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47 Cards in this Set

  • Front
  • Back
key role of potassium in the body
regulates RMP
potassium distribution is regulated by
Na/K ATPase, which pumps Na out and K into cells
intracellular potassium level
140 (98% of total body potassium is intracellular)
extracellular potassium level
3.5-5
Things that can cause hyperkalemia
artifact, redistribution, decreased renal excretion
artifact
hemolysis, leukocytosis, thrombocytosis (500K+), increased tourniquet time
Things that cause redistribution from ICF >> ECF
AIDS: metabolic Acidosis, insulin defic/hyperglycemia, Drugs (digoxin, nonselective beta blockers), hyperkalemic periodic paralysis
hyperglycemia and insulin
K+ follows water moving out of cells in response to high ECF tonicity; insulin encourages cellular uptake of K
digitalis and nonselective beta blokers
block Na/K ATPase
Potassium reabsorption in the nephrob
600-700 mEq filtered daily and 60-70% reabsorbed in PCT, 20-30% in loop of henle
Where excreted K+ comes from
secreted from CD - usually 70mEq per day but can be up to 280.
Things that increase CD secretion of K+
increased flow of tubular fluid (osmotic diuresis) ; increased lumen negativity, aldosterone
role of osmotic diuresis
more water means K+ concentration in lumen is less, favoring secretion
role of lumen negativity
promotes efflux into lumen; if more Na is reabsorbed, the lumen is more neg and K+ secretion favored
role of aldosterone
induces expression of Na+ channels on apical surface of principle cells, leading to more uptake, making lumen more neg. Also induces expression of K+ channels on apical membrane of principle cells, promoting excretion
Hyperkalemia
serum K > 5
risk factors for hyperkalemia
eGFR <20; DM, HIV, CHF, older pts, meds
signs/sx of hyperkalemia
ascending muscle weakness, EKG changes, arrhythmia, paralysis
what happens to K in diabetic ketoacidosis
hyperkalemia b/c high glucose pulls water/K+ out of cells and insulin is low, so less cellular uptake
Plan:
assess EKG, consider redistribution if no major sx
EKG changes
As serum K rises, see peaked T wave w/ short QT, followed by long PR and QRS, decreased p wave amplitude, then see sinoventricular pattern. EMERGENCY
Things that decrease renal excretion of K
Renal failure, low flow (hypovolemia), distal RTA
NSAIDS/Cox inhib, beta blockers, DM and HIV
inhibit renin, so less K+ secretion
ACE Inhib, ARB, heparin
ACE inhib block Angio II, ARB and heparin lower aldo >> so less K+ secretion
Amiloride
Blocks ENAC >> tubule more positive, so less K+ secretion
Spironolactone
K-sparing diuretic; decrease aldo >> less k+ secretion
Intake and hyperkalemia
high intake could cause hyperkalemia in setting of kidney defect, like RAAS problem or low GFR
Treating symptomatic hyperkalemia
treat promptly and provide continuous cardiac monitoring. Must stabilize MP, enhance uptake, decrease total body K
IV Ca chloride/Ca gluconate
Stabilize membrane potential. give every 5 min until EKG returns to baseline (contraindicated in pt w. digitalis tox)
IV insulin
enhances cellular uptake; give w/ nebulized albuterol
therapy to decrease total body K
dialysis, sodium polystyrene
treating mild dz
dietary changes - restrict to 2500 mg/day (60mEQ) avoid contributing meds.
hypokalemia
serum K <3.5
diff dx for low serum K
redistribution, kidney/GI losses, decreased intake
signs and sx of low serum K
abnormal skeletal/cardiac muscle function, usually when level dips below 3. See arrhythmia, muscle cramps, ascending weakness, resp weakness, paralysis, glucose intolerance, impaired urinary concentration. See U waves on EKG.
most common cause of low serum K
diuretics
things that can cause redistribution: ECF to ICF
B2 agonists, epineph, insulin, systemic alkalosis, barium intox, hypokalemic periodic paralysis, treating DKA
urine potassium-creatinine ratio
(urine K+ x 100 ) / urine Cr
treating hypokalemia - large deficit
give IV potassium chloride, avoid glucose and bicarb.
treating asx
potassium citrate for those w/ concurrent met acidosis due to RTA
loop diuretics
block Na/K/2Cl reabsorption in loop of henle
bartter's deficiency
looks like a loop diuretic; see hypoK, hypoCl, high renin, high aldo, metabolic alkalosis
thiazides
block Na/Cl reabs in DCT
Gitelman's
presents like thiazide
what these diuretics do
impair Na uptake and induce hypovolemia >> increase Aldosterone (also transient increase in flow) leads to more K secretion
24hr urine K <20; Urine K/Cr <13
think diarrhea, prior diuretics, decreased intake, redistribution
24hr urine K >30, urine K/Cr >20
think diuretics