Electrolytes
Electrolyte Main function in the Body
Sodium The most abundant
extracellular cation. It
contributes to the
osmolality of extracellular
fluid and maintains the
volume of ECF and cell
size and shape. Sodium is
essential for transmitting
nerve impulses.
Potassium The major intracellular
cation that regulates
activity at the
neuromuscular
Renal Regulation Causes of high blood levels Causes of low blood levels
1. Approximately 70% Excess water loss Increased sodium loss
of the Na+ in the - Diabetes Insipidus - Hypoadrenalism
filtrate is reabsorbed - Renal tubular disorder - Potassium deficiency
in the proximal - Prolonged diarrhea - Diuretic use
tubules by iso- - Profuse sweating - Ketonuria
osmotic - Severe burns - Salt-losing
reabsorption. It is Decreased water intake nephropathy
limited, however, by - Older persons - Prolonged vomiting or
the availability of Cl- - Infants diarrhea
to maintain electrical - Mental impairment - Severe burns
neutrality. Increased intake or retention Increased water retention
2. Na+ is reabsorbed in - Hyperaldosteronism - Renal failure
exchange for H+. This - Sodium bicarbonate - Nephrotic syndrome
reaction is linked excess - Hepatic cirrhosis
with HCO3- and - Dialysis fluid excess - Congestive heart
depends on carbonic failure
anhydrase. Water imbalance
3. Stimulated by - Excess water intake
aldosterone, Na+ is - SIADH
reabsorbed in - Pseudohyponatremia
exchange for K+ in
the distal tubules.
(H+ competes with K+
for this exchange.)
1. Aldosterone induces Decreased renal excretion GI Loss
K+ reabsorption and - Acute or chronic renal - Vomiting
secretion by the failure (GFR, <20 - Diarrhea
renal tubules by mL/min) - Gastric suction
 junction, as well as exchanging it for
cardiac muscle Na+ .
contraction and pH.
2. A high concentration
of hydrogen ions
keeps K+ out of cells
and induces its renal
retention. Low
hydrogen ion
concentration allows
more K+ ions to enter
cells, which lowers
serum K+ . Low
hydrogen ion
concentration also
allows more K+ to be
excreted by the
kidney.
Chloride The major extracellular Cl- is reabsorbed, in part, by
anion that acts to passive transport in
maintain osmotic the proximal tubule along
pressure, keeps the concentration gradient
the body hydrated, and created by Na+ .
maintains electric
neutrality via interaction
with sodium or
carbon dioxide.
- Hypoaldosteronism - Intestinal tumor
- Addison’s disease - Malabsorption
- Diuretics - Cancer-therapy-
Cellular shift chemotheraphy,
- Acidosis radiation therapy
- Muscle/cellular injury - Large doses of
- Chemotherapy laxatives
- Leukemia Renal Loss
- Hemolysis - Diuretics (thiazides,
Increased intake mineralocorticoids)
- Oral or IV potassium - Nephritis
replacement therapy - Renal tubular acidosis
Artifactual (RTA)
- Sample hemolysis - Hyperaldosteronism
- Thrombocytosis - Cushing’s syndrome
- Prolonged tourniquet - Hypomagnesemia
use or excessive fist - Acute leukemia
clenching Cellular Shift
- Alkalosis
- Insulin overdose
Decreased Intake
Chloride disorders are often a Chloride disorders are often a
result of the same causes that result of the same causes that
disturb Sodium levels because disturb Sodium levels because
Chloride passively follows Chloride passively follows
Sodium; Few exceptions are: Sodium; Few exceptions are:
Excess loss of HCO3- Excessive loss
- GI losses - Prolonged vomiting
- RTA - Diabetic ketoacidosis
- Metabolic acidosis - Aldosterone
deficiency
- Salt-losing renal
diseases such as
 pyelonephritis
High serum HCO3-
concentrations
- Compensated
respiratory acidosis
- Metabolic alkalosis

Bicarbonate The second most
abundant anion in the
extracellular fluid. It is a
major component of the
blood buffering system,
accounts for 90% of total
blood carbon
dioxide, and maintains
charge neutrality in the
cell.
Bicarbonate is recovered Metabolic alkalosis Metabolic acidosis
from the glomerular filtrate - Severe vomiting
and converted to CO2 when - Hypokalemia
H+ is excreted in - Excessive alkali intake
the urine.
Henle’s loop: With normal
AVP function, it creates
an osmotic gradient that
enables water reabsorption
to be increased or decreased
in response
to body fluid changes in
osmolality.

Collecting ducts: Also under

Magnesium The second most
abundant intracellular
cation. Cofactor of many
enzymes (for glycolysis,
transcellular ion
transport, neuromuscular
transmission, synthesis of
carbs, proteins, lipids,
AVP influence, this
is where final adjustment of
water excretion is made
Overall regulation is
controlled by the kidney, it
can reabsorb Mg2+ in
deficiency states or readily
excrete Mg2+ in overload
states.
Non-protein bound
Decreased excretion
Acute or chronic renal failure
Hypothyroidism
Hypoaldosteronism
Hypopituitarism (decreased
growth hormone)
Increased intake
Antacids
Reduced Intake
- Poor diet/Starvation
- Prolonged
magnesium-deficient
IV therapy
- Chronic alcoholism
Decreased absorption
- Malabsorption
 nucleic acids, hormone magnesium is filtered in Enemas syndrome
activity). glomerulus, 25%-30% is Cathartics - Surgical resection of
reabsorbed by the PCT, 50%- Therapeutic-eclampsia, intestine
60% by the loop of Henle cardiac arrythmia - Nasogastric suction
(reabsorption mostly occurs Miscellaneous - Pancreatitis
here) and 2%-5% by the DCT. Dehydration - Vomiting
Bonce carcinoma - Diarrhea
Slight excesses of Bone metastases - Laxative abuse
Mg2+ in serum are rapidly - Neonatal
excreted by the kidneys. - Primary
Normally, only about 6% of - Congenital
filtered Mg2+ is excreted in Increased Excretion-Renal
the urine per day. - Tubular disorder
- Glomerulonephritis
- Pyelonephritis
Increased Excretion –
Endocrine
- Hyperparathyroidism
- Hyperaldosteronism
- Hyperthyroidism
- Hypercalcemia
- Diabetic ketoacidosis
Increased Excretion – Drug
induced
- Diuretics
- Antibiotics
- Cyclosporin
- Digitalis
Miscellaneous
- Excess lactation
- Pregnancy

Calcium Important activator in the Regulated by PTH, Vitamin D Primary hyperparathyroidism- Primary hypoparathyroidism-
coagulation system and calcitonin. adenoma or glandular glandular aplasia, destruction,
 hyperplasia or removal
Acts as an enzyme 98% of calcium is reabsorbed Hyperthyroidism Hypomagnesemia
activator within cells at the kidneys Benign familial hypocalciuria Hypermagnesemia
Malignancy Hypoalbuminemia (total
Maintains stability of Calcium is reabsorbed under Multiple myeloma calcium only, ionized not
nerve membrane the influence of PTH and Increased vitamin D affected by)-chronic liver
1,25- Thiazide diuretics disease, nephrotic syndrome,
Required for muscle cell dihydroxycholecalciferol. Prolonged immobilization malnutrition
contraction Calcitonin stimulates Acute pancreatitis
excretion of calcium. Vitamin D deficiency
Contributes to skeletal Renal Disease
growth Rhabdomyolysis
Pseudohypoparathyroidism

Phosphate Important in structural Phosphate reabsorption is Highest risk to those with acute Caused by increased renal
integrity of cell inhibited by PTH and or chronic renal failure excretion and decreased
membrane and surfactant increased by 1,25- Causes: intestinal absorption
furnishing to the lungs dihydroxycholecalciferol. - Increased intake of Occurs in about 1% to 5% of
phosphate hospitalized patients
Excretion of PO4 is
- Increased released of Occurs to 20% to 40% in patients
Involved in the stimulated by calcitonin cellular phosphate with:
intermediary metabolism - Increased breakdown of - Diabetic ketoacidosis
of the carbohydrate cells found in: severe - Chronic obstructive
component of nucleoside infections, intensive pulmonary disease
and ATP exercise, neoplastic (COPD)
disorders, intravascular - Asthma
hemolysis and - Malignancy
lymphoblastic leukemia) - Long term treatment
with Total Parenteral
Nutrition (TPN)
- Inflammatory bowel
disease
- Anorexia nervosa
- Alcoholism
Occurs to 60% to 80% in ICU
patients