Hemostasis: Lesson 5 - Antiplatelet Meds (Part 1 of 2)
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- เผยแพร่เมื่อ 3 ก.ค. 2024
- An overview of antiplatelet medications. Part 1 covers on aspirin. Part 2 covers P2Y12 inhibitors (e.g. clopidogrel, prasugrel, ticagrelor), IIb/IIIa inhibitors, dipyridamole, and cilostazol.
Excellent video, as always! Yours are definitely among the best videos I've ever seen to learn medicine. Thank you very much for all the effort you put into making them.
dear Dr. strong you are the best teacher I've ever met in my life. Thank you, God bless you. Best regards from Croatia
thanks from irak
Thank you. Good lecture.
Great lecture, thank you. But I think you should also mention the risk for acute kidney injury (with higher doses of aspirin) among side effects. It's a very common complication that people tend to forget.
+Caravanaserai Thanks for the comment. I'm going to discuss NSAID-related AKI in an upcoming video, but you're right that I should have mentioned it here too. In the US, it's my observation that aspirin-associated AKI isn't as commonly observed as it apparently once was, because people are favoring other NSAIDs (e.g. ibuprofen, naproxen) for chronic pain management; but we still see it occasionally.
+Eric's Medical Lectures I guess the reason I'm writing this comment is that (in EU, especially in Slovenia where I currently work as an internal medicine fellow) aspirin is widely marketed as if it was the analgesic/antipyretic drug of choice. It's when people start to rationalize like this: "since my grandpa can take an aspirin a day and he's just fine, so can I". But grandpa takes 100 mg (for CV prevention), and you 500 mg (analgesia). And that's the difference. What about the ulcer? "No problem, I'll take PPI (it's also over-the-counter medicine) and I'll be fine." So the patient is on higher doses of aspirin permanently with false sense of safety and years later ends develops chronic kidney disease, possibly due to chronic interstitial nephritis, if not sooner with AKI.
I agree with you, there are probably more acute kidney injuries (as well as chronic kidney disease) due to newer and more widely used NSAIDs, but since aspirin has a different indication (secondary prevention of CV events) it is the false general perception that leads people to believe that aspirin is OK to take on each and every occasion. In my opinion the aspirin should only be used for its antithrombotic properties.
Hi Dr. Strong, appart from the loading dose , what's the rationale for the higer aspirin doses in the first days\weeks after an ACS\ischemic stroke?
Excellent lectuew, Dr Strong! I am looking forward to the video about new new generation anticoagulants. Also, about the role of aspirin in acute ischemic stroke: in your opinion should it be given even when the patient is going to receive alteplase?
Please keep up the great work
That's a good question that I could have addressed...in general, aspirin should not be considered as a contraindication to alteplase (thrombolysis). For example, imagine a patient who arrives to the ER with signs of a stroke, receives aspirin immediately, and then has a head CT which rules out a intracranial bleed as the etiology of symptoms. In that circumstance, the prior aspirin administration should not be used to significantly argue against thrombolysis (given the potential benefit of thrombolysis outweighs any possible risk from the aspirin). However, one trial (ARTIS), found that coadministering aspirin with thrombolysis led to an increased risk of symptomatic intracranial hemorrhage compared to thrombolysis alone. Therefore, I wouldn't intentionally give both at the same time. I don't know if there is specific evidence for this, but in common practice, if aspirin is not given up front in a patient who receives thrombolysis, it's typically not started for 24 hrs after thrombolysis is given.
Excellent Dr, I am looking forward for part 2 and please be more specific for clopidogrel Many Thanks From Egypt
I'm not so sure about that. Personally for me, aspirin works more quickly and the effect lasts longer as far as pain relief is concerned. I have had experience taking ibuprofen, acetaminophen, and aspirin for headache relief and this is what I found:
Acetaminophen has a delay of up to half an hour and works for about 6 hours, just as the instructions say. Also, there is still residual pain after the dose
Ibuprofen has about the same delay and effective length as acetaminophen and there is residual pain
Aspirin works in 2 minutes and lasts all day. No residual pain whatsoever.
I hope you respond to me, 13:54
you said ''high dose ASA needed to achieve antiinflammatory and antipyretic effects to be evident''.
however you wrote Pain and Fever, which would be countercted by analgesic and antripyretic effects of a drug.
COuld you clear this up please? It'sconfusing.
LOW dose (baby ASA) 81mg (low) is surely for long term use for patients with anamnesia of CVD(so it's 2ndary PPX against CVDs)
maybe im just wrong as i think inflammation(oedema)(tumor), fever(calor), pain(dolor), redness(rubor) are seperate progresses that are all initated from the same endothelial damage, collagen exposre.
If we think about it tissue damage causes antiinfammatory mediators to released,
tldr: when you said antiinflammatory and antipyretic effects to be evident:
Do you (or in general in this field), refer antiinflammatory and analgesic as the same? (interchangeable)? I doubt it.
All due respect, great video. I hope you can elaborate under my comment.
thanks!
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ok but when you stop the synthesis of TXA2 , you untouched he effects of adp + thrombin and others , so how aspirin alone is effective ????
Thoughts on vorapaxar?
Nyc
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