1st part of the chapter, goes up to blood typing.
Okay… we are starting blood. I've got two
videos here and I'm going to get all the way
to the beginning of blood typing in this
first one. I want to take you to two
really excellent websites. Again, I've got
these websites in, oops– the wrong one–in GREAT
WEBSITES (in eCampus) linked so you can see it in more
detail. This one is called Red Gold, the Epic
Story of Blood. A really excellent website
put together by PBS. They had a
presentation on this on television and
they put together a really detailed
website on it. So you can look at it in
more detail. It does a really good job–also
has some videos and things like that. And the
other one that's just excellent is Blood
Book.com. Over on the left you see a
menu and it's got all sorts of
information about blood types and how
blood typing is done, transfusions, all
sorts of things like that. So really–2
great, great, great resources. There's lots
more than that, but I'm just going to
take you over there.
Alright, so let's go back to blood then.
Um, alright.
Okay, so…… at the end of this chapter in
lecture, we're going to talk about some
weird stuff related to blood like
leeches and bloodletting–references on
these two pictures over here. But let's
get into the meat of this material. We're
in the area called hematology—study
about blood.
Remember your tissues–nervous, muscle, epithelial, connective. Blood is a
specialized connective tissue. Its
functions—well, it has got lots. It carries
gases, it carries hormones,
it has buffers for pH maintenance to
keep your tissues in a kind of a neutral pH
range, it carries nutrients and waste
products and heat (by-product of
respiration), maintains your core body
temperature. So anyway, there is a bunch of them right there. Alright, so let me point
out a couple things here. You are looking
at a cut section of a (let me change colors)
cut section of a blood vessel, with an electron
micrograph right over here. And, here is
the blood vessel, and there is a white
blood cell right there. This is a color
enhanced photo, by the way. And these are
your red blood cells. It does a
really nice job of showing you shape. Here is your typical shape. From the edge,
it is called by concave because it is
concave on both sides. That is because
its nucleus has been extruded. We will
talk about that more coming up. But
notice the way these red blood cells
kind of stack like coins. If you were
to put coins in a, like, a little
sleeve like nickels or dimes or
something, they would kind of fit together. Blood cells do the same thing. That
allows them to go through very tiny
blood vessels.
Sometimes the blood vessels may only be
the thickness of the width of a red
blood cell. The amount of blood that you
have—you've got around four
or five liters. That's about a gallon and
a half of blood. PH not exactly 7:
it is a tad alkaline, about 7.4. Okay,
so let's get moving a little bit more.
There are some things in your notes, some
features of blood: be sure to take a look
at them. I am not going to spend any
time going over them now. All right, so
we are going to start with plasma first and
what you see in the picture is plasma.
Here is the plasma, right there. Now notice
that all the cells and the elements of
blood have settled down at the bottom.
Now, there are two ways that this
can happen. Number one–you can actually
put the tube in a centrifuge and spin it
down, so all the red cells and white
cells, and the platelets end up at the bottom.
Or you could let this tube sit for many
hours, and all of those all of the cells
and the formed elements will–because
they are heavier than plasma—will settle
down to the bottom. We will talk more about that coming up, so let's talk about
what is in this plasma. Okay. Mainly water,
lots of plasma proteins. There are 3
major groups. Let us go with the easy one
first. Fibrinogen and it's relatives–clot.
These are clotting proteins. They
come from the liver. Albumins—this is the
biggest group of the plasma proteins,
comes from the liver. Also, these are very
important in maintaining osmotic
pressure in the blood, that is, to keep
blood plasma– water– from leaking out of
the blood vessels into your tissues.
We are going to talk about that way more when we get into the circulatory system.
Albumins are large proteins: they
can't get out of the blood.
Generally, they cannot get out of the
capillary walls, so they are stuck inside
the blood. Now, the third group is the
globulin group. You have heard of these
before. You may have heard of gamma
globulin, another name for antibody.
Antibodies are in this group. There are
some odds and ends globulins like transferrin,
we will talk about more in just a minute.
Some are made in the liver , some not made in
the liver. Antibodies are not made in the
liver. Other things in plasma –there are
some dissolved things in plasma: oxygen
and carbon dioxide, nutrients, hormones,
waste products, bile pigments–things like
that. Okay, so let us talk about plasma
versus serum. All right–so. In order to understand this, you need
to go back to this fibrinogen right here,
and we need to talk about this area—the
plasma that I highlighted here. (And let
me just erase that right there). Okay, so
in the plasma that you see here, in
addition to all that other stuff. (I'm just
going to center on fibrinogen now), is
clotting factor. i It is up in here. All
right. It is not doing anything: it's inactive.
All right, so it's just floating around
in plasma, doing nothing. Now, let us say
that I take another tube of blood–here is
a tube of blood (and change to red here).
And here is my tube, here is my blood right
there, and this tube is a plain glass
tube that has no anticoagulant in it.
Now this other tube right here has an
anticoagulant in it. It has to because, if
there wasn't an anticoagulant there, that
blood would have clotted and there is
no clot in this tube. But in this tube
that we are talking about now– we are going to make a clot. All right, so. Just a plain
glass tube, we put the blood in and what
will happen is the fibrinogen, which is
normally floating around free in the
plasma, gets involved in binding to other
proteins involved in clotting and we end
up. That catches red blood cells and
forms a large clot material that looks
like this. Right? Now, there is still going
to be some some fluid up here at
the top, but it's not going to be called
plasma: it is going to be called serum. It is
different from plasma. Remember, this is
called plasma over here. Now the
difference–everything is exactly the
same. All the plasma proteins of albumin
and globulin and waste products and
bilirubin and glucose and all that , but
the big difference is this fibrinogen
group. In the tube that had an
anticoagulant on the right, where there
is no clot, the fibrinogen and the other
clotting proteins were floating around
in the plasma. No clot, not involved in a clot. But in this tube
right here, that has no anticoagulant,
where is the fibrinogen? (I am going to make…
I'm going to go to blue now). The
fibrinogen is now involved down here in
the clot. It is what is causing the clot
so the fibrinogen is not floating around
free anymore in the fluid: it is down here
in the clot. Now, as a result of that, this
area up here is no longer called plasma
because it has no fibrinogen in it,
It is called serum. So you could say that
serum
is plasma without any clotting proteins
in it, because the clotting proteins are
involved in the clot. It is a fine point, you may be thinking, but those terms are
used a lot– serum versus plasma–and they
are not the same term. Okay
Remember I said you could take a blood
sample and spin it down in a centrifuge?
Well, there is a centrifuge right there.
We are going to be doing it this in a lab. That is
what has been done in this tube. So
remember, this tube is coated with or the
blood has added to it an anticoagulant.
That is what is keeping this from clotting.
This is unclotted blood. All right. So
what happens then is all the solid
elements of blood get pulled down to the
bottom. You see all the red: this is where
the RBCs are, down here. The white blood
cells and platelets are lighter than red
blood cells: they hang out right here at
the interface between plasma and the red
cells. And all this stuff up here is
plasma. It can sit there forever: it's
never going to clot. This process of
separating out the formed elements from
the plasma is a very important test It is
called a hematocrit, and we are going to be
doing it in lab. The hematocrit measures
packed cell volume, in other words, what
percent of the whole blood is packed
cells. That is, the have been packed down
here because they have been centrifuged,
so all the red cells are pulled down,
white cells and platelets also— packed cell
volume. Normally, it is about 40%, which
means that, let's say, your hematocrit is 42, which is average for a woman. 42
percent of your blood is packed cell
volume: 58 percent is plasma. Now, 42
% is right at the average for a
woman–plus or minus 5%. So, in
other words,
5% more–5% less, that
would take you from about 37 % up
to 47%. It is normal for a female:
that's your normal range, with the
average being 4.2 But a male males
have more red cells–47% plus or
minus 5 %. So 42% lower
range up to 52% for higher range,
for a male.
So, although 44–nah, let's go 40. Although
40 percent might be normal for a female,
that is not normal for a male. We are out
of the range. Okay—views of red blood
cells. I mentioned biconcave. Notice they
have no nucleus. We'll talk more about.
Notice that when you're looking at
them straight on they look round, but
they are biconcave. They are amitotic:
they do not reproduce. A red cell cannot
make baby red cells: they all come from
bone marrow and that's because they have
no nucleus, and they have no DNA and no chromosomes and I they have
genetic blueprint for reproduction. They are basically oxygen carriers and
co2 carriers via hemoglobin. That is it.
Because they have to carry oxygen to
their target site to your tissues,
you don't want red cells to use up their
own oxygen load. That would be like you
delivering Blue Bell ice cream in a
truck and multiple times during the day
you go to the back and eat bunches of
ice cream. By the time you get to
your place where you are going to drop it
off, you have eaten half the ice cream.
Same thing. Therefore, red blood cells do
not undergo aerobic respiration: they
undergo an anaerobic way of making ATP
so they don't use up their oxygen load. Counts… counts are given per cubic
millimeter–men about a million higher
than women. Again, you see the range.
Newborns have a very high red cell
count because they are compensating.
Their bone marrow puts out a bunch of
red cells right at birth to pick up any
available oxygen molecules that might be
hanging out. Because the newborns are
transitioning from getting oxygen from
the mom via the placenta to picking up
their own oxygen out of the air, and so
they have a higher count it. It goes down.
All right… so let's go more into that.
Okay….hemoglobin. You are looking at a
hemoglobin molecule up here. (Get rid of
that) All right.. so here is a hemoglobin
molecule. There are four chains here— two
different kinds of chains, alpha chains
and beta chains. Here is an alpha chain…
here is an alpha chain. Here is a beta
chain… here is a beta chain. The alphas are the same and the betas are the same but
they are not similar to each other. All
right. Iin the middle of each of these
chains is this guy in green which you
see over on the right. It is called a
heme molecule and right in the center of
that heme (oops, it's not marking right)
there is an iron. You see it in the very
center and that is where oxygen is going to
bind. Remember that (let me get rid of all
these lines… there) we are.
Well…..
Okay, all the lines are gone now.
Where was I? Oxygen is going to bind to the heme. Carbon
dioxide also binds to hemoglobin but it
doesn't bind anywhere on this guy.
Whoopsie…get back over to that other picture here.
There we go.
CO2 binds on the globin molecule… these
chains. So again, globin refers to the amino acid
chains of the alpha and beta…. the
polypeptide chains.
Those are globin structures. And the heme is that structure right there. Okay.
Hemoglobin is given per hundred milliliters
of blood. Most of the levels of things
that are in blood, like cholesterol
levels and triglycerides and all that
stuff are given in 100ml amounts or
what's called a deciliter. That is a
hundred mil amount. Hemoglobin is 12 to 18 grams per hundred mls…. women 12 to 14,
men 16 to 18. Again, men have higher
hemoglobin counts. Hemoglobin that has a
high level of oxygen is oxyhemoglobin:
hemoglobin that's bound to carbon
dioxide is carbaminohemoglobin. We are
going to talk about them in the
respiratory system. Now, there is a view
down here showing you a nucleotide base
sequence. You can see ATG bla bla bla bla
bla: this is the sequence along a DNA
molecule for a beta chain for normal
hemoglobin. Look right here and you
see a GAG with an amino acid called
glycine, that will be coded for,
you know, when the mRNA is read with
ribosomes. But look down below
at sickle cell anemia (hemoglobin) and you'll see that instead of GAG you get GTC and that
codes for the amino acid called
valine instead of glycine, which totally
changes your hemoglobin. So sickle cell
hemoglobin is a defective hemoglobin. It
doesn't carry the right amount of oxygen. It tends to stack up in kind of a plate
form as if you were stacking a bunch of
plates on top of each other and it
causes the red cell to get stretched out
in an odd shape. It is called a
sickle shape…it is that sickle cell hemoglobin
doing it. Also notice that there are some
other different kinds of hemoglobin and
another variation of one is a fetal
hemoglobin. Hemoglobin F, F for fetus, you made it when you were a fetus. It latches on
to free oxygen molecules that have come
across from the mother a lot better than
adult or after birth hemoglobin. So this
is a another type of hemoglobin that you
just find in the fetus. By the way, this
is supposed to be HGB not HBG but
anyway. We are going to be measuring hemoglobin in lab. This is a hemoglobinometer
right here— a handheld one. Ours has been broken for many years so
we'll do it a different way. Okay.
Let's go through the life of a red blood
cell. The life of a red blood cell is
only (oops) about a hundred and
twenty days. Let me get rid of that guy
right there… get my blue back again. Okay.
So we are going to start out over here at
bone marrow where the red blood cells
are produced. They go out into the
blood and they now travel around in the
blood, going to all the organs (your blood
goes to organs many times during the day).
And a couple of really important organs
you see here are the liver and spleen.
And in the liver and spleen you have a
bunch of these cells right here and
notice this guy is called a macrophage. He
is a large phagocytic cell. He is a
relative of a monocyte in the blood,
which we'll talk about later. His job is
to remove bacteria and viruses and dead
cells and things that are not supposed
to be there, but in addition to all that
these phagocytic macrophages remove dead and dying red blood cells. You don't want
these defective dying red cells to stay
in circulation: they could stack up and
obstruct, start to obstruct, blood flow,
promote clotting, bla bla bla. All right.
So, at about 120 days these red blood cells are living on borrowed time.
Their membranes have become very
delicate, prone to self-destructing. They
change their shape, and they are like
nabbed in your liver and spleen by these
macrophages. So the macrophage now
destroys the red blood cells and that
frees up the hemoglobin….. right, and the
hemoglobin now is going to break down.
It is going to break down into heme and
then break down to globin, the two
components. Now the globin molecules….
remember they are 4 alpha and beta, two
of each type. The globin molecules are
made,
remember, of just chains of amino acids.
So the globin ends up as individual
amino acids , which can be used by the
liver to make more proteins…the
liver makes a lot of proteins. Or the
amino acids can go out into the blood
and be used by your cells to make their
proteins or they can go any number of
places. Okay, so that's the globin. Now the
heme portion… all right.
Remember heme–primary thing is iron. So
the heme gets broken down to iron and
the rest of the heme ends up as biliverdin and bilirubin. Tthese two guys
are bile pigments. not bile. Do not
confuse bile pigments with bile. Bile
pigments end up in bile, but bile has much
more than just bile pigments. Now, the bile
pigments— I'll get back to heme in a
minute-. The bile pigments go out into the
blood and you have some bile pigments
running around in your blood. But most of
them, as they go through the liver, are
taken out. Your liver uses those bile
pigments to make bile, which you are going to hear more about, and get to the digestive
system. Some of that bile is going to end
up in your large intestine. This is the
large intestine…. well, this is the small
intestine over here and here is the large
intestine over here. Bile gets dumped
right at the.. or into the small intestine,
mixes up with stuff that's ultimately
going to become feces, and what you see
going out down here is fecal matter.
Right here… the green arrow, and the point
they are making here is that the bile
pigments get incorporated into the
pigment that you see in feces, which is a
kind of a green brown pigment. All right.
Now, let's go back to iron, but before we go back to iron, notice also that some of
the bile pigments end up over here in
the kidneys. And there, they are converted
to another variation of a bile pigment
called urobilinogen. And urobilinogen
goes out in urine, giving urine a kind of a yellowish color.
So bile pigments are in urine, at least
they are kid molecules that
they are converted into, in urine and
feces. Okay. Now, let's go back to this
iron right there. The iron needs to
be recycled in the body because remember
that iron is going to be incorporated into
new hemoglobin, in new red cells in
bone marrow. But not all the iron is
going to go to bone marrow. Some of the iron
is going to stay in the liver, where it is
bound in the liver with one of two
protein molecules, either hemosiderin or
ferritin. "Fer" should always tell you iron.
Iron cannot be hanging out by itself.
Iron tends to rust when it comes in
contact with oxygen. You don't want that
happening, so it is actually bound with a
protein in the liver so it doesn't do
liver damage. Now, the same thing with
transport… this iron that has to go
back to the bone marrow is going to be
carried by blood, and of course, there is a
lot of oxygen in blood. You don't want oxygen and iron meeting
because, again, that would promote rust.
The iron that is being transported in
the blood, not as hemoglobin, has to be
bound to a carrier molecule. It is called
transferin and it comes from the liver.
It is the little carrier molecule,
protein carrier molecule, in blood and
that's the way iron gets transported back
to bone marrow. The last the views you're are looking at over here…. normal liver at the
top and hemochromatosis at the bottom. Sometimes
called iron overload disease, you can see
how red brown that liver is. Ultimately
damages and destroys your liver. Okay. We kind of talked about some of this
already. In fact, I think I have talked
about all of this already.
Ferritin is the major storage protein
for iron in the liver. The little kid you
see over here…. look at his eyes, the
whites of his eyes. This has not been
photo-edited. You see kind of a yellow
greenish color—that is jaundice. You can
see it in fingernails and whites of the
eye, and pale skin people. That is from
excess bile pigments that are not being
removed by the liver. Okay…
blood cell production. I've already
introduced you to this. This happens in
bone marrow. We are going to be starting
with a precursor cell called a
hemocytoblast, which is the mother of all blood cells. This is the cell that becomes
white cells, platelets, and everything. But
they develop through difference cells, what are
called stem cell lines. So a
hemocytoblast develops into one
cell line that is going to become red
cells going that way. Aother
hemocytoblast line will develop along
another route. Another one develops
along another route. These would become,
for example, white blood cells. We are
going to follow these red cells over here.
You are looking at bone marrow, by the way,
right over here,
and you can see red cells being produced
right in here. Okay. So this is a scaled
down view of erythropoiesis. Hemopoiesis
means making things from blood, in blood.
There is hemopoiesis, which is the overall.
There is erythropoiesis, making of red
cells. There is leucopoiesis, making white
cells. "Leuco" means white. There is thrombopoiesis, making thrombocytes, which is the
other name for platelets. So thrombopoiesis, erythropoiesis leucopoisis….you will
be seeing these as we move along. Okay.
So where is this bone marrow that's
making red cells? Well, back in 2401 you found out about
the epiphysis and the cancellous bone,
and those are major locations for red
cell production. As an adult, you make them at the ends of
your long bones or you make them in some of the irregular bones, particularly the
os coxa– the pelvic bones–your cranial
bones, your sternum. Those are primary
areas for red cell production, so if
someone is going to get a… if you are a
bone marrow transplant donor,
primarily they would probably either get
that specimen from your sternum
cancellous bone or from your os coxa
pelvic bones, also cancellous bone. They
wouldn't go to the proximal head of your
humerus and get it. I mean that would be
the epiphysis, which is also cancellous
bone, but that is a secondary location for
red cell production. It is much easier to
get it from a sternum. The fetus also makes its own red cells: they don't come from
the mother. There are no maternal red cells that cross the placenta in the fetus.
The
yolk sac makes red cells and the liver
does some also, until its own bone marrow
develops. Alright. So we're going to start
out with a hemocytoblast, which
you see here and you see right there…
okay. So we' are going to skip over some of
these in between stages. They are only
about four stages you need to know… okay.
Let's jump over to this guy right
here and this is called an erythroblast.
Notice that it still has a nucleus. There it
is right there. He is making hemoglobin
and bunches of it, and it's filling up in
the cell. You can see the cell changing
its size and the nucleus is getting smaller.
and it is just basically just making tons
of hemoglobin and eventually right here
is about the point at which it is going to
go from bone marrow out into the blood.
All right… we cross over now into the
blood and at this time this nucleus now
is extruded. That is what you see
happening right there. It then is called
a reticulocyte: it's this guy right here.
He has little bits of, it looks like
maybe bits of nucleus, you can see
there's one right there and one to the
left.
Whereas, this is just a plain Jane
erythrocyte: he has no nuclear material
at all. So that the nuclear material
disintegrated and ejected, and you end up
then with your last phase, which is the
one you know—an erythrocyte.
Erythrocytes are the carriers of oxygen,
obviously, and CO2. Reticulocytes are
important not for any function, but
there's is important test called a
reticulocyte count, which gives a
clinician an idea about how fast bone
marrow is making red blood cells. It is
usually somewhere around 1/2 to 1% of
all your red cells. We will talk more about
it in lecture. Ok. So to make these red
blood cells, what do you need? To go
through this process, obviously you need
iron and you need B complex vitamins in
order to make DNA, in order to make
hemoglobin. And there's another thing
over here you are going to see later. We will
talk about it. It is coming from the
stomach–called intrinsic factor.
Your stomach actually makes it. You don't
get it in your diet. This intrinsic
factor is needed for the absorption of
B12. B12 vitamins come in meat and they
may come in your vitamins that you are taking. But in order to absorb them efficiently,
you have to have intrinsic factor. If you don't have that intrinsic factor,
then you cannot absorb B12 and then you
have an anemia. By the way, the guy down
here is a nucleated red blood cell.
That is this guy right here. You are really
not supposed to see many of these at all.
Okay. What tells bone marrow to make
more or less red cells? EPO, a hormone,
comes from the kidney. You see the kidney
right here, so here is the kidney. It makes
erythropoietin (EPO) or EPO, sometimes you see it talked about. It tells bone marrow to
pick up the pace of red cell production.
More red cells… more ability to carry oxygen.
Blood oxygen levels go up, so
that should tell you now why the kidney
makes EPO. It does it when there is
a drop in oxygen getting to the kidney,
because the kidney cells need oxygen.
If there is not enough blood flow to the
kidney or there is not enough oxygen in
the blood getting to the kidney, it
starts making EPO. Okay…variables again. We have talked about EPO's
function and the kidney. Hypoxia (kind of off the screen) means low oxygen .
Testosterone
plays a factor here, because males need
more oxygen carrying capacity for their
greater percentage of lean muscle mass,
compared to women. So they have
testosterone to increase that lean
muscle mass. So…problems. Let us go too
many…polycythemia. Remember that the norm is around 5 million per cubic millimeter.
You can have counts of over 10 million per cubic millimeter.
That's twice as many (as normal). So what is going to happen is your blood will be much thicker.
That makes for slower circulation. That
makes for harder pumping of the heart to
get that thicker blood around. You can
see what that would do the heart. How does
that happen? Well, you could have
a hereditary problem
causing polycythemia or you could be
getting blood donations a lot, or you
could be blood doping, which is where you
purposefully get blood to increase your
oxygen carrying capacity. That is also
illegal in the Olympics. Let's go
the flip side, which is more common… the
anemias. There are different kinds of
anemias here. Hemorrhagic is the number
one: it is blood loss. It could be anything…
car accident. It could be, you know, cut
yourself on a piece of glass. It could be
heavy menstrual flow. Okay.
Easy treatment. Let's go "easy treatment"
things. Hemorrhagic… just talked about it.
Okay, let me get rid of all that… right. So we
talked about that (oops, too big.. make
smaller ones). Right …so we talked about
that. Let's go down to pernicious anemia.
Pernicious means deadly.
This is anemia that I've already
actually talked about. It is due to a lack
of intrinsic factor being made in your
stomach or a lack of vitamin B complex.
Vitamins easily treat it: you can either
increase your B vitamins or you can take
intrinsic factor. They give it to you by
shot. Okay… let's go down to hypochromic
anemia. This is low iron or what is
sometimes called iron deficiency anemia.
You are not, let's say you're a vegan.
You are not taking iron
supplements. Okay, that would be yours anemia. Now, there's another one here called
nutritional….nutritional anemia. This is
kind of a catch-all of everything else.
If you are lacking any nutrients, like if
you are starving to death.
Or you are protein malnutritioned,
and you're not getting enough protein.
You have to have proteins to make
hemoglobin protein… that's nutritional.
So those are all pretty much easy
to treat. Okay… so let's go
hemoglobinopathies. These are not easy to treat: this is a hereditary gene related
disorder of hemoglobin. hemoglobinopathy…. "path" means disease. Sickle cell
anemia and thalassemias… they would look like the picture to the right. The
thalassemias are related to
middle-eastern inheritance patterns and
sickle cell in African and
african-american inheritance patterns.
The same kind of thing though, basically,
not treatable. Well, I mean you could
give them blood transfusions but there is
no treatment, there is no cure.
Then we have hemolytic anemias. This is
where your blood blood cells are being
destroyed or lysed
and we're going to talk about one cause,
transfusions, in a minute. That would
be transfusion reactions or things like
snake venoms, spider venom.. those
can cause hemolytic anemia. And then we
have aplastic anemia…due to
problems in bone marrow. The bone marrow is
not making red cells. Usually it is due
to, maybe drug treatments, antibiotic– long
term treatment. It does damage to the
bone marrow. Bone marrow can't keep up
with red cell production. Okay… moving on.
I already mentioned hemochromatosis:
that is iron overload disease. So let me
go on. Alright. Let me get you into
this and then we'll stop. I am going to introduce you into blood typing,
and then the second video will pick up
with it. Really good tutorial at, I think,
University of Arizona, as opposed to
Arizona State. Okay.
Let me introduce some things
here.
On your red blood cells (here is a red
blood cell) right there… RBC, you can have
special markers out here… carbohydrate
protein markers. There are many many many
of them, dozens of them all over the
outside of the membrane. All right? Now
these markers, or sometimes they're
may be called fingerprints by people, are
actually called antigens. An antigen is a
marker, a fingerprint, or a receptor on the
outside of a cell. You have them all
over your cells. You have them on your
kidney cells and liver cells and
blood cells. You inherit them from your
parents…mother and father, All
right. When they are on red blood cells,
they are called agglutinogens. You will
see why in a minute or so.
Agglutinogens are red cells, oh sorry, the
agglutinogens are antigens specifically
on red blood cells. Remember "gen". Okay. Now, obviously your immune system… you
don't want your immune system to react
to these antigens on your own red cells.
Right…. if you've got a markers which
makes you a A type blood, you don't want your
own immune system to make antibody that
would attack your own cells. That would
be foolish and stupid and
self-destructive, so your immune system
does not make antibody against your own
self antigens. These are self antigens
that I'm talking about. Okay….. now on the
other hand, in your blood you have
antibody to various things. Not your own
markers, though. Again, that would be
self-destructive. But you do have
antibodies against markers you don't
have so. So, in other words, if this is you
and here's some bacterium that gets into
your body. Bacteria have these antigens
also. Your immune system, when it sees
this bacterium— it gets into you.
You want your immune system to attack
that– right? But those are not self
antigens: they are foreign. They are not
part of you But remember, your red blood
cell? Here's an RBC. Here are your a"A"
antigens or agglutinogens that are on
the outside of your red cells. You don't
want your immune system to see these…
right? To react to them? So you obviously
would not have antibody to those "A"
markers, but you would have, for example,
anti-B antibodies to your blood.
That is already in your blood.
You don't have "B" markers on your red
cells but you make antibody to those "B"
markers that are not on your red cells.
So if you ever came in contact with "B"
markers, you can see the problem. You
would already have antibody to those
markers. If, by some weird chance, you
are given the wrong blood… okay?
Here is you. There is your red blood
cell here, "A" markers on your red blood
cells. You have "A" blood type right
there, and you are given the wrong blood….
let's say you are given "B" blood. All
right?
There is going to be a problem because in
your body, remember you are the person on
the right…. you are the recipient. You would have anti B, correct?
Remember, that is the antibody floating
around in your blood. Well, if you are
give n"B" blood…here's a red
blood cell with a B marker… there's your
problem right there. If you were given that blood, if nobody
caught it, you would have agglutination
of these "B" cells, with your antibody
floating around in your plasma. That is
called agglutination. It is the reaction
between antigen and antibody, and you see
it right here on a blood test.
Look right here, for example. Here is
the same blood put on–three drops— on
a card, same blood exactly. Then anti-A antibody. …a drop of
anti-A has been added here. A drop of anti-B added there.
This is Rh antibody right there. " Anti" in
front of the "A" means antibody to "A"
markers. "Anti" front of "B" means
antibody to "B" markers. You can see
these clumps of red cells right here. You
can see more clumps over here, you can
see more clumps over here. It is where
they've been mixed together between the
antibody and the blood and that's the
agglutination reaction. You will see more
of it coming up. Okay…. so that's an
introduction. So one last thing then.
Alright.. we are going to look at only two
major blood types ABO blood types and Rh
blood types. There are many more, many
more different kinds of agglutinogins—not
going to go into them. If you are going to
end up a medical technologist or
clinical lab scientist, you have to take
a blood banking course and you spend way
more time going over the different blood
types. Okay… so the last thing all of this
was figured out– blood typing stuf—f the
ABO blood groups in the early 1900s. Two
important laws of Karl Landsteiner, who is
the pivotal guy. He won the Nobel Prize and all that.
If a marker is present on red blood
cells in blood, that is, if you are a
blood type and you've got those "A"
markers on your red cells, you are not
going to be making anti-A. Your blood
would agglutinate, and you would be dead.
That's what one says. Two says that if
you are missing an agglutinogen,
on your red cells…….. like, remember you're "A" blood. You have "A" markers but you don't
have "B" markers… right? If you don't have "B" markers, then you will have anti-B
floating around in your body. You make
antibody to the antigens you do not have
OK, that's the end right now.

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