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regulation of K, Mg, Ca, phosphate

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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
K permeability
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)
Ca absorption sites
70% prox (active), 20% TAL
excrete 1%
Mg absorption site
majority in TAL
paracellular uptake along cation selective tight junctions
(lumen positive drives)
phosphate balance sites
actively transported in prox (80%)
urine buffer but unregulated
10% excretion
prox tubule has monobasic and dibasic transporters