Hyper/Hypo- kalemia

Question 1

2 mechanisms leading to hyperkalemia

Answer 1

redistribution from or into cells

decreased urinary excretion

Question 2

5 factors driving K into cells, hypokalemia

Answer 2

insulin, B2 stimulation, alkalosis, anabolism, hypoK periodic paralysis

Question 3

6 factors driving K out of cells, hyperK

Answer 3

insulin deficit, increased tonicity, cell injury, nonselective B blocker, alpha stimulation, mineral acidosis

Question 4

contrast mineral and organic acidosis w/ cellular K shift

Answer 4

mineral: causes hyperkalemia as H+ are exchanged for K+ to maintain neutrality, Cl- cant enter cell
organic: no hyperkalemia because organic anions can enter cell w/ H+, maintining neutrality w/o k+ exiting

Question 5

3 factors impairing K+ excretion

Answer 5

• more positive lumen
• low flow and Na delivery to CCD
• low aldo or aldo activity

Question 6

describe the effects of amiloride on CCD and pH/electrolytes

Answer 6

block ENaC channels:

• lumen more positive
• less K+ excretion (K sparing diuretic)
• higher serum K+
• less H+ secretion
• lower arterial pH

example of a hyperkalemic distal RTA, type IV

Question 7

risk factors for hyperkalemia

Answer 7

low eGFR

anything that interferes with RAAS- HIV, DM, meds like ACE inhibs, heparin, NSAIDs, ketoconazle

CHF

Question 8

causes of psueodhyperK, lab errors

Answer 8

hemolysis w/i tube, excess tourniquet, severe leukocytosis/thrombocytosis (plts clump and relaese K+ in tube)

Question 9

after ruling out a solely cellular redistribution cause of hyperK, what is the next step?

Answer 9

problem of low renal excretion:

• renal failure w/ low GFR
• low urine flow from hypovolemia
• hyperK distal RTA

Question 10

6 categories of hyperK distal RTA causes

Answer 10

interference w/ RAAS pathway or end target ENaC

1. impaired renin- HIV, DM, NSAIDs, tacrolimus
2. ACE inhibs
3. ARBs
4. impaired aldo metabolism- adrenal disease, heparin, ketoconazole
5. aldo receptor blockers- spironolactone and eplerinone
6. ENaC blockers- amiloride, triamterene, pentamidine (also pseudohypoaldo type I- loss of fn at ENaC)

Question 11

2 types of hypoaldo found in hyperK distal RTA

Answer 11

low renin- blocking RAAS upstream of renin release (DM, HIV, UTO, NSAIDs)

high renin- problem downstream of renin, up of aldo (ACEi, ARBs, heparin, adrenal insufficiency)

Question 12

what can make excess K intake a problem

Answer 12

w/o normal kidney fn, healthy kidney can excrete most excess K

salt subs, juice, clay, burnt matches, excess bananas can be problems

Question 13

describe the EKG changes from hyperK

Answer 13

tall peaked T wave w/ short QT at K=6, gets worse w/ higher K values, eventually lose p wave and have ventricular block then v-fib around K=9

causes by increased membrane potential, eventually this is above the threshold and no regulation against firing potentials

Question 14

protective therapy w/ EKG changes

Answer 14

IV Ca, brings threshold for depolariztion back above the membrane potential that has been elevated by high K

Question 15

3 categories of hyperK tx

Answer 15

stabilize Em: IV Ca

increase cellular entry: insulin, B2 agonist (albuterol), bicarb (w/ pH lower than 7.2)

K removal: dialysis, exchange resin (Na polystryrene sulfnonate), maybe loop/thiazide diuretics

Question 16

DDx of hypokalemia (3)

Answer 16

increased cell entry, low intake or GI loss, renal losses

Question 17

3 factors enhancing K+ renal excretion

Answer 17

more negative CCD lumen, more flow/Na delivery to CCD, more aldo

Question 18

how to distinguish b/w GI loss (and prior diuretic use), redistribution and kidney loss (or current diuretic use)

Answer 18

urine K/Cr ratio: K/Crx100

below 13-15= GI loss or redistribution

above 20= renal loss or current diuretics

Question 19

which diuretics/ syndromes cause hypoK

Answer 19

loop (bartters syndrome): less Na and K reabsorption at NKCC

thiazide (Gitelman): less Na reabsorb at NCC

both cause increase Na delivery and flow rate to CCD (more K secretion) and volume loss which stimulates RAAS, aldo to secrete more K

Question 20

what should be considered w/ hypoK w/o HTN

Answer 20

assess urinary K excretion w/ K/Cr ratio: distinguish b/w GI and renal losses

if renal, determine acid base status

• acid: RTA, toulene, DKA
• alkali: diuretics, vomiting, NG suction, Bartter/gitelman
• neutral: leukemia, polydipsia, tylenol OD

Question 21

what should be considered w/ hypoK w/ HTN

Answer 21

measure renin and aldo

high in both: renal HTN, renin tumor, malignant HTN

high aldo low renin: primary aldo

low both: SAME, Liddle, cushings

ALL w/ HTN will have alkalosis (either aldo or aldo effects cause more H+ secretion)

Question 22

tx of hypoK

Answer 22

hard to estimate K deficit, dont want to overshoot

give KCl 40-60 mEq at a time