Had virtually no hemostasis and thrombosis lectures in my residency! Thank you for breaking it down to the point where anyone can understand your material! THANK YOU!!!!!
+zoink540 Thanks. It wasn't until I started looking into this topic in depth in preparation for this video, did I realize how confusing the relevant review papers were!
Thank you for the remarkable videos. Is there a way to share part of the video (the fantastic animation) in a lecture ? thank you for further information.
This is a great video. However something remains unclear. As far as I am aware, the vWF mediated adhesion occurs under high shear rates. This binding isn't enough, despite it's necessity under high shear. Following the vWF is the neighbouring binding to GPVI, which signalls the platelet to activate integrins (Ia/IIb a.k.a GPIa/IIa]) which tightly fixes the platelet to the adhered surface. Under low shear, as far as I know, binding to collagen is also mediated via GPIIb-IIIa and fibrinogen - but I cannot find any information on this. Your lecture states GPIb-IX-V-vWF-collagen binding occurs as well as direct GPIa-collagen and GPVI-collagen without the mention of fibrinogen. Is this the case and is the direct binding viable? 🤔
Thank you for yet another great video. At 3.00, as I can guess without subtitles, you say "While the vasospasam of the endothelial cells..." What type of cell really contracts to provide vasospasam?
+Fabian Balderrama The terminology is confusing. Alpha granules release coagulation factor V (Roman numeral), as well as platelet factor 4 (Arabic numeral). Whereas factor V plays a critical role in the coagulation cascade (discussed in lesson 3), the role of platelet factor 4 (PF4) in normal physiology is less clear. The only major reason to know about PF4 as a practicing clinician is due to its role in the development of a condition called heparin-induced thrombocytopenia (which will be discussed in a future video on hypercoagulable states - which I just haven't had time yet to make).
This is really helpful, thanks a lot for this good explanations. Just one question: do you have any references? I'm writing my thesis atm and I can't really cite a youtube video :(
Had virtually no hemostasis and thrombosis lectures in my residency! Thank you for breaking it down to the point where anyone can understand your material! THANK YOU!!!!!
This is great. Really clarifies some concepts that are not laid out all that well in peer reviewed publications. Many thanks!
+zoink540 Thanks. It wasn't until I started looking into this topic in depth in preparation for this video, did I realize how confusing the relevant review papers were!
Clear and concise, a great presentation which I shall recommend to all my students. Thank you for this effort.
Thank you for this leacture. The animations really helped piece all the information together.
Thank you for the remarkable videos. Is there a way to share part of the video (the fantastic animation) in a lecture ? thank you for further information.
Thank you very much for the amazing approach
Is that possible to have the slides?
ADAMST13 .. lol .... I keep enjoying your videos, pls keep up the great work.
Excellent and clear explanation of a difficult topic. Thank you
Thank you for the response!!!! You're amazing!
Absolutely love your content! Thank you
Amazing! Incredible! Fantastic! Wonder! Super!
Brilliant lectures Eric
Thank you so much. These videos are incredibly helpful.
AMAZING video!!
Very nice Eric! Thank you so much
Beautiful videos. Keep going.
Wow Nice animation in between!!
Brief, well explained, fine diagrams
Very helpful for medical students
Thank you!!!!!!!.....After 15 years...I now understand this!!!!
Thank you so much for this simple explanation of such detailed information 🙏🙏🙏
You are in a different level ,,,
This is a great video.
However something remains unclear.
As far as I am aware, the vWF mediated adhesion occurs under high shear rates. This binding isn't enough, despite it's necessity under high shear.
Following the vWF is the neighbouring binding to GPVI, which signalls the platelet to activate integrins (Ia/IIb a.k.a GPIa/IIa]) which tightly fixes the platelet to the adhered surface.
Under low shear, as far as I know, binding to collagen is also mediated via GPIIb-IIIa and fibrinogen - but I cannot find any information on this.
Your lecture states GPIb-IX-V-vWF-collagen binding occurs as well as direct GPIa-collagen and GPVI-collagen without the mention of fibrinogen.
Is this the case and is the direct binding viable? 🤔
Super good lecture. Your lecture is the best in education for intend audiences.
Thank you Dr. Strong! I am Pediatrics resident in Colombia. Your videos are very clear and informative :)
Thank you, doc. From School of Medicine in University of Hargeisa
movable video or diagram about plat.activation is wonderful
at 9.45 min
awesome video. thank you!
So I just want to make sure that the platelets also secret vWf? And thanks very much for your lectures.
Brilliant lekture
thank you very much for clarification
Thank you for yet another great video. At 3.00, as I can guess without subtitles, you say "While the vasospasam of the endothelial cells..." What type of cell really contracts to provide vasospasam?
pericytes
Every blood vessel (except for the miniscule capillaries) has it's own muscular elements myocytes.
Awesome 👌🏼
Great lecture ,
neatly presented :)
this makes so much more sense than our lectures
Thank you, it was very instructive. However, I still have a shadowy area. What is the flip-flop ??
Is where Calcium cause the platelets to expose their serine substrates which causes clotting factors to bind to the platelets
I promise u, this is exactly what u need :) :)
So good. thank you
Awesome video.... but the alpha granules have/release Factor 4 (IV), not Factor 5 (V) I think.... let me know if I'm wrong :-)
+Fabian Balderrama The terminology is confusing. Alpha granules release coagulation factor V (Roman numeral), as well as platelet factor 4 (Arabic numeral). Whereas factor V plays a critical role in the coagulation cascade (discussed in lesson 3), the role of platelet factor 4 (PF4) in normal physiology is less clear. The only major reason to know about PF4 as a practicing clinician is due to its role in the development of a condition called heparin-induced thrombocytopenia (which will be discussed in a future video on hypercoagulable states - which I just haven't had time yet to make).
Excellent thank you too much doctor
THANK YOU!!!
Thank you so much
very good!
Too good
These are great! Just an aside, around 13:22 GP VI is written "GP IV."
Grrr...that's annoying...thanks for letting me know! (I really need to find someone willing to proofwatch these...)
+Eric's Medical Lectures you are great!
Thank you :)
Wow please how can I download this video
Excellent
Well .... It is still very difficult, but easier than the book though... So thank you !
Great. Is there anywhere that the PowerPoint is accessible?
All the pdfs I have for my videos are available here (which I believe includes this one): drive.google.com/drive/folders/0B9SDUwepGWeUTmtscnJSSjR5OE0
marvelous 🌺🌺🌺🌺
This is really helpful, thanks a lot for this good explanations. Just one question: do you have any references? I'm writing my thesis atm and I can't really cite a youtube video :(
Great question. I could use links to the source material too, especially when the explanations need context or further reading. 😎
I can only view 4 videos in Haematology, Am i missing some? can i find the whole series anywhere else?
Many Thanks
Sorry, I've only posted the first 4. Still working on the others. The next one in the series should be posted within a few days.
splendid!
ManyThanks
Can you share the PowerPoint here?
I'm very sorry, but I stopped sharing my PPT files many years ago after finding them incessantly plagiarized.
9:37
excellent
*ANO NE ANO NE*
..that must be one of the ridiculous enzyme names in the body.. völlig korrekte
this topics are very frustating tho -_-