Electrolytes and Acid-Base Disorders Flashcards
1
Q
TBW of term infants
A
75%
2
Q
TBW from the first year of life until puberty
A
60%
3
Q
TBW at the end of puberty, males
A
60%
4
Q
TBW at the end of puberty, females
A
50%
5
Q
ICF is ___% of TBW
A
30-40
6
Q
ECF is ___% of TBW
A
20-25
7
Q
Plasma is ___% of TBW
A
5
8
Q
IF is ___% of TBW
A
15
9
Q
Normal plasma osmolality
A
285-295 mOsm/kg
10
Q
Formula for osmolality
A
2Na + Gluc/18 + BUN/2.8
11
Q
Formula for effective osmolality
A
2Na + Gluc/18
12
Q
Effective osmolality is aka
A
Tonicity
13
Q
Determines the osmotic force that is mediating the shift of water between the ICF and ECF
A
Effective osmolality (tonicity)
14
Q
Formula for corrected Na in hyperglycemia
A
Measured sodium + [1.6 (glucose – 100) / 100]
15
Q
Osmolal gap is a clinical clue to
A
Presence of unmeasured osmoles and may indicate poisoning with methanol or ethylene glycol
16
Q
Osmolal gap is present if
A
Measured osm exceeds calculated osm bby >10 mOsm/kg
17
Q
Elevated effective osmolality leads to secretion of what hormone
A
ADH
18
Q
Most important determinant of renal Na excretion
A
Volume status of the child
19
Q
Main sites for precise regulation of Na balance in the kidney
A
Distal tubule and collecting duct
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
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
22
Q
Na intake is recommended not to exceed
A
2500mg/day
23
Q
T/F Presence of glucose enhances Na absorption in the GIT
A
T
24
Q
Most devastating consequence of hypernatremia
A
Brain hemorrhage
25
Goal in hypernatremia is to decrease Na by ___
<12meq/L every 24 hrs or 0.5meq/L/hr
26
In hypernatremic dehydration, first priority is to
Restore intravascular volume with ISOTONIC solution, preferably normal saline
27
Why is NSS>LR in restoration of intravascular volume in hypernatremic dehydration
Low Na concentration of LR can cause serum Na to decrease too rapdily
28
Formula for water deficit
Weight x 0.6 (1-145/Na)
29
MCC of hypovolemic hyponatremia
Diarrhea
30
Type of hyponatremia seen in heart failure and renal failure
Hypervolemic hyponatremia
31
Type of hyponatremia seen in SIADH
Euvolemic hyponatremia
32
Responsible for most of the symptoms of hyponatremia
Brain cell swelling
33
Traditional first step in the diagnostic process in hyponatremia
Determination of plasma osmolality
34
Low vs normal osmolality vs high osmolality: True hyponatremia
Low
35
Low vs normal osmolality vs high osmolality: Pseudohyponatremia
Normal
36
Low vs normal osmolality vs high osmolality: Elevation of another effective osmole, e.g. glucose
High
37
To prevent central pontine myelinosis, correction of hyponatremia should not be more than ___meq/L in 48 hours
18
38
Each mL of 3% NaCl (HTS) increases Na by approximately
1 meq/L
39
Insulin increases movement of K into the cells by activating
Na-K-ATPase
40
T/F Decrease in pH drives potassium extracellularly
T
41
Mechanism of beta agonist in cases of hyperkalemia
Increases movement of K into the cells by activating Na-K-ATPase
42
T/F α-agonists causes a net movement of K out of the cell
T
43
T/F Exercise causes a net movement of K out of the cell
T
44
Principal hormone regulating potassium secretion
Aldosterone
45
Most important effects of hyperkalemia are due to
Role of K in membrane polarization
46
ECG changes in hyperkalemia begins with
Peaking of T waves --> OTHER: ST depression, increased PR, flattening of P, widening of QRS --> Vfib
47
Useful method to evaluate renal response to hyperkalemia
TTKG (Transtubular potassium gradient)
48
Formula for TTKG
Kurine/Kplasma x (plasma osm/urine osm)
49
TTKG value when there is normal renal excretion of K
>10
50
TTKG value when there is a defect in renal excretion of K
<8 (such as in lack of aldosterone)
51
Treatment of hyperkalemia that RAPIDLY decreases the risk of life-threatening arrhythmias: Shift potassium intracellularly
Insulin, beta agonist, NaHCO3
52
Treatment of hyperkalemia that RAPIDLY decreases the risk of life-threatening arrhythmias: Cardiac membrane stabilization
IV Calcium
53
Treatment of hyperkalemia that removes potassium from the body
Loop diuretic, SPS (Kayexalate), dialysis
54
MOA of SPS
Na is exchanged for K and K-containing resin is excreted from the body
55
Met alk + hypoK + high urine chloride + normal BP
Bartter, Gitelman, diuretic use
56
ECG changes in hypoK
Flattened T, ST depression, U wave
57
Paralysis is possible only at K level of
<2.5meq/L
58
TTKG of ___ in the presence of hypoK suggests excessive urinary losses of K
>4
59
4th MC cation in the body
Mg
60
3rd MC intracellular cation
Mg
61
MCC of hypomag
GI and renal losses
62
Drugs that cause significant Mg wasting
Amphotericin and Cisplatin
63
Hypomag causes secondary hypocal bby
Impairing release of PTH and blunting of tissue response to PTH
64
Symptoms of hypermag do not occur until plasma Mg is
>4.5
65
Effect of hypermag on muscles and reflexes
Inhibits Ach release at the NMJ --> hypotonia, hyporeflexia, weakness
66
Effect of hypermag on BP
Associated with hypotension because of vascular dilation
67
Level of hypermag that causes complete heart block and cardiac arrest
>15mg/dL
68
Aprox 65% of plasma phos is in
Phospholipids
69
Most plentiful intracellular anion
Phosphate
70
Effect of PTH on serum phos
Decreases serum and increases urinary phosphate by decreasing resorption in the kidneys
71
Body's compensatory mechanism for hypophos
Stimulates 1α-hydroxylase --> 25-D to 1,25-D (calcitriol) --> increase intestinal absorption and renal resorption of phos
72
Effect of Phosphatonin
Inhibits renal resorption of phos causing phosphaturia and hypophosphatemia
73
Mechanism of hypophos in refeeding syndrome
Anabolism --> significant cellular demand for phos
74
Mechanism of hypophos in respi alk
Glycolysis > intracellular use of phos
75
Avid uptake of phos along with Ca and Mg which can produce plasma deficiency of all 3 ions
Hungry bone syndrome (seen after parathyroidectomy)
76
MCC of severe hypophos in adults
Alcoholism
77
Severe hypophos is defined as a level of
1-1.5mg/dL
78
MC complication of acute hypophos
Rhabdomyolysis
79
MCC of hyperphos
Renal insufficiency
80
Principal clinical consequence of hyperphosphatemia
Hypocalcemia and systemic calcification
81
Mechanism of Sevelamer
An ORAL phosphate binder given in significant hyperphosphatemia that prevents absorption of dietary phosphorus by binding it in the GIT
82
Henderson-Hasselbbach equation
pH = 6.1 + log [HCO3-]/[CO2]
83
Rapid pulmonary response to changes in CO2 concentration occurs via
Central sensing of pCO2 and subsequent increase or decrease in ventilation
84
3 principal sources of hydrogen ions
1) Dietary protein metab 2) Incomplete metab of carbb (lactic acid) and fats (ketones) 3) Stool losses of bicarb
85
Necessary 1st step in renal regulation of acid-base balance
Resorption of filtered bicarbonate
86
Reclaims ~85% of filtered HCO3
Proximal tubule
87
Most important regulator of renal acid excretion
Extracellular pH
88
Respiratory compensation for a metabolic process happens quickly and is complete within
12-24 hours
89
Renal compensation for a metabolic process is completed within
3-4 days
90
Expected compensation: Met acid
pCO2 = 1.5 x HCO3 + 8±2
91
Expected compensation: Met alk
pCO2 increases by 7mmHg for every 10meq/L increase in serum HCO3
92
Expected compensation: Respi acid, acute
HCO3 increases by 1 for each 10mmHg increase in pCO2
93
Expected compensation: Respi acid, chronic
HCO3 increases by 3.5 for each 10mmHg increase in pCO2
94
Expected compensation: Respi alk, acute
HCO3 falls bby 2 for each 10mmHg decrease in pCO2
95
Expected compensation: Respi alk, chronic
HCO3 falls by 4 for each 10mmHg decrease in pCO2
96
MC etiology of met acid
Diarrhea
97
Serum pH ___ may impair cardiac contractility and increase risk of arrhythmia
<7.2
98
Effect of acidemia on cardiovascular response to catecholamines
May decrease
99
Effect of acidemia on pulmonary vasculature
VASOCONSTRICTION
100
Acute effect of acidemia on action of insulin
Insulin resistance
101
Acute effect of acidemia on ATP
Reduced ATP synthesis
102
Anion gap formula
Na - Cl - HCO3
103
Normal AG
4-11
104
Met acid resulting from increase in unmeasured anions
HAGMA
105
Met acid resulting from decrease in bicarbonate concentration without an increase in unmeasured anions
NAGMA
106
Approx 11 meqs of anion gap is normally sec to
Albumin
107
1g/dL decrease in albumin decreases anion gap by
~2.5meq/L
108
Met alkalosis is MC secondary to
Emesis or diuretic use
109
pCO2 increases by 7mmHg for each 10meq/L increase in serum HCO3 but pCO2 never exceeds
55-60
110
Etiologies of met alkalosis are divided into 2 categories babsed on
Urinary chloride level
111
Etiology of met alkalosis: Does not respond to volume repletion
Elevated urinary chloride
112
Etiology of met alkalosis: Responds to volume repletion
Low chloride level
113
Mechanism of tetany in alkalemia
iCa decreases as a result of increased binding of Ca to albumin
114
Intervention is usually necessary with moderate or severe met alkalosis, that is with a HCO3 level of
>32
115
T/F In a patient breathing room air, hypoxia is always present if a respiratory acidosis is present
T
116
Effect of hypercapnia on pulmonary vasculature
Vasoconstriction
117
Effect of hypercapnia on cerebral vasculature
Vasodilation
118
T/F In patient with chronic respi acid, respiratory drive is often less responsive to hypercarbia and more responsive to hypoxia
T
119
Effects of hypoxemia on ventilation begins when O2sat decreases to approx ___ and pO2 ___
90%, 60mmHg
