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symptoms of hypokalemia
low K hyperpolarizes cell (need greater stim)
< 3.5 mM
flattens T wave, arrythmias, paralysis & death
decreases excitability of nerve & muscles
symptoms of hyperkalemia
high K brings closer to depolarization threshold
> 5.5 mM
causes V fib around 10 mM
K uptake in diet
avidly uptaken by GI & Na/K ATPase into cells
stimulated by insulin (largest), aldosterone (stimulated in hyperkalemia), epi (α decrease, β2 increase)
physiological modulators of K balance
acidosis associated with increase [K]
hypertonicity associated with high [K]
cell lysis releases internal K
exercise stimulates release of K from cells
management of external K balance
excretion must match dietary intake
absorbed in proximal tubule & loop
variable transport in distal tubule & collecting duct
(up to 80% can be excreted, 99% can be absorbed)
K tubular transport
taken up with NKCC and paracellularly in TAL
principal cell main excretion - K channel in parallel with eNaC (secretion of K with absorption of Na)
α intercalated cell absorbs K with H/K ATPase (for severe hypokalemia)
critical factors for K secretion
activity of Na/K ATPase
electrochemical gradient for K
secretion induced > 4 mM
hyperkalemia induces increased Na/K, permeability, release of aldosterone (coupling)
acidosis inhibits secretion, alkalosis increases secretion (hypokalemic alkalosis)
increased tubular fluid flow also increases secretion (keeps gradient high)
Mg absorption site
majority in TAL
paracellular uptake along cation selective tight junctions
(lumen positive drives)
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