear nuclei look weird. |
|
| 70:01 | right. They look like they've been and pinched and so they have what |
|
| 70:05 | called lobes to them. So sometimes see um Lobular granule sites is sometimes |
|
| 70:13 | term that you'll see. All So neutral Phyllis feels the difference between |
|
| 70:18 | is which dye binds them. All . So we're gonna start with the |
|
| 70:24 | . The most common type. It's lobed. So you can see I've |
|
| 70:29 | done you're not gonna have to identify . Alright. I'm not gonna I'm |
|
| 70:32 | pointing them out so that you can in the spread which ones they |
|
| 70:34 | All right. They're fake acidic in . Alright. So what they're looking |
|
| 70:38 | is they're looking for that first line bacterial infection. Do you have a |
|
| 70:43 | inside you? I'm gonna kill All right. So that's what we're |
|
| 70:47 | to deal with. They play an role in your inflammatory response. The |
|
| 70:52 | to fill about 4%. Alright. job is to deal with parasites. |
|
| 70:58 | right. In the Western World. World Western World. Do you think |
|
| 71:02 | have to deal with a whole bunch parasites? So what do you think |
|
| 71:06 | see NFL counselor like. Low very . Very low. Alright. If |
|
| 71:12 | go to India or Southeast Asia, do you expect in that population? |
|
| 71:18 | . Okay. They also play a in allergic reactions to some degree. |
|
| 71:22 | right now they're called because they get by an acidic um a die. |
|
| 71:28 | you've heard of H. And Standing Standing standing okay. Don't worry |
|
| 71:37 | if you haven't taken microbiome then. haven't seen this stuff yet but this |
|
| 71:43 | and purple stuff H. And Alright. So the sn is the |
|
| 71:48 | stuff besa fills. Besa fills again smaller portion. They play a major |
|
| 71:56 | in um uh allergic reactions. But I was trying to get here is |
|
| 72:01 | a dilation and heparin. So you imagine here is when an infection occurs |
|
| 72:06 | if there's damage there these cells show and they say ah this is the |
|
| 72:10 | of damage starts releasing. The histamines starts releasing the heparin Heparin. Its |
|
| 72:15 | is to serve as an anticoagulants. it allows fluid to come into that |
|
| 72:18 | and not create a clot. The causes days of dilation and inflammation so |
|
| 72:23 | the fluid shows up. All You can remember what histamine is because |
|
| 72:28 | you get all topped up you take of that. Okay. Monitor sites |
|
| 72:35 | baby macrophages. So again is the largest population. Um They basically are |
|
| 72:43 | circulation. And then what will happen they'll differentiate into the macrophage. Macrophage |
|
| 72:47 | kind of like the neutrophils and that looking for bacteria but typically you'll have |
|
| 72:52 | different types of macrophages. One that as a population that doesn't migrate through |
|
| 72:58 | . It becomes a stationary macrophage and monitors its environment or what it can |
|
| 73:03 | is it can migrate from tissue to to tissue. It can also serve |
|
| 73:06 | an androgen presenting cell which is more we need to know. That's basically |
|
| 73:11 | you alert your other uh how you the lymphocytes lymphocytes um This is the |
|
| 73:21 | the second largest I should have said the the previous not the manga sites |
|
| 73:27 | most of these are hidden up. . They're they're they're kind of sequestered |
|
| 73:32 | a way away in um your lymphatic looking for the presence of pathogen. |
|
| 73:40 | . So you have two different populations cells and T cells and this is |
|
| 73:45 | specific line of defense against specific foreign . B cells are the antibody producing |
|
| 73:52 | . All right. So what they're is that each of these cells are |
|
| 73:55 | to a specific pathogen. They're just and if that specific pathogen comes along |
|
| 74:01 | to the B. Cell that causes B cell to differentiate become a plasma |
|
| 74:05 | and it starts producing that antibody that's that specific antigen, that specific pathogen |
|
| 74:12 | has that response to that particular Alright. So it plays a role |
|
| 74:17 | antibody mediated or what you'll see sometimes mediated defense. T cells on the |
|
| 74:24 | hand and their names come from the . And T. Come from where |
|
| 74:28 | where they mature. So B cells and bone marrow T cells are made |
|
| 74:32 | bone but then they go to the and that's where they're selected for |
|
| 74:37 | What they're doing is they recognize the themselves through their receptor recognizes the |
|
| 74:44 | So this is what is called cell immunity. Alright. There's different types |
|
| 74:48 | T cells T helper cells to killer um side of toxic T cells um |
|
| 74:54 | there's like three or four others that now that when I was in school |
|
| 74:58 | exist so. Alright. But their is they act directly they're not producing |
|
| 75:03 | to bind things up there recognizing the and then they say hey come kill |
|
| 75:08 | thing, this thing needs to be . And that's how um how they |
|
| 75:13 | work. That is your kindergarten exposure the immune system. Yes ma'am. |
|
| 75:30 | asking a question that has a 45 answer and I mean and it's a |
|
| 75:35 | good question. I'm not trying to . I mean it is an incredibly |
|
| 75:39 | question which is why all our topics to do with the immune system. |
|
| 75:44 | immune system is grossly complex. And essence what you have is for the |
|
| 75:49 | . Cell and T. Cell. each have their own specific receptor called |
|
| 75:52 | B cell receptor in the T. receptor. Very complex part right? |
|
| 75:55 | what this is is it's a piece D. N. A. That |
|
| 75:59 | these regions that are variable regions and reorganize themselves during the process of |
|
| 76:05 | And so every one of your T and every one of your B cells |
|
| 76:09 | unique in that they recognize a specific antigen. Right. And so this |
|
| 76:17 | a roll of the dice. Let's out um trying to be very careful |
|
| 76:23 | trying to go too far. It's basically a random process of what you're |
|
| 76:28 | to be able to recognize. So and I may be able to recognize |
|
| 76:31 | same pathogen. But the way that do our through different antigens, |
|
| 76:36 | determinants, different episodes. Alright. the way that we go to make |
|
| 76:41 | that the B. Cell and Cell they go through a process of |
|
| 76:45 | which basically says can you recognize something now? Are you recognizing self? |
|
| 76:52 | . Okay. We don't want you die go die in a fire. |
|
| 76:55 | we select away from those things that attack ourselves. And then those things |
|
| 77:01 | can both recognize uh an antigen and something that's not self are the ones |
|
| 77:07 | stick around and I can't remember what total number of combinations are. But |
|
| 77:11 | like ridiculously high. It's not But it's it's crazy now just to |
|
| 77:17 | you a sense. Alright, so For the vaccine that was for the |
|
| 77:23 | that we the COVID-19 right. What did was we created a a very |
|
| 77:30 | small molecule right, a very small genic piece of. Well it was |
|
| 77:37 | RNA that could make a small And so the idea was is do |
|
| 77:42 | have an antibody that can be produced can recognize that episode? And if |
|
| 77:50 | did then you created a monoclonal A single antibody that can recognize it |
|
| 77:56 | for those who got exposed to the virus has many many proteins, many |
|
| 78:03 | different shapes on those proteins. And we created a massive polyclonal attack. |
|
| 78:11 | , we basically created a defense that much, much greater than those that |
|
| 78:16 | just being exposed with that little tiny . And I went way too far |
|
| 78:21 | that. So, immunology is a of fun and very, very |
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| 78:26 | I know. What do I Like zero seconds left. Two |
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| 78:29 | Alright. I think this is the slide I'll do right here, I |
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| 78:37 | . Yeah, well, we'll leave that. We're gonna stop here with |
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| 78:43 | platelet one. All right. what is the platelet? A platelet |
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| 78:48 | a portion of the mega carrier site off. All right. So, |
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| 78:53 | make a carrier site. Remember was down the same path as the original |
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| 78:57 | . And then you got it gave a different hormone. It's that causes |
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| 79:04 | mega carrier site to start doing this of weird, shimmy shake. And |
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| 79:07 | it's plasma membrane starts doing this kind weird stuff. And the sheer force |
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| 79:11 | the blood going by that thrombosis site that mega carrier site rips off a |
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| 79:17 | tiny piece of that plasma and within plasma void or within that plasma. |
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| 79:23 | the plasma membrane within that structure are that the platelet needs in order to |
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| 79:29 | its function. Alright. So, a whole bunch of Granules in there |
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| 79:33 | you can see right here, here's little blab and they're they're being torn |
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| 79:36 | . So this is the structure. what you're gonna have, you're gonna |
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| 79:39 | these alpha Granules in these dense core . And what these do is within |
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| 79:44 | structures, the alpha Granules. Those all the elements you're gonna need to |
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| 79:47 | a blood clot and then you have molecules that regulate where those are gonna |
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| 79:54 | how they work. So, the platelet plays a role in this process |
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| 79:59 | homeostasis. Alright, Homeostasis is the word for saying, creating blood clots |
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| 80:05 | scabs. Alright, They exist in blood for about 10 days. How |
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| 80:09 | the red blood cells stay in the ? 120. So, I want |
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| 80:13 | to see those two differences. Don't the two, once three months. |
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| 80:16 | is just about a week. All . And then after about 10 days |
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| 80:19 | kind of fall apart. Macrophages come and show them all up and get |
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| 80:22 | of them. All right. And , what when we do we'll start |
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| 80:25 | the most cases when we get back Thursday. All right. And so |
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| 80:30 | kind of what this is the start . We get to talk about |
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| 80:36 | You Yeah, don't talk to me the Dodgers going based on my email |
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| 80:46 | yesterday? The reason I asked is I remember seeing on |
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