Transcription
Anteye fibrinolytic therapy. In the previous video in this amazing playlist about bleeding and coagulation disorders, we have talked about tranexamic acid. If you have understood the previous video, this one's gonna be a piece of cake. I've told you before that we have anti-platelets, such as aspirin, so just copy Degrelle, such as lots of other stuff, and we have the fibrinolytic therapy, such as TPA. What's the antidote for aspirin? It doesn't exist. What's the antidote to TPA? The answer is tranexamic acid and aminocaproic acid.
What's the name of this Greek letter? It's Epsilon. I know Greek, of course, because I'm an Egyptian guy, and Greece is just like, there are neighbors on the opposite side of the Mediterranean Sea. We love each other; we both can get thalassemia and G6PD deficiency, and this is none of anybody else's business. Okay, so epsilon aminocaproic acid, that's why the abbreviation is EACA, and this is not Obamacare. With that being said, now let's get started. [Music]
Haemostasis has main steps: tempura, apply coagulation, etc. What was the job of TPA? To destroy the clot, causing fibrinolysis. What is the job of tranexamic acid or aminocaproic acid? It is to preserve the clot and prevent fibrinolysis. So this is the TPA that destroys the clot and causes fibrinolysis, but not under aminocaproic acid watch, because it's gonna preserve the fibrin meshwork. As you know, in fibrinolysis, we have plasmin that destroys the fibrinogen and the fibrin and the stabilized fibrin, producing fibrinogen degradation products, fibrin degradation products, and D-dimer, respectively. Plasmin is not left free all the time; it comes from plasminogen. TPA converts plasminogen to plasmin, but not under aminocaproic acid watch; we're gonna preserve the clot, baby; we gonna preserve it. So here's the whole story: plasminogen to plasmin, then plasmin dissolves the fibrin into fibrin degradation products and the stabilized fibrin to the dimer. What's the name of this process? Fibrinolysis. Who stimulates this process? TPA. Who inhibits this process? Something from within, something from without. What's from within? Plasminogen activator inhibitors 1 & 2. What's from without, or from outside of your body? Anti-fibrinolytic therapy, such as the famous aminocaproic acid and tranexamic acid. These guys will inhibit the conversion of plasminogen to plasmin, therefore preserve the fibrin and inhibit its dissolution.
In brief, anti-fibrinolytic therapy is anti-TPA and has two main members: epsilon aminocaproic acid and tranexamic acid. They do what? They prevent fibrinolysis. How? By preventing conversion of plasminogen to plasmin. So what? They preserve the fibrin meshwork. So therefore, they reduce bleeding, but as a side effect, if you reduce bleeding, you will cause thrombosis. Aminocaproic acid prevents the conversion of plasminogen into plasmin, therefore preserves the fibrin and inhibits its degradation. Okay, so it's an anti-fibrinolytic therapy. Yep. It's used to treat acute bleeding. How? By preserving the fibrin meshwork; no one is going to destroy this beautiful meshwork under my watch, said the aminocaproic acid. Therefore, it can cause persistence of blood clots. If you are going to preserve the clot and prevent bleeding, you will cause clotting and thrombosis, because actions have consequences.
Indications: bleeding, of course; severe thrombocytopenia; bleeding coagulation disorders; bleeding cardiac surgery, which can cause bleeding; invasive dental procedures if the patient is on anticoagulant #bleeding; acute promyelocytic leukemia, because in APL there is risk of catastrophic hemorrhage #bleeding; and aminocaproic acid is the hero to decrease the risk of this catastrophe. In the previous video, we had some bullet points about tranexamic acid; for example, it inhibits the conversion of plasminogen to plasmin via competitive inhibition. Bleeding during a dental procedure in case of a hemophilia patient warrants the use of tranexamic acid or aminocaproic acid. Never ever give anti-fibrinolytic to control hematuria; it doesn't work and it can cause that problem to be worse. Severe DIC + confer fibrinolysis; please give antifibrinolytic, but be very careful because this can lead to thrombosis. In this case, give heparin. Antifibrinolytics can be used in von Willebrand disease adjunctively; they are not the main dish, they are not the main entree, they are just helping other therapies to control mucosal bleeding or procedures because these can lead to bleeding.
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