Potassium control Flashcards
Describe the distribution of potassium in the body. (2)
98% ICF, 2% ECF. Mainly stored in skeletal muscle cells, but also liver RBC bone.
Explain how and why the body maintains [K+]e. (2)
Through the Na+/K+ ATPase.
Maintained because hypo- or hyperkalaemia can have drastic effects on the resting membrane potential, and the excitability of cardiac tissue.
Describe the internal balance of potassium. (2)
Normally there’s a balance between the electrical gradient for positive potassium to enter the negative cell, and the chemical gradient of low [K+]e for K+ to leave the cell.
Describe how [K+]e is regulated. (2)
Short term - internal balance changes - moves K+ from ECF to ICF.
Long term - external balance changes - changes in renal excretion.
Explain 5 things that increase [K+]i. (10)
Insulin - K+ in splanchnic blood stimulates insulin secretion, which increases Na+/K+ activity, increases K+ uptake into cells, increases [K+]i. (This is why insulin + dextrose is a treatment for hyperkalaemia).
Aldosterone - K+ in blood stimulates aldosterone secretion, increases Na+/K+ activity, increases K+ uptake into cells, increases [K+]i.
Catecholamines - stimulates B2 adrenoceptors, which increases Na+/K+ activity, increases K+ uptake into cells, increases [K+]i.
High [K+]e - increased concentration gradient leading to more diffusion, which increases K+ uptake into cells, increases [K+]i.
Alkalosis - low [H+] drives K+ into cells.
Explain 4 things that decrease [K+]i. (8)
Exercise and cell lysis - net release of [K+] from within the cell during recovery phase of action potential. Cell lysis from muscle damage also releases all of the [K+]i. (Catelochamines are also released in exercise to offset this change).
Increase in ECF osmolarity eg in diabetes - water moves out of cells, lowers concentration of [K+]e, so K+ moves out of cell.
Low [K+] in the ECF.
Acidosis - high [H+] in ECF drives K+ out of cells.
Explain the relationship between acid base disturbances and internal balance of potassium. (8)
Acidosis - too much H+ in ECF - H+ moves into cells - reciprocal K+ shift out of cells - hyperkalaemia.
Alkalosis - too little H+ in ECF - H+ moves out of cells - recirpocal K+ shift into cells - hypokalaemia.
Hyperkalaemia - shift of K+ into cells - reciprocal H+ shift out of cells - acidosis.
Hypokalaemia - shift of K+ out of cells - reciprocal H+ shift into cells - alkalosis.
Describe external K+ balance. (3)
Control of the total body potassium over the long term. Regulates K+ secretion into the late DT and collecting duct. Slower - 6-12 hours. Secreted K+ can be 15-120% of filtered amount.
Describe 5 factors affecting K+ secretion into the lumen. (5)
Tubular features
High [K+]e - directly stimulates Na+/K+ ATPase and stimulates aldosterone. Increases loss.
Aldosterone - increased translation of proteins like Na+/K+ ATPase, ENaC, and K+ channels. Increases loss.
Acid base status - acidosis decreases K+ secretion, alkalosis increases K+ secretion.
Luminal factors
Increased flow rate - increases loss because K+ is washed away.
Increased Na+ delivery - more Na+ reabsorbed = more K+ lost.
Describe the clinical causes of hyperkalaemia (5)
Inappropriate IV K+.
Drugs that increase K+ retention (ACE inhibitors and K+ sparing diuretics)
Diabetic ketoacidosis - acidosis and reduced insulin.
Cell lysis due to trauma.
Metabolic acidosis
Exercise.
Describe the clinical features of hyperkalaemia. (4)
Reduced excitability of cardiac muscle leading to arrhythmia sand heart block.
Paralytic ileus
Acidosis
ECG changes - high T wave, depressed ST segement - ventricular fibrillation.
Describe the emergent treatment of hyperkalaemia. (3)
Calcium gluconate - Reduce K+ effect on the heart.
IV glucose and insulin to shift K+ into cells.
Dialise excess K+.
Describe the long term treatment of hyperkalaemia. (3)
Treat cause - stop medication, treat DKA.
Reduce intake.
Measures to remove excess K+ - dialysis, oral binding drugs.
Describe the causes of hypokalaemia. (2)
Excessive loss - GI (D+V) or renal (diuretics, osmotic diuresis).
Things that shift K+ into cells (metabolic alkalosis).
Describe the clinical features of hypokalaemia. (6)
Heart - raised excitability leading to arrhythmias because more Na+ channels remain open.
Paralytic ileus.
Muscle weakness
Nephrogenic diabetes insipidus due to unresponsive ness to ADH.
ECG - low T wave, high U wave, low ST segment.