Secondary Hemostasis - How Your Blood Clots (Coagulation) - Hematology
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- Опубліковано 30 вер 2024
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►👨🏫💊Antibiotics Lectures: www.medicosisp... ... Check out my brand new "Electrolytes" course at www.medicosisp... and use the PROMO code: ELECTROLYTES50 to get a 50% discount. Platelet plug formation is also known as primary hemostasis.
Secondary hemostasis, on the other hand, deals with converting fibrinogen into fibrin via the coagulation cascade to form a strong plug to stop bleeding.
Too little coagulation and you'll bleed. Too much coagulation and you will thrombose. Both extremes are bad.
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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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/...
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he died
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Amazing video as usual thank you, for the answer I think it has to do with stasis, when blood doesn't move that cases the platelets to aggregate and get activated this releasing the granules and factor 3 causing the cascade to start
Hi ! Do you have videos on carbohydrate metabolism ?
Not yet
Thank you man
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my only question doctor is, why is there no hemarthrosis in platelet disorders/thrombocytopenia, but there is in coagulation deficiencies, if as you say, you cannot have coagulation without a primary platelet plug?
Sometimes you can have good 2ry hemostasis without good primary hemostasis.
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what about that factor xii (12) is not working in vivo but in vitro? i read it today while sloving MCQS . this confused me .
Sorry, I don’t understand your question
Medicosis Perfectionalis Factor XII is part of the coagulation cascade and activates factor XI and prekallikrein in vitro.Factor XII itself is activated tofactor XIIa by negatively charged surfaces, such as glass. This is the starting point of the intrinsic pathway @medicosis perfictionalis my colleague said to me factor xii work in vitro not in vivo
Then who is going to activate factor XI in vivo?
are platelet factors (platelet factor 3 and 4) the same as clotting factors (factor 1 - 12)?
Nope
Thanks
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I think that’s fair!
Actually there are 20 factors since last year.. c mon
20 factors of what?
Of coagulation.. Like protein C.. Protein S.. Even vW factor is number 13
Do you have any reference so that I can check it out?
@@MedicosisPerfectionalis I will try to find those news. I recently learned at university that since last year there are 20factors of coagulation. The 19th is protein C, the 20st is protein S. Anyway you can search on google
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How?
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