Transcription
Hey, guys. It's Medicosis Perfectionel. It's where medicine makes perfect sense. This is the eleventh video in my series on bleeding and coagulation. In the previous video, we talked about primary hemostasis, also known as platelet plug formation. Today, we have a crazy mnemonic, so let's get started.
Here are my previous videos in this playlist, so make sure to subscribe. Quick recap of what happened in the previous video. We start with an injury; then the endothelium is removed, and the subendothelial collagen is exposed. The platelets start to swell, and they form pseudopods. Then, contractile protein contracts. Thanks to the calcium canalicular system, when they contract, they release granules like thromboxane A2 and ADP. Platelets become sticky. The tissue leaks von Willebrand factor. Platelets adhere to the von Willebrand factor, and fibrinogen can be converted into fibrin through the secondary hemostasis.
Let's make this clear. We have three processes: We have adhesion, and we have activation, and we have aggregation. Different sources have different opinions. Some sources will say they activate first. Others will say they adhere first. Others will say they aggregate and then adhere and activate. Doesn't matter. Okay? I like adhesion, activation, aggregation. The sequence doesn't matter that much, as long as you know what the mechanism is.
In the previous video, I had 10 steps of platelet plug formation. But let's summarize them into three main steps: first, platelet adhesion. The platelet adheres to the subendothelial collagen. What helps is the von Willebrand factor. Where did it come from? From the endothelium and the platelets—both of them. What's the receptor that helps the platelet here? GP Ib. GP stands for glycoprotein. If there is Ib, there will be IIb. Yes, indeed. There is IIb. GP IIb/IIIa—who expresses this enzyme or this receptor? ADP; so we call this ADP-dependent expression of GP IIb/IIIa receptor. What else we have? Thromboxane A2, which is a vasoconstrictor and a vasoconstrictor and a platelet aggregator par excellence. So here is platelet activation.
Then we have platelet aggregation. They will aggregate together. Each platelet will express its own GP IIb/IIIa receptor. A molecule of fibrinogen happens to exist in between, and then we will convert fibrinogen into fibrin, and this will be secondary hemostasis, which is the topic of the next video.
The upcoming mnemonic is not for everyone. Some people will like it; some people won't, and that's okay. Here's the real story, and here's the mnemonic. Injury leads to the endothelium being removed. Yes, this piece is removed. SEC is exposed. SEC is the subendothelial collagen. Here we have FCO exposed. Then the platelets swell. Yes, the MCO will exactly swell. Yeah, absolutely. Pseudopods, pseudobrain. Nobody is thinking at that moment. Contractile proteins contract. The PC muscle contracts, the pubococcygeus muscle. After contraction, release. Absolutely. Platelets become sticky. Yes. Everything is sticky. Tissue leaks. Yes, it does. Then adheres. Mhmm. Fibrinogen is converted into fibrin, forming a strong plug. Here we have a strong bond. This strong plug will trap the red blood cells. Trap my heart.
To get all of my notes from my bloody Dropbox folders, go to patreon.com/medicosus. Please consider subscribing. We are on YouTube, Facebook, Instagram. We're everywhere. Thank you guys for watching. Until next time. Be safe, stay happy, and study hard. In the next video, we'll talk about secondary hemostasis and the coagulation cascade.