Transcription
It's Medicos is Perfectional is resuming our bleeding and coagulation series of lectures. In the previous video, we have talked about the antithrombin 3. Today, I'll talk about fibrinolysis, or as Merriam-Webster's say, fibrinolysis or fibrin alysus. I don't care how you pronounce it; I just care you know what the flip you're talking about. Now, with that being said, let's get started. [Music]
Here are just some of my previous bleeding and coagulation videos in my bleeding and coagulation playlist. So please subscribe and save the playlist; otherwise, you're missing out on a lot of goodies. Hemostasis: blood stable, i.e., stopping the bleeding; prevention of blood loss. Steps of hemostasis: vasoconstriction, temporary platelet plug, coagulation. This is primary hemostasis; this is secondary hemostasis. Of course, we have talked about all of these before. Now we have fibrinolysis: we should dissolve the clot and restore the function and restore the normal blood flow, because baby, it's over; the party is over; history will remember me for my words of wisdom.
Primary hemostasis is balanced on the dynamic harmonious antagonism between the smooth endothelium, which wants the blood to flow, and the thrombosis, which demand blood clotting. So here is the story, Morning Glory. You injure yourself; vasoconstriction of the vessel occurs; temporary platelet plug known as primary hemostasis. Depending on the time for the trauma, if the trauma is very small, such as a paper cut, the platelet plug is sufficient; primary hemostasis is more than enough. Thank you so much. But if it's larger, we need the coagulation cascade, the second-row hemostasis, to convert fibrinogen into fibrin, laying down a strong mesh work, trapping the red blood cell, forming a clot. This clot is stronger; then the clot will contract producing the serum. Then we have fibrinolysis, which is the topic of today, to destroy the fibrin clot and restore, regenerate, and restore the function, and then we will regenerate the tissue.
We have talked about vasoconstriction before. I know that repetition is the mother of pedagogy, but I'm not gonna repeat myself; just remember that it's a local myogenic spasm. The platelet is just floating around checking the gate; if the gate is secure and the layer underneath is not exposed, everything is fine, okay? But if the gate is cracked open and the sub-indusial collagen is exposed, maybe it's the same thing with the engineer in the post-earthquake inspection; he is looking at the two walls; if the wall is fine, probably not much damage has been done to the building. I'm not an engineer, but I okay, I just have an opinion, and then but if the walls are cracked like this and the sub-endothelial collagen is exposed, okay, the earthquake was so bad in this building; it's not fun. So here's the platelet, and here's the platelets, and they are activated when the sub-in detail collagen is exposed because it means that the end is here is damaged because it means there is a trauma, baby.
Here is the process of primary hemostasis. We start with platelet adhesion thanks to the GP 1p receptor on the plate and the von Willebrand factor on the sub-endothelial collagen. Then we have the platelet activation; they are active; they start to secrete thromboxane A2 and ADP. ADP will express the receptor called GP 2b3a, a GP for glycoprotein, and this GP 2b3a is important because this plate is gonna attach this plate thanks to this receptor. Then there is a molecule fibrinogen in between; so this is primary hemostasis. Secondary hemostasis is converting this fibrinogen into strong fibrin mesh work. Do you know how does that protein called thrombin? Why do we call thrombin? Because this is the protein of thrombosis; mark my words. There are only two ways to coagulate: the intrinsic and the extrinsic; but there are several ways to bleed. This is physiology; this is pathology.
Secondary hemostasis or the coagulation cascade: we start from here. What's the goal? Fibrin; because successful people begin with the end in mind, as Stephen Covey said. So fibrin is here; it comes from fibrinogen, which is inactive. Who activates it to fibrin? Thrombin. Thrombin is now active, but it's present in an inactive form called prothrombin. This is the president; we call it factor 1. This is the vice-president; we call it factor 2, because we discovered this first, then this first; then we go upwards; that's why factor 1 is here and factor 12 is here; something your professor will never tell you, okay? Then let's go to the prothrombinase complex. We need two numbers and two words. What are the two numbers? Ten and five. What are the two words? Calcium and phospholipids. Cool.
Now the extrinsic, which is the easiest one. You injure yourself; here's the trauma. Extrinsic means we need something from outside of us, outside of the vessel, to activate this cascade. What kind of thing do you mean? How about the tissue factor coming from the tissue? Yes, it works. Why? Because if there is a trauma, the tissue factor is gonna come in contact with the blood here, okay? You mean the presence of the tissue factor in the blood is an evidence of trauma? Indeed. Okay, now we have the chief factor, also known as tissue thromboplastin or tissue phospholipid TPL, activating factor 7 into 7a. 7a is gonna activate 10, and 10a. 10a is the most important factor; this is Leo Messi, and it's gonna is part a crucial part of the prothrombinase complex that's gonna activate prothrombin into thrombin. Thrombin is gonna convert fibrinogen into fibrin; that's the extrinsic. How about the intrinsic? Okay, it's longer. We need something from within, something intrinsic to the blood vessel. How about the sub-in detail collagen? Okay, that works. How about the high molecular weight kininogen? It works. How about the plasma collection? Also works. All of these are activating the factor twelve into twelve a. Twelve a is gonna activate eleven. Eleven will activate ten. No, ten is here, baby; ten is here; forget about ten now, okay? Nine and then eight; yes, you got it. This is fast; they act quickly; the House of Representatives; these guys are very slow and old people called the Senate; they are slow but more efficient. Now we're done. And the most or the highest number was factor 12; then we discovered factor 13, because some people after forming fibrin would bleed to death and die. Yes, why? Because you didn't stabilize the fibrin. So there is factor 13, called the fibrin stabilizing factor; what a glorious name! It's going to activate the fibrin into fibrin. How would you stabilize a fibrin? It's called cross-linking.
Fibrinolysis: let's break it down. What does fibrin mean? They are fibers; I N protein. So fibrin is the fiber allure or fibrous protein; lysis: breakdown. So fibrinolysis is the breakdown of the fibrin. I have prepared 50 hematology cases in the same manner as the ten cases about Hodgkin's lymphoma that was in my hematology playlist. These 50 cases cover bleeding disorders. Go to patreon.com/scishow for the courses, and thank you in advance. What's the goal of fibrinolysis? What is the why? Because Friedrich Nietzsche said, "He who has a why to live can bear almost any how." Now I'm gonna borrow his thoughts. Medicos is Perfection Alice says, "He who has a why to fibrinolysis can bear almost any mechanism." The mechanism is gonna be easy if you understand the why; if you understand the purpose of fibrinolysis or fibrinolysis. So why the flip do we need fibrinolysis or thrombolysis or thrombolysis? Because if you leave the clot alone, the clot will grow and grow and grow, and it will press on the local structures; it's gonna cause lots of problems; it can occlude the vessel leading to heart attacks, every kind, like you know, many people die of heart attack, stroke, etc. This is gonna happen if you do not break them down, because it's over, like okay, we need a clot to stop bleeding, but once you have a clot, please break it down; otherwise, it will grow and grow and grow.
Now here is the purpose of fibrinolysis: if you don't break the clot, it's gonna grow and kill you. So now you should be interested in learning about fibrinolysis, because without fibrinolysis, your blood clot will grow until you suffer. Now you better bloody be excited about fibrinolysis. Okay, I'm super, super excited. Fibrinolysis! The hell! The mechanism: primary and secondary. Primary is physiology; secondary is pathology and pharmacology, which are kind of the same thing. I love to mess with pharmacists. Primary fibrinolysis: be--how? First, which enzyme breaks the clot down? Okay, you've told us that the purpose of fibrinolysis is to break that clot down lest it should grow and grow and grow and kill us and make us suffer. Okay, so what enzyme breaks down this clot? It's called plasmin. The protein that's in the plasma; it's a proteolytic enzyme. No kidding, because these are protein fibers; they end in I N. If there is an enzyme to break them them down, it better bloody be a proteolytic enzyme; makes perfect sense. Then what? After the plasmin breaks the clot, the clots broken down into fragments; we call them degradation products; we call them also split products; same exact thing. You break down fibrin into fibrin degradation products, and you break down fibrinogen into fibrinogen degradation products; same thing. Okay, what will happen to the fragments? They are cleared by your sewage system: the liver and the kidney; they get rid of every stuff. Don't you just keep eating and destroying your health, and these poor guys are suffering. Fibrinolysis is not over yet; we shall continue in the next video. Please subscribe; hit the bell; follow me on Facebook, Instagram; get all of my notes, all the cases, and support this channel on patreon.com/medicosis, so that I can send you my bloody Dropbox links. Thank you for watching; be safe; stay happy, and study hard. This is Medicos is Perfectional, a loss for medicine; makes perfect sense.