In my university, the lecturer explains all of this in a difficult way that only if you have studied everything you will know what he's talking about . Even though we study pharmacology for the first time this year . Nobody gets to the roots of subjects like you do . Thank you ❤️
Not only are you extremely effective at simplifying and making this content digestible, but you also share an incredible amount of enthusiasm when presenting your main points. I believe this is one of the reasons why people praise your work in every single video I watch. Thank you for that.
Thank you so much for all you explain. Many universities don’t have professors with the capacity to explain things the way you do, a way we all understand. drawing is the best source to remember things. Thank you thank you.
Thank you for this great lecture! I appreciate much your work. There is one little mistake at 12:00. The adrenal gland's average secretion is 80% epi and 20% NE
Right on time! Im struggling on my uni with pharmacology cause lectures are bad and there is not enough study material. Thank you ninja nerd for teaching us everything
I saw those graphs about adrenergic agonists in first aid .. I couldn't understand anything from those pictures . .. after watching this lecture when I go back to first aid.. I wondered how easy was that.. this is his magic.. full of concepts..thank you
Honestly, I'm in a class that has NO lecture on pharmacology whatsoever. It's a "read the book and take the quizzes" kind of class. Thank you so much, I would send you my tuition money if I could.
Thank you so much for this video! Helped me get through my Pharmacology exams! Would really appreciate another lecture with you about NSAIDS and DMARDS :>
This is very interesting to someone who has high blood pressure. I found out last year that drinking alcohol reduces my pressure significantly. Couldn't figure out why that is, but watching this video made me think it has something to do with the alpha 2 receptors. Is that right? Does whiskey act like Clonidine?
Alcohol is a ligand of GABA receptor (much stronger ligand than GABA itself) so it reduces the action potential of the cell, better said it calms you down. I guess the effect comes from that overall sedative effect it has on your CNS and all other subsystems being downregulated. That's my guess.
I am actually blown away by your brain and how it can remember all of this info. I am watching your videos in hope they can teach me what my pharmacology lecturer cannot.....however its still way over my head. )-:
An alpha 2 agonist I’d also add that we use quite frequently in the ICU is dexmetetomidine. We run it as a drip for sedation. Works great for patients who we need sedated but still need a respiratory drive. Definitely see the effect on heart rate and blood pressure at times.
@@BarrelCollective It’s a direct alpha 2 agonist, which inhibits the release of catecholamines from neurons which leads to bradycardia/hypotension. Sometimes quite profound.
I had a patient in the ICU who experienced intense reflex bradycardia from norepi! BP would increase significantly and then HR dropped into the 40's and occassionally patient would convert into a junctional rhythm! Very interesting to put two and two together!
As your video lectures are very very informative Please make video lecture on Oncology topics like Breast Cancer colorectal Cancer Leukaemia lymphomas … highly requested
I wish you would’ve touched on dexmetotomidine while you were talking about Alpha 2 agonists. I think it’s sedative nature and adverse affects are confused in most people outside of those prescribing it
I have question! On the timeline the event that starts at 1:25:39: Systolic blood pressure going up it's for two effects: alpha-1 receptors on arteries and veins, alpha-1 receptors that are present on veins that's going to increase venous return, increase preload, INCREASE CARDIAC OUTPUT! The other thing is that there's beta-1 receptors and there is little bit of beta-1 receptor effect and you can increase contractility and INCREASE CARDIAC OUTPUT!! How the hack could be at 1:27:40 that CARDIAC OUTPUT HAPPENS TO BE NEUTRAL???? 1:27:56 now we have alpha-1 receptors ONLY on arteries (not on veins anymore?) that increases afterload and if we increase afterload, we DROP CARDIAC OUTPUT???? How could that be?
I request you to upload videos about Drugs for respiratory disorder and git disorders ,autacoids and related drugs . I'm completely dependent upon you🥺
Take Guanfacine for Autonomic Dysfunction. Used to take Clonidine but was changed to avoid rebound hypertension. Autonomic Dysfunction due to removal of bilateral carotid body tumors and resultant vagus nerve damage.
I appreciate your effort very much. But what I am asking is to let us take full picture of your note please leave board fully visible after lecture. Thank you
Perfect video, amazing breakdown of content. I love your videos. Keep it up please. Thank you for everything you and your team are doing to make our studying more amenable.
This might be the only lecture that I've left feeling confused about. In the beginning, you noted that norepi caused decreased HR, decreased contractility, decreased CO@ and also decreased SVR and BP, but then in the comparisons it was not the same. Was this ONLY for higher doses of norepi??
Can the B3 agonits ,since they're located within the adipose tissues and helps breaing down triglycerides , be used to lose weight or to reduce fatts in our body ?
if systolic blood pressure depends from cardiac output and systolic blood pressure increases with Norepinephrine then the cardiac output must increase as well!
