Potassium Flashcards
intracellular potassium is maintained at?
140 mEq/L
transcellular distribution of K+ is largely determined by the _______
Na/K ATPase
acidemia can result in potassium ____ due to ____ exchange
efflux from the cell; H+/K+ exchange (usually with HCl retention rather than organic acid)
what happens to ingested K+?
some is distributed into cells with help in insulin; most of it is excreted into urine due to aldosterone (6-8 hours)
high levels of insulin have what effect on K+?
increased cellular uptake of potassium and decreased serum potassium
activation of beta-adrenergic receptors has what effect on K+?
uptake into cells
how to non-selective beta-blockers affect potassium levels?
cause hyperkalemia (beta agonists cause hypokalemia)
digitalis toxicity and hyperglycemia cause ____kalemia
hyper-kalemia (the first inhibits Na/K ATPase, in the second K+ follows water out of cells)
how does DKA affect potassium levels?
patients have hyperkalemia initially (from decreased insulin + hyperglycemia) but an overall low level of potassium and ultimate hypokalemia once insulin corrects the hyperglycemia (due to osmotic diuresis)
key site of potassium excretion regulation
cortical collecting duct
name three mechanisms for increased excretion of potassium in the CCD
increased flow; increased tubular lumen negativity; aldosterone (through increased Na reabsorption and increased potassium channels on principle cells)
clinical signs of hyperkalemia
ascending muscle weakness, ECG changes, cardiac arrhythmias, paralysis when severe
ECG signs of hyperkalemia
peaked T waves with a shortened QT interval initially, followed by increased PR interval and QRS duration, eventually V fib
potential causes of pseudohyperkalemia
thrombocytosis, leukocytosis
healthy adults should be able to secrete up to ___mEq potassium without developing hyperkalemia
280 (normal = 70)
causes of impaired excretion of potassium
defect in RAAS, decreased GFR, defect in the CCD, drugs that cause any of these three things
causes of redistributive hyperkalemia
tissue injury, insulin deficiency, metabolic acidosis, hyperosmolarity, drugs (digoxin, octreotide, beta blockers, somatostatin), oleandar toxicity
causes of hypoaldosteronism in setting of high renin
adrenal insufficiency, enzyme defects, meds (ACE inhibitors, ARBs, heparin, ketoconazole)
causes of hypoaldosteronism in setting of low renin
diabetes mellitus, HIV, meds (NSAIDs, Cox-2 inh, calcineurin inh)
causes of collecting duct defects
meds (amiloride, triamterene, spirinolactone, eplerenone, trimethoprim, pentamidine), tubulointerstitial dz, urinary tract obstruction, defective mineralocorticoid receptor, Gordon syndrome
tx of symptomatic hyperkalemia (or with ECG changes)
IV calcium-chloride or calcium-gluconate (antagonize depolarization) every 5 minutes (unless digoxin toxicity) and insulin, sodium bicarb, and/or nebulized albuterol all temporarily correct hyperkalemia by pulling K+ into cells
tx of hyperkalemia in pt with kidney failure
hemodialysis, loop diuretics to decrease total K+, (sodium bicarb won’t help)
differential for hypokalemia
redistribution, kidney or GI losses, or decreased intake
clinical signs of hypokalemia
abnormal skeletal and cardiac muscle function, including arrhythmias, ECG changes, muscle cramps and weakness, ileus, glucose intolerance
what is the most common cause of hypokalemia?
diuretics
drugs that cause hypokalemia
beta2 agonists, epinephrine, insulin, vit B12
intoxication with the following cause hypokalemia
barium, chloroquine, quietapine, risperidone
when does hypokalemic periodic paralysis present?
after a high-carb meal or strenuous exercise
acidosis/alkalosis can cause hypokalemia
alkalosis
assessment of these three things is imporant in a patient with hypokalemia
urinary potassium excretion, blood pressure, acid-base status
in patients with hypokalemia, urinary potassium-creatinine ratio >20 suggests?
kidney potassium wasting
in patients with hypokalemia, urinary potassium-creatinine ratio <13 suggests?
redistribution, decreased intake, extrarenal loss
how to calculate urine potassium-creatinine ratio
urine K x 100/urine Cr
if a pt is determined to have potassium wasting, what is the next step?
determine whether they have hypertension
if a pt with potassium wasting is hypertensive, what should be measured next?
aldosterone and renin levels
if a pt with potassium wasting is not hypertensive, what should be evaluated next?
acid-base status, urinary sodium and chloride levels
overall flow diagram for hypokalemia
- diuretic use?, 2. hypertension?, IF NO then: redistribution?, assess K+ excretion, assess acid-base status if increased; IF YES HTN: measure renin and aldosterone
tx of hypokalemia
IV KCl (avoid NaHCO3 and glucose in IV solutions); if mild can use oral tx; give magnesium repletion (potassium-citrate if also have RTA)
causes of true hypovolemic metabolic alkalosis & hypokalemia
loss of gastric secretions, diuretics, Bartter’s & Gitelman’s, calcium-alkali syndrome
urine composition during generation phase of vomiting
low chloride, high concentrations of sodium and potassium being lost with bicarb (high pH)
urine composition during maintenance phase of vomiting
continued excretion of bicarb results in volume contraction, which triggers reabsorption of bicarb, and thus sodium and chloride AND aldosterone release – the result is continued metabolic alkalosis, low urine chloride, sodium, and bicarb, plus increased reabsorption of sodium which increases secretion of K+ and H+ due to negative lumen (paradoxical aciduria, urine pH low again)
tx of metabolic acidosis due to vomiting/nasogastric suction
normal saline +/- KCl (if concurrent hypokalemia)
diuretic-induced metabolic alkalosis and hypokalemia
diuretic blocks reabsorption of Na+ and Cl-, which stimulates aldosterone, resulting in H+ and K+ secretion, resulting in hypochloremia, hypokalemia, and alkalosis (as bicarb is released in the body for each H+ lost)
describe the defect in Bartter’s syndrome
defect in Na-K-2Cl transporter in thick ascending limb; acts like constant loop diuretic causing metabolic alkalosis, hypokalemia, normal BP
describe the defect in Gitelman’s syndrome
defect in distal convoluted tubule at NaCl transport site; acts like a constant thiazide diuretic causing metabolic alkalosis, hypokalemia, normal BP
why does calcium-alkali syndrome cause metabolic alkalosis and hypokalemia?
hypercalcemia acts on receptor in thick ascending limb, leading to inhibition of Na-K-2Cl transporter, and thus effect of loop diuretic (which causes hypovolemia, alkalosis and hypokalemia)
tx of calcium-alkali syndrome
normal saline to restore ECF and EABV to normal, prevent/reverse azotemia
causes of metabolic alkalosis in setting of low EABV but high ECF
heart failure, cirrhosis, nephrotic syndrome
tx of metabolic alkalosis in setting of low EABV but high ECF
normal saline WON’T work; use acetazolamide (carbonic anhydrase inhibitor) in severe cases to tx alkalosis
what causes primary hyperaldosteronism?
adrenal tumors or hyperplasia
why don’t pts with primary hyperaldosteronism have edema?
“aldosterone escape” or down-regulation of thiazide-sensitive Na-Cl cotransporters in the distal tubule result in diuresis (this is how it can cause alkalemia despite normal or high EABV and ECF)
when might urinalysis show high sodium but low chloride?
only during generation phase of vomiting, otherwise they track together
