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Renal Test 2 > Regulating K+ Balance > Flashcards

Regulating K+ Balance Flashcards

1
Q

normal K+ value in blood

A

3.5-5.0 mEq/L

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2
Q

where is the highest amt of K+ found in the body

A

muscle (2700 mEq)

followed by:
bone
liver
RBCs

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3
Q

major route of K+ loss in the body

A

major: urine
minor: feces

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4
Q

value for hypokalemia

A

<3.7 mEq/L

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5
Q

causes of hypokalemia

A

loss of GI fluids
high insulin
*alkalosis

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6
Q

value for hyperkalemia

A

> 5.2 mEq/L

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7
Q

value for lethal hyperkalemia

A

> 10 mEq/L

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8
Q

causes of hyperkalemia

A 
high K+ dietary intake
burns
rhabdomyolysis
hemolysis
acidosis
tissue damage
low insulin
hyperglycemia
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9
Q

pseudohyperkalemia

A

falsely high K+ levels

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10
Q

cause of pseudohyperkalemia

A

RBC lysis during blood draw

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11
Q

how does hyperkalemia affect cardiac cells

A

decreases firing, leading to hyperpolarization and bradycardia

Note: cardiac cells match the name (hypErkalemia and hypErpolarization)

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12
Q

how does hyperkalemia affect other cells

A

leads to hypopolarization

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13
Q

how does hypokalemia affect cardiac cells

A

increases firing, leading to hypopolarization, and tachycardia

Note: cardiac cells match the name (hypOkalemia and hypOpolarization)

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14
Q

how does hypokalemia affect other cells

A

hyperpolarization

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15
Q

role of epinephrine on K+ in the body

A

lowers serum K+

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16
Q

how does epinephrine alter K+ levels in the serum

A

stimulating K+ uptake into kidney cells/tissues causing K+ excretion into the urine

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17
Q

role of insulin on K+ in the body

A

stimulates Na/K ATPase
K+ influx into kidney cells
Na+efflux to interstitium/blood

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18
Q

treatment for hyperkalemia and how it works

A

Tx: insulin

Remember: Hyperkalemia is high plasma K+

How: Insulin moves K+ out of blood and into the kidney cells/TF to be excreted from body

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19
Q

role of aldosterone on K+ in the body (3 things)

A

renal: increases K+ excretion (lowers plasma K+)

extra-renal: increases K+ secretion into intestinal fluids & saliva

enhances acid excretion via alkalosis

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20
Q

what 3 factors enhance K+ uptake into the K+ cells (known as secretion)

A
  1. insulin
  2. B-catacholamines
  3. alkalosis (“K is lo”)
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21
Q

what channel/pump does insulin work on to decrease plasma K+ levels

A

Na/K ATPase pump

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22
Q

what channel/pump do B-catecholamines work on to enhance K+ uptake into renal cells/TF

A

Na/K ATPase pump via cAMP

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23
Q

what 3 factors impair K+ uptake into the K+ cells

A
  1. alpha-catecholamines
  2. acidosis
  3. cell damage
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24
Q

how does acidosis impair K+ uptake into cells

A

inhibition of Na/K ATPase (Donnan Effect)

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25
Q

what 2 factors enhance K+ efflux out of the K+ cells (known as reabsorption)

A
  1. hyperosmolality
  2. strenuous exercise

Note: strenuous exercise is also a stimulus for hypOnatremia (low plasma Na+)

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26
Q

how does hypErosmolality contribute to K+ efflux from cells

A

ICF contraction and high intracellular [K+]

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27
Q

how does strenuous exercise contribute to K+ efflux from cells

A

+ alpha-catecholamines which inhibit cell uptake therefore K+ goes away from cells

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28
Q

ADH affect on K+

A

increase K+ secretion

via Na+ reabsorption
via K+ channel stimulation (adds K+ channels)

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29
Q

luminal flow rate affect on K+

A

increase K+ secretion

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30
Q

Alkalosis affect on K+

A

increase K+ secretion

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31
Q

glucocorticoids affect on K+

A

increase K+ secretion

via binding of mineralcorticoid receptor
increase GFR
increase Tubular flow rate (TFR)

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32
Q

anion delivery affect on K+

A

increase K+ secretion

how:
acts as osmotic diuretic
increases Tubular flow rate (TFR)
impacts electrochemical differences

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33
Q

acidosis affect on K+

A

decrease K+ secretion

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34
Q

total body K+

A

3500 mEq

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35
Q

equation for K+ filtered load

A

K filtered load = GFR x Plasma [K+] x % filterability

36
Q

equation for GFR when you are given filtered fraction

A

GFR = filtered fraction x RBF

37
Q

equation for GFR if you are given Kf

A

GFR = Kf x Puf

note: Kf = Lf x Sf

38
Q

equation for GFR if GFR = clearance

A

GFR = Cx = Ux * V
_______
Px

39
Q

what substances are filtered and reabsorbed in the PT

A 
***K+
water
Cl-
HCO3-
Ca2+
Pi
glucose (100%)
amino acids (100%)
40
Q

what is secreted in the PT

A 
organic anions
organic cations (metabolites, creatinine, urate, drugs)
41
Q

major mechanism facilitating movement of substances in the PT

A

Na/K ATPase pump

located in basolateral membrane

42
Q

compare K+ and Na+ reabsorption in PT

A

K+ and Na+ reabsorption is similar in the PT

*no direct role on K+ balance. only an INDIRECT role for what happens with K+ later in the nephron

43
Q

how does TEPD change from the early to the late PT

A

early PT (PCT) has a NEGATIVE TEPD bc Na+ is reabsorbed first leaving Cl- behind

the buildup of NEG TEPD repels Cl- OUT of the cell to be reabsorbed

Na+ combines with Cl- to make NaCl (salt)

water follows the salt and a POSITIVE TEPD builds up in the late PT (straight tubule)

POSITIVE TEPD repels K+ out of the cell to be reabsorbed

44
Q

how does K+ move in the PT

A

moves paracellularly to be reabsorbed

45
Q

what 2 substances are always reabsorbed together

A

Na+ and HCO3-

46
Q

how is the medullary presence of K+ increased (4 steps)

A
  1. K+ secreted into cortical collecting duct
    (travels down deeper down the CD)
  2. K+ reabsorbed by OMCD and IMCD
    (now K+ floating in interstitium)
  3. K+ floats in the interstitium all the way over to the PT
  4. K+ secreted back into the TF of the LATE PD/Des LoH
47
Q

how does increased medullary K+ affect NKCC2

A

lots of medullary K+ decreases NKCC2 reabsorption

48
Q

where is the NKCC2 located

A

TAL

49
Q

how does increased medullary K+ affect Na+

A

lots of medullary K+ triggers Na+ reabsorption and K+ excretion

+enhance Na delivery to the distal tubule

*you have enough K+ in the interstitium/blood so you don’t need to reabsorb any more. In order to secrete K+ in to the TF to be excreted into the urine, you need to reabsorb Na+

50
Q

what determines whether K+ is secreted or absorbed in the late DT and Cortical CD

A

the body’s needs

51
Q

where does K+ “fine-tuning” occur

A

late DT

cortical CD

52
Q

Function of principal cells

A

secrete K+ (to tubular fluid to be excreted in urine)

53
Q

what channels are found in principal cells

A

Na/K ATPase pump (basolateral)

ENaC (apical/luminal)
BK=”big” K+ channel (apical)
ROMK = renal outer medullary K+ channel (apical)

54
Q

function of beta-intercalated cells

A

secrete K+ (to tubular fluid to be excreted in urine)

55
Q

what channels are found in B-intercalated cells

A

H+ ATPase (basolateral)
H+/K+ ATPase (basolateral)

Cl- channel (basolateral)

HCO3-/Cl- antiporter (apical)
K+ channel (apical)

56
Q

what is REABSORBED in B-intercalated cells

A

Cl-

H+

57
Q

what is SECRETED in B-intercalated cells

A

HCO3-

K+

58
Q

where does the HCO3- that is secreted by B-intercalated come from

A

CO2 diffuses into the B-intercalated cell
v
CO2 combines with H2O to form carbonic acid (H2CO3)
v
H2CO3 dissociates into H+ and bicarbonate (HCO3-)
v
the HCO3- is secreted into the tubular lumen via the HCO3-/Cl- antiporter
v
the H+ is reabsorbed into the blood via the H+ATPase and the H+/K+ ATPase

59
Q

3 most important factors that stimulate K+ secretion

A
  1. increased ECF [K+] ****#1 factor
  2. aldosterone
  3. increased tubular flow rate
60
Q

what channels are found in A-intercalated cells

A

HCO3-/Cl- antiporter (basolateral)
K+ channel (basolateral)

H+ ATPase pump (apical)
H+/K+ ATPase pump (apical)
Cl- channel (apical)

61
Q

function of A-intercalated cells

A

REABSORB K+ (back into the bloodstream which will increase plasma K+)

62
Q

what is REABSORBED in A-intercalated cells

A

K+

HCO3-

63
Q

what is SECRETED in A-intercalated cells

A

H+

Cl-

64
Q

3 most important factors that stimulate K+ reabsorption

A
  1. K+ deficiency (hypOlakemia)
  2. low diet K+
  3. K+ loss via severe diarrhea (must be very significant to cause change)
65
Q

What is SECRETED in principal cells

A

K+

66
Q

what is REABSORBED in principal cells

A

Na+

H2O

67
Q

How is K+ secretion regulated

A
  1. high ECF [K+] *****
  2. Na/K ATPase (basolateral side)
  3. reduced K+ back-leakage of K+ from ICF –> interstitium
  4. Adding K+ channesl into apical/luminal membrane
  5. increase aldosterone secretion
  6. increase DT flow rate
68
Q

how does increasing DT flow rate impact K+ secretion

A

increasing DT flow rate –> dilutes tubular lumen K+–> increases the [K+] gradient –>K+ washed away –> increase Na to the DT for reabsorption –> K+ SECRETION

69
Q

what happens to the concentration gradient if you decrease flow rate

A

K+ secretion slows down

70
Q

alkalosis vs alkalemia

A

alkalosis pertains to the ECF

alkalemia pertains to the blood pH and is the physiologic response)

71
Q

alkalosis

A

low [H+] in the ECF

72
Q

alkalemia

A

high blood pH (bc low concentration of H+ therfore basic)

73
Q

how does acute alkalosis (dealing w/the ECF) affect K+ levels

A

low [H+] leads to increased activity of Na/K ATPase pump

increased [K+]i

increased passive diffusion of K+ into TF/lumen

increased K+ channels

increased K+ secretion –> excretion in urine

Final result: HYPOKALEMIA (K+ is “lo” in the blood)

74
Q

how does acute acidosis (dealing w/the ECF) affect K+ levels

A

high [H+] leads to decreased activity of Na/K ATPase pump

decreased [K+]i

decreased passive diffusion of K+ into TF/lumen

decreased K+ channels

decreased K+ secretion –> K+ retained in blood

Final result: HYPERKALEMIA (high K+ levels in the blood)

75
Q

acidosis (ECF)

A

high [H+] concentration in the ECF

76
Q

acidemia (physiologic)

A

physiological low blood pH (acidic)

77
Q

normal vs acidotic and alkolotic pH levels

A 
normal = 7.41
acidotic = 7.17
alkalotic = 7.57
78
Q

which acute process is associated with K+ secretion – alkalemia or acidemia

A

alkalemia

(need to increase H+ reabsorption which will increase K+ secretion)

H+/K+ ATPase pump in B-intercalated cells

79
Q

what does chronic acidosis to do K+

A

stimulates K+ secretion (more excretion in the urine)

How?

  • decrease water reabsorption in PT
  • inhibits Na/K ATPase pump
  • increase RTF to DT and CD
  • stimulates RAAS (bc of low water reabsorption/low ECFV)
80
Q

opposing factors in acidosis that stabilize K+ secretion

A

(–) low intracellular [K+]
- paired with-
(++) low PT reabsorption & high distal flow

81
Q

opposing factors in volume explansion that stabilize K+ secretion

A

(–) low aldosterone
-paired with-
(++) low PT reabsorption & high distal flow

82
Q

opposing factors in water diuresis that stabilize K+ secretion

(high water intake)

A

(–) low ADH
- paired with -
(++) low DT reabsorption & high distal flow

83
Q

opposing factors in volume contraction that stabilize K+ secretion
(review slide 30)

A

(–) low GFR & low distal flow
- paired with -
(++) high renin & high Ang II & high aldosterone

84
Q

which K+ status induces aldosterone secretion

A

hyperkalemia

85
Q

aldosterone paradox

A

sodium balance can be maintained without effects on K+ homeostasis

ex: dietary Na restriction
ex: marked induction of aldosterone

86
Q

effect of diuretics on Na+ and K+

A

they inhibit Na+ reabsorption and promote K+ secretion

  • loop and thiazide diuretics increase Na+ delivery to the distal segment of the distal tubule
  • this increases K+ loss (potentially causing hypokalemia)
  • the increase in distal tubular Na+ concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine.
  • increased hydrogen ion loss can lead to metabolic alkalosis
87
Q

effect of K+ sparing drugs

A

spare K+ from being excreted without messing w/Na

ex: spironolactone

mechanism:
antagonize the actions of aldosterone (aldosterone receptor antagonists) at the distal segment of the distal tubule. This causes more sodium (and water) to pass into the collecting duct and be excreted in the urine. They are called K+-sparing diuretics because they do not produce hypokalemia like the loop and thiazide diuretics. The reason for this is that by inhibiting aldosterone-sensitive sodium reabsorption, less potassium and hydrogen ion are exchanged for sodium by this transporter and therefore less potassium and hydrogen are lost to the urine. Other potassium-sparing diuretics directly inhibit sodium channels associated with the aldosterone-sensitive sodium pump, and therefore have similar effects on potassium and hydrogen ion as the aldosterone antagonists.

Renal Test 2 (9 decks)

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