More questions from the minds of the M2s at OUWB
The minds of OUWB continue to provide thoughtful questions.
My roommate and I have encountered a question regarding the content on Sodium/Water Balance and also its application to SIADH. We have been using some outside resources to supplement the learning in class, and I feel that they have been somewhat contradictory in these 2 scenarios. The following are the scenarios that I am trying to think through
1) Patient eats a high salt meal, increasing total body Na+, resulting in an increase in ADH release (via increased plasma osmolarity) and eventually reaching baseline Na+ concentration and osmolarity at a higher ECV. Now, the increase in ECV would result in a down regulation of Sympathetic NS and RAAS; however, what I am hearing is that this down regulation would just return the kidney to Na+ in = Na+ out and would not actually return the individual to the original ECV. So, my question is how does this person get back to original ECV? What I am reading is that the person will continue to operate at this higher ECV until sodium restriction takes place. However, I am wondering how decreased RAAS (decrease aldosterone – decrease Na+ reabsorption – increase sodium excretion) wouldn’t do this, and also if pressure natriuresis wouldn’t do this also? Basically, why don’t these mechanisms do the work automatically, and why do you have to sodium restrict?
You have it right. That is the currently accepted understanding of sodium metabolism. It is not quite complete, because, though some subjects increase their blood pressure with increased sodium intake, not all patients increase their blood pressure. As to why the renin-angiotensin aldosterone system does not down regulate itself sufficiently to fully correct the volume overload situation, it is not well understood. The sodium regulating systems in the body strive to match sodium absorption with sodium excretion. With an increase in sodium intake there will be a modest expansion of the extracellular compartment until the sodium excretion is upregulated to match sodium intake. We can see evidence of the increase total body sodium with an increase in body weight associated with increased sodium intake.
2) In SIADH – high levels of ADH cause increased water reabsorption but euvolemic hyponatremia. Fitting in with my previous questions in the earlier scenario, how does the patient maintain euvolemic status? If increased water reabsorption occurs and the ECV is increased, the same down regulation of Sympathetic NS and RAAS would occur. Now, the outside resources in this case state that a decreased RAAS would actually cause increased sodium excretion that would allow for increased water excretion that would maintain euvolemic status. This makes sense because then the hyponatremia that results is not only an effect of the dilution from increased water reabsorption, but also from the increased excretion of Na+. But, this goes directly against the whole logic of needing to sodium restrict in the earlier case (i.e. RAAS can’t do the work to return the individual in scenario 1 back to a normal ECV).
So again you are well versed in what is happening in SIADH. SIADH is largely euvolemic and largely is a situation where patients are in sodium balance, i.e. sodium = sodium out. However if you do meticulous metabolic balance studies you will find that patients do gain weight during SIADH. There is excess water and this does serve to expand the patient’s extracellular volume. This also will suppress the renin-angiotensin-aldosterone-system so that patients will get a modest increase in urine sodium excretion. But I don’t quite understand how you think this is any different than the first scenario. There is a modest increase in sodium excretion but in the presence of continued unremitting ADH activity the patient continues to deal with the modest increase in volume. So like the first scenario, the modulation of the RAAS is unable to fully restore euvolemia.
For more on SIADH and volume status see this post.
Metabolic Alkalosis, the emergency lecture
“I thought you were going to do metabolic alkalosis?”
“Me? I thought you were going to do metabolic alkalosis.”
So here is a quick lecture on metabolic alkalosis.
I believe my chapter on metabolic alkalosis in the fluids book holds up and is appropriate for second year medical students.
Chapter 14. Metabolic Alkalosis
The lecture I am going to try to give on Tuesday:
Video of the lecture:
The Hypernatremia Lecture for OUWB
Las\\t Wednesday I was unable to get through the entire Sodium and Water lecture. Here is the last 17 minutes that I was not able to get to in class.
The full slide set is available here
Introduction to Acid-Base and Metabolic Acidosis
Today’s lecture, in PowerPoint, no less.
OUWB Question about pseudohyponatremia
First catch of the year.
I have a question regarding your OUWB lectures. I’m trying to grasp why hyperglycemia causes an increase in serum tonicity and decrease in serum sodium, but hyperlipidemia causes no change in serum tonicity and a decrease in serum sodium. For hyperglycemia, I understand that the glucose contributes to the serum osmolarity and can’t passively cross the membrane so causes water to move. However, I’m confused with the situation with lipids and was wondering if you could clarify. Thank you so much!
I may have over indexed on false hyponatremia stuff. This is something you need to be familiar with but a detailed understanding of the mechanism of pseudohyponatremia.
The student had perfect knowledge of the mechanism behind hyperglycemia induced hyponatremia associated with hyperglycemia.
The lipid situation is just a lab error. The lipids fool the lab machine into thinking the sodium is low. It is not low. That is why the osmolality is normal. The osmolality detector is not fooled by the high fats (or proteins) in the blood.
You will not need to know the mechanism for the lab error. I tried to explain it but that may be a situation where I causes more confusion than provided clarity.
All my Posts for Medical Students at OUWB
I have had the honor to teach the M2s since the medical school opened it’s doors. Here are the blog posts I have written to answer medical students questions or to post the latest materials (Handouts, Keynotes).
OUWB Question: What’s going on with this mess?
I create all of my presentations in Keynote. In
You cannot tell if a respiratory acid-base disorder from the ABG
This is a frequent cause of confusion. I know
OUWB Student question: Do I need to memorize all of these equations?
No. You will be provided an equation cheat.
OUWB student question on ammonium production and potassium
How does hyperkalemia or even alkalosis suppress
OUWB: So you’re lost in renal and looking for a map
If you are a reader and need a book to help you
OUWB: Podcasts of interest
If you are taking the M2 renal class and are
OUWB 2023: Regarding the upcoming TBL
I received an email questioning what to read in
More OUWB M2 questions and Answers
The question: I am going through the real well
OUWB SoM Sodium and Water Lecture
So drop box behaves strangely with Keynote files. When you get to this page by clicking the above links, press the Download button.
Here is a link to the Keynote presentation exported to powerpoint.
The TTKG is dead, now what?
Halperin has declared the TTKG dead.
And therefore never send to know for whom the bell tolls; It tolls for the TTKG
However we still need to assess patients for hypokalemia and differentiate between renal and extra-renal losses.
Measuring a fractional excretion of potassium (FEK) doesn’t physiologically make sense. The idea behind the fractional excretion calculation is calculating what percentage of the filtered potassium (in this case, but can be anything) ends up in the urine. But potassium doesn’t work that way. Essentially all of the filtered potassium is reabsorbed in the proximal tubule and thick ascending limb of the loop of Henle so that the fractional excretion of potassium is zero at that point. Then in the late distal convoluted tubule and the medullary collecting duct all of the potassium that is destined for the toilet is secreted. So all of the potassium that is cleared by the kidney is secreted but the distal nephron/tubules not filtered by the glomerulus. That said the FEK is just a calculation and you can do it. I reviewed the the best data on it here:
So what calculation do I use? I use the TTKG, but that’s because I’m a dinosaur. What I should be doing is the urine potassium to creatinine ratio.
The answer is 13 mEq/g creatinine.
In this study of hypokalemic periodic paralysis versus patients with increased renal potassium excretion, the K:Cr ratio neatly divided the two groups.
If you know of a better reference for the potassium to creatinine ratio, tweet me up.
Some addenda to my Curbsiders podcast on NAGMA
In my discussion on The Curbsiders I talked about the urine anion gap as a way to estimate urine ammonium. Here are the figures I would have shown for the urine anion gap, if the Curbsiders was a television show rather than a podcast:
The urine anion gap is wildly inaccurate at estimating urine ammonium. In this study of 1,044 people with chronic kidney disease, the urine anion gap was 42, while the urine ammonium was only 21:
Would you trust a technique to measure serum sodium if it was twice the actual serum sodium?
There is a second way to estimate the urine ammonium, the urine osmolar gap. The urine osmolar gap was devised to escape a different weakness in the urine anion gap, the problem with large amounts of urine anions, like ketones or hippurate.
The osmolar gap assumes that the difference between the measured and calculated osmolality will largely be made up by ammonium salts.
Here is a tweetorial about this, if that is your thing:
Part One: Don’t trust equations:
One of the weird truths about nephrology is that you spend your fellowship learning all of the equations and then for the first few years after fellowship you learn that they are rubbish.
Don't believe me…
— Joel M. Topf, MD FACP (@kidney_boy) August 2, 2018
Part Two: But you need to understand the equations so you can use them properly, the urine anion and osmolar gap:
I spoke about the urine anion gap with the @curbsiders but I want to emphasize what is oing on here:
In metabolic acidosis the kidneys try to excrete excess acid as ammonium NH4+. This is essential because even at a pH of 4.4, the hydrogen concentration is
— Joel M. Topf, MD FACP (@kidney_boy) August 2, 2018
The other mistake I made was an over simplification on how NH4+ is made. I said NH3 was made in the proximal tubule but it is more complicated than that. A lot more complicated. From David Goldfarb:
The proximal tubule makes 2 molecules of NH4+ via Glutaminase which also produces a 1 alpha-ketaglutamate (AKG). The AKG generates 2 molecules of HCO3 which is added to the blood. The NH4 gets tossed into the tubular fluid. So for every NH4+ created in the proximal tubule, one bicarb gets added to the blood.
