So you have your NaCl which is your crystalloid.
Take a look at what colloids are in summary. Everything
we have done here, we're pretty much finished.
A table to summarize everything we discussed.
Colloid, packed RBCs, albumin, FFP. Where
are colloids always located? Really a good
component to then fill up the plasma compartment.
Next, packed RBCs, what does it do? Well, you
give packed RBCs, this then increases hemoglobin
now. A couple of things that I wish to bring
to your attention. You are going to like this.
Okay. If you have packed RBCs and you are
giving this two patient, is there any point
in time in which perhaps you have an athlete?
They might be taking RBCs or not exactly may
be an athlete but something that is equivalent
to giving an RBC or production of RBC. EPO
perhaps, or erythropoietin. So the reason I say
this is because maybe you are making better
sense of what is going on here? Why an athlete
might want to be taken EPO is because that
athlete especially let us, say oh! our lovely
friend Neil Amstrong, and he have got a script
of awards because of blood
doping, is well you give the EPO or packed
RBCs, what are you trying to do? Increase
production of, well what is it called? The
erythropoiesis, RBCs. And when you and whatever
means either through hormone, EPO or packed
RBCs, you are going to increase hemoglobin
thus increase oxygen carrying capacity. Now
obviously this isn't a clinical setting.
So forget about that athlete, but as to the clinical
setting, this is a patient that has had acute
blood loss, severe anemia. What kind? We will
get into that later. But severe anemia here
would in fact be normocytic and you will call
it nonhemolytic. But Dr. Raj, how can you call
this nonhemolytic? Well, let us see. Did the
RBCs perish within the body when you lose
your blood? You see the blood spurting out
right now. The RBCs didn't die inside your body.
I don't care if the RBCs has die
that on the floor. Hence, you have to call
it nonhemolytic. Is that dramatic enough for
you? Put yourself, give yourself clinical
attacks every step of the way. Platelets,
what is going on here? Stop significant bleeding,
in quantitative and qualitative platelet dysfunctions
or dysfunctional conditions. For example,
Let me give you one quantitative. What is that
one in which that patient, unfortunately, looks
close to death, bleeding from orifice, mucous
membrane, PT, PTT, BT were all elevated and
you find your platelet count to be decreased?
So thrombocytopenia, is quantitative, decreased
platelet count. Would you tell me what normal
platelet count is? 150,000 to 400,000. That
you have memorized. 150/400. So what are the
boards going to give you? They will give you
50,000, which is clinically significant. You
will know that your patient has a quantitative
decrease in platelet. What about qualitative?
Give me an example of qualitative? How about
this one? One in which you find your bleeding time
to be elevated. PT, PTT is normal. Actually
any time that you have a platelet defect,
what should be the major test that is going
to be affected? Is it? I am giving the options.
Is it BT, is it PT or PTT? Good. BT What is BT?
Bleeding time. When you are only dealing with
platelet dysfunction either quantitative or
qualitative, it is bleeding time that you
know being elevated. That is it. So qualitative,
bleeding time is elevated, what if I told you
that your patient has a hard time binding
your platelet to your von Willebrand factor.
You know the name of that glycoprotein? You
better. It is called glycoprotein Ib. What
is the name of that disease? Bernard–Soulier.
So that is a qualitative disease. Are we
clear? Let us move on. FFP, that patient who
had DIC, you want to make sure that you do
what? You give FFP, which is filled with coagulation
factors. Now I want to be more technical now
because if we have DIC, late stages, well how's my
patient presenting? Oh! my goodness, every
single coagulation factor has been consumed.
Hence, it is called consumption coagulopathy.
So thus you want to give FFP as being your
mode of treatment. Cryoprecipitates , I told
you that this is a form of your plasma components,
but take a look at many of these factors here.
Many of the factors begin with the letter F.
Use that to your advantage. Fibrinogen,
fibronectin. Next, make your life easier.
This is important. What if you find a patient,
I am giving a lot of clinical correlation,
but this is good, right, because of reinforcement
and summary. Otherwise, you are just reading
through this and what is the point. I mean you
can do this on your own. So here is your patient.
A patient comes in and there's bleeding taking
place. There is even hemarthrosis. What does
that mean? Bleeding into the joints. Okay.
Now you take a look at the labs and all that
you find is an increase in PTT. PT is normal,
bleeding time is normal. Further investigation
then shows you that your patient has deficiency
of factor VIII. What is my diagnosis please?
Hemophilia A or B? A. Now work with me, ready,
pay attention. A comes before B, 8 comes before
9, what am I getting at? I think you know.
Hemophilia A is issues with factor VIII deficiency.
Hemophilia B, which is the next letter is
hemophilia B is your factor IX, the number
after 8. Are we okay? That is imperative
that you know. Next von Willebrand factor.
You want to put those together. How in the
world can you possibly have factor VIII work
together? How can you possibly of optimum
factor VIII functioning? You must have von Willebrand factor.
What is all this? This
is all cryoprecipitate. Fibrinogen, fibronectin,
factor VIII, von Willebrand factor. Take a
look at my pathologies, factor VIII dysfunction,
hemophilia A, and von Willebrand disease.
Once again, close your eyes, von Willebrand
disease. Who is your patient that I gave you?
Female, menses, menorrhagia. Blood test came
back to be positive for well remarkable for
a prolonged PTT and a prolonged BT, bleeding
time. Welcome to von Willebrand disease.
Now blood transfusions themselves have particular
issues and you will be asked the following.
The most updated information in terms of feedback
and such that you need to make sure that you
are quite comfortable with. One is called
TACO, the other one is called TRALI. What
is going on here? These are transfusion reactions.
We have transfusion associated circulatory
overload and that is going to be TACO and
the other one is called transfusion related
acute lung injury. So once the circulatory
overload, at least pay attention to CO and
TACO, and at least pay attention to LI, lung
injury, and TRALI. Keep those in mind. Those
are important transfusion reaction issues
if your patient requires transfusion. Why
do we even need a transfusion perhaps? Maybe
there's blood loss. Maybe there is iron deficiency
anemia that was so bad and once your hemoglobin levels
start dropping, at 8 maybe even 7 g/dL,
not good. Hemochromatosis. I am sorry.
What is going on here? Listen. The way to
read this, interpret this, by giving your blood
transfusion, you might then be introducing
what? Too much iron. What is this? Secondary
hemochromatosis. Are we clear? What else
may happen upon administering transfusion?
Citrate chelation of calcium. Hyperkalemia
that is the big one okay. A lot of times what
ends up happening is that say that your patient,
take a look at the very first row, what kind
of component was that? Packed RBCs. Where
do you store them? Where do you store packed
RBCs? In a blood unit that is rather cold.
If it is sitting there for a long period of
time, is it just possible that some of those
RBCs might actually die? Yes, and may result
in? Release of potassium. Does that make
sense to you? I hope so. Inside the cell,
what is the most abundant electrolyte? Potassium.
So hyperkalemia. For you, I will take a second
here to make sure that you are completely
comfortable with those reactions and those
side effects that may commonly occur by giving
transfusions. Now, the one that we really don't
have as much anymore of course, would then be your
hepatitis C. You know we have enough measures
where that rarely occur, we will
just put it that way.