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Chemistry 2 > electrolytes 2 (Na+, K+, Cl-,HCO3-) > Flashcards

electrolytes 2 (Na+, K+, Cl-,HCO3-) Flashcards

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1
Q

major cation ECF

A

Na+ ( 90%)

  • maintains water distribution & osmotic pressure
  • intake 130-260 mmol NaCl
  • body uses 1-2 mmol/day the rest is excreted
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2
Q

ATPase ion Pump

A

Na+ & K+ move between ICF & ECF by Na+/K+ ATPase ion pump

  • 3 Na+ ions move out in exchange for 2 K+ ions as ATP is converted to ADP
  • water follows Na+ out of cell which prevents osmotic rupture*
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3
Q

3 processes for regulation of sodium

A
  1. intake of H2O in response to thirst
    - stimulated/supppressed by plasma osmolality
  2. excretion of H2O
    - in response to AVP ( causes water to be reabsorbed)
  3. excretion of Na+
    - involves aldosterone, angiotensin ll & atrial natiuretic peptide (ANP)
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4
Q

sodium specimen collection

A
  • serum
  • heparinized plasma ( lithium heparin )
  • urine ( random or 24hr)
  • not significantly affected by hemolysis ( but if grossly hemolyzed Na+ decreased
    bc of dilution)
  • refrigerate or freeze for delayed analysis
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5
Q

methods of analysis - sodium

A

chemical methods- outdated
flame emission spectrophometry
atomic absorption spectrophotometry (AAS)

ion- selective electrodes (ISEs)
- most common method in clinical labs

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6
Q

Sodium electrode

A
  • a glass ion-exchange membrane is used for Na+ measurement
  • Na+ interacts with the tip ( measuring electrode) producing a potential that is dependent on the activity/concentration of Na+
  • reference electrode maintains a constant potential
  • difference in potential between the reference & measuring electrodes = the activity of Na+
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7
Q

direct vs indirect measurement for ISEs

A

Direct

  • undiluted
  • elevated lipid/proteins don’t interfere
  • more accurate

Indirect

  • diluted
  • increased lipids & proteins cause electrolyte exclusion effect

electrolyte exclusion effect

  • excess lipids or proteins displace plasma water
  • less aqueous phase gets added to the diluent
  • causes Pseudohyponatremia***- falsely decreased Na+ concentration
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8
Q

Sodium electrode -sources of error

A

protein build up on electrode membranes through continuous use
- causes poor selectively & poor reducibility for results

solution
- routine maintenance to remove protein build up

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9
Q

VITROS analyzers slide

A

use disposable ISE slides

  • drop of sample & reference fluid are applied at same time
  • dry slide technology
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10
Q

Hyponatremia

A

Na+ level < 135 mmol/L

caused by
- increased Na+ loss ; hypoaldsosteronism, K+ deficiency, diuretics, ketonuria

  • Increased H2O retention; renal failure, nephrotic syndrome, CHF
  • water imbalance; excessive water intake, pseudohyponatremia
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11
Q

hypernatremia

A

Na+ >145mmol/L

caused by
- increased intake or retention; hyperaldosteronism, excess salt ingestion

  • excess H2O loss; diabetes insipidus, profuse sweating
  • decreased H2O intake; older ppl or infants, mental impairment
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12
Q

Sodium reference ranges

  • serum/plasma
  • critical
A

serum/plasma: 135-145 mm/L ( CSF is around the same)

critical <120 or >160 mmol/L

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13
Q

major cation in ICF

A

potassium (K+)

  • dietary requirement : 50-150mmol/day
  • small amount used, most excreted by kidneys ( not stored well)
  • K+ conc regulates neuromuscular excitability, heart contractions
  • too low or too high can lead to cardiac arrest
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14
Q

regulation of potassium

A
  • nearly all K+ is reabsorbed in the proximal tubules of the kidney
  • additional K+ is secreted into urine in exchange for Na+
  • any excess K+ consumed in the diet is excreted in the urine; can accumulate to toxic levels in renal failure
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15
Q

factors that influence distribution of K+

A

K+ loss due to Na+, K+ ATPase pump inhibition
- hypoxia, hypomagnesemia, digoxin overdose

Insulin promotes acute entry of K+ into skeletal muscle & liver by increase Na+,K+ATPase activity

Catecholamines like epinephrine ( beta- stimulator) promote entry of K+ into cells

Propanolol ( beta-blocker) impairs entry of K+ into cells

excercise

  • K+ released from muscle cells during excercise
  • fist pumping during venipuncture can cause falsely high K+ levels

cellular breakdown
- damage to RBCs releases K+ into ECF

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16
Q

Specimen collection - potassium

A

serum

plasma ( heparin preferred)

don’t use EDTA ( K2 EDTA contains potassium )

urine ( random or 24 hr)

Minimize hemolysis ( hemolysis falsely increases K+ results )

separate plasma/ serum from cells ASAP or may give false increased K+

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17
Q

methods of measurement for Potassium

A

flame photometry
-older method q

ion-selective electrodes (ISEs)
-most routinely used

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18
Q

Potassium electrode

A

ion-exchange electrode

solid plastic membrane contianing valinomycin
- an antibiotic that will selectively bind with K+

KCL is the inner electrolyte solution

Can be direct or indirect mode
- difference between the two method is only slight compared to Na+

19
Q

clinical significance of potassium

A

increased or decreased concentration of K+ will affect muscle irritability = cardiac arrest

20
Q

K+ reference ranges
serum
critical

A

serum : 3.5-5.1 mmol/L

critical: < 2.8 or >6.0
- always check for hemolysis first

21
Q

Major anion in ECF

A

Chloride

- major contributor to osmolality ( with Na+ )

22
Q

Regulation of Chloride

A

Cl- usually shifts due to changes in Na+ or HCO3-

Cl- in the diet

  • absorbed by intestinal tract
  • then filtered by glomerulus
  • then passively reabsorbed ( with Na+) by proximal tubules

excess Cl- is ecreted in urine & sweat

excessive sweating stimulates aldosterone to act on the sweat glands to conserve Na+ & Cl-

23
Q

How Chloride maintains Electroneutrality

A
  1. Na+ is reabsorbed along with Cl- in proximal tubules
    - Na+ reabsorption is limited by amount of Cl- available
  2. Chloride shift ( hamburger phenomenon)
    - CO2 from cellular metabolism in tissues moves into the plasma & the red cells
    - in RBCs, CO2 form carbonic acid which splits into H+ & HCO3-
    - Deoxyhemoglobin (HHb) buffers H+
    - HCO3- moves diffuses into plasma
    - Cl- dissuses into RBC & electric balance is maintained
24
Q

Chloride specimen collection

A

serum/plasma ( separate from cells)

lithium heparin ( best anticoagulant)

urine ( 24hr is best )

CSF ( decreased CL in bacterial meningitis ; glucose also decreased in bacterial meningitis)

Sweat ( screen for cystic fibrosis )
- >60 mmol/L is positive for CF

25
Q

Chloride methods of analysis

A
  • amperometric -coulometric titration
  • mercurimetric titration
  • colorimetry
  • ion -selective electrode (ISE)
26
Q

Amperometric - coulometric titration analysis of chloride

A

• Silver ions are generated coulometrically from a silver electrode
and combine with chloride ions in the patient sample.
• Ag+ + Cl- → AgCl
• When all of the Cl- in the sample has bound to Ag+, the free Ag+
indicates the endpoint.
• The coulometric generator and timer shut off and the amount of
time elapsed is used to calculate the Cl- in the sample.
• An example of this is the Cotlove Chloridometer.

26
Q

Amperometric - coulometric titration analysis of chloride

A

• Silver ions are generated coulometrically from a silver electrode
and combine with chloride ions in the patient sample.
• Ag+ + Cl- → AgCl
• When all of the Cl- in the sample has bound to Ag+, the free Ag+
indicates the endpoint.
• The coulometric generator and timer shut off and the amount of
time elapsed is used to calculate the Cl- in the sample.
• An example of this is the Cotlove Chloridometer.

27
Q

Ion selective electrode for chloride

A

• Most common method
• Uses an ion-exchange membrane to selectively bind Cl- via a redox
reaction
• Used in clinical chemistry analyzers

28
Q

Chloride clinical significance

A

Cl- passively follows Na+ therefore Cl- disorders often have the same causes as Na+ disorders

causes of Hypochloremia

  • increased Cl- ( vomiting, diabetic ketoacidosis, aldosterone deficiency,Pyelonephritis)
  • high serum HCO3- ( respiratory acidosis, metabolic alkalosis)

causes of hyperchloremia

  • increased intake
  • excess loss of HCO3- ( renal tubular acidosis, metabolic acidosis, through GI tract)
29
Q

Chloride references ranges

A

serum/ plasma 98-107mmol/L

30
Q

Bicarbonate (HCO3-) or total CO2 (TCO2)

A

bicarbonate is the 2nd most abundant anion in ECF

total CO2 is comprised of

  • dissolved CO2
  • carbonic acid ( H2CO3)
  • bicarbonate

bicarbonate accounts for 90% of total CO2

31
Q

Bicarbonate importance in the body

A

HCO3- is a major component of buffer systems in blood.
• NaHCO3-/H2CO3 (sodium bicarbonate/carbonic acid)

Chloride Shift in the tissues and lungs
• This maintains electroneutrality (pluses = minuses on either side of the cell membrane)
• If           HCO3-   →   into cell
    Then           out   ←   Cl-
And vice versa
32
Q

Regulation of Bicarbonate (HCO3-)

A

• 85% of HCO3- is reabsorbed by proximal tubules in kidneys;
15% by distal tubules.

• Tubules are only slightly permeable to bicarb, so usually 
reabsorbed as CO2.
-  HCO3- combines with H+ to form H2CO3
-  H2CO3 dissociates into H2O and CO2
-  CO2 diffuses back into ECF

• Excess HCO3- flows into the urine

  • In alkalosis:
  • Kidneys increase excretion of HCO3- in urine to correct pH

• In acidosis:
• HCO3- is reabsorbed by the proximal and distal tubules to
correct pH.

33
Q

Bicarbonate Specimen Collection

A
  • Serum and lithium heparin plasma• (arterial and whole blood measurements were discussed last chapter)
  • Analyze ASAP
  • Keep anaerobic
  • i.e. Don’t decap specimen
  • Exposure to air causes a loss of CO2 = ↓TCO2
  • Can ↓ by 6 mmol/L per hour
34
Q

TCO2 Methods of Analysis

A
  • ISE Method (pCO2)
  • Combination pH electrode
  • Silicon rubber membrane which is permeable to CO2 gas
  • pH sensitive glass electrode detects a change in pH (↓ pH is measured)

OR
• Gas-sensing electrode

35
Q

PCO2 (Bicarbonate) pH Glass Electrode

A

The sample is acidified
first to convert all froms
of CO2 to CO2 gas

↓ in pH measured
i.e. H+ ions that are produced

36
Q

Gas-Sensing CO2 Electrode

A

same equation as ISE

The membrane is in contact with a 
solution that is permeable only to 
CO2.
The change in pH of the HCO3- is 
detected by a pH electrode.
TCO2
37
Q

TCO2 enzyme method

A

• Sample is alkalinized to convert all forms of CO2 to HCO3-

Phosphoenolpyruvate + HCO3- ——-> Oxaloacetate + H2PO4-

Oxaloacetate + NADH + H+ ———> Malate + NAD+

The rate of change in absorbance of NADH ~ [HCO3-]

38
Q

TCO2 /HCO3- - Clinical Significance

A 
Causes of Decreased HCO3-
Metabolic acidosis
Renal Tubular Failure with Hyperchloremia
Compensated Respiratory Alkalosis
Severe Diarrhea
Causes of Increased HCO3-
Metabolic Alkalosis
   - Severe vomiting
   - Excessive intake of alkali
Compensated Respiratory Acidosis
39
Q

CO2 reference ranges

A

Plasma / serum TCO2 (venous) 23-29 mmol/L

Plasma / serum HCO3- 21-28 mmol/L

40
Q

Anion Gap

A
  • A number that represents the concentration of unmeasured anions (proteins, phosphates, sulfates and organic acids)
  • Not a real Gap in anions and cations
  • Created by concentration differences between commonly measured cations (Na+ + K+) and anions (Cl- + HCO3-)

• Useful for:
- Indicating an increase in one or more unmeasured anions in serum (Metabolic Disorders)** if an increased anion gap usually indicates a metabolic disorder

  • Quality control for analyzer used to measure electrolytes** should never be a negative number if negative indicates a problem with the analyzer
41
Q

Anion gap calculation

A

Calculation: measured cations – measured anions

Na+) - (Cl- + HCO3-) OR
(Na+ + K+ ) - (Cl- + HCO3-

42
Q

Anion Gap refernece range

A

Anion Gap (AGap) should be positive
• 7 - 16 mmol/L or
• 10 - 20 mmol/L if K+ included

43
Q

Abnormal anion gap

A

Low(rare)

  • multiple myeloma
  • analyzer error
High 
• Methanol
• Uremia
• Diabetic ketoacidosis
• Paraldehyde
• Iron, inhalants, ibuprofen
• Lactic acidosis
• Ethylene glycol, ethanol ketoacidosis
• Salicylates, starvation ketoacidosis

Chemistry 2 (30 decks)

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