01-07 Potassium Flashcards
hormonal regulation of [K+]
—w/in mins: insulin, epi; w/in hrs: aldo
—cause muscle, liver, bone and RBCs to uptake excess K+ in serum via upreg of Na+/K+-ATPase, Na+/K+/2Cl- and Na+/Cl-
—∆s in serum [K+] ∆ the rate of secretion of these hormones
INSULIN: most import; pts w/ DM have ↑er [K+] rise s/p eating than non-DM pts; used in tx of hyperkalemia
EPI: ↑ uptake via β2; α → release
—β-blocker can be slow absorption of K+ into cell s/p meal
ALDO: slower but acts to both ↑ cell uptake and urinary excretion
—Addisonian crisis (low aldo) → hyperkalemia
Acid-Base and K+
—In METABOLIC (i.e. usu. not resp) acidosis → hyperkalemia b/c cells uptake H+ and secrete K+ to maintain electroneutrality
Effect of Plasma osmolality on [K+]
hyper-omolarity (e.g. ↑ [glucose]) → hyperkalemia
—hypertonic plasma shrinks cells ↑ intracell [K+] creating gradient for more K+ to leave cell
—also solvent drag (H2O pulls K+ w/ it)
—double-whammy for diabetics b/c of decr levels of/sensitivity to insulin which also leads to hyperkalemia
10mOsm ↑ → 0.4-0.8 ↑ [K+]
Effect of cell lysis on [K+]
—trauma, burns, tumor lysis syndrome and rhabdo all ↑ [K+]
—ulcers → bleed → RBCs lyse → reabsorb K+ in GI tract
Effect of exercise on [K+]
exercise releases K+ from muscles
—can be up to 2.0mEq/L w/ vigorous exercise
—only problematic in: β-blockers, renal failure, d/o affecting release of epi, aldo or insulin (Addison’s, DM, etc.)
filtering of K+
freely filtered b/c no protein bound
—can also be secreted
PT handling
—67% reabsorbed here (constant fraction of filtered load)
LoH handling
—20% reabsorbed here (constant fraction of filtered load)
DCT and CT/CD handling
—where?
—by what mech?
—resorbs AND secretes
—regulated by aldo, serum [K+] and, to a lesser extent ADH
—∆s in tubular flow rate and acid-base imbalances can ∆ K+ handling but in non-homeostatic ways
SECRETION: The Principal Cell
—first basolateral Na+/K+ ATPase moves K+ into princ. cell
—second, K+ diffuses out through channels into tubular fluid
REABSORPTION: The Intercalated Cell
—H+/K+-ATPase (Exchanger)
[IMAGE]
Mechanism of [K+] regulation of [K+]
∆s: —speed of Na+/K+-ATPase —electrochecmical gradient —aldosterone secretion —flow rate
Mechanism of Aldo regulation of [K+]
∆s:
—expresion of basolater Na+/K+-ATPase
—expression of ENaC both directly and indirectly via (SGK1 and CAP1)
—the permeability of the apical membrane by ∆ing # of channels
—takes ~24hrs b/c its effect on K+ is initially cancelled by ↑ Na+ reabsorption → decr H2O delivery to distal nephron
Regulation of aldosterone secretion
↑: A2 and hyperkalemia
↓: natruetic peptides (e.g. ANP) and hypokalemia
Mechanism of ADH regulation of [K+]
—stimulates K+ secretions by DCT/CD basically by ∆ing intracellular [Na+] altering electrochem gradient
—makes up for the decreased flow it causes, so there is constant urinary K+ excretion despite ∆s in water handling
Effect of tubular flow rate on K+
Tubular flow rates bend 1° cilia on principal cells ↑ing [Ca2+]intracell → depolarizes apical membrane → K+ channels activated
—↑ flow → ↑ K+ secretion
Effect of ∆ing pH on [K+]
acidosis: HYPERkalemia —inhibits basolateral Na+/K+-ATPase —reduces permeability of apical membrane alkalosis: HYPOkalemia —opposite above
When acidosis is chronic, kidney can once again secrete K+ b/c of alterations in tubular flow 2°to ↓ed
Effect of glucocorticoids on [K+]
glucocorticoids ↑ K+ secretion → HYPOkalemia
—↑ GFR → ↑ flow rate → ↑ K+ secretion
—stimulate Sgk1
Hyperkalemia 101: —[K+] cut-off? —How common? —Severity? —Symptoms?
– Serum [K+] > 5 mEq/L
– Relatively uncommon
– Often life-threatening: severity depends on speed of ∆ in serum [K+]
– Often asymptomatic: 1st sx may be cardiac arrest
Clinical Manifestations of HYPERkalemia
—S/Sx
—EKG ∆s?
—Mechanism for these ∆s?
S/Sx: muscle weakness EKG ∆s by frequency: —1. Peaked Ts —2. PR prolongation/QRS widening —3. sine wave/asystole Mechanism: —depolarization because [K+]_out is now closer to [K+]_in —Na+ channels become paralyzed —No APs/contractions
Tx for arrythmias 2° to HYPERkalemia
Ca2+ stabilized membrane
Causes of HYPERkalemia by category of distrurbance
INCREASED INTAKE
—problematic only when output decreased
—foods, meds (abx, K+ supplement), salt substitutes
DECREASED OUTPUT
—Decreased GFR
—Hypoaldosteronism (1°, 2° or Hyporeninemic)
—Meds
CELL SHIFT
—e.g. exercise (many others see list card)
SPURIOUS
—pseudohyperkalemia due to cell lysis from improper phlebotomy
Foods high in K+
Potatoes, tomatoes, citrus fruits, melons, milk
How does hypoaldosteronism (or resistance to aldo) effect [K+]? Mechanism?
Lack of aldosterone or aldosterone resistance closes the distal Na+ channel
—Inability to absorb Na+ = inability to generate negative electrical gradient for K+ secretion
