Potassium Disorders Flashcards
What is the physiology of normal potassium regulation?
freely filtered by glomerulus but reabsorbed by proximal tubule and loop of Henle so little reaches distal
what reaches distal is secreted by CCD and excreted - amt excreted determined by rate of secretion
What are the major physiologic determinants of renal potassium excretion?
mineralocorticoids
distal delivery of Na and water
nonreabsorbable anions
How does the potassium cross the CCD?
transcellular (major) or paracellular
pumped in by NaK pump on BL membrane - diffuses out down conc gradient using K channel on luminal
paracellular driven by lumen negative voltage from Na being pumped in
What are factors that influence the internal distribution of potassium?
insulin
b2 stimulation
What are the cellular determinants of potassium secretion?
cell K concentration
luminal K concentration
Potential difference across luminal membrane
permeability of luminal membrane for K
How do mineralocorticoids determine K excretion?
Aldo released with hyperkalemia - increases Na absorption through luminal channel and increases K secretion through NaK pump (increases in cell)
H+ secretion in intercalated duct also increased
also increase K permeability of luminal membrane
How does distal delivery of Na affect K excretion?
more distal delivery means more uptake into cell - increases lumen negative potential
also causes NaK pump to go faster
luminal K concentration also lowered by more volume
How do nonreabsorbable anions affect K excretion?
not absorbed proximally - increase distal delivery of Na and volume - increases K secretion
also increase lumen negative voltage because they can’t enter cell with Na like Cl can
What are examples of non reabsorbable anions?
sulfate
phosphate
carbenicillin
sometimes bicarb
When are abnormalities in renal K secretion seen?
when mineralocorticoids and distal Na delivery shift in same direction - primary mineralocorticoid excess, primary increase in distal Na delivery, primary decreases in either
What physiologic factors increase cell K uptake?
plasma K
insulin - prevents post meal hyperkalemia
B adrenergic catecholamines - prevents post exercise hyperkalemia
What findings are present in Conn’s syndrome?
low renin, high aldo
HTN
hypokalemic alkalosis
How can Conn’s syndrome be differentiated from bilateral adrenal hyperplasia?
conn’s HTN corrects with tumor removal
HTN in bilateral won’t respond even to bilateral adrenalectomy
How does 11betaHSD2 act in hypokalemia development?
usually converts cortisol to cortisone def allows cortisol to activate receptor
What is Liddle syndrome?
low renin and aldo
no response to inhibitor of aldo secretion or spironolactone
triamterene/transplant normalizes BP and K
What is Bartter’s syndrome?
genetic condition with primary defect in loop of Henle salt reabsorption
hypokalemic with high R and A
What is Gitelman’s syndrome?
defect in DCT reabsorption of NaCl
Hypokalemic with high R and A
What happens to K secretion in CKD?
decreased distal Na delivery and nephron dropout
but remaining nephrons develop increased ability to secrete K
What two defenses against hyperkalemia do patients with CKD have?
Redistribute K faster into cells with K load
Increase rate of K excretion in stool
What are the neuromuscular manifestations of hypo and hyperkalemia?
hypo - weakness leading to flaccid paralysis, rhabdo
hyper - paresthesias leading to paralysis
What are cardiac manifestations of hypo and hyperkalemia?
hypo - arrhythmia, ST depression, T wave flattening, U wave
hyper - cardiac arrest
How does hypokalemia affect the kidney?
concentrating defect
can cause hypernatremia by inducing nephrogenic DI
What are the EKG changes in hyperkalemia?
peaked t wave first, then widening QRS, then sine wave
What are the general rules of treatment for potassium disorders?
all patients should have serum K corrected, but those with EKG changes treated emergently
if hypokalemia AND acidosis - treat hypokalemia first, isolated treatment for acidosis can worsen hypokalemia
