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FHB Mikayla > Unit 2, L18 Renal Regulation of Electrolytes > Flashcards

Unit 2, L18 Renal Regulation of Electrolytes Flashcards

1
Q

What functions is K critical for?

A

Regulation of cell volume, regulation of intracellular pH, resting membrane potential, and cardiac and neuromuscular activity

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2
Q

What is the percentage of K found in the ICF

A

98%

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3
Q

What percentage of total body K is located in the ECF

A

2%

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4
Q

Value of K+ in ECF for hyperkalemia

A

Exceeding 5.0 mEq/L

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5
Q

Value of K+ in ECF for hypokalemia

A

Less than 3.5 mEq/L

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6
Q

The standard diet means consuming what amount of K per day

A

100 mEq of K per day

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7
Q

How much K gets absorbed in the intestines per day, assuming 100 mEq diet

A

90 mEq of K per day

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8
Q

How much K gets excreted through feces per day, assuming 100 mEq diet

A

5-10 mEq per day

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9
Q

Of the 90 mEq we absorb, how much of it is in the extracellular fluid initially?

A

65 mEq

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10
Q

What facilitates the movement of K from the extracellular fluid to the tissue stores?

A

Insulin, epinephrine, and aldosterone

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11
Q

After movement form extracellular fluid to the tissue stores, what is the concentration of K per day in the tissue stores

A

3435 mEq/day

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12
Q

What facilitates the excretion of extracellular fluid K?

A

Plasma K concentration, AVP, and aldosterone

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13
Q

How much K gets excreted through the urine, assuming a 100 mEq diet?

A

90-95 mEq

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14
Q

How much K is reabsorbed in the proximal tubule

A

67%

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15
Q

How much K is reabsorbed in the TAL of the loop of Henle

A

20%

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16
Q

K can be secreted where and through what cells

A

K is secreted in the distal tubule and collecting duct, and principal cells secrete K

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17
Q

What type of cells reabsorb K?

A

Alpha intercalated cells

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18
Q

In a normal diet, what is the percentages for K reabsorption and excreteion

A

85% is reabsorbed and 15% is excreted

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19
Q

If you have decreased dietary K, what happens to reabsorptionb

A

Increased reabsorption to 99%

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20
Q

If you have increased dietary K, what happens to excretion

A

Increased excretion, up to 80%

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21
Q

What are the factors that regulate the rate of K secretion from principal cells?

A

Na/K/ATPase pumps
Electrochemical gradient of K+ across the apical membrane
Permeability of the apical membrane to K

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22
Q

Increased K concentration outside of the cell will activate what signaling pathway for K secretion?

A

Increased extracellular K leads to stimulation of Na/K/ATPase, which leads to increased K inside of the cell, which increases K permeability of the apical membrane, which leads to increased K secretion

Additionally, increased extracellular K concentration can lead to increased aldosterone, which increases K secretion by inserting Na/K/ATPase pumps into the membrane

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23
Q

Physiological factors that keep plasma K constant

A

Epinephrine
Insulin
Aldosterone

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24
Q

Pathophysiological: displace plasma K from normal

A

Acid base disorders
Plasma osmolality
Cell lysis
Vigorous exercise

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25
Q

Drugs that induce hyperkalemis

A

Dietary K supplements
ACE inhibitors
K sparing diuretics

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26
Q

What will alpha 1 receptor stimulation do in terms of K

A

Release K from the cells

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27
Q

What will beta 2 receptor stimulation do in terms of cells

A

Uptake K into cells

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28
Q

What is the most important hormone that shifts K into cells

A

Insulin

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29
Q

Function of aldosterone

A

Stimulation of Na/K/ATPase pump, increases urinary excretion of K

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30
Q

In hyposmolality, what happens to K?

A

Cells swell, so intracellular K concentration is diluted, increasing the driving force moving K into the cell

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31
Q

In hyperosmolality, what happens to K

A

The cells will shrink, so the intracellular K concentration is concentrated, which will increase the driving force to move K out of the cells

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32
Q

What conditions/events will cause K to shift out of cells (aka hyperkalemia)

A 
Insulin deficiency 
Beta 2 adrenergic antagonists
Alpha adrenergic agonists
Acidossi
Hyperosmolarity
Cell lysis
Exercise
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33
Q

What conditions causes K to shift into cells (hypokalemia)

A 
Insulin
Beta 2 adrenergic agonists
Alpha adrenergic antagonists
Alkalosis
Hyposmolarity
34
Q

What hormones will alter K secretion

A

Aldosterone, glucocorticoids (increased K excretion), and AVP

35
Q

What happens to tubular flow when you have water diuresis

A

More water is in the tubular fluid, so you have an increase in urinary flow rate. You then get an increase in K secretion in the DT and CCD, as luminal K is being diluted because you have more water, so you have a larger concentration gradient by the time you reach the principal cells.

36
Q

What happens to tubular flow rate if you are in a state of antidiuresis

A

There is decreased urinary flow rate, as you have less water, and this concentrates the luminal K concentration, decreasing the concentration gradient for K, which will decrease DT/CCD K secretion

37
Q

What happens to AVP if you are in a state of water diuresis

A

Decreased AVP, so no additional AQP channels are being inserted into the apical membrane of the principal cells, and less Na movement into the cell, so there is decreased K secretion

38
Q

What happens to AVP when you are in a state of antidiuresis

A

Increased AVP, means more AQP channels are being inserted into the apical membrane of the principal cells, allowing for more Na movement into the cell. Because you are moving more Na, this will also allow for more K movement out, so you get increased K secretion

39
Q

Sensitivity of K secretion to tubular flow rate is ____________ to K amount in diet

A

Proportional

40
Q

K wasting diuretics

A

Furosemide, acetazolamide, and mannitol

41
Q

K sparing diuretics

A

Spironolactone, amiloride, and triamterene

42
Q

What are the main two mechanisms behind K wasting diuretics?

A

1) In principal cells, increased Na uptake, as well as more activity of Na/K/ATPase. K is being pumped into cells, increasing driving force for K secretion from principal cells
2) Increased flow rate; luminal K is diluted, thus increasing driving force for K secretion from the principal cells

43
Q

What are the three mechanisms for loop-specific diuretics

A

1) In principal cells, increased Na uptake, as well as more activity of Na/K/ATPase. K is being pumped into cells, increasing driving force for K secretion from principal cells
2) Increased flow rate; luminal K is diluted, thus increasing driving force for K secretion from the principal cells
3) Direct inhibition of the Na/K/Cl co-transporter

44
Q

What do loop diuretics and thiazide diuretics inhibit

A

Na upstream of K secretion sites

45
Q

What is the mechanism behind K sparing diuretics?

A

These diuretics act on the actions of the cells that are affected by aldosterone sensitive cells, ie on principal cells
The K sparing diuretics inhibit Na transport in the principal cells, and Na/K/ATPase activity is downregulated, so K secretion is decreased

46
Q

Acute metabolic acidosis will cause what for K secretion and excretion

A

Acute metabolic acidosis will decrease Na/K/ATPase activity as well as K permeability in the apical membrane of the pincipal cells in the distal tubule and collecting duct, both of which will lead to decreased K secretion and decreased K excretion

47
Q

If you have chronic metabolic acidosis, what will happen to K secretion and excretion

A

For chronic, it comes from acute, which has decreased K excretion. If there is decreased K excretion, then there will be increased plasma K concentration. (There will also be increased plasma K concentration because of an increase in the H+/K exchanger). This leads to activation of aldosterone, which will act in the distal tubule and the collecting duct on the principal cells to increase Na/K/ATPase activity and K permeability in the apical membrane, thus increasing K secretion and excretion. Additionally, in the proximal tubule, you will have decreased NaCl and H2O reabsorption and increased tubular fluid flow rate, both of which will contribute to the effects seen in the distal tubule and collecting duct

48
Q

What are the cellular processes in which Ca2+ plays an important role

A

Bone formation, cell division and growth, blood coagulation, hormone-response coupling, and electrical stimulus-response coupling

49
Q

What percentage of Ca is found in ICF and ECF

A

1% in ICF and 0.1% in ECF

50
Q

What percentage of Calcium is ionized, complexed, or protein bound?

A

Ionized: 50%
Complexed: 10%
Protein bound: 40%

51
Q

In acidosis, what happens to ionized Ca

A

Increased ionized Ca, so hypercalcemia

52
Q

In alkalosis, what happens to ionized Ca

A

Decreased ionized Ca, so hypocalemia

53
Q

How does acidosis increase plasma Ca

A

H can compete with Ca for binding to anionic sites on proteins or small molecules so it can displace the Ca and pushes it into the ECF

54
Q

Acute alkalosis can cause signs and symptoms mimicking what

A

Hypocalemia

55
Q

Ca binding to plasma proteins depends on _____

A

Protein concentration, especially albumin

56
Q

What percentage of Pi is stored in

Bone
ICF
ECF
Protein bound

A

Bone is 86%
ICF is 14%
ECF is 0.03%
Protein bound is 10%

57
Q

Dietary intake of phosphate is how much per day

A

1400 mg/day

58
Q

GI excretion of phosphate per day

A

500 mg/day

59
Q

In adults, the kidneys maintain total body Pi balance bt

A

Excreting an amount of Pi in the urine equal to the amount absorbed by the intestinal tract (900 mg/day)

60
Q

If Pi is moving from intestine to phosphate pool, what is that called

A

Absorption

61
Q

If Pi is moving from bone and soft tissue to the phosphate pool, what is that called

A

Resorption

62
Q

What will Calcitriol do for Pi

A

Calcitriol will have 2 actions

1) when paired with PTH, will faciliate resorption of Pi from bone to phosphate pool
2) Will inhibit excretion from kidneys in the urine

63
Q

What will PTH do to Pi

A

Two actions

1) When paired with Calcitriol, will facilitate resorption from bone and soft tissue to phosphate pool
2) When paired with FGF-23, will increase excretion from kidneys in urine

64
Q

Dietary intake of Ca per day

A

1000 mg

65
Q

Amount of Ca excreted out of the feces

A

800 mg

66
Q

Amount of Ca excreted through urine

A

200 mg

67
Q

What does Calcitriol do for Ca

A

3 actions

1) With PTH, will facilitate resorption from bone to calcium pool
2) Will inhibit excretion of Ca through urine
3) Will increase Ca absorbed from intestine

68
Q

What will PTH do for Ca

A

2 things

1) With calcitriol, will inhibit excretion of Ca from kidneys as urine
2) With calcitriol, will facilitate resorption from bone to calcium pool

69
Q

How much filtered Ca is reabsorbed by the nephron

A

About 99%

70
Q

The proximal tubule reabsorbs what percentage of Ca

A

50-70%

71
Q

The TAL reabsorbs what percentage of Ca

A

20%

72
Q

The distal tubule reabsorbs what percentage of Ca

A

9-10%

73
Q

Increased plasma Pi does what to plasma Ca, PTH, and Pi excretion

A

Reduces plasma Ca concentrations, therefore increases plasma PTH, which increases Pi excretion by the kidneys

74
Q

What is the most important hormone to control Pi excretion and how does it work

A

PTH is the most important hormone and it inhibits Pi reabsorption by the proximal tubule and thereby increases Pi excretion

75
Q

Increased plasma Pi will also do what to FGF-23 and calcitriol

A

Increased plasma Pi increases FGF-23, which increases Pi excretion and increases calcitriol production by the proximal tubule

However, will also suppress calcitriol production, which results in a decrease in intestinal Pi reabsorption

76
Q

Function of FGF-23

A

Inhibits Pi reabsorption and inhibits calcitriol production
Secretion is stimulated by sustained hyperphosphatemia, PTH, and calcitriol

FGF-23 is the brake

77
Q

Calcitriol’s effect on Ca and phosphate

A

Stimulates Ca and phosphate uptake from GI tract, and stimulates renal reabsorption of Ca and phosphate. Maintains normal bone remodeling

78
Q

PTH’s effect on Ca and phosphate

A

Stimulates rapid transfer of Ca and phosphate from bone and stimulates slower bone resorption. Also increases renal excretion of phosphate and stimulates renal reabsorption of Ca

79
Q

FGF-23’s effect on Ca and Phosphate

A

Increases renal excretion of phosphate, and increases renal reabsorption of Ca

80
Q

Effect of Calcitriol on other hormones

A

Suppresses PTH synthesis, stimulates FGF-23 secretion

81
Q

PTH’s effect on other hormones

A

Stimulates renal production of calcitriol

82
Q

FGF-23’s effect on other hormones

A

Decreases renal production of calcitriol

FHB Mikayla (26 decks)

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