ACUTE TUBULAR INJURY/NECROSIS or ACUTE KIDNEY INJURY - Pathology
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- Опубликовано: 3 авг 2024
- Tubulointerstitial disorders:1- ACUTE TUBULAR INJURY/NECROSIS
Tubular and Interstitial Diseases • (1) ischemic or toxic tubular injury, leading to acute kidney injury (AKI) or ATN and acute renal failure, and • (2) inflammatory reactions of the tubules and interstitium (tubulointerstitial nephritis).
ACUTE KIDNEY INJURY (AKI) (ACUTE TUBULAR NECROSIS, ATN) ATN is a clinicopathologic entity characterized clinically by Acute reduction of renal function and often, but not invariably, morphologic evidence of tubular injury.
ATI / ATN • It is the most common cause of acute renal failure, which signifies rapid reduction of renal function and urine flow
Causes of AKI 1. Ischemia due to decreased or interrupted blood flow, 2. Direct toxic injury to the tubules 3. Acute tubulointerstitial nephritis 4. Urinary obstruction
Types of ATN1. Ischemic 2. Nephrotoxic 3. Mixed
Pathogenesis
Tubular injury and (2)Disturbances in blood flow
Morphology Ischemic AKI
• focal tubular epithelial necrosis at multiple points along the nephron, with large skip areas in between, often accompanied by
• rupture of basement membranes (tubulorrhexis) and
• occlusion of tubular lumens by casts.
There is also evidence of epithelial regeneration: Flattened epithelial cells with hyperchromatic nuclei and mitotic figures are often present. In the course of time this regeneration repopulates the tubules so that, no residual evidence of damage is seen.
Clinical Course 1.initiation, 2. maintenance, and 3.recovery stages.
The initiation phase Lasting for about 36 hours, is dominated by the inciting medical, surgical, or obstetric event in the ischemic form of AKI.
The Initiation Phase • The only indication of renal involvement is a slight decline in urine output with a rise in BUN. • At this point, oliguria could be explained on the basis of a transient decrease in blood flow and declining GFR.
The maintenance phase • is characterized by sustained decreases in urine output to between 40 and 400 mL/day (oliguria), salt and water overload, rising BUN concentrations, hyperkalemia, metabolic acidosis, and other manifestations of uremia.
The recovery phase • a steady increase in urine volume that may reach up to 3 L/day. • The tubules are still damaged, so large amounts of water, sodium, and potassium are lost in the flood of urine.
The recovery phase •Hypokalemia, rather than hyperkalemia, becomes a clinical problem. There is a peculiar increased vulnerability to infectionat this stage.
Clutch video! Perfectly concise, detailed pathophys and well explained! Thank you!
Sir, please make such videos on all systems, bones, respiratory system, CNS, etc. Your crystal clear explanationations are unmatchable. Please Sir, it'll be of great great help then.
Yeah sir please,it will be very helpful to our upcoming exams
This was great, I’m sharing it with the nursing students in my class. THANK YOU!!!
Never understood this topic from Robbins. Saw this video and literally got the concepts. Thankyou Sir!
Thank you :-) am glad that it helped :-)
Straight to the point.... thanks man
What a beautiful video…thank you so much
To the point, and well explained 🎉🎉
Thank you so much sir ❤! You have no idea how your way of teaching is ! Its outstanding 😊🎉 ❤
😊 thank you
Very gud class..... I was searching for this complete section thank u very much
sir ur videos are the concised version of Robbins, tnx a lot sir🙏
you are an excellent teacher
Thank you 😊
Excellent video
Please make such videos more and more
Very helpful ✌
Thank you very much, Explains it nicely
you are the best man
Extremely informative and well-made - following this channel from now on - KEEP up the good work sir :D
Thank you 😊 Glad it was of some help.
Great video
Thank you!
Loved it!
What a flow chart appreciate
Thank you so much sir🙏
Very good explanation ❤️
Thank you so much
Thank you 😊
Thanks sir!
Thankue so much sir 👍
Cotran in HD! Thank you 😊
I was diagnosed with atypical anti-glomerular basement membrane disease about 18 months ago. With two kidney biopsy the Doctors still aren't sure what's up and sent to the Mayo Clinic for a third opinion. I looked at the pathology report and it says acute tubular injury. They have had me on rituximab and prednisone now they want on cellcept. My question is would you be willing to look at the pathology report and give your opinion? I was in great shape before covid at 65 my egfr was 82. Now it is 27 and not sure that my doctors have seen this before. This happened after covid, but my covid symptoms were very slight. Any help would be appreciated. David.
Thanks man,💥🎉🎊👌👌
Best video ever on this topic, thank you sir.,
Lovely
Sir can you do a tutorial on glomerulonephritis
That's good
Sir nice video
in pathogenesis ,
Stimulation of RAAS cause efferant vasoconstriction there by increase gfr for sometime and then due to hyperfiltration injury cause decrease in gfr?
THIS IS MOST CONFUSING PART .
RAAS cause affarent vasoconstriction and decrease renal perfusion
Just wow
Hi... Nice video... Thanks...👍👍👍
@9:00 In explanation of the pathophysiology, you've said that the tubular obstruction & deceased tubular flow causes decreased GFR, but I think both of them directly causes oliguria with nothing to do with GFR...
This is the first video I saw & yes.. subscribed 👍👍
It has to do with gfr
Becoz increase in tubular pressure is oppposing pressure to netf iltration pressure
GFR=FILTRATION COEFFICIENT X NET PRESSURE(oncotic and hydrostatic )
@@doraemonnobita9513 Hi... What you've explained is explained prior to 9:00 min time stamp.... @ 9:00, he's explaining about tubular obstruction ➡️ causing a Dec GFR ➡️ Oliguria... But I'm saying that, even if GFR is high, oliguria would happen because of of tubular obstruction.....
Thanks for the response, though ☺️☺️
Sir kindly uplode vedio from renal system
Sir can u please explain microscopy
Sir, in reversible injury there is loss of function of Na - K pump ...but here...why does this pump redistribute to luminal side and works...??
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Really via ur videos ..
I love pathology ..
Help Line to line understanding of Robbins ..
...
Eagerly waiting for more to come .
Thanks for this great job
Sir why in recovery phase there is increase in urine output??
Sir how hypertrophy occur s
Sir videos on nephrotic syndrome
Why does some ischemia cause tubular injury while other ischemia causes papillary damage?
i think depends on the amount of the blood reaching.. like renal papilla is closer to the main artery and tubules would be affected more
correct me if I'm wrong pls
Papillary necrosis is primarily anti prostaglandin mediated injury caused by NSAIDs which affect the countercurrent mechanism of Vasa recta.
While tubular necrosis is caused by nephrotoxins that affect cell integrity either by impacting cell protein metabolism or cell wall integrity.
How increased nacl delivery to distal tubules stimulate RAAS?
macula densa cells sense it and cause RAAS activation to reduce GFR so there would be more time to absorb NaCl.. it'll get it as if GFR is high and no time for reabsorption
🙏🙏🙏🙏
Part 2 ???
ruclips.net/video/jAC-mfChY4c/видео.html
why you don't answer questions
Go and read more books on your own 😂😂
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