Hi. Welcome to our video series
on interpreting lab values.
In this particular video, we're going
to take a look at platelets from a CBC.
Now if the normal range of platelets isn't
met, you're either going to be high or low.
Low platelets is thrombocytopenia.
That means the platelet -- the count
that's lower than normal.
Thrombocytosis is a platelet count
that's higher than normal.
Now, keep in mind, anytime a platelet count
is abnormal, there's something else going on.
Might be an underlying medical condition,
or it may be some kind of side
effect from medication.
Either way, we're going to have to do
some additional investigating to figure out
what the causes of either the
high or the low platelets.
Now let's look how the
platelets become a plug.
I mean, this is a really important job of the platelets.
When you have some damage to the
endothelium, you start to have the bleeding.
Look at the picture and you see the red
cells oozing out along with the platelets.
So the platelets' job is to protect us from
that, otherwise we'd hemorrhage to death.
So it works with a coagulation cascade
to form a platelet plug.
Now, the coagulation cascade
is pretty complex.
I'm just going to keep you
kind of a big picture view.
Now, I'm going to break it down into
3 steps and each one of the steps
will start with a letter A.
So step 1, the platelets adhere to
the damaged endothelium.
So just go ahead and underline
the word "adhere."
Step 2, they activate themselves.
That's the really cool part. It's
like they have superpowers
and when they start sticking to
that damage in the endothelium,
they activate themselves, make
themselves really sticky.
Now, now that they're super sticky,
they aggregate. That's just another word
for collect or clump to form a plug.
So the 3 As of the coagulation
cascade: they adhere,
they activate, and they aggregate.
So when you're thinking about what goes on,
what saves us from hemorrhaging to death?
It's our platelets. When we
have normal levels
and functioning platelets, they
adhere to the damage,
they activate themselves, and
then they aggregate.
They collect and clump. That forms a
plug and should stop the bleeding.
Now, let's break it down a little bit more.
When the platelets stick, it's when
the von Willebrandt factor connects
collagen and platelets. That's
what really helps them stick.
So it's the von Willebrandt factor --
it's got that name because
that's who discovered it --
connects collagen and platelets.
Next, the platelets release ADP and
thromboxanes and some other chemicals.
We'll just call them "other chemicals" for now.
But what this does is it causes other
platelets to activate and release ADP, etc.,
and on, and so on, and so on.
That's the cascade effect.
are really critical concepts, so just
kind of underline that word.
You'll see it again when we
talk about NSAIDS
and how they impact those
other types of things.
So people who are on NSAIDS,
non-steroidal anti-inflammatory drugs,
have less prostaglandins and less
thromboxanes, and that's why
they have a tendency to bleed.
They start interrupting that cascade.
So step 1, the platelets stick. We
got that von Willebrandt factor,
connects the collagen and the platelets.
Step 2. The platelets release
ADP and thromboxanes
and those other chemicals,
and that cascade effect just
That's what causes the platelets to
clump together or aggregate together.
Think of it as a platelet party. Like, it's --
everything is going on, everybody's having
a good time, and so they all race together.
Because activated platelets have a
surface receptors that bind fibrinogen --
it's a protein in plasma --
and the fibrinogen forms a bridge between
the platelets to actually make the plug.
Okay. That may be more than
you wanted to know,
but understanding that concept
helps you understand how
medications might affect this, like
we talked about the NSAIDS,
and how other diseases might affect
this ability of a patient to stop bleeding.