Friday, September 2, 2016

Question from OUWB M2 on SIADH

Another question from the e-mail
I am trying to understand why SIADH does not cause edema. I understand that in SIADH, there is an increase in Total Body Water, as the increased ADH causes increased water reabsorption. However, there is no change in total body sodium. This implies that the issue is a euvolemic hyponatremia. I would imagine that with total body water increase, there is increased ECF and therefore increased capillary hydrostatic pressure. How come this doesn't result in edema?
This is a question I get every year.

The question comes from a student with clear thinking about SIADH. And it is true that careful and precise measurements of total body water will show that people with SIADH have excess total body water, so they are not truly "euvolemic." But we use the term euvolemia here because they are in sodium balance. Their sodium intake equals their sodium excretion:


This is very different than patients with hypervolemic hyponatremia (heart failure and liver failure) where sodium intake is much greater than sodium excretion. With positive sodium balance (total body sodium increases everyday) heart failure patients develop progressive and clinically evident edema.

The other way to look at the increased water that patients have with SIADH is to quantify it. If a patient with SIADH drops their sodium from 140 to 120 they have dropped there sodium by 14%. This comes from an increase in total body water of 14%, so in a 70 kg young man (42 liters total body water), this represents a increase in total body water of 5.88 liters. Two thirds of this water would be intracellular, so only 2 liters would be extracellular. In heart failure, dogma states people gain 5 kilograms of body weight before they develop clinically evident edema. Since the edema is from excess sodium all of this fluid gain is extracellular. So the amount of water that needs to be retained to lower the sodium 20 points, is less than half the amount that is needed to cause clinically evident edema.

Question from OUWB M2s on potassium excretion

Here is the question:
Regarding potassium secretion, I'm having a little trouble understanding one concept: increased flow rates with the collecting tubules results in increased potassium secretion. Say a person is on a loop diuretic and their flow rates are increased. I understand that increasing sodium delivery will result in more potassium secretion, but how does the flow rate affect it? 
I would've guessed high flow rates would decrease sodium re-absorption and therefore decrease potassium secretions.

My answer was just a figure from The Fluid and Electrolyte Acid Base Companion:

  The idea is that increased tubular flow has two interrelated explanations for why it increases potassium excretion. 
  1. The first is that when potassium excreted by either the ROMK or Big K channel, potassium in the tubule then will decrease the chemical gradient from in the cell to out of the cell. By increasing the tubular  flow potassium is quickly washed away, maintaining (or refreshing) the chemical gradient. 
  2. The second is that increased tubular flow is really synonymous with increased sodium delivery. This sodium is then sucked up by the eNaC allowing the generation of the electronegative tubule increasing the excretion of potassium.

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Monday, August 22, 2016

Question from the OUWB M2s

This question came via e-mail:
A couple of my classmates and I had a question regarding one of your slides (slide 39 on the Potassium, Metabolic Alkalosis presentation). We were unsure of the mechanisms that prevented bicarbonate excretion with hypokalemia, specifically decreased NaK2Cl activity in the loop of Henle and decreased NaCl resorption in the distal convoluted tubule. Could you please give us an explanation for these mechanisms?
So the reason you can't remember a mechanism is I gave the old "just because" mechanism without much explanation.

The first step of why the the Na-K-2Cl transporter slows own in response to a low K is pretty sraight forward. Tubular potassium will fall as patients get hypokalemia. As the plasma potassium falls, less and potassium is filtered and then less potassium will be available to cycle the Na-K-2Cl pumps. The decreased activity in the loop of Henle results in more distal delivery of sodium and that drives move acid secretion and maintenance of the metabolic alkalosis.

The distal convoluted tubule is a bit more complex. Here is a diagram:

The hypokalemia stimulates the hydrogen-potassium exchanger. This generates intracellular acidosis, even though the patient has alkalosis. In order to correct the acidosis the cell slows sodium-chloride co transport so more sodium washes down stream and stimulates the hydrogen secretion, maintaining the alkalosis.

If you are looking for a deeper dive into metabolic alkalosis I recommend this review by Galla in JASN
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