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IRA ASTUTI HASIBUAN

POSTGRADUATE OF BIOMEDICAL SCIENCE


FACULTY OF MEDICINE
UNIVERSITY SUMATERA UTARA

ELECTROLYTE
A substance whose components dissociate in solution into
positively (cation) and negatively (anion) charged ions. For
example, sodium chloride in solution (saline), dissociates into
Na and Cl. Other electrolytes of physiological importance
include Ca, PO42-, etc.

Glucose is not an electrolyte since it does not dissociate in


solution. At all times the total number of positive charges
balances the number of negative charges to achieve electrical
neutrality.

Non Electrolyte
dextrose

Electrolyte
Cation : Na, K,
Ca, Mg

ureum
kreatinin

Anion : HCO3,
Cl, HPO4

ELECTROLYTE
Kation/anion

Na +

Ekstra selular ( mEq/L )


142
142

Intraselular ( mEq/L )
15

K+

150
150

Ca ++

Mg ++

27

Total

154

194

HCO3-

24

10

Cl -

105105
105

HPO4 =

100
100

SO4 =

20

Asam Org

Protein

16

63

Total

154

194

Water and electrolyte in the body


The total body water is divided functionally into the
extracellular (20% of body weight) and the intracellular
fluid spaces (40 of body weight) separated by the cell
membrane with its active sodium pump which ensures
that sodium remains largely in the ECF

The cell contains large anions such protein and glycogen, which
cannot escape and therefore draw in K ions to maintain
electrical neutrality.

These mechanism ensure that Na and its balance anions Cl and


HCO, are the mainstay of ECF osmolality, and K has
corresponding function in the ICF

SODIUM
Normal range: 136145 mEq/L or 136145 mmol/L

The total body sodium is 3000-4000 mmol, of which only 60%


is exchangeable, the remainder being locked mainly in bone

The principal role of sodium is to regulate serum osmolality as


well as fluid balance.

Changes in body water and plasma volume can directly or


indirectly affect the serum sodium concentration.

PHYSIOLOGY OF SODIUM

As a result of changes in effective circulating volume,


baroreceptors and osmoreceptors will respond
accordingly in an attempt to restore an isovolemic state of
the body.
Baroreceptors are located in the carotid sinus, aortic
arch,
cardiac
atria,hypothalamus,
and
the
juxtaglomerular apparatus in the kidney.
Stimulation of these receptors will promote urinary
loss of water and sodium.

PHYSIOLOGY OF SODIUM

Osmoreceptors are present


primarily in the hypothalamus.
The three major mediators
involved include vasopressin or
antidiuretic hormone (ADH),
The
renin-angiotensinaldosterone System (RAAS),
And Natriuretic peptides.
The Resultant Renal Effects
From These Three Distinct
Pathways
Will
Alter
the
homeostasis Of Water and
sodium.

Homeostatic mechanisms involved in sodium, potassium,


and water balance.

SIGN AND SYMPTOM OF HYPONATREMIA


AND HYPERNATREMIA
HYPONATREMIA
Abnormal sensor
Agitation
Anorexia
Apathy
Cheyne-Stokes respiration
Depressed deep-tendon
reflexes
Disorientation
Hypothermia
Lethargy
Muscle cramps
Nausea
Seizures

HYPERNATREMIA
Thirst
Restlessness
Irritability
Lethargy
Muscle twitching
Seizures
Hyperreflexia
Coma
Death

CAUSES OF HYPONATREMIA

SIADH

The syndrome of inappropriate antidiuretic hormone secretion


(SIADH) is the most common cause of hyponatremia in
hospitalized patients

Normally, ADH is secreted from the posterior lobe of the


pituitary gland in response to decrease in plasma volume or
increase in serum osmolality.

In SIADH, secretion of ADH is not caused by hemodynamic


disturbance and is mediated through nonosmotic receptors,
resulting in water retention and dilutional hyponatremia.

The key points in diagnosing SIADH are the serum


sodium concentration, tonicity of plasma and urine,
urine sodium concentration and clinical volume
status.

Finding of hyponatremia ( serum sodium


concentration < 135 mEq/L ), hypotonicity plasma
osmolality ( <280 mOsm/kg) inappropriate
concentrated urine ( > 100 mOsm/kg ), elevated
urine sodium concentration (>20mEq/L) are
constant with SIADH

SIADH is a diagnosis of exclusion, and adrenal,


cardiac, liver, kidney, and thyroid dysfunction
must be ruled out.

TREATMENT
Mild asymptomatic hyponatremia (serum sodium > 125
mEq/L) is treated with fluid restriction.
Severe symptomatic hyponatremia is treated with
hypertonic saline in addition to fluid restriction. In treating
SIADH, the osmolality of the infused saline must exceed the
osmolality of the patients urine.
To avoid neurologic complications due to rapid shifts in
sodium, the serum sodium level should be raised no faster
than 1 to 2 mEq per hour, and no faster than 8 to 12 mEq per
day.

CAUSES OF HYPERNATREMIA

HYPERNATREMIA
Na > 145 mmol/L

HYPOVOLEMIA

EUVOLEMIA

Diabetic incipidus

increased
insensible
water loss

profuse sweating
diarrhea

HYPERVOLEMIA

Primary
hyperaldosteronism
Cushing disease
Sea water, near
drowning

fever,
extensive burns,
mechanical ventilation

Resuscitative efforts
using hypertonic
sodium bicarbonate

POTASSIUM
The total body K lies between 3000 and 3500 mmol and is
contained in the intracellular space at a concentrastion of 120145 mmol/L

Only a very small proportion is in the ECF, where its


concentration lies crucially in the narrow range 3.5-5.2
mmol/L.

The major physiological role of potassium is in the


regulation of muscle and nerve excitability. It also play
important roles in control intracellular volume, protein
synthesis, enzymatic reaction, and carbohydrate metabolism

Na-K-ATPase pump is principally responsible for regulating


potassium entry into cell. Potassium is primarily excreted by
the kidneys

Potassium homeostasis is altered by insulin, aldosterone,


changes in acid-base balance, renal function, or
gastrointestinal and skin loses

Although potassium may affect different body functions,


its effect on cardiac muscle is the most important due to
the potential life threatening effect of arrhytmia as a result
of either high or low serum potassium concentration

The acute homeostatic sequence of events in the body to


maintain serum potassium within a narrow concentration range.

HYPOKALEMIA
Hypokalemia is defined as a serum potassium concentration less
than 3.5 mEq/L (<3.5 mmol/L).
ETIOLOGY : clinicians should determine whether hypokalemia is
due to intracellular shifting of potassium (apparent deficit) or
increased loss from the body (true deficit)

True
deficit
Alkalosis
2adrenergic
stimulation
insulin

Apparent
deficit

Decreased intake :
Tea and toast diet, alcoholism,
indigence, potassium-free IV fluids,
anorexia nervosa, bulimia
Increased output :
Extrarenal : vomiting, diarrhea, laxative
abuse, intestinal fistules
Renal : corticosteroids, amphotericin B,
diuretics, hyperaldosteronism, cushings
syndrome, licorice abuse

Signs, Symptoms, and Effects of Hypokalemia on Various


Organ Systems
CARDIO
VASCULAR

METABOLIC/
ENDOCRINE

NEURO
MUSCULAR

Decreased in
T-wave
amplitude
Development
of U waves
Hypotension
Increased risk
of digoxin
toxicity
PR
prolongation
Rhytm
disturbances
ST segment
depression
QRS widening

Decreased
aldosterone
release
Decreased
insulin release
Decreased
renal
responsiveness
to ADH

Areflexia
Cramps
Loss of
smooth
muscle
function
weakness

RENAL

Inability to
concentrate
urine
nephropathy

HYPERKALEMIA

Hyperkalemia is defined as serum potassium concentration


greater then 5.0 mEq/L (> 5.0 mmol/L )

Hypokalemia may indicate a true or apparent potassium


imbalance

Renal failure is the most common causes of hyperkalemia

ETIOLOGIES OF HYPERKALEMIA

Apparent
excess
( extracellular
shifting )

True excess

Metabolic
acidosis
INCREASED INTAKE

DECREASED OUTPUT

Endogenous causes :
Hemolysis
Rhabdomyolysis
Muscle crush injuries
Burns

Chronic or acute renal


failure
Drugs : potassiumsparing diuretics, ACEinhibitors, NSAID,
Angiotensin II receptor
antagonist, heparin,
trimethoprim
Deficiency of adrenal
steroids
Addisons disease

Exogenous causes :
Salt subtitutes
Drugs ( e.g. penicillin
potassium )

SIGN AND SYMPTOM OF HYPERKALEMIA

Symptom of hyperkalemia usually do not developed until


serum potassium concentration reach 5.5 mEq/L.

Symptoms are caused by changes in neuromuscular and


cardiac function and include muscle twitching, cramping,
weakness and paralysis.

The most concerning symptoms are cardiac abnormalities :


peaked T waves, widened QRS complexes, prolonged PR
interval, shortened QT interval, this can lead to cardiac
arrhytmias.

Normal range : 96-106 mEq/L or 96-106 mmol/L

Chloride is passively absorbed from the upper small intestine. In the


distal ileum and large intestine., its absorbtion is coupled with
bicarbonate ion secretion
Chloride is influenced by the extracellular fluid balance and acid-base
balance.
The physiological role of chloride is primarily passive. It balances out
positive charges in the extracellular fluid and, by passively following
sodium, helps to maintain extracellular osmolality

HYPOCHLOREMIA

Causes :
A patient is on acid-suppressive therapy (e.g., high-dose
H2-blockers or proton pump inhibitors)
Patient who is receiving continuous or frequent
nasogastric suction
Person whose has profuse vomiting, a greater loss of
chloride than sodium can occur because gastric fluid
contains 1.53 times more chloride than sodium.
Gastric outlet obstruction, protracted vomiting and selfinduced vomiting
Metabolic alkalosis

HYPERCHLOREMIA

The most causes : saline infusion in hospitalized patient


parenteral nutrition solutions with high chloride
concentrations
Drug : acetazolamide
Metabolic and respiratoric acidosis

CALCIUM

Ninety-nine percent of total body calcium resides in


bone. Less than 1 % exist in the extracellular fluid.

Normal serum calcium concentration in the extracellular


between 8.6 and 10.2 mg/dL. Nearly 50 % of serum calcium
is protein bound, primarily to albumin.

Calcium is essential to many body function, including bone


metabolism, neuromuscular activity, electrical conduction
in the heart and smooth muscle, coagulation, and exocrine
and endocrine functions.

CALCIUM
HOMEOSTASIS

Calcium homeostasis is regulated by parathyroid hormone,


calcitonin and vitamin D.

For every 1 g/dL decrease in serum albumin concentration


below 4 g/dl serum calcium concentration will decrease by
0,8 mg/dl, therefore serum calcium concentration should be
corrected in patient with hypoalbuminemia

Corrected calcium = ( 0,8 ( 4 albumin )) + serum calcium

source : https://quizlet.com/31186621/endocrine-06-bone-mineral-homeostasis-flashcards/

HYPOCALCEMIA

CAUSES

Diminished intake
Medications : calcitonin
Ethylenediaminetetraacetic acid ( EDTA )
Glucocorticoid
Loop diuretics
Phosphate salts
Picamycin
Hyperphosphatemia
Hypoalbuminemia
Hypomagnesemia
Hypopharatiroidism
Pancreatitis
Renal failure
Secondary hyperpharathyroidism
Vitamin D deficiency

HYPERCALCEMIA

CAUSES

The most causes is malignancy and primarily


hyperparathyroidism

Hypercalcemia can also result from:


Excessive administration
Of IVcalcium salts
Calcium supplements
Chronic immobilization
Pagetsdisease
Sarcoidosis
Hyperthyroidism
Acute adrenal insufficiency
Somer espiratory diseases

Lithiuminducedrenalcalciumreabsorption
ExcessivevitaminD,vitaminA,or
thyroidhormone,which increases
intestinal absorption
Tamoxifen
Androgenichormones
Estrogen
Progesterone

SIGNS AND SYMPTOMS

HYPOCALCEMIA

HYPERCALCEMIA

Tetany characteristic symptom


Neuromuscular disfunction
Cardiovascular disfunction
Central nervous system dysfunction
Chronic hypocalcemia : hair loss,
dermatitis, eczema, grooved nails

Fatigue
Confusion
Bradycardia
Arrhytmia
chronic hypercalcemia :
nephrolithiasis, metastatic calcification,
renal failure

MAGNESIUM

Magnesium is found primarily in the bone,


muscle and soft tissue. Approximately 1 % of total
body stores present in extracellular fluid

The normal serum magnesium concentration is


1.5 to 2.4 mg/dl.

Magnesium is utilized throughout the body as a


cofactor for enzyme and is required in reaction
involving adenosine triphosphatase ( ATP )

REGULATION

Largely regulated by the kidney


Other factors including :
gastrointestinal function,
parathyroid hormone activity,
patient condition

HYPOMAGNESEMIA
Defined as serum magnesium concentration less than 1.5
mg/dl and is severe when the serum concentration is
below 1 mg/dl
CAUSES

symptoms

Excessive
gastrointestinal
loses
Renal losses
Surgery
Trauma

Burns
Sepsis
Pancreatitis
Malnutrition
alcoholism

Arrhytmias, torsades de pointes, seizures,


coma and death

HYPERMAGNESEMIA

Defined as serum magnesium concentration greater than 2.4


mg/dl. Most patients remain asymptomatic until serum
magnesium concentration exceed 4 mg/dl.

CAUSES

Renal insufficiency
iatrogenic

SIGNS AND SYMPTOMS OF HYPERMAGNESEMIA

2-5 mEq/L

Bradycardia, flushing, sweating,


sensation of warmth, nausea, vomitting,
decreased serum calcium and decreased
clotting mechanism

6 mEq/L

Drowsiness and decreased deep tendon


reflexes

10-15
mEq/L

Flaccid paralysis and increased PR and


QRS intervals

> 15
mEq/L

Respiratory distress and asystole

PHOSPHATE
Normal range serum phosphate concentration : 2.64.5
mg/dL or 0.841.45 mmol/L for adults
It is important for intracellular metabolism of proteins,
lipids, and carbohydrates and it is a major component in
phospholipid membranes, RNAs, nicotinamide diphosphate
(an enzyme cofactor), cyclic adenine and guanine nucleotides
(second messengers), and phosphoproteins.
Phosphate absorption is diminished when a large amount of
calcium or aluminum is present in the intestine due to the
formation of insoluble phosphate compounds.

PHOSPHATE REGULATION

Serum phosphate and calcium concentrations as well as PTH


and vitamin D levels are intimately related with each other.
Serum phosphate indirectly controls PTH secretion via a
negative feedback mechanism. With a decrease in the serum
phosphate concentration, the conversion of vitamin D to 1,25DHCC increases (which increases serum concentrations of both
phosphate and calcium). Both the intestinal absorption and
renal reabsorption of phosphate is increased.
The concomitant increase in serum calcium then directly
decreases PTH secretion. This decrease in serum PTH
concentration permits a further increase in renal phosphate
reabsorption.

HOMEOSTASIS REGULATION OF CALCIUM AND


PHOSPHATE BY PTH, VITAMIN D DAN FGF23

From the following article:


The skeleton as an endocrine organ

Douglas J. DiGirolamo, Thomas L. Clemens & Stavroula Kousteni .Nature Reviews


Rheumatology 8, 674-683 (November 2012) doi:10.1038/nrrheum.2012.157

HYPOPHOSPHATEMIA
Hypophosphatemia indicates a serum phosphate
concentration
less than 2.6 mg/dL (<0.84 mmol/L).
Common causes of decreased serum phosphate
concentrations:
1. Increased renal excretion
2. Intracellular shifting
3. Decreased phosphate or vitamin D intake
Infusion of concentrated glucose solutions, especially when
accompanied by insulin, can produce hypophosphatemia
through intracellular phosphate shifting refeeding
syndrome

SIGNS AND SYMPTOMS OF


HYPOPHOSPHATEMIA
Patients with moderate reduction in serum phosphate
(22.5 mg/dL or 0.640.81 mmol/L) are often asymptomatic.
Neurological irritability may occur as the serum phosphate
concentration
Drops below 2 mg/dL(<0.64 mmol/L )
Severe hypophosphatemia is often associated with muscle
weakness, rhabdomyolysis, paresthesia, hemolysis, platelet
dysfunction, and cardiac and respiratory failure. CNS effects
often include encephalopathy, confusion, obtundation,
seizures, and ultimately, coma

HYPERPHOSPHATEMIA
Hyperphosphatemia indicates a serum phosphate
concentrationgreater
Than 4.5 mg/Dl (>1.45 mmol/L).
There are three basic causes for elevated serum
phosphate concentrations:
1.Decreased renal phosphate excretion
2. Shift of phosphate from intracellular to extracellular
fluid
3. Increased intake of vitamin D or phosphate-containing
products (orally, rectally, or intravenously)
THE MOST CAUSE

RENAL
DYSFUNCTION

SIGNS AND SYMPTOMS

Signs and symptoms of hyperphosphatemia commonly


result from the accompanying hypocalcemia and
hyperparathyroidism
Renal function may diminish if hyperphosphatemia is
left untreated.
In the presence of renal dysfunction, phosphate
excretion is further reduced to cause an even greater
increase of serum phosphate concentration and a further
decline in serum calcium concentration

REFFERENCES
Lau A., Chan L., Electrolyte, Other minerals, and
Trace Elements
Lobo D., Lewington A., Allison S., Basic Concepts of
Fluid and Electrolyte Therapy
Bartel B., Gau E., Fluid and Electrolyte Management
Balasubramanian A., Flareau B., Sourbeer J.,
2007.,Syndrome of Inappropriate Antidiuretic Hormone
Secretion