CLINICAL CHEMISTRY 2

Electrolytes

I. Introduction
Ions capable of carrying an electric charge
Two types of Ions:
A. Anions
Carry (-) charge and move toward the anode
E.g. Cl-, HCO3-, PO4

Functions of Electrolytes
1. Volume and osmotic regulation (Na+, Cl-, K+)
2. Myocardial rhythm and contractility (K+, Mg2+, Ca2+)
3. Neuromuscular Excitability (K+ ,Mg2+, Ca2+)
4. Cofactors in enzyme activation (Mg2+, Ca2+, Zn2+)

B. Cations
Carry (+) charge and move toward the cathode
E.g. Na+, K+, Mg2+, Ca2
5. Regulation of ATPase ion pumps (Mg2+)
6. Acid-base balance (HCO3-, K+, Cl-)
7. Production and use of ATP from glucose (Mg2+, PO4-)

II. Water
A. Introduction
40-75% of body weight
Function
Location:

Transport nutrients to the cells and Removes waste products

ICF: 2/3 E CF: 1/3 Intravascular (25%) and interstitial fluid (75%)

B. Osmolality:

Concentration of ions is maintained by:

1. Passive Transport
Passive movement of ions across a membrane
2. Active Transport
Requires energy to move ions across a membrane
ATPase-dependent ion pumps
i. Definition: Conc. of solutes per Kg of solvent (millimoles/kg)
ii. Regulation
a. Thirst Sensation
Response to consume more fluids
Prevents water deficit
b. Arginine vasopressin hormone (AVP)
Antidiuretic Hormone (ADH)
rea sorptio of ater i kid e s
Suppressed in excess H2O load
Activated in water deficit
c. Renin-angiotensin-aldosterone
Na+ retention, aldosterone release, vessel constriction
system
d. Atrial natriuretic Peptide (ANP)
Na+ excretion in the kidney
e. Glomerular Filtration Rate (GFR)
/ ol. e pa sio a d / ol. depletio
iii. Determination
Any substance dissolve in a solvent will:
freezing point by 1.858C
boiling point by 0.52C
Main contributors are Na, Cl, Urea and Glucose
Distribution of Body Water in Adult
Compartment
(%) of Body Weight
Extracellular
Plasma
5
Interstitial
15
Intracellular
40
Total Body Water
60
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freezing point by 1.858C

boiling point by 0.52C

(%) of Total Body H2O

8
25
67
100
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CLINICAL CHEMISTRY 2
II. Electolytes
A. Sodium (Na+)
i.
Description and Regulation
The most abundant cation
in the ECF
Major Extracellular cation
Na+, K+ -ATPase ion pump
moves 3 Na+ ions out of the
cell in exchange for 2 K+ ions

Plasma concentration depends in renal regulation

a. Intake of water
Thirst
b. Excretion of water
AVP H2O reabsorption)
c. The blood volume status
A giote si II aldostero e
Aldostero e Na+ reabsorption in kidney)
ANP Uri ar Na + Excretion )

ii. Clinical Applications

Causes of Hypo atre ia ( Na+)
. Sodiu (Na+) Loss
a. Hypoaldosteronism
b. K+ Deficiency
c. Diuretic Use
d. Salt-losing nephropathy
e. Severe Burns

. Water Rete tio

a. Renal failure
b. SIADH
c. Nephrotic syndrome
d. Chronic heart failure
e. Hepatic cirrhosis

iii. Determination of Sodium

Specimen
a. Serum, Plasma (heparin and oxalate)
b. False ith arked he ol sis

Causes of Hyper atre ia ( Na+)

1. Excess Water Loss
a. Diabetes insipidus
b. Profuse sweating
c. Severe burns

2. Decreased Water Intake

a. Old/Infant/Mentally Impaired
3. Increased Intake or Retention
a. Cushing Syndrome
b. Hyperaldosteronism
c. Hypertonic Salt Solution

Methods
a. FES
b. AAS
c. ISE (Glass ion-exchange membrane)

B. Potassium (K+)
i. Description and Regulation
Major Intracellular cation
Regulation of neuromuscular
excitability, contraction of
heart, ICF volume, H+ conc.
K+, ell e ita ility
(muscle weakness)
K+ , ell e ita ilit
(arrhythmia/paralysis)

1. Aldosterone
K+ excretion in urine)
2. Na+, K+ -ATPase pump
( fu tio ellular e tr )
( fu tio ellular e tr )
3. ith e er ise, dia etes
mellitus and cell breakdown

ii. Clinical Applications

Causes of Hypokalemia (K+)
1.
a.
b.
c.
d.
2.

GI Loss
Vomiting
Diarrhea
Gastric suction
Laxatives
Cellular Shift K+ uptake
a. Alkalosis
b. Insulin Overdose

3. Renal Loss
a. Diuretics
b. Renal Tubular Acidosis
c. Cushi gs s dro e
d. Hyperaldosteronism
e. Hepatic cirrhosis
4. Decreased Intake

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iii. Determination of Potassium

Specimen
a. Serum, Plasma (heparin)
b. False ith he ol sis
c. 24 hour urine
Methods
a. FES
b. AAS
c. ISE (valinomycin membrane)
Causes of Hyperkalemia (K+)

1. Decreased Renal Excretion

a. Renal Failure
b. Hypoaldesteronism
. Addiso s Disease
2. Increased Intake
a. Oral/IV K+ replacement

3. Cellular Shift
a. Acidosis
b. Muscle/cellular injury
c. Chemotherapy / Leukemia
4. Artifactual
a. Hemolysis, Thrombocytosis
b. Prolonged tourniquet

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CLINICAL CHEMISTRY 2

C. Potassium (K+)
i. Description and Regulation
Major Extracellular anion
Involve in maintaining
Osmolality,blood volume
and electric neutrality
(Chloride shift)
Rate limiting component
in Na+ reabsorption

ii. Clinical Applications

Causes of Hyperchlore ia (Cl-)
1. Excess Loss of HCO3a. GI Losses
b. Metabolic acidosis

1. Aldosterone
K+ excretion in urine)
2. Na+, K+ -ATPase pump
( fu tio ellular e tr )
( fu tio ellular e tr )
3. ith e er ise, dia etes
mellitus and cell breakdown

Cause of Hypochlore ia (Cl-)

2. Excess Loss of Cla. Prolonged Vomiting
b. Aldosterone Deficiency
c. Salt-losing pyelonephritis

iii. Determination of Potassium

Specimen
a. Serum, Plasma (lithium heparin)
b. False ith arked he ol sis
c. 24 hour urine
Methods
a. ISE ( Use ion exchange membrane)
b. Amperometric-coulometric
(Cotlove Chloridometer)
Ag2+ +2Cl- -> Ag Cl2
c. Scales and Schales
Titration with mercuric nitrate

D. Bicarbonate (HCO3-)
i. Description and Regulation
2nd Most Abundant anion in
the ECF
Accounts for more than
80% of total CO2
(Chloride shift)
Major buffering system
of the blood
ii. Clinical Applications
Metabolic Alkalosis HCO3a. Severe vomiting
b. Hypoventilation
c. Excessive alkali intake

1. Aldosterone
K+ excretion in urine)
2. Na+, K+ -ATPase pump
( fu tio ellular e tr )
( fu tio ellular e tr )
3. ith e er ise, dia etes
mellitus and cell breakdown

iii. Determination of Bicarbonate

Specimen
a. Serum, Plasma (heparin)
b. False if left uncapped
6
ol/L per hr
Methods
a. Enzyme method

Metabolic acidosis HCO3a. Hyperventilation

E. Magnesium (Mg)
i. Physiology and Regulation
2nd Major Intracellular cation
Neuromuscular conduction
Enzyme cofactor and
ATPase ion pump
53% (Bone), 46% (muscle,
soft tissues), <1% (Blood)
Serum: 33% (protein bound),
61% (ionized),5% (complexed

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1. Parathyroid Hormone (PTH) - Mg2+

Promotes Ca + renal reabsorption
2. Aldosterone and thyroxine - Mg2+
Promotes Na + renal reabsorption

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CLINICAL CHEMISTRY 2
ii. Clinical Applications
Causes of Hypomagnesemia (Mg+)
1. Reduced Intake
2. Absorption
a. Poor diet/starvation
a. Malabsorption synd.
b. Prolonged Mg+- deficient IV b. Diarrhea
3. Others
c. Vomiting
a. Excess lactation
d. Laxative
b. Pregnancy

Causes of Hyper ag ese ia ( Mg 2+ )

a. E retio , Re al failure
b. Hypoparathyroidism
c. Hypoaldosteronism
e. Bone carcinoma and bone metastases

Cause of Hypo ag ese ia ( Mg+) - Excretion

4. Renal
5. Endocrine
a. Tubular disorders,
a. Hyperparathyroidism
Pyelonephritis
b. Hyperaldosteronism
b. Glomerulonephritis
c. Hyperthyroidism
6. Drug Induced
d. Hypercalcemia
a. Furosemide, Thiazide
e. Diabetic ketoacidosis
b. Gentamicin, Cyclosporin
c. Digitales and Digoxin

iii. Determination of Magnesium

Specimen
a. Serum, Plasma (lithium heparin), 24 hr urine
b. He ol sis ause False
Method
a. Calmagite Mtd.
Mg2+ + CalmagiteReddish-violet (532nm)
b. Formazen Dye Mtd.
Mg2+ + DyeColored complex (660 nm)
c. Methylthymol blue Mtd. Mg2+ + ChromogenColored complex
d. Titan Yellow
Serum TCA filtrate+titan yellowRed cmpd.

F. Calcium (Ca+2)
i. Physiology and Regulation
For muscle contraction and blood coagulation
99% in bone and teeth and 1% in blood and ECF
Calcium in the blood is distributed as
1. Ionized
Unbound/ free, physiologically active
45% of Total Calcium
2.Protein bound Bound to protein (E.g. albumin)/40%
3. Complex Ca+2 Bound to anions
(E.g. HCO3-, PO4- & lactate)/15%

Causes of Hypocalcemia
( Ca+)

Cause of Hypercalcemia
( Ca+)

a.
b.
c.
d.
e.
e.

a. Hyperparathyroidism
b. Malig a
PTHrP
c. Vita i D
d. Thiazide diuretics
e. Prolonged immobilization

Hypoparathyroidism
Hypo/hypermagnesemia
Hypoalbuminemia
Acute pancreatitis
Vitamin D deficiency
Rhabdomyolysis

iii. Determination of Calcium

Specimen
a. Serum, Plasma (Dry lithium heparin), 24 hr urine
Method
a. AAS, ISE
b. Ortho-cresolphthalein complexone (CPC)
c. Alizarin, Arsenzo III dye, Methyl phenol blue

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Factors affecting Ca+2 level in blood:

1. Bone resorption
Cause Ca+2 in blood
PTH mobilizes Ca+2 from the bone
2. Bone deposition
Cause Ca+2 in blood
Calcitonin inhibits PTH and Vit.D
3. Intestinal absorption Vitamin D Ca+2 in the intestine

b. Hemolysis cause False

d. Clark and Collip (Redox Titration method)
e. Ferro and Ham (Precipitation with Chloranilic acid)

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CLINICAL CHEMISTRY 2
F. Phosphate
i. Physiology and Regulation
Major Intracellular anion
Component of phospholipids, nucleic acids, creatine phosphate and ATP
80% - bone, 20% - soft tissues, 1% - serum/plasma
GH re al e retio of phosphate

ii. Clinical Applications

Causes of Hypophosphate ia ( PO4-)
a. Hyperparathyroidism
b. Vitamin D Deficiency
iii. Determination of Sodium
Specimen
Serum, Plasma (lithium heparin), 24 hour urine
He ol sis ause False

Cause of Hyperphosphate ia ( PO4-)

a. I take
b. release of cellular phosphate
c. breakdown of cells

Methods
Ammonium phosphomolybdate comp.(340nm)
Fiske-Subbarow Method (Final product: Molybdenum blue)

G. Lactate
i.

Description and Regulation

Indicator of severity of O2 deprivation (hypoxia)
Li er o erts la tate a k to glu ose Glu o eoge esis

ii. Clinical Applications

Hypoxic Conditions (Type A)
a. Lactate Acidosis
b. Shock, MI, Severe CHF
c. Pulmonary edema, severe blood loss

Lactate Acidosis
Metabolic Origin (Type B)
a. Diabetes Mellitus, Liver disease
b. Toxins (ethanol, methanol or salicylate poisoning)

IV. Anaion Gap

Mathematical approximation of difference between the concentration of unmeasured cations & unmeasured anions
(Na+) (Cl- + HCO3-)
7-16 mEq/L
A io gap
u easured a io s

Uremia

Ketoacidosis

Lactic acidosis
i
easured atio s

Hypernatremia
A io gap
u easured a io s

Hypoalbuminemia
i u easured atio s:
Hypermagnesemia
Hypercalcemia

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