Potassium Lecture Flashcards

Vocabulary flashcards about Potassium regulation, measurement, and related conditions.

Potassium

First discovered in 1807 by Sir Humphrey Davy. Named potassium in English from pot-ash extracted from wood and leaves. Symbol K (Kalium) derived from Arabic word for alkali.

Resting Membrane Potential

Potassium plays a key role in determining the resting membrane potential of cells at -70mV, important for action potential propagation in neurons, muscle, and cardiac tissues.

Hyperkalaemia

Results in a decrease of resting membrane potential, leading to increased excitability of cells.

Hypokalaemia

Gives the opposite cellular effect to hyperkalaemia, i.e., decreased excitability of the cells.

Intracellular Potassium Concentration

Approximately 150 mmol/L.

Extracellular Potassium Concentration

Ranges from 3.6 – 5.0 mmol/L.

Acidosis and Potassium

H+ ions move from ECF to ICF in exchange for K, often leading to hyperkalaemia.

Alkalosis and Potassium

H+ ions move from ICF to ECF in exchange for K, often leading to hypokalaemia.

Regulation of Potassium

Insulin, adrenaline, and aldosterone increase K transport into the cell. Intracellular K is maintained by the Na/K ATPase pump.

Aldosterone's Role in Potassium Regulation

Released from the adrenal cortex in response to increased K concentration, acting on the kidney to increase K excretion, hydrogen secretion, and Na reabsorption.

RAAS and Potassium

The Renin-Angiotensin-Aldosterone System regulates K balance in addition to Na balance. Angiotensin II stimulates aldosterone secretion, increasing renal K excretion.

Potassium selective electrode

Operates via potentiometry, measuring the potential difference between two electrodes. The indicator electrode contains valinomycin, which allows K ions to pass through.

Valinomycin

A mobile carrier ionophore with selective affinity for potassium ions, derived from Streptomyces. It facilitates potassium transport across membranes.

In vitro haemolysis

Rupture of erythrocytes during specimen collection, leading to release of K into the plasma, artificially increasing measured K.

Serum vs Plasma Potassium

K in serum can be 0.1 – 0.2 mmol/L higher than in plasma because K is released by platelets during clotting.

K2-EDTA contamination

Specimen collected into a tube containing potassium salt of EDTA artificially increasing measured K, while also causing artefactual ↓ serum Mg and ↓ alkaline phosphatase (ALP).

Cold Sample and Potassium

The Na/K/ATPase pump activity is reduced at low temperatures, leading to falsely increased K levels.

Hyperkalaemia Symptoms

Severe hyperkalaemia can lead to muscular weakness and dangerous cardiac arrhythmia, potentially resulting in cardiac arrest.

Causes of Hyperkalaemia

Redistribution of K from ICF to ECF, decreased K excretion, and excessive K intake.

Potassium-Sparing Diuretics

Medications like spironolactone that inhibit the action of aldosterone, causing potassium retention.

ACE Inhibitors

Inhibit the conversion of angiotensin I to angiotensin II, preventing aldosterone activation and causing potassium retention.

Digoxin's Effect on Potassium

Inhibits the Na+/K+-ATPase, reversing cellular distributions of Na and K, leading to hyperkalaemia. Digoxin has a narrow therapeutic index, and high serum K is lethal.

Digibind

Antibody against Digoxin used as antidote.

Hypokalaemia Symptoms

Muscle weakness, hyporeflexia, and cardiac arrhythmia.

Causes of Hypokalaemia

Redistribution of K from ECF to ICF, increased K excretion, and certain medications.

Thiazide and Loop Diuretics

Increase renal potassium excretion, leading to hypokalaemia. Thiazides inhibit Na-Cl cotransport, promoting K excretion.

Conn's Syndrome

Primary hyperaldosteronism is characterized by excessive aldosterone secretion, leading to Na retention and K loss, resulting in hypertension.

Liddle Syndrome

Inherited disorders of renal tubular function associated with hypokalaemic alkalosis

Gitelman Syndrome

Inherited disorders of renal tubular function associated with hypokalaemic alkalosis

Bartter Syndrome

Inherited disorders of renal tubular function associated with hypokalaemic alkalosis

Key points of Potassium lecture

Potassium excretion is regulated by aldosterone and extracellular hydrogen ion concentrations. Serum potassium measurement is conducted by the potentiometric method with valinomycin. Pre-analytical factors must be ruled out before diagnosis. Hyperkalaemia is most frequently due to decreased renal excretion. Hypokalaemia is most frequently a result of renal / gastrointestinal loss.

Addison's Disease and Potassium

Primary adrenal insufficiency leading to decreased aldosterone production, resulting in hyperkalaemia due to reduced potassium excretion.

Causes of Pseudohyperkalaemia

In vitro haemolysis, K2-EDTA contamination, prolonged tourniquet use or fist clenching during venipuncture, extreme thrombocytosis or leucocytosis.

Treatment of Acute Hyperkalaemia

Calcium gluconate (to stabilize cardiac membrane), insulin with glucose (to shift K+ into cells), sodium bicarbonate (to shift K+ into cells), loop diuretics (to enhance K+ excretion), dialysis (in severe cases).

Magnesium Deficiency and Potassium

Magnesium depletion increases renal potassium secretion, leading to hypokalaemia that is often resistant to potassium supplementation unless magnesium is also repleted.

Refeeding Syndrome and Potassium

During refeeding after starvation, insulin secretion increases, driving potassium and phosphate into cells, potentially causing severe hypokalaemia and hypophosphataemia.

Diabetic Ketoacidosis (DKA) and Potassium

Although total body potassium is depleted in DKA due to osmotic diuresis, initial serum potassium levels may be normal or elevated due to extracellular shift caused by insulin deficiency and acidosis.

Potassium and Rhabdomyolysis

Muscle damage can cause hyperkalaemia due to the release of intracellular potassium stores into the circulation.

Chloride depletion and Potassium

Contraction alkalosis and hypokalaemia resulting from vomiting, compensation with ECF volume contraction by the kidney and preferentially reabsorb Na+ to the detriment of K+.