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Nelson - Fluids > Electrolytes and Acid-Base Disorders > Flashcards

Electrolytes and Acid-Base Disorders Flashcards

1
Q

TBW of term infants

A

75%

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2
Q

TBW from the first year of life until puberty

A

60%

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3
Q

TBW at the end of puberty, males

A

60%

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4
Q

TBW at the end of puberty, females

A

50%

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5
Q

ICF is ___% of TBW

A

30-40

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6
Q

ECF is ___% of TBW

A

20-25

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7
Q

Plasma is ___% of TBW

A

5

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8
Q

IF is ___% of TBW

A

15

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9
Q

Normal plasma osmolality

A

285-295 mOsm/kg

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10
Q

Formula for osmolality

A

2Na + Gluc/18 + BUN/2.8

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11
Q

Formula for effective osmolality

A

2Na + Gluc/18

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12
Q

Effective osmolality is aka

A

Tonicity

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13
Q

Determines the osmotic force that is mediating the shift of water between the ICF and ECF

A

Effective osmolality (tonicity)

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14
Q

Formula for corrected Na in hyperglycemia

A

Measured sodium + [1.6 (glucose – 100) / 100]

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15
Q

Osmolal gap is a clinical clue to

A

Presence of unmeasured osmoles and may indicate poisoning with methanol or ethylene glycol

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16
Q

Osmolal gap is present if

A

Measured osm exceeds calculated osm bby >10 mOsm/kg

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17
Q

Elevated effective osmolality leads to secretion of what hormone

A

ADH

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18
Q

Most important determinant of renal Na excretion

A

Volume status of the child

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19
Q

Main sites for precise regulation of Na balance in the kidney

A

Distal tubule and collecting duct

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20
Q

Accounts for elevated BUN and uric acid in dehydration

A

Resorption of uric acid and urea in the proximal tubule when Na retention increases

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21
Q

Increase in blood volume stimulates release of what hormone

A

ANP –> increase in GFR –> inhibition of Na resorption in the medullary portion of the collecting duct

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22
Q

Na intake is recommended not to exceed

A

2500mg/day

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23
Q

T/F Presence of glucose enhances Na absorption in the GIT

A

T

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24
Q

Most devastating consequence of hypernatremia

A

Brain hemorrhage

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25
Q

Goal in hypernatremia is to decrease Na by ___

A

<12meq/L every 24 hrs or 0.5meq/L/hr

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26
Q

In hypernatremic dehydration, first priority is to

A

Restore intravascular volume with ISOTONIC solution, preferably normal saline

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27
Q

Why is NSS>LR in restoration of intravascular volume in hypernatremic dehydration

A

Low Na concentration of LR can cause serum Na to decrease too rapdily

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28
Q

Formula for water deficit

A

Weight x 0.6 (1-145/Na)

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29
Q

MCC of hypovolemic hyponatremia

A

Diarrhea

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30
Q

Type of hyponatremia seen in heart failure and renal failure

A

Hypervolemic hyponatremia

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31
Q

Type of hyponatremia seen in SIADH

A

Euvolemic hyponatremia

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32
Q

Responsible for most of the symptoms of hyponatremia

A

Brain cell swelling

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33
Q

Traditional first step in the diagnostic process in hyponatremia

A

Determination of plasma osmolality

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34
Q

Low vs normal osmolality vs high osmolality: True hyponatremia

A

Low

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35
Q

Low vs normal osmolality vs high osmolality: Pseudohyponatremia

A

Normal

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36
Q

Low vs normal osmolality vs high osmolality: Elevation of another effective osmole, e.g. glucose

A

High

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37
Q

To prevent central pontine myelinosis, correction of hyponatremia should not be more than ___meq/L in 48 hours

A

18

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38
Q

Each mL of 3% NaCl (HTS) increases Na by approximately

A

1 meq/L

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39
Q

Insulin increases movement of K into the cells by activating

A

Na-K-ATPase

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40
Q

T/F Decrease in pH drives potassium extracellularly

A

T

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41
Q

Mechanism of beta agonist in cases of hyperkalemia

A

Increases movement of K into the cells by activating Na-K-ATPase

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42
Q

T/F α-agonists causes a net movement of K out of the cell

A

T

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43
Q

T/F Exercise causes a net movement of K out of the cell

A

T

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44
Q

Principal hormone regulating potassium secretion

A

Aldosterone

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45
Q

Most important effects of hyperkalemia are due to

A

Role of K in membrane polarization

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46
Q

ECG changes in hyperkalemia begins with

A

Peaking of T waves –> OTHER: ST depression, increased PR, flattening of P, widening of QRS –> Vfib

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47
Q

Useful method to evaluate renal response to hyperkalemia

A

TTKG (Transtubular potassium gradient)

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48
Q

Formula for TTKG

A

Kurine/Kplasma x (plasma osm/urine osm)

49
Q

TTKG value when there is normal renal excretion of K

A

> 10

50
Q

TTKG value when there is a defect in renal excretion of K

A

<8 (such as in lack of aldosterone)

51
Q

Treatment of hyperkalemia that RAPIDLY decreases the risk of life-threatening arrhythmias: Shift potassium intracellularly

A

Insulin, beta agonist, NaHCO3

52
Q

Treatment of hyperkalemia that RAPIDLY decreases the risk of life-threatening arrhythmias: Cardiac membrane stabilization

A

IV Calcium

53
Q

Treatment of hyperkalemia that removes potassium from the body

A

Loop diuretic, SPS (Kayexalate), dialysis

54
Q

MOA of SPS

A

Na is exchanged for K and K-containing resin is excreted from the body

55
Q

Met alk + hypoK + high urine chloride + normal BP

A

Bartter, Gitelman, diuretic use

56
Q

ECG changes in hypoK

A

Flattened T, ST depression, U wave

57
Q

Paralysis is possible only at K level of

A

<2.5meq/L

58
Q

TTKG of ___ in the presence of hypoK suggests excessive urinary losses of K

A

> 4

59
Q

4th MC cation in the body

A

Mg

60
Q

3rd MC intracellular cation

A

Mg

61
Q

MCC of hypomag

A

GI and renal losses

62
Q

Drugs that cause significant Mg wasting

A

Amphotericin and Cisplatin

63
Q

Hypomag causes secondary hypocal bby

A

Impairing release of PTH and blunting of tissue response to PTH

64
Q

Symptoms of hypermag do not occur until plasma Mg is

A

> 4.5

65
Q

Effect of hypermag on muscles and reflexes

A

Inhibits Ach release at the NMJ –> hypotonia, hyporeflexia, weakness

66
Q

Effect of hypermag on BP

A

Associated with hypotension because of vascular dilation

67
Q

Level of hypermag that causes complete heart block and cardiac arrest

A

> 15mg/dL

68
Q

Aprox 65% of plasma phos is in

A

Phospholipids

69
Q

Most plentiful intracellular anion

A

Phosphate

70
Q

Effect of PTH on serum phos

A

Decreases serum and increases urinary phosphate by decreasing resorption in the kidneys

71
Q

Body’s compensatory mechanism for hypophos

A

Stimulates 1α-hydroxylase –> 25-D to 1,25-D (calcitriol) –> increase intestinal absorption and renal resorption of phos

72
Q

Effect of Phosphatonin

A

Inhibits renal resorption of phos causing phosphaturia and hypophosphatemia

73
Q

Mechanism of hypophos in refeeding syndrome

A

Anabolism –> significant cellular demand for phos

74
Q

Mechanism of hypophos in respi alk

A

Glycolysis > intracellular use of phos

75
Q

Avid uptake of phos along with Ca and Mg which can produce plasma deficiency of all 3 ions

A

Hungry bone syndrome (seen after parathyroidectomy)

76
Q

MCC of severe hypophos in adults

A

Alcoholism

77
Q

Severe hypophos is defined as a level of

A

1-1.5mg/dL

78
Q

MC complication of acute hypophos

A

Rhabdomyolysis

79
Q

MCC of hyperphos

A

Renal insufficiency

80
Q

Principal clinical consequence of hyperphosphatemia

A

Hypocalcemia and systemic calcification

81
Q

Mechanism of Sevelamer

A

An ORAL phosphate binder given in significant hyperphosphatemia that prevents absorption of dietary phosphorus by binding it in the GIT

82
Q

Henderson-Hasselbbach equation

A

pH = 6.1 + log [HCO3-]/[CO2]

83
Q

Rapid pulmonary response to changes in CO2 concentration occurs via

A

Central sensing of pCO2 and subsequent increase or decrease in ventilation

84
Q

3 principal sources of hydrogen ions

A

1) Dietary protein metab 2) Incomplete metab of carbb (lactic acid) and fats (ketones) 3) Stool losses of bicarb

85
Q

Necessary 1st step in renal regulation of acid-base balance

A

Resorption of filtered bicarbonate

86
Q

Reclaims ~85% of filtered HCO3

A

Proximal tubule

87
Q

Most important regulator of renal acid excretion

A

Extracellular pH

88
Q

Respiratory compensation for a metabolic process happens quickly and is complete within

A

12-24 hours

89
Q

Renal compensation for a metabolic process is completed within

A

3-4 days

90
Q

Expected compensation: Met acid

A

pCO2 = 1.5 x HCO3 + 8±2

91
Q

Expected compensation: Met alk

A

pCO2 increases by 7mmHg for every 10meq/L increase in serum HCO3

92
Q

Expected compensation: Respi acid, acute

A

HCO3 increases by 1 for each 10mmHg increase in pCO2

93
Q

Expected compensation: Respi acid, chronic

A

HCO3 increases by 3.5 for each 10mmHg increase in pCO2

94
Q

Expected compensation: Respi alk, acute

A

HCO3 falls bby 2 for each 10mmHg decrease in pCO2

95
Q

Expected compensation: Respi alk, chronic

A

HCO3 falls by 4 for each 10mmHg decrease in pCO2

96
Q

MC etiology of met acid

A

Diarrhea

97
Q

Serum pH ___ may impair cardiac contractility and increase risk of arrhythmia

A

<7.2

98
Q

Effect of acidemia on cardiovascular response to catecholamines

A

May decrease

99
Q

Effect of acidemia on pulmonary vasculature

A

VASOCONSTRICTION

100
Q

Acute effect of acidemia on action of insulin

A

Insulin resistance

101
Q

Acute effect of acidemia on ATP

A

Reduced ATP synthesis

102
Q

Anion gap formula

A

Na - Cl - HCO3

103
Q

Normal AG

A

4-11

104
Q

Met acid resulting from increase in unmeasured anions

A

HAGMA

105
Q

Met acid resulting from decrease in bicarbonate concentration without an increase in unmeasured anions

A

NAGMA

106
Q

Approx 11 meqs of anion gap is normally sec to

A

Albumin

107
Q

1g/dL decrease in albumin decreases anion gap by

A

~2.5meq/L

108
Q

Met alkalosis is MC secondary to

A

Emesis or diuretic use

109
Q

pCO2 increases by 7mmHg for each 10meq/L increase in serum HCO3 but pCO2 never exceeds

A

55-60

110
Q

Etiologies of met alkalosis are divided into 2 categories babsed on

A

Urinary chloride level

111
Q

Etiology of met alkalosis: Does not respond to volume repletion

A

Elevated urinary chloride

112
Q

Etiology of met alkalosis: Responds to volume repletion

A

Low chloride level

113
Q

Mechanism of tetany in alkalemia

A

iCa decreases as a result of increased binding of Ca to albumin

114
Q

Intervention is usually necessary with moderate or severe met alkalosis, that is with a HCO3 level of

A

> 32

115
Q

T/F In a patient breathing room air, hypoxia is always present if a respiratory acidosis is present

A

T

116
Q

Effect of hypercapnia on pulmonary vasculature

A

Vasoconstriction

117
Q

Effect of hypercapnia on cerebral vasculature

A

Vasodilation

118
Q

T/F In patient with chronic respi acid, respiratory drive is often less responsive to hypercarbia and more responsive to hypoxia

A

T

119
Q

Effects of hypoxemia on ventilation begins when O2sat decreases to approx ___ and pO2 ___

A

90%, 60mmHg

Nelson - Fluids (4 decks)

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