There's two major classes of anti-platelet medications.

One is simply just one drug.

It's an N-Said aspirin therapy there.

And then we've got a bunch of P2-Y12 inhibitors.

So I'll go through those in the anti-platelet section here.

All right, so first and foremost, we've got aspirin.

So this can basically act as a blood thinner.

It can help reduce the risk of stroke and heart attacks and blood clots.

It's a mechanism of action in cardioporphylaxis, so how it protects the heart and reduces the risk of a future,

you know, heart attack or stroke, it irreversibly inhibits Cox 1. So that's cyclooxygenase. That's a specific enzyme there.

And ultimately, by inhibiting this enzyme, we reduce the production of thrombocene A2.

Thrombocene A2 is a potent vaso, excuse me, not a vasoconstrictor, but a platelet aggregator.

It makes and helps platelets stick together.

So by reducing thromboxane A2, we have anti-platelet activity,

which makes the blood a little bit thinner, if you will,

and ultimately its mechanism leads to the inhibition of platelets action, which they

stick together and begin the formation of a blood clot.

Also, we use aspirin not just on a chronic basis, but we also use it in acute management of MI.

For most patients, the low dose, 81 milligrams, is going to be okay.

Occasionally, you may see 325 milligrams once a day, maybe even twice a day in some rare circumstances.

So more of a clinical judgment type of situation.

The higher the dose of aspirin we go, the more and more likely that we can run into

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