ELECTROLY

TE

LOCATION

MAIN FUNCTIONS

REFERENCE RANGE

DISORDERS CAUSING AN
INCREASE

DISORDERS CAUSING
A DECREASE

METHODS OF
DETERMINATION

SODIUM

ECF(major
)
90%

Serum
(275295
mOsm/kg)
*3.8-5 mmonl/L
K>7.5mmol/l(eleva
ted)

Urine (24-h)
300900 mOsm/kg

Urine/serum
ratio 1.03.0

Random urine
501200
mOsm/kg

Osmolal gap
510 mOsm/kg

EXCESS WATER LOSS

INCREASED SODIUM
LOSS

(FES)----YELLOW
(AAS)
ALBANESE-LEIN
(colorimetric)
Reagent: uranyl
acetate
Product: sodium
uranyl acetate ppt
Color: +H2O =
YELLOW

ECF
(135-145
mmol/L)
ICF
(4-10
mmol/L)

Water pull
(Osmotic
activity of
extracellular
fluid, blood vol.
regulation
neuromuscular
excitability
combine w/
HCO3 &Cl (acidbase balance)

Diabetes insipidus
Renal tubular disorder
Prolonged diarrhea
Profuse sweating
Severe burns
DECREASED WATER
INTAKE

Older persons
Infants
Mental impairment
INCREASED INTAKE OR
RETENTION

Hyperaldosteronism
Sodium bicarbonate
excess
Dialysis fluid excess

Hypoadrenalism
Potassium deficiency
Diuretic use
Ketonuria
Salt-losing
nephropathy
Prolonged vomiting or
diarrhea
Severe burns
INCREASED WATER
RETENTION

Renal failure
Nephrotic syndrome
Hepatic cirrhosis
Congestive heart
failure

HORMONES
INVOLVED IN
THE
ELECTROLYTE
Aldosterone
ANF/ANH
ADH

ISEs- most routinely

used method in clIN
LAB

WATER IMBALANCE

Excess water intake

SIADH
Pseudohyponatremia
POTASSIUM

Major ICF

ECF
(4
mmol/L)

ICF
(110
mmol/L)

neuromuscula
r excitability,
contraction of
the heart
&skeletal
ICF volume,
and H_
concentration

Serum: 3.5-5.5
mmol/L

Acidosis
Renal Failure
Hypoaldosteronism
Defects in renal tubular
potassium secretion
Diuretics that block the
DCT potassium secretion

HYPOKALEMIA
GI LOSS

Vomiting
Diarrhea
Gastric suction
Intestinal tumor
Malabsorption
Cancer therapy
chemotherapy,

Direct and Indirect ISE

for Na and K
EFP
AAS
Lockhead and Purcell

Aldosterone

->20X
inside

radiation therapy
Large doses of
laxatives
RENAL LOSS

Diureticsthiazides,
mineralocorticoids
Nephritis
Renal tubular acidosis
(RTA)
Hyperaldosteronism
Cushings syndrome
Hypomagnesemia
Acute leukemia
CELLULAR SHIFT

Alkalosis
Insulin overdose
DECREASED INTAKE

CHLORIDE

CALCIUM

-Maintenance of
Electolyte balance
-Hydration
-Maintenance of
osmotic pressure

Bone

-Structural
Neuromuscular( con
trol of excitability,
release of
neurotransmitters,
initiation of muscle
contraction)
-Enzymatic
( coenzyme for
coagulation factors)
Signaling
(intracellular second

Serum: 98-108
mmol/L
CSF: 115-132
mmol/L
Urine: 110-250
mmol/L
Sweat: 5-40 mmol/L
Serum: 8.5-10.4
mg/dL

Dehydration
Renal tubular acidosis
Congestive heart failure
Respiratory alkalosis

acidosis

Metabolic acidosis
Diarrhea
Profuse sweating
Increased gastric juice
sec
Salt-losing nephritis
Addisons disease
alkalosis

ISE
Coulometricamperometric method
Zall color reaction
Mercuric nitrate
titration method
ISE
AAS
EFP
Precipitation by
a. Ammonium
oxalate
b. Chloronilic
acid
c. Picrolonic acid
For mation of colored
complexes bet
calcium and a variety
of dyes
(alizarin, o-

Parathyroid
hormone
Calcitriol or
act. Vit D3
Calcitonin

messenger)

PHOSPHAT
E

Bone
Inside the
cell

MAGNESIU
M

Inside the
cell

COPPER

IRON

-Transfer of energy
during metabolism
-Maintenance of pH
of body fluids
-Constituents of
bones
-Membrane
structure
-Essential activator
of several enzymes.
-Oxidative
phosphorylation
-Therapeutic agent

Important in
Erythropoiesis and
catalytic activity of
several enzymes

cresolpthalein
complexone,calcein,
murexide, nuclear fast
red)
Removal of calcium
from a colored
complex by titration
with chelating agent
(EDTA, EGTA, dyes)
Fiske-subbarow
method
Daly-Ertinghausen
method
Enzymatic method

Hypothyroidism
Chronic
glomerulonephritis
Uremia

Hyperthyroidism
Avitaminosis D
Rickets
Osteomalacia

1.3-2.1 mEq/L or
0.65-1.05 mmol/L

Chronic renal disease

Severe dehydration
Aldosterone deficiency

Gastrointestinal
disorders
Acute alcoholism
Prolonged parenteral
fluid therapy without
magnesium
supplementation
Use of diuretics

ISE
AAS
Colorimetric analysis
(calgamite,
methylthymol blue,
Titan yellow)
Fluorometric analysis

Infants: 20-70 g/ L
Children: 80-190
Men: 70-140
Non-preg women:
80-155
Pregnant: 120-300

Acute copper poisoning

Pregnancy
Estrogen therapy
Lymphomas
Leukemias
RA
Systemic lupus
erythematosus
Thalassemia

Menkes syndrome
Kwashiorkor
Nephrosis
Sprue
Celiac disease
Wilsons disease

AAS

Total: 3-5 g

Hemolytic anemia

IDA

Serum iron:

Parathyroid
hormone
Growth
hormone

Aldosterone

Serum:
Male- 65-165 g/l
Female- 45-160

ZINC

MANGANESE

COBALT
MOLYBDENUM

plasma

-Activator of
enzymes
-Insulin and
porphyrin
metabolism
-Growth and sexual
maturation
Wound healing and
sensory perception.
-essential for lipid
and carbohydrate
metabolism, bone and
tissue formation, and
reproductive process.
-also a component of
enzymes
-a component of vit.
B12
-help from the active
sites of certain
enzymes

70-150 g/dL

Pernicious anemia
Aplastic anemia
Marrow damage by
toxins
Lead poisoning
Pyridoxine def.
Acute hepatic cell
necrosis
Hemochromatosis
Hemosiderosis

Iron malabsorption
Blood loss
Late Pregnancy
Infection
Neoplasia
RA

Zinc toxicity

Ferrozine method
TIBC and Transferrin
Saturation
Zinc
Protoporphyrin/Heme
ratio

AAS

Pernicious anemia

CHROMIUM

NICKEL

IODIDE

SELENIUM

-an essential
component of the
glucose tolerance
factor
-stabilizes the nucleic
acid structure
allowing the
synthesis of proteins
-linked to iron
metabolism
-component of
thyroid hormones T3
and T4
-component of the
enzyme glutathione
peroxidase.

-insulin become less

effective in reducing
hyperglycemia
1-4g/dL

Iron deficiency

Goiter

Malnurishment
Chronic bowel disease
Hyperalimentration.

AAS