A review of the normal physiology of sodium, potassium, and water. Major topics covered include the renin angiotensin aldosterone system, the hypothalamic pituitary adrenal axis, ADH (antidiuretic hormone), and the natriuretic peptides.
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.
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.
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.
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
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
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.
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! 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 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 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?
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
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?
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?
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)
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.
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...
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 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 :)
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.
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!
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.
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??
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.
