Potassium

Question 1

what does Na/K ATPase do to electrochem potential

Answer 1

K in, but can’t then get back out

Question 2

what does nernst equation tell us

Answer 2

transmembrane potential based on the [k] in and out of cell

Question 3

what is normal potential

Answer 3

-90mV - negative inside compared to out

Question 4

what is K role in action potential?

Answer 4

as it is pumped back into the cell, the action potential repolarizes

Question 5

what happen in hypokalemia

Answer 5

Na permiability increases > membrane more excitable

Question 6

what happen in hyperkalemia

Answer 6

Na permiability dec > membrane less excitable

Question 7

effect of hyperkalemia on action potential (2)

Answer 7

1, resting potential closer to 0

2. conduction slowed

Question 8

what are effects on heart, mucsle, brain on hyperkalemia

Answer 8

heart - heart slows down,
muscle - weakness and stiffness
brain - minimal

Question 9

what are effects on heart, mucsle, brain on hypokalemia

Answer 9

heart - premature beats, tachy
muscle - weakness and breakdown
brain - minimal

Question 10

where is most body K

Answer 10

in ICF - 99%

Question 11

3 relevant K transporters in cells

Answer 11

1. Na in/ H out is stimulated by insulin
2. Na/K ATPase, stimulated by high ICF Na or Beta-2
3. K in/ H out pump

Question 12

what is effect of cells death/buiding on K

Answer 12

lysis - K into blood, buiding uses up K

Question 13

what is effect of acid-base on K

Answer 13

1. HCO3- in ECF, pulls H out and K in

2. HCl in ECF, pushes H into cell and K out

Question 14

what happens to K in lactic acid

Answer 14

H enters the cell, but so does lactate, so K is not changed

Question 15

average K intake

Answer 15

50-150 mmol

Question 16

how does aldosterone reg K

Answer 16

1. in CCD adosterone inserts eNaC into lumenal membrane
2. Na reabsorbed faster than Cl leaving lumen -ve
3. K secretion into lumen favored
4. K washed away by flow

Question 17

2 stim for aldosterone release

Answer 17

1. K levels

2. angiotensin 2

Question 18

2 responses to ingested K

Answer 18

1. acute - eat and insulin released which pulls K into cells

2. chronic - slightly higher ECF K leads to aldosterone release

Question 19

3 causes of hyperkalemia

Answer 19

1. high intake
2. shift K out of cells
3. failure of renal excretion

Question 20

ways of k intake having negative effect

Answer 20

1. usually okay because excreted

2. can cause problems if there are other issue

Question 21

4 ways K can be shifted out of cells

Answer 21

1. insulin def
2. hyperglycemia - pull water out of muscle and K follows
3. beta-blockers
4. widespread cell death

Question 22

2 ways of reduced renal excretion

Answer 22

1. lower flow through CCD - renal failure

2. lowered secretion - hypoaldosteronism, aldo antagonists, tubular disease

Question 23

2 mechs behind hypoaldosteronism

Answer 23

1. loss of signal - problem with RAAS

2. adrenal disease

Question 24

3 antagonists of aldosterone (K sparing diuretics)

Answer 24

1. spironolactone - aldo receptor antagonist
2. triamterine, amiloride - Na channel blocker
3. trimethoprim - antibiotic that acts like amiloride

Question 25

4 treatments of hyperkalemia

Answer 25

1. antagonize adverse effects of K - calcium gluconate 2. shift K into cells - insulin and glucose 3. increase urine K - non- K sparing diuretics 4. reduce K intake

Question 26

3 causes of K deficiency

Answer 26

1. reduced intake - rare 2. shift into cells 3. excess elim (gut or urine)

Question 27

3 causes of shift into cells

Answer 27

1. insulin 2. giving NaHCO3 (base) 3. Beta 2 stim

Question 28

2 GI losses

Answer 28

1. diarrhea | 2. vomiting - via bicarbonaturia

Question 29

2 causes of urine losses

Answer 29

1. high flow through CCD | 2. high K secretion - bicarbonaturia, hyperaldosterone

Question 30

how does vomiting cause bicarbonaturia

Answer 30

1. rise in HCO3- as lose HCl 2. increases flow through CCD and pulls water with it 3. increased K secretion in CCD as HCO3- make lumen more neg.

Question 31

what is primary hyperaldo

Answer 31

tumor makes aldo in unregulated way

Question 32

Sx of hyperaldo

Answer 32

1. high ECF 2. hypertension 3. hypokalemia

Question 33

causes of secondary hyperaldo

Answer 33

1. high renin 2. high angiotensin 3. high aldo

Question 34

what happens to plasma [k] in PT with ECF vol depletion

Answer 34

no change - proximal water absorb causes CCD flow down which evens it out

Question 35

what happens to [k] in PT with high salt diet

Answer 35

no change - high volume leads to low resorption of water and high CCD flow which leads to maintained K loss even though aldo is low

Question 36

treatment of hypokalemia (3)

Answer 36

1. treat underlying cause 2. prevent further loss - k sparing diuretics 3. replace K