UNIVERSITY OF PORTHARCOURT

FACULTY OF BASIC MEDICAL SCIENCES .

DEPARTMENT OF HUMAN PHYSIOLOGY

ASSIGNMENT ON

THE PHYSIOLOGY OF EACH ELECTROLYTE,

THEIR FUNCTIONS, MECHANISM OF ACTION

AND EFFECTS OF EXCESS AND LOW LEVELS

BY

PATRON LISA OGHENEMARO

U2021/4797150

COURSE CODE/ TITLE: PHS 321.1 /BODY FLUID

PHYSIOLOGY

DR. BRUNO CHINKO

What are electrolytes?

Electrolytes are substances that have a natural positive or negative electrical

charge when dissolved in water. An adult’s body is about 60% water, which
means nearly every fluid and cell in your body contains electrolytes. They
help your body regulate chemical reactions, maintain the balance between
fluids inside and outside your cells, and more.

Roles of Electrolytes

These six ions aid in nerve excitability, endocrine secretion, membrane

permeability, buffering body fluids, and controlling the movement of fluids
between compartments. These ions enter the body through the digestive
tract. More than 90 percent of the calcium and phosphate that enters the
body is incorporated into bones and teeth, with bone serving as a mineral
reserve for these ions. In the event that calcium and phosphate are needed
for other functions, bone tissue can be broken down to supply the blood and
other tissues with these minerals. Phosphate is a normal constituent of
nucleic acids; hence, blood levels of phosphate will increase whenever
nucleic acids are broken down.

Excretion of ions occurs mainly through the kidneys, with lesser amounts lost
in sweat and in feces. Excessive sweating may cause a significant loss,
especially of sodium and chloride. Severe vomiting or diarrhea will cause a
loss of chloride and bicarbonate ions. Adjustments in respiratory and renal
functions allow the body to regulate the levels of these ions in the ECF.

Table 1. Electrolyte and Ion Reference Values

Chemical Symbol Plasma. CSF.

Urine

Sodium Na+ |136.00–146.00 (mM) 138.00–150.00 (mM)

40.00–220.00

(mM)

Potassium. K+. 3.50–5.00 (mM) 0.35–3.5 (mM) .

25.00–125.00

)mM (

Chloride Cl- 98.00–107.00 (mM) 118.00–132.00

(mM) 110.00–250.00

.)mM(

Bicarbonate HCO3- 22.00–29.00 (mM) ----

Calcium Ca2+ 2.15–2.55 ----

Up to 7.49

.
(mmol/ day)

Phosphate HPO4- 0.81_ 1.45. -----

12.9-42.00
( mmol/day)

What are the key electrolyte components?

There are several key elements that your body needs to maintain normal
electrolyte levels. The following section includes the major elements, marked
as positive (+) or negative (-), and what happens when there’s too much or
too little of that element.

Sodium

Sodium is the major cation of the extracellular fluid. It is responsible for one-
half of the osmotic pressure gradient that exists between the interior of cells
and their surrounding environment. People eating a typical Western diet,
which is very high in NaCl, routinely take in 130 to 160 mmol/day of sodium,
but humans require only 1 to 2 mmol/day. This excess sodium appears to be
a major factor in hypertension (high blood pressure) in some people.
Excretion of sodium is accomplished primarily by the kidneys. Sodium is
freely filtered through the glomerular capillaries of the kidneys, and although
much of the filtered sodium is reabsorbed in the proximal convoluted tubule,
some remains in the filtrate and urine, and is normally excreted.

Hyponatremia is a lower-than-normal concentration of sodium, usually

associated with excess water accumulation in the body, which dilutes the
sodium. An absolute loss of sodium may be due to a decreased intake of the
ion coupled with its continual excretion in the urine. An abnormal loss of
sodium from the body can result from several conditions, including excessive
sweating, vomiting, or diarrhea; the use of diuretics; excessive production of
urine, which can occur in diabetes; and acidosis, either metabolic acidosis or
diabetic ketoacidosis.

A relative decrease In blood sodium can occur because of an imbalance of

sodium in one of the body’s other fluid compartments, like IF, or from a
dilution of sodium due to water retention related to edema or congestive
heart failure. At the cellular level, hyponatremia results in increased entry of
water into cells by osmosis, because the concentration of solutes within the
cell exceeds the concentration of solutes in the now-diluted ECF. The excess
water causes swelling of the cells; the swelling of red blood cells—decreasing
their oxygen-carrying efficiency and making them potentially too large to fit
through capillaries—along with the swelling of neurons in the brain can result
in brain damage or even death.

Hypernatremia is an abnormal increase of blood sodium. It can result from

water loss from the blood, resulting in the hemoconcentration of all blood
constituents. Hormonal imbalances involving ADH and aldosterone may also
result in higher-than-normal sodium values.

Potassium

Potassium is the major intracellular cation. It helps establish the resting

membrane potential in neurons and muscle fibers after membrane
depolarization and action potentials. In contrast to sodium, potassium has
very little effect on osmotic pressure. The low levels of potassium in blood
and CSF are due to the sodium-potassium pumps in cell membranes, which
maintain the normal potassium concentration gradients between the ICF and
ECF. The recommendation for daily intake/consumption of potassium is 4700
mg. Potassium is excreted, both actively and passively, through the renal
tubules, especially the distal convoluted tubule and collecting ducts.
Potassium participates In the exchange with sodium in the renal tubules
under the influence of aldosterone, which also relies on basolateral sodium-
potassium pumps.

Hypokalemia is an abnormally low potassium blood level. Similar to the

situation with hyponatremia, hypokalemia can occur because of either an
absolute reduction of potassium in the body or a relative reduction of
potassium in the blood due to the redistribution of potassium. An absolute
loss of potassium can arise from decreased intake, frequently related to
starvation. It can also come about from vomiting, diarrhea, or alkalosis.

Some insulin-dependent diabetic patients experience a relative reduction of

potassium in the blood from the redistribution of potassium. When insulin is
administered and glucose is taken up by cells, potassium passes through the
cell membrane along with glucose, decreasing the amount of potassium in
the blood and IF, which can cause hyperpolarization of the cell membranes of
neurons, reducing their responses to stimuli.

Hyperkalemia, an elevated potassium blood level, also can impair the

function of skeletal muscles, the nervous system, and the heart.
Hyperkalemia can result from increased dietary intake of potassium. In such
a situation, potassium from the blood ends up in the ECF in abnormally high
concentrations. This can result in a partial depolarization (excitation) of the
plasma membrane of skeletal muscle fibers, neurons, and cardiac cells of the
heart, and can also lead to an inability of cells to repolarize. For the heart,
this means that it won’t relax after a contraction, and will effectively “seize”
and stop pumping blood, which is fatal within minutes. Because of such
effects on the nervous system, a person with hyperkalemia may also exhibit
mental confusion, numbness, and weakened respiratory muscles.

Chloride

Chloride is the predominant extracellular anion. Chloride is a major

contributor to the osmotic pressure gradient between the ICF and ECF, and
plays an important role in maintaining proper hydration. Chloride functions to
balance cations in the ECF, maintaining the electrical neutrality of this fluid.
The paths of secretion and reabsorption of chloride ions in the renal system
follow the paths of sodium ions.

Hypochloremia, or lower-than-normal blood chloride levels, can occur

because of defective renal tubular absorption. Vomiting, diarrhea, and
metabolic acidosis can also lead to Hypochloremia. Hyperchloremia, or
higher-than-normal blood chloride levels, can occur due to dehydration,
excessive intake of dietary salt (NaCl) or swallowing of sea water, aspirin
intoxication, congestive heart failure, and the hereditary, chronic lung
disease, cystic fibrosis. In people who have cystic fibrosis, chloride levels in
sweat are two to five times those of normal levels, and analysis of sweat is
often used in the diagnosis of the disease.

Bicarbonate
Bicarbonate is the second most abundant anion in the blood. Its principal
function is to maintain your body’s acid-base balance by being part of buffer
systems.

Bicarbonate ions result from a chemical reaction that starts with carbon
dioxide (CO2) and water, two molecules that are produced at the end of
aerobic metabolism. Only a small amount of CO2 can be dissolved in body
fluids. Thus, over 90 percent of the CO2 is converted into bicarbonate ions,
HCO3–, through the following reactions:

CO2+ H 2 ↔ H2 + CO3 ↔ H2 + CO3− + H +

The bidirectional arrows indicate that the reactions can go in either direction,
depending on the concentrations of the reactants and products. Carbon
dioxide is produced in large amounts in tissues that have a high metabolic
rate. Carbon dioxide is converted into bicarbonate in the cytoplasm of red
blood cells through the action of an enzyme called carbonic anhydrase.
Bicarbonate is transported in the blood. Once in the lungs, the reactions
reverse direction, and CO2 is regenerated from bicarbonate to be exhaled as
metabolic waste.

Calcium

About two pounds of calcium in your body are bound up in bone, which
provides hardness to the bone and serves as a mineral reserve for calcium
and its salts for the rest of the tissues. Teeth also have a high concentration
of calcium within them. A little more than one-half of blood calcium is bound
to proteins, leaving the rest in its ionized form. Calcium ions, Ca2+, are
necessary for muscle contraction, enzyme activity, and blood coagulation. In
addition, calcium helps to stabilize cell membranes and is essential for the
release of neurotransmitters from neurons and of hormones from endocrine
glands.

Calcium is absorbed through the intestines under the influence of activated

vitamin D. A deficiency of vitamin D leads to a decrease in absorbed calcium
and, eventually, a depletion of calcium stores from the skeletal system,
potentially leading to rickets in children and osteomalacia in adults,
contributing to osteoporosis.

Hypocalcemia, or abnormally low calcium blood levels, is seen in

hypoparathyroidism, which may follow the removal of the thyroid gland,
because the four nodules of the parathyroid gland are embedded in it.
Hypercalcemia, or abnormally high calcium blood levels, is seen in primary
hyperparathyroidism. Some malignancies may also result in hypercalcemia.

Phosphate

Phosphate is present in the body in three ionic forms: H2PO4, H2PO4 ² -,

PO4 ³- . The most common form is H2PO4 ²- . Bone and teeth bind up 85
percent of the body’s phosphate as part of calcium-phosphate salts.
Phosphate is found in phospholipids, such as those that make up the cell
membrane, and in ATP, nucleotides, and buffers.

Hypophosphatemia, or abnormally low phosphate blood levels, occurs with

heavy use of antacids, during alcohol withdrawal, and during
malnourishment. In the face of phosphate depletion, the kidneys usually
conserve phosphate, but during starvation, this conservation is impaired
greatly. Hyperphosphatemia, or abnormally increased levels of phosphates
in the blood, occurs if there is decreased renal function or in cases of acute
lymphocytic leukemia. Additionally, because phosphate is a major
constituent of the ICF, any significant destruction of cells can result in
dumping of phosphate into the ECF.

Regulation of Sodium and Potassium

Sodium is reabsorbed from the renal filtrate, and potassium is excreted into
the filtrate in the renal collecting tubule. The control of this exchange is
governed principally by two hormones—aldosterone and angiotensin II.

Aldosterone

This flow chart shows how potassium and sodium ion concentrations in the
blood are regulated by aldosterone. Rising K plus and falling NA plus levels in
the blood trigger aldosterone release from the adrenal cortex. Aldosterone
targets the kidneys, causing a decrease in K plus release from the kidneys,
which reduces the amount of K plus in the blood back to homeostatic levels.
Aldosterone also increases sodium reabsorption by the kidneys, which
increases the amount of NA plus in the blood back to homeostatic levels.

Recall that aldosterone increases the excretion of potassium and the

reabsorption of sodium in the distal tubule. Aldosterone is released if blood
levels of potassium increase, if blood levels of sodium severely decrease, or
if blood pressure decreases. Its net effect is to conserve and increase water
levels in the plasma by reducing the excretion of sodium, and thus water,
from the kidneys. In a negative feedback loop, increased osmolality of the
ECF (which follows aldosterone-stimulated sodium absorption) inhibits the
release of the hormone.

Angiotensin II

Angiotensin II causes vasoconstriction and an increase in systemic blood

pressure. This action increases the glomerular filtration rate, resulting in
more material filtered out of the glomerular capillaries and into Bowman’s
capsule. Angiotensin II also signals an increase in the release of aldosterone
from the adrenal cortex.

In the distal convoluted tubules and collecting ducts of the kidneys,

aldosterone stimulates the synthesis and activation of the sodium-potassium
pump. Sodium passes from the filtrate, into and through the cells of the
tubules and ducts, into the ECF and then into capillaries. Water follows the
sodium due to osmosis. Thus, aldosterone causes an increase in blood
sodium levels and blood volume. Aldosterone’s effect on potassium is the
reverse of that of sodium; under its influence, excess potassium is pumped
into the renal filtrate for excretion from the body.

Regulation of Calcium and Phosphate

Calcium and phosphate are both regulated through the actions of three
hormones: parathyroid hormone (PTH), dihydroxyvitamin D (calcitriol), and
calcitonin. All three are released or synthesized in response to the blood
levels of calcium.
PTH is released from the parathyroid gland in response to a decrease in the
concentration of blood calcium. The hormone activates osteoclasts to break
down bone matrix and release inorganic calcium-phosphate salts. PTH also
increases the gastrointestinal absorption of dietary calcium by converting
vitamin D into dihydroxyvitamin D (calcitriol), an active form of vitamin D
that intestinal epithelial cells require to absorb calcium.

PTH raises blood calcium levels by inhibiting the loss of calcium through the
kidneys. PTH also increases the loss of phosphate through the kidneys.

Calcitonin is released from the thyroid gland in response to elevated blood

levels of calcium. The hormone increases the activity of osteoblasts, which
remove calcium from the blood and incorporate calcium into the bony
matrix.

Chapter Review

Electrolytes serve various purposes, such as helping to conduct electrical

impulses along cell membranes in neurons and muscles, stabilizing enzyme
structures, and releasing hormones from endocrine glands. The ions in
plasma also contribute to the osmotic balance that controls the movement of
water between cells and their environment. Imbalances of these ions can
result in various problems in the body, and their concentrations are tightly
regulated. Aldosterone and angiotensin II control the exchange of sodium
and potassium between the renal filtrate and the renal collecting tubule.
Calcium and phosphate are regulated by PTH, calcitrol, and calcitonin.