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47 Cards in this Set
- Front
- Back
key role of potassium in the body
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regulates RMP
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potassium distribution is regulated by
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Na/K ATPase, which pumps Na out and K into cells
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intracellular potassium level
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140 (98% of total body potassium is intracellular)
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extracellular potassium level
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3.5-5
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Things that can cause hyperkalemia
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artifact, redistribution, decreased renal excretion
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artifact
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hemolysis, leukocytosis, thrombocytosis (500K+), increased tourniquet time
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Things that cause redistribution from ICF >> ECF
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AIDS: metabolic Acidosis, insulin defic/hyperglycemia, Drugs (digoxin, nonselective beta blockers), hyperkalemic periodic paralysis
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hyperglycemia and insulin
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K+ follows water moving out of cells in response to high ECF tonicity; insulin encourages cellular uptake of K
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digitalis and nonselective beta blokers
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block Na/K ATPase
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Potassium reabsorption in the nephrob
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600-700 mEq filtered daily and 60-70% reabsorbed in PCT, 20-30% in loop of henle
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Where excreted K+ comes from
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secreted from CD - usually 70mEq per day but can be up to 280.
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Things that increase CD secretion of K+
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increased flow of tubular fluid (osmotic diuresis) ; increased lumen negativity, aldosterone
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role of osmotic diuresis
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more water means K+ concentration in lumen is less, favoring secretion
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role of lumen negativity
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promotes efflux into lumen; if more Na is reabsorbed, the lumen is more neg and K+ secretion favored
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role of aldosterone
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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
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Hyperkalemia
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serum K > 5
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risk factors for hyperkalemia
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eGFR <20; DM, HIV, CHF, older pts, meds
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signs/sx of hyperkalemia
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ascending muscle weakness, EKG changes, arrhythmia, paralysis
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what happens to K in diabetic ketoacidosis
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hyperkalemia b/c high glucose pulls water/K+ out of cells and insulin is low, so less cellular uptake
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Plan:
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assess EKG, consider redistribution if no major sx
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EKG changes
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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
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Things that decrease renal excretion of K
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Renal failure, low flow (hypovolemia), distal RTA
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NSAIDS/Cox inhib, beta blockers, DM and HIV
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inhibit renin, so less K+ secretion
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ACE Inhib, ARB, heparin
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ACE inhib block Angio II, ARB and heparin lower aldo >> so less K+ secretion
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Amiloride
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Blocks ENAC >> tubule more positive, so less K+ secretion
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Spironolactone
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K-sparing diuretic; decrease aldo >> less k+ secretion
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Intake and hyperkalemia
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high intake could cause hyperkalemia in setting of kidney defect, like RAAS problem or low GFR
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Treating symptomatic hyperkalemia
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treat promptly and provide continuous cardiac monitoring. Must stabilize MP, enhance uptake, decrease total body K
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IV Ca chloride/Ca gluconate
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Stabilize membrane potential. give every 5 min until EKG returns to baseline (contraindicated in pt w. digitalis tox)
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IV insulin
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enhances cellular uptake; give w/ nebulized albuterol
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therapy to decrease total body K
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dialysis, sodium polystyrene
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treating mild dz
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dietary changes - restrict to 2500 mg/day (60mEQ) avoid contributing meds.
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hypokalemia
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serum K <3.5
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diff dx for low serum K
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redistribution, kidney/GI losses, decreased intake
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signs and sx of low serum K
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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.
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most common cause of low serum K
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diuretics
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things that can cause redistribution: ECF to ICF
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B2 agonists, epineph, insulin, systemic alkalosis, barium intox, hypokalemic periodic paralysis, treating DKA
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urine potassium-creatinine ratio
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(urine K+ x 100 ) / urine Cr
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treating hypokalemia - large deficit
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give IV potassium chloride, avoid glucose and bicarb.
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treating asx
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potassium citrate for those w/ concurrent met acidosis due to RTA
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loop diuretics
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block Na/K/2Cl reabsorption in loop of henle
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bartter's deficiency
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looks like a loop diuretic; see hypoK, hypoCl, high renin, high aldo, metabolic alkalosis
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thiazides
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block Na/Cl reabs in DCT
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Gitelman's
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presents like thiazide
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what these diuretics do
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impair Na uptake and induce hypovolemia >> increase Aldosterone (also transient increase in flow) leads to more K secretion
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24hr urine K <20; Urine K/Cr <13
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think diarrhea, prior diuretics, decreased intake, redistribution
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24hr urine K >30, urine K/Cr >20
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think diuretics
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