Lecture 8: Regulation of potassium and magnesium Flashcards
What are the main extracellular and intracellular ions?
Sodium= extracellular Potassium= intracellular
Why is potassium important?
- very important in function of excitable tissues (nerves and muscles)
- determines the resting membrane potential
What is the concentration of potassium in the body and its distribution?
Total body K+: 3-4 mmol/L
Intracellular fluid: 98%
Extracellular fluid: 2%
How does K+ conc affect the resting membrane potential?
Extracellular K+ rises: resting membrane potential becomes less negative (depolarized)
Extracellular K+ falls: resting membrane potential becomes more negative (hyperpolarised) so are less sensitive to depolarising stimuli and less excitable
How is potassium concentration managed?
Via the kidney
- K+ is freely filtered by the glomerulus
- in PCT 65% is reabsorbed: passive, through the tight junctions via concentration gradient/solvent drag
- TAL 20% is reabsorbed: transcellular/paracellular
- DCT, K+ reabsorption and leakage back are equal
- late DCT and CD: secretion by principle cells if you have normal/high potassium levels and reabsorption by intercalated cells
Are principle cells affected by aldosterone?
Yes, it has an aldosterone receptor
-increased in ion channels
What cells in the kidney are responsible for reabsorption or secretion?
Reabsoprtion: intercalated cells
Secretion: principal cells
What are the causes of hypokalaemia?
(Low K+ concentration)
- excess insulin (glucose is taken into cell along with potassium)
- alkalosis (pH in blood is too high), to correct this K+ moved into cells in exchange for H+
- insufficient intake (anorexia nervosa/prolonged fasting)
- some catecholamines
- too much aldosterone (primary aldosteronism/activated RAS system)
- diuretics (large amount of K+ lost in the urine)
- vomiting/diarrhoea
- sweat
Do you get symptoms with hypokalaemia?
It is asymptomatic until K+ concentration falls below 2-2.5 mmol/L
-can get paralysed as less action potentials are generated
What are some clinical effects of hypokalaemia?
- muscle weakness/cramps/tetany
- impaired liver conversion of glucose to glycogen
- vasoconstriction and cardiac arrythmia
- impaired ADH action causing thirst, polyuria
- metabolic alkalosis due to increase in intracellular H+
How is hypokalaemia treated?
Treat underlying cause
-oral/intravenous K+ required
What causes hyperkalaemia?
- reduced renal excretion due to acute kidney injury or chronic kidney disease
- increased plasma load due to dietary changes/IV infusion/cellular tissue breakdown
- insulin deficiency
- transcellular shift of K+ out of cells due to metabolic acidosis
- catecholamines
- hypoaldosteronism
What is pseudohyperkalaemia?
Due to haemolysis during venipuncture or storage of a sample
not expected patient to be hyperkalaemic
What are the clinical features of hyperkalaemia?
- can be asymptomatic
- muscle weakness
- cardiac arrythmias
How do you treat hyperkalaemia?
Emergency treatment (>6.5mmol/L or ECG changes)
- calcium gluconate (Ca2+ satbailises the myocardium)
- insulin to drive potassium into cells , and this is given alongside glucose to avoid hypoglycemia
- calcium resonium- removes K+ by increasing excretion from the bowels
Other treatments:
- salbutamol, drives K+ into cells (should not be used on patients with ischaemic heart disease/arrythmias)
- sodium bicarbonate: corrects acidosis and would drive K+ into cell
- renal replacement therapy
