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Outline
I.
II.
III. IV.
Introduction
Electrolytes
Anions
Ions that carry (-) charge and move toward the anode E.g. Cl-, HCO3-, PO4Cations Ions that carry (+) charge and move toward the cathode E.g. Na+, K+, Mg2+, Ca2+
B.
Introduction
Functions of Electrolytes
1.
2. 3.
4.
5. 6.
7.
Volume and osmotic regulation (Na+, Cl-, K+) Myocardial rhythm and contractility (K+ , Mg2+, Ca2+) Neuromuscular Excitability (K+ , Mg2+, Ca2+) Cofactors in enzyme activation (Mg2+, Ca2+, Zn2+) Regulation of ATPase ion pumps (Mg2+) Acid-base balance (HCO3-, K+, Cl-) Production and use of ATP from glucose (Mg2+, PO4-)
Outline
I.
II.
III. IV. V.
Introduction Water The Electrolytes Anion Gap Electrolytes and Renal Function
Outline
II.
Water
A.
B.
i.
Introduction Osmolality
ii.
iii. iv.
Water
A.
Introduction
b.
c. d.
Transport nutrients to the cells Determines cell volume Removes waste products Act as bodys coolant Intracellular Fluid (ICF) 2/3 Extracellular Fluid 1/3
Location:
a. b.
Water
A.
Introduction
Distribution of Body Water in Adult
Compartment Percent (%) of Body Weight 5 15 40 60 Percent (%) of Total BodyWater 8 25 67 100
Water
A.
Introduction
Passive Transport
2.
Active Transport
Outline
II.
Water
A.
B.
i.
Introduction Osmolality
ii.
iii. iv.
Water
B.
Osmolality
i.
1. 2.
Definition
Physical property of a solution based on concentration of solutes per kilogram of solvent (millimoles/kg) Blood osmolarity is regulated by:
a. b.
Water
B.
Osmolality
ii.
1.
Clinical Significance
Blood osmolarity is regulated by:
a.
b.
Thirst Sensation Response to consume more fluids Prevents water deficit or dehydration Arginine vasopressin hormone (AVP) Antidiuretic Hormone (ADH) reabsorption of water in kidneys Suppressed in excess water load ( POSM) Activated in water deficit ( POSM)
Water
B.
Osmolality
iii.
Water
B.
Osmolality
iii.
Water
B.
Osmolality
iv.
Serum or urine
Osmolality
Indicates number of molecules per Kg of solvent Any substance dissolve in a solvent will: 1. the freezing point by 1.858C 2. the boiling point by 0.52C 3. vapor pressure (Dew point) by 0.3 mmHg 4. the osmotic pressure by 17,000 mmHg Main contributors are Na, Cl, Urea and Glucose
Outline
II.
Water
A.
B.
i.
Introduction Osmolality
ii.
iii. iv.
Outline
I.
II.
III. IV. V.
Introduction Water The Electrolytes Anion Gap Electrolytes and Renal Function
Outline
II.
The Electrolytes
Concentration of Cations and Anions in Extracellular and Intracellular Water Concentration of Water Concentration of Water Extracellular Intracellular Extracellular Intracellular Cation Anion (mmol/L (mmol/L) (mmol/L (mmol/L) Na+ 136-145 15 HCO323-29 10 K+ 3.5-5.1 150 Cl98-107 1 Ca2+ 2.15-2.5 1 HPO420.78-1.42 50 Mg2+ 0.63-1 13.5 SO420.5 10
Outline
II.
The Electrolytes
A.
B. C.
D.
E. F.
G.
H.
The Electrolytes
A.
Sodium (Na+)
i.
ii. iii.
The Electrolytes
A.
Sodium (Na+)
i.
Description and Regulation The most abundant cation in the ECF Major Extracellular cation Na+, K+ -ATPase ion pump moves 3 Na+ ions out of the cell in exchange for 2 K+ ions
The Electrolytes
A.
Sodium (Na+)
i.
Description and Regulation Plasma concentration depends in renal regulation a. Intake of water in response to thirst b. Excretion of water as affected by AVP H2O reabsorption c. The blood volume status, which affects Na excretion through: a. Aldosterone ( Na+ reabsorption in the kidneys) b. Angiotensin II ( aldosterone) c. ANP ( Urinary Na + Excretion )
The Electrolytes
A.
Sodium (Na+)
i.
The Electrolytes
A.
Sodium
i.
ii. iii.
The Electrolytes
A.
Sodium
ii.
Clinical Applications
Causes of Hyponatremia ( Na+)
Sodium (Na+) Loss Water Retention Hypoadrenalism ( aldosterone) Renal failure (dilution of Na+) Potassium (K+) Deficiency Nephrotic s. (COP - PV, AVP) Diuretic Use (Thiazide) CHF, Hepatic cirrhosis Ketonuria (Na+ lost with ketones) Water Imbalance Salt-losing nephropathy Prolonged vomiting or diarrhea
The Electrolytes
A.
Sodium
ii.
Clinical Applications
Causes of Hypernatremia ( Na+)
Decreased Water Intake Diabetes insipidus ( AVP) Old/Infants / Mental Impairment Renal tubular dis. ( urine conc.) Increased Intake or Retention Cushing Syn. ( Na+ reabs.) Prolonged diarrhea
The Electrolytes
A.
Sodium
i.
ii. iii.
The Electrolytes
A.
Sodium (Na+)
iii.
Determination of Sodium Specimen a. Serum, Plasma (lithium heparin, ammonium heparin and lithium oxalate) b. False with marked hemolysis Methods a. FES b. AAS c. ISE (Glass ion-exchange membrane)
Outline
II.
The Electrolytes
A.
B. C.
D.
E. F.
G.
H.
The Electrolytes
B.
Potassium (K+)
i.
ii. iii.
The Electrolytes
B.
Potassium (K+)
i.
Description and Regulation Major Intracellular cation Regulation of neuromuscular excitability and contraction of heart, ICF volume, H+ conc. K+, cell excitability (muscle weakness) K+, cell excitability (arrhythmia or paralysis)
The Electrolytes
B.
Potassium (K+)
i.
Description and Regulation Aldosterone K+ excretion in urine in exchange for Na+ Na+, K+ -ATPase pump function cellular entry hypoxia, digoxin overdose, hypomagnesemia, propanolol (-blocker) function cellular entry insulin, epinephrine with exercise, hyperosmolality (DM) and cellular breakdown
The Electrolytes
B.
Potassium (K+)
i.
The Electrolytes
B.
Potassium (K+)
i.
ii. iii.
The Electrolytes
B.
Potassium
ii.
Clinical Applications
Causes of Hypokalemia ( K+) Renal Loss Diuretics, Nephritis, CHF RTA (H+,K+ excretion) Cushings syn. (Na+,K+ reabs.) Hyperaldosteronism
GI Loss Vomiting, Diarrhea Gastric suction Intestinal tumor, malabsorption Cancer therapy, laxatives Cellular Shift - K+ uptake Alkalosis (Plasma)-H+Na+K+ Insulin Overdose
Hypomagnesemia: aldosterone
Decreased Intake
The Electrolytes
B.
Potassium
ii.
Clinical Applications
Cause of Hyperkalemia (K+) Cellular Shift Acidosis (Plasma H+, K+) Muscle/cellular injury Chemotherapy / Leukemia Hemolysis
The Electrolytes
B.
Potassium (K+)
i.
ii. iii.
The Electrolytes
B.
Potassium (K+)
iii.
Determination of Potassium Specimen a. Serum, Plasma (heparin) b. False with hemolysis c. 24 hour urine Methods a. FES b. AAS c. ISE (Use valinomycin membrane)
Outline
II.
The Electrolytes
A.
B. C.
D.
E. F.
G.
H.
The Electrolytes
C.
Chloride
i.
ii. iii.
The Electrolytes
C.
Chloride
i.
Description and Regulation Major Extracellular Anion Involve in maintaining osmolality blood volume and electric neutrality (Chloride shift) Rate limiting component in Na+ reabsorption
The Electrolytes
C.
Chloride
i.
ii. iii.
The Electrolytes
C.
Chloride
ii.
Clinical Applications
Cause of Hypochloremia (Cl-) Excess Loss of ClProlonged Vomiting Diabetic Ketoacidosis Aldosterone Deficiency Salt-losing pyelonephritis
Cause of Hyperchloremia (Cl-) Excess Loss of HCO3GI Losses RTA Metabolic acidosis
The Electrolytes
C.
Chloride
i.
Determination of Chloride Specimen a. Serum, Plasma (lithium heparin) b. False with marked hemolysis (dilution) c. 24 hour urine Methods a. ISE (Use ion exchange membrane) b. Amperometric-coulometric (Cotlove Chloridometer)
The Electrolytes
C.
Chloride
i.
Determination of Chloride Methods c. Schales and Schales Titration with mercuric nitrate Indicator S-diphenylcarbazone
d.
Colorimetric
Outline
II.
The Electrolytes
A.
B. C.
D.
E. F.
G.
H.
The Electrolytes
D.
Bicarbonate (HCO3-)
i.
ii.
The Electrolytes
D.
Bicarbonate (HCO3-)
i.
Regulation and Clinical Applications 2nd Most Abundant anion in the ECF Accounts for more than 80% of total CO2 with HCO3Major component of the buffering system of the blood
HCO3 HCO3Metabolic acidosis
Metabolic Alkalosis
Hyperventilation
The Electrolytes
D.
Bicarbonate (HCO3-)
i.
ii.
The Electrolytes
D.
Bicarbonate (HCO3-)
ii.
Determination of Sodium Specimen a. Serum, Plasma (heparin) b. False if left uncapped ( 6mmol/L per hour) Methods a. ISE (Use of pCO2 electrode) b. Enzyme method
Outline
II.
The Electrolytes
A.
B. C.
D.
E. F.
G.
H.