Hi, I'm a huge fan of your vids. Thank you for all the effort. One correction: around min 30 it is said that in henoch shonlein purpura there's no joint pain, whereas in fact about 60-80% of kids have joint pain, mostly knees and ankles. (a typical case being a kid that "started not walking well/refuses to walk and has a rash on the buttocks)
Great videos Dr. Bolin. Small correction: "Membranous glomerulonephritis is the most common cause of nephrotic syndrome in adults," the most common cause in adults Focal Segmental Glomerulosclerosis (FSGS) as of 2018.
This is just superb, I been tryin to find out about "what is the creatinine level for kidney failure?" for a while now, and I think this has helped. Have you heard people talk about - Aiyibestoen Phenomenal Asset - (search on google ) ? It is an awesome exclusive product for discovering how to improve your kidney function without the normal expense. Ive heard some decent things about it and my colleague got excellent results with it.
Thanks for the awesome content i consider you as one of the Best studying sources In min 21 the traid of TTP and HUS Should be 1 renal insufficiency 2 thrombocytopenia 3 hemolytic anemia You mention thrombocytopenia and low platlets instead of renal insufficiency Thanks again big love big support ♥️
: Eight months after an attack of acute glomerulonephritis 38 year old woman was hospitalized for investigation of progressive bilateral leg oedema. On examination ,she was normotensive and exhibited pitting oedema of both ankles and dullness over her lung bases. Her face was pale and puffy and she admitted to frequent minor intercurrent infections. 1.What is your tentative Diagnosis?explain (10 marks) 2.What Biochemical analysis would you request, and in what order)please give the nomals in a healthy patient
Nephrology: Glomerulonephritides. Signs/Symptoms (SSx); Diagnosis (Dx), Differential Diagnosis (DDx); Treatment/Management (Tx/Mx); This is always a Nephritic Syndrome (Hematuria [Microhematuria]) with a Possibility for Nephrotic Syndrome (Edema, Proteinuria and Hypertension) coexistence. Complement Levels (C3) can be a distinguishing feature as well as the Pathology, namely Multisystemic Involvement or Renal Morphology only. Goodness, Glomerulonephritis is such a devastating disease process and a morbid Pathogenesis (Disease progression). MD Paul Bolin, Leben Lebe rein und heil gut ist immer. Prost!
After watching many of your videos i can hear angels singing in my head! Thank you thank you!. I was taught in the same manner as Dr. Cordova, and also glomerulonephritis is accompanied by hypertension and nephrotic syndrome don't. Could that be a fair statement?
+Maria Carbo It's not really a rule, but non-proliferative GMN like Minimun changes, focal-segmentary and membranous tend to do nephrotic syndrome, whereas proliferative GMN like IgA, extracapilar or mesangio-proliferative do more nephritic syndrome and hypertension.
Atypical nephrotic syndrome is accompanied by hypertension. After all, nephrotic syndrome causes fluid overload via third spacing. Compensatory mechanisms of the body can lead to hypertension. However, typical nephrotic syndrome doesn’t normally have hypertension as part.
Hi Dr. Paul. One question, why is Henoch Shonlein classified as "limited to the kidneys" if it also affects the skin, GI & apparently the joints as someone pointed out below. Shouldn't it be part of the systemic group then ? Thank you for all your videos, I watched all of them during my internal medicine course and made notes of it, it was a great help ! Keep it up
Hi Dr. Bolin thank you for this nephrology summary. If I could I wanna ask why did you consider Membranous GN as a systemic disease if it is idiopathic and only affects the kidney? Does that * mean something I missed? It seems a little off to me.
+Joaquín Alonso Córdova Linares Thanks for pointing that out. It is included it here because there is a tendency, though not in all cases, for membranous glomerulonephritis to be diagnosed in association w/ an autoimmune condition or with various other processes including infection and malignancy. Hence it is quite possible for this to show up with a myriad of other symptoms affecting other organ systems. Pathogenically, MGN is caused by immune-complex deposition. Just as a side note, I adapted this classification table from somewhere else...I think Kaplan, but I'm not sure. Really, though, the line between those that are "renal only" and those that are "systemic" is a lot more blurry than this might suggest.
Paul Bolin I had that feeling too. When I was taught GN the nephrologist classified it wether it is primary or secondary, proliferative or non-proliferative, and if it developed as nephritic or nephrotic syndrome. I am not familiar with Kaplan or the USMLE because I'm not from USA, nonetheless thank you for the clarification.
Question... could Nephrotic eventually lead to nephritic because of the permeability during filtration and having protein eventually causing gaps to gradually increase (assuming if there is no medical intervention). Resulting in the leak of RBC which are notably larger in size than that of protein, in the urine. Awesome Vid BTW!
I just want to make a clarification regarding rapidly progressing crescentic glomerulonephritis. According to Robbins and Coltran Pathologic Basis of Disease, 9e, roughly half of RPGN are manifestations of small vessel vasculitis or polyangiitis. This is ANCA-positive.
Thank you, your video has the best classification I've ever seen, inambiguous, crystal clear, thank you very much.
Hi, I'm a huge fan of your vids. Thank you for all the effort. One correction: around min 30 it is said that in henoch shonlein purpura there's no joint pain, whereas in fact about 60-80% of kids have joint pain, mostly knees and ankles. (a typical case being a kid that "started not walking well/refuses to walk and has a rash on the buttocks)
Great videos Dr. Bolin. Small correction: "Membranous glomerulonephritis is the most common cause of nephrotic syndrome in adults," the most common cause in adults Focal Segmental Glomerulosclerosis (FSGS) as of 2018.
This is just superb, I been tryin to find out about "what is the creatinine level for kidney failure?" for a while now, and I think this has helped. Have you heard people talk about - Aiyibestoen Phenomenal Asset - (search on google ) ? It is an awesome exclusive product for discovering how to improve your kidney function without the normal expense. Ive heard some decent things about it and my colleague got excellent results with it.
you have done a great effort to put it together in a very nice and high quality job. Thanks a lot for your excellent presentation
Really appreciate your hard work. excellent as always
Incredible animation, thank you.
Simply excellent. Very grateful for clear, concise and well presented video. Thank you for the great channel. 11/8/2018 😊
There can be joint pain in HSP btw
thank you so much for posting those videos they are of great benefit
Thanks for the awesome content i consider you as one of the Best studying sources
In min 21 the traid of TTP and HUS Should be 1 renal insufficiency 2 thrombocytopenia 3 hemolytic anemia
You mention thrombocytopenia and low platlets instead of renal insufficiency
Thanks again big love big support ♥️
: Eight months after an attack of acute glomerulonephritis 38 year old woman was hospitalized for investigation of progressive bilateral leg oedema. On examination ,she was normotensive and exhibited pitting oedema of both ankles and dullness over her lung bases. Her face was pale and puffy and she admitted to frequent minor intercurrent infections.
1.What is your tentative Diagnosis?explain (10 marks)
2.What Biochemical analysis would you request, and in what order)please give the nomals in a healthy patient
Nephrology: Glomerulonephritides. Signs/Symptoms (SSx); Diagnosis (Dx), Differential Diagnosis (DDx); Treatment/Management (Tx/Mx); This is always a Nephritic Syndrome (Hematuria [Microhematuria]) with a Possibility for Nephrotic Syndrome (Edema, Proteinuria and Hypertension) coexistence. Complement Levels (C3) can be a distinguishing feature as well as the Pathology, namely Multisystemic Involvement or Renal Morphology only. Goodness, Glomerulonephritis is such a devastating disease process and a morbid Pathogenesis (Disease progression). MD Paul Bolin, Leben Lebe rein und heil gut ist immer. Prost!
After watching many of your videos i can hear angels singing in my head! Thank you thank you!. I was taught in the same manner as Dr. Cordova, and also glomerulonephritis is accompanied by hypertension and nephrotic syndrome don't. Could that be a fair statement?
+Maria Carbo It's not really a rule, but non-proliferative GMN like Minimun changes, focal-segmentary and membranous tend to do nephrotic syndrome, whereas proliferative GMN like IgA, extracapilar or mesangio-proliferative do more nephritic syndrome and hypertension.
Atypical nephrotic syndrome is accompanied by hypertension. After all, nephrotic syndrome causes fluid overload via third spacing. Compensatory mechanisms of the body can lead to hypertension. However, typical nephrotic syndrome doesn’t normally have hypertension as part.
Thank you so much
AFAIK the name "lupus" comes from the heavy facial wounds that can appear in patients (the wounds resembling a wolf's bite).
27:17 Amyloid protein simply deposits in the tongue.
Thankyou so much for these videos !
Hi Dr. Paul. One question, why is Henoch Shonlein classified as "limited to the kidneys" if it also affects the skin, GI & apparently the joints as someone pointed out below. Shouldn't it be part of the systemic group then ?
Thank you for all your videos, I watched all of them during my internal medicine course and made notes of it, it was a great help ! Keep it up
Hi Dr. Bolin thank you for this nephrology summary. If I could I wanna ask why did you consider Membranous GN as a systemic disease if it is idiopathic and only affects the kidney? Does that * mean something I missed? It seems a little off to me.
+Joaquín Alonso Córdova Linares Thanks for pointing that out. It is included it here because there is a tendency, though not in all cases, for membranous glomerulonephritis to be diagnosed in association w/ an autoimmune condition or with various other processes including infection and malignancy. Hence it is quite possible for this to show up with a myriad of other symptoms affecting other organ systems. Pathogenically, MGN is caused by immune-complex deposition. Just as a side note, I adapted this classification table from somewhere else...I think Kaplan, but I'm not sure. Really, though, the line between those that are "renal only" and those that are "systemic" is a lot more blurry than this might suggest.
Paul Bolin I had that feeling too. When I was taught GN the nephrologist classified it wether it is primary or secondary, proliferative or non-proliferative, and if it developed as nephritic or nephrotic syndrome. I am not familiar with Kaplan or the USMLE because I'm not from USA, nonetheless thank you for the clarification.
Joaquín Alonso Córdova
Excellent as always dr.Paul
Question... could Nephrotic eventually lead to nephritic because of the permeability during filtration and having protein eventually causing gaps to gradually increase (assuming if there is no medical intervention). Resulting in the leak of RBC which are notably larger in size than that of protein, in the urine. Awesome Vid BTW!
Same q!
hey dr.bolin, great video ! where does microscopic polyangitis fit ?
I just want to make a clarification regarding rapidly progressing crescentic glomerulonephritis. According to Robbins and Coltran Pathologic Basis of Disease, 9e, roughly half of RPGN are manifestations of small vessel vasculitis or polyangiitis. This is ANCA-positive.
Wow man thanks ! :)
Hello Dr.Bolin. What are the reasons, if any, for complement to have low leves?Thank you:)
SLE!
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10:19