potassium + discussion grp

what is the life-threatening range of potassium

>6 and <2

what common hormone/medication can affect potassium, what does it do to potassium

insulin; drives K into the cells indirectly by stimulating Na-H antiporter and directly by stimulating Na-K-ATPase

explain what is happening to potassium in the nephron tubules

majority is being reabsorbed except at the very end in the collecting duct where 2-5% of K is secreted in exchange for Na reabsorption via aldosterone

what are the four most common “shifts” of K to leave the cell

• hyperglycemia

• cell necrosis

• fasting

• acidosis

how does hyperglycemia cause a K shift out of the cells

inc osmolarity in the ECS draws water out of the cells, and K follows by solvent drag

how does cell necrosis cause a K shift out of the cell

potassium is normally contained but with necrotic cells/tissues, the barriers won’t funx properly so there is not regulation of K leaving the cell

how does fasting cause K shift out of the cell

dec basal insulin levels, reduces insulin-stimulated intracellular K uptake; insulin usually pushes K in the cells, so low insulin will result in higher K out of the cells

how does acidosis cause K shift out of the cell

in some forms of acidosis, H ions move intracellularly in exchange for K ions

what is the rationale for tx of hypertension w diuretics

diuretics enhance sodium loss causing small volume depletion that is enough to ease the resistance in the arteries → can result in a dec of BP for some people

what is the most common used diuretic

thiazide (hydrochlorothiazide)

where do thiazide diuretics act in the nephron

DCT to dec sodium reabsorption

if thiazide is one of the more common diuretics, when would you use furosemide- a loop diuretic

reserved for acute conditions like inc edema w congestive heart failure, or in cases of resistant edema→ nephrotic syndrome; inc urine output and dec pressure

what is the most common side effect of thiazides

hypokalemia

what can hypokalemia lead to

arrhythmias→ fatal arrhythmias

besides hypokalemia, what are other side effects of thiazide

• too much diuresis → too much volume depletion

• poor perfusion to kidney → “pre-renal” uremia

• hyperglycemia

• gout

what are the two main mechanisms of hypokalemia due to thiazides

• since Na reabsorption is inhibited in DCT → inc Na delivered downstream → more exchange of K secretion and Na reabsorption in collecting duct via principal cells

• thiazides cause volume contraction → inc aldosterone → K excretion in the urine

what are the potassium sparing diuretics

• amiloride

• triamterene

• spironolactone eplerenone

how do potassium sparing diuretics work

prevent K loss in the urine by inhibiting Na absorption and K secretion in the CCD and block actions of aldosterone

how can hypokalemia be managed

w oral potassium supplements, or if you need to prevent renal loss → K sparing diuretics, these can be paired w potassium wasting meds sometimes too

common symptoms of volume depletion

orthostatic hypotension, tachycardia, poor skin turgor

how to tell on a basic metabolic panel if a pt is volume depleted

BUN:creatinine ratio is greater than 20:1 but not always a dependable finding

what is Addison’s disease

an autoimmune disease that cripples the adrenal glands, causes low aldosterone (hypoaldosteronism) which will cause hyperkalemia