Potassium Flashcards

1
Q

what does Na/K ATPase do to electrochem potential

A

K in, but can’t then get back out

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2
Q

what does nernst equation tell us

A

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

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3
Q

what is normal potential

A

-90mV - negative inside compared to out

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4
Q

what is K role in action potential?

A

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

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5
Q

what happen in hypokalemia

A

Na permiability increases > membrane more excitable

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6
Q

what happen in hyperkalemia

A

Na permiability dec > membrane less excitable

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7
Q

effect of hyperkalemia on action potential (2)

A

1, resting potential closer to 0

2. conduction slowed

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8
Q

what are effects on heart, mucsle, brain on hyperkalemia

A

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

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9
Q

what are effects on heart, mucsle, brain on hypokalemia

A

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

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10
Q

where is most body K

A

in ICF - 99%

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11
Q

3 relevant K transporters in cells

A
  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
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12
Q

what is effect of cells death/buiding on K

A

lysis - K into blood, buiding uses up K

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13
Q

what is effect of acid-base on K

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

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

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14
Q

what happens to K in lactic acid

A

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

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15
Q

average K intake

A

50-150 mmol

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16
Q

how does aldosterone reg K

A
  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
17
Q

2 stim for aldosterone release

A
  1. K levels

2. angiotensin 2

18
Q

2 responses to ingested K

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

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

19
Q

3 causes of hyperkalemia

A
  1. high intake
  2. shift K out of cells
  3. failure of renal excretion
20
Q

ways of k intake having negative effect

A
  1. usually okay because excreted

2. can cause problems if there are other issue

21
Q

4 ways K can be shifted out of cells

A
  1. insulin def
  2. hyperglycemia - pull water out of muscle and K follows
  3. beta-blockers
  4. widespread cell death
22
Q

2 ways of reduced renal excretion

A
  1. lower flow through CCD - renal failure

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

23
Q

2 mechs behind hypoaldosteronism

A
  1. loss of signal - problem with RAAS

2. adrenal disease

24
Q

3 antagonists of aldosterone (K sparing diuretics)

A
  1. spironolactone - aldo receptor antagonist
  2. triamterine, amiloride - Na channel blocker
  3. trimethoprim - antibiotic that acts like amiloride
25
Q

4 treatments of hyperkalemia

A
  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
26
Q

3 causes of K deficiency

A
  1. reduced intake - rare
  2. shift into cells
  3. excess elim (gut or urine)
27
Q

3 causes of shift into cells

A
  1. insulin
  2. giving NaHCO3 (base)
  3. Beta 2 stim
28
Q

2 GI losses

A
  1. diarrhea

2. vomiting - via bicarbonaturia

29
Q

2 causes of urine losses

A
  1. high flow through CCD

2. high K secretion - bicarbonaturia, hyperaldosterone

30
Q

how does vomiting cause bicarbonaturia

A
  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.
31
Q

what is primary hyperaldo

A

tumor makes aldo in unregulated way

32
Q

Sx of hyperaldo

A
  1. high ECF
  2. hypertension
  3. hypokalemia
33
Q

causes of secondary hyperaldo

A
  1. high renin
  2. high angiotensin
  3. high aldo
34
Q

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

A

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

35
Q

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

A

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

36
Q

treatment of hypokalemia (3)

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