MLAB 2401: CLINICAL CHEMISTRY
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Transcript of MLAB 2401: CLINICAL CHEMISTRY
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MLAB 2401:CLINICAL CHEMISTRY
WATER BALANCE & ELECTROLYTES
Part Two
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ELECTROLYTES
Electrolytes Substances whose molecules dissociate into
ions when they are placed in water.Osmotically active particlesClassification of ions: by charge
CATIONS (+) In an electrical field, move toward the cathode Sodium (Na), Potassium (K), Calcium(Ca), Magnesium(Mg)
ANIONS (-) In an electrical field, move toward the anode Chloride(Cl), Bicarbonate, PO4, Sulfate
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ELECTROLYTES
General dietary requirementsMost need to be consumed only in small
amounts as utilizedExcessive intake leads to increased
excretion via kidneysExcessive loss may result in need for
corrective therapy loss due to vomiting / diarrhea; therapy required - IV replacement, Pedilyte, etc.
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ELECTROLYTE FUNCTIONS
Volume and osmotic regulation Myocardial rhythm and contractility Cofactors in enzyme activation Regulation of ATPase ion pumps Acid-base balance Blood coagulation Neuromuscular excitability Production of ATP from glucose
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ELECTROLYTE PANEL
Panel consists of:sodium (Na) potassium (K)chloride (Cl)bicarbonate CO2 (in its ion form = HCO3
- )
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ANALYTES OF THE ELECTROLYTE PANEL
Sodium (Na)– the major cation of extracellular fluidMost abundant (90 %) extracellular cationDiet
Easily absorbed from many foods
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FUNCTION: SODIUM
Influence on regulation of body water Osmotic activity
Sodium determines osmotic activity Main contributor to plasma osmolality
Neuromuscular excitability extremes in concentration can result in
neuromuscular symptoms Na-K ATP-ase Pump
pumps Na out and K into cells Without this active transport pump, the cells would
fill with Na+ and subsequent osmotic pressure would rupture the cells
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REGULATION OF SODIUM Concentration depends on:
intake of water in response to thirst excretion of water due to blood volume or
osmolality changes Renal regulation of sodium
Kidneys can conserve or excrete Na+ depending on ECF and blood volume by aldosterone and the renin-angiotensin system
this system will stimulate the adrenal cortex to secrete aldosterone.
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REFERENCE RANGES:SODIUM
Serum 136-145 mEq/L or mmol/L
Urine (24 hour collection) 40-220 mEq/L
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SODIUM
Urine testing & calculation:Because levels are often increased, a dilution
of the urine specimen is usually required.
Once a number is obtained, it is multiplied by the dilution factor and reported as (mEq/L or mmol/L) in 24 hr.
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DISORDERS OF SODIUM HOMEOSTASIS Hyponatremia: < 136 mmol/L
Causes of: Increased Na+ loss Increased water retention Water imbalance
Hypernatremia:> 150 mmol/L Causes of:
Excess water loss Increased intake/retention Decreased water intake
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HYPONATREMIA
1. Increased Na+ lossAldosterone deficiency
hypoadrenalismDiabetes mellitus
In acidosis of diabetes, Na is excreted with ketones
Potassium depletion K normally excreted , if none, then Na
Loss of gastric contents12
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HYPONATREMIA
2. Increased water retentionDilution of plasma Na+
Renal failureNephrotic syndromeHepatic cirrhosisCongestive heart failure
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HYPONATREMIA
3. Water imbalanceExcess water intakeChronic condition
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SODIUM
Note: Increased lipids or proteins may cause false
decrease in results. This would be classified as artifactual/pseudo-hyponatremia
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CLINICAL SYMPTOMS OF HYPONATREMIA
Depends on the serum levelCan affect
GI tractNeurological
Nausea, vomiting, headache, seizures, coma
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HYPERNATREMIA
1. Excess water loss SweatingDiarrheaBurnsDiabetes insipidus
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HYPERNATREMIA
2. Increased intake/retention• Excessive IV therapy
3. Decreased water intake• Elderly• Infants• Mental impairment
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CLINICAL SYMPTOMS OF HYPERNATREMIA
Involve the CNS Altered mental status Lethargy Irritability Vomiting Nausea
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SPECIMEN COLLECTION: SODIUM
Serum (slt hemolysis is OK, but not gross) Heparinized plasma Timed and random urine SweatGI fluidsLiquid feces (would be only time of excessive loss)
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ANALYTES OF THE ELECTROLYTE PANEL
Potassium (K+)the major cation of intracellular fluid
Only 2 % of potassium is in the plasmaPotassium concentration inside cells is 20 X greater than it is outside.
This is maintained by the Na-K pumpexchanges 3 Na for 1 K
Diet easily consumed by food products such as bananas 21
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FUNCTION: POTASSIUM Critically important to the functions of
neuromuscular cellsAcid-base balanceIntracellular fluid volumeControls heart muscle contractionPromotes muscular excitability
Decreased potassium decreases excitability (paralysis and arrhythmias)
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REGULATION OF POTASSIUM
Kidneys Responsible for regulation. Potassium is readily
excreted, but gets reabsorbed in the proximal tubule - under the control of ALDOSTERONE
Diet Cell Uptake/Exchange
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REFERENCE RANGES: POTASSIUM Serum (adults)
3.5 - 5.1 mEq/L or mmol/L Newborns
3.7 - 5.9 mEq/L Urine (24 hour collection)
25 - 125 mEq/L
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DISORDERS OF POTASSIUM HOMEOSTASIS Hypokalemia
< 3.5 mmol/L Causes of:
Non-renal loss Renal Loss Cellular Shift Decreased intake
Hyperkalemia >5.1 mmol/L Causes of
Decreased renal excretion Cellular shift Increased intake Artifactual/False elevations
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HYPOKALEMIA
1. Non-renal loss Excessive fluid loss ( diarrhea,
vomiting, diuretics ) Increased Aldosterone promote
Na reabsorption … K is excreted in its place
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HYPOKALEMIA
2. Renal Loss Nephritis, renal tubular acidosis,
hyperaldosteronism, Cushing’s Syndrome
3. Cellular Shift Alkalosis, insulin overdose
4. Decreased intake27
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MECHANISM OF HYPOKALEMIA
Increased plasma pH ( decreased Hydrogen ion )
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K+ moves into RBCs to preserve electrical balance,causing plasma potassium to decrease.( Sodium also shows a slight decrease )
H+
K+
RBC
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CLINICAL SYMPTOMS OF HYPOKALEMIA
Neuromuscular weakness Cardiac arrhythmia Constipation
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HYPERKALEMIA
1. Decreased renal excretion Renal disease Addison’s disease Hypoaldosteronism
2. Cellular Shift Such as acidosis, chemotherapy, leukemia,
muscle/cellular injury Hydrogen ions compete with potassium to get
into the cells
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HYPERKALEMIA
3. Increased intake Insulin IVs promote rapid cellular
potassium uptake
4. Artifactual• Sample hemolysis• Prolonged tourniquet use• Excessive fist clenching
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CLINICAL SYMPTOMS OF HYPERKALEMIA
Muscle weakness Tingling Numbness Mental confusion Cardiac arrhythmias Cardiac arrest
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SPECIMEN COLLECTION: POTASSIUM
Non-hemolyzed serum heparinized plasma 24 hr urine
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ANALYTES OF THE ELECTROLYTE PANEL
Chloride (Cl-) The major anion of extracellular fluid
Chloride moves passively with Na+ or against HCO3
- to maintain neutral electrical charge
Chloride usually follows Na if one is abnormal, so is the other
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FUNCTION: CHLORIDE
Body hydration/water balanceOsmotic pressureElectrical neutrality
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REGULATION OF CHLORIDE
Regulation via diet and kidneys In the kidney, Cl is reabsorbed in the renal
proximal tubules, along with sodium. Deficiencies of either one limits the reabsorption
of the other.
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REFERENCE RANGES: CHLORIDE Serum
98 -107 mEq/L or mmol/L
24 hour urine 110-250 mEq/L varies with intake
CSF 120 - 132 mEq/L Often CSF Cl is decreased when CSF protein is
increased, as often occurs in bacterial meningitis.
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DETERMINATION: CHLORIDE
Specimen type Serum Plasma 24 hour urine CSF Sweat
Sweat Chloride Test Used to identify cystic fibrosis patients
Increased salt concentration in sweat Pilocarpine= chemical used to stimulate sweat
production Iontophoresis= mild electrical current that stimulates
sweat production
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DISORDERS OF CHLORIDE HOMEOSTASIS
Hypochloremia Decreased blood chloride Causes of :
Conditions where output exceeds input
Hyperchloremia Increased blood chloride Causes of:
Conditions where input exceeds output
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HYPOCHLOREMIA
Decreased serum Cl loss of gastric HCl salt loosing renal diseases metabolic alkalosis/compensated respiratory
acidosis increased HCO3- and decreased Cl-
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HYPERCHLOREMIA
Increased serum Cl dehydration (relative increase) excessive intake (IV) congestive heart failure renal tubular disease metabolic acidosis
decreased HCO3- & increased Cl-
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ANALYTES OF THE ELECTROLYTE PANEL
Carbon dioxide/bicarbonate (HCO3-)
2nd most abundant anion of extracellular fluidTotal plasma CO2= HCO3
- + H2CO3- + CO2
HCO3- (bicarbonate ion)
accounts for 90% of total plasma CO2
H2CO3- (carbonic acid)
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FUNCTION:BICARBONATE ION
CO2 is a waste product continuously produced as a result of cell
metabolism, the ability of the bicarbonate ion to accept a
hydrogen ion makes it an efficient and effective means of buffering body pH
dominant buffering system of plasma
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REGULATION OFBICARBONATE ION
Bicarbonate is regulated by secretion / reabsorption of the renal tubules
Acidosis: decreased renal excretion
Alkalosis: increased renal excretion
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REGULATION OF BICARBONATE ION
Kidney regulation requires the enzyme carbonic anhydrase - which is present in renal tubular cells & RBCs
carbonic anhydrase
Reaction: CO2 + H2O ⇋ H2CO3 → H+ + HCO–3
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Pulmonary ControlRenal Control
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REFERENCE RANGE:BICARBONATE ION
Total Carbon dioxide (venous) 23-29 mEq/L or mmol/L
includes bicarb, dissolved and undissociated H2CO3 - carbonic acid (bicarbonate)
Bicarbonate ion (HCO3–)
22-26 mEq/L or mmol/L
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SPECIMEN COLLECTION: BICARBONATE ION
heparinized plasma arterial whole blood fresh serum Anaerobic collection preferred
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ELECTROLYTE BALANCE
Anion gap – an estimate of the unmeasured anion concentrations such as sulfate, phosphate, and various organic acids.
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ELECTROLYTE SUMMARY
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cations (+) Na 142 K 5 Ca 5 Mg 2 154 mEq/L
anions (-) Cl 105 HCO3- 24 HPO4- 22 SO4-2 1 organic acids 6 proteins 16
154 mEq/L
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ANION GAP Anion Gap Calculations
1. Na - (Cl + CO2 or HCO3-)
Reference range: 7-16 mEq/L
Or
2. (Na + K) - (Cl + CO2 or HCO3-)
Reference range: 10-20 mEq/L
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FUNCTIONS OF THE ANION GAP Causes in normal patients
what causes the anion gap?
2/3 plasma proteins & 1/3 phosphate& sulfate ions, along with organic acids
Increased AG –
uncontrolled diabetes (due to lactic & keto acids) severe renal disorders Hypernatremia lab error
Decreased AG -
a decrease AG is rare, more often it occurs when one test/instrument error
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REFERENCES Bishop, M., Fody, E., & Schoeff, l. (2010). Clinical
Chemistry: Techniques, principles, Correlations. Baltimore: Wolters Kluwer Lippincott Williams & Wilkins.
http://thejunction.net/2009/04/11/the-how-to-authority-for-donating-blood-plasma/
http://www.nlm.nih.gov/medlineplus/ency/article/002350.htm
Sunheimer, R., & Graves, L. (2010). Clinical Laboratory Chemistry. Upper Saddle River: Pearson .
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