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As we all know, aspirin doesn't actually thin the blood, as it has been explained to me, it makes it "slippery". Slippery blood doesn't stick to itself hence this helps prevent internal blood clots (or allows blood to pass more easily around an existing clot). I also understand that having your blood too "slippery" can lead to the body attempting to counteract that and making it too "sticky".

Anyhow, my question regarding that is this, how does aspirin work? How does it make the blood "slippery"? (If there is a more medically correct term for "slippery" and "sticky", I'm all ears).

P.S. I paid the Mayo Clinic's website a visit before coming here, the information about aspirin's mechanism wasn't particularly helpful to me.

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    $\begingroup$ Aspirin doesn't make blood slippery (like lubricant's might allow machinery to work.) Blood clots require thrombocytes (aka platelets) and blood proteins to form. Too many platelets and clotting is more likely; not enough (or inactivation of some of the platelets) and clots don't form as easily. Anything that activates platelets (as described below) can result in a clot. Aspirin inhibits that. $\endgroup$ – anongoodnurse Aug 31 '16 at 16:14
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Aspirine irreversibly inhibits the enzyme cyclooxygenase. This enzyme facilitates the reaction from arachidonic acid to prostaglandin G2/H2. The further reaction leads to the generation of Thromboxane A2 which is important for the activation and aggregation of platelets. See the figure (from here) for an overview:

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Thromboxane A2 usually stimulates the activation of new platelets and increases their aggregation, with a shortage of this compound these activations are not possible and the coagulation of blood is reduced.

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