Pro-clotting Mechanisms

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  • Опубликовано: 16 июл 2024
  • 😍🖼Animated Mnemonics (Picmonic): www.picmonic.com/viphookup/me...
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    Disclaimer: I use affiliate links....
    ►👨‍🏫💊Antibiotics Lectures: www.medicosisperfectionalis.c... ... Check out my brand new "Electrolytes" course at www.medicosisperfectionalis.c... and use the PROMO code: ELECTROLYTES50 to get a 50% discount. Blood coagulation is the most important decision in your body...Too much coagulation and you form an unwanted clot (such as myocardial infarction, DVT/PE or a stroke)...Too little coagulation and you may bleed to death.
    That's why blood clotting/coagulation is balanced by anti-clotting mechanisms VS pro-clotting mechanisms counteracting each other.
    In the previous video of this series, I have discussed the anti-clotting mechanisms (such as heparin, heparan sulfate, prostacyclin,...etc): • Anti-clotting Mechanisms
    To watch all of my bleeding and coagulation videos, click here: goo.gl/Dt41Bg
    Primary hemostasis is balanced on the dynamic harmonious antagonism between the smooth endothelium (that prefers laminar blood flow) and thrombocytes (which favor clotting and thrombosis).
    Platelets are called thrombocytes "cells of thrombus".
    The smooth endothelium is squamous epithelium that lines the blood and lymphatic vessels from the inside.
    When platelets roll over the smooth endothelium, nothing happens.
    But, once there is an injured endothelium, platelets adhere, activate and aggregate to form a temporary platelet plug (primary hemostasis).
    Then, the coagulation factors are stimulated "thanks to subendothelial collagen, tissue thromboplastin and platelet factor 3), coagulation cascade ensues until fibrinogen is converted into fibrin fibers trapping the RBCs and forming a stronger thrombus (secondary hemostasis).
    After that, fibrinolysis occur (thanks to tissue plasminogen activator or tPA) to destroy the clot and restore function and flow.
    Hemostasis is defined as “cessation of blood bleeding”.
    There are 2 types of hemostasis:
    1. Primary hemostasis: formation of weak, temporary platelet plug (by platelets).
    2. Secondary hemostasis: formation of stronger fibrin meshwork (by coagulation factors).
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    Disclaimer 1: The information provided here is for educational purposes only, and not to provide medical advice…If you have any symptoms or medical questions, you should talk to your doctor.
    Disclaimer 2: I use affiliate links.
    To be able to answer exam questions, Try to think of primary hemostasis and secondary hemostasis as two separate entities. 1ry hemostasis involves platelets and 2ry hemostasis involves the coagulation cascade. If you like my videos, please consider leaving a tip at www.paypal.me/perfectionalis/
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Комментарии • 19

  • @MedicosisPerfectionalis
    @MedicosisPerfectionalis  5 лет назад +4

    What are you waiting for?!!... My 50 hematology *cases* (vignettes) are waiting for you...board-style questions...www.patreon.com/medicosis/

  • @adrianpop4427
    @adrianpop4427 4 года назад +6

    Hi, love your vids, especially those in the coagulation playlist, but I would like to add a couple of things. First von Wilebrand factor is also produced in the megakaryocytes, that's why you find it in platelets as well ( makes things clearer for people who wonder how does it get in the platelet in the first place ). Secondly after many hours of searching in articles and books I couldn't find any mention that factor VIII cannot be activated without the vWF. High clearance of factor VIII is responsible for its lower activity in vWD. Also only in type 3 vWD there is a complete lack of vWF ( which are less than 5% percent of cases ), so it would be more accurate to say " lower levels or modified activity of vWF" rather than " you don't have the vWF". Hope that you can tell me where you read about factor VIII not being able to be activated without vWF, that would make all that searching worth while. Cheeers!!

  • @kckckrc
    @kckckrc 5 лет назад +3

    Great video with great information!

  • @shumailairshad8775
    @shumailairshad8775 3 месяца назад +1

    You are simply amazing 😍

  • @randomps3gamerx
    @randomps3gamerx 3 года назад +1

    Isn't VWF also made in megakaryocytes?

  • @paulhetherington3854
    @paulhetherington3854 2 года назад

    PRO-- Powered memories, of optics? Swedish--- THROM- Thrice recon, this is! movements of! Royal islanders. "Don't have a, Thrombone!" Austin Powers

  • @deepikayadav2363
    @deepikayadav2363 5 лет назад +3

    Why effect of aspirin last for 48 hrs if it inhibits platelets irreversibly and life of plt is 8 to 12 days?

    • @MedicosisPerfectionalis
      @MedicosisPerfectionalis  5 лет назад +7

      Because the bone marrow doesn’t wait for 8 to 12 days until all platelets die and then decide to produce new ones...It’s a 24/7 process...After 48 hours, you have a sufficient number of new platelets that are capable of primary hemostasis...Excellent question by the way!

    • @deepikayadav2363
      @deepikayadav2363 5 лет назад

      @@MedicosisPerfectionalis thanks a lot...u are awesome...but I m still confused...why do we stop aspirin 5 to 7 days before any surgery if 48 hrs is all it takes to wear off it's effect...

    • @MedicosisPerfectionalis
      @MedicosisPerfectionalis  5 лет назад +1

      Because you will have more platelets if you wait more, which makes the surgery safer. Please watch my video on thrombocytopenia where I discuss the difference between a platelet count of 150,000 , 90,0000, 50,000 , 20,000, etc...It will start to make more sense then.

    • @deepikayadav2363
      @deepikayadav2363 5 лет назад +2

      @@MedicosisPerfectionalis ok thanks a lot...please make more rheumatology videos...sincere request🙏

    • @MedicosisPerfectionalis
      @MedicosisPerfectionalis  5 лет назад

      I will...Thank you, dear!