explained nicely. post obstruction failure not explained elsewhere like you did. great job brother.
@absolutetuber3 жыл бұрын
this guy is going to make a great IM subspecialist
@hendalsh22707 жыл бұрын
Yeeeey finally I'm gonna understand this topic 😍😍
@Meetpatel-pu6me7 жыл бұрын
Hend alsh haha i am happy :))
@pubalidola38294 жыл бұрын
Thank u so much for this video... u saved me from my exam🙏🙏❤
@taracunningham1364 жыл бұрын
Thank you for this video. I was having difficulty understanding these concepts. Very well presented.
@freethinker34954 жыл бұрын
the BUN in prerenal azotemia increases because decreased perfusion stimulates RAAS. ADH augments urea reabsorption and not crearinine hence increased bun to cr. tatio
@hassanmohamedahmedomar5935 Жыл бұрын
Really this video helped me , thanks for your simplified exaplanation.
@doctorkhizar3 жыл бұрын
Salam bro why you stop making videos. You are very good in clearing the issues.
@DrNiteshRaj6 жыл бұрын
what a superb concept sir.....
@madhuekanayake57214 жыл бұрын
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
@soumitradas61603 жыл бұрын
Its a good one...most importantly palatable one😀👍👍👍 Please upload the "CKD" as well thank you 🙏
@pritishrestha53102 жыл бұрын
Thanx a lot Dr Patel for the first time understood the concept....
@susanharvey35934 жыл бұрын
Thank you so much for this, I understand it better than I ever have!!!
@62.sayantikadhar494 жыл бұрын
Great explanation👏, please make videos on general pharmacology 🙂
@Meetpatel-pu6me4 жыл бұрын
Sure. Will try to do it in the future
@muzdalfaibadullah95894 жыл бұрын
Finally I find the great vedio
@tayebahchaudhry80657 жыл бұрын
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!
@Meetpatel-pu6me7 жыл бұрын
Tayebah Chaudhry thank you.... yess i will try to make a video on that.
@tayebahchaudhry80657 жыл бұрын
Thank u again!
@Yupi2148 ай бұрын
Can u plz make video on step1 acid base concept and winter formula
@monika2465 жыл бұрын
Ur all explanations are just perfect😊
@heyitsdiamedico55386 жыл бұрын
Very clear explanation. Thank you so much ❤️ ❤️
@meghasa84164 жыл бұрын
Beautifully explained. Thank you so much :)
@ujjawalshriwastav.11154 жыл бұрын
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.
@B_hope1 Жыл бұрын
Great explanation 😍😍
@srinivasanaravindhasamy55753 жыл бұрын
Which book are you referring
@fatimaahmarZ Жыл бұрын
but in acute tubular necrosis and post renal azotemia when BUn :cr ratio is decreased then why we call it azotemia ????
@rahulranganathan1076 жыл бұрын
Excellent videos bro...god bless you and fr your journey
@spookypineapple6 жыл бұрын
You're the man.
@lukabatrovic60093 жыл бұрын
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?
@azharkhan-fr4vl2 жыл бұрын
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
@ritumaida69133 жыл бұрын
Keep it up .....great explanation☺
@pavitrahegde30632 жыл бұрын
Nicely explained, thanks!!
@deepaksingh-ut7lh6 жыл бұрын
Keep it up bro....... Excellent Explanation
@sameersagarsinghsonkar97162 жыл бұрын
1st discuss what's AKI,...after that discuss further it's better to understand
@indiandoctorsaiims1736 жыл бұрын
Too much helpful and yr acid base balance video is awesome 💪💪👌👌👌👌
@janhaviborkar82872 жыл бұрын
Amazing explaination 💯
@steamergamer42494 жыл бұрын
Why a cardiothoracic surgeon watching this 😂😂
@nileshmane64765 жыл бұрын
Excellent explanation sir
@jeanner73066 жыл бұрын
great video, thanks for posting!!!
@raahilatheist42586 жыл бұрын
Best expanation thanku sir plz contiue to make more videos
@lrs16756 жыл бұрын
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).
@cutiecouplecheekybubble2 жыл бұрын
As in comparison of na more water is excreted into urine as water couldn't absorb as tubular epithelium is damaged
@argumentumadbaculum6 жыл бұрын
All your videos are gems
@dktreat94624 жыл бұрын
very clear explanation. Keep it up
@sarahNnazim7 жыл бұрын
dr.patel would u be kind to us and make a video on fluid electrolyte distribution, please.
@Meetpatel-pu6me7 жыл бұрын
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.
@maryammohammad22823 жыл бұрын
Why creatinine dosent get reabsorbed in prerenal I couldn’t get it?
@jashankparwani1824 жыл бұрын
What was your step1 score and when did you take the exam?
@Meetpatel-pu6me4 жыл бұрын
Step 1 score - 249. I took it in 2016
@IJAZ-o4n4 жыл бұрын
excelent lecture
@Sunitasingh123754 жыл бұрын
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
@Meetpatel-pu6me4 жыл бұрын
B&B videos(based on reviews) , FA and UW should be enough. Supplement it with BRS Physiology if needed.
@ridazahra20094 жыл бұрын
Explained really well
@medicss18363 жыл бұрын
Much helpful then any other video
@AbdurRahman-pn4qi6 жыл бұрын
Great job sir!!
@muhammadmehdi57523 жыл бұрын
amazing explanation (y)
@davidmbeckmann6 жыл бұрын
Very good, sir!
@oliverpapa77165 жыл бұрын
Very clear and helpful , good explaination .
@kholailyas8204 жыл бұрын
Best lecture
@rebazaped16754 жыл бұрын
Well done Dr
@basildabbah38517 жыл бұрын
nice man :)) can u please explain renal tubular acidodis !!!!
@Meetpatel-pu6me7 жыл бұрын
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 !
@basildabbah38517 жыл бұрын
thanks doc much appreciate
@aleezasyed9353 жыл бұрын
it realy helped me awesome 👌👌
@shkooling3 жыл бұрын
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!
@shridhardodamani77523 жыл бұрын
Filtration is affected in all the three causing azotemia . Thats why we talk in ratios to differentiate the three
@tranminhnghia54983 жыл бұрын
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.