Amazing explanation, clear and informative diagrams. I was watching a lecture at my university and didn't really understand primary hemostasis, but this video really cleared it up.
for the last part of this video, isn't it fibrin instead of fibrinogen? i thought fibrinogen needs to be converted to fibrin and then it can form cross-linked mesh?
I don't know why people are complaining about the voice over. I thought it was perfect. She was talking like an actual person does when they are talking to you. And personally, that helps me listen better. Would people rather it be completely monotone? To each their own I suppose.
Great video however I'm not an engineer but if a bridge falls out or half of it does it would be common sense that you don't use the bridge because the integrity of the bridge is no longer intact
its cool to learn here definitely....but the high speed video and high speed talking of a person who knows everything about the topic makes learning harder (have to constantly stop video) teaching is not just spewing out stuff as fast has humanly possible....but actually considering who is watching....of course IMHO
Thank you so much, amazing video. I have a question if someone can help me with it - When an injury occurs, why do we only lose NO and prostacyclin (vasodilators) with the blood and not the vasoconstrictor, endothelin?
because the winner is endothelin :) I mean like vasoconstrictor more stronger while injured, so the vasodilators gonna fail with it. Hope it's gonna help u,guys😊
First response to vascular injury is vascular spasm or vasoconstriction to reduce bleeding. Then platelet plug, aggregation, and thrombus form. Injured or damaged endothelial cells release endothelin which will act on smooth muscles to contract and ultimate goal will be vascular spasm. Particularly endothelin will trigger release of calcium in smooth muscles which will cause contraction
Thanks pretty darn good overview. My Lippincott Pharmacology text fills in some details but your narration and illustration make the concepts and substances a bit easier to latch on to...One small note of criticism, meant constructively, the "hole" in the vessel is called the lumen.
The alpha granules contain fibronectin, not fibrinogen - fibrinogen itself has to be activated by thrombin to become FIBRIN and is stickier - it polymerises with other fibrins and stuff, and only binds to fibronectin when mediated by factor VIII. Fibronectin... don't polymerise, they bind to fibrin when Factor VIII comes into play and catalyse the process (factor VIII stabilises fibrin and 'contracts' it, closing up wounds), Fibronectin mainly binds cell membranes through connecting with integrin molecules, which means it binds cells to cells. Platelets basically start working on long term healing the moment the are activated, but is relatively inefficient until fibroblast cells come in and form huge amounts of connective tissue etc.
It is a very good video but please, please, please stop moving the cursor around when you are not writing! You wiggle it around and shake it constantly, it is distracting and annoying. I would quit watching this video except it was assigned by my instructor.
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THIS VIDEO IS ABSOLUTELY AMAZING!!!! I actually am understanding!! :D THANK YOU KHAN ACADEMY!! :D
i wish u were my professor :(
You saying fibrinogen leads to platelet aggregation? Doesnt have to be cleaved to fibrin by thrombin first?
Amazing explanation, clear and informative diagrams. I was watching a lecture at my university and didn't really understand primary hemostasis, but this video really cleared it up.
for the last part of this video, isn't it fibrin instead of fibrinogen? i thought fibrinogen needs to be converted to fibrin and then it can form cross-linked mesh?
I know I'm late but fibrin only exists in secondary hemostasis.
Thank you for your simple explanation
thank you khan academy, for helping me with almost every exam TT
I don't know why people are complaining about the voice over. I thought it was perfect. She was talking like an actual person does when they are talking to you. And personally, that helps me listen better.
Would people rather it be completely monotone? To each their own I suppose.
Great explanation. Really helped explain the details of primary hemostasis from First Aid 2017
I absolutely love khansacademy ☺️☺️☺️
Great video however I'm not an engineer but if a bridge falls out or half of it does it would be common sense that you don't use the bridge because the integrity of the bridge is no longer intact
Really thank u... God bless ya❤️❤️
thankzz
great video!!
Fantastic video! Thanks
i love this video thanks!!!!
this is outstanding. very concise, understandable, easy to remember
great work ..
Thank you so much for blowing up my mind, this video is super amazing and easy to be understood!!!!
its cool to learn here definitely....but the high speed video and high speed talking of a person who knows everything about the topic makes learning harder (have to constantly stop video) teaching is not just spewing out stuff as fast has humanly possible....but actually considering who is watching....of course IMHO
Thank you so much, amazing video. I have a question if someone can help me with it -
When an injury occurs, why do we only lose NO and prostacyclin (vasodilators) with the blood and not the vasoconstrictor, endothelin?
because the winner is endothelin :)
I mean like vasoconstrictor more stronger while injured, so the vasodilators gonna fail with it.
Hope it's gonna help u,guys😊
great! i almost got it! thank you
Great information
what is the program for the drawings?
This video is so helpful, thank you
Excellent !
the content is good but the voice over is so poor!
No its not
thank you! very helpful video, i recommend also watching the 2ndary hemostasis video by Khan Academy
First response to vascular injury is vascular spasm or vasoconstriction to reduce bleeding. Then platelet plug, aggregation, and thrombus form. Injured or damaged endothelial cells release endothelin which will act on smooth muscles to contract and ultimate goal will be vascular spasm. Particularly endothelin will trigger release of calcium in smooth muscles which will cause contraction
Awesome! Thank you so much!
pravo... thx thx thx ❤❤❤❤❤
I can be clear with u guys I wouldn't make it through one day before exam without u 😭🙏
Thanks pretty darn good overview. My Lippincott Pharmacology text fills in some details but your narration and illustration make the concepts and substances a bit easier to latch on to...One small note of criticism, meant constructively, the "hole" in the vessel is called the lumen.
thank you for your sharing ms, this is best, i really analyze the process of primary hemostasis, thank you, i hope for you response 😇
Wonderful amazing thanks
The alpha granules contain fibronectin, not fibrinogen - fibrinogen itself has to be activated by thrombin to become FIBRIN and is stickier - it polymerises with other fibrins and stuff, and only binds to fibronectin when mediated by factor VIII.
Fibronectin... don't polymerise, they bind to fibrin when Factor VIII comes into play and catalyse the process (factor VIII stabilises fibrin and 'contracts' it, closing up wounds),
Fibronectin mainly binds cell membranes through connecting with integrin molecules, which means it binds cells to cells. Platelets basically start working on long term healing the moment the are activated, but is relatively inefficient until fibroblast cells come in and form huge amounts of connective tissue etc.
Alpha granules contain both: fibronectin AND fibrinogen
They have both, actually.
Fibrinogen is produced by the liver. I think you meant to say "Fibronectin".
fibrinogen and fibronectin both are present in alpha granules of platelets
I can get sound on other videos but not the primary and secondary hemostasis?
Great explanation. Thank you!
Gorgeous 🤝🏻✨
Best
Really good explanation, thank you
So nice!
Str8 fantastic video thnx so much for explaining this in a simple manner
nice helpful vedio thanks alot
I don't understand the purpose if vasoconstriction as a result of damage to collagen. Wouldn't this cause more blood to be lost?
Vasoconstriction will increase the flow resistance therefore reducing the flow of blood to the wound site.
Great, thank you! What is the name of this software?
Thank you and love you 😍
I love you !
Hey, do u com(ment) here often?
These are really helpful......thank you
Great work thank you
YOU ARE BRILLIANT!
y are amazing tnx
Thankyou!
Thank you 🙏
very good job !!!
this is really helpful!
thanks a lot 😊
So just to clarify, does fibrinogen not fibrin aggregate platelets via their activated 2b/3a receptors?
Fibrinogen aggregates the platelets via their receptors. Fibrin is formed from fibrinogen by thrombin.
thankyou
great vedio
Thank you
thank you!!!!
THANK YOU
thank you!
too fast, too fast! lol but still helpful
THANK YOU!!!
thank you!
I think ..stop saying that .. Plz .
your constant pausing in your sentences is killing me.
no she is cute u fuck
The voiceover/dictation of the topic is SO distracting... still, helpful information..
It is a very good video but please, please, please stop moving the cursor around when you are not writing! You wiggle it around and shake it constantly, it is distracting and annoying. I would quit watching this video except it was assigned by my instructor.
You're so hard to understand it makes me sleepy. Prolly because of how you talk. But thanks for the effort