Electrolyte:

SODIUM
JAI ANTHONY F. CUEVAS, RMT
 Sodium (Na+)

-major extracellular cation.

-responsible for plasma osmolality (physical property

of a solution that is based on the concentration of
solutes).
NV: 136 – 145 mmol/L
 Sodium (Na+)

-regulation depends greatly in the intake and

excretion of water and renal regulation.

Importance of Regulation:
1.The intake of water in response to thirst, as
stimulated or suppressed by plasma osmolality.
 Sodium (Na+)

Importance of Regulation:
2.The excretion of water is largely affected by
Antidiuretic Hormone release in response to
changes in blood volume or osmolality.

3.The blood volume status, which affects sodium

excretion through aldosterone, angiotensin II, and
ANP (atrial neuretic peptide).
 Sodium (Na+)

Clinical Significance:
I. Hyponatremia
s/s: nausea, vomiting, coma, respiratory depression (difficulty in
breathing).
Due:
a. Hypovolemic-Hyponatremia
-low sodium and low water volume in the body.
-excessive loss of water along with the loss of sodium.
Urine Na+= >20 mmol/L
***Low sodium in blood delivered in kidney to be excreted in urine.
 Sodium (Na+)

Clinical Significance:
I. Hyponatremia
Due:
a. Hypovolemic-Hyponatremia (cont)
Renal Causes:
i. Thiazide diuretics
ii. Diseases associated with polycystic kidney disease.
Etrarenal Causes:
i. Insuficiency of aldosterone (low Na+ in blood)
-deficiency of cortisol (influence low flow of sodium in renal tubules).
ii. Cellular shift
-happens when there is low K+ in the blood. Causes hypochloremia.
 Sodium (Na+)

Clinical Significance:
I. Hyponatremia
Due:
b. Normovolemic/Euvolemic Hyponatremia
-caused by Syndrome of Inapropriate ADH (SIADH).
defect in regulation and secretion of ADH seen in
malignancy, CNS disorders, AIDS, pulmonary disease)
-brings mild hypervolemia, leads to the release of antineuretic
peptide (ANP) which brings about the secretion of sodium and
water in the kidneys, there is inhibition of sodium, potassium and
ATPase.
 Sodium (Na+)

Clinical Significance:
I. Hyponatremia
Due:
b. Normovolemic/Euvolemic Hyponatremia
Causes:
i. Artifactual Hyponatreimia- high lipids and CHONS.
ii. Severe Hyperglycemia- high plasma osmolality due to DM causing mild
hypervolemia.
iii. Chronic intake of water.
iv. Renal insufficiency- low cortisol leading to low aldosterone secretion
that triggers release of ADH causing dilution of plasma.
 Sodium (Na+)

Clinical Significance:
I. Hyponatremia
Due:
c. Hypervolemic Hyponatremia
-caused by water overload which further causes
edema.
-seen in nephrotic syndrome (advance renal disease),
and liver cirrhosis which brings low serum protein
synthesis.
 Sodium (Na+)

Clinical Significance:
I. Hyponatremia
Categorization of Diseases:
Increase sodium loss.
-decrease aldosterone production,certain
diuretics, ketonuria(sodium loss with ketones), salt
losing neuropathy, vomiting, burns, and diarrhea.
 Sodium (Na+)

Clinical Significance:
I. Hyponatremia
Categorization of Diseases:
Increased Water Retention.
-dilution of serum/plasma sodium due to acute or
chronic renal failure. Low plasma level of ADH
causing water retention, Liver cirrhosis, congestive
heart failure.
 Sodium (Na+)

Clinical Significance:
I. Hyponatremia
Categorization of Diseases:
Water Imbalance.
-increase water intake in polydypsia (increased
thirst), Syndrome of Inappropriate ADH secretions
(SIADH), Pseudonatremia (hemolysis)
 Sodium (Na+)

Clinical Significance:
II. Hypernatremia
-increase plasma sodium level >140 mmol/L
Categorization of Diseases:
Excess water loss.
-Diabetes Insipidus, Renal Tubular Disorder,
Profuse Sweating, Severe Burns.
 Sodium (Na+)

Clinical Significance:
II. Hypernatremia
Categorization of Diseases:
Diabetes Insipidus
-production of diluted urine. May caused either:

Nephrogenic Diabetes Insipidus- kidneys doesn’t response to ADH.

Central Diabetes Insipidus- impaired ADH production.

ADH=Vasopressin
 Sodium (Na+)

Clinical Significance:
II. Hypernatremia
Categorization of Diseases:
Decrease water intake.
-older person, infancy, mental impairment.
 Sodium (Na+)

Clinical Significance:
II. Hypernatremia
Categorization of Diseases:
Increase intake or retention of sodium.
-Hyperaldosteronism, sodium-bicarbonate excess, dialysis fluid
excess.
 Sodium (Na+)

Methods of Determination:
1. Ion Selective Electrode (ISE)
2. Flame emission spectrophotometry
3. Atomic absorption spectrophotometry (AAS)
4. Colorimetric Assays
-Determination by Trinder and Maruna (Triple Salt)
5. Enzymatic Reaction
-used the ability of sodium to activate the enzyme galactosidase.
Substrate: o-nitrophenyl-β-D-galactoside (ONPG)
ONPG –Galactosidase, Na+ o-nitrophenol (Yellow) + D-galactopyranoside
Absorbance= 405 nm
Sodium (Na+)

End
Electrolyte:
POTASSIUM
JAI ANTHONY F. CUEVAS, RMT
 Potassium

-Major intracellular cation.

-function: regulation of neuromascular excitability, contraction of the heart
(along with calcium and magnesium), intracellular fluid volume^, and
hydrogen ion concentration, and regulation of Resting Membrane Potential
(RMP).
>K+= low RMP
<K+= high RMP
***cell excitability causes arrhythmia of the heart with muscle fatigue
movement.
NV: 3.5 – 5.3 mmol/L
***Increase or decrease may manifest condition of the heart. Levels of >6
indicates “Panic Value”.
 Potassium

Regulation:
Kidneys: reabsorption in the proximal convoluted
tubule in exchange to hydrogen ions (H+).

Aldosterone: potassium is secreted in the urine in

exchange to sodium reabsorption in the distal
convoluted tubule and collecting ducts.
 Potassium

Clinical Significance:
I. Hypokalemia
Gastrointestinal loss.
-vomiting, diarrhea, gastric suctions, intestinal
tumors, malabsorption, cancer theraphy, large
dosage of laxatives.
 Potassium

Clinical Significance:
I. Hypokalemia
Renal loss.
-diuretics, nephritis, renal tubular acidosis,
hyperaldosteronism, Cushing’s syndrome,
hypomagnesemia, acute leukemia.

***Cushing’s syndrome- increase production of

glucocorticoids.
 Potassium

Clinical Significance:
I. Hypokalemia
Cellular shift.
-alkalosis, insulin overdose.

Decrease inake.
 Potassium

Clinical Significance:
II. Hyperkalemia
Decrease renal excretion.
-Acute or chronic renal failure,
hypoaldosteronism, Addison’s disease.

***Addison’s disease- disease in the production of

adrenocortical hormones.
 Potassium

Clinical Significance:
II. Hyperkalemia
Cellular shift.
-metabolic acidosis, muscle/cellular injury,
hemolysis, diabetes mellitus.
 Potassium

Clinical Significance:
II. Hyperkalemia
Increase intake.
-oral or IV potassium replacement theraphy.
 Sodium (Na+)

Methods of Determination:
1. Ion Selective Electrode (ISE)
2. Flame emission spectrophotometry
3. Atomic absorption spectrophotometry (AAS)
4. Turbidimetric Method
Potassium

END
Electrolyte:
CHLORIDE
JAI ANTHONY F. CUEVAS, RMT
 Chloride

-major extracellular anion.

function: electric neutrality of the blood, osmolality

regulation together with sodium, and maintaining
blood volume.
NV: Serum: 98 – 106 mmol/L
Sweat: 5 – 35 mmol/L
Urine: 110 – 250 mmol/L
 Chloride

Chloride Shift Mechanism:

-important in the metabolism and regulation of acid base balance.
1st: Intracellular
CO2 + H2O Carbonic Anhydrase H2CO3 Carbonic Anhydrase H+ + HCO3-
2nd: Excretion of HCO3- by the cell.
3rd: Kidney
Glomeruli Filtrate  Tubules (Na+ is actively reabsorbed, Cl-
passively reabsorbed)
or Cl is secreted and/or HCO3- is reabsorbed (vice versa)
 Chloride

Methods of Determination:
Specimen Consideration:
-Lithium Heparin is the recommended anticoagulant
for chloride determination.
Gross Hemolysis
-induce gross dilution of Cl-
 Chloride

Methods of Determination:
1. ISE
2. AMPOTHERIC method
-generates silver (Ag+) ion complex with
chloride using AgNO3 producing AgCl amplified
by Iron (Fe3+).
-Equipment used: Cotlove Chloridometer
 Chloride

Methods of Determination:
3. Colorimetric Method
Schales-Schales Method
Hg(NO3)2 + Cl-  HgCl2 + NO3-
Excess Hg + diphenylcarbazone  colored complex
 Chloride

Methods of Determination:
3. Colorimetric Method (cont)
Zall-Garner Method
 Modification by Skeggs
Cl- + Mercuric Thiocyanate  HgCl2
Excess Thiocyanate + Fe(NO3)3  Reddish Brown Color
 Chloride

Methods of Determination:
3. Colorimetric Method (cont)
Fingerhut Reaction
Cl- + Ferric Perchlorate  Colored product
 Chloride

Methods of Determination:
4. Iontophoresis (on sweat)
Gibson-Cooke Method
-for the diagnosis of cystic fibrosis.
Instrument: Pilocarpine
introduced to the forearm of the patient.
Sweat on pilocarpine will be tested with the iontophoresis
through chloride release in sweat in an absorbent pad. 
produce elution of Cl- and determined.
Chloride

END