9. Regulation of potassium and magnesium Flashcards
What is the main intracellular cation?
potassium
What does potassium determine?
resting membrane potential
What are the body concentrations of potassium?
Total body K+: 3-4mmol/L
• Intracellular fluid: 98%: 150-160mmol/L
• Extracellular fluid: 2%: 4-5mmol/L
What is the effect on resting membrane potential if extracellular K+ rises and falls?
- If extracellular [K+] rises, the resting membrane potential is decreased (i.e. depolarized)
- If extracellular [K+] falls, the resting membrane potential is increased (i.e. hyperpolarized)
Where in the nephron is potassium reabsorbed?
65% in PCT, 20% in TAL
How is potassium reabsorbed in the PCT?
- Passive
- Through tight junctions (paracellular movement)
- Via concentration gradient/solvent drag
How is potassium reabsorbed in the TAL?
- Transcellular - Na+K+ ATPase on basement membrane maintains gradient of Na+ by pumping Na+ out of tubular cell to blood and K+ in. Na+K+Cl- cotransporter on apical membrane transport the ions into the cell. ROMK channels and Cl-K+ channels on the basal membrane move potassium and chloride out of the cell into blood
- Paracellular - ROMK channels on apical membrane also transport K+ out of cell into lumen and the positive charge in lumen repels cations so potassium and other cations move paracellularly to the blood.
Why is there not a lot of reabsorption of potassium in the DCT?
K+ reabsorption and leakage back are approximately equal in early DCT
Where does secretion of K+ occur and in which cells?
In the late DCT and collecting duct
Describe how secretion of K+ occurs
ENaC channels on apical surface move Na into cell. Na+K+ ATPase on basal membrane moves Na into blood and K+ in. the K+ is the then pumped into the lumen through the (ATP dependent) K+ pump
What cells are involved in reabsorption of K+ in late DCt and collecting duct?
intercalated cells
• 10-12% reabsorbed if body trying to preserve K+
Describe how reabsorption of K+ occurs at late DCT and CD
- H+ATPase on apical membrane moves H+ into lumen.
- H+K+ATPase moves H+ into lumen and K+ into cell.
- on the basal surface, Na+K+ ATPase moves K+ out into blood and Na+ into cell
- ROMK channels on basal surface also help move K+ into blood
What are the causes hypokalaemia??
• Excess insulin • Alkalosis • Certain catecholamines (beta-2- adrenergic agonists and alpha- adrenergic antagonists • Insufficient intake - Anorexia nervosa - Prolonged fasting • Too much aldosterone - Primary aldosteronism - Compensated heart failure - Cirrhosis • Diuretics e.g. loop and thiazides • Vomiting • Diarrhoea (lead to metabolic alkalosis) • Sweat – excessive exercise, hot climate
How does alkalosis lead to hypokalaemia?
To lower blood pH K+ moved into cells in exchange for H+
How does increased aldosterone lead to hypokalaemia?
aldosterone causes proliferation of carriers on principal cells so increased secretion
What is the pathophysiology behind hypokalaemia?
- Low K+ results in decreased resting potential – nerve and muscle cells are hyperpolarized
- Less sensitive to depolarizing stimuli and less excitable
- Less action potentials generated and paralysis ensues
Below which levels does hypokalaemia become symptomatic?
Hypokalemia is asymptomatic until K+ concentration falls below 2- 2.5mmol/L
WHat are the Clinical effects of hypokalemia?
- Muscle weakness, cramps and tetany (starts in lower extremities)
- Impaired liver conversion of glucose to glycogen
- Vasoconstriction and cardiac arrythmias
- Impaired ADH action causing thirst, polyuria and no concentration of urine
- Metabolic alkalosis due to increase in intracellular H+ concentration
What is the treatment for hypokalaemia?
treating underlying cause. Oral or intravenous K+ may also be required
What may cause hyperkalaemia?
• Reduced renal excretion • Increased plasma load • Insulin deficiency – Type 1 diabetes • Transcellular shift of K+ out of cells • Pseudohyperkalemia, an artifact: • Certain catecholamines (beta-2- adrenergic antagonists and alpha- adrenergic agonists • Hypoaldosteronism and drugs which reduce effect of aldosterone (renin inhibitors, ACE inhibitors etc.)
What may lead to reduced renal excretion of potassium?
AKI or CKD, mineralocorticoid deficiency (e.g. Addison’s disease), K+ sparing diuretics or renal tubular defects
What may lead to increased plasma load of potassium?
due to dietary changes, IV infusion or cellular tissue breakdown
What may lead to Transcellular shift of K+ out of cells?
due to metabolic acidosis, insulin deficiency, exercise or drugs (digoxin)
What may lead to Pseudohyperkalemia?
due to hemolysis during venipuncture or storage of the sample, a high white cell or platelet count
