The physiological difference between anticoagulant “blood thinners” like warfarin, and anti-platelet drugs like aspirin.

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After some research all the sources I’ve found either gave a very vague “they slow down clot formation” or went into explicit detail that I’d need a PhD to understand. What’s the actual difference in how they work.

Bonus ELI5- How does alcohol thin blood? This was actually the original question I wanted answered but my curiosity went a step further.

In: Biology

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Anonymous 0 Comments

Blood clotting stands on two big things: the platelets, which are little cells made by the bone marrow, and coagulation factors, which are proteins created by the liver with the use of vitamin K. These two mechanisms act together as such: the platelets initially stick to the damaged blood vessel and patch it up, and then the coagulation factors are activated by the platelets and by the damaged cells of the vessel and consolidate the blood cloth by sticking to everything (platelets, red blood cells etc.). Aspirin in an antiplatelet therapy, which means it doesn’t let platelets stick to stuff. Warfarin is an anti vitamin K drug: it stops the production of coagulation factors by the liver, so less coagulation factors means less stickiness overall.

Bonus: long term alcohol intake damages the liver, so less coagulation factors, as well as damages the bone marrow cell production: it gives a megaloblastic anemia (less red blood cells means less things to stick) and thrombopenia (which means less plateles); moreover, it damages the blood vessel wall, so it’s less resistant to tearing. However, acute alcohol intake gives dehydration (because you piss a lot) and inflammation, which are both pro clotting risk factors.

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