Errata: @9:38, juxtaglomerular cells are adjacent to the endothelium, but they themselves are derived from smooth muscle. @17:10, aldosterone's indirect effect on serum potassium is to decrease it, NOT increase it.
Respected Sir, at 15:22 , it should be that ADH inserts Aquaporins-2 into the Epithelium of collecting tubules and ducts rather than endothelium. Please reply.
wooowww! I've read countless times the chapters in Guyton regarding these topics yet i was still confused until i watched this lecture. you're my savior, Sir. continue making videos such as this. it saves a lot of medical students from confusion and doubt. thank you so much. -A medical student from the Philippines.
Thanks so much for your passion and dedication to teaching others. It is wonderful to have people like you around Eric and I am so appreciative of the amount of thought you have put into summarizing such complex topics.
Thank you Doctor Strong , this is a wonderful lecture, unrivaled by any. I listen to this the third time. I listened to this topic many time in my life to a degree :)
I greatly enjoy your teaching style and method. Your e-lectures alway have helped me to maintain 4.0 GPA in A&P and Pathophysio. Thank you very much, Dr. Strong!!!!!!!! - a nursing student from the SF Bay Area
That's a great question. I've never been satisfied with published explanations of this phenomenon that I've come across. However, I would hypothesize it's because the H2O retention that comes with SIADH is spread across all body compartments, whereas the H2O retention that is secondary to disorders of sodium retention (e.g.. hyperaldo., etc...) is disproportionately distributed to the intravascular space due to the osmotic pressure of excess Na+, which can't freely move between compartments.
Uncomparable quality of lectures.. I have watched your lectures since last year and I never had a chance to express how I appreciate. Thank you so much, professor.
Thanks! There's an annotation that points this out, but unfortunately annotations don't show up on mobile. Glad to know viewers are keeping me honest! =)
I am very looking forward to your hypo/hyperkalemia videos! Thank you soooo much! Going from big picture to details is extremely helpful in understanding as a first year medical student. And your diagrams are superb
I am watching this vid because I am a psychopharmacology fellow. We have a patient on lithium who has long standing borderline high potassium. I am thnking he has hypoaldostertonemia beccause his TTKG is 4.8. I think normal TTKG is 7. And especially in the face of borderline high potassium, that TTKG should be even higher. Those are my thoughts. BTW. u r a god of renal physiology! Holy shiit. U really got that stuff down pat!
A small doubt.. At 19:32, you say Increased serum Glucose leads to increased extra cellular oncotic pressure. Doesn't oncotic pressure depend on the protein content? Glucose being an osmolyte, shouldn't the more appropriate term me "increased osmotic pressure"?
Hi Simply simplified. One small error, in one of the penultimate charts describing the RAA axis and ADH, under aldosterone , increased potassium is mentioned, should have been decreased. Regards and thanks. Dr Samir Dasgupta MD
Thank You sooooo much for this lecture. You are the man; You are the doctor!! I have two questions: 1. Where does maxzide act on nephron, in particular, Triamterene, K^+ spare? 2. What's the relationship to ACE Inhibitors and chronic cough?
9:38 I think juxtaglomerular cells are not endothelial cells, but rather sit right next to the arteriolar endothelium and constitute specialized smooth muscle cells!
Rise in glucose in the extracellular space results in the increase in OSMOTIC PRESSURE but not the ONCOTIC pressure (protein base pressure). Otherwise a brilliant lecture. Recommend any day...
Hi Dr. Strong. When talking about ABG disturbance causing hypo/hyperkalemia, what are other mechanism of change in plasma potassium beside H+/K+ cellular exchange? Because since H+ concentration is cca 10 milion x lower than plasma K+ concentration, change in pH from e.g. 7,4 (H+ conc. 40nmol/l) to pH 7,3 ( H+ conc. 50nmol/l) means difference of just 10nmol/L, there is also only 10nmol/l change in patassium concentration, which is clinically irrelevant. Therefore I'd say primary potassium disorder can cause ABG disorder but not reverse (by celular exchange of H+/K+). Am I wrong? I hope I just didn't miss something that will cause me to look like a fool :)
Hi, thanks for the lecture, around about 14.00 I think you say cortisol dilates the afferent arteriole of the kidney would,this not increase exertion in kidneys and reduce blood pressure, when cortisol,increases BP?
Also would you be able to make a video on 1. the communication of the kidney and the heart. 2. Hemodynamics of valvular heart disease: pressure overload v. volume overload 3. Factors that alter preload, afterload, and contractility of the heart and its effects Thank you!
I hope to get to all of these at some point. Unfortunately, I'm very behind on fulfilling requests, so I wouldn't want to estimate when I'll get to those specific topics. Thanks for watching!
Great explanation dr. Eric ! Btw, i read an article about hyponatremia, and it's said that ADH also promotes sodium excretion as well as water reabsorption. What's your comment on this?
Steps: 1. For a basic science topic (e.g. sodium & potassium metabolism), I'll start with an old-school textbook - yes, some of us still use those! ;) While for a clinical topic, I'll start with the relevant UpToDate article. 2. Using one of those resources, build a general outline of what I want to talk about. 3. Create the figures/tables, supplementing with other resources when necessary. 4. Anticipate what questions I would have if someone were presenting the topic to me, and then I look those up - either in a textbook, or from the primary literature. And work the answer into the video outline/slides. 5. Trim down the topic to the minimum necessary to convey the information without oversimplifying it. 6. If it's a video with "live action" (i.e. I'm speaking on camera), I usually write a literal script because its incredibly painful to have to rerecord a whole section because I realize that I misspoke while I'm editing later 7. Record the video.
This video was great and helped me a lot! Thank you! I have a question about loop diuretics - I've read that they can cause both hyponatremia and hypernatremia - hyponatremia from volume depletion causing the release of ADH, and hypernatremia from lowering the corticomedullary osmolar gradient by disrupting countercurrent multiplication; which do you more commonly see in clinical practice?
I have never once seen hypernatremia caused by loop diuretics in clinical practice. In contrast, maybe 1/3-1/2 of all patients on loop diuretics are hyponatremic, though whether the diuretic is the direct cause, or the hyponatremia is being caused by the disease for which the diuretic has been prescribed (e.g. heart failure, cirrhosis) is usually unclear.
if u could do a seperate lecture on renal physiology that u haven't included in those lectures ,it will be helpful.ex.counter current mechsnism,renal clearence,GFR.
Wow, great information but also quite overwhelming, need to study more :) Where do you start looking for the right tests? I am chronic low sodium for no obvious reason, (now diagnosed with hashimotos, adrenal fatigue etc.) I personally think, the low sodium and low blood pressure is a key to my health but the GP has no answers. Do I look for a metabolic doctor here in Sydney??
Awsm lecture...best for the topic...in ur chart it is writen in indirect effects of aldosterone tht it increases serum potassium....shouldnt it decrease?? Because aldosterone increases excreation of potassium in principal cell??
Yes you are correct. There is an annotation that pops up over top of the chart pointing out this error, but if you have annotations turned off, you won't see it.
Sorry they aren't posted yet. Last week, I had a fatal operating system/software problem on the computer I use for recording the audio, and decided that the computer was old enough that it made more sense to replace it instead of the pain of reinstalling the OS or reformating the hard drive. May take another week or two...
For most videos, I start with creating a slide set in PowerPoint, and export them as high-resolution jpgs. (PowerPoint, at least older versions like mine, defaults to exporting them as low resolution jpgs. Changing them to higher resolution literally requires altering the Windows registry; there are sites on line that explain how to do this - See: support.microsoft.com/kb/827745 , but any manual change of the registry is risky, and you should only attempt it if you know what you are doing) The majority of original images and diagrams I use are drawn directly in PowerPoint (it's actually half decent as a drawing program, once you figure out the work-arounds for things it can't do, like any complex 3 dimensional structure). More complicated pictures are drawn in Adobe Fireworks or Illustrator. I then record the narration using a free program called Audacity, exported as a wav file. The music is arranged and rendered in Finale, and also exported as a wav. The jpg version of the slides, and the wav files for the narration and music are stitched together and synched up in Premiere Pro. For the videos that include animation (e.g. chest X-rays, PFTs), these are created in Premiere itself. Animations in Premiere may be much more limited than in Flash or a dedicated animation program, but are also much simpler/faster to create. I experimented with trying to use Blender with the intention of mind-blowing animations, but quickly realized that if I spent 90% of the creative process on the animation, my priorities were probably misplaced.
And all I am trying to find out is do I need to take in more potassium than sodium. (yea, I know I need to have a low sodium diet. But just how much potassium)
Evelynn, thanks for the feedback. Unfortunately, I'm pretty unimpressed with the available textbooks out there that cover electrolyte disorders, and don't have a specific recommendation. When I was a med student (1998-2003), most students used either Renal Pathophysiology: The Essentials or Fuids and Electrolytes in the Surgical Patient (choice depending upon anticipated specialty); however I was quite underwhelmed by both books. I honestly don't know what most students use these days, other than First Aid for Step 1 (which I don't recommend for the purpose of studying for a physiology course). The professional standard text is Clinical Physiology of Acid Base and Electrolyte Disorders by Burton Rose, but it weighs at at 1000 pages, and I can't imagine a non-nephrologist having enough patience and interest to get through it. If anyone else on here has a recommendation for Evelynn, feel free to list it here!
I think that might be the first time anyone has asked what animal I keep in that tank! It was actually a Xenopus frog (it unfortunately died about 2 years ago.)
Errata:
@9:38, juxtaglomerular cells are adjacent to the endothelium, but they themselves are derived from smooth muscle.
@17:10, aldosterone's indirect effect on serum potassium is to decrease it, NOT increase it.
Respected Sir, at 15:22 , it should be that ADH inserts Aquaporins-2 into the Epithelium of collecting tubules and ducts rather than endothelium. Please reply.
I was about to write it in comments then I read it😂
wooowww! I've read countless times the chapters in Guyton regarding these topics yet i was still confused until i watched this lecture. you're my savior, Sir. continue making videos such as this. it saves a lot of medical students from confusion and doubt. thank you so much. -A medical student from the Philippines.
+aspiring MD I'm glad you found it helpful!
Yeah true at time guyton gets really confusing
Amazing video. You have no idea how much this video has help finally understand the whole mean process. A big thank you sir.
WOW! What an incredible breakdown! You did great, I was feeling overwhelmed and you summarized it right up.
Better than most, if not all other video tutorials that I've seen.
High quality, clear and accurate. Excellent!!
I've admired your dedication to med ed since 2013. Thank you Dr. Eric.
Rawdon Waller You're very welcome!
Thanks so much for your passion and dedication to teaching others. It is wonderful to have people like you around Eric and I am so appreciative of the amount of thought you have put into summarizing such complex topics.
Thank you Doctor Strong , this is a wonderful lecture, unrivaled by any. I listen to this the third time. I listened to this topic many time in my life to a degree :)
I greatly enjoy your teaching style and method. Your e-lectures alway have helped me to maintain 4.0 GPA in A&P and Pathophysio. Thank you very much, Dr. Strong!!!!!!!! - a nursing student from the SF Bay Area
The above video is the first I've watched of what you contribute. I was most impressed, it was so way, way cool.
Thank you, Paul
That's a great question. I've never been satisfied with published explanations of this phenomenon that I've come across. However, I would hypothesize it's because the H2O retention that comes with SIADH is spread across all body compartments, whereas the H2O retention that is secondary to disorders of sodium retention (e.g.. hyperaldo., etc...) is disproportionately distributed to the intravascular space due to the osmotic pressure of excess Na+, which can't freely move between compartments.
Uncomparable quality of lectures.. I have watched your lectures since last year and I never had a chance to express how I appreciate. Thank you so much, professor.
"In reality the pituitary gland is much much smaller than the brain." A great lecture with some sense of humor! Thank you!
THANK YOU SO MUCH for the lectures and your devotion in doing medical videos! I hope you will make more.
Perfect level of detail for someone with a background!
First week into my Chemical Pathology rotation for my MPath degree. I find this very helpful. Thank you.
Thank you Dr Strong , you are superb clinician, teacher, instructor. Thanks very much.
By far the best lecture on this topic
My new favorite med youtube channel ❤🎉
At 17.20 there is a mistake i guess. Aldosterone leads to a decrease in serum potassium, not an increase as shown. But what a great great video!!!
Thanks! There's an annotation that points this out, but unfortunately annotations don't show up on mobile. Glad to know viewers are keeping me honest! =)
9 years later, this is still viewed :) and it's very helpful. Thank you!
Subscribed straight away thanks to the channel name "strong medicine" i thought yeah this is something i need
At first look this seemed too complicated.
But your step by step explanation was excellent and the topic is easy to understand.
Thanks
By far the best lecture !!! Thanks ... keep it strong !!!
I am very looking forward to your hypo/hyperkalemia videos! Thank you soooo much! Going from big picture to details is extremely helpful in understanding as a first year medical student. And your diagrams are superb
What a brillian summary! Thankyou
You have some bad ass videos! Best channel for medical students. Respect!
Thank you! I found this useful even while reviewing for medicine clerkship and step2! (also, sherlock is THE BEST!)
Sophie, that was a very Holmesian observation! Good luck with step 2!
Thanks you sir for your effort to make these wonderful lectures and make it free for us. Dr. Nahid, Bangladesh.
Very helpful and detailed. Thank you so much for this educational video.
Nice way of explanation with simple & easy way with complete information 🙏🙏
Amazing explanation of a complex and disputed topic .Thank you .
Thanks Doctor. Greetings from Mexico.
Best Video ever!!!! I loved, very didactic and complete at the same time.
this is really helpful. u simplified it and make it easy to understand! everythg just make sense..
Thank you so much.
I am watching this vid because I am a psychopharmacology fellow. We have a patient on lithium who has long standing borderline high potassium. I am thnking he has hypoaldostertonemia beccause his TTKG is 4.8. I think normal TTKG is 7. And especially in the face of borderline high potassium, that TTKG should be even higher. Those are my thoughts. BTW. u r a god of renal physiology! Holy shiit. U really got that stuff down pat!
Thank you so much. Finally, I got right lecture. you relived my symptoms of back itching~~~Thank you again~
You are such a great teacher. I wish you were my attending.
Sir a sublime video for non practitioner too..just as easy you have made👍
Now I know I will make an A on this next Exam!!! Thank you, Thank you, Thank you.
Thanks Dr.
Easily understandable way of explanation
Of this lectures 👍👍
It was very helpful and well explained ,,, thank u !
Thanks for these series of videos they are very helpful.
OMG... You are my guardian angel..... Great breakdown!!!!!!!!!!!!
So useful. Thank you Dr. Strong!
Wow!! So wonderfully simplified! Thank you.
Thank you Doctor. This lecture is the best !
Verry very fantastic. .. thanks alot may allah bless you sir
You're amazing! Thank you so much for sharing your expertise with us!!
you are amazing, thanks for dedicating your precious time.
Thank you for your thorough review!
A small doubt.. At 19:32, you say Increased serum Glucose leads to increased extra cellular oncotic pressure. Doesn't oncotic pressure depend on the protein content? Glucose being an osmolyte, shouldn't the more appropriate term me "increased osmotic pressure"?
Extremely helpful video. Thank you!!
great lecture, congratulations and thank you! keep up
Hi
Simply simplified.
One small error, in one of the penultimate charts describing the RAA axis and ADH, under aldosterone , increased potassium is mentioned, should have been decreased.
Regards and thanks.
Dr Samir Dasgupta MD
very nice explanation
Thank You sooooo much for this lecture. You are the man; You are the doctor!! I have two questions: 1. Where does maxzide act on nephron, in particular, Triamterene, K^+ spare? 2. What's the relationship to ACE Inhibitors and chronic cough?
That was brilliant - subscribed!
Very good lecture! Is it possible to add subtitles in order to enhance the good quality?
9:38 I think juxtaglomerular cells are not endothelial cells, but rather sit right next to the arteriolar endothelium and constitute specialized smooth muscle cells!
Thanks for pointing that out! I've added it to the pinned comment above.
Very good lecture! Is it possible to add English subtitles in order to enhance the good Quality?
Thank you! please place more lectures.
Rise in glucose in the extracellular space results in the increase in OSMOTIC PRESSURE but not the ONCOTIC pressure (protein base pressure). Otherwise a brilliant lecture. Recommend any day...
Perfect! Thank you for all of these!
This is beautiful. Thank you so much!
lot of love and plenty of respect
thanks a lot.
I love you man, thank you soo much man, this is priceless
Hi Dr. Strong. When talking about ABG disturbance causing hypo/hyperkalemia, what are other mechanism of change in plasma potassium beside H+/K+ cellular exchange? Because since H+ concentration is cca 10 milion x lower than plasma K+ concentration, change in pH from e.g. 7,4 (H+ conc. 40nmol/l) to pH 7,3 ( H+ conc. 50nmol/l) means difference of just 10nmol/L, there is also only 10nmol/l change in patassium concentration, which is clinically irrelevant. Therefore I'd say primary potassium disorder can cause ABG disorder but not reverse (by celular exchange of H+/K+). Am I wrong? I hope I just didn't miss something that will cause me to look like a fool :)
Thanks for the Videos and hard work doc!
Hi, thanks for the lecture, around about 14.00 I think you say cortisol dilates the afferent arteriole of the kidney would,this not increase exertion in kidneys and reduce blood pressure, when cortisol,increases BP?
Thank you alot .Very informative
Also would you be able to make a video on
1. the communication of the kidney and the heart.
2. Hemodynamics of valvular heart disease: pressure overload v. volume overload
3. Factors that alter preload, afterload, and contractility of the heart and its effects
Thank you!
I hope to get to all of these at some point. Unfortunately, I'm very behind on fulfilling requests, so I wouldn't want to estimate when I'll get to those specific topics. Thanks for watching!
thank you for the update!
AT 21:11 didyou mean severe dehydration instead of severe hydration?
Yes, thanks for pointing that out!
Could you please explain how do the NSAIDS blunt the effect of ACEI/ARBS? Thanks.
I LOVE YOU RIGHT NOW!!
Thank you!
excellent presentation. thanks
Great explanation dr. Eric ! Btw, i read an article about hyponatremia, and it's said that ADH also promotes sodium excretion as well as water reabsorption. What's your comment on this?
please can you show us how you prepared this lecture , your approach for the subject you want to learn
Steps:
1. For a basic science topic (e.g. sodium & potassium metabolism), I'll start with an old-school textbook - yes, some of us still use those! ;) While for a clinical topic, I'll start with the relevant UpToDate article.
2. Using one of those resources, build a general outline of what I want to talk about.
3. Create the figures/tables, supplementing with other resources when necessary.
4. Anticipate what questions I would have if someone were presenting the topic to me, and then I look those up - either in a textbook, or from the primary literature. And work the answer into the video outline/slides.
5. Trim down the topic to the minimum necessary to convey the information without oversimplifying it.
6. If it's a video with "live action" (i.e. I'm speaking on camera), I usually write a literal script because its incredibly painful to have to rerecord a whole section because I realize that I misspoke while I'm editing later
7. Record the video.
Extraordinary sir
Hello, Isn't the glucose effecting the Osmotic pressure and not the Oncotic pressure(which is determined by plasma proteins)?
Super excellent Prof
This video was great and helped me a lot! Thank you! I have a question about loop diuretics - I've read that they can cause both hyponatremia and hypernatremia - hyponatremia from volume depletion causing the release of ADH, and hypernatremia from lowering the corticomedullary osmolar gradient by disrupting countercurrent multiplication; which do you more commonly see in clinical practice?
I have never once seen hypernatremia caused by loop diuretics in clinical practice. In contrast, maybe 1/3-1/2 of all patients on loop diuretics are hyponatremic, though whether the diuretic is the direct cause, or the hyponatremia is being caused by the disease for which the diuretic has been prescribed (e.g. heart failure, cirrhosis) is usually unclear.
Please add transcript of the video. It will help in understanding better.
if u could do a seperate lecture on renal physiology that u haven't included in those lectures ,it will be helpful.ex.counter current mechsnism,renal clearence,GFR.
Wow, great information but also quite overwhelming, need to study more :) Where do you start looking for the right tests? I am chronic low sodium for no obvious reason, (now diagnosed with hashimotos, adrenal fatigue etc.) I personally think, the low sodium and low blood pressure is a key to my health but the GP has no answers. Do I look for a metabolic doctor here in Sydney??
Trollbead M Hi, I am in Sydney with similar issue. Wondering if I can get in touch to help each other.
Awsm lecture...best for the topic...in ur chart it is writen in indirect effects of aldosterone tht it increases serum potassium....shouldnt it decrease?? Because aldosterone increases excreation of potassium in principal cell??
Yes you are correct. There is an annotation that pops up over top of the chart pointing out this error, but if you have annotations turned off, you won't see it.
Thanku sir....u r the best teacher....hope t see more new awsm videos....
fabulous video, thank you
Hi Doctor,,i couldn"t find your lecture on hypokalaemia and hyperkalaemia
Sorry they aren't posted yet. Last week, I had a fatal operating system/software problem on the computer I use for recording the audio, and decided that the computer was old enough that it made more sense to replace it instead of the pain of reinstalling the OS or reformating the hard drive. May take another week or two...
Eric Strong Doctor, eagerly waiting for ur videos on hypo and hyperkalaemia...when will it be posted..
I am just wondering what program you use to build presentations like Dr. Erick's. Does anyone know?
For most videos, I start with creating a slide set in PowerPoint, and export them as high-resolution jpgs. (PowerPoint, at least older versions like mine, defaults to exporting them as low resolution jpgs. Changing them to higher resolution literally requires altering the Windows registry; there are sites on line that explain how to do this - See: support.microsoft.com/kb/827745 , but any manual change of the registry is risky, and you should only attempt it if you know what you are doing) The majority of original images and diagrams I use are drawn directly in PowerPoint (it's actually half decent as a drawing program, once you figure out the work-arounds for things it can't do, like any complex 3 dimensional structure). More complicated pictures are drawn in Adobe Fireworks or Illustrator. I then record the narration using a free program called Audacity, exported as a wav file. The music is arranged and rendered in Finale, and also exported as a wav. The jpg version of the slides, and the wav files for the narration and music are stitched together and synched up in Premiere Pro. For the videos that include animation (e.g. chest X-rays, PFTs), these are created in Premiere itself. Animations in Premiere may be much more limited than in Flash or a dedicated animation program, but are also much simpler/faster to create. I experimented with trying to use Blender with the intention of mind-blowing animations, but quickly realized that if I spent 90% of the creative process on the animation, my priorities were probably misplaced.
Very helpful! A little higher volume would be nice.
Lovely, thank you so much xxx
And all I am trying to find out is do I need to take in more potassium than sodium. (yea, I know I need to have a low sodium diet. But just how much potassium)
Why do people who consume too much salt in their diet have HBP? Wouldn't the body exrete extra sodium and not pick it up unless it sensed a low BP?
HI Eric, Thanks for the great lectures! What textbook do you recommend specifically for lytes disorders?
Evelynn, thanks for the feedback. Unfortunately, I'm pretty unimpressed with the available textbooks out there that cover electrolyte disorders, and don't have a specific recommendation. When I was a med student (1998-2003), most students used either Renal Pathophysiology: The Essentials or Fuids and Electrolytes in the Surgical Patient (choice depending upon anticipated specialty); however I was quite underwhelmed by both books. I honestly don't know what most students use these days, other than First Aid for Step 1 (which I don't recommend for the purpose of studying for a physiology course). The professional standard text is Clinical Physiology of Acid Base and Electrolyte Disorders by Burton Rose, but it weighs at at 1000 pages, and I can't imagine a non-nephrologist having enough patience and interest to get through it. If anyone else on here has a recommendation for Evelynn, feel free to list it here!
Great video! Thanks!
Does transmembrane H20 shift occur in uremia too?
Aldosterone indirect effect lowers potassium in serum,or not?
sooo strong , many thanks
best explained
I assume that tank is an atoloxyl tank. I am inspired to move one of my tanks near my workstation now. :) thank you
I think that might be the first time anyone has asked what animal I keep in that tank! It was actually a Xenopus frog (it unfortunately died about 2 years ago.)