the BUN in prerenal azotemia increases because decreased perfusion stimulates RAAS. ADH augments urea reabsorption and not crearinine hence increased bun to cr. tatio
Thanks a lot for sparing ur time to help others!!! Very helpful videos. Any lecture on basal ganglia. That inhibition, dis-inhibition always confuses me. thanks!
Really informative lecture..thank you very much sir..🙂 Can you please tell the answer for this too.. True or false Increase serum Creatinine seen in b)Myocardial infarction d) Early DM nephropathy
Can you tell regarding Urine creatinine/Plasma creatinine ? Can't get it for pre renal, renal and post renal. You missed this one in the video. Rest all are clear.
dr. Sarah....I would love to make new videos but because of final exams and step 2 preparation I am having difficult time making new videos....will try to resume soon after final exams...sorry for that.
basil dabbah thank you.... actually i am making video on whatever topic i am prepared with and fortunately i am doing RTA so video will be ready in few hours..cheers !
Dr. Patel, can you explain one thing to me. If in prerenal AKI, urine sodium is decreased, then how is osmol. od the increased? Where does osmol. comes from?
Increased Osmolality doesn't always means that ions should be increased.. it is a ratio of ions(solute) dissolved in a solvent.. as there is decrease in urine sodium concentration but at the same time water absorption due to ADH ( released due to low plasma volume) is more as compared to decrease in urinary sodium.. as a result osmolality increases
If urine FeNa increases >2% in Intrinsic Renal azotemia how does osmolality decrease? I thought Urine Osmolality = 2 x (urine Na) + Urine K + (urinary urea nitrogen/2.8) + (urine glucose/18).
Thank you for the video! I liked the video! I still have some confusion and am hoping someone can help me. So with intrinsic AKI, the tubular epithelium is damaged, so they can not reabsorb things back into the blood. I still don't understand why BUN and Cr are building up in the blood? Is it because in intrinsic AKI it can't get filtered as well?? Any help would be appreciated thank you!
I don't know if you still require answer to this question, what I understand is: - Prerenal AKI makes GFR drops because of lack of blood flow. - Intrinsic AKI makes GFR drops because of direct damage, like inflammation, ischemia, which affects both the tubules (reabsorption and concentration) and the glomeruli (filtration). - Post renal AKI, I assume, in the early stage does not drop GFR, but later the built up fluid damages the glomeruli and tubules, leading to the same issues as intrinsic AKI. All three got problems with excreting BUN and creatinine and various azote byproducts either because of compromised glomeruli function or reduced kidney blood flow (which might in turn creates glomeruli damage). So how do we distinguish them? - Prerenal AKI got distinctively high BUN/creatinine ratio (in blood) > 20 from the start, and maintained tubular function (urine osmolality > 500), and raised ADH, aldosterone (effort to raise renal blood flow) (Fe Na < 1% and urine Na < 20). - Intrinsic AKI got low BUN/creatinine ratio < 15 all the way (BUN got lost via GI tract and skin, creatinine got no other exits), disrupted tubular function all the way so no concentration, no Na reabsorption (urine osmolality < 350, urine Na > 40, Fe Na > 2%). - Post renal AKI got BUN/creatinine ratio that is > 15 early because maintained tubular function + increase hydrostatic pressure in the tubules making BUN reabsorption increases (creatinine remains unabsorbed), then BUN/creatinine ratio drops < 15 when tubular damage occurs. Since we can still properly filter fluid and have no need to increase blood flow, aldosterone and ADH do not rise, leading to urine Na > 40 and Fe Na > 1% or 2%; tubular damage might play a role as in intrinsic AKI, in not reabsorbing Na properly.
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Thank you so much for this, I understand it better than I ever have!!!
Thank you for this video. I was having difficulty understanding these concepts. Very well presented.
Excellent videos bro...god bless you and fr your journey
Beautifully explained. Thank you so much :)
Thank u so much for this video... u saved me from my exam🙏🙏❤
Yeeeey finally I'm gonna understand this topic 😍😍
Hend alsh haha i am happy :))
Very clear explanation. Thank you so much ❤️ ❤️
Ur all explanations are just perfect😊
what a superb concept sir.....
great video, thanks for posting!!!
explained nicely. post obstruction failure not explained elsewhere like you did. great job brother.
Allah must bless you sir for making topic simpler.
You're the man.
this guy is going to make a great IM subspecialist
Really this video helped me , thanks for your simplified exaplanation.
Thanx a lot Dr Patel for the first time understood the concept....
Keep it up bro....... Excellent Explanation
Its a good one...most importantly palatable one😀👍👍👍
Please upload the "CKD" as well thank you 🙏
Too much helpful and yr acid base balance video is awesome 💪💪👌👌👌👌
Excellent explanation sir
Great job sir!!
Salam bro why you stop making videos. You are very good in clearing the issues.
Nicely explained, thanks!!
Finally I find the great vedio
All your videos are gems
Best expanation thanku sir plz contiue to make more videos
very clear explanation. Keep it up
Keep it up .....great explanation☺
Very good, sir!
Amazing explaination 💯
Thank u for this explanation
the BUN in prerenal azotemia increases because decreased perfusion stimulates RAAS. ADH augments urea reabsorption and not crearinine hence increased bun to cr. tatio
Thanks a lot for sparing ur time to help others!!! Very helpful videos.
Any lecture on basal ganglia. That inhibition, dis-inhibition always confuses me. thanks!
Tayebah Chaudhry thank you.... yess i will try to make a video on that.
Thank u again!
Great explanation 😍😍
Really informative lecture..thank you very much sir..🙂
Can you please tell the answer for this too..
True or false
Increase serum Creatinine seen in
b)Myocardial infarction
d) Early DM nephropathy
Good job. Thanks
Explained really well
thank you so much its so helpful
Gud work machaa
amazing explanation (y)
Great explanation👏, please make videos on general pharmacology 🙂
Sure. Will try to do it in the future
great job brother.:)
thanks
Rahul Tiwari thank you bro :)
Well done Dr
Much helpful then any other video
Best lecture
Nice explaination.....
excelent lecture
Thank you !
Can u plz make video on step1 acid base concept and winter formula
excellently explained...
thank you :))
Thank you so much
it realy helped me awesome 👌👌
Thank you 🙏🏻
Thanks you sir
Can you tell regarding Urine creatinine/Plasma creatinine ? Can't get it for pre renal, renal and post renal. You missed this one in the video. Rest all are clear.
Thank you 💙👏👏
Thanks 🙏🏼
dr.patel would u be kind to us and make a video on fluid electrolyte distribution, please.
dr. Sarah....I would love to make new videos but because of final exams and step 2 preparation I am having difficult time making new videos....will try to resume soon after final exams...sorry for that.
good work
thankyou:) this was useful
zara you are welcome :))
Very clear and helpful , good explaination .
Thank you
great!
nice man :)) can u please explain renal tubular acidodis !!!!
basil dabbah thank you.... actually i am making video on whatever topic i am prepared with and fortunately i am doing RTA so video will be ready in few hours..cheers !
thanks doc much appreciate
Thank u bro
Amazing
very nice
but in acute tubular necrosis and post renal azotemia when BUn :cr ratio is decreased then why we call it azotemia ????
awesome
Which book are you referring
thank u
Thnx:)
Dr. Patel, can you explain one thing to me. If in prerenal AKI, urine sodium is decreased, then how is osmol. od the increased? Where does osmol. comes from?
Increased Osmolality doesn't always means that ions should be increased.. it is a ratio of ions(solute) dissolved in a solvent.. as there is decrease in urine sodium concentration but at the same time water absorption due to ADH ( released due to low plasma volume) is more as compared to decrease in urinary sodium.. as a result osmolality increases
Why creatinine dosent get reabsorbed in prerenal I couldn’t get it?
Why a cardiothoracic surgeon watching this 😂😂
What was your step1 score and when did you take the exam?
Step 1 score - 249. I took it in 2016
❤
If urine FeNa increases >2% in Intrinsic Renal azotemia how does osmolality decrease? I thought Urine Osmolality = 2 x (urine Na) + Urine K + (urinary urea nitrogen/2.8) + (urine glucose/18).
As in comparison of na more water is excreted into urine as water couldn't absorb as tubular epithelium is damaged
1st discuss what's AKI,...after that discuss further it's better to understand
Sir please tell me all the sources needed to score high in step 1 for PHYSIOLOGY:please reply Sir things are confusing on u tube
Please do reply sir
B&B videos(based on reviews) , FA and UW should be enough. Supplement it with BRS Physiology if needed.
nice pencil
sha A haha
Thank you for the video! I liked the video!
I still have some confusion and am hoping someone can help me. So with intrinsic AKI, the tubular epithelium is damaged, so they can not reabsorb things back into the blood. I still don't understand why BUN and Cr are building up in the blood? Is it because in intrinsic AKI it can't get filtered as well?? Any help would be appreciated thank you!
Filtration is affected in all the three causing azotemia . Thats why we talk in ratios to differentiate the three
I don't know if you still require answer to this question, what I understand is:
- Prerenal AKI makes GFR drops because of lack of blood flow.
- Intrinsic AKI makes GFR drops because of direct damage, like inflammation, ischemia, which affects both the tubules (reabsorption and concentration) and the glomeruli (filtration).
- Post renal AKI, I assume, in the early stage does not drop GFR, but later the built up fluid damages the glomeruli and tubules, leading to the same issues as intrinsic AKI.
All three got problems with excreting BUN and creatinine and various azote byproducts either because of compromised glomeruli function or reduced kidney blood flow (which might in turn creates glomeruli damage).
So how do we distinguish them?
- Prerenal AKI got distinctively high BUN/creatinine ratio (in blood) > 20 from the start, and maintained tubular function (urine osmolality > 500), and raised ADH, aldosterone (effort to raise renal blood flow) (Fe Na < 1% and urine Na < 20).
- Intrinsic AKI got low BUN/creatinine ratio < 15 all the way (BUN got lost via GI tract and skin, creatinine got no other exits), disrupted tubular function all the way so no concentration, no Na reabsorption (urine osmolality < 350, urine Na > 40, Fe Na > 2%).
- Post renal AKI got BUN/creatinine ratio that is > 15 early because maintained tubular function + increase hydrostatic pressure in the tubules making BUN reabsorption increases (creatinine remains unabsorbed), then BUN/creatinine ratio drops < 15 when tubular damage occurs. Since we can still properly filter fluid and have no need to increase blood flow, aldosterone and ADH do not rise, leading to urine Na > 40 and Fe Na > 1% or 2%; tubular damage might play a role as in intrinsic AKI, in not reabsorbing Na properly.
Kindly upload more content
Sure. Will give my best
Niiiice👍👍👍👍😭
👍👌
D. Y. Shah thank you :))
kidly uplod ckd plzzzzz
So easily made for us