Last updated on May 23, 2020 at 15:19
Potassium in the body
98% of all potassium in the body is intracellular. In the intracellular space is the concentration 140 – 160 mM, while in the extracellular space is it just 3.5 – 5.5 mM.
The serum potassium level depends in two things:
- The internal potassium balance, the balance between the intracellular and extracellular compartments
- The external potassium balance, the balance between potassium intake and potassium loss
The internal potassium balance
The internal balance depends on 6 things:
- Tonicity of the extracellular space
- Physical activity
pH: Cells have the possibility to excrete K+ in exchange for H+ and visa versa. If the extracellular H+ concentration is low (alkalosis) will H+ be pumped out of cells while K+ will be pumped into cells. If the extracellular H+ level is high (acidosis) will H+ be pumped into cells while K+ will be pumped out. Acidosis can therefore cause hyperkalaemia while alkalosis can cause hypokalaemia.
Tonicity: When the extracellular space is hypertonic (due to increased sodium or glucose concentration for example) will water flow out of cells and into the EC space. Because the K+ level inside the cell doesn’t change will the K+ concentration increase, as the cells have lost water. This concentration increase causes K+ to flow out of the cell, potentially causing hyperkalaemia.
Insulin enhances Na+/K+ ATPase activity, causing K+ to enter the cells. In fact, when there is a hyperkalaemia that should be quickly normalized it is common to give insulin and glucose simultaneously. This doesn’t really fix the elevated K+ level in the body though, it just “hides” the potassium inside cells.
Catecholamines also enhances Na+/K+ ATPase activity, via β2-receptors. α-receptors decrease the activity.
Mineralocorticoids contribute to the balance. I don’t know how (book doesn’t explain). Probably not too important.
Physical activity causes K+ outflow from muscle cells.
The external potassium balance
The daily intake of food is ca 40 – 120 mmol K+. This extra potassium reaches the extracellular space and not the cells in normal cases. 90% of the lost potassium is excreted by the kidneys, the remaining through the GI tract.
The external balance depends on 5 things:
- K+ intake
- GI excretion
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 GFR < 5 mL/min can even a few bananas cause severe hyperkalaemia.
Mineralocorticoids play a much larger role in the external balance than the internal. Aldosterone and some of its weaker precursors enhance Na+/K+ and Na+/H+ exchange in the distal tubules and collecting duct. This causes K+ and H+ loss.
The GFR determines how much K+ is filtered. When it’s increased will more water and sodium reach the distal tubules, which increases Na+/K+ exchange, causing sodium to be reabsorbed and more potassium to be excreted. Increased flow rate, such as in osmotic diuresis, inhibits K+ reabsorption. Increased level of anions in the filtrate, like bicarbonate, increases K+ excretion because of electroneutrality.
pH also influences the potassium excretion. Renal K+ excretion decreases in acidosis and increases in alkalosis.
GI excretion only accounts for 10% of potassium loss in healthy people, but in severe renal failure may this number go up to 50% to compensate for the failing kidneys.
Most important causes:
- Metabolic alkalosis
- Cushing syndrome
- Conn syndrome
- Insulin treatment
- β2-receptor agonist
- Osmotic diuresis
- Increased mineralocorticoid activity
- Extreme sweating
- Renal tubular acidosis I
- Renal tubular acidosis II
Consequences of hypokalaemia:
- Development of metabolic alkalosis
- Hyperpolarized membranes (membrane potential becomes more negative)
- Muscle weakness
- Polyuria (hypokalaemia causes nephrogenic diabetes insipidus where the kidney responds less to ADH)
- Metabolic acidosis
- Chronic renal failure
- Diabetes mellitus type 1 (lack of insulin)
- Mass cell destruction (tumor treatment, haemolytic anaemia)
- Hypoaldosteronism (Addison)
- Renal tubular acidosis IV
- Drugs that inhibit aldosterone or RAAS
- Hypopolarized membranes (more positive membrane potential)
- Muscle weakness
- Respiratory depression
79. Respiratory acidosis and alkalosis. Causes, compensation, consequences
81. States of decreased extracellular volume, and their consequences