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Potassium: Difference between revisions
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== Regulation of potassium level == | == Regulation of potassium level == | ||
The potassium level is mainly regulated by the renin-angiotensin-aldosterone system in the kidneys. Increasing levels of potassium stimulates RAAS and therefore aldosterone production, which in turn stimulates the [[Na+/K+-ATPase]] in the distal tubules and collecting duct. This causes K+ and H+ loss. This system is very effective and therefore prevents hyperkalaemia from developing, as long as the kidneys are functioning. | The potassium level is mainly regulated by the [[renin-angiotensin-aldosterone system]] in the kidneys. Increasing levels of potassium stimulates RAAS and therefore aldosterone production, which in turn stimulates the [[Na+/K+-ATPase]] in the distal tubules and collecting duct. This causes K+ and H+ loss. This system is very effective and therefore prevents hyperkalaemia from developing, as long as the kidneys are functioning. | ||
The daily intake of potassium in the diet is approximately 40 – 120 mmol K+. This extra potassium reaches the extracellular space and not the cells in normal cases. 90% of excreted potassium is excreted by the kidneys, the remaining through the <abbr>GI</abbr> tract. | The daily intake of potassium in the diet is approximately 40 – 120 mmol K+. This extra potassium reaches the extracellular space and not the cells in normal cases. 90% of excreted potassium is excreted by the kidneys, the remaining through the <abbr>GI</abbr> tract. | ||
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==== pH ==== | ==== pH ==== | ||
When acidosis occurs, the body attempts to buffer the increasing plasma H+. One of these is the intracellular buffer, where H+ in the plasma is moved inside cells. To maintain electroneutrality, the cells exchange K+ to the plasma. The total amount og potassium ion in the body doesn’t change, but a larger fraction of it is moved to the plasma, potentially causing hyperkalaemia. Hyperkalaemia reduces the kidney’s ability to excrete ammonia, which may further worsen the acidosis. For every 0.1 unit reduction in blood pH the plasma potassium concentration increases by approximately 0.2 – 2 mM. | When [[acidosis]] occurs, the body attempts to buffer the increasing plasma H+. One of these is the intracellular buffer, where H+ in the plasma is moved inside cells. To maintain electroneutrality, the cells exchange K+ to the plasma. The total amount og potassium ion in the body doesn’t change, but a larger fraction of it is moved to the plasma, potentially causing hyperkalaemia. Hyperkalaemia reduces the kidney’s ability to excrete ammonia, which may further worsen the acidosis. For every 0.1 unit reduction in blood pH the plasma potassium concentration increases by approximately 0.2 – 2 mM. | ||
The opposite can occur in case of alkalosis. Hydrogen ions are buffered out of the cells, requiring cells to move K+ ions into the cells, potentially causing hypokalaemia. | The opposite can occur in case of [[alkalosis]]. Hydrogen ions are buffered out of the cells, requiring cells to move K+ ions into the cells, potentially causing hypokalaemia. | ||
Reciprocally, an increase in plasma K+ concentration (hyperkalaemia) causes cells to buffer this change by moving K+ ions into the cells. To maintain electroneutrality, the cells exchange H+ to the plasma, potentially causing acidosis. The opposite can occur in case of hypokalaemia. | Reciprocally, an increase in plasma K+ concentration (hyperkalaemia) causes cells to buffer this change by moving K+ ions into the cells. To maintain electroneutrality, the cells exchange H+ to the plasma, potentially causing acidosis. The opposite can occur in case of hypokalaemia. | ||
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==== Insulin ==== | ==== Insulin ==== | ||
Insulin enhances Na+/K+ ATPase activity, causing K+ to enter the cells. We use the fact that insulin causes intracellular movement of H+ in the management of [[hyperkalaemia]]. | Insulin enhances Na+/K+ ATPase activity, causing K+ to enter the cells. We use the fact that insulin causes intracellular movement of H+ in the management of [[hyperkalaemia]]. | ||
==== Beta-2-receptor ==== | |||
[[Catecholamine|Catecholamines]] enhance [[Na+/K+ ATPase]] activity, via [[β2-receptors]], causing potassium to enter cells. α-receptors decrease the activity. | |||
==== Others ==== | ==== Others ==== | ||
[[Mineralocorticoid|Mineralocorticoids]] contribute to the balance. I don’t know how it contributes to the internal balance (book doesn’t explain). Their effect on the external balance is much more important. | |||
Mineralocorticoids contribute to the balance. I don’t know how it contributes to the internal balance (book doesn’t explain). Their effect on the external balance is much more important. | |||
Physical activity causes K+ outflow from muscle cells. | Physical activity causes K+ outflow from muscle cells. | ||
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==== Potassium intake ==== | ==== Potassium intake ==== | ||
K+ intake is counter-regulated by kidney and GI excretion, so even a high potassium intake isn’t dangerous (unless it’s intravenous). In end-stage renal failure, when the <abbr>GFR</abbr> < 5 mL/min even a few bananas can cause severe hyperkalaemia. | K+ intake is counter-regulated by kidney and GI excretion, so even a high potassium intake isn’t dangerous (unless it’s intravenous), unless there is severe kidney failure. In [[end-stage renal failure]], when the <abbr>GFR</abbr> < 5 mL/min even a few bananas can cause severe hyperkalaemia. | ||
==== Mineralocorticoids ==== | ==== Mineralocorticoids ==== | ||