6. Electrolytes

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



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+)


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)


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)



C. Potassium (K+)


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-)


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


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


Metabolic Alkalosis HCO3- Metabolic acidosis HCO3- a. Severe vomiting a. Hyperventilation

b. Hypoventilation

c. Excessive alkali intake




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

)


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



F. Phosphate


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


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


Indicator of severity of O2 deprivation (hypoxia) Lier oerts latate ak to gluose Gluoeogeesis


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

6. Electrolytes

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