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
I have my Step 1 in a few weeks and Osmosis is my "go to" when I don't get a concept. It makes the learning process so so much simpler and we don't even realise the number of high yield points they cover because all of it just sounds like a seamless story! Keep up the good job guys! What you're doing here is just incredible.
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.
Hi! i just want to say thanks, you videos had save me a lot of times, for exams, and other Stuff. In Mexico, e here im studyng medicine, a lot of students watch your videos. Everybody loves them, thank you.
I love your videos! and your sense of humour is just perfect! I love you guys! I'm currently studying for my state exams and your videos are great for revising some things I've forgotten from pathology!
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.
That's the plan! We’re glad you’re finding the videos useful! If you haven’t yet checked out our educational platform we have a bunch of tools that 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
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
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.
I really hope you don't stop making these videos. I honestly find them to be the best medicine videos on youtube, and I've watched many channels but the way you guys do it is just so clear and easy to understand. Just know you are making a difference in someone's life to become a better student and a better doctor. Thank you sir
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.
Thanks for watching, AK G! Did you know that if you like & review us on Facebook then you’ll get access to our videos a day before they’re published on RUclips? Check it out here: bit.ly/2u35D6J
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?
Thanks for the kind words, Agnese! Did you know that if you like & review us on Facebook then you’ll get access to our videos hours or even days before they’re published on RUclips? Check it out here: facebook.com/pg/OsmoseIt/reviews
I hve a doubt ...at the beginning of d video u said that in intrarenal we see azotemia but at the u said that BuN:creatinine falls....plz tell me actually wat happens.....
Agreed... I think they didn't make the distinction between the 3 pathologies at the end when they made the statement about a reduced BUN:Cr, but azotemia being present. I think we can all agree that in acute interstitial nephritis the interstitium becomes damaged and inflamed, so REABSORPTION cannot take place, and whatever is filtered gets excreted (Na, Urea, H2O). This is in contract to glomerulonephritis and tubular necrosis, where pressure builds up in Bowman's capsule bc too much gets Filtered, leading to a reduced pressure difference, In the end leading to reduced filtration and a buildup in Urea etc
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.
I don't understand how glomerularnephritis causes decrease in GFR - don't feel like you properly explained it in the video. Could someone explain? Thanks 🙂 (really like your vids!)
Thank you for this video,but i don't understand that why fluid leak form Glomerulonephritis lead to differential pressure , and result in low GFR (i guess that because low blood pressure,but i think wrong?)
จิรโชติ ธนผลผดุงกุล In the process of glomerular filtration, the amount of proteins in the blood that is to be filtered constitute the blood colloidal osmotic pressure. When there are more proteins, the BCOP is high, that enables fluid to move from its region of higher concentration to its region of lower concentration. (simple basic osmosis) so good amount of fluid is filtered out because of this. But what happens here is, the proteins are leaking out, so the BCOP has reduced. So naturally the osmotic pressure difference has reduced, now the fluid doesn't have enough concentration gradient to be filtered out, and that's why lesser fluid gets filtered. Lesser GFR. Hope that clears your doubt :)
Wouldn't it be due to the increase of Hydrostatic pressure in Bowman's Capsule? The colloid osmotic pressure actually keeps the fluid in the blood vessel, it doesn't push it out to be filtered. The protein that is lost would actually cause more fluid to come out of the vessel. The hydrostatic pressure (about 50 mmHg) in the glomerular capillaries and the colloid pressure in Bowman's capsule (should be 0 because there should not be any proteins there) are 2 forces in favor of filtration, while the hydrostatic pressure in Bowman's Capsule (about 10mmHg) and the plasma colloid pressure (about 30 mmHg) are 2 forces against filtration, so normally there is a force of about 10 mmHg favoring filtration. What happens is that your proteins leak out so your plasma colloidal pressure goes down leading to an increase in filtration because this force goes against it, so if you decrease it you increase filtration, but this leads to an increase of hydrostatic pressure in the glomerular space which is another force that goes against filtration and I believe this is the force that would ultimately decrease the GFR, but only if there is a blockage further down in the tubule, so this would be the case in ATN if your PCT cells form a brown muddy cast and block the passage of the filtrate., and again in this case there wouldn't really be proteins leaking out. So in the case of RPGN it would be the crescents that form which can get scarred and block the passage of filtrate into the tubule. Hopefully this helps you out and maybe someone else can help out in case I'm incorrect in my thinking.
Are penicillins really considered nephrotoxic? I thought It would be more so aminoglycoside drugs like vancomycin and gentamicin that caused nephrotoxicity?
could you please tell me in case of excessive urination without any other symptoms how polyuria can be stopped any safe treatment for such patient who cannot have normal life bec of polyuria
this video hints at an answer, but i still don't understand why, in glomerular nephritis when membrane permeability increases, water isn't able to escape if protein and glucose are able to? shudnt we see an increase in water output with GN? = / additionally, if protein/glucose attracts water, again, id expect more urine output. lastly, i was under the impression that altho osmotic pressure is important to push blood thru the glomerulus, hydrostatic pressure was of bigger impact. so again, id expect increase in urine output
See, the main force responsable for water secretion is pressure gradient. Yes, you would have water scaping through glomeruli, but then the difference of pressure would be significantly reduced. Therefore, you will have a congestion (excess of water not moving), but not a increase of volume being excreted for a unit of time, because you don't have a force able to (deltaP).
I'm really confused because of your lab results and your explanation. You say the three causes of AKI all result in Azotemia but at the end you contradict yourself by sating the BUN:CR falls as less urea is absorbed? Also, how is the osmorality of the urine decreased yet sodium concentration in the the urine is increased? Help!
The amount of urea reabsorbed is relatively lesser compared to the amount of creatinine that is being excreted by the muscle cells. (since there is dysfunctional filtration) so in blood, creatinine levels build up relatively more, and thats why the BUN:Creatinine ratio decreases. This is how I understood it
Uzma Roshan's answer is true. Regarding your second question, acute tubular necrosis will damage tubular cells (either ischemically or nephrotoxically). These cells of the tubules are responsible for concentrating the urine filtrate by reabsorbing MOST of the water. So when these cells are damaged, there will be no reabsorption of water which is why the urine is hyposmotic even though more Na is excreted.
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!
6.00.... due to fluid leakage . why GFR decreases .?,, actually due to the increased permeability the GFR should increase know..... plz any one clear my dought
because due to fluid leakage there is loss of gradient(pr. becomes nearly same on both sides) and it is the gradient which leads to filteration of many substances
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
I wish that you will NEVER stop making videos
thanks a lot, I know how time consuming making this kind of videos and I cant thank you enough
Thanks! Its a full-time job for some of us!
Osmosis : I am so happy to read this . . Thank you guys
I would always prefer to listen for hours of these videos rather than a one hour of my professors
Hahahhah looking boring 😂
you guys are so good for putting up these videos on youtube for free! God bless you!
I have my Step 1 in a few weeks and Osmosis is my "go to" when I don't get a concept. It makes the learning process so so much simpler and we don't even realise the number of high yield points they cover because all of it just sounds like a seamless story! Keep up the good job guys! What you're doing here is just incredible.
these videos are literally gold, renal path is one of the hardest to grasp and this does amazing job with animations. GOD BLESS.
I'm a final year med student and i generally watch one of these before a new chapter because it's just so easy and such a clear base to start off with
Glad that our videos are able to help with your medical studies, Anna! 💕
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.
you guys can explain it way better than my clinical instructor
Thanks - I'm glad you found the video helpful.
I love osmosis Tqsm for helping me throughout ❤
Always our pleasure! 💕🥰🫀
Bless you all you all are getting me through pathophysiology in nursing school!
pls upload more videos on hypernatrimia ,and hyperkalmia and all fluid electrolyte imbanaces
I literally have no words to express how much I love Osmosis♥️
🫀❤️💕
Hi! i just want to say thanks, you videos had save me a lot of times, for exams, and other Stuff. In Mexico, e here im studyng medicine, a lot of students watch your videos. Everybody loves them, thank you.
I love your videos! and your sense of humour is just perfect! I love you guys! I'm currently studying for my state exams and your videos are great for revising some things I've forgotten from pathology!
Honestly, you guys are the best. I hope guys get paid well for this type of job. Keep it up.
Thanks
Just recently got iut the hospital due to this 😊. Very informative video
We hope this video helped! 💕
You are more than great in explaining these causes of acute kidney injury I've been struggling in order to understand them 👍👍👍
Thanks so much! It would be awesome if you could review us on our Facebook page. facebook.com/OsmoseIt/
Osmosis OK 👍👌
whenever i want to see any educational video, i want to see the first name as osmosis!! and most of the times it is..very well explained :)
thanks for sharing! I really needed this for tomorrow's midterm.
Thank you for the useful video, I also have some kidney disease
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.
Excellent videos. Hands down. The narrator's voice is just
Literally a life saver thank you
Glad to help, Jacie! ❤️
Where were you when I was in med school!!!! Thank you so much.
This helps me so much. Please don't ever stop making videos
That's the plan! We’re glad you’re finding the videos useful! If you haven’t yet checked out our educational platform we have a bunch of tools that 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
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.
u r doing very good job...it's more useful for my xams ....I m expecting more videos from u
THANKS !! DO NOT STOP !!! PLEASE !!!
your videos are amazing and so much fun i wish people like you could be in our clg
These 45 unlikes jealous of ur work
I really hope you don't stop making these videos. I honestly find them to be the best medicine videos on youtube, and I've watched many channels but the way you guys do it is just so clear and easy to understand. Just know you are making a difference in someone's life to become a better student and a better doctor. Thank you sir
You and your team have dedicated a lot of time to make many educated videos, thank you so much
Thanks for the kind words, Khairul!
This is saving my life.
People subscribing to this channel with lightning speed !
Osmosis will become finest med school 😘
Thanks! (+ an acute tubular necrosis video would be great!)
excellent video. . please don't stop making more.. thank you so much!
Thank you guys! This is brilliant
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.
LOVE YOU GUYS! THANKS FOR THE AWESOME VIDEOS! HELP SO MUCH!
thank you for the great explanation :D
Thank you thank you thank you very much
Thanks for watching, AK G! Did you know that if you like & review us on Facebook then you’ll get access to our videos a day before they’re published on RUclips? Check it out here: bit.ly/2u35D6J
this is so helpful thank u so much
im confuse..at first it says azotemia..then in general they say that the BUN to creatinine ratio reduce..so which one is it?
Does ultravist damage kidney?
nice graphics and good presentation. Great work. really appreciate the efforts; thumbs up
guys do you have video about ARDs ? amd i really love the way you make your explaination . thanksssomats
We have set up a Patreon page to allow folks to vote on upcoming topics: www.patreon.com/osmosis?ty=h
me salvas la vida con estos videos!
Good integration . Thank you .
Best explanation 😍
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?
those damn sound effects had me dying.
Thank you osmosis Bro. You are awesome 😀
excellent job ! thank you so much
done :D
Great job 👍🏻👍🏻
Thanks!
thanks, it was really helpful
You guys are the best!!!!
Beautiful videos! Much simpler than reading Robbins n number of times! :D
The 2 people who hated this video are jealous of this tremendous work .
YOU ARE AMAZING
thank you....
Besides the great content you provide ...these drawings are SOOO adorable. Keep up the awesome work!
Thanks for the kind words, Agnese! Did you know that if you like & review us on Facebook then you’ll get access to our videos hours or even days before they’re published on RUclips? Check it out here: facebook.com/pg/OsmoseIt/reviews
Thanks, I'll definitely check it :)
you are the best ever
amazing! keep it up! you guys rock!
wow I didn't know Pakistanis are helping soo much
I hve a doubt ...at the beginning of d video u said that in intrarenal we see azotemia but at the u said that BuN:creatinine falls....plz tell me actually wat happens.....
Bhargavi Puppala same doubt me too
Agreed...
I think they didn't make the distinction between the 3 pathologies at the end when they made the statement about a reduced BUN:Cr, but azotemia being present. I think we can all agree that in acute interstitial nephritis the interstitium becomes damaged and inflamed, so REABSORPTION cannot take place, and whatever is filtered gets excreted (Na, Urea, H2O). This is in contract to glomerulonephritis and tubular necrosis, where pressure builds up in Bowman's capsule bc too much gets Filtered, leading to a reduced pressure difference, In the end leading to reduced filtration and a buildup in Urea etc
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.
I don't understand how glomerularnephritis causes decrease in GFR - don't feel like you properly explained it in the video. Could someone explain?
Thanks 🙂 (really like your vids!)
Also, why does the concentration of serum urea and creatinine increase? - isn't water not filtrated too?
It's a great video!!!!!!!!
Osmosis we need more KIDNEY pathology videos please bro :)
Working on it!
Thanks a lot guys ! :)))
Thank you for this video,but i don't understand that why fluid leak form Glomerulonephritis lead to differential pressure , and result in low GFR (i guess that because low blood pressure,but i think wrong?)
จิรโชติ ธนผลผดุงกุล In the process of glomerular filtration, the amount of proteins in the blood that is to be filtered constitute the blood colloidal osmotic pressure. When there are more proteins, the BCOP is high, that enables fluid to move from its region of higher concentration to its region of lower concentration. (simple basic osmosis) so good amount of fluid is filtered out because of this. But what happens here is, the proteins are leaking out, so the BCOP has reduced. So naturally the osmotic pressure difference has reduced, now the fluid doesn't have enough concentration gradient to be filtered out, and that's why lesser fluid gets filtered. Lesser GFR.
Hope that clears your doubt :)
Wouldn't it be due to the increase of Hydrostatic pressure in Bowman's Capsule? The colloid osmotic pressure actually keeps the fluid in the blood vessel, it doesn't push it out to be filtered. The protein that is lost would actually cause more fluid to come out of the vessel. The hydrostatic pressure (about 50 mmHg) in the glomerular capillaries and the colloid pressure in Bowman's capsule (should be 0 because there should not be any proteins there) are 2 forces in favor of filtration, while the hydrostatic pressure in Bowman's Capsule (about 10mmHg) and the plasma colloid pressure (about 30 mmHg) are 2 forces against filtration, so normally there is a force of about 10 mmHg favoring filtration. What happens is that your proteins leak out so your plasma colloidal pressure goes down leading to an increase in filtration because this force goes against it, so if you decrease it you increase filtration, but this leads to an increase of hydrostatic pressure in the glomerular space which is another force that goes against filtration and I believe this is the force that would ultimately decrease the GFR, but only if there is a blockage further down in the tubule, so this would be the case in ATN if your PCT cells form a brown muddy cast and block the passage of the filtrate., and again in this case there wouldn't really be proteins leaking out. So in the case of RPGN it would be the crescents that form which can get scarred and block the passage of filtrate into the tubule. Hopefully this helps you out and maybe someone else can help out in case I'm incorrect in my thinking.
Are penicillins really considered nephrotoxic? I thought It would be more so aminoglycoside drugs like vancomycin and gentamicin that caused nephrotoxicity?
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
I still don't understand why damaged podocyte can lower the GFR. Doesn't fluid leakage increase GFR?
DD I too had the same doubt
4:09
Thank u......
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Perfect , thank you
🙌🏼 💕 ✨
could you please tell me in case of excessive urination without any other symptoms how polyuria can be stopped any safe treatment for such patient who cannot have normal life bec of polyuria
I believe you need to find out the cause of the polyuria, As it can be caused by Diabetes mellitus, Diabetes insipidus, or simply a cold weather
thanks a lot
I will :)
Please do hyponatremia :)
That's fabulous.
Thanks!
Splendid 💙
Thanks, Fatima! 💖
Great video
nice.. very nice
you are awesome
you are amazing 💪😎
this video hints at an answer, but i still don't understand why, in glomerular nephritis when membrane permeability increases, water isn't able to escape if protein and glucose are able to? shudnt we see an increase in water output with GN? = / additionally, if protein/glucose attracts water, again, id expect more urine output.
lastly, i was under the impression that altho osmotic pressure is important to push blood thru the glomerulus, hydrostatic pressure was of bigger impact. so again, id expect increase in urine output
please anyone reply on this question I have the same problem .
See, the main force responsable for water secretion is pressure gradient. Yes, you would have water scaping through glomeruli, but then the difference of pressure would be significantly reduced. Therefore, you will have a congestion (excess of water not moving), but not a increase of volume being excreted for a unit of time, because you don't have a force able to (deltaP).
Can you please make videos about metabolic acidosis, alkalosis, and respiratory acidosis and alkalosis 😭
Medcram he make a great lecturs on that ****ruclips.net/video/4wMEMhvrQxE/видео.html** **
Thank you
Awesome videos but just a detail: Certain toxines, like aminoglycosides cause non-oliguric intra renal AKI.
What's the treatment
excellent!
Hey I think you forgot about PPI (the most common cause) for Acute interstitial nephritis
awesome!!!!
I'm really confused because of your lab results and your explanation. You say the three causes of AKI all result in Azotemia but at the end you contradict yourself by sating the BUN:CR falls as less urea is absorbed? Also, how is the osmorality of the urine decreased yet sodium concentration in the the urine is increased? Help!
I was thinking the same thing when he finally wrapped it up, very confusing.
The amount of urea reabsorbed is relatively lesser compared to the amount of creatinine that is being excreted by the muscle cells. (since there is dysfunctional filtration) so in blood, creatinine levels build up relatively more, and thats why the BUN:Creatinine ratio decreases.
This is how I understood it
Uzma Roshan's answer is true. Regarding your second question, acute tubular necrosis will damage tubular cells (either ischemically or nephrotoxically). These cells of the tubules are responsible for concentrating the urine filtrate by reabsorbing MOST of the water. So when these cells are damaged, there will be no reabsorption of water which is why the urine is hyposmotic even though more Na is excreted.
amazing!
Thanks Monica. =)
Thanks ❤
Welcome! 🥰
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!
The best!!!
Well-done
Thank you! 🙌🏼
Proton-pump inhibitors are an important cause of acute interstitial nephritis too.
Thanks a lot for your work !
6.00.... due to fluid leakage . why GFR decreases .?,, actually due to the increased permeability the GFR should increase know..... plz any one clear my dought
because due to fluid leakage there is loss of gradient(pr. becomes nearly same on both sides) and it is the gradient which leads to filteration of many substances
I love the kidney, it's so cute