#2 - Disorders of Fluid and Potassium Flashcards
Normal K+ concentration
3.5-5.3 mEq/L
K+ distribution in body
98% in cells, 2% ECF
K+ excretion
90% in urine, 10% in stool
GI excretion can increase in kidney failure to 50%
K+ is reabsorbed by proximal tubule but
secreted by cortical collecting duct - rate of secretion determines K+ excretion rate
K crosses collecting duct in 2 ways
Transcellular > paracellular
- Transcellular route - Na/K-ATPase on basolateral side makes high intracellular concentration, then diffuses along gradient into lumen which is less negative but conc. gradient favors it
Rate of transcellular K secretion =
rate of K diffusion across luminal membrane
Increased by:
- Increased intracellular [K], permeability of luminal membrane to K, decreased luminal [K], and more negative lumen
Insulin and B2-adrenergic stimulation both
shift K+ into cells, insulin after eating and B2/epinephrine during exercise
Mineralocorticoid - Aldosterone
Secreted from zona glomerulosa of adrenal cortex in response to hyperkalemia and Ang. II
- Increases rate of Na+ absorption through luminal channel (makes lumen more negative)
- Increases K+ secretion through Na/K pump
- Increase K+ permeability of luminal membrane
- Increases H+ secretion by intercalated cell
Decreased EABV normally causes
- Increased aldosterone from increased JG, renin, AII activity
- Decreased distal Na+ delivery due to increased proximal absorption
Increased EABV normally causes
- Decreased aldosterone from decreased JG activity
- Increased distal Na delivery from decreased proximal absorption
Distal delivery of Na and H2O are
correlated together
- Increased delivery of Na stimulates distal Na absorption which makes lumen more negative and increases K secretion, also making Na/K pump work faster
- Higher flow rates also remove positive charges in lumen more so more K can be secreted
Non-reabsorbable anions effect on Na and volume
increase distal Na delivery because coupled with it, secondarily increasing K secretion, also making lumen more negative. More poorly reabsorbable anions will increase it more.
Primary mineralocorticoid excess
E.g. aldosterone secreting tumor, primary aldosteronism - benign tumor of zona glomerulosa = Conn’s syndrome
- Increased aldosterone activity and distal delivery causes K+ loss and hypokalemia
Primary increase in distal delivery
E.g. diuretics
- Increase distal delivery and Na loss with volume depletion and increased aldosterone causing K loss and hypokalemia
Primary decrease in mineralocorticoid activity or distal Na delivery
Seen in destruction of adrenal gland, acute renal failure
- Cause decreased distal delivery and aldosterone causing K+ retention and hyperkalemia
Hyperkalemia stimulates
cell K+ uptake directly, and also through hormones such as insulin and epinephrine
Hypokalemia disorder causes
inadequate intake, GI loss, renal loss, cellular redistribution
Hypokalemia from inadequate dietary intake because
some K always lost, unlike Na which can go to virtually zero excretion if necessary
2 Most common causes of hypokalemia
- Diarrhea - fecal K+ wasting and acidosis causes K+ out of cells which partially helps
- Vomiting - greater K+ depletion, not from gastric loss but metabolic alkalosis which causes kidney to not reabsorb HCO3-, causing K+ wasting. Alkalosis also causes redistribution of K into cells worsening the hypokalemia
- Urinary K+ < 20 mEq
Acidosis and alkalosis cause K+ to redistribute
out of and into cells, respectively
Hypokalemic periodic paralysis
intermittent attacks of muscle weakness triggered by large carb meals (insulin) or rest post-exercise (epinephrine) where K+ gets acutely shifted into cells
- Inherited form - dominant a-1 mutation in Ca channel
- Acquired - hyperthyroidism
Conn’s Syndrome
benign tumor of zone glomerulosa - produces excess aldosterone in absence of volume contraction > K+ loss and hypokalemia
- resolves if tumor removed
Bilateral adrenal hyperplasia
HTN will not respond even to bilateral removal
Primary aldosteronism
conditions where excess aldosterone secretion is cause of primary adrenal disease, e.g. Conn’s Syndrome and bilateral adrenal hyperplasia