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
what 2 factors enhance K+ efflux out of the K+ cells (known as reabsorption)
1. hyperosmolality 2. strenuous exercise Note: strenuous exercise is also a stimulus for hypOnatremia (low plasma Na+)
26
how does hypErosmolality contribute to K+ efflux from cells
ICF contraction and high intracellular [K+]
27
how does strenuous exercise contribute to K+ efflux from cells
+ alpha-catecholamines which inhibit cell uptake therefore K+ goes away from cells
28
ADH affect on K+
increase K+ secretion via Na+ reabsorption via K+ channel stimulation (adds K+ channels)
29
luminal flow rate affect on K+
increase K+ secretion
30
Alkalosis affect on K+
increase K+ secretion
31
glucocorticoids affect on K+
increase K+ secretion via binding of mineralcorticoid receptor increase GFR increase Tubular flow rate (TFR)
32
anion delivery affect on K+
increase K+ secretion how: acts as osmotic diuretic increases Tubular flow rate (TFR) impacts electrochemical differences
33
acidosis affect on K+
decrease K+ secretion
34
total body K+
3500 mEq
35
equation for K+ filtered load
K filtered load = GFR x Plasma [K+] x % filterability
36
equation for GFR when you are given filtered fraction
GFR = filtered fraction x RBF
37
equation for GFR if you are given Kf
GFR = Kf x Puf note: Kf = Lf x Sf
38
equation for GFR if GFR = clearance
GFR = Cx = Ux * V _______ Px
39
what substances are filtered and reabsorbed in the PT
``` ***K+ water Cl- HCO3- Ca2+ Pi glucose (100%) amino acids (100%) ```
40
what is secreted in the PT
``` organic anions organic cations (metabolites, creatinine, urate, drugs) ```
41
major mechanism facilitating movement of substances in the PT
Na/K ATPase pump | located in basolateral membrane
42
compare K+ and Na+ reabsorption in PT
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
how does TEPD change from the early to the late PT
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
how does K+ move in the PT
moves paracellularly to be reabsorbed
45
what 2 substances are always reabsorbed together
Na+ and HCO3-
46
how is the medullary presence of K+ increased (4 steps)
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
how does increased medullary K+ affect NKCC2
lots of medullary K+ decreases NKCC2 reabsorption
48
where is the NKCC2 located
TAL
49
how does increased medullary K+ affect Na+
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
what determines whether K+ is secreted or absorbed in the late DT and Cortical CD
the body's needs
51
where does K+ "fine-tuning" occur
late DT | cortical CD
52
Function of principal cells
secrete K+ (to tubular fluid to be excreted in urine)
53
what channels are found in principal cells
Na/K ATPase pump (basolateral) ENaC (apical/luminal) BK="big" K+ channel (apical) ROMK = renal outer medullary K+ channel (apical)
54
function of beta-intercalated cells
secrete K+ (to tubular fluid to be excreted in urine)
55
what channels are found in B-intercalated cells
H+ ATPase (basolateral) H+/K+ ATPase (basolateral) Cl- channel (basolateral) HCO3-/Cl- antiporter (apical) K+ channel (apical)
56
what is REABSORBED in B-intercalated cells
Cl- | H+
57
what is SECRETED in B-intercalated cells
HCO3- | K+
58
where does the HCO3- that is secreted by B-intercalated come from
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
3 most important factors that stimulate K+ secretion
1. increased ECF [K+] ******#1 factor 2. aldosterone 3. increased tubular flow rate
60
what channels are found in A-intercalated cells
HCO3-/Cl- antiporter (basolateral) K+ channel (basolateral) H+ ATPase pump (apical) H+/K+ ATPase pump (apical) Cl- channel (apical)
61
function of A-intercalated cells
REABSORB K+ (back into the bloodstream which will increase plasma K+)
62
what is REABSORBED in A-intercalated cells
K+ | HCO3-
63
what is SECRETED in A-intercalated cells
H+ | Cl-
64
3 most important factors that stimulate K+ reabsorption
1. K+ deficiency (hypOlakemia) 2. low diet K+ 3. K+ loss via severe diarrhea (must be very significant to cause change)
65
What is SECRETED in principal cells
K+
66
what is REABSORBED in principal cells
Na+ | H2O
67
How is K+ secretion regulated
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
how does increasing DT flow rate impact K+ secretion
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
what happens to the concentration gradient if you decrease flow rate
K+ secretion slows down
70
alkalosis vs alkalemia
alkalosis pertains to the ECF | alkalemia pertains to the blood pH and is the physiologic response)
71
alkalosis
low [H+] in the ECF
72
alkalemia
high blood pH (bc low concentration of H+ therfore basic)
73
how does acute alkalosis (dealing w/the ECF) affect K+ levels
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
how does acute acidosis (dealing w/the ECF) affect K+ levels
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
acidosis (ECF)
high [H+] concentration in the ECF
76
acidemia (physiologic)
physiological low blood pH (acidic)
77
normal vs acidotic and alkolotic pH levels
``` normal = 7.41 acidotic = 7.17 alkalotic = 7.57 ```
78
which acute process is associated with K+ secretion -- alkalemia or acidemia
alkalemia (need to increase H+ reabsorption which will increase K+ secretion) H+/K+ ATPase pump in B-intercalated cells
79
what does chronic acidosis to do K+
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
opposing factors in acidosis that stabilize K+ secretion
(--) low intracellular [K+] - paired with- (++) low PT reabsorption & high distal flow
81
opposing factors in volume explansion that stabilize K+ secretion
(--) low aldosterone -paired with- (++) low PT reabsorption & high distal flow
82
opposing factors in water diuresis that stabilize K+ secretion (high water intake)
(--) low ADH - paired with - (++) low DT reabsorption & high distal flow
83
opposing factors in volume contraction that stabilize K+ secretion (review slide 30)
(--) low GFR & low distal flow - paired with - (++) high renin & high Ang II & high aldosterone
84
which K+ status induces aldosterone secretion
hyperkalemia
85
aldosterone paradox
sodium balance can be maintained without effects on K+ homeostasis ex: dietary Na restriction ex: marked induction of aldosterone
86
effect of diuretics on Na+ and K+
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
effect of K+ sparing drugs
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.