Ultimately, let's take a look at the stages of hemostasis here.
So remember, we began way back where we caused damaged to the vascular phase.
What happened here?
Endothelial cell was damaged and when endothelial cell was damaged, what did they express?
Von Willebrand factor. Good.
Where do they bind to? Glycoprotein Ib.
Next, what made then happen?
This was adhesion, wasn't it?
Process called adhesion.
What if there is a defect in von Willebrand factor?
So now I'm gonna give you a fourth test.
The fourth test is called bleeding time.
The time that you'll have to memorize here will be 2 to 7 minutes, okay?
2 to 7 minutes.
In other words, the bleeding time is going to tell you how well is my platelet working only.
May I ask you a very important question?
Can you form a plug without the coagulation cascade?
Technically speaking, yes you can, right?
All you need is platelet and fibrinogen without the coagulation cascade
and you can form a temporary hemostatic plug.
I bring this to your attention because if you're missing von Willebrand factor here
and it cannot bind and you don't even have it,
the bind the glycoprotein Ib, the test that you'll find to be elevated will be bleeding time.
Remind me one more time that von Willebrand factor stabilizes which coagulation cascade?
Which coagulation cascade component is von Willebrand factor stabilized?
Factor VIII is part of which coagulation pathway?
The intrinsic will be measured by which test?
So when a patient, a young lady with menorrhagia has von Willebrand disease.
What will be the only two test that'll be elevated? Bleeding time.
Because you don't have the von Willebrand factor binding like glycoprotein Ib
and number two an increase in PTT because you don't have the von Willebrand factor II
stabilize factor VIII.
That must be understood.
What's the next step after adhesion?
It's called aggregation.
What do you need for aggregation?
What's the glycoprotein receptor here?
Initially, what is it going to bind to?
Those beads that were called fibrinogen.
What else helps you with aggregation?
TXA2 stands for thromboxane.
Give me a drug that you should know.
We even recommend this.
A little controversy but point being is aspirin.
Baby aspirin, 81mg.
Why do you wanna give aspirin to a patient who may be at risk of developing,
let's say, coronary arterial disease?
Oh, because it inhibits what's known as your COX, cyclooxygenase.
When you inhibit cyclooxygenase then you might be inhibiting the synthesis of thromboxane
in which you will then not have aggregation.
But if you continue forward physiologically, you may then form what kind of plug?
A temporary hemostatic plug.
Stop there mentally because at this point we form temporary hemostatic plug.
What's my next step?
The fibrinogen must be cleaved.
What's the name of that enzyme that cleaves fibrinogen?
So now with thrombin we get into our coagulation cascade.
We have two branches, intrinsic and extrinsic.
It converges about which factor please?
Factor X, remember that, factor X.
And then with this you activate your prothrombin and that thrombin will then cleave the fibrinogen.
Now that you formed a proper stable clot, you must then have your factor XIII to make it insoluble.
Mentally stop there.
What's next, now that you formed a clot?
Well, you gotta break it down.
What do we call this?
Ah, the final phase.
They're all part of proper hemostasis.
Proper, balance, a seesaw.
And who then is the enzyme that activates your or degrades your fibrin?
It's called plasmin and this factor is factor XII.
This is then called the fibrinolytic phase.
What's the name of the test in which you made them have excessive thrombi breakdown?
To summarize the plugs, here they are.
The one on the left is your temporary.
Remind me again, what are those receptors on the platelet here that are binding those beads?
What are those beads?
Any coagulation components?
While the one on the right is your stable.
What's the difference?
Take a look at the beads.
Hah! It became a concrete brick.
How did that happen?
The concrete brick was developed due to cleavage of the fibrinogen with the help of which enzyme?
Is it thrombin or plasmin please?
And you cleave up the ogen to form your fibrin which is your stable clot
and the factor XIII will come in to make it insoluble.
Is that understood?
Remind me again, what is then going to break down this fibrin clot?
Factor XII will then activate your plasminogen
and the plasmin will then start breaking down your stable clot
all to make sure that you maintain homeostasis because if you then form too many thrombi,
you may then have pathologies such as DIC, TTP, if it's a young child maybe HUS.