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Urinary & Renal > Potassium > Flashcards

Potassium Flashcards

1
Q

intracellular potassium is maintained at?

A

140 mEq/L

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2
Q

transcellular distribution of K+ is largely determined by the _______

A

Na/K ATPase

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3
Q

acidemia can result in potassium ____ due to ____ exchange

A

efflux from the cell; H+/K+ exchange (usually with HCl retention rather than organic acid)

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4
Q

what happens to ingested K+?

A

some is distributed into cells with help in insulin; most of it is excreted into urine due to aldosterone (6-8 hours)

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5
Q

high levels of insulin have what effect on K+?

A

increased cellular uptake of potassium and decreased serum potassium

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6
Q

activation of beta-adrenergic receptors has what effect on K+?

A

uptake into cells

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7
Q

how to non-selective beta-blockers affect potassium levels?

A

cause hyperkalemia (beta agonists cause hypokalemia)

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8
Q

digitalis toxicity and hyperglycemia cause ____kalemia

A

hyper-kalemia (the first inhibits Na/K ATPase, in the second K+ follows water out of cells)

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9
Q

how does DKA affect potassium levels?

A

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)

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10
Q

key site of potassium excretion regulation

A

cortical collecting duct

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11
Q

name three mechanisms for increased excretion of potassium in the CCD

A

increased flow; increased tubular lumen negativity; aldosterone (through increased Na reabsorption and increased potassium channels on principle cells)

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12
Q

clinical signs of hyperkalemia

A

ascending muscle weakness, ECG changes, cardiac arrhythmias, paralysis when severe

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13
Q

ECG signs of hyperkalemia

A

peaked T waves with a shortened QT interval initially, followed by increased PR interval and QRS duration, eventually V fib

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14
Q

potential causes of pseudohyperkalemia

A

thrombocytosis, leukocytosis

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15
Q

healthy adults should be able to secrete up to ___mEq potassium without developing hyperkalemia

A

280 (normal = 70)

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16
Q

causes of impaired excretion of potassium

A

defect in RAAS, decreased GFR, defect in the CCD, drugs that cause any of these three things

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17
Q

causes of redistributive hyperkalemia

A

tissue injury, insulin deficiency, metabolic acidosis, hyperosmolarity, drugs (digoxin, octreotide, beta blockers, somatostatin), oleandar toxicity

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18
Q

causes of hypoaldosteronism in setting of high renin

A

adrenal insufficiency, enzyme defects, meds (ACE inhibitors, ARBs, heparin, ketoconazole)

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19
Q

causes of hypoaldosteronism in setting of low renin

A

diabetes mellitus, HIV, meds (NSAIDs, Cox-2 inh, calcineurin inh)

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20
Q

causes of collecting duct defects

A

meds (amiloride, triamterene, spirinolactone, eplerenone, trimethoprim, pentamidine), tubulointerstitial dz, urinary tract obstruction, defective mineralocorticoid receptor, Gordon syndrome

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21
Q

tx of symptomatic hyperkalemia (or with ECG changes)

A

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

22
Q

tx of hyperkalemia in pt with kidney failure

A

hemodialysis, loop diuretics to decrease total K+, (sodium bicarb won’t help)

23
Q

differential for hypokalemia

A

redistribution, kidney or GI losses, or decreased intake

24
Q

clinical signs of hypokalemia

A

abnormal skeletal and cardiac muscle function, including arrhythmias, ECG changes, muscle cramps and weakness, ileus, glucose intolerance

25
Q

what is the most common cause of hypokalemia?

A

diuretics

26
Q

drugs that cause hypokalemia

A

beta2 agonists, epinephrine, insulin, vit B12

27
Q

intoxication with the following cause hypokalemia

A

barium, chloroquine, quietapine, risperidone

28
Q

when does hypokalemic periodic paralysis present?

A

after a high-carb meal or strenuous exercise

29
Q

acidosis/alkalosis can cause hypokalemia

A

alkalosis

30
Q

assessment of these three things is imporant in a patient with hypokalemia

A

urinary potassium excretion, blood pressure, acid-base status

31
Q

in patients with hypokalemia, urinary potassium-creatinine ratio >20 suggests?

A

kidney potassium wasting

32
Q

in patients with hypokalemia, urinary potassium-creatinine ratio <13 suggests?

A

redistribution, decreased intake, extrarenal loss

33
Q

how to calculate urine potassium-creatinine ratio

A

urine K x 100/urine Cr

34
Q

if a pt is determined to have potassium wasting, what is the next step?

A

determine whether they have hypertension

35
Q

if a pt with potassium wasting is hypertensive, what should be measured next?

A

aldosterone and renin levels

36
Q

if a pt with potassium wasting is not hypertensive, what should be evaluated next?

A

acid-base status, urinary sodium and chloride levels

37
Q

overall flow diagram for hypokalemia

A
  1. diuretic use?, 2. hypertension?, IF NO then: redistribution?, assess K+ excretion, assess acid-base status if increased; IF YES HTN: measure renin and aldosterone
38
Q

tx of hypokalemia

A

IV KCl (avoid NaHCO3 and glucose in IV solutions); if mild can use oral tx; give magnesium repletion (potassium-citrate if also have RTA)

39
Q

causes of true hypovolemic metabolic alkalosis & hypokalemia

A

loss of gastric secretions, diuretics, Bartter’s & Gitelman’s, calcium-alkali syndrome

40
Q

urine composition during generation phase of vomiting

A

low chloride, high concentrations of sodium and potassium being lost with bicarb (high pH)

41
Q

urine composition during maintenance phase of vomiting

A

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)

42
Q

tx of metabolic acidosis due to vomiting/nasogastric suction

A

normal saline +/- KCl (if concurrent hypokalemia)

43
Q

diuretic-induced metabolic alkalosis and hypokalemia

A

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)

44
Q

describe the defect in Bartter’s syndrome

A

defect in Na-K-2Cl transporter in thick ascending limb; acts like constant loop diuretic causing metabolic alkalosis, hypokalemia, normal BP

45
Q

describe the defect in Gitelman’s syndrome

A

defect in distal convoluted tubule at NaCl transport site; acts like a constant thiazide diuretic causing metabolic alkalosis, hypokalemia, normal BP

46
Q

why does calcium-alkali syndrome cause metabolic alkalosis and hypokalemia?

A

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)

47
Q

tx of calcium-alkali syndrome

A

normal saline to restore ECF and EABV to normal, prevent/reverse azotemia

48
Q

causes of metabolic alkalosis in setting of low EABV but high ECF

A

heart failure, cirrhosis, nephrotic syndrome

49
Q

tx of metabolic alkalosis in setting of low EABV but high ECF

A

normal saline WON’T work; use acetazolamide (carbonic anhydrase inhibitor) in severe cases to tx alkalosis

50
Q

what causes primary hyperaldosteronism?

A

adrenal tumors or hyperplasia

51
Q

why don’t pts with primary hyperaldosteronism have edema?

A

“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)

52
Q

when might urinalysis show high sodium but low chloride?

A

only during generation phase of vomiting, otherwise they track together

Urinary & Renal (22 decks)

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