Transcription
Hey guys, it's Medicosis Perfection Alice, where medicine makes perfect sense. Today, we'll continue discussing our bleeding and coagulation series of lectures. This is the 18th video in my series. We'll talk about a comparison between the intrinsic and the extrinsic coagulation pathways, and let's get started. [Music]
As I've told you before, hemostasis is prevention of blood loss by stopping the bleeding. Steps of hemostasis: we have vasoconstriction, then temporary plug hole zone as primary hemostasis. The hero here is the platelet. Then coagulation, or secondary hemostasis; the heroes here are the coagulation factors. The coagulation factors are… are they albumin or globulin? The answer is globulin. But we have different types of globulin: we have alpha globulin, beta globulins, and gamma globulins. What kind of globulin are those coagulation factors? The answer is beta globulin. How about the gamma globulins? No, no. The gamma globulins are the immunoglobulins, also known as the antibodies. Cool.
Then we have fibrinolysis as the cat that cleans after itself. The body is like a nice cat; it dissolves the clots and restores the function, restoring the normal blood flow. Then regeneration and repair the injured, traumatized tissue. Primary hemostasis is balanced on the dynamic, harmonious antagonism between the smooth endothelium, which wants the blood to flow, and the thrombocytes, which want blood clotting. This is anticoagulation; these are procoagulation. It's a balance. When you have less platelets, you'll bleed. When you have more platelets, theoretically, you will thrombose.
Here is the story: you injure yourself; vasoconstriction of the blood vessel occurs. Then temporarily plug holes, also known as primary hemostasis. Depending on the type of trauma, if it's a small trauma, the platelet plug is sufficient. I'm done. Thank you. Primary hemostasis, and that's it. If it's a larger trauma, we need the secondary hemostasis, also have the coagulation cascade—lay down the fibrin meshwork to trap the red blood cells. Then the clot will contract, providing the serum, and then fibrinolysis to clean this mess, restore the blood flow, and regenerate the tissue.
Here is the first step, called also known as vasoconstriction. I'm not going to talk about this anymore because I've talked about it before, but just remember it's a local automatic myogenic spasm, like the policeman who checks the security gate and like the engineer in a post-earthquake inspection who checks the painting on the wall. The platelets are floating in the blood; when they see a cracked endothelial layer and an exposed subendothelial collagen underneath, they go nuts and start their primary hemostasis.
Primary hemostasis: first platelet adhesion. They adhere to the subendothelial collagen thanks to the von Willebrand factor, which is synthesized by the endothelium and stored in the platelets. The platelets use their nice receptor GP1b to adhere to this von Willebrand factor. Then we have the platelet activation; they get active and they release stuff such as the ADP and thromboxane A2. ADP will express this nice receptor called GPIIb/IIIa, so we call this ADP-dependent expression of GPIIb/IIIa receptor. Thromboxane A2 again will help platelet aggregation and will cause vasoconstriction because vasoconstriction helps the blood clot by decreasing the surface area. Remember, here is GP1b, here is GPIIb/IIIa. Adhesion first, then aggregation later. One comes before two; makes it easier for you.
Then we have platelet aggregation; that's platelets displaying that each one has its own GPIIb/IIIa receptor, and then there is a molecule of fibrinogen in between. The next step is to convert this fibrinogen into nice fibrin fibers to form a meshwork, that's called the secondary plug, and then trap the red blood cells, and here we have a strong plug. Remember my words of wisdom: there are only two ways to coagulate, but there are several ways to bleed. This is so deep. What are the two ways to coagulate? The intrinsic pathway and the extrinsic pathway.
Why did I write the intrinsic pathway in a larger font? It's bigger than this because the intrinsic pathway is longer than the extrinsic. Everything in my slides is for a reason. I have great news for you: I have 50 hematology cases on the topic of platelets and bleeding disorders. They are on Patreon. Go to patreon.com/scishowsays. They are $15, and I promise you will never answer the 15 correctly; you will always have mistakes. I will write more cases later about more subjects, so go to Patreon. At least, if you don't want to purchase these cases, at least follow me on Patreon. That's why… that's how you get notified when I release new cases. Following on Patreon is free.
Let's talk about the extrinsic pathway. Why called extrinsic? Because we need something from outside of the blood vessel, i.e., tissue, to provide us with tissue factor. And this tissue factor will activate factor VII. Factor VII is now active; look, it's going to activate factor X, and boom! Prothrombin, thrombin, fibrin, fibrin traps the red blood cells, forms a secondary clot. Very nice.
Let's talk about the intrinsic pathway. More steps. We start with factor XII. We need something from within the vessel, so the subendothelial collagen to activate factor XII into factor XIIa, XI, then we have IX, then VIII. So VIII, IX, XI, XII. How about X? X is here. After this, you have prothrombin, thrombin, fibrinogen, fibrin, and boom, we are done. By the way, here also we have the high molecular weight kininogen activating factor XII. Also, we have prekallikrein doing the same stuff.
Now the big comparison: intrinsic versus extrinsic. What do you mean by intrinsic? It's something from within us, within the vessel, such as the subendothelial collagen or the high molecular weight kininogen or prekallikrein. So the intrinsic is self-sufficient; something from within. Extrinsic, on the other hand, something from without, from outside of the blood, from outside the vessel, which we mean the tissue. That's why we call the factor that comes from the tissue, tissue factor. So then the next thing is: intrinsic has more steps, a longer cascade. If it's long, it's going to be more efficient. Why? I remember the cascade; it's like a small waterfall; it gains gravity acceleration and momentum as it goes down. Boom, boom, boom, boom, boom, boom, boom. #gravity. Extrinsic, on the other hand, has less steps, shorter cascade; it's faster, but it lasts… it's less efficient. Intrinsic starts with factor XII. Who activates factor XII? The subendothelial collagen and you have the high molecular weight kininogen and plasma prekallikrein. Cool. This starts with factor VII. Who activates factor VII? The tissue factor, also known as tissue thromboplastin or tissue phospholipid (TPL). Cool.
Factors in the intrinsic: we have II before X and II after X. We have VIII, IX, XI, XII. How about X? Ten is here. It's written in the center; it's in the common pathway. Extrinsic involves only factor VII. The intrinsic, we use to measure it, the PTT test. The PTT measures the intrinsic pathway and the common pathway. This is very important. The PT measures only the extrinsic pathway and the common pathway.
Thank you for watching. Again, there are 50+ hematology cases on Patreon. Go to patreon.com/medicosis. Also, you'll get all of my notes; you'll get other topics such as scombroid poisoning. It's only on Patreon, anyways. Thank you for watching. Please subscribe, and as always, be safe, stay happy, and study hard. This is Medicosis Perfection Alice, where medicine just makes perfect sense.