potassium balance Flashcards
what is the importance of maintaining K+ balance?
the kidneys maintain K+ balance in order to maintain plasma [K+] within the narrow concentration range of 3.5-5mmol/L
plasma [K+] within this range is essential for the normal functioning of neurons and muscle, in particular, cardiac muscle
how much K+ do we consume daily?
100mol/day with 90mml absorbed through the GIT daily
how is a rise in plasma [K+] after a meal prevented?
K+ homestasis maintained by regulation of plasma [K+] in the ECF and regulation of Renal K+ excretion by kidneys to match the dietary K+ intake
regulation of plamsa K+ controlled by?
- epinephrine
- insulin
- aldosterone
increase uptake of K+ into skeletal muscle, liver, bone and RBS
increased turnover rate of Na/K/ATPase, Na/K/2Cl, and Na/Cl transporters (acute)
increased quantitiy of na/K/ATPase (Chronic)
What can alter plasma [K+]?
- acid base balance - metabolic acidosis increases plamsa K+
- increase in plasma osmolaltiy causes a release of K+ from cells
- cell lysis
- exercise
describe K+ excreiton by the kidneys
- k+ uptake from the blood by the cells of Collecting ducts
- K+ is secreted down concentration gradient from these cells into the filtrate and excreted in the urine
- secretion is regulated by K+ itself and hormones
describe the regulation of K+ excretion by the DT and CD
when plasma [K+] increases
- hyperkalaemia quickly stimulates K+ secretion -
- stimulates Na+/K+ pump
- increases permeability of apical membrane to K+
- stimulates aldosterone secretion by adrenal cortex (which increases number of Na/K pumps and increases epithelial sodium channels thus increasing permability of apial membrane to K+
- increases flow rate of tubular fluid
- ADH- stimulates secretion of K+ by DT and CD but decreases urinary flow rate
hypokalaemia has the opposite effects
what is the overall effect of acute vs. chronic metabolic acidosis?
Acute = decreases K+ excretion
chronic = increases K+ excretion- due to associated increase in aldosterone levels
what concentration incidates hypokalemia? What concentration incidates hyperkalema?
Hypokalemia < 3.5 mEq/L
due to diuretics, excess aldosterone, metabolic alkalosis, severe diarrhoea, and vomiting
hyperkalemia > 5mEq/L
due to renal failure, adrenal insufficiency, acute acidosis, tissue destruction like burns or trauma
how does severe diarrhoea result in hypokalemia?
diarrhoea results in K+ loss via
- direct K+ loss via GIT
- indirect K+ loss via kidneys - decreases ECF volume, stimulates Aldosterone, cuases excretion of K+ by kidneys
*severe vomitting cuases the same thing to happen*
what are the symptoms of hypokalemia?
usually aymptomatic - but if sever
- weakness of skeletal muscle
- cardiac arrhythmias- but usually only in those with cardiac disease -
*changes in K+ can have effects of excitable cells- hypokalemia hyperpolarizes the membrane voltage making it more difficult to generate an action potention b/c a larger depolarizing current is needed to reach threshold
why does acute renal failure cuase hyperkalemia?
when the glomerular filtration rate falls to about 25% of normal
plasma K+ rises
hyperkalaemia reduces RMP
decreases excitablility of neurons, cardiac cells, and muscle cells, causes cardiac arrest and death
why does hyperkalaemia cause a decrease in excitability of neurons?
the membrane potential at the onset of depolarization determines the number of sodium channels activated during depolarization - which in turn determines the magnitude of the inward sodium current and the Vmax of the action potential
as the resting membrane potential becomes less negative (as with hyperkalemia) the percentage of available sodium channels decreases and leads to a decremetn in the inward sodium current (decrease in Vmax)
therefore, as resting membrane potential becomes less negative - Vmax decreases and causes a slowing of impulse conduction through the myocardium and prolongation of membrane depolarization (arrythmia)
why does tissue destruction cause hyperkalemia?
when cells lyse and K+ is released into ECF