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
major stimuli for aldosterone release?
hyperkalemia
26
aldosterone mechanism
more Na and K channels on luminal membrane increase Na/K ATPase activity
27
Conns disease
primary hyperaldosteronism -tumor in adrenal cortex leads to hypokalemia -high K secretion
28
Addisons disease
destruction of adrenal gland -hypoaldosteronism decreased K secretion -hyperkalemia
29
why no hypernatremia in hyperaldosteronism?
water follows Na | -therefore, body sense increased volume and increase Na excretion
30
diuretics
drugs that increase urine excretion -inhibit solute and water reabsorption to help eliminate excess volume ex/ edema and CHF
31
osmotic diuretic
ex/ mannitol inhibit reabsorption of water and secondarily Na -proximal tubule leads to downstream increase in reabsorption therefore, they don't work too well
32
mannitol
osmotic diuretics
33
carbon anhydrase inhibitor
ex/ acetazolamide inhibit NaHCO3- reabsorption -proximal tubule altitude sickness
34
acetazolamide
carbonic anhydrase inhibitor
35
loop diuretics
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
furosemide
loop diuretic
37
bumetanide
loop diuretic
38
ethacrynic acid
loop diuretic
39
thiazide diuretic
act in distal convoluted tubule inhibit Na/Cl cotransport -increased Na, Cl, K excretion ex. HCTZ
40
hydrochlorothiazide
thiazide diuretic
41
potassium sparing diuretics
work in collecting duct -inhibit Na reabsorption and K secretion often used with other diuretics that increase K excretion
42
amiloride
K sparing diuretic
43
triamterene
K sparing diuretic | -blocks Na channels
44
spironolactone
K sparing diuretic | -aldosterone antagonist
45
collecting duct sodium channels?
due to aldosterone - blocked by K sparing diuretics - little affect on K channels**
46
further down nephron?
better affect of diuretic
47
K sparing diuretics
block sodium channels | or inhibit aldosterone
48
hypocalcemic tetany
muscles lock off and don't work
49
PTH
regulates calcium levels | -thyroid surgery can mess up Ca levels
50
plasma Ca
some bound to protein -cannot be flitered at glomerulus -only free calcium is filtered and biologically active
51
normal total plasma levels
4.5-5 mEq/L
52
effect of pH on Ca levels?
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
PTH
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
high levels of Ca?
leads to decreased PTH levels
55
Ca handling in kidney?
70% reabsorbed in proximal tubule | 20% reabsorbed in TAL
56
proximal tubule Ca reabsorption mechanism
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
TAL Ca reabsorption
paracellular reabsorption bc of + luminal potential pushes positive ions through cells for reabsorption Ca, Mg, Na, NH2, K all reabsorbed this way
58
change in luminal potential?
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
distal tubular Ca reabsorption
tight junctions - no paracellular transport have Vit D dependent Ca binding protein - pulls Ca intracellulary - Ca ATPase then moves Ca to blood
60
physiological control of Ca
control in TAL and distal convoluted tubule
61
stimulation of Ca reabsorption?
PTH, calcitriol PTH released with decreased plasma Ca levels
62
increased Ca in plasma
PTH goes down | calcitonin goes up
63
calcitonin
acts to oppose PTH
64
phosphate handling in kidney?
80% reabsorbed in proximal tubule | 10% reabsorbed in distal tubule
65
proximal tubule reabsorption in proximal tubule?
Na/K symporter luminal membrane basolateral membrane P/A- counterexchange -inhibited by PTH** this transport is saturable (like glucose) -has a Tm
66
PTH and phosphate?
increases excretion lowers Tm of transport - more excretion
67
renal handling of Mg
only 25% reabsorbed in proximal tubule bulk reabsorbed in thick ascending limb (~60%) -paracellular movement due to positive luminal potential
68
Mg carrying in plasma?
60% free (can be filtered) 20% complexed 20% bound to proteins
69
loop diuretics
change the luminal potential get increased excretion of positive cations in urine
70
PTH
suppress PO4 reabsorption in PCT decreased Tm for symporter
71
Mg reabsorption?
mainly in TAL
72
hypokalemia EKG?
flat T | depressed ST
73
hyperkalemia EKG?
broad QRS tall T prolonged PR
74
neuromuscular symptoms?
hypokalemia | muscle weakness, paralysis
75
cardiac symptoms
hyperkalemia | arrhythmias
76
H/K ATPase
in intercalated cells of collecting duct K reabsorption and H secretion
77
vigorous exercise
can lead to hyperkalemia
78
loop diuretics and Ca?
large increase in Ca excretion | -reducing TAL potential
79
thiazide diuretics and Ca?
reduce Ca excretion -increase Ca reabsorption in distal convoluted tubule used to treat hypercalcuria
80
intercalated cells?
collecting duct K reabsorption and H secretion -H/K ATPase
81
principal cells
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
hypocalcemia
slowed HR
83
hypercalcemia
fast HR
84
shift K into ICF?
insulin epinephrine aldosterone
85
acid-base status and K movement?
acidosis increases ECF K | alkalosis decreases ECF K
86
hypocalcemia
can lead to hypocalcemic tetany | -increased excitability
87
hypercalcemia
depressed neuromuscular excitability | -cardiac arrhythmias