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Important Electrolytes Flashcards

1
Q

Major extracellular cation

A

Sodium

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2
Q

Renal threshold for sodium

A

110-130 mmol/L (120 mmol/L)

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3
Q

Reference range for sodium

A

136–145 mmol/L (mEq/L)

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4
Q

Panic values for sodium

A

</= 120 mmol/L (hyponatremia), >/= 160 mmol/L (hypernatremia)

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5
Q

Most common method for sodium measurement

A

Ion-selective electrode (ISE) with glass silicate electrode

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6
Q

Difference between direct and indirect ISE

A

Direct measures undiluted, indirect measures diluted (prone to pseudohyponatremia)

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7
Q

Color observed in flame photometry for sodium

A

Yellow

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8
Q

Rarely used colorimetric method for sodium

A

Albanese-Lein (produces yellow color)

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9
Q

Causes of absolute sodium loss in hyponatremia

A

Addison’s disease, salt-losing nephropathy, ketonuria, prolonged vomiting or diarrhea, severe burns, diuretics

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10
Q

Cause of dilutional hyponatremia with water retention

A

Renal failure, CHF, nephrotic syndrome, hepatic cirrhosis

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11
Q

Condition causing water imbalance in hyponatremia

A

SIADH, increased water intake

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12
Q

Effect of SIADH on sodium and water

A

Increased ADH retention, relative water excess, pseudohyponatremia

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13
Q

Causes of high plasma osmolality in hyponatremia

A

Hyperglycemia, mannitol infusion

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14
Q

Causes of hypernatremia with absolute sodium increase

A

NaHCO3 excess, hyperaldosteronism (Conn’s syndrome)

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15
Q

Urine osmolality < 300 mOsm/kg in hypernatremia

A

Diabetes insipidus (low urine SG and Osm)

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16
Q

Urine osmolality 300–700 mOsm/kg in hypernatremia

A

Partial AVP defect, osmotic diuresis

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17
Q

Urine osmolality > 700 mOsm/kg in hypernatremia

A

Loss of thirst, insensible water loss, GI fluid loss, excess sodium intake

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18
Q

Direct ISE measures sodium in

A

Undiluted samples

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19
Q

Indirect ISE measures sodium in

A

Diluted samples (prone to pseudohyponatremia)

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20
Q

Causes of absolute sodium loss in hyponatremia

A

Addison’s disease, salt-losing nephropathy, ketonuria (DKA), prolonged vomiting or diarrhea, severe burns, diuretics

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21
Q

Pathophysiology of sodium loss in Addison’s disease

A

Primary adrenalism; decreased aldosterone leads to reduced sodium retention and increased potassium

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22
Q

Causes of dilutional hyponatremia due to water retention

A

Renal failure, CHF, nephrotic syndrome, hepatic cirrhosis

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23
Q

Causes of dilutional hyponatremia due to water imbalance

A

Increased water intake, SIADH

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24
Q

Mechanism of SIADH in hyponatremia

A

Increased ADH retention caused by tumors; hydrostatic pressure exceeds osmotic pressure, leading to pseudohyponatremia

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25
Q

Potassium concentration in cells compared to extracellular fluid

A

20x higher intracellularly; major intracellular cation

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26
Q

Reference range for potassium in serum

A

3.5–5.1 mmol/L

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27
Q

Reference range for potassium in plasma

A

3.5–4.5 mmol/L

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28
Q

Potassium level due to platelet release after clotting

A

5.1 mmol/L

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29
Q

Panic values for potassium

A

≤2.8 mmol/L (hypokalemia); ≥6.2 mmol/L (hyperkalemia)

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30
Q

Most common method for potassium measurement

A

ISE using valinomycin

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31
Q

Flame photometry flame color for potassium

A

Violet

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32
Q

Lockhead-Purcell method result for potassium

A

Color/Spectrophotometry = blue

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33
Q

Primary cause of hypokalemia in cellular shifts

A

Influx due to increased pH (alkalosis), insulin overdose

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34
Q

Mechanism of potassium influx in alkalosis

A

Increased pH causes hydrogen ion movement out of cells, driving potassium into cells

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35
Q

Effect of insulin overdose on potassium levels

A

Promotes cellular uptake of potassium, leading to hypokalemia

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36
Q

Effect of alkalosis on potassium distribution

A

Potassium increases inside RBCs (cellular influx)

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37
Q

Causes of hypokalemia due to GI loss

A

Vomiting, diarrhea, gastric suction, laxatives, malabsorption

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38
Q

Causes of hypokalemia due to renal loss

A

Renal tubular acidosis, hyperaldosteronism (↑ Na reabsorption, ↓ K excretion), thiazide diuretics

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39
Q

Hyperkalemia mechanism: cellular shift

A

Potassium moves outside cells (efflux) during acidosis, chemotherapy, muscle injury, leukemia, or hemolysis

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40
Q

Hyperkalemia mechanism: increased intake

A

Oral or IV potassium replacement

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41
Q

Hyperkalemia mechanism: decreased renal excretion

A

Renal failure, hypoaldosteronism, K-sparing diuretics

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42
Q

Causes of pseudohyperkalemia

A

Sample hemolysis, hemoconcentration/venous stasis, thrombocytosis, use of EDTA anticoagulant

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43
Q

Major extracellular anion

A

Chloride

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44
Q

Relationship with Sodium and HCO3-

A

Direct relationship with Sodium; inverse relationship with HCO3- (chloride shift)

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45
Q

Reference values for Serum (mEq/L)

A

98–107 mmol/L

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46
Q

Reference values for Sweat Chloride

A

<40 mmol/L

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47
Q

Panic values for Serum Chloride

A

≤80 mmol/L or ≥120 mmol/L

48
Q

Panic values for Sweat Chloride

A

≥60 mmol/L (indicative of cystic fibrosis)

49
Q

Method for sweat chloride analysis

A

Gibson and Cooke’s method (pilocarpine iontophoresis)

50
Q

Common method for Chloride measurement

A

ISE with ion exchange membrane

51
Q

Mercurimetric titration method for chloride

A

Schales-Schales method (blue-violet color with diphenylcarbazone)

52
Q

Spectrophotometric chloride assay

A

Whitehorn titration (red complex with mercuric thiocyanate)

53
Q

Hypochloremia causes

A

Same as sodium: aldosterone deficiency, salt-losing nephropathy, DKA, vomiting, diarrhea, severe burns, diuretics; metabolic alkalosis, compensated respiratory acidosis

54
Q

Hyperchloremia causes

A

Same as sodium: renal tubular acidosis, GI loss of HCO3-, metabolic acidosis, compensated respiratory alkalosis

55
Q

Inverse changes between Bicarbonate and Chloride

A

Increased bicarbonate = decreased chloride; decreased bicarbonate = increased chloride

56
Q

Major extracellular anion

57
Q

Relationship with Sodium and HCO3-

A

Direct relationship with Sodium; inverse relationship with HCO3- (chloride shift)

58
Q

Reference values for Serum (mEq/L)

A

98–107 mmol/L

59
Q

Reference values for Sweat Chloride

A

<40 mmol/L

60
Q

Panic values for Serum Chloride

A

≤80 mmol/L or ≥120 mmol/L

61
Q

Panic values for Sweat Chloride

A

≥60 mmol/L (indicative of cystic fibrosis)

62
Q

Method for sweat chloride analysis

A

Gibson and Cooke’s method (pilocarpine iontophoresis)

63
Q

Common method for Chloride measurement

A

ISE with ion exchange membrane

64
Q

Mercurimetric titration method for chloride

A

Schales-Schales method (blue-violet color with diphenylcarbazone)

65
Q

Spectrophotometric chloride assay

A

Whitehorn titration (red complex with mercuric thiocyanate)

66
Q

Hypochloremia causes

A

Same as sodium: aldosterone deficiency, salt-losing nephropathy, DKA, vomiting, diarrhea, severe burns, diuretics; metabolic alkalosis, compensated respiratory acidosis

67
Q

Hyperchloremia causes

A

Same as sodium: renal tubular acidosis, GI loss of HCO3-, metabolic acidosis, compensated respiratory alkalosis

68
Q

Inverse changes between Bicarbonate and Chloride

A

Increased bicarbonate = decreased chloride; decreased bicarbonate = increased chloride

69
Q

Second major extracellular anion

A

Bicarbonate

70
Q

Percentage of total CO2 at physiological pH

A

> 90% of the total CO2

71
Q

Reference values for measured TCO2

A

23–27 mmol/L

72
Q

Reference values for calculated HCO3–

A

22–26 mmol/L

73
Q

Panic values for HCO3–

A

≤10 mmol/L or ≥40 mmol/L

74
Q

Method for Total CO2 measurement

A

ISE (acidification of sample followed by electrode-based CO2 detection)

75
Q

Enzymatic method for HCO3– measurement

A

Involves alkalinization to convert CO2 and H2CO3 to HCO3– followed by enzymatic reaction with PEP carboxylase and malate dehydrogenase (decreased absorbance at 340 nm)

76
Q

Clinical significance of ↓ HCO3–

A

Metabolic acidosis, compensated respiratory alkalosis, RTA, GI loss of HCO3–

77
Q

Clinical significance of ↑ HCO3–

A

Metabolic alkalosis, compensated respiratory acidosis

78
Q

Cofactor of enzymes Magnesium

A

> 300 enzymes

79
Q

Magnesium distribution

A

55% ionized, 30% bound to proteins, 15% bound to ions

80
Q

Reference values for magnesium (mEq/L)

A

1.26–2.1 mEq/L

81
Q

Reference values for magnesium (mg/dL)

A

1.51–2.52 mg/dL

82
Q

Panic values of magnesium(mg/dL)

A

≤1 or ≥4.7 mg/dL

83
Q

Reference method for magnesium

A

AAS (Atomic Absorption Spectrophotometry)

84
Q

Dye-binding methods for magnesium

A

Calmagite (Red Violet), formazan, methylthymol blue, xylidyl blue

85
Q

Dye-lake methods for magnesium

A

Titan yellow (ACD lake), Clayton yellow, thiazole yellow dye

86
Q

Clinical significance of Hypomagnesemia

A

↓ intake (poor diet, starvation, chronic alcoholism), ↓ absorption (vomiting, diarrhea, malabsorption), ↑ excretion (renal, endocrine, drug-induced)

87
Q

Clinical significance of Hypermagnesemia

A

↑ intake (antacids, enemas), ↓ excretion (renal failure, hypoaldosteronism)

88
Q

Calcium - Plasma level regulation

A

PTH (Bone resorption, Vitamin D activation, Ca2+ reabsorption in kidneys), Active Vitamin D (intestinal calcium absorption), Calcitonin (inhibits PTH)

89
Q

Calcium - Distribution

A

50% ionized, 40% bound to proteins (albumin), 10% bound to ions

90
Q

Calcium - Reference values (total)

A

4.3-5 mEq/L (8.6-10 mg/dL)

91
Q

Calcium - Panic values

A

≤6 mEq/L

92
Q

Calcium - Methods (AAS)

A

Lanthanum oxide to chelate phosphates (PO4)

93
Q

Calcium - Methods (ISE)

A

PVC membrane impregnated with calcium ion exchanger for ionized Ca measurement

94
Q

Calcium - Methods (Dye-binding)

A

O-cresolphthalein complexone (CPC) method, Arsenazo III (violet color for Ca2+)

95
Q

Calcium - Methods (Precipitation)

A

Clark-Collip oxalic acid precipitation, Ferro-Ham chloranilic acid precipitation

96
Q

Calcium - Clinical significance (Hypocalcemia)

A

Primary hypoparathyroidism, secondary hyperparathyroidism, chronic renal failure, hypomagnesemia, ↓ albumin, pseudohypoparathyroidism, vitamin D deficiency, pancreatitis

97
Q

Calcium - Clinical significance (Hypercalcemia)

A

Primary hyperparathyroidism, hypercalcemia of malignancy, multiple myeloma, vitamin D excess, prolonged immobilization

98
Q

Phosphate - Classification

A

Major intracellular anion, component of essential biomolecules, measured as inorganic PO4

99
Q

Phosphate - Reference range

A

2.4–4.4 mg/dL

100
Q

Phosphate - Panic values

A

≤1 mg/dL; ≥8.9 mg/dL

101
Q

Phosphate - Method (Fiske-Subbarow/Ammonium Molybdate)

A

PO4 + ammonium molybdate → Ammonium phosphomolybdate, UV: ↑ APM @ 340 nm, C/S: Phosphomolybdenum (Blue) A ↑ 600-700 nm

102
Q

Phosphate - Clinical significance (Hypophosphatemia)

A

Diabetic ketoacidosis, long-term TPN, IBD, anorexia nervosa, alcoholism, hyperparathyroidism, vitamin D deficiency

103
Q

Phosphate - Clinical significance (Hyperphosphatemia)

A

Renal failure, milk or laxatives, neoplastic disorders, intravascular hemolysis, lymphoblastic leukemia

104
Q

Phosphate - Transcellular shifts

A

Intracellularly and extracellularly depending on where it is needed, influenced by bicarbonate

105
Q

Phosphate - Regulation

A

Proximal Convoluted Tubule: reabsorption site, PTH: decreases reabsorption, Calcitonin: increases excretion, Vitamin D: increases absorption and reabsorption, Growth hormone: decreases renal excretion

106
Q

Phosphate - Pre-Analytical Considerations

A

Avoid hemolysis, do not use Citrate, Oxalate, or EDTA plasma, circadian rhythm (low in evening, high in late morning)

107
Q

Phosphate - Measurement/Analysis Methods

A

Ammonium phosphomolybdate (340 nm), Fiske and Subbarow (600 nm)

108
Q

By-product of anaerobic glycolysis, indicates hypoxia

109
Q

Lactate - Reference values (venous blood)

A

Colorimetric (POD - complexed): 8.1-15.3 mg/dL; UV (enzymatic): 4.5-19.8 mg/dL

110
Q

Lactate - Method (POD-coupled reaction)

A

Lactate + O2 → Lactate oxidase → pyruvate + H2O2 → H2O2 + chromogen (POD) → oxidized chromogen + H2O

111
Q

Lactate - Method (Enzymatic-UV)

A

Lactate + NAD → Lactate dehydrogenase → pyruvate + NADH

112
Q

Lactate - Type A Lactic Acidosis: Hypoxic/Ischemic

A

Shock, MI, severe CHF, pulmonary edema, severe blood loss

113
Q

Lactate - Type B Lactic Acidosis Metabolic:

A

Diabetes mellitus, severe infection, leukemia, liver or renal disease, toxins (ethanol, methanol, salicylate poisoning)

114
Q

Major extracellular cation

115
Q

Major intracellular cation

116
Q

Major extracellular anion

117
Q

Major intracellular anion

Clinical Chemistry (43 decks)

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