Potassium Handling and Potassium Diseases Flashcards
What is likely the most important aspect of maintaining proper potassium levels?
• Potassium conentration maintains the resting membrane potential of excitable cells
○ Not having the right amount of potassium can result in cardiac arrhythmias or neuronal dysfunction
• Potassium also has an important role in acid/base balance
• A third thing to notice is that potassium plays a large role in determining the intracellular osmotic environment (enriched in cells)
What is the normal range of ECF potassium concentration?
• 3.5 - 5mM
* more than 6 and we are worried and more than 6.5 death is imminent so get the ECG
The range of potassium excretion is 0 - 45grams a day but only 30 grams are filtered. How can there be more excretion than filtration?
- Potassium is both filtered AND secreted
- Both reabsorption and secretion take place in the tubule
- Potassium is passively reabsorbed in the proximal tubule and loop of henle
Where is the bulk of filtered potassium reabsorbed?
- In the proximal tubule, 80% is reabsorbed
* The mechanism is paracellular and passive, driven by the bulk flow of water through the tight junctions
In the loop of henle, how is potassium normally reabsorbed?
- Na/K/2Cl co-transporter in the apical membrane first
- Potassium is high concentraion in the cell so it will trundle out through the basolateral membrane according to gradient
- 10-15% of filtered load happens this way in the loop of henle
- The last little bit is resorbed in the principal cells
What assumption can pretty safely be made according to potassium reabsorption?
• All of the filtered potassium is obligatorily reabsorbed, hence regulated potassium secretion in the fine tuning segments also determines potassium excretion and ECF potassium balance
If you ingest potassium and that raises your ECF potassium, what happens in the kidney?
- Simply by mass action the Na/K ATPase turns faster and there is more potassium that enters the tubule cells
- More potassium entering the basolateral side of the cells means more potassium that trundles down through the apical side into the lumen
how does tubular flow affect potassium reabsorption/secretion?
the slower flow is, the more time there is for potassium to leak accross (secretion) the apical membrane. Thus, the concentration of potassium in the urine increases with slow flow, which pushes “lower” secretion “back”
When does potassium secretion take place?
After much of the filtered water has been obligitorily reabsorbed, meaning that there is more electrochemical pushback across the apical membrane. With an abnormally higher flow, the potassium would get “sucked out” more. Thus, with more water in the urine (diuretics) higher flow and more hypokalemia worry
Loop diuretics inhibit the Na/K/2Cl channel in the TALH. You’d expect this to block how much potassium reabsorbtion?
You’d expect it to interfere with about 15% of the total potassium reabsorbtion. However, it’s more like 100% plus of the filtered load of potassium gets excreted in loop diuretic use.
* this is because of hte 15% blocking reabsorption and the tons of extra water and flow sucking potassium out, increasing potassium secretion
What role does aldosterone play in potassium regulation?
• Increased potassium works directly on the adrenal zona glomerulosa (the same ones that will secrete aldosterone for water-handling reasons)
• Aldosterone works at several levels, categorized as step1 or step 2 effects
• It increases the number of Na/K ATPase pumps on the basolateral surface
• Also increases potassium channels on apical surface, allowing a “passive” influx of sodium to drive potassium out
• The net effect is, with mass action, aldosterone-mediated rise in potassium excretion and more fine-tuning of ECF potassium
- Increased potassium works directly on the adrenal zona glomerulosa (the same ones that will secrete aldosterone for water-handling reasons)
- Aldosterone works at several levels, categorized as step1 or step 2 effects
- It increases the number of Na/K ATPase pumps on the basolateral surface
- Also increases potassium channels on apical surface, allowing a “passive” influx of sodium to drive potassium out
- The net effect is, with mass action, aldosterone-mediated rise in potassium excretion and more fine-tuning of ECF potassium
What is the potassium specific concern in primary hyperaldosteronism?
Since aldosterone increases the apical membrane potassium channels, it increases potassium secretion and excretion.
- this is balanced by the low tubular flow that is a result of sodium and water reabsorbtion in the tubule
- however, in this disease the net result is potassium loss and potential hypokalemia due to overall increased or normal tubular flow plus the added K secretion
Cardiac disease can lead to RAAS activation and eventually “secondary hyperaldosteronism”. Concerning potassium, what happens here vs. primary aldosteronism?
You’d expect the overall situation of expanded ECF and RAAS activation to result in the same overall net loss of potassium, but in this case GFR is overall reduced (constriction of vessels by overall SNS tone) and the low flow leads to overall LESS potassium secretion
What is the basic rule of thumb for acid/base problems and potassium levels?
Alkalosis increases potassium secretion and tends to produce hypokalemia.
*thus gitelman’s and barter’s messing with sodium reabsorbtion, causing metabolic alkalosis and eventually hypokalemia
Why (brief) does alkalosis increase potassium secretion?
high pH causes shift of ECF potassium INTO (accross basolateral membrane) cells of the tubule.
- this shift is shared by all cells, leading to overall hypokalemic state as potassium goes intracellular
- apical potassium channels are inhibitied by protons, so less protons means more open potassium channels
