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
Hi. Medical student here.
Clot formation has several steps.
1) Injury
2) Vessel constriction
3) Platelets become sticky and adhere to the injury
4) Platelets that are stuck to the injury grow a web to keep them in place.
Anticoagulants interfere with step 4. Antiplatelets interfere with step 3.
Alcohol is an antiplatelet.
So, blood clotting works by a whole cascade of clotting factors – which are little proteins in the blood. When one is activated, it then activates the next, which activates the next, which activates the next. This makes a *cascade* so that your blood clots very very quickly. They also all tend to enhance one another and “egg each other on” in many ways.
Different blood thinners target different clotting factors. Aspirin targets platelets and prevents them from clumping together, while warfarin blocks an enzyme called *vitamin k epoxide reductase* which is responsible for “turning on” factors II, VII, XI, and X when the blood needs to clot.
By targeting different areas, the blood thinners work in very different ways. Warfarin is much stronger than aspirin, and can also be reversed by giving someone a huge dose of vitamin k. This is very important if the person is bleeding a lot – like if they have been in a car crash or something.
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.
I think anticoagulants prevent fibrin from forming with the blood clot. When you get a tear in a blood vessel, the first thing that happens is that some platelets in your blood stick to the site of the tear, then they will slowly start attracting more platelets to stick together and soon there will be a temporary patch over the hole in the blood vessel. This is not a very strong patch and the patch will need some help from fibrin if it is going to completely stop the bleeding and hold together for any meaningful amount of time. That’s where the anticoagulants come in and hinder the process. Fibrin is a protein produced but the platelets in the clot that makes the clot stronger and more permanent and without it the clot will essentially fall apart.
Antiplatelets, on the other hand, prevent the blood clots from sticking together to allow the clots to grow in size.
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