You would be the reason I graduate from med school.Thank you so much for making this course so much easier. I wouldn't be able to do this if it wasn't for your tutorials.
Thanks for the review! Just want to add a few things now that things are coming back to me: PGE2 --> uterine contraction; NSAIDs might be good for menstrual cramps. Prostaglandin also affects the kidneys; NSAIDs can cause kidney failure/damage.
Created an account just to say thank you so much for making this video. Was super helpful since I had no idea what my lecturer was on about. Really easy to understand and saved me listening to an hour long lecture. Thank you!
Thank you, 6 weeks of hard to understand lectures condensed into 7 mins of easy to understand video. University lecturers should be afraid of these videos, they could easily take their jobs!
Hello. Can anyone tell me what's the sentence on 7:04 'this is because the protective ________ of the prostaglandin on the stomach......' Thank you in advance
Fantastic explanations & easy to understand. Thank you sooo much & I'm hoping with enough practice these short vids will really help with my Pharmacology exam :-)
I am doing a project on Aclovate, a topical corticosteroid. Now, you mentioned that non-steroidal anti inflammatory inhibit the production of COX. However, what do steroidal anti-inflammatory inhibit?
COX 1 and COX2, acylation by aspirin, time course of action compared between Aspirin and other NSAIDS ? What I understand is that when COX is inhibited, the AA is shunted to make more leukotrienes and that is the cause of the broncoconstriction. Where does the Phospholipase A2 come from? I know some comes from the pancreas but I assume that is not the source here.
Thank you so much you helped to find out what was actually the role of COX but i heard that painkillers may also have effect on the kidney. Can someone please explay me short why ? ( sorry for my bad english i'm actually french )
I have one question but i am not sure whether its related and it is really confusing me . I want to know that if Arachidonic acid and the cyclooxygenas enzyme could be produced from the same cell . Does COX and AA could have same site of production ? Ok even i could include LOX.
thanks fr the video bt i have one question. i didnt get how aspirin was gud fr heart ?if it inhibits activity of cyclooxygenase so how could it possibly produce prostacyclins?plzz HELP !!
it inhibits Cox pathway in both platelts and endothelial cell..however endothelial cell has nucleus, thus able to regenerate the COX...soo aspirin will shift towards anti coagulant state..I think
AS i bodybuilder, i supplement with AA at 1000mg before every workout! Its a product called X-factor by molcular nutrition. Well the point is to cause inflammation in the muscles, which in results tells to body to send nutrients and blood into them, this then has a positive effect on muscle building. Any thought on this kind of use of AA ?
While I would thanks for your best and easy explanation ,could you please explain how prostaglandin H2 turns into platelets,I really did not get that.As far as I know platelets are produced from megakaryocytes
To state that Thromboxane A2 is 'bad for the heart' and therefore harmful to the body is an oversimplification. Thromboxane A2 (TXA2) is released by platelets once they are activated- that is, once they have bound to damaged blood vessels and are in the process of creating a 'platelet plug' as the first step in repairing that damage. The released TXA2 recruits other platelets from circulating blood to assist in covering the site of damaged blood vessel. In this case, TXA2 is very GOOD for the cardiovascular system and the body as it allows for efficient blood vessel repair. However, individuals who have an increased risk of thrombus formation (blood clots) can reduce this risk by inhibiting the release of TXA2 and thus reducing platelet accumulation. Aspirin is given on a regular basis to people with this risk to reduce TXA2 production, not to reduce inflammation. Although aspirin and ibuprofen are both NSAIDs, they have very different pharmacokinetics as aspirin covalently binds to COX (disabling it entirely) whereas other NSAIDs only competitively bind to it. The covalent bond to COX allows for aspirin to effectively disable platelet aggregation (thus why it is known as an antiplatelet drug) whereas other NSAIDs only have a mild inhibitory effect on platelets. In general, any substance produced by the body isn't purely 'harmful', and if it is, it's because not creating that substance would have meant something much worse for the body. For example, harmful substances are created when you are starving as a byproduct of trying to produce energy, but if you didn't create these byproducts you would die much more quickly from lack of energy. The only exception to this rule is during a pathology when inappropriate amounts of something harmful, or production of something harmful at the wrong time, is occurring. Hope this helps :).
Steroids inhibit the key enzyme Phospholipase A2, so the entire cascade is blocker, thereby Streroids can play a beneficial role both in Asthma and Inflammation. :)
You would be the reason I graduate from med school.Thank you so much for making this course so much easier. I wouldn't be able to do this if it wasn't for your tutorials.
At the end of the video would you consider zooming all the way out so that I can see the entire picture and make sure I can see/talk it out to myself?
@@louie188 thanks~~
Instablaster...
Thanks for the review! Just want to add a few things now that things are coming back to me: PGE2 --> uterine contraction; NSAIDs might be good for menstrual cramps. Prostaglandin also affects the kidneys; NSAIDs can cause kidney failure/damage.
I have always found it easier to understand what I am reading with the aid of visuals
, Thank you very much for making these videos.
added to my pharmacy playlist! awesome vid
wow! the way you link everything together, makes everything just click!. thank you sooo much!
Created an account just to say thank you so much for making this video. Was super helpful since I had no idea what my lecturer was on about. Really easy to understand and saved me listening to an hour long lecture. Thank you!
u alive ?
Wonderful overview. Amazing that weeks of lectures couldn't convey what you did in 7.5 minutes. Keep up the great work.
OMG, you are a savior! Thanks from the Vet student from Latvia!
This video is amazing, just watched it for fun a year after I found it for physiology homework.
Very useful video. Keep uploading many more like this in medical physiology.
Amazing tutorial, the explanation was simple and informative. Keep up the good work
Thank you, 6 weeks of hard to understand lectures condensed into 7 mins of easy to understand video. University lecturers should be afraid of these videos, they could easily take their jobs!
Thank you! So straightforward when you explain it!
Amazing. You just saved me for my Cell and Molec test!!
Keep on making these videos.
You are getting me through my MPHARM degree!!! thankyou so much.
how can these videos have unlike??? omgg ure amazing
Some Haters ...
Brilliant ! thanks for making this subject clear and simple...
Marvelous! very clear voice which makes it easy to understand the process.. thanks a bunch!
This is my first time understanding very well thanks from Egypt ❤❤❤
Really helpful, simple and easy to understand. Thanks a lot.
Well done... So neat and organized! Thank you :-)
wya rn
thanks alot! this vid helped me understand our eicosanoid lesson in my metabolism subject
Hello. Can anyone tell me what's the sentence on 7:04 'this is because the protective ________ of the prostaglandin on the stomach......'
Thank you in advance
protective effect
thank you for this. brief, clear and simple..
Hi Leandra, I'm from Melbourne, Australia.
Thank god 2011 is over and people dont still make writing videos!
Fantastic explanations & easy to understand. Thank you sooo much & I'm hoping with enough practice these short vids will really help with my Pharmacology exam :-)
hey I am a post graduate and was still fumbling with that.. appreciate your efforts, it certainly did help....
Thanks !! :)
defo post post graduate rn
this is a wonderful video do you have any videos on Glycolysis, ETC, Oxidative Phoshorlyation
Far out...if only you were my lecturer...I'd be less confused during class! Thank you!
I am doing a project on Aclovate, a topical corticosteroid. Now, you mentioned that non-steroidal anti inflammatory inhibit the production of COX. However, what do steroidal anti-inflammatory inhibit?
Phospholipase A2
one of the best videos .. great work !!
COX 1 and COX2, acylation by aspirin, time course of action compared between Aspirin and other NSAIDS ?
What I understand is that when COX is inhibited, the AA is shunted to make more leukotrienes and that is the cause of the broncoconstriction. Where does the Phospholipase A2 come from? I know some comes from the pancreas but I assume that is not the source here.
abelincolnparth hi, phospholipase A2 is released due to any stress to phospholipid layer (the cell membrane)..
This is gold! I finally get it thanks to u:)
Thank you so much you helped to find out what was actually the role of COX but i heard that painkillers may also have effect on the kidney. Can someone please explay me short why ? ( sorry for my bad english i'm actually french )
From where do phospholipase A2 come from?
amazing videos, I have seen a few and you make something that looks hard look so easy, thank you so much!
agreed
AMAZING!!! I'll never forget it!!!
funtastically explained A.A acid...a great help thank you sir
DUDE... YOU'RE A GENIUS !!!
That was GLORIOUS.
Omg man I’m studying Pharma and I just got these point only from you
This was an excellent video... thank you
Was easy to understand n recall!! thank u 😊
to answer my own question.... definitely Australian!!!! Thanks so much!!! ive watched it many times xx
I have one question but i am not sure whether its related and it is really confusing me . I want to know that if Arachidonic acid and the cyclooxygenas enzyme could be produced from the same cell . Does COX and AA could have same site of production ? Ok even i could include LOX.
+Black Mimosa I can't find those either..where does COX come from?
+Darrell Ng COX 2 is selectively produced by the enterocytes but COX 1 can be produced in any cell under inflammatory conditions.
Very good. However, I do think that you are missing a step between the production of arachadonic acid and PGH2. The formation of PGG2.
Very easy to understand like this!
very helpful video explained brilliantly and in a sequence thankyou :)
thanks fr the video bt i have one question. i didnt get how aspirin was gud fr heart ?if it inhibits activity of cyclooxygenase so how could it possibly produce prostacyclins?plzz HELP !!
it inhibits Cox pathway in both platelts and endothelial cell..however endothelial cell has nucleus, thus able to regenerate the COX...soo aspirin will shift towards anti coagulant state..I think
Finally! I understand this yessss
AS i bodybuilder, i supplement with AA at 1000mg before every workout! Its a product called X-factor by molcular nutrition. Well the point is to cause inflammation in the muscles, which in results tells to body to send nutrients and blood into them, this then has a positive effect on muscle building. Any thought on this kind of use of AA ?
WOW! very good and educational video. Thanks alot!!
very educational, easy to understand
THANK YOU!! where are you from I wonder? I cant place your accent for sure?
I don't understand how can arachidonic acid give thromboxane and prostaglycin which would work in opposite manner ?!
Excellent video, thank you!
super helpful, thank you!
Very useful... Thank you
Thank you this has really helped!!!
Watch at 1.5x speed. You’re welcome
amazing explanation. Thank you a lot
Best explanation, thanks
Great video!
dude you are a genius!!! thank you!!!
understaning pharmacology abit better now, thanks!
Very well described thanks!!!
this was golden. thank yoU!
This is so good
Thank you
i love this explanation.. very useful.. thank you =)
Thank you!! This saved my fine ass
😂
Really helpful thank you
helped me a lot.....thanks
Thank you so much❤❤❤❤❤❤❤
IT WAS REALLY HELPFUlLL .AHMAD AFGHA
Fantastic, thankyou
Thank you very much!
While I would thanks for your best and easy explanation ,could you please explain how prostaglandin H2 turns into platelets,I really did not get that.As far as I know platelets are produced from megakaryocytes
Im not sure you heard him correctly. What he said was that inside the platelets, Prostaglandin H2 is converted into thromboxane A2.
thank you mate ,yeah I got it now
Awesome! Thanks heaps!
Thank you!
best video 👍
Thank you
Thank you so much,this helped me a lot :)
donated five bucks! keep making 'em :)
Wow! your The best!
Thnx....God bless u.
Sir. Why does the body produce substances which is harmful to it ?
To state that Thromboxane A2 is 'bad for the heart' and therefore harmful to the body is an oversimplification. Thromboxane A2 (TXA2) is released by platelets once they are activated- that is, once they have bound to damaged blood vessels and are in the process of creating a 'platelet plug' as the first step in repairing that damage. The released TXA2 recruits other platelets from circulating blood to assist in covering the site of damaged blood vessel. In this case, TXA2 is very GOOD for the cardiovascular system and the body as it allows for efficient blood vessel repair. However, individuals who have an increased risk of thrombus formation (blood clots) can reduce this risk by inhibiting the release of TXA2 and thus reducing platelet accumulation. Aspirin is given on a regular basis to people with this risk to reduce TXA2 production, not to reduce inflammation. Although aspirin and ibuprofen are both NSAIDs, they have very different pharmacokinetics as aspirin covalently binds to COX (disabling it entirely) whereas other NSAIDs only competitively bind to it. The covalent bond to COX allows for aspirin to effectively disable platelet aggregation (thus why it is known as an antiplatelet drug) whereas other NSAIDs only have a mild inhibitory effect on platelets.
In general, any substance produced by the body isn't purely 'harmful', and if it is, it's because not creating that substance would have meant something much worse for the body. For example, harmful substances are created when you are starving as a byproduct of trying to produce energy, but if you didn't create these byproducts you would die much more quickly from lack of energy. The only exception to this rule is during a pathology when inappropriate amounts of something harmful, or production of something harmful at the wrong time, is occurring.
Hope this helps :).
Thank you!!!
Snape?
Steroids inhibit the key enzyme Phospholipase A2, so the entire cascade is blocker, thereby Streroids can play a beneficial role both in Asthma and Inflammation. :)
Thank you .well done
Only if our lecturers explained things this clearly, they just assume that you know the basics and overload you information right from the start :(
thank you sir
But PGE2 is for pain and fever not D2
the first pathway is 5-lipxygenase
thaaanx
watch at 1.5x
thank you soooooo much (:
Thanks.