An excellent explanation of the pathophysiology of Nephropathy in Hypertension & at a steady pace- allowing for an understanding without pausing &going back again & again.
andrew- this video was SO helpful. i actually get it!! the explanation of the hyaline substance leading to decreased flow to efferent arteriole, eventually causing tubular necrosis helped a lot.
Thank you for creating this content! I am a nursing student in OB rotation and we're going over how preeclampsia/HTN cause proteinuria. I wanted to know exactly how high blood pressure caused glomerular damage and your visuals and explanation was really helpful. Thanks again and God bless!
Good Job!, this video helps me to clearly understand the pathogenesis of Hypertensive Nephropathy. I am more confident now in my upcoming report. Continue sharing your easy-to-understand lecture. Keep it up!
Actually I'm a bit confused with the urine concentration thing, but I find this video very helpful. Thanks for sharing your knowledge to us. It's great help. :)
Thank you so much for your excellent presentations. To have your input on my Masters Pathophysiology revision is an absolutely fabulous resource. Yours JP Liverpool UK.
thank you for your lecture; it is very helpful. The reason I was looking for your video was to look for answer on what medications can prevent or delay nephropathy in hypertensive patient.
Thank you for these videos. With my pathophysiology course online, your lectures are very helpful. Quick question, do you have a video or videos on interpreting lab values?
I am not seeing a playlist link 😕. Wonderful video by the way. I realise you didn’t go through the theory of glomerular htn and glomerular hyperfiltration. Is there any videos on that?
We are working on cleaning up the channel and creating new playlists:). Not any videos on that, but we will add it to the list! Thanks for the feedback, we appreciate it.
Great video. Also kind of explains the interaction with NSAIDs and ACE-I. Ive seen pts come in for acute kidney injury on ACE-I and wonder why they have AKI and then you ask them if they pop ibuprofen and they say yes and I go no duh! lol
At least a contributing factor is that increased SGLT2 proximal reabsorption of Na in hyperglycaemia causes reduced tubular salt at the macula densa, leading to false detection of reduced flow and RAAS activation.