Important Electrolytes Flashcards
1
Q
Major extracellular cation
A
Sodium
2
Q
Renal threshold for sodium
A
110-130 mmol/L (120 mmol/L)
3
Q
Reference range for sodium
A
136–145 mmol/L (mEq/L)
4
Q
Panic values for sodium
A
</= 120 mmol/L (hyponatremia), >/= 160 mmol/L (hypernatremia)
5
Q
Most common method for sodium measurement
A
Ion-selective electrode (ISE) with glass silicate electrode
6
Q
Difference between direct and indirect ISE
A
Direct measures undiluted, indirect measures diluted (prone to pseudohyponatremia)
7
Q
Color observed in flame photometry for sodium
A
Yellow
8
Q
Rarely used colorimetric method for sodium
A
Albanese-Lein (produces yellow color)
9
Q
Causes of absolute sodium loss in hyponatremia
A
Addison’s disease, salt-losing nephropathy, ketonuria, prolonged vomiting or diarrhea, severe burns, diuretics
10
Q
Cause of dilutional hyponatremia with water retention
A
Renal failure, CHF, nephrotic syndrome, hepatic cirrhosis
11
Q
Condition causing water imbalance in hyponatremia
A
SIADH, increased water intake
12
Q
Effect of SIADH on sodium and water
A
Increased ADH retention, relative water excess, pseudohyponatremia
13
Q
Causes of high plasma osmolality in hyponatremia
A
Hyperglycemia, mannitol infusion
14
Q
Causes of hypernatremia with absolute sodium increase
A
NaHCO3 excess, hyperaldosteronism (Conn’s syndrome)
15
Q
Urine osmolality < 300 mOsm/kg in hypernatremia
A
Diabetes insipidus (low urine SG and Osm)
16
Q
Urine osmolality 300–700 mOsm/kg in hypernatremia
A
Partial AVP defect, osmotic diuresis
17
Q
Urine osmolality > 700 mOsm/kg in hypernatremia
A
Loss of thirst, insensible water loss, GI fluid loss, excess sodium intake
18
Q
Direct ISE measures sodium in
A
Undiluted samples
19
Q
Indirect ISE measures sodium in
A
Diluted samples (prone to pseudohyponatremia)
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
21
Q
Pathophysiology of sodium loss in Addison’s disease
A
Primary adrenalism; decreased aldosterone leads to reduced sodium retention and increased potassium
22
Q
Causes of dilutional hyponatremia due to water retention
A
Renal failure, CHF, nephrotic syndrome, hepatic cirrhosis
23
Q
Causes of dilutional hyponatremia due to water imbalance
A
Increased water intake, SIADH
24
Q
Mechanism of SIADH in hyponatremia
A
Increased ADH retention caused by tumors; hydrostatic pressure exceeds osmotic pressure, leading to pseudohyponatremia
25
Potassium concentration in cells compared to extracellular fluid
20x higher intracellularly; major intracellular cation
26
Reference range for potassium in serum
3.5–5.1 mmol/L
27
Reference range for potassium in plasma
3.5–4.5 mmol/L
28
Potassium level due to platelet release after clotting
5.1 mmol/L
29
Panic values for potassium
≤2.8 mmol/L (hypokalemia); ≥6.2 mmol/L (hyperkalemia)
30
Most common method for potassium measurement
ISE using valinomycin
31
Flame photometry flame color for potassium
Violet
32
Lockhead-Purcell method result for potassium
Color/Spectrophotometry = blue
33
Primary cause of hypokalemia in cellular shifts
Influx due to increased pH (alkalosis), insulin overdose
34
Mechanism of potassium influx in alkalosis
Increased pH causes hydrogen ion movement out of cells, driving potassium into cells
35
Effect of insulin overdose on potassium levels
Promotes cellular uptake of potassium, leading to hypokalemia
36
Effect of alkalosis on potassium distribution
Potassium increases inside RBCs (cellular influx)
37
Causes of hypokalemia due to GI loss
Vomiting, diarrhea, gastric suction, laxatives, malabsorption
38
Causes of hypokalemia due to renal loss
Renal tubular acidosis, hyperaldosteronism (↑ Na reabsorption, ↓ K excretion), thiazide diuretics
39
Hyperkalemia mechanism: cellular shift
Potassium moves outside cells (efflux) during acidosis, chemotherapy, muscle injury, leukemia, or hemolysis
40
Hyperkalemia mechanism: increased intake
Oral or IV potassium replacement
41
Hyperkalemia mechanism: decreased renal excretion
Renal failure, hypoaldosteronism, K-sparing diuretics
42
Causes of pseudohyperkalemia
Sample hemolysis, hemoconcentration/venous stasis, thrombocytosis, use of EDTA anticoagulant
43
Major extracellular anion
Chloride
44
Relationship with Sodium and HCO3-
Direct relationship with Sodium; inverse relationship with HCO3- (chloride shift)
45
Reference values for Serum (mEq/L)
98–107 mmol/L
46
Reference values for Sweat Chloride
<40 mmol/L
47
Panic values for Serum Chloride
≤80 mmol/L or ≥120 mmol/L
48
Panic values for Sweat Chloride
≥60 mmol/L (indicative of cystic fibrosis)
49
Method for sweat chloride analysis
Gibson and Cooke's method (pilocarpine iontophoresis)
50
Common method for Chloride measurement
ISE with ion exchange membrane
51
Mercurimetric titration method for chloride
Schales-Schales method (blue-violet color with diphenylcarbazone)
52
Spectrophotometric chloride assay
Whitehorn titration (red complex with mercuric thiocyanate)
53
Hypochloremia causes
Same as sodium: aldosterone deficiency, salt-losing nephropathy, DKA, vomiting, diarrhea, severe burns, diuretics; metabolic alkalosis, compensated respiratory acidosis
54
Hyperchloremia causes
Same as sodium: renal tubular acidosis, GI loss of HCO3-, metabolic acidosis, compensated respiratory alkalosis
55
Inverse changes between Bicarbonate and Chloride
Increased bicarbonate = decreased chloride; decreased bicarbonate = increased chloride
56
Major extracellular anion
Chloride
57
Relationship with Sodium and HCO3-
Direct relationship with Sodium; inverse relationship with HCO3- (chloride shift)
58
Reference values for Serum (mEq/L)
98–107 mmol/L
59
Reference values for Sweat Chloride
<40 mmol/L
60
Panic values for Serum Chloride
≤80 mmol/L or ≥120 mmol/L
61
Panic values for Sweat Chloride
≥60 mmol/L (indicative of cystic fibrosis)
62
Method for sweat chloride analysis
Gibson and Cooke's method (pilocarpine iontophoresis)
63
Common method for Chloride measurement
ISE with ion exchange membrane
64
Mercurimetric titration method for chloride
Schales-Schales method (blue-violet color with diphenylcarbazone)
65
Spectrophotometric chloride assay
Whitehorn titration (red complex with mercuric thiocyanate)
66
Hypochloremia causes
Same as sodium: aldosterone deficiency, salt-losing nephropathy, DKA, vomiting, diarrhea, severe burns, diuretics; metabolic alkalosis, compensated respiratory acidosis
67
Hyperchloremia causes
Same as sodium: renal tubular acidosis, GI loss of HCO3-, metabolic acidosis, compensated respiratory alkalosis
68
Inverse changes between Bicarbonate and Chloride
Increased bicarbonate = decreased chloride; decreased bicarbonate = increased chloride
69
Second major extracellular anion
Bicarbonate
70
Percentage of total CO2 at physiological pH
>90% of the total CO2
71
Reference values for measured TCO2
23–27 mmol/L
72
Reference values for calculated HCO3–
22–26 mmol/L
73
Panic values for HCO3–
≤10 mmol/L or ≥40 mmol/L
74
Method for Total CO2 measurement
ISE (acidification of sample followed by electrode-based CO2 detection)
75
Enzymatic method for HCO3– measurement
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
Clinical significance of ↓ HCO3–
Metabolic acidosis, compensated respiratory alkalosis, RTA, GI loss of HCO3–
77
Clinical significance of ↑ HCO3–
Metabolic alkalosis, compensated respiratory acidosis
78
Cofactor of enzymes Magnesium
>300 enzymes
79
Magnesium distribution
55% ionized, 30% bound to proteins, 15% bound to ions
80
Reference values for magnesium (mEq/L)
1.26–2.1 mEq/L
81
Reference values for magnesium (mg/dL)
1.51–2.52 mg/dL
82
Panic values of magnesium(mg/dL)
≤1 or ≥4.7 mg/dL
83
Reference method for magnesium
AAS (Atomic Absorption Spectrophotometry)
84
Dye-binding methods for magnesium
Calmagite (Red Violet), formazan, methylthymol blue, xylidyl blue
85
Dye-lake methods for magnesium
Titan yellow (ACD lake), Clayton yellow, thiazole yellow dye
86
Clinical significance of Hypomagnesemia
↓ intake (poor diet, starvation, chronic alcoholism), ↓ absorption (vomiting, diarrhea, malabsorption), ↑ excretion (renal, endocrine, drug-induced)
87
Clinical significance of Hypermagnesemia
↑ intake (antacids, enemas), ↓ excretion (renal failure, hypoaldosteronism)
88
Calcium - Plasma level regulation
PTH (Bone resorption, Vitamin D activation, Ca2+ reabsorption in kidneys), Active Vitamin D (intestinal calcium absorption), Calcitonin (inhibits PTH)
89
Calcium - Distribution
50% ionized, 40% bound to proteins (albumin), 10% bound to ions
90
Calcium - Reference values (total)
4.3-5 mEq/L (8.6-10 mg/dL)
91
Calcium - Panic values
≤6 mEq/L
92
Calcium - Methods (AAS)
Lanthanum oxide to chelate phosphates (PO4)
93
Calcium - Methods (ISE)
PVC membrane impregnated with calcium ion exchanger for ionized Ca measurement
94
Calcium - Methods (Dye-binding)
O-cresolphthalein complexone (CPC) method, Arsenazo III (violet color for Ca2+)
95
Calcium - Methods (Precipitation)
Clark-Collip oxalic acid precipitation, Ferro-Ham chloranilic acid precipitation
96
Calcium - Clinical significance (Hypocalcemia)
Primary hypoparathyroidism, secondary hyperparathyroidism, chronic renal failure, hypomagnesemia, ↓ albumin, pseudohypoparathyroidism, vitamin D deficiency, pancreatitis
97
Calcium - Clinical significance (Hypercalcemia)
Primary hyperparathyroidism, hypercalcemia of malignancy, multiple myeloma, vitamin D excess, prolonged immobilization
98
Phosphate - Classification
Major intracellular anion, component of essential biomolecules, measured as inorganic PO4
99
Phosphate - Reference range
2.4–4.4 mg/dL
100
Phosphate - Panic values
≤1 mg/dL; ≥8.9 mg/dL
101
Phosphate - Method (Fiske-Subbarow/Ammonium Molybdate)
PO4 + ammonium molybdate → Ammonium phosphomolybdate, UV: ↑ APM @ 340 nm, C/S: Phosphomolybdenum (Blue) A ↑ 600-700 nm
102
Phosphate - Clinical significance (Hypophosphatemia)
Diabetic ketoacidosis, long-term TPN, IBD, anorexia nervosa, alcoholism, hyperparathyroidism, vitamin D deficiency
103
Phosphate - Clinical significance (Hyperphosphatemia)
Renal failure, milk or laxatives, neoplastic disorders, intravascular hemolysis, lymphoblastic leukemia
104
Phosphate - Transcellular shifts
Intracellularly and extracellularly depending on where it is needed, influenced by bicarbonate
105
Phosphate - Regulation
Proximal Convoluted Tubule: reabsorption site, PTH: decreases reabsorption, Calcitonin: increases excretion, Vitamin D: increases absorption and reabsorption, Growth hormone: decreases renal excretion
106
Phosphate - Pre-Analytical Considerations
Avoid hemolysis, do not use Citrate, Oxalate, or EDTA plasma, circadian rhythm (low in evening, high in late morning)
107
Phosphate - Measurement/Analysis Methods
Ammonium phosphomolybdate (340 nm), Fiske and Subbarow (600 nm)
108
By-product of anaerobic glycolysis, indicates hypoxia
Lactate
109
Lactate - Reference values (venous blood)
Colorimetric (POD - complexed): 8.1-15.3 mg/dL; UV (enzymatic): 4.5-19.8 mg/dL
110
Lactate - Method (POD-coupled reaction)
Lactate + O2 → Lactate oxidase → pyruvate + H2O2 → H2O2 + chromogen (POD) → oxidized chromogen + H2O
111
Lactate - Method (Enzymatic-UV)
Lactate + NAD → Lactate dehydrogenase → pyruvate + NADH
112
Lactate - Type A Lactic Acidosis: Hypoxic/Ischemic
Shock, MI, severe CHF, pulmonary edema, severe blood loss
113
Lactate - Type B Lactic Acidosis Metabolic:
Diabetes mellitus, severe infection, leukemia, liver or renal disease, toxins (ethanol, methanol, salicylate poisoning)
114
Major extracellular cation
Sodium
115
Major intracellular cation
Potassium
116
Major extracellular anion
Chloride
117
Major intracellular anion
Phosphate
