Potassium Flashcards
normal plasma K
3.5-5
handling of an acute K load vs acute K deprivation
handling of acute K load is quick: 75% of K load is taken up acutely into cells very quickly, followed by relatively reapid incr in renal K excretion (urinary K excretion can exceed filtered K load due to tubular K secretion); handling of K deprivation is slow (days to weeks) and therefore substantial K defecit can occur in meantime, also kidney cannot decr K excretion to the same level it decr Na excretion (minmum urine K is 5-15 mEq)
total body K vs plasma K
reduced TBK doesn’t affect plasma K as much as increased TBK does b/c cells can release K if plasma is deficient (but can’t take up K as easily); thus, if plasma is hypokalemic than the body must be severely TBK deprived
hormones that affect K
insulin, catecholamines, and aldosterone all send K into cells by incr Na/K pump activity (aldosterone also causes K excretion in kidney) and can be used to tx hyperkalemia and/or can cause side effects of hypokalemia (i.e. beta agonist side effect = hypokalemia)
factors affecting internal K balance (6)
plasma K concentration (high K stims Na/K pump and thus sends K into cells, high K in plasma also incr concen gradient for K to enter cells); hormones (insulin, catecholamines, aldo all send K into cells); exercise (K release from muscle); plasma tonicity (hypertonicity shrinks cells, thus incr. K concentration and creating a large concentration gradient for K to leave cells, also K leaves w/ water via solvent drag); acid-base balance (acidemia = hyperkalemia as H+ enters cells in return for K); cell lysis (rhabdomyolysis, hemolysis dump K into plasma)
hypertonicity effects on K balance (3)
hypertonicity shrinks cells, thus incr. K concentration and creating a large concentration gradient for K to leave cells, also K leaves w/ water via solvent drag –> hyperkalemia (incr by 1 mEq for each 20 mOsm incr) - most often seen w/ acute hyperglycemia (further impacted by lack of insulin in T1DM to send K back into cells)
glucose load effects on K in normals and diabetics
normal: glucose load induces insulin -> hypokalemia; diabetic: glucose load causes hypertonicity -> hyperkalemia
diabetics and K
glucose load in diabetes causes hyperkalemia b/c hypertonicity sends K out of cells and b/c insulin can’t send it back inside; however, kidneys in DKA tend to excrete K b/c ketoanions reach distal tubule and incr K excretion (more neg lumen) and b/c osmotic diuresis (glucose, ketones) -> may cause hypokalemia, particularly after hyperglycemia corrected w/ insulin; overall, diabetics have TBK deficit (loss in urine) but hyperkalemia in plasma (insulin lack, hypertonicity)
organic vs inorganic acidosis and K balance
organic acidosis (lactic acidosis, alcoholic ketosis, DKA) causes less hyperkalemia than inorganic acidosis (HCl, H2SO4, H3PO4), perhaps b/c organic acids enter cell as anion w/ H+ and thus K+ doesn’t need to leave
K reabsorption throughout kidney (%s)
prox nephron not regulated: 80% in PT, 10% in TAL; collecting duct regulated: in hyperkalemia, 20-180% can be secreted in initial collecting duct (20-40% will be reabsorbed again in CD despite hyperkalemia) -> total 10-150% filtered load excreted, vs. in hypokalemia, 2% will be reabsorbed in initial CD w/ 6% reabs in late CD -> total 2% filtered load excreted
K handling in PT (3)
in early prox tubule, reabs paracellularly due to solvent drag; in late tubule, small positive lumen V drives K reabs paracellularly; there is minimal secretion to lumen through luminal K channels
K handling in loop of Henle: thin descending limb, thin ascending limb, TAL
K passively secreted in thin descending limb (driven by high K permeability and high medullary K concentration); K passively reabs in thin ascending limb (this traps K in medullary interstitium -> incr capacity to secr K in distal tubule and CD during hyperkalemia); TAL reabs K both actively (accounts for 50%, via NK2Cl) and passively (accounts for 50%, due to positive lumen), some reabs K is secreted back into lumen through ROMPK while some exits the cell basolaterally
reabs and secretion of K in CD - what cells/channels are responsible?
principal cells secr K through aldo-sensitive channels and thru apical K-Cl synporter (driven by concentration gradient maintained by fast urine flow and by neg lumen V est by ENAC Na reabs); alpha IC cells reabs K through HK antiporter channels
reqs for K secretion into CD (3, lab values to get K secr)
aldo; Na delivery to CD (Na reabs through ENAC makes lumen negative and drives K secretion - need urine Na > 10-20 mEq/L to get K secretion); high urine flow rate (maintains concen. gradient; need urine V > 300-500 mL/day to get K secretion)
factors affecting distal nephron K secretion (4)
incr plasma K -> incr K excretion (independent of aldo); aldo -> incr K secretion; incr distal tubule Na delivery (-> neg lumen) and incr flow (maintain K concen gradient) -> incr K secretion; anions in tubular fluid (if NaCl delivered to tubule, Cl- absorbed relatively easily and tubule doesn’t get negative; if Na-sulfate delivered, sulfate is not as permeable as Cl- and thus is left behind -> more negative lumen = more K secr – we see this clinically w/ ketoanions, HCO3-, and anionic meds like penicillin)
non-reabsorbable anions: what do they do, what are they (4)
if NaCl delivered to tubule, Cl- absorbed relatively easily and tubule doesn’t get negative; if Na-sulfate delivered, sulfate is not as permeable as Cl- and thus is left behind -> more negative lumen = more K secr; we see this clinically w/ ketoanions, HCO3- (metabolic alkalosis kidney compensation, prox RTA), and anionic meds like penicillin or hippopurate (toluene, glue sniffing)
why doesn’t hypovolemia lead to hypokalemia via aldo?
hypovolemia -> RAAS -> AgII -> NaH in PT upregulated -> avid PT Na reabsorption -> low distal Na delivery -> no K secretion despite high aldo levels
hyperkalemia consequences (7)
cell swelling; cell alkalosis (K enters cells in exchange for H+); plasma acidosis (decr renal ammoniagenesis -> impaired urinary acidication); cell depolarization; muscle weakness and paralysis (initially incr muscle excitability followed by Na channel inactivation) which can lead to respiratory muscle failure; vasodilation (SMC relaxation); cardiac conduction disturbances and ventricular arrhythmias
hyperkalemia ECG
peaked T waves -> long PR w/ flattened p -> QRS wide -> sine wave (VF)
pseudohyperkalemia (4)
in vitro hemolysis assoc w/ leukocytosis (serum K high, plasma K normal), thrombocytosis (serum K high, plasma K normal), fist clenching during blood draw (exercise), fragile RBC in genetic disorders (hereditary spherocytosis)
dietary potassium (4)
potatoes, bananas, oranges, tomatoes
causes of hyperkalemia: 3 general classes w/ specifics
high K intake (us. needs impaired K excretion or internal K balance probs to cause hyperkalemia tho); impaired K excretion due to low GFR (AKI/CKD), RAAS probs (hypoaldo in Addison’s, type IV RTA, and meds; aldo resistance due to meds or tubulointerstitial CKD), inadeq distal tubule Na delivery and urine flow; abnormal internal balance due to insulin deficiency, hypertonicity, metabolic acidosis, drugs (beta antagonists, severe digoxin toxicity, succinylcholine), exercise, tissue damage/cell lysis
AKI effects on K balance (4)
causes hyperkalemia: decr distal Na delivery and urine flow; distal tubule dysfn prevents K secretion; tissue breakdown/catabolic state/metabolic acidosis lead to hyperkalemia; no adapative mechs to incr K secr in distal tubule and colon
CKD effects on K balance
can cause hyperkalemia, but only if GFR severely depressed (<15-20) b/c compensation occurs (distal nephron hypertrophy w/ incr. principle cell area, incr NK pump activity, and incr apical K channel activity; colon K secr incr.)
