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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.
Non Electrolyte
dextrose
Electrolyte
Cation : Na, K,
Ca, Mg
ureum
kreatinin
Anion : HCO3,
Cl, HPO4
ELECTROLYTE
Kation/anion
Na +
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
The cell contains large anions such protein and glycogen, which
cannot escape and therefore draw in K ions to maintain
electrical neutrality.
SODIUM
Normal range: 136145 mEq/L or 136145 mmol/L
PHYSIOLOGY OF SODIUM
PHYSIOLOGY OF SODIUM
HYPERNATREMIA
Thirst
Restlessness
Irritability
Lethargy
Muscle twitching
Seizures
Hyperreflexia
Coma
Death
CAUSES OF HYPONATREMIA
SIADH
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
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
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
ETIOLOGIES OF HYPERKALEMIA
Apparent
excess
( extracellular
shifting )
True excess
Metabolic
acidosis
INCREASED INTAKE
DECREASED OUTPUT
Endogenous causes :
Hemolysis
Rhabdomyolysis
Muscle crush injuries
Burns
Exogenous causes :
Salt subtitutes
Drugs ( e.g. penicillin
potassium )
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
CALCIUM
CALCIUM
HOMEOSTASIS
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
Lithiuminducedrenalcalciumreabsorption
ExcessivevitaminD,vitaminA,or
thyroidhormone,which increases
intestinal absorption
Tamoxifen
Androgenichormones
Estrogen
Progesterone
HYPOCALCEMIA
HYPERCALCEMIA
Fatigue
Confusion
Bradycardia
Arrhytmia
chronic hypercalcemia :
nephrolithiasis, metastatic calcification,
renal failure
MAGNESIUM
REGULATION
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
HYPERMAGNESEMIA
CAUSES
Renal insufficiency
iatrogenic
2-5 mEq/L
6 mEq/L
10-15
mEq/L
> 15
mEq/L
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
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
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
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