Let's talk about that bleeding time.
Now, before we take a look at that bleeding time.
What is my actual time?
Two to 7 minutes.
What is bleeding time measuring?
Let me give you three options.
Is it measuring the activity of your platelet?
Is it measuring the activity of your coagulation cascades, intrinsic or extrinsic?
It's only measuring the activity of your platelet.
There are two reasons as to why bleeding time could be elevated.
Meaning to say above 7 minutes.
One could be, the platelet itself was improperly aggregating or adhering,
or number two, the platelet wasn't present.
We call that thrombocytopenia.
Let's take a look at aspirin.
What does aspirin do?
Remember, NSAIDs and aspirin inhibit COX.
In the COX pathway of the arachidonic acid pathway.
What was the component responsible for platelet aggregation?
Remind me. Thromboxane. TXA2. Thromboxane.
So therefore, let me ask you another important question.
You think that aspirin will cause a decrease in platelet count?
What's my platelet count again?
At least 150,000 to 400,000, right?
Will aspirin and NSAID cause a decrease in platelet count?
Never. Right? Never.
All it does is inhibit thromboxane synthesis.
It inhibits aggregation.
You'll never find clinically petechia, you'll never find clinically once again, petechia with aspirin or NSAIDs.
Why? Because a platelet count remains normal.
Renal failure will cause thrombocytopenia.
We're not sure exactly why.
Once again, I repeat, renal failure may then cause thrombocytopenia or platelet aggregation defect.
When it does, you'll have an increase in bleeding time. Look for that.
Please do not confuse renal failure with nephrotic syndrome, okay?
In nephrotic syndrome, you may lose in maybe about 5 to 10% of your patient's antithrombin III.
If you lose antithrombin III, your patient is in a state of hypercoagulation.
Fascinating, isn't it?
Whereas if it's renal failure, like I said, we don't know exactly what the signaling is yet,
but we definitely know that the platelets are not functioning properly.
And then for whatever reason that cause thrombocytopenia.
For example, you've heard of immune thrombocytopenic purpura,
you've heard of thrombotic thrombocytopenic purpura,
ITP, TTP, or even in DIC, disseminated intravascular coagulopathy.
Those are conditions in which your platelet count is going to drop. No doubt.
Those are conditions in which you would find an elevated bleeding time.
And be careful here, von Willebrand disease, now, the type that I'm only going to focus upon,
is the type of von Willebrand disease where the patient is deficient of von Willebrand factor.
Now, our topic for this discussion is only bleeding time.
So therefore, von Willebrand factor if it's not present, now you remind me,
the fact that we an elevated bleeding time is that due to not binding to glycoprotein Ib,
or is it due to the fact that factor VIII will not be stabilized.
That's the prior, isn't it?
So when you don't have the von Willebrand factor binding to glycoprotein Ib,
you can expect the bleeding time to be elevated.
To make it complete, when that von Willebrand factor is not present,
you can't stabilize factor VIII.
Which test will be elevated as well in von Willebrand disease?
Topic here? Only bleeding time.