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Physiology > Control of Potassium, Calcium, Phosphate, & Magnesium > Flashcards

Control of Potassium, Calcium, Phosphate, & Magnesium Flashcards

1
Q

Potassium

 Tightly controlled – Usually changes less than

A

± 0.3 mEq/liter

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2
Q

Cell functions very sensitive to

A

changes  Resting membrane potentials

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3
Q

98% of potassium located

A

intracellularly

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4
Q

Daily intake usually ranges between

A

50 mEq/liter to 200 mEq/liter

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5
Q

Small changes in extracellular K+ can

A

easily lead to hyper or hypokalemia

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6
Q

Only 5 to 10% of intake of K removed by

A

feces – rest must be removed by kidneys

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7
Q

After ingesting 40 mEq of K+ into ECF – [K+] would increase

A

by 2.8 mEq/liter

 Most ingested K+ quickly moves into the cellular volume

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8
Q

moves potassium AND glucose into the cells following a meal

A

INSULIN

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9
Q

secretion stimulated by increased [K+]

A

aldosterone. In disease state, ability to move K+ into the cells AND K+ reabsorption are affected

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10
Q

Epinephrine stimulates

A

β2-adrenergic receptors increasing movement of K+ into the cell. β2-adrenergic blocking agents (treat hypertension) can lead to hyperkalemia

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11
Q

Factors that shifts K+ into cells (Potential hypo)

A

insulin, Aldosterone (also increases K+ secretion), Β-adrenergic stimulation, Alkalosis

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12
Q

Factors that shifts K+ out of cells (Potential hyper)

A

• Insulin deficiency (diabetes mellitus)
• Aldosterone deficiency (Addison’s disease)
• Β-adrenergic blockade• Acidosis
• Cell lysis • Strenuous exercise • Increased extracellular
fluid osmolarity

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13
Q

Potassium

 Increased [H+] will reduce

A

action of Na-K ATPase with less transfer of K+ into the cells

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14
Q

Cell lysis dumps intracellular K+ in

A

extracellular compartment

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15
Q

Potassium. With an increase in extracellular osmolarity, water moves out of the cell which

A

increasing intracellular [K+] which increases the rate of K+ diffusion out of the cell

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16
Q

Excretion rate of K determined by:

A

 Rate of potassium filtration  Rate of potassium reabsorption  Rate of potassium secretion

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17
Q

Constant fraction of filtered load reabsorbed in

A

proximal tubule and the loop of Henle – Does not change day-to-day

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18
Q

Renal Excretion of Potassium daily Filtration

A

180 liter/day x 4.2 mEq/liter = 756

mEq/day

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19
Q

consistent reabsorption of k percentage per part of kidney

A

 65% proximal tubule

 25 to 30% in loop (mainly thick ascending segment)

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20
Q

Flexible Reabsorption & Secretion

A

Principle cells of distal tubule and cortical collecting tubule

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21
Q

With normal K+ intake of 100 mEq/day  Feces removes

A

8 mEq  Kidneys must remove 92 mEq

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22
Q

Proximal tubule removes how much potassium

A

491 mEq leaving 265 mEq

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23
Q

Loop removes how much K

A

204 mEq leaving 61 mEq

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24
Q

Distal tubule & cortical collecting tubule MUST secrete how much K

A

31 mEq Approximately 1/3 of excreted potassium

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25
Q

During High potassium intake  Distal tubule & cortical collecting tubule increase

A

potassium secretion

 Very strong mechanism – rate of potassium excretion can exceed amount of potassium being filtered

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26
Q

during Low potassium intake secretion rate

A

decreases
 Can decrease secretion to point where there is net reabsorption
 Excretion can fall to 1% of filtered potassium (756 mEq/day x 0.01 = 8 mEq/day)

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27
Q

Principal Cells Make up

A

90% of cells in late distal and cortical collecting tubule

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28
Q

principal cells Secretion driven by

A

Na-K ATPase in basolateral border of cells
 Move K+ into cell setting up concentration gradient
 Concentrationgradientdrives diffusion from cell into tubular lumen

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29
Q

Tubular membrane contains

A

special channels for K+ diffusion

 Usually provide high permeability for K+ movement out of the cell

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30
Q

Intercalated Cells

A

Reabsorb potassium especially during potassium depletion

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31
Q

Intercalated Cells Could be related to H-K ATPase

A

 Located tubular membrane  Pumps H+ from tubular cell into lumen (secretion)
 Pumps K+ from tubular lumen into cell (reabsorption)  K+ diffuses from cell into interstitial space via basolateral membrane
 Major effect only during potassium depletion

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32
Q

Control of Potassium Secretion

Three factors control rate of K+ secretion

A

 Activity of Na-K ATPase
 Electrochemical gradient for K+ movement from the blood to the tubular lumen
 Permeability of tubular membrane to K+

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33
Q

Stimulation of Potassium Secretion

A

 Increased extracellular [K+]  Increased [aldosterone]  Increased tubular flow rate
 Increased [H+] will DECREASE potassium secretion

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34
Q

Increased Plasma Potassium

 Important control mechanism  Always a certain level

A

of secretion even at normal [K+]

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35
Q

Increased [K+] stimulates action

A

Na-K ATPase. More K+ moved into cell from interstitial space which increased gradient from cell interior to tubular lumen

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36
Q

[K+] of renal interstitial fluid increases

A

(increased plasma concentration) which decreases amount of K+ diffusing from cell interior into interstitial space Increase [K+] in plasma stimulated release of aldosterone

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37
Q

Increased aldosterone increases

A

rate of sodium reabsorption by late distal tubule and collecting duct
 Increases activity of Na-K ATPase – so an increase in sodium reabsorption will also increase potassium secretion
 Increases tubular membrane permeability for potassium

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38
Q

Plasma Potassium & Aldosterone

 Great example of

A

negative feedback control system
 Factor being controlled (potassium) as feedback effect on controller (aldosterone)
 Small change in plasma [K+] produced huge change in aldosterone concentration

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39
Q

Normal aldosterone level is approximately

A

6 nag/dL

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40
Q

Anything that affects our ability to produce aldosterone will have a big effect

A

on potassium excretion!!

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41
Q

High aldosterone (primary aldosteronism)=

A

Hypokalemia

42
Q

Low aldosterone (Addison’s disease) =

A

Hyperkalemia

43
Q

ncreased K+ intake with intact aldosterone feedback

 Big change in intake (x7 increase)

A

mall change [K+] (4.2 to 4.3 mEq/liter)

44
Q

Increased K+ intake with blocked aldosterone feedback

 Big change in intake (x7 increase)

A

big change in [K+] (3.8 to 4.7 mEq/liter)

45
Q

Increased distal tubular flow rate will

A

increase potassium secretion

46
Q

Increased tubular flow rate can be caused by

A

volume expansion; high sodium intake; specific diuretics

47
Q

Relationship between tubular flow rate and potassium secretion greatly affected

A

by potassium intake

 Higher the intake, the greater the effect created by tubular flow

48
Q

As potassium diffuses into tubular lumen, the increase in luminal concentration will

A

will decrease the gradient thus decreasing the movement of potassium

49
Q

Increased tubular flow carries

A

potassium away thus helping to preserve the gradient. The higher the flow the better the gradient is preserved, the more potassium is secreted

50
Q

Preserving K+ Excretion With Changing Na+ Intake
Assume high Na+ intake
 Aldosterone secretion decreases which will produce

A

a decrease K+ secretion
 BUT since sodium reabsorption is decreased, overall distal tubular flow is increased which results in an increase in K+ secretion
 THE TWO OFF SET EACH OTHER

51
Q

Acute Acidosis Decreases K secretion by…

A

 Reduces the activity of Na-K ATPase – decreases driving force for moving potassium from cell interior to tubular lumen
 Prolonged acidosis produces increased potassium excretion – Result of decreased reabsorption of sodium chloride and water in proximal tubule and increased distal tubular flow
 Alkalosis (H+) increases potassium secretion

52
Q

Total calcium in plasma:

A

5 mEq/liter
 50% in ionized form
 40% bound to plasma protein  Amount bound to protein decreases with an increase in [H+]. Patients with
alkalosis more susceptible to hypocalcemic tetany  10% bound in non-ionized form to other ions (phosphate, citrate)

53
Q

Normal ion concentration:

A

2.4 mEq/liter (1.2 mmol/liter)

54
Q

Hypocalcemia:

A

: increases muscle and nerve excitability

hypocalcemic tetany

55
Q

Hypercalcemia

A

epressed neuromuscular excitability which can lead to cardiac arrhythmias

56
Q

99% of calcium stored

A

in bone
 HUGE reservoir – if plasma concentration drops, body will move calcium from the bone – if plasma concentration rises, body will move calcium back into the bone

57
Q

1% of calcium in

A

intracellular space and cell organelles  0.01% present in extracellular fluid

58
Q

PTH most important control agent for

A

Ca. 90% excreted via gastrointestinal tract (feces) (≈900 mg/day)  10% excreted via kidneys (urine) (≈100 mg/day)

59
Q

PTH regulation accomplished through 3 actions:

A

 Stimulation of bone resporption of calcium
 Stimulation of vitamin D which stimulates calcium reabsorption by intestines
 Direct stimulation of renal tubule reabsorption of calcium

60
Q

PTH Affect on Bone

 As extracellular calcium concentration falls:

A

 Parathyroid gland directly stimulated to increase secretion of
PTH
 Increased PTH concentration stimulates bone to increase release of bone salts (resporption) which includes the release of large amounts of calcium

61
Q

PTH Affect on Bone. As extracellular calcium concentration increases:

A

 Parathyroid gland decreases PTH secretion

 Decreased PTH concentration decreases salt resporption to point where calcium will be added to the bone

62
Q

Calcium Excretion

A

 Freely filtered, reabsorbed BUT NOT secreted
 Excretion rate = Filtration – Reabsorption
 Only filtering a very small percentage of the calcium that is actually present in the body!!!!!

63
Q

Calcium Excretion proximal tubule, LOH, Distal/collecting tube

A

 Proximal tubule: 65% filtered load reabsorbed
 Loop of Henle: 25 to 30% filtered load reabsorbed
 Distal tubule / Collecting tubule: 4 to 9% filtered load reabsorbed
 Normally only 1% of filtered load is excreted  Changes as plasma concentration changes (i.e. intake changes)

64
Q

Proximal Tubule Reabsorption of Ca++

80% of amount

A

reabsorbed carried by water via paracellular pathway

20% of amount reabsorbed via a transcellular pathway

65
Q

Proximal Tubule Reabsorption of Ca++ . Diffusion through luminal membrane into cell driven by

A 
chemical gradient (higher [Ca++] in lumen than inside cell) AND by electrical gradient (interior of cell negative with respect to lumen
 Pumped out of cell across basolateral membrane via Ca ATPase pump and Na-Ca counter-transport mechanism
66
Q

Thick Ascending Loop – Ca++ Reabsorption

 Paracellular pathway accounts for

A

50% of reabsorption in loop

 Passive diffusion down electrical gradient – lumen has slight positive charge compared to interstitial fluid

67
Q

Thick Ascending Loop transcellular pathway accounts for

A

0% of reabsorption in loop

 Active process stimulated by PTH, Vitamin D (Calcitrol), and calcitonin (PTH concentration most important)

68
Q

Distal Tubule – Ca++ Reabsorption

 Almost all transport via

A

Transcellular pathway  Active transport across basolateral membrane –
diffusion into cell

69
Q

i distak tubule increased [PTH] increases

A

Ca++ reabsorption

 Reabsorption also increased by Vitamin D and calcitonin

70
Q

REMINDER: increased Reabsorption =

A

increased Excretion

71
Q

Regulation of Ca++ Reabsorption / Excretion. PTH is primary controller and stimulates

A

increased reabsorption in Loop and Distal Tubule

72
Q

Regulation of Ca++ Reabsorption / Excretion. PTH has no effect in

A

Proximal Tubule (Following sodium and water reabsorption)

73
Q

regulation of Ca++ Reabsorption / Excretion. Δ in EC fluid volume and blood pressure cause

A

inverse changes in sodium & water reabsorption which causes parallel changes in calcium reabsorption

74
Q

regulation of Ca++ Reabsorption / Excretion. [H+] major affect is on the transport mechanisms in the

A

Distal Tubule

75
Q

regulation of Ca++ Reabsorption / Excretion. [Phosphate] affects [PTH] – As [Phosphate] increases

A

[PTH] increases

76
Q

things that increase Ca++ Reabsorption

A 
increase [PTH]
decrease EC Fluid Volume
 decrease Blood Pressure
 increase Plasma Phosphate
Metabolic Acidosis
77
Q

things that decrease Ca reabsorption

A 
decrease [PTH]
increase EC Fluid Volume
increase Blood Pressure
decrease Plasma Phosphate
Metabolic Alkalosis
78
Q

Phosphate

 Normal tubular maximum of

A

0.1 mMol/minute  If filtered load under Tmax, all phosphate reabsorbed  If filtered load over Tmax, phosphate is excreted

79
Q

Phosphate. Plasma threshold level approximately

A

0.8 mMol/liter

80
Q

phosphate Normal plasma concentration around

A

1 mMol/liter – Large intake of phosphate each day (milk & meat)

81
Q

Phosphate Reabsorption

 Proximal Tubule: percentage of filtered plasma reabsorbed and how

A

75 to 80%

82
Q

Phosphate Reabsorption enters cells from

A

lumen via Na-Phosphate co-transport mechanism

83
Q

Phosphate Reabsorption exits cells from

A

leaves cell via counter-transport mechanism across basolateral membrane ?????

84
Q

Phosphate Reabsorption in LOH

A

Very small amounts

85
Q

Phosphate Reabsorption in Distal tubule

A

10% of filtered phosphate reabsorbed

86
Q

Phosphate Reabsorption in collecting tubule

A

Very small amounts

87
Q

Approximately 10% of filtered phosphate is

A

excreted

88
Q

Regulation of Phosphate

 Tmax can change based

A

on intake  Low intake, Tmax will increase over time

89
Q

Regulation of Phosphate arathyroid Hormone  As PTH increases bone resorption of

A

calcium,

phosphate is also resorbed

90
Q

Regulation of Phosphate. increasing [PTH] decreases the

A

Tmax for phosphate so less phosphate is reabsorbed and more is excreted

91
Q

Magnesium

 >50% stored in

A

bone

92
Q

Magnesium. Most of what is left is located in the

A

intracellular volume  <1% located in extracellular volume

93
Q

TOTAL plasma magnesium =

A

1.8 mEq/liter BUT >50% is bound to plasma proteins so free ionized is 0.8 mEq/liter

94
Q

magnesium Daily intake

A

≈ 250 to 300 mg/day BUT only 50% is actually absorbed by the gastrointestinal tract (125 to 150 mg/day)
 The amount absorbed is the amount the kidneys must excrete each day

95
Q

Renal excretion of magnesium is ≈

A

10 to 15 of filtered load

96
Q

Magnesium Reabsorption

 Proximal Tubule:

A

25% of filtered load

97
Q

Magnesium Reabsorption. Loop of Henle:

A

Primary site of reabsorption – 65% of

filtered load

98
Q

Magnesium Reabsorption. distal Tubule / Collecting Tubule:

A

<5% of filtered load

99
Q

Magnesium Reabsorption. Control mechanisms not clearly defined increase [Magnesium] results in

A

decrease reabsorption and increase excretion

100
Q

Magnesium Reabsorption. increase EC fluid volume results in  reabsorption and  excretion

A

decrease reabsorption and increase excretion

101
Q

Magnesium Reabsorption. increase [Ca++] results in

A

decrease reabsorption and increase excretion

Physiology (27 decks)

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