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Electrolytes
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CLINICAL CHEMISTRY 2
aaronjanpalmares_02.08.15 Page 1
I. Introduction
Ions capable of carrying an electric charge Two types of Ions:
Functions of Electrolytes 1. Volume and osmotic regulation (Na
+, Cl
-, K
+) 5. Regulation of ATPase ion pumps (Mg
2+)
2. Myocardial rhythm and contractility (K+, Mg
2+, Ca
2+) 6. Acid-base balance (HCO3
-, K
+, Cl
-)
3. Neuromuscular Excitability (K+
,Mg2+
, Ca2+
) 7. Production and use of ATP from glucose (Mg2+
, PO4-)
4. Cofactors in enzyme activation (Mg2+
, Ca2+
, Zn2+
)
II. Water
A. Introduction
40-75% of body weight Function Transport nutrients to the cells and Removes waste products Location: ICF: 2/3 E CF: 1/3 Intravascular (25%) and interstitial fluid (75%)
B. Osmolality:
Concentration of ions is maintained by:
1. Passive Transport
Passive movement of ions across a membrane 2. Active Transport
Requires energy to move ions across a membrane ATPase-dependent ion pumps
i. Definition: Conc. of solutes per Kg of solvent (millimoles/kg) ii. Regulation
a. Thirst Sensation Response to consume more fluids Prevents water deficit
b. Arginine vasopressin hormone (AVP) Antidiuretic Hormone (ADH) reasorptio of ater i kides Suppressed in excess H2O load Activated in water deficit
c. Renin-angiotensin-aldosterone
system
Na+ retention, aldosterone release, vessel constriction d. Atrial natriuretic Peptide (ANP) Na+ excretion in the kidney e. Glomerular Filtration Rate (GFR) / ol. epasio ad / ol. depletio
iii. Determination
Any substance dissolve in a solvent will:
freezing point by 1.858C freezing point by 1.858C boiling point by 0.52C boiling point by 0.52C Main contributors are Na, Cl, Urea and Glucose
Distribution of Body Water in Adult
Compartment (%) of Body Weight (%) of Total Body H2O
Extracellular
Plasma 5 8
Interstitial 15 25
Intracellular 40 67
Total Body Water 60 100
A. Anions
Carry (-) charge and move toward the anode E.g. Cl-, HCO3-, PO4-
B. Cations
Carry (+) charge and move toward the cathode E.g. Na+, K+, Mg2+, Ca2
Electrolytes
CLINICAL CHEMISTRY 2
aaronjanpalmares_02.08.15 Page 2
II. Electolytes
A. Sodium (Na+)
i. Description and Regulation
The most abundant cation Plasma concentration depends in renal regulation in the ECF a. Intake of water Thirst
Major Extracellular cation b. Excretion of water AVP H2O reabsorption) Na+, K+ -ATPase ion pump c. The blood volume status Agiotesi II aldosteroe
moves 3 Na+
ions out of the Aldosteroe Na+ reabsorption in kidney) cell in exchange for 2 K
+ ions ANP Uriar Na + Excretion )
ii. Clinical Applications
Causes of Hypoatreia ( Na+) Causes of Hyperatreia ( Na+) . Sodiu (Na+) Loss . Water Retetio 1. Excess Water Loss 2. Decreased Water Intake a. Hypoaldosteronism a. Renal failure a. Diabetes insipidus a. Old/Infant/Mentally Impaired
b. K+ Deficiency b. SIADH b. Profuse sweating 3. Increased Intake or Retention
c. Diuretic Use c. Nephrotic syndrome c. Severe burns a. Cushing Syndrome
d. Salt-losing nephropathy d. Chronic heart failure b. Hyperaldosteronism
e. Severe Burns e. Hepatic cirrhosis c. Hypertonic Salt Solution
iii. Determination of Sodium
Specimen Methods
a. Serum, Plasma (heparin and oxalate) a. FES
b. False ith arked heolsis b. AAS c. ISE (Glass ion-exchange membrane)
B. Potassium (K+)
i. Description and Regulation
Major Intracellular cation 1. Aldosterone Regulation of neuromuscular K+ excretion in urine)
excitability, contraction of 2. Na+, K+ -ATPase pump
heart, ICF volume, H+ conc. ( futio ellular etr) K+, ell eitaility ( futio ellular etr)
(muscle weakness) 3. ith eerise, diaetes K+ , ell eitailit mellitus and cell breakdown
(arrhythmia/paralysis)
ii. Clinical Applications
Causes of Hypokalemia (K+) Causes of Hyperkalemia (K+) 1. GI Loss 3. Renal Loss 1. Decreased Renal Excretion 3. Cellular Shift
a. Vomiting a. Diuretics a. Renal Failure a. Acidosis
b. Diarrhea b. Renal Tubular Acidosis b. Hypoaldesteronism b. Muscle/cellular injury
c. Gastric suction c. Cushigs sdroe . Addisos Disease c. Chemotherapy / Leukemia d. Laxatives d. Hyperaldosteronism 2. Increased Intake 4. Artifactual
2. Cellular Shift - e. Hepatic cirrhosis a. Oral/IV K+ replacement a. Hemolysis, Thrombocytosis K+ uptake 4. Decreased Intake b. Prolonged tourniquet a. Alkalosis
b. Insulin Overdose
iii. Determination of Potassium
Specimen a. Serum, Plasma (heparin)
b. False ith heolsis c. 24 hour urine
Methods a. FES
b. AAS
c. ISE (valinomycin membrane)
CLINICAL CHEMISTRY 2
aaronjanpalmares_02.08.15 Page 3
C. Potassium (K+)
i. Description and Regulation
Major Extracellular anion 1. Aldosterone Involve in maintaining K+ excretion in urine)
Osmolality,blood volume 2. Na+, K+ -ATPase pump
and electric neutrality ( futio ellular etr) (Chloride shift) ( futio ellular etr) Rate limiting component 3. ith eerise, diaetes in Na
+ reabsorption mellitus and cell breakdown
D. Bicarbonate (HCO3-)
i. Description and Regulation
2nd Most Abundant anion in 1. Aldosterone the ECF K+ excretion in urine)
Accounts for more than 2. Na+, K+ -ATPase pump 80% of total CO2 ( futio ellular etr)
(Chloride shift) ( futio ellular etr) Major buffering system 3. ith eerise, diaetes of the blood mellitus and cell breakdown
E. Magnesium (Mg)
i. Physiology and Regulation
2nd Major Intracellular cation 1. Parathyroid Hormone (PTH) - Mg2+ Neuromuscular conduction Promotes Ca + renal reabsorption
Enzyme cofactor and 2. Aldosterone and thyroxine - Mg2+ ATPase ion pump Promotes Na + renal reabsorption
53% (Bone), 46% (muscle, soft tissues), Ag Cl
2
c. Scales and Schales
Titration with mercuric nitrate
ii. Clinical Applications
Causes of Hyperchloreia (Cl-) Cause of Hypochloreia (Cl-) 1. Excess Loss of HCO3
- 2. Excess Loss of Cl
-
a. GI Losses a. Prolonged Vomiting
b. Metabolic acidosis b. Aldosterone Deficiency
c. Salt-losing pyelonephritis
iii. Determination of Bicarbonate
Specimen a. Serum, Plasma (heparin)
b. False if left uncapped 6ol/L per hr Methods a. Enzyme method
ii. Clinical Applications
Metabolic Alkalosis HCO3- Metabolic acidosis HCO3- a. Severe vomiting a. Hyperventilation
b. Hypoventilation
c. Excessive alkali intake
CLINICAL CHEMISTRY 2
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ii. Clinical Applications
Causes of Hypomagnesemia (Mg+) Cause of Hypoageseia ( Mg+) - Excretion 1. Reduced Intake 2. Absorption 4. Renal 5. Endocrine a. Poor diet/starvation a. Malabsorption synd. a. Tubular disorders, a. Hyperparathyroidism
b. Prolonged Mg+- deficient IV b. Diarrhea Pyelonephritis b. Hyperaldosteronism
3. Others c. Vomiting b. Glomerulonephritis c. Hyperthyroidism
a. Excess lactation d. Laxative 6. Drug Induced d. Hypercalcemia
b. Pregnancy a. Furosemide, Thiazide e. Diabetic ketoacidosis
b. Gentamicin, Cyclosporin
c. Digitales and Digoxin
Causes of Hyperageseia ( Mg 2+ ) iii. Determination of Magnesium a. Eretio, Real failure Specimen b. Hypoparathyroidism a. Serum, Plasma (lithium heparin), 24 hr urine
c. Hypoaldosteronism b. Heolsis ause False e. Bone carcinoma and bone metastases Method a. Calmagite Mtd. Mg
2+ + CalmagiteReddish-violet (532nm)
b. Formazen Dye Mtd. Mg2+
+ DyeColored complex (660 nm) c. Methylthymol blue Mtd. Mg
2+ + ChromogenColored complex
d. Titan Yellow Serum TCA filtrate+titan yellowRed cmpd.
F. Calcium (Ca+2
)
i. Physiology and Regulation
For muscle contraction and blood coagulation Factors affecting Ca+2 level in blood: 99% in bone and teeth and 1% in blood and ECF 1. Bone resorption Cause Ca+2 in blood Calcium in the blood is distributed as PTH mobilizes Ca+2 from the bone 1. Ionized Unbound/ free, physiologically active 2. Bone deposition
Cause Ca+2 in blood
45% of Total Calcium Calcitonin inhibits PTH and Vit.D
2.Protein bound Bound to protein (E.g. albumin)/40% 3. Intestinal absorption
Vitamin D Ca+2 in the intestine 3. Complex Ca
+2 Bound to anions
(E.g. HCO3-, PO4
- & lactate)/15%
Causes of Hypocalcemia
( Ca+) Cause of Hypercalcemia
( Ca+) a. Hypoparathyroidism
a. Hyperparathyroidism
b. Hypo/hypermagnesemia b. Maliga PTHrP c. Hypoalbuminemia c. Vitai D d. Acute pancreatitis d. Thiazide diuretics
e. Vitamin D deficiency e. Prolonged immobilization
e. Rhabdomyolysis
iii. Determination of Calcium
Specimen a. Serum, Plasma (Dry lithium heparin), 24 hr urine b. Hemolysis cause False Method
a. AAS, ISE d. Clark and Collip (Redox Titration method)
b. Ortho-cresolphthalein complexone (CPC) e. Ferro and Ham (Precipitation with Chloranilic acid)
c. Alizarin, Arsenzo III dye, Methyl phenol blue
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F. Phosphate
i. Physiology and Regulation
Major Intracellular anion Component of phospholipids, nucleic acids, creatine phosphate and ATP 80% - bone, 20% - soft tissues, 1% - serum/plasma GH real eretio of phosphate
ii. Clinical Applications
Causes of Hypophosphateia ( PO4-) Cause of Hyperphosphateia ( PO4-) a. Hyperparathyroidism a. Itake
b. Vitamin D Deficiency b. release of cellular phosphate c. breakdown of cells
iii. Determination of Sodium
Specimen Methods
Serum, Plasma (lithium heparin), 24 hour urine Ammonium phosphomolybdate comp.(340nm)
Heolsis ause False Fiske-Subbarow Method (Final product: Molybdenum blue)
G. Lactate
i. Description and Regulation
Indicator of severity of O2 deprivation (hypoxia) Lier oerts latate ak to gluose Gluoeogeesis
ii. Clinical Applications
Lactate Acidosis
Hypoxic Conditions (Type A) Metabolic Origin (Type B)
a. Lactate Acidosis a. Diabetes Mellitus, Liver disease
b. Shock, MI, Severe CHF b. Toxins (ethanol, methanol or salicylate poisoning)
c. Pulmonary edema, severe blood loss
IV. Anaion Gap
Mathematical approximation of difference between the concentration of unmeasured cations & unmeasured anions (Na+) (Cl- + HCO3-) 7-16 mEq/L
Aio gap ueasured aios
Uremia Ketoacidosis Lactic acidosis i easured atios
Hypernatremia Aio gap
ueasured aios Hypoalbuminemia i ueasured atios:
Hypermagnesemia Hypercalcemia