FAR EASTERN UNIVERSITY MANILA – DEPARTMENT OF MEDICAL TECHNOLOGY

ELECTROLYTES – PART 1
I. Introduction
A. Ions capable of carrying an electric charge
• Two types of Ions:
1. Anions
Anions Cations
2. Cations
• Carry (-) charge and move toward the anode • Carry (+) charge and move toward the cathode
• Eg., Cl-, HCO3-, PO4- • Eg., Na+, K+, Mg2+, Ca2+
• Functions of Electrolytes
1. Volume and osmotic regulation (Na Na++, Cl
Cl--, K+
K +) 5. Regulation of ATPase ion pumps (Mg 2+
Mg2+ )
+ - + -
2. Myocardial rhythm & contractility (K Mg2+, Ca2+
K+, Mg2+ Ca2+) 6. Acid-base balance (HCO 3 , K+
HCO3- K , Cl
Cl )
2+ -
3. Neuromuscular Excitability (K
K++ Mg22+ Ca2+
, Mg , Ca2+) 7. Production and use of ATP from glucose (Mg Mg2+ , PO
PO44)
2+ Ca2+
4. Cofactors in enzyme activation (Mg
Mg2+ , Ca2+, Zn2+
Zn2+)
II. Water
A. Introduction:
• 40-75% of body weight
• Function: a. Transport nutrients to the cells b. Removes waste products
• Location: a. ICF: 2/3;
2/3 b. ECF: 1/3
1/3 - Intravascular, 25%; 75%
25% interstitial fluid, 75%
• Distribution of Body Water in Adult
Compartment (%) of Body Weight (%) of Total Body H2O
Extracellular 20
20 33
33
Plasma 5
5 8
Interstitial 15
15 25
25
Intracellular 40
40 67
67
Total Body Water 60
60 100
100
B. Osmolality and Blood Volume:
• Concentration of ions is maintained by:
1. Passive
Passive Transport: Passive movement of ions across a membrane
2. Active
Active Transport: Requires energy to move ions across a membrane. ATPase ATPase - dependent
dependent ion pumps
ion pumps
i. Definition
1. Concentration of solutes / Kg of solvent (mmol/kg)
2. Regulated by:
a. Thirst Sensation
b. Arginine vasopressin hormone (AVP)
ii. Regulation
1. Thirst Sensation: Response to consume more fluids. Prevents water deficit
Thirst Sensation
2. Arginine
Arginine vasopressin hormone (AVP):
vasopressin hormone AVP Antidiuretic Hormone (ADH). ↑ reabsorption of water in kidneys
• Suppressed
Suppressed in excess H2O H2O load
load and Activated
Activated in water deficit
water deficit
3. Renin-angiotensin-aldosterone system: a. Angiotensinogen
Renin angiotensin aldosterone Angiotensinogen –Renin Renin→ b. Angiotensin
Angiotensin II –ACE
CE→ c. Angiotensin
Angiotensin IIII
–AT1 receptor→ i. Adrenal gland aldosterone release (kidney sodium retention) + ii. vessel constriction
aldosterone release constriction
+
4. ANP:
ANP ↑ Na Na+ and H 2O excretion
H2O excretion in the kidney
5. GFR:
H2O ↑ w/ vol. expansion & ↓ w/ vol.
vol. expansion vol. depletion
depletion
iii. Determination: Osmolality (Serum or urine).
Any substance dissolve in a solvent will:
1. ↓ freezing point by 1.858°C
freezing point 1.858°C
2. ↑ boiling point by 0.52°C
boiling point 0.52°C
3. ↓ vapor pressure (dew point) by 0.3
vapor pressure 0.3 mmHg
mmHg
4. ↑ osmotic pressure by 17,000
osmotic pressure mmHg
17,000 mmHg
• Main contributors are Na Na++ Cl-
, Cl-, Urea
Urea and Glucose
Glucose

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 FAR EASTERN UNIVERSITY MANILA – DEPARTMENT OF MEDICAL TECHNOLOGY

III. Electrolytes
Cation (mmol/L) Anion (mmol/L)
Na+ (136-145);
136 145 K+ (3.5-5.1);
3.5 5.1 Ca2+ (2.15-2.5);
2.15 2.5 Mg2+ (0.63-1)
0.63 1 HCO3- (23-29);
23 29 Cl- (98-107);
98 107 HPO42- (0.78-1.42);
0.78 1.42 SO42- (0.5)
0.5

A. Sodium (Na+)
i. Description and Regulation
• The most abundantcation
most abundant cation • Plasma concentration depends in:
in the ECF a. Intake of water Thirst
• Thirst
• Major
Major extracellular cation
extracellular cation b. Excretion of water AVP
• AVP (↑ H2O reabsorption)
• Na+, K+ -ATPase ion pump c. The blood volume • Angiotensin
AngiotensinII II (↑ aldosterone)
moves 33 NaNa++ ions out
ions out of the status Aldosterone
• Aldosterone (↑ Na+ reabsorption in kidney)
K+ ions
cell in exchange for 22 K+ ions • ANP
ANP (↑ Urinary Na + Excretion )
ii. Clinical Applications
Causes of Hyponatremia (↓ Na+) Causes of Hypernatremia (↑ Na+)
1. ↑↑ Sodium (Na+)+
Sodium (Na )Loss
Loss 2. ↑↑ Water
Water Retention
Retention 1. Excess
Excess Water Loss
Water Loss Decreased Water
2. Decreased WaterIntake
Intake
Hypoaldosteronism
a. Hypoaldosteronism a. Renal failure a. Diabetes insipidus
Diabetes insipidus a. Old/Infant/Mentally Impaired
b. Potassium Deficiency
Potassium Deficiency b. SIADH b. Profuse sweating Increased Retention
3. Increased Retention or Intake
Intake
c. Diuretic Use (Thiazide) c. Nephrotic (fever and diarrhea) CushingSyndrome
a. Cushing Syndrome
d. Vomiting and diarrhea syndrome c. Severe burns Hyperaldosteronism
b. Hyperaldosteronism
e. Addison's dse.
Addison's dse. d. Hepatic cirrhosis c. Hypertonic Salt Solution

iii. Determination of Sodium

• Specimen • Methods
a. Serum, Plasma (heparin and oxalate) a. FES
b. False ↓↓ with marked hemolysis (dilutional effect) b. AAS
marked hemolysis
c. ISE (Glass
Glass ion-exchange membrane)
ion exchange membrane

B. Potassium (K+)

i. Description and Regulation

• Major
Major Intracellular cation
Intracellular cation 1. Aldosterone
Aldosterone iii. Determination of Potassium
• Regulation of neuromuscular (↑ K+ excretion in urine) • Specimen
excitability, contraction of 2. Na+,
Na+ K+K+ -ATPase
-ATPase pump
pump a. Serum, Plasma (heparin)
heart, ICF volume, H+ conc. (↓ function ↓ cellular entry) b. False ↑ with hemolysis
• ↑ K+, ↑ cell excitability (↑ function ↑ cellular entry) c. 24-hour urine (diurnal variation)
diurnal variation
(muscle weakness)
muscle weakness • Methods
+
• ↓ K , ↓ cell excitability a. FES
(arrhythmia/paralysis)
arrhythmia paralysis b. AAS
c. ISE (Use valinomycin membrane)
valinomycin membrane
ii. Clinical Applications
Causes of Hypokalemia (↓K+) Causes of Hyperkalemia (↑K+)
1. GI Loss
GI Loss Renal Loss
3. Renal Loss DecreasedRenal
1. Decreased RenalExcretion
Excretion 3. Cellular
CellularShift
Shift
a. Vomiting a. Diuretics a. Renal Failure a. Acidosis
Acidosis
b. Diarrhea b. Renal Tubular Acidosis b. Hypoaldesteronism
Hypoaldesteronism b. Muscle/cellular injury
Muscle cellular injury
c. Laxatives c. Cushing’s syndrome
Cushing’s syndrome c. Addison’s
Addison’s Dse. c. Chemotherapy/Leukemia
Chemotherapy Leukemia
2. Cellular Shift -
Cellular Shift d. Hyperaldosteronemia
Hyperaldosteronemia 2.. Increased Intake
Increased Intake 4. Artifactual
Artifactual / Pseudo
Pseudo-
↑ + uptake
↑ K uptake
K+ e. Hypomagnesemia a. Oral/IV – K +
a. Hemolysis/Thrombocytosis
Hemolysis Thrombocytosis
Alkalosis
a. Alkalosis 4. Decreased Intake replacement b. Prolonged
Prolonged tourniquet
tourniquet
Insulin Overdose
b. Insulin Overdose

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 FAR EASTERN UNIVERSITY MANILA – DEPARTMENT OF MEDICAL TECHNOLOGY

C. Chloride (Cl-)
i. Description and Regulation iii. Determination of Chloride
• Major Extracellular
Major Extracellular Anion
Anion • Specimen
• Involve in maintaining osmolality,
osmolality blood volume and
blood volume a. Serum, Plasma (lithium heparin)
lithium heparin
electric neutrality (Chloride
electric neutrality shift)
Chloride shift b. False ↓ w/ marked
marked hemolysis
hemolysis (dilution)
dilution
• Rate limiting component in Na +
Na+reabsorption
reabsorption c. 24-hour urine
ii. Clinical Applications • Methods
Causes of Hyperchloremia (↑Cl-) Causes of Hypochloremia (↓Cl-) a. ISE (Use ion
ion exchange
exchange membrane)
membrane

1. Excess Loss of HCO3HCO3- 2. Excess

ExcessLoss Cl-
Lossof Cl b. Amperometric-coulometric
Amperometric coulometric

a. GI Loss a. Prolonged vomiting (Cotlove chloridometer)

Cotlove chloridometer

b. Metabolic acidosis
Metabolic acidosis Aldosterone deficiency
b. Aldosterone deficiency Ag2+ + 2Cl- → Ag Cl2
c. Salt-losing pyelonephritis c. Schales and schales
Schales and schales
d. Metabolic alkalosis
Metabolic alkalosis Titration with mercuric nitrate

d. Skeggs and Hochestrasser

(Colorimetric)
e.

Review Quiz - Part 1

1 - 6. Identify the hormone that:
1. ↑ reabsorption of water in the kidneys. Arginine vasopressin
Arginine vasopressin hormone
hormone
2. ↓ reabsorption of water in the kidneys. Atrial natriuretic
Atrial natriuretic peptide
peptide
3. ↑ reabsorption of Sodium in the kidneys. Aldosterone
Aldosterone
4. ↓ reabsorption of Sodium in the kidneys. Atrial Atrialnatriuretic
natriuretic peptide
peptide
5. Promotes vasocontriction. Angiotensin
Angiotensin IIII
6. Promotes vasodilation. Atrial
Atrial natriuretic peptide
natriuretic peptide
7. ANP is secreted by what organ? HeartHeart
8 - 9. Angiotensinogen is converted into Angiotensin II by participation of what organs? KidneysKidneys, Lungs
Lungs
10 - 11. Blood osmolality is mainly regulated by what mechanism and hormone. Thirst Sensation, AVP
Thirst Sensation AVP
12 - 13. Electrolytes involved BOTH in the regulation of myocardial rhythm and as enzyme cofactor. Calcium, Magnesium
Calcium Magnesium
14 - 15. Electrolytes involved BOTH in the regulation of blood volume and acid-base balance. PotassiumPotassium, Chloride
Chloride

Review Quiz - Part 2

1. Electrolyte involved BOTH in the regulation of neuromuscular excitability and blood volume. Potassium Potassium
2. Electrolyte involved in the regulation of the ATPase Ion Pump. Magnesium
Magnesium
3. The major intracellular anion. Phosphate
Phosphate
4. Angiotensinogen is converted into Angiotensin I by what hormone? Renin Renin
5. It refers to the diffusion of ions across a cellular membrane. Passive Transport
Passive Transport
6. Angiotensin I is converted into Angiotensin II by what enzyme? Angiotensin Converting
Angiotensin Converting Enzyme
Enzyme
7 - 8. Any substance dissolve in a solvent (solution) will ↑ what colligative properties? Boiling Point, Osmotic
Boiling Point OsmoticPressure
Pressure
9 - 10. Any substance dissolve in a solvent (solution) will what colligative property? Freezing
Freezing point, VaporPressure
point Vapor Pressure
11 - 14. What analytes are the main contributors to plasma Osmolality? Sodium, Chloride, Ureas
Sodium Chloride Ureas, Glucose
Glucose
15. Refers to ions capable of carrying an electric charge. Electrolytes
Electrolytes

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