Aspirin, so we know that it irreversibly inhibits COX pathway both one and two,
and so therefore without this, you don't have the thromboxane,
guess what you'd lose?
Bleeding time is the only thing to be affected,
and increase in, but no change in PT, PTT, why please? Why?
Because we're only dealing with platelets.
Is that clear?
May I ask another important question?
Will there be a decrease in platelet count if all that you do
is inhibit thromboxane formation, of course not.
The platelet count will be perfectly normal.
Clinical use, antipyretics, so for example,
patient has fever, analgesia, anti-inflammatory, and antiplatelet.
Toxicity here, you're thinking about bleeding.
Now, this is interesting.
I need you to memorize this.
In physiology and in a patient that unfortunately may be popping in too many aspirin pills,
over the counter, popping these like crazy
maybe because they're wishing to take care of a headache
and unfortunately, the first thing that may happen for reasons that we're quite unsure of
but please memorize that aspirin up in the respiratory center will stimulate it.
Yes, stimulate it acutely.
So one of the first things that you're going to find with aspirin toxicity
if a patient is taking too many, it actually stimulates the respiratory center
which means that the patient has hyperventilation.
Now, what does that mean to you?
On your labs, what are you looking for?
An ABG has been done.
An ABG, what are you going to find in terms of your carbon dioxide?
Decrease in carbon dioxide. Welcome to respiratory alkalosis.
Keep that in mind, very important.
In addition, they're taking aspirin.
Who is? A child.
Maybe the child has, who's this patient?
The child, eight years of age, fever, big time.
Take a look at the tongue, it looks like a peel of a strawberry in a child.
Fever, strawberry tongue.
Take a look at the skin of this child.
It looks like the skin is falling off.
It's called a desquamating rash.
Maybe you have lymphadenopathy.
You put all this together, you should be thinking Kawasaki.
But with Kawasaki, maybe this child has been taking aspirin.
Right? It could be.
Now, I know in clinical practice, we use IVIG granted.
However, you might be given a situation where such a child is given aspirin.
You think that child may ever, ever experience a viral infection?
Influenza, maybe chicken pox, what have you, and the patient's taking aspirin.
Now, for reasons that once again are unclear but yet we know is that in that child,
a virus plus aspirin may result in death of the liver,
highlight, it makes you pay attention to Reye's syndrome
and it also has a side effect, Tinnitus.
It may affect your vestibulocochlear nerve.
Told you earlier whenever you see the letters GREL, G-R-E-L, what exactly are you doing?
Good, you are then inhibiting your P2Y12 receptors.
You see where it says irreversibly blocking ADP receptors?
The name of those receptors are P2Y12 receptors.
Once you inhibit those receptors and then, what are you doing?
You're inhibiting the activation of the platelet.
If you inhibit the activation of platelet, obviously,
I am going to then inhibit aggregation.
Welcome to Clopidogrel, Prasugrel, Ticagrelor, or Ticlopidine.
Clinical use once again as an alternative for aspirin.
So therefore, you're thinking about acute coronary syndrome once again.
Let it be unstable angina, maybe coronary stenting,
and increased incidence of recurrence of thrombotic stroke, a thrombotic stroke.
Not embolic but thrombotic.
In other words, maybe a thrombi formation in the middle cerebral artery.
Those are clinical uses.
The toxicity especially Ticlopidine, would be neutropenia.
Look for a patient that has susceptibility to infection.
Let's take a look at Abciximab here.
Abciximab is going after what?
A glycoprotein IIb/IIIa, picture that for me one more time.
You have one IIb here and we have another IIb/IIIa here.
And you have Dr. Roger's ugly face.
My ugly face is fibrinogen.
You'll never forget that.
Welcome to Abciximab.
Clinical use, as an alternative for aspirin would be acute coronary syndrome.
It could be part of the regimen of percutaneous coronary angioplasty when you need to go in there
and open up and balloon your coronary to make it easier.
And then, toxicity here may be bleeding and thrombocytopenia.