Hello and welcome to this video on chapter 18 on blood or hematology, the study of blood. So we'll go right into PowerPoint. All right, we take a look at the functions of blood that we're going to discuss here.
The first one is Describe the composition and physical characteristics of blood. So we'll take a look at what is blood like? Why is it a connective tissue?
What are the functions of blood? Composition functions of plasma. Then we'll go into the formed elements, erythrocytes and hemoglobin and leukocytes and platelets.
Then we'll talk about abnormalities of such. And then hemostasis, we'll probably do in the second video. And hemostatic disorders like rhombi and emboli. and hemophilias and things like that.
And then we'll talk about the significance of blood typing and why we get transfusion reactions when we do. All right, so if we take a look at this table, here's something that you'll want to know. That blood is never blue. It's very bright red.
If you've seen blood leaving an artery, excuse me, it's a very bright red color. And then we've all seen blood coming out of a vein because typically when we have a bleed, that's where the blood is coming from. It's just kind of oozing out of our body. It's not shooting out like it would be in an artery.
So our blood is only scarlet red to dark red or brick red. It's never blue. That's just what our blood vessels look like.
You know, it's like, why is the sky blue? Just depends on how the light gets bent. All right. So volume of blood is going to vary between males and females. Females...
between four and five liters, males between five and six liters, because males are bigger and they have a greater body mass and therefore they need more blood to carry out the functions, deliver oxygen and other nutrients and carry waste products away. We're going to use this number, 5.25 liters of blood in our body, kind of as an average, but this is the number that we typically use. And the reason why It's because when we talk about cardiac output, which is how much blood our heart delivers.
So this is going to be liters per minute. It's going to be 5.25 liters per minute. So our entire blood supply is circulating throughout our body in a minute. All right. Now we're going to worry about the viscosity.
Now, plasma concentration. When I took this from the previous edition, it was wrong. But if you look in your book, it's right. 0.9% concentration. And typically we're talking about what saline concentration is.
So if you have IV saline that you're giving your patient, it's going to be 0.9% saline. And then the temperature of our blood is about 38 degrees Celsius, 37. We can say that that would be 98.6. degrees Fahrenheit.
And then here, we're going to remember this number for later on at the end of the semester. This pH range is 7.35 to 7.45, but yet we want to be right at 7.4. That is our normal pH of our blood. But of course, because of homeostasis, that we can have a range that those are in.
And I just did that again right here. So our blood is composed of formed elements. Those are the cellular components of blood. and then the plasma. So we have scarlet to dark red, and then there's that, and then here is that 5.25 liters that we need to remember.
So if we spin down blood, we're going to get it to separate according to weight. So if we centrifuge it, and here's what we're going to see, these percentages. Now it doesn't matter, this is going to be any volume of blood. we're going to get these percentages. So 55% is plasma, less than 1% is going to be what's known as our buffy coat, which we'll discuss in a minute.
And then 44% is going to be our erythrocytes. All right. So a lot of times you'll see 45 as a number because this is less than one. So I know 55 and 45 add up to one with this being a little bit less. So we can go anywhere between 44 and you'll see well i'm going to go to this next thing so our hematocrit you've probably heard of somebody having their hematocrit taken this is the percentage of red blood cells in a sample so there are no units on a hematocrit because it's just merely a percentage.
So here is the normal hematocrit for a male 47 plus or minus five and females 42 plus or minus five. So as you can see that this 44 and this 55 those are kind of generalized but if we had a male with a hematocrit of 47 then his plasma would have to be right around 52 percent. And then his buffy coat, I'm just going to put BC, is always going to be right around 1%, a little bit less than 1%.
And then as this number increases, the plasma will decrease. And as your hematocrit decreases, then your plasma increases because it's all relative. It's a percentage.
And so these numbers are never, never concrete. They're always, and they're going to fluctuate probably within a week, depending on how much water you might have and different kinds of things. So.
So in your plasma, it's going to be 92% water by weight. We're going to have proteins in here, about 7% of our blood. And then the other solutes, 1%, of course, when we're talking about plasma. So what are the proteins that we find within plasma? Albumin, we'll discuss shortly.
Globulins, those are the antibodies. And alpha, beta, gamma globulins. And fibrinogen, that's a clotting protein. And then other regular...
regulatory proteins that could be hormones those could be carrier proteins like we saw with the lipid soluble hormones that they need to have a carrier protein in there just a whole bunch of other kinds of proteins that could be in there and then what are the other solutes they're going to be the electrolytes primarily sodium is going to be in our plasma because it's an extracellular fluid potassium would be intracellular um calcium in here we put magnesium in here put chloride in there uh nutrients so oxygen carbohydrates amino acids whatever fatty acids probably not a lot of fatty acids but still fatty acids respiratory gases so co2 and o2 and then um the waste product so these would be CO2, urea, uric acid, those kinds of things. All right. So if we take a look at the formed elements, then the formed elements are the cellular components of our blood. In the Buffy coat, we are just going to have the white blood cells and the platelets or thrombocytes.
Here you can see their numbers. We went over the numbers in lab notes. So. four and a half or 4.8 to 10,800 or 11,000. This is not going to be an absolute number.
So per cubic millimeter, also known as a microliter. Okay. So those units are synonymous. And then 150 to 400,000 per cubic milliliter or cubic microliter. For now, I'm not going to have you learn.
Oh, maybe I am. We'll see as we get into the notes. I'm just going to tell you right now.
So as far as white blood cells are concerned, the neutrophils are the most abundant. The lymphocytes are next. The monocytes are third.
The eosinophils and then the basophils are last. So there's a little demonic never let monkeys eat bananas as the order of the white blood cells that we have. And you will not need to know the percentages at all, just the relative, just who's the most abundant, who's the least abundant in the order in which they come. And then erythrocytes.
So we're going to have, what is this, a hundred times more? One thousand, ten thousand, million. Yeah. So there's a hundred times more erythrocytes than we have leukocytes. And erythrocytes, of course, are the red blood cells.
So erythro means red and leuko means white. OK. moving on. So here's a blood smear that shows all of the components of blood. So we have the erythrocytes, as you can see, the most abundant in a blood smear.
Then we would have monocytes. Oh, here's the neutrophils. We actually have two monocytes and a lymphocyte in this picture, but you can see that their numbers are far less than what we find in the red blood cells.
And then platelets are actually fragments of cells. that we'll look at how they get produced. All right. Why is blood considered a connective tissue?
Because it's made from embryonic stem cells that reside in the bone marrow. We can either call it hematopoietic stem cells, or we can call them hemocytoblasts. I'm not sure how you learned that tissue in 201, or in the AMP1, when you did tissue types.
or even with connective tissue. I guess that's probably where you would have discussed it. But those are the cells that are going to give rise to all blood cells, and it comes from mesenchyme.
So mesenchyme is the embryonic connective tissue that will give rise to fibroblasts, chondroblasts, osteoblasts, and hemocytoblasts. And what's interesting, when we take a look at the cell formation line, you'll see how osteoclasts actually come from hemocytoblasts and not from osteoprogenitor cells, which is really kind of interesting. Okay, so what are the functions of blood?
We have a distribution function to carry everything through the blood. We have a regulation function to regulate body temperature, pH, fluid, volume, among others, but those are the three most important, and then protection. So it's really neat that... Because blood is being carried in a vessel that can be damaged, that the blood itself has the ability to plug up the hole while we wait for the blood vessel to heal itself. And then we also have the ability within our blood to prevent and combat infection so that we're protecting against infection, we're protecting against blood loss.
Okay, so here's our plasma, as we saw in the... Or in this next slide, well actually we did see in the first slide that the plasma is about 92% water, so we're going to go with 90% water. Upwards of 100 different dissolved substances or solutes that we can have in different categories.
See this isn't right so from the video before or from the book before so we're going to cross that out and we're going to put 0.9% saline. is isotonic so that's going to be the same as what our plasma is greater than this is hypertonic and and we'll talk a lot about this when we get into water balance and with the urinary system so if we're dehydrated we'll have a hypertonic plasma we drink too much water and our kidneys are not able able to eliminate all that water then we'll have over hydration so albumin uh most of plasma proteins are made by the liver with the exception of um of the globulins which are going to be made by um uh leuko or i mean lymphocytes uh but albumin is the most abundant to maintain something called osmotic pressure of the blood and then we have shuttles so we have the ubers for our um for our lipid soluble hormones then buffers and clotting proteins and then our globulins So really quickly, I want to show you the significance of albumin because we're going to talk about this again with cardiovascular system and capillary dynamics. But it is vital that we and then again, when we do urinary system, but it's vital that we understand the role of albumin within a capillary.
So here is our capillary. We're over here on the arterial end. And this is this will be the venule end. So as blood is entering a capillary, we'll label it. the pressure of the presence of the blood in that capillary is going to push against the wall.
So we can essentially say this is capillary blood pressure. We call it hydrostatic pressure. So HP stands for hydrostatic pressure. And that is pressure just due to the presence of blood within the vessel.
And what it's going to do is push water. and the dissolved substances out into the interstitial fluid. And if we draw a capillary, that's not very even.
Divide that very evenly. But as we move down a capillary over to the venule end, we can see that hydrostatic pressure is decreasing just due to the fact that we have a volume of blood that's leaving, plus we have more resistance happening. And as our blood is becoming more viscous because we're losing more water, But what it, oh, so then this process of the water moving out of the capillary we call filtration.
So on the arterial end. of a capillary, filtration is going to be the dominant force. And then we get to about the middle of the capillary bed and we can see, it should be a little bit higher up here, that hydrostatic pressure or hydrostatic pressure down here and whatever this pressure is up here are going to be equal.
But then as we move towards the venule end, then we start to get into whatever this pressure was that's all the way up here. Down here that is the prevailing pressure at the venule end of a capillary and that's called osmotic pressure. So OP stands for osmotic pressure. Now, or we can also call it oncotic pressure. You might have seen that before.
All right. So what osmotic pressure is going to do is draw water back in. So we had filtration on the arterial end. We're going to have reabsorption on the venule end. And the reason why we have absorption is the presence of albumin.
So here's just in my world, in case you don't know, this is a protein. When I was in grad school, my cell biology class, a professor comes in one day. We're talking about proteins and he goes, how do you draw a protein? And we're just kind of sitting there going, I don't know. And so he just went up to the board and he drew a scribble.
And so this is really, if you, if you look at any, um, you Google any plasma protein or any protein, sorry, not just plasma protein, any protein structure, it's three-dimensional structure. It's tertiary structure, uh, looks very much like a scribble. And, um, and so with my albumin, I always make my albumin little clouds, but it's a protein because I always like to write albumin inside.
So that's why it's a cloud. So there's our proteins. Now, albumin was down here, and albumin is a non-diffusible protein. So, albumin needs to be non-diffusible.
So, it has to remain, I don't know. So, albumin is going to be present in the blood, but it will not leave the bloodstream. So, we can't rely on sodium.
As we said before, water always follows salt. Well, guess what? Water's leaving, but so is sodium too. So I can't rely on sodium within the capillary to draw the water back in.
So I have to use another substance, another solute, that's going to increase the likelihood for osmosis to happen. And that's what osmotic pressure is, is that it generates osmosis. So once the water decreases as we move towards the venule end of the capillary, sorry.
the albumin concentration increases. So we have a higher albumin concentration on the venule end of the capillary than we do on the arterial end of the capillary. And therefore, water will be drawn toward the albumin and it's a pull.
So this is a pull back into the capillary. This is a push out of the capillary. So that's the significance of albumin. And we absolutely have to have albumin. We can see in people with liver...
failure. You might've seen people with the CDs, uh, where they have that very swollen abdomen, or they may have, um, um, swollen appendages. So ankles and wrists may be very swollen, um, because the liver isn't functioning properly. It can't, doesn't make enough albumin.
And therefore you don't, the water gets pushed out. The hydrostatic pressure pushes it out, but the osmotic pressure doesn't bring it back. Excuse me. Um, my son is a funeral director.
had a client, patient, and he's not a patient anymore. I don't know what he calls them. Anyway, he picked up an individual at the hospital that had passed away and he was getting ready to embalm him. And he says, mom, I've never seen anybody with an abdomen as distended as that.
And I said, did he die of liver failure? And he said, yeah. And I said, well, there you go.
And so my son did not take A&P 2 with me. He took A&P 1 with me, but he didn't do A&P 2 because he got married and then went off to mortuary school. And so he didn't know what the purpose of the albumin was.
So there you go. Also, kwashiokor. So if you have... protein malnutrition those you've seen malnourished children with those very distended bellies and very thin arms and legs due to their lack of protein in their diet they will get kwashiorkor.
And that's why it's because now all of that fluid is deposited abdominally and not brought back into their vasculature. So there's a whole bunch of that, most of which is not going to be on the exam, just what's in your notes. But we will absolutely talk about this again.
So the more you're exposed to how this works, so much better is it going to be for you, especially you. as you move on from, from AMP2 into other classes, especially if you're going into the nursing program and you've got fluid shifts and things that you need to be aware of with your patient, this is a very, very important component of how fluid shifts happen in the body. So there that is.
All right. So we can take a look at the components. So we, we talked about that albumin. It exerts osmotic force to retain fluid within the blood, contributes to blood viscosity if we're concerned about blood pressure, which we'll talk about later, and then can also be responsible for the transports of some ions and lipids and hormones.
Then the globulins, especially these gamma globulins, are going to be the antibodies. And then the fibrinogen is part of clotting. And then regulatory proteins, as I said, were enzymes and hormones. Then here's the electrolytes, nutrients, respiratory gases, and wastes.
And then here are the electrolytes that we primarily find within the blood. Oh, forgot hydrogen. Sorry about that, friends. Oh, and bicarbonate. I forgot about that.
Now, okay, not very little. We're going to put very little, very little phosphate in your plasma because it binds with calcium. And then now you don't have free calcium for...
uh whatever we need it to be so um release a neurotransmitter muscle contraction blood clotting second messenger to get into our into our cells if it's bound with phosphate then it's done and so parathyroid hormone is going to cause our kidneys to eliminate phosphate from the body okay then here are the nutrients and other molecules our lipids found within then lactate the same as lactococci Okay, let's put that in there. All right. So formed elements of hematocrit are the number of erythrocytes or the concentration of erythrocytes that we have, approximately 5 million per microliter or cubic millimeter, same thing. Now, one thing about red blood cells, they are biconcave disks. We're going to talk about why they are biconcave disks.
They are a nucleate. And they are flexible for travel through the capillaries. And so let's just go ahead and talk about why they need to be biconcave discs.
So biconcave means that it dips in on both sides. So if we looked at it from a side view, if we looked at it from a top view, it would look like this. Not a complete hole, just a depression inside of there. Now, we would think, oh, and let's just talk about anucleate, which means no nucleus.
Why would you not want to have a nucleus in your red blood cells? More room for hemoglobin. And because your red blood cells come from the bone marrow, they do not have to repair themselves.
They do not have to mitotically divide. So therefore, you do not need to have a red blood cell with a nucleus. Now, this is really important. Why it's biconcave disc. So it's all about gas exchange.
So notice right here, we said a huge surface area to volume ratio suited for gas exchange. So if you've seen the movie Divergent or you've read the book, it's about Chicago after this post-apocalyptic Chicago. And there are these four groups of children and you have the Dauntless. And this particular group is characterized by their ability to drive to jump on the L.
So the L never stopped. It just it never stops at any stops. It's just always traveling the elevated railroad.
Anyway, passenger train subway. There we go. It's an L.
It's an elevated subway. And so the L is always traveling. And so they have to learn how if they want to be part of that group, they have to learn how.
to jump onto the train and off of the train. So if you're a little dauntless person or you're a hemoglobin with oxygen, carrying, or whoops, if you're in your tissues, or you're a little hemoglobin without oxygen, deoxyhemoglobin, you need to be right next to the edge. And you want to have lots of your train car doors, you want them to be open all the time, so that you can get on and off.
And so you want to be right next to the edge or right next to the platform if you want to jump onto the red blood cell, or like this. You want to be next to the platform if this is an alveolus. And so our red blood cells are such that there's lots of surface area, lots of places to put hemoglobin. Because if I have a hemoglobin in the middle, he's not going to be able to exchange anything.
So we've given up the volume. Sure, I could put a lot more hemoglobin in here if I had a spherical red blood cell, but These are the only ones that could be against the edge. And then these guys that are in the middle are never going to be able to get any oxygen.
So by maximizing the surface area or the perimeter of our red blood cell, then we have more places for gas exchange to take place. And that is why a red blood cell is a biconcave disc. This video, if you click on it in the PowerPoint, it'll show you. a capillary.
And one thing about red blood cells is they pass through a capillary. A capillary is the barely larger than the width of a red blood cell. And so the red blood cells have to stack up in a stack. We call it a rouleau. And so that's their stack of red blood cells as they're passing through.
And this just shows that happening. Okay. Oh, red blood cells live about 120 days.
And here is hematocrit. Okay. Well, not hematocrit, but actual number. So 4.8 million males have 5.4 because they have more oxygen demand.
And so they tend to have a little bit more. Leukocyte. So here are the groups and they're larger.
They initiate the immune response, defend against harmful substances. How long do they live? 12 hours, especially if they're in... If they're engaged in an active infection, they eat up a little bit of stuff and then they die. And then they turn into pus.
And so neutrophils are pus. Well, that's part of the pus. And then lymphocytes, though, we hope they last for years because those are the ones that are going to confer lifelong immunity to things once we've been exposed to it.
So they should last our entire lifetime. Some of them. You don't always just have one, but we'll talk more about that with immunity.
And then the platelets, they're smaller than a red blood cell and participate in hemostasis. And they'll live about eight to 10 days. And then there's their numbers and then there's their numbers. All right. This just shows the path of development from a hemocytoblast.
OK, so hemopoiesis. So you've got two cell lines. Don't even worry about that. Just how we develop.
from our progenitor cell into a red blood cell. You can see we go through a lot of changes. We kick out the nucleus here when we're a reticulocyte as we're becoming a reticulocyte. But we did have a nucleus for a long time.
And then here's platelets. Notice that platelets are going to come from a big giant cell called a mycocaryocyte. And they're actually going to be fragments of cells down there. And then the white blood cells are going to come. some from this myeloid stem cell, some from the lymphoid stem cell.
So these are going to be the lymphocytes. And then everybody else are going to come from also the same cells that red blood cells and platelets came from. And then here is what's crazy.
So this monocyte, this progenitor cell, is also going to give rise to osteoclasts. bone cells that take the calcium out of the bone and put it into the bloodstream, which is really crazy. But yeah, they have very similar functions, so it makes sense.
Okay, so here is the structure of a red blood cell. Notice we're going to have a lot of surface area here and about 280 million hemoglobin molecules in a red blood cell. And then here is that rouleau where they stack up as they're passing through a capillary. All right, hemoglobin, it will bind easily and reversibly to oxygen. So four globins and four hemes.
We'll take a look at that picture in just a minute. So four molecules of oxygen combined to one hemoglobin molecule. Here is our level of hemoglobin in our bloodstream is 12 to 18 grams per deciliter.
A lot of times we'll take a look at like blood sugar is milligrams. This is actually grams. per deciliter of blood, 100 milliliters of blood.
Oxyhemoglobin is when hemoglobin is bound to oxygen. It looks like this. This is the formula that we use for that.
It's oxygenated and bright red. Deoxyhemoglobin is deoxygenated and dark red. And hemoglobin is never going to be by itself.
So if there isn't an oxygen molecule bound to hemoglobin, it'll bind to a hydrogen ion or atom and hydrogen ion. Yeah. And so it can be a buffer as well.
All right, so there are two alpha chains, two beta chains with the central heme molecule with an iron in the middle. And O2 will bind to the iron. And I have a picture of that. Carbon dioxide will also bind to hemoglobin, but it will bind to the globin. And it forms this molecule called carbon aminohemoglobin.
But we're just going to do that with respiration. So you don't need to know that right now. So here is one hemoglobin molecule. So you can see we have two alpha chains, alpha one and alpha two. We have two beta chains, beta one and beta two.
And then we have a heme. So each globin molecule has a heme in the middle with a central iron. And that's what the oxygen is going to bind to. And so we have four oxygen atoms or molecules, oxygen molecules binding to the hemes in the hemoglobin. OK, hematopoiesis, specifically erythropoiesis.
So this is the formation of blood. Erythropoiesis is the formation of red blood cells. We know that it occurs in the bone marrow.
Cells arise from hematopoietic pluripotent stem cells, which means that they can make different cells. So if we go back and just really quickly take a look at this one hemocytoblast, this is what it begins. can become so one two three four five six seven eight nine different cells so that makes it pluripotent that it can end up being a variety of cell types okay what do we need for um uh erythrocyte production we absolutely have to have iron we must have vitamin b12 and we must have folic acid for proper formation and Talk more about that, what happens if you don't have it in a little bit. All right, 120 days removed from circulation by the spleen.
My on-campus students always refer to the spleen as the red blood cell graveyard because they just get taken out of circulation. And like we said, due to the lack of nucleus, red blood cells cannot repair themselves. But when we... we get into immunity, then we'll talk more, or the lymphatic system, we'll talk more about the spleen and how it's going to break down the components of hemoglobin and what it's going to save.
The iron, namely the rest of the material, will be broken down and eliminated from our body in bio. All right, so what stimulates red blood cell production is erythropoietin or EPO that's released from the kidneys. And what is the stimulus is hypoxia.
So lack of O2 in your tissues. So how can I have a lack of O2? How can I have hypoxia? Hypoxia?
Not enough red blood cells. So maybe I'm hemorrhaging. Maybe I have excessive red blood cell production or destruction.
What's going to cause that? I may have malaria. So I can have the plasmodium organism in there can cause. hemolysis. Maybe I have a strep infection that can cause hemolysis.
Maybe I've been exposed to chemotherapy. Mostly ionizing radiation though is going to cause our red blood cells to be destroyed. So those things will account for a reduced red blood cell number.
Erythropretin will also be stimulated if I'm it. if I don't have enough O2. So maybe I'm at a high elevation or maybe I have pneumonia. And so my blood is not being oxygenated like it should, because I don't have, I have too much fluid in my lungs and the oxygen can't pass through the fluid and get into the bloodstream as quickly as it needs to, because the blood never stops moving as it's passing through the lungs.
And so you have a quarter of a second to fully oxygenate the blood. red blood cells that are passing by in that amount of time. And so if pneumonia is causing too much fluid in the way, then the O2 was not going to be able to load onto the red blood cells.
And then also increased tissue demands, aerobic exercise, or some other kind of homeostatic imbalance, but primarily aerobic exercise. If you're training for a marathon, you're going to make more red blood cells for that. And just because your body keeps saying, I need O2, I need O2, I need O2, and that will be one of the effects of training for a marathon. Especially if you train for a marathon at a high altitude, then you're really going to have enough, lots of red blood cells.
And that's why our Olympic teams train in Colorado Springs, because of the high elevation. So here is just showing all of that happen. So you can take a look at that. And then this is the recycling of blood.
So this is taking it out in the spleen and what we're doing with everything. And I don't need you to know any of these steps, but you can take a look at that at your leisure. It's in the book. OK, erythrocyte disorders continued.
So anemia is low oxygen carrying capacity due to insufficient red blood cell numbers. So hemorrhagic anemia is blood loss. hemolytic anemia well i guess this is the first of the disorders but we're talking about hypoxia so hemolytic anemia the red blood cells lice maybe you have abnormal hemoglobin in sickle cell anemia for example or thalassemia uh transfusion mismatch if you don't get the right red blood cells then um you're gonna eat them the macrophages are gonna eat them up complement can attack them and And and then we can get anemia and that because we're lysing the red blood cells and then parasitic or bacterial infections, like I said, with malaria or strep infections and then aplastic anemia. So this is the destruction or inhibition of the bone marrow.
So I can't even make it to begin with. So a lot of things, toxins, drugs, ionizing radiation also can destroy the red blood or the bone marrow. A decreased hemoglobin content can also cause this to be anemic.
So maybe I have iron deficiency anemia. I'm going to make little tiny cells if I don't have the iron that I need. We call them microsites.
If I have pernicious anemia, lack of vitamin B12, the cells are inefficient in carrying oxygen because they haven't gone from that. Let's go back here really quick. If we look at the steps, vitamin B12 is necessary to go.
down this pathway. And if I don't have vitamin B12, then I can't make my red blood cells and they're going to stay arrested up in this level. And so they're not going to be efficient in carrying out to you. And we'll get those macrocytes, those big cells forming. Okay.
And then abnormal hemoglobin that could cause this hemolytic anemia, we can get lysis of the red blood cells. But also, if the hemoglobin isn't formed properly, then it won't be able to carry the oxygen either. And we will get sickle cell anemia, which I'll show you a picture of in a minute, or thalassemia. I have a really cool story to tell you about thalassemia in just a second.
And then polycythemia, this is what if I have too many. So this before was not enough. So I didn't have enough red blood cells.
I get anemia. But if I have too many, because maybe I've been blood doping, so I've been cheating. We talked about that with the EPO in the hormone chapter. Too many red blood cells makes the blood more viscous and sludgy and it's hard to push blood around.
But you can be naturally polycythemic if you are an Olympic athlete. And I and I would hazard a guess that any of our Olympic athletes that train at. Colorado Springs, if we measured their blood, they would definitely have a hematocrit of over 50, all of them. So more red blood cells than they actually do plasma. But their cardiovascular system is strong enough because they've been training to push that thick and sludgy blood around.
Okay, so let me just tell you this quick story about thalassemia. So both thalassemia and sickle cell anemia are... typically found in individuals of other than Caucasian ancestry to Western European.
I shouldn't say that. Not British Isles. Just let's leave it that way. So sickle cell anemia, typically African-American black populations are.
This is where we find the gene for sickle cell anemia, which we'll talk more about in just a minute. But I want to tell my thalassemia story. So thalassemia is from Eastern European Greece and the diaspora from the Holy Land from Israel out into the world so a lot of times with Ashkenazi Jews that moved to Romanian and Greece and Albanian countries over there had a thalassemia gene just like African descent people have sickle cell anemia gene so so I have a friend who is a um oh she's very scandinavian she's very blonde hair blue height blue eyed and um married a jensen who was also very blonde hair blue eyed so their kids are all recessive they're all blonde hair blue eyed and um uh so we were talking one day and she said something about her sister's thalassemia i was like wait a minute your sister has thalassemia she said yeah my grandma has thalassemia too So, you know, I just kind of stood there with my mouth open. She goes, OK, let me tell you the story. So when her great grandmother was coming across to America on the boat, she ended up in America pregnant with her grandma and my friend's grandma and her friends, her biological father.
was a Greek sailor on the ship at the time. And, and so he was carrying a thalassemia gene and, and her grandma got it and then passed that gene on to her sister. And so I was like, oh, that's really interesting.
Because if she had been Northern, you know, like Scandinavia, Northern Europe, chances of having her, of her having thalassemia in her family are very, very low. Um, so anyway, I just, I always like that kind of thing. I love that kind of thing.
All right. So with sickle cell anemia, what happens is the gene, we have one base pair mismatch. Um, so in the sixth, um, amino acid that comes for glutamate, we actually substitute one base pair.
So it's a substitution, not mismatch, but a substitution. And you get a, I don't know, it's either an A and a T instead of a C and a G. And I think, and you get valine in the place, in the sixth amino acid out of 146 amino acids.
This is all it takes is one base pair substitution and you get this valine right here. And that will cause this misshapen erythrocytes. And they get plugged up in capillaries.
They can't get transported through. We get oxygen deprivation in our organs. Very, very painful and ultimately death. And. just from one mistake in your DNA out of 146 amino acids.
So that's 438 codons, or I mean, base pairs. So just one out of 438 base pairs makes this mistake, which is crazy. Okay, so let's talk really quickly about blood typings. So I think we'll go over this more in the lab video. So I just want to reiterate what we have with blood typing.
So if you're a blood type A individual, you are going to have an antigen on the surface, which we refer to as antigen A, and it has a particular shape. And in your plasma, you will have antibodies that will attach to the B antigen. So you have the opposite antibody.
to the antigens that you possess. Then if you are a type B person, you are going to have a B antigen, which has a structure different from A, and you will have the antibodies that will bind to the A antibodies or the A antigens. Okay.
So type A people can't get type B blood. Type B people can't get type A blood. Type AB people have both antigens, and so they can't have either antibodies. And therefore...
they can take any blood type. And so they are known as the universal recipient. So they can get any of the blood types. And then a type O person has no antigens on the surface.
And so these guys have both. These guys have nobody. And so they have both antibodies because they have no antigens. And so this... is not going to elicit.
So this type O red blood cell will not elicit an immune response from any of the other blood types. So we call them the universal donor. Now, to truly be the universal donor and the universal recipient, you have to be AB positive, which means you have another antigen. You have the RH antigen on the surface or the D antigen.
And therefore, they don't have any antibodies. So they will not attack in a positive blood type. And so the universal recipient is truly AB positive. And then an RH negative has no antibodies unless exposed to RH positive blood. We'll talk about in the lab video.
And and so the universal donor is actually O negative because they don't have anything to trigger an immune response and cause a tissue mismatch in a in a in a blood transfusion rejection. So this just shows what it looks like if you get the right blood type. There's no agglutination, so there's no clumping of blood.
But if you get the wrong blood type, so you have the antibodies in here that are going to bind to it. So if you take A to a B recipient, so an A donor to a B recipient, then the B antibodies are going to attack the A antibodies or the antibodies. against A that the B type person has. And then you'll get clumping and hemolysis and then unsuccessful blood type match.
Okay. And then I'm going to leave this for talking about in lab. And this is why an Rh negative mother needs to have a RhoGAM shot with her pregnancies.
Okay. Leukocytes. so leukocytes the white blood cells there's there we just put 4 500 whatever so just as long as we're in the 4 000 range to the 11 000 range i'm okay with that their job is defense against disease and um their job they must leave so extravasation means to leave the blood vessel so in order to do that There are three processes, margination, diapedesis, and chemotaxis is movement towards the chemical.
Once they have stuck to the capillary wall and move through the capillary wall, and then they travel to where the infection is. And I will make that so that you can watch that. And then leukopoiesis is white blood cell production. from the bone marrow and this is usually due during infection or during we'll put infection and um inflammation so those are the triggers and and they will secrete um leukocytosis uh stimulating factors so that the bone marrow will produce the white blood cells during an infection and so A greater than 11,000 number is a normal homeostatic response to invasion.
We're just fine with that. And like I said, we'll talk a lot more about white blood cells when we get into immunity. This just shows what they look like, but you're not ever going to have to identify them or know any really specific characteristics like lobed nuclei, that the cytoplasmic granules are.
stain and eosinthes stain so they look red you're not going to need to know any of that but there that is if you care okay so um white blood cells come in two versions they come in granulocytes so let's just go back to this picture so these right here the eosinophils or i mean the neutrophils the eosinophils and the basophils if we look in here there's little dots in their cytoplasm so this is a neutral stain so they're kind of a purpley color. This is a eosin stain. So these are, this is a neutral stain, eosin stain.
So they're red and this is a basophil stain or a basic stain. So they're purple. They have, and here you can see in the drawings.
So inside of them, they're going to have enzymes that are going to help digest things, help destroy what they're trying to attack. Lymphocytes and monocytes on the other hand are the agranulocytes. So right here, the agranulocytes, they do not have cytoplasmic granules. Okay, so A means without, so without granules. The granulocytes, at least the neutrophils, are primarily phagocytic.
They are the most numerous, and so here's never let monkeys eat bananas. Granules contain peroxidases and hydrolytic enzymes. They are definitely attracted to a site of acute infection, because remember they only live about 12 hours.
And so as soon as that inflammation is happening, they're going to be there. They are very phagocytic, as I said, and they love to eat bacteria. That's what they're going to eat up. Okay, granulocytes, no, eosinophils, sorry, they attack parasitic worms, also help lessen the severity of allergies.
If I have, let's say I have a hookworm or a pinworm that's traveling through my bloodstream, what they're going to do is the eosinophils because they're much smaller than the hookworms. I mean, they're not probably not even that big compared to the hookworm. What they're going to do is sit on the outside and then they're going to release their hydrolytic enzymes from their cytoplasmic granules on top of the parasitic worm. And then basophils contain histamine usually during allergies, but we're just know that they have histamine in them.
And then when we talk about allergies, then we'll talk more about them. So there are the three. So this would be a neutrophil.
This would be a vasophil. This would be an eosinophil. Okay.
And then the agranulocytes will be the lymphocytes. They are the second most. There are T lymphocytes and there are B lymphocytes.
And the monocytes are the largest of cells. They become macrophages when they leave the bloodstream. Okay, and again, we will discuss these at length when we do immunity. All right, leukocyte disorders, leukopenia, if I do not have, so anytime you see penia, it's a low amount. It's a lack of.
So a lot of times when people are taking medications, particularly anti-cancer drugs, they will end up with leukopenia and they'll be very susceptible to infection. Okay, so that's why a lot of times they, well, not all the time. A lot of times, all the time. If you have a person who is under chemotherapy living in your home, you can get a vaccination exemption for your children.
Because if they have any live vaccines that they're taking, they can shed live viruses and the attenuated ones. And then the person on chemotherapy could get an infection from that. And so we have to be careful with the kind of vaccines that we give.
um individuals when they when they live with people who are immunocompromised or immunosuppressed um leukemia is a is cancer where we have a single white blood cell that just went crazy just went haywire and just started making multiple copies of itself because it has nucleus and therefore it can divide and so those oncogenes turned on and it just made lots and lots of copies of itself um infectious mononucleosis. This is if you get the Epstein-Barr virus. So mono can reside in your cells for the rest of your life and excess agranulocytes will result and they will impair your, you know, when you feel like you're just tired and you may have a sore throat and different kinds of symptoms that you get with Epstein-Barr.
But I just need you to know mono is Epstein-Barr and you get more agranulocytes. Okay, then thrombocytes are the platelets. They are actually fragments of cells called megakaryocytes.
They're the big cells, and they will form platelet plugs in hemostasis. We'll talk about that with hemostasis. Their job is to bind to collagen fibers to become active, and we'll discuss that as how they work.
They also work by a positive feedback mechanism. The more platelets begin to cling in a damaged area, the more platelets will cling. So it just accelerates the clotting process. And they also provide a site for the activation of inactive clotting factors so that a clot may happen.
And this is just what they look like as they're entering the blood cell. They're just little fragments of cells. And that's where we're going to leave this video.
And we'll take up in the next video with hemostasis.