Aspirin, also known as acetylsalicylic acid, is a commonly used medication for pain relief, fever reduction, and anti-inflammatory purposes. However, one of the potential side effects of aspirin is an increased risk of bleeding. Understanding the mechanism behind aspirin-induced bleeding requires examining the effects of aspirin on blood clotting and platelet function.

Aspirin works by inhibiting the enzyme cyclooxygenase (COX), specifically COX-1 and COX-2, which are responsible for the production of prostaglandins and thromboxane A2 (TXA2) [2]. TXA2 is a potent vasoconstrictor and platelet aggregator that promotes blood clotting [2]. By inhibiting COX-1, aspirin reduces the production of TXA2, leading to decreased platelet aggregation and blood clot formation [2][3].

However, aspirin's antiplatelet effect is not limited to the duration of its presence in the body. Aspirin irreversibly acetylates COX-1, which means that the inhibition of platelet function persists even after the drug has been cleared from the body [2]. This prolonged antiplatelet effect is due to the irreversible inhibition of COX-1 in platelets, which prevents the production of TXA2 for the lifespan of the platelet (around 7-10 days) [2][3].

The reduced production of TXA2 and the inhibition of platelet aggregation by aspirin can lead to an increased risk of bleeding. Platelets play a crucial role in the formation of blood clots, and their reduced function makes it more difficult for the body to form clots and stop bleeding [2][3]. This effect is particularly relevant in situations where bleeding occurs, such as injuries, surgeries, or ulcers.

It is important to note that the risk of bleeding associated with aspirin use varies depending on the dose and duration of treatment. Low-dose aspirin, commonly prescribed for cardiovascular protection, has a lower risk of bleeding compared to higher doses used for pain relief [2]. Additionally, individuals with certain medical conditions, such as bleeding disorders or gastrointestinal ulcers, may be at a higher risk of aspirin-induced bleeding [2].

In conclusion, the mechanism of aspirin-induced bleeding is primarily related to its inhibition of platelet function by irreversibly inhibiting COX-1 and reducing the production of TXA2. This prolonged antiplatelet effect can increase the risk of bleeding, particularly in situations where clotting is necessary. It is important to consider the dose and duration of aspirin treatment, as well as individual risk factors, when assessing the potential for aspirin-induced bleeding.

Sources:
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1852201/
[3] https://pubmed.ncbi.nlm.nih.gov/6499/