Tag: OUWB

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#OUWB Questions

This question came in after class from a couple of students.

If the urine sodium in volume depletion and the great edematous states (heart failure, liver failure, and nephrotic syndrome) is low how can the urine osmolality be high?

The osmolality of the urine is made up of electrolytes (sodium, potassium and chloride) and non-electrolytes. The non-electrolytes like urea and ammonia will make up the bulk of the osmolality in the small volume of urine that is seen in this clinical setting.

In the advanced electrolyte class (nephrology and critical are fellowship) we look at the electrolyte content of the urine and use it to look at hypo- and hypernatremia more sophistically. For the purpose of medical school, SHELF exams, and USMLE parts 1, 2, 3 you can safely just look at the osmolality of the urine. We are trying to build a model that is understandable and good enough to predict how patients will behave in health and illness. This works pretty good.

The next question also came from a couple of people in class.

In SIADH, you say that the patients are euvolemic, but then you say they retain water via ADH in the medullary collecting duct. How can both of these be true? Won’t they become volume overloaded if they retain water.

This is a common question. The key to understanding this takes a bit of a leap of faith. First off, there is no slight-of-hand here. If you do careful water measurements as patients develop SIADH you can measure an increase in total body water. But critically, the increase in water is not progressive and it does not cause clinically significant volume overload. It does not cause pulmonary edema, it does not cause peripheral edema and it does not cause hypertension, all consequences of true volume overload from a positive sodium balance. 
One of the reasons that excessive water intake does not cause volume overload is that most of that water (two-thirds) disappears into the intracellular compartment. Just like no one complains of their rings not fitting after drinking a lot of water, having high ADH does not cause interstitial edema.
This image from the lecture needs to be front and center when you think about SIADH: water out of balance, sodium in balance:

The last question for now comes from an e-mail (jtopf@mac.com):

I had a question from the second half of the lecture about treating euvolemic hyponatremia in the case of adrenal insufficiency. I’m having a hard time understanding why urea and salt tablets would help to reverse the hyponatremia. If solute in = solute out and the kidneys are already in sodium balance, how would it increase the solute load in the case of salt tablets? Even if the urine output goes up, won’t there still be non-physiological ADH release and concentration of the urine?

So the best way to think about salt and urea tablets is be visualizing this slide from this SIADH lecture:

In SIADH, the secretion of ADH is fixed and maximal. It’s like somone is stepping on the gas and can’t remove his foot.

Normally the ADH slides from minimal to maximal in order to balance water excretion with variable water intake:

The ADH slider is supposed to indicate that the ADH can slide from minimal activity, resulting in large volumes of urine, to maximal activity, resulting in minimal urine output. As the questioner correctly intuited, the osmolar load is fully excreted. In euvolemic hyponatremia, the slider is jammed to the right. If the urine osmolality (the denominator) is fixed the only way to adjust the urine volume will be to adjust the osmolar load (the numerator). Increasing the osmolar load with a high protein diet or salt tablets or urea pills will raise the numerator and hence increase the urine volume. It’s just math. Yes, taking sodium tablets will just result increase the sodium excretion since these patients are in sodium balance, but this additional sodium excretion increases the urine output making it easier for the patient to have less water intake than excretion, the goal for the treatment of hyponatremia.

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OUWB Acid base question

The e-mail:

Hi Dr. Topf,

We were going through the acid-base study guide and Prince Harry has us all out of sorts. His scenario is this: 

Your first mistake. It is Prince William not Harry. Know your Royals. (Though I do not think royal genealogy is a board eligible topic.)

7.42 | 32 | 76
Na – 148
Cl – 98
K – 5.8
HCO3 – 28 

For the primary acid-base disturbance, I would think it is respiratory alkalosis because the pH is elevated, the PCO2 is decreased, and the HCO3 is elevated.  

You are correct

Then for the second acid base disturbance, I thought it would be metabolic alkalosis. His PCO2 is 32, which is down about 10. So, his bicarb should go down either 2 if acute or 4 if chronic, to either 22 or 20. Instead it is 28 which means he has excess HCO3 (base) and so has an additional alkalosis. 

Correct again

I tried doing the anion gap (22) and the bicarb before (38) but my understanding is that a bicarb before of 38 would also be metabolic alkalosis.  

Yes

In the answers, it says that if you have an AG with alkalosis or a primary acid-base disorder, that it would be an acidosis.  

If you have time, can you help me understand why his primary disorder is metabolic alkalosis, and how to apply the anion gap and bicarb before formulas to this case?  

Thanks for your time. 

Best regards,

This refers to this question in the handout:
There is an error in the ABG. Using the Henderson Hasselbalch equation it is obvious that this ABG is impossible, as pointed out by +MedCalc on twitter:

@kidney_boy Threw @medcalc at it. Don’t know how HCO3 could be 28 as Henderson (The Law) says it should be 21. pic.twitter.com/ilqD1l3Qec
— MedCalc (@MedCalc) August 23, 2014

So the actual pH should be 7.51. But that doesn’t change the rest of the answer or the calculations.
To get this problem right, it breaks one of the rules I established and uses another rule that was not discussed. This is failure on my part and I will fix this.
The rule that it breaks is the rule that compensation is always in the same direction as the primary disorder. Obviously with a pCO2 of 32 and bicarbonate of 28 the two independent Henderson-Hasselbalch variables are moving in discordant directions.
This is a great guideline, it just isn’t always true. In cases where patients have two primary disorders the pCO2 and bicarbonate can move in opposite directions. This is not the typical finding but when it occurs it is simple to interpret:
If the pCO2 falls it is respiratory alkalosis and if it rises it is respiratory acidosis. If the bicarbonate falls it is metabolic acidosis and if it rises it is metabolic alkalosis. So in the case of Prince William, his bicarb is up and pCO2 is down so he has both a metabolic and respiratory alkalosis. The reason I do not include this is that it is an additional complexity that if you follow the algorithm that I taught you will get the right answer without knowing this exception. I choose to streamline the teaching rather than teach this shortcut.
The rule that was not discussed is in regards to the anion gap. In my booklet I never discuss that the presence of an anion gap regardless of the pH or serum bicarbonate always indicates a metabolic acidosis. The hierarchy of acid interpretation that I showed in the booklet should include that right at the top and has been updated to reflect that:
So Prince William is rocking an anion gap of 22, this means he has an anion gap metabolic acidosis. If you use the bicarbonate before formula you see that his bicarbonate was 38 excluding his anion gap metabolic acidosis indicating a truly wicked metabolic alkalosis.
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OUWB School of Medicine Materials 2014

The Potassium and Metabolic Alkalosis lecture:

The Acid Base Lecture

  • Keynote (480 MB)
  • PDF (51 MB)
  • Extra lecture only about non-anion gap metabolic acidosis


The Potassium lecture (on your own)


The Sodium and Water Handout


The Electrolyte and Acid Base Companion


Acid Base Workshop
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Team based learning, reason for optimism about medical education

In general, as I have progressed through my education, I have felt that the quality of education has been on a downward vector.

  • I believe that duty hour work restrictions have diminished continuity of care and reduced the drive for residents to read and learn about their patients, because the patients feel less like “their patients.”
  • I think the emphasis on fraud prevention that has meant that attendings need to see and be present for all of the meaningful aspects of patient encounters has diminished fellow autonomy and delayed the maturation process that senior residents and fellows undergo.
  • I think the addition of alternative medicine curriculum to medical schools is an inexcusable retreat from the goal of medical scientists.

But I have recently experienced a vision for the future of medical education at Oakland University William Beaumont Medical school and I am blown away. Don’t worry future doctors are going to be just fine.

OUWB is one of the newest medical schools in the country and has it’s first two classes of medical students enrolled, classes of 2015 and 2016. The second years are finishing up the renal section. It is an integrated unit including histology, pathology, physiology and pathophysiology. I was privileged to have an integral role in developing the curriculum. One of the parts that I spent hours on was developing Team Based Learning modules (TBL).

Typical MD Lab from Scott Hall
(http://conjoint.med.wayne.edu/mdlabs.php)

Team based learning is OUWB’s version of the small group learning sessions that have always been a part of the first two years of medical school. During my years at Wayne State they were called MD Labs. The sessions were sprinkled through out the curricula. I went to a few and they were of widely variable quality. I didn’t go to many, because they didn’t count toward your grade. That told me that The Dean didn’t think they were important enough to count so I took the hint spent my limited hours cranking on stuff that counted.

The TBL is a reinterpretation of those small group sessions that I see as wildly successful. The success is not by accident and comes from the novel structure of the sessions. A TBL is made up of preparation and three segments:

Prep

The preparatory reading is a chapter, or article or handout that covers all of the main ideas of the session. For proteinuria and glomerular disease the students were assigned a chapter in Harrison’s. For CKD and AKI the students were given review articles in BMJ (Hilton R. 2006) and NEJM (Abboud, Henrich 2010). For Sodium and Water, I wrote a 41 page chapter on the subject. Be warned I have been told that it has a lot of typos.


    Individual Readiness Assessment Test (iRAT)

    As soon as the session starts the students have a multiple choice test of 10 questions. All of the answers should be found in the assigned reading. The test score is part of the students grade in the section. This means that all of the students need to do the prep work and all of the students need to show up for the session. Two huge improvements to the Wayne State MD labs.
    Gunning for grades on the iRAT

      Team Readiness Assessment Test (tRAT)

      After completing the fill-in-the-bubble iRAT, the students then work in 5 person teams on the exact same questions they just answered. The teams have scratch off pads that work like instant lottery tickets with the correct answers. When the team answers a question they get instant feedback if they were right or wrong. This is closed book but the students all work together. After the all of the teams complete their tRAT there is a brief discussion of any questions that were troubling. The proctors walk around the room during the exercise and listen to the team discussions to they get a sense of what questions are difficult/poorly written.
      If you scratch off three horse shoes you win $60.
        Look at her notes. Every tricky nephrology
        question starts with “let’s draw a nephron.”

        Application Exercise

        Application questions are complex questions that supposed to integrate physiology and clinical medicine in to a complex multiple choice question. The questions are all open book, and in this age of WiFi, laptops and the WWW, we should really rename open book as open Google. The teams get 15-20 minutes per question and then simultaneously display their answer. Then the proctors lead a discussion on the reasoning behind the answers and different strategies the teams used to get to the answer.

        The things I love about the TBL

        • It is part of the grade. Curriculum directors need to understand that the medical school curriculum has more information than is possible to learn and students are rational actors. They will sacrifice important but uncounted learning opportunities in order to prepare for counted exams. There is no way to make something meaningful without making it part of the grade.
        • The iRAT happens right when the students walk in to the room. I love how this makes it clear that the students are being graded on preparation. The important thing is getting the students to learn the material before the session starts. This paragraph from Regis School of pharmacy states it perfectly:

        “To promote active and collaborative learning, students are sometimes asked to work in groups in class or on projects outside of class. While group work does benefit student learning, unfortunately it is often plagued by “social loafers”, or students who do not pull their weight in terms of helping the group. As a result, many students learn to dislike group work and may seek to avoid it. TBL is different. TBL ensures that each member of the team is held accountable for their own learning outside of class. Students who do not prepare adequately before class will perform poorly on the iRAT and will not be able to contribute in a meaningful manner to the tRAT and application exercises. As a result, most students who would normally remain “social loafers” in a group learning project are instead quickly motivated to do the assigned work out of class in order to perform well on the iRAT. In addition, as teams work together and compete with other teams in the class, loyalty to the team develops among each member. This further motivates the “social loafers” to prepare outside of class so that they can contribute and help the team succeed.“

        In the cut throat world of medical school any system that allowed a “social loafer” to benefit from the group while contributing nothing would be a recipe for a short lived project. The iRAT gives a clear message: come to class prepared, or you will suffer.

        • The application exercises are open google. To me, this was the most interesting part of TBL. Clinical medicine is, of course, open book. Everyday I am consulting Dr. Google, Epocrates and UpToDate. My information gathering strategies were developed on the fly in my clinical practice. No one taught me these types of skills and no where in medical school were there any opportunities to practice hone them. The students of OUWB are working together, comparing notes, seeing which resources work best. I heard students explain the virtues of DynaMed (a POS in my opinion). I spoke with students who distanced themselves from Wikipedia until I told them I was a fan and had no reservations about using the crowd sourced encyclopedia. After hearing me extol its virtues they quickly changed their tune and agreed that it was easy to filter good from bad wiki pages (referenced, with mainstream journals, avoid political topics) and that the good ones never steered them wrong.

        People used, Google, Wikipedia, UpToDate and a strange
        resource called a “book” 

        Summary

        The portable computer revolution of iPads and smart phones allows us to bring the library to the bedside, it is time for medical schools to appreciate and embrace this pivot in the history if medicine. TBLs are the best example I have seen of of this.

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        OUWB MS2 Renal Section Course Materials

        I am teaching at the Oakland University Beaumont Medical School in August. Here are the lecture materials I used.

        Sodium and Water PDF (for medical students, longer than the hand out of the same name I use for third years). This is the 40+ page handout for the TBL on sodium and water. Here is the file from pages in case you wanted to fix some of my typos: Pages

        Acid Base Long-ass lecture PowerPoint (3 hours of Acid-Base fun)

        Acid Base hand out for workshop pdf | pages

        NAGMA Cases this is the brief powerpoint of NAGMA cases as part of the Acid-Base workshop

        Excel table for doing Henderson-Hasselbalch, anion gap and adjusted sodium. Useful if you need to rite a lot of acid-base problems and you are stickler for ABGs that are, you know, possible.

        Fluids and Electrolyte Companion This is a 500 page opus I wrote a decade ago. Most of the pictures and concepts that I taught from come right from this book. The acid-base section holds up pretty well, as does the potassium section. The Sodium section is a bit more variable.