Potassium Flashcards
what does Na/K ATPase do to electrochem potential
K in, but can’t then get back out
what does nernst equation tell us
transmembrane potential based on the [k] in and out of cell
what is normal potential
-90mV - negative inside compared to out
what is K role in action potential?
as it is pumped back into the cell, the action potential repolarizes
what happen in hypokalemia
Na permiability increases > membrane more excitable
what happen in hyperkalemia
Na permiability dec > membrane less excitable
effect of hyperkalemia on action potential (2)
1, resting potential closer to 0
2. conduction slowed
what are effects on heart, mucsle, brain on hyperkalemia
heart - heart slows down,
muscle - weakness and stiffness
brain - minimal
what are effects on heart, mucsle, brain on hypokalemia
heart - premature beats, tachy
muscle - weakness and breakdown
brain - minimal
where is most body K
in ICF - 99%
3 relevant K transporters in cells
- Na in/ H out is stimulated by insulin
- Na/K ATPase, stimulated by high ICF Na or Beta-2
- K in/ H out pump
what is effect of cells death/buiding on K
lysis - K into blood, buiding uses up K
what is effect of acid-base on K
- HCO3- in ECF, pulls H out and K in
2. HCl in ECF, pushes H into cell and K out
what happens to K in lactic acid
H enters the cell, but so does lactate, so K is not changed
average K intake
50-150 mmol
how does aldosterone reg K
- in CCD adosterone inserts eNaC into lumenal membrane
- Na reabsorbed faster than Cl leaving lumen -ve
- K secretion into lumen favored
- K washed away by flow
2 stim for aldosterone release
- K levels
2. angiotensin 2
2 responses to ingested K
- acute - eat and insulin released which pulls K into cells
2. chronic - slightly higher ECF K leads to aldosterone release
3 causes of hyperkalemia
- high intake
- shift K out of cells
- failure of renal excretion
ways of k intake having negative effect
- usually okay because excreted
2. can cause problems if there are other issue
4 ways K can be shifted out of cells
- insulin def
- hyperglycemia - pull water out of muscle and K follows
- beta-blockers
- widespread cell death
2 ways of reduced renal excretion
- lower flow through CCD - renal failure
2. lowered secretion - hypoaldosteronism, aldo antagonists, tubular disease
2 mechs behind hypoaldosteronism
- loss of signal - problem with RAAS
2. adrenal disease
3 antagonists of aldosterone (K sparing diuretics)
- spironolactone - aldo receptor antagonist
- triamterine, amiloride - Na channel blocker
- trimethoprim - antibiotic that acts like amiloride
4 treatments of hyperkalemia
- antagonize adverse effects of K - calcium gluconate
- shift K into cells - insulin and glucose
- increase urine K - non- K sparing diuretics
- reduce K intake
3 causes of K deficiency
- reduced intake - rare
- shift into cells
- excess elim (gut or urine)
3 causes of shift into cells
- insulin
- giving NaHCO3 (base)
- Beta 2 stim
2 GI losses
- diarrhea
2. vomiting - via bicarbonaturia
2 causes of urine losses
- high flow through CCD
2. high K secretion - bicarbonaturia, hyperaldosterone
how does vomiting cause bicarbonaturia
- rise in HCO3- as lose HCl
- increases flow through CCD and pulls water with it
- increased K secretion in CCD as HCO3- make lumen more neg.
what is primary hyperaldo
tumor makes aldo in unregulated way
Sx of hyperaldo
- high ECF
- hypertension
- hypokalemia
causes of secondary hyperaldo
- high renin
- high angiotensin
- high aldo
what happens to plasma [k] in PT with ECF vol depletion
no change - proximal water absorb causes CCD flow down which evens it out
what happens to [k] in PT with high salt diet
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
treatment of hypokalemia (3)
- treat underlying cause
- prevent further loss - k sparing diuretics
- replace K
