Test 2: Wk7: 2 Tubular transport of K/Ca/Mg - Mangiarua Flashcards

1
Q

Plasma K conc.

Range

A

4 meq/L

3.4-4.5 meq/L

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2
Q

fatal plasma K conc.

A

8 meq/L

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3
Q

Intracellular K conc.

A

145 meq/L

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4
Q

primary regulator of K

A

kidneys

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5
Q

K transport is

A

bidirectional

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6
Q

% K reabsorbed in proximal tubule

A

67%

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7
Q

% K reabsorbed in thick ascending limb

A

20%

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8
Q

% K remaining at start of distal convoluted tubule

A

13%

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9
Q

% of filtered K is reabsorbed prior to distal tubule regardless of dietary K

A

87%

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10
Q

K has a — reabsorption

A

net

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11
Q

proximal tubule K transport

A

active - pump on luminal and basolateral

passive - most reabsorption in PT is passive

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12
Q

Distal tubule and cortical collecting duct K transport

A

perform the fine-tuning of K+ excretion to

maintain K+ balance

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13
Q

a person on a low K+ diet, there is further reabsorption of K+ by the — of the late distal tubule and collecting ducts

A

α-intercalated cells

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14
Q

persons on a normal or high K+ diet, K+ is secreted by the — of the late distal tubule and collecting duct

A

principal cells

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15
Q

The principal cells, in the connecting tubule and cortical and medullary collecting duct, when stimulated by — will secrete —.

A

aldosterone

K+

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16
Q

— dominate the overall transport of K+ unless — is inhibited

A

Principal cells

Aldosterone

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17
Q

— secretion is increased by Na entrance through —

A

K; ENaC

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18
Q
sodium entrance through ENaC sodium
channels causes (2)
A
  1. NA,K-ATPase stimulation

2. Depol of luminal membrane

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19
Q

Potassium entering via the Na,K-ATPase that is not secreted

A

recycles through basolateral channels.

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20
Q

amiloride inhibits

A

inhibits sodium entry, and therefore inhibits potassium

secretion

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21
Q

stimulates both sodium reabsorption and potassium secretion at multiple points.

A

Aldosterone

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22
Q

ROMK and BK Low K excretion

A

ROMK - sequestered

BK - closed

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23
Q

ROMK and BK Normal K excretion

A

ROMK - open

BK - Closed

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24
Q

ROMK and BK High K excretion

A

ROMK - open

BK - open

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25
Q

5 factors that alter K secretion

A

(1) Sodium Delivery to the Distal Nephron
(2) Aldosterone
(3) Plasma Potassium
(4) GI Hormones
(5) Angiotensin II

26
Q

Sodium Delivery to the Distal Nephron on K secretion

A

High sodium delivery stimulates potassium secretion; low

sodium delivery inhibits it.

27
Q

Aldosterone on K secretion

A

Increases Na-K-ATPase which supplies more potassium from the interstitium to the cytosol of the principal cells.

Stimulates the activity of ROMK channels in principal cell of the distal nephron

28
Q

Plasma Potassium on K secretion

A

The Na-K-ATPase that takes up potassium in principal cells is highly sensitive to the potassium concentration

Plasma potassium concentration exerts an influence on potassium excretion but is not the dominant factor under normal conditions.

29
Q

GI Hormones on K secretion

A

Gastrointestinal peptide hormones released in response to ingested potassium may be responsible for the response to dietary intake.

30
Q

Angiotensin II on K secretion

A

Inhibitor of potassium secretion; decrease the activity of ROMK channels in principal cells.

31
Q

Alkalosis results in — K from principal cells which leads to —

A

⬆ K secretion and depletion of K

32
Q

elevated plasma pH is often associated with

A

hypokalemia.

33
Q

Low plasma pH is often associated with

A

hyperkalemia

34
Q

Total plasma calcium has 3 components

A
  1. 40% protein bound - no filter
  2. 50% ionized Ca and biologically active - filters
  3. 10% complexed with anions - filters
35
Q

As the plasma H+ concentration increases, the concentration of ionized calcium —

A

increases

36
Q

In acidosis, as more H+ are buffered by plasma proteins, bound calcium is
displaced from proteins causing plasma Ca to

A

increase

37
Q

in alkalosis the release of H+ from plasma proteins causes the plasma
Ca to

A

decrease

38
Q

% of filtered Ca reabsorbed

A

98-99%

39
Q

PTH — Ca++ reabsorption in the kidney and increases [Ca++ ]ECF

A

increases

40
Q

Ca paracellular reabsorption in proximal tubule

A

driven by solvent drag

41
Q

Ca transcellular reabsorption in proximal tubule

A

uptake across the brush border via Ca permeable ion channel and exit across basolateral membrane via Ca ATPase

42
Q

Ca reabsorption in thick ascending limb

A

paracellular - driven by the transepithelial electrochemical gradient

43
Q

Ca reabsorption in distal tubule

A

transcellular
1 Ca enter through apical Ca ion channels
2 Ca binds calbindin and complex diffuses across the cell to deliver Ca to basolateral
3 Ca transported across basolateral by 3NaCa antiporter and Ca-ATPase

44
Q

distal tubule is the site of Ca

A

Ca reabsorption regulation

45
Q

— regulates calcium homeostasis

A

PTH

46
Q

PTH action

A

increases plasma Ca conc.

47
Q

PTH renal effects (3)

A
  1. promotes calcitriol formation
  2. increase Ca reabsorption
  3. increase phosphate excretion
48
Q

PTH increases Ca++ reabsorption by: (2)

A

Increasing the transcription and open probability, and inhibition of endocytosis of the Ca++-permeable ion channel.

  • Upregulating the expression of calbindin and NCX1.
49
Q

% of plasma phosphate is unbound and — filtered

A

90%; freely

50
Q

% of the filtered load of phosphate is —

A

90%; actively reabsorbed from the nephron

51
Q

phosphate is Co-transported with Na+ across — driven by —

A

the luminal plasma membrane.

intracellular Na+ gradient.

52
Q

Pi is reabsorbed via three sodium phosphate cotransporters

A

Npt2a, Npt2c and PiT-2.

53
Q

sodium phosphate cotransporters, which are positioned in the — of —

A

apical membrane of renal proximal tubule cells

54
Q

PTH inhibits reabsorption of phosphate in the

A

the proximal tubule

55
Q

PTH stimulates the removal of — from the brush border of the —

A

NPT2; proximal tubule

56
Q

% of plasma magnesium is protein bound

A

30% of plasma magnesium is protein bound ➞ non filterable.

57
Q

% of plasma magnesium is ionized

A

60% of plasma magnesium is ionized ➞ filterable.

58
Q

% of plasma magnesium is complexed to anions such as phosphate, citrate, and oxalate

A

10% of plasma magnesium is complexed to anions such as phosphate, citrate, and oxalate➞ filterable.

59
Q

Mg reabsorption in proximal tubule is believed to be

A

paracellular aided by a chemical gradient generated by Na gradient

60
Q

Mg reabsorption in Thick ascending limb

A

paracellular

61
Q

Mg2+ reabsorption along the DCT, which is predominantly —

A

transcellular

62
Q

Mg2+ entry across the DCT apical membrane may take place via the

A

TRPM6 cation channel; the key driving force is the inside-negative membrane potential.