Intrarenal acute kidney injury (acute renal failure) - causes, symptoms & pathology
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- Опубліковано 15 лип 2024
- What is intrarenal acute kidney injury? Acute kidney injury (AKI) describes when the kidneys aren't functioning optimally, usually brought about within a few days. Find our full video library only on Osmosis: osms.it/more.
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Let me paraphrase: ARF can be categorises with prerenal, intrarenal & post renal. Prerenal is caused by HoTN, CO, haemorrhage, reduced fluid. Intrarenal mainly caused by infections, and post renal caused by urinary track obstruction. Clinical manifestations can be oliguria, oedema, vomiting, fatigue and weakness. The goal of management is to maintain the renal function during caring and restore the fluid balance, treating infections and other causes of ARF
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Totally agree. I come to Osmosis first for the visual explanation of the physiology, anatomy, etc., then hit up UpToDate for the nitty gritty details. Really helpful.
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Thank you for the useful video, I also have some kidney disease
Literally a life saver thank you
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Thanks
Best explanation 😍
Thank you
excellent. thank u
What us the best way to diagnose if AKi is due to prerenal or post renal what is causing it.
Perfect , thank you
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Splendid 💙
Thanks, Fatima! 💖
Well-done
Thank you! 🙌🏼
So... What i didn't get Is in nephrotic sindrome the GFM become more ''leacky'' and there is high proteinuria sholuldn't also the urinary output be high?
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Does ultravist damage kidney?
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8:00 why na can’t be absorbed as well as urea
.. previously u said that urea in blood will be increased and edema will occur
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why is there eosinophilia ?
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The explaination of reduced GFR in glomerulonephritis doesnt make sense. If more fluid is leaking from the capillaries into Bowmans capsule, there should be more primary urine and definitely no oliguria. However, inflammation of the glomerulus can explain reduced GFR. Nice video otherwise, thanks for sharing!
Same question
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pls upload more videos on hypernatrimia ,and hyperkalmia and all fluid electrolyte imbanaces
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Terrific work, I hope you demonstrate the introduction for a common subject in one video for example here in AKI you explained renal functions 3 times in each of the 3 videos of AKI, I think you can explain the intro once and then in other related videos mention where to find the intro, keep on the good work.
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Great video!!! But Unclear how to fluid leakage reduced pressure difference?
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Thank you, TwinkleTwinkle! We're glad you're finding our videos useful. If you haven't yet checked out our educational platform we have a bunch of tools that we think you'd like. These include unreleased videos, tens of thousands of flashcards and multiple choice practice questions, study workspaces, and daily exam schedule organizers to help you learn medicine. You can sign up for a free trial of Osmosis Prime here: bit.ly/2ut5ZEJ
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This video is useful and help me in the pathology study 👌👌👌👌
Good integration . Thank you .
You are more than great in explaining these causes of acute kidney injury I've been struggling in order to understand them 👍👍👍
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nice graphics and good presentation. Great work. really appreciate the efforts; thumbs up
Thanks! (+ an acute tubular necrosis video would be great!)
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In the summary of IntraRenal AKI it says the BUN:Creatinine ratio decreases due to impaired reabsorption of Urea in tubular damage. How then does Azotaemia result?
Is this in fact just in reference to IntraRenal AKI resulting in Renal Papillary Necrosis but not in reference to glomerular issues or acute tubular necrosis where the BUN is referenced to increase?
Normally, more urea (BUN) is reabsorbed than creatinine so the ratio BUN:Cr will be around 15. The ratio will decrease in intrarenal azotemia because there will be less excretion of BUN. So, both of them are not excreted in this case which will increase BOTH of their concentrations in blood but the RATIO will be less.
guys do you have video about ARDs ? amd i really love the way you make your explaination . thanksssomats
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This helps me so much. Please don't ever stop making videos
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excellent!
Thank you thank you thank you very much
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Thanks!
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Hi, would you mind easing my mind about something? Why is it that we can expect intrarenal AKI to generally cause a different presentation to something like acute tubular necrosis, which I believe you mentioned would be a cause of intrarenal AKI? I had thought in tubular necrosis, for example, reabsorption and secretion is affected, but there you would see azotemia and edema? Likewise, I thought glomerulopathies (at least those causing nephritic syndrome) often result in azotemia (and rarely edema)? Just wondering where I'm going wrong. Thanks!
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Awesome video!!! Do you have video on Acid-Base distrubances?
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I really love this channel But some major mistakes in the video... actually edema in glomerunephiritis is because of hypoproteinemia and decrease plasma oncotic pressure... and metabolic acidosis don't just happen due to build up of acids it's because of complex mechanisms involving potassium sodium and hydrogen ion transport
edema due to proteinuria is in nephrotic and nephritic syndrome.
I KNEW IT! I know this comment is 4 years old, but it was driving me crazy none of that made sense to me! I had to go back to the anatomy and physiology of the kidney/filtrates and what GFR actually is. Iv been going over notes and different videos for about 10 hours...I thought I had misinterpreted something somewhere. Your comment is like a breath of fresh air.
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I will :)
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Thanks!