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MSS Renal Exam 2 > Regulation of K, Ca, PO4, and Mg > Flashcards

Regulation of K, Ca, PO4, and Mg Flashcards

1
Q

high aldosterone

A

can feedback to cut off renin release

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2
Q

aldosterone release?

A

adrenal gland

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3
Q

normal range of K

A

3.5 - 5

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4
Q

hyperkalemia

A

more excitable
-raises RMP

ventricular fib

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5
Q

hypokalemia

A

less excitable
-decreased RMP

low T wave ST depression

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6
Q

K distribution in body

A

higher in ICF

-muscle, liver, RBCs

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7
Q

insulin

A

stimulates K move into ICF

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8
Q

epinephrine

A

stimulates K move into ICF

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9
Q

renal K handling?

A

67% reabsorbed proximal tubule
20% reabsorbed TAL (Na/K/2Cl cotransport)

physiological control in collecting duct
-principal cells reabsorb or secrete

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10
Q

dietary K depletion

A

reabsorption DT and CD

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11
Q

normal or increased K

A

secreted DT and CD

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12
Q

principal cells in CD mechanism?

A

Na/K ATPase

  • negative luminal potential
  • attracts K to lumen
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13
Q

factors affecting K secretion in collecting duct

A 
extracellular [K+]
negative luminal potential
luminal flow rate (increase flow)
extracellular pH - K/H exchanger
aldosterone - stimulates K secretion
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14
Q

aldosterone and K

A

stimulates K secretion

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15
Q

luminal fluid flow rate

A

diuretic state increases flow

  • washes out gradient
  • increased secretion
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16
Q

acidema

A

increases K/H exchanger

  • more H out of cell
  • more K into cell

leads to hyperkalemia**

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17
Q

alkalemia

A

-H into cell, K out of cell

leads to hypokalemia**

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18
Q

hyperkalemia

A

leads to aldosterone release

-Na and K exchange to maintain electroneutrality

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19
Q

urinary K secretion

A

increases with plasma K increase

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20
Q

low sodium diet

A

may lead to hyperkalemia

  • less Na to DT and CD
  • less reabsorption, therefore less K secretion
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21
Q

diuretics

A

may lead to hypokalemia

-most classes increase Na and volume reabsorption, increasing K secretion

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22
Q

tubular flow rate?

A

increases flow rate results in more K secretion

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23
Q

pH affect on K?

A 
increased pH (alkalosis) increases K secretion
decreased pH (acidosis) decreased K secretion
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24
Q

collecting duct principal cells?

A

Na/K exchanger

H/K exchanger

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25
Q

major stimuli for aldosterone release?

A

hyperkalemia

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26
Q

aldosterone mechanism

A

more Na and K channels on luminal membrane

increase Na/K ATPase activity

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27
Q

Conns disease

A

primary hyperaldosteronism
-tumor in adrenal cortex

leads to hypokalemia
-high K secretion

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28
Q

Addisons disease

A

destruction of adrenal gland
-hypoaldosteronism

decreased K secretion
-hyperkalemia

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29
Q

why no hypernatremia in hyperaldosteronism?

A

water follows Na

-therefore, body sense increased volume and increase Na excretion

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30
Q

diuretics

A

drugs that increase urine excretion
-inhibit solute and water reabsorption

to help eliminate excess volume
ex/ edema and CHF

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31
Q

osmotic diuretic

A

ex/ mannitol

inhibit reabsorption of water and secondarily Na
-proximal tubule

leads to downstream increase in reabsorption
therefore, they don’t work too well

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32
Q

mannitol

A

osmotic diuretics

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33
Q

carbon anhydrase inhibitor

A

ex/ acetazolamide

inhibit NaHCO3- reabsorption
-proximal tubule

altitude sickness

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34
Q

acetazolamide

A

carbonic anhydrase inhibitor

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35
Q

loop diuretics

A

ex/ furosemide (lasix), bumetanide (bumex), ethacrynic acid

inhibit Na/K/2Cl cotransport in TAL
-compete with Cl

increased RBF and dissipate medullary concentration gradient

powerful - need to monitor**

36
Q

furosemide

A

loop diuretic

37
Q

bumetanide

A

loop diuretic

38
Q

ethacrynic acid

A

loop diuretic

39
Q

thiazide diuretic

A

act in distal convoluted tubule

inhibit Na/Cl cotransport
-increased Na, Cl, K excretion

ex. HCTZ

40
Q

hydrochlorothiazide

A

thiazide diuretic

41
Q

potassium sparing diuretics

A

work in collecting duct
-inhibit Na reabsorption and K secretion

often used with other diuretics that increase K excretion

42
Q

amiloride

A

K sparing diuretic

43
Q

triamterene

A

K sparing diuretic

-blocks Na channels

44
Q

spironolactone

A

K sparing diuretic

-aldosterone antagonist

45
Q

collecting duct sodium channels?

A

due to aldosterone

  • blocked by K sparing diuretics
  • little affect on K channels**
46
Q

further down nephron?

A

better affect of diuretic

47
Q

K sparing diuretics

A

block sodium channels

or inhibit aldosterone

48
Q

hypocalcemic tetany

A

muscles lock off and don’t work

49
Q

PTH

A

regulates calcium levels

-thyroid surgery can mess up Ca levels

50
Q

plasma Ca

A

some bound to protein
-cannot be flitered at glomerulus

-only free calcium is filtered and biologically active

51
Q

normal total plasma levels

A

4.5-5 mEq/L

52
Q

effect of pH on Ca levels?

A

H+ compete for binding sites of Ca on plasma proteins

lower pH - increased H+, more free Ca
higher pH - less H+, less free Ca

53
Q

PTH

A

released in response to lower Ca levels

  • releases Ca from bone (osteoclast activity)
  • kidney activates Vit D (hydroxylated) which goes to gut as calcitriol to increase gut absorption
  • also causes increased reabsorption of Ca in kidney

leads to increased Ca levels in plasma

54
Q

high levels of Ca?

A

leads to decreased PTH levels

55
Q

Ca handling in kidney?

A

70% reabsorbed in proximal tubule

20% reabsorbed in TAL

56
Q

proximal tubule Ca reabsorption mechanism

A

low intracellular Ca

  • goes from lumen to cell
  • Na/Ca exchanger
  • can also go down gradient paracellularly
  • not in distal tubule (bc tighter junctions)
57
Q

TAL Ca reabsorption

A

paracellular reabsorption bc of + luminal potential pushes positive ions through cells for reabsorption

Ca, Mg, Na, NH2, K all reabsorbed this way

58
Q

change in luminal potential?

A

no driving force for cation reabsorption in TAL

positive luminal potential bc of K leak channels
-loop diuretics stop this, disrupting the potential

results in increase excretion of these cations

59
Q

distal tubular Ca reabsorption

A

tight junctions - no paracellular transport

have Vit D dependent Ca binding protein

  • pulls Ca intracellulary
  • Ca ATPase then moves Ca to blood
60
Q

physiological control of Ca

A

control in TAL and distal convoluted tubule

61
Q

stimulation of Ca reabsorption?

A

PTH, calcitriol

PTH released with decreased plasma Ca levels

62
Q

increased Ca in plasma

A

PTH goes down

calcitonin goes up

63
Q

calcitonin

A

acts to oppose PTH

64
Q

phosphate handling in kidney?

A

80% reabsorbed in proximal tubule

10% reabsorbed in distal tubule

65
Q

proximal tubule reabsorption in proximal tubule?

A

Na/K symporter luminal membrane
basolateral membrane P/A- counterexchange

-inhibited by PTH**

this transport is saturable (like glucose)
-has a Tm

66
Q

PTH and phosphate?

A

increases excretion

lowers Tm of transport - more excretion

67
Q

renal handling of Mg

A

only 25% reabsorbed in proximal tubule

bulk reabsorbed in thick ascending limb (~60%)

-paracellular movement due to positive luminal potential

68
Q

Mg carrying in plasma?

A

60% free (can be filtered)
20% complexed
20% bound to proteins

69
Q

loop diuretics

A

change the luminal potential

get increased excretion of positive cations in urine

70
Q

PTH

A

suppress PO4 reabsorption in PCT

decreased Tm for symporter

71
Q

Mg reabsorption?

A

mainly in TAL

72
Q

hypokalemia EKG?

A

flat T

depressed ST

73
Q

hyperkalemia EKG?

A

broad QRS
tall T
prolonged PR

74
Q

neuromuscular symptoms?

A

hypokalemia

muscle weakness, paralysis

75
Q

cardiac symptoms

A

hyperkalemia

arrhythmias

76
Q

H/K ATPase

A

in intercalated cells of collecting duct

K reabsorption and H secretion

77
Q

vigorous exercise

A

can lead to hyperkalemia

78
Q

loop diuretics and Ca?

A

large increase in Ca excretion

-reducing TAL potential

79
Q

thiazide diuretics and Ca?

A

reduce Ca excretion
-increase Ca reabsorption in distal convoluted tubule

used to treat hypercalcuria

80
Q

intercalated cells?

A

collecting duct

K reabsorption and H secretion
-H/K ATPase

81
Q

principal cells

A

collecting duct

K secretion

  • Na/K ATPase creates high intracellular [K]
  • driving force for K secretion through channels

aldosterone - causes increased Na/K ATPase

(+) increased ECF K, increased aldosterone, increased tubular flow rate
(-) acidosis

82
Q

hypocalcemia

A

slowed HR

83
Q

hypercalcemia

A

fast HR

84
Q

shift K into ICF?

A

insulin
epinephrine
aldosterone

85
Q

acid-base status and K movement?

A

acidosis increases ECF K

alkalosis decreases ECF K

86
Q

hypocalcemia

A

can lead to hypocalcemic tetany

-increased excitability

87
Q

hypercalcemia

A

depressed neuromuscular excitability

-cardiac arrhythmias

MSS Renal Exam 2 (7 decks)

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