2. Objectives
What is electrolyte?
Which are imp electrolytes in our body?
What are the functions of particular electrolyte?
Regulation in body
Sample collection
Method of estimation
Errors which can affect the result
Pathological alteration
3. What are they??
Electrolytes are minerals found in body fluids that carry an
electrical charge and are essential to keeping the heart, nerves
and muscles functioning properly.
As such, it is important to maintain a precise and constant
balance of electrolytes.
CATION - positively charged electrolyte
ANION - negatively charged electrolyte
Cations = Anions for homeostatsis to exist in each fluid
compartment.
Commonly measured in mEq/L.
6. • Most prevalent cation in the ECF.
• Total body Sodium is about 5000 mEq in an adult.
• Daily requirement of sodium is about 100 mEq.
• In normal individuals, the kidney strives to achieve
Na+ balance – that is, to have Na+ excretion equal to
Na+ ingestion.
A. Sodium (Na+)
Introduction
7. Maintain balance of extracellular fluid, thereby it
controls the movements of the water between fluid
compartments.
Transmission of nerve impulses
Neuro muscular and myocardial impulse
transmission
A. Sodium (Na+)
FUNCTIONS
8. A. Hormones increasing sodium reabsorption:
1. Renin:
Released from the juxtaglomerular apparatus of the kidney
Release is stimulated by: raised sympathetic tone, falling
plasma volume, and certain prostaglandins, such as PGE2
No direct effects promoting Na+ retention, it controls the renin-
angiotensin-aldosterone axis
2. Angiotensin II:
Levels rise as result of renin release
In turn, it stimulates the release of aldosterone
Also increases tone in the efferent glomerular arteriole. The net
effect is to enhance Na+ reabsorption from the proximal tubule.
A. Sodium (Na+)
REGULATION
9. 3. Aldosterone:
Steroid hormone released from the adrenal cortex
End product of the RAAS system
Acts on the distal tubule and collecting duct to increase Na+ and
water reabsorption (proportionately more Na+ than water)
4. Arginine vasopressin (AVP), anti-diuretic hormone (ADH):
Neuron cell bodies in supra-optic and paraventricular nuclei of the
Hypothalamus,
Stored in posterior pituitary.
Passive absorption of water from the collecting ducts along with a
small degree of Na+ re-absorption, concentrating the urine
A. Sodium (Na+)
REGULATION
11. B.Hormones increasing sodium excretion:
1.Atrial Natriuretic Peptide (ANP):
A small peptide produced from the atrial wall as
a result of atrial stretching.
Increase Na (and hence water) excretion by
increasing GFR and blocking Na reabsorption in
PCT
2.Brain Natriuretic Peptide (ANP):
secreted by the hypothalamus, termed brain
natriuretic peptides (BNP)
Have a similar roles.
A. Sodium (Na+)
REGULATION
12. Serum: venous blood sample in gel vaccutainer
Urine:
24 hrs urine collection
No preservative is required
Store at 2-8 degree
Sample collection
Method of estimation
Ions selective electrode
A. Sodium (Na+)
14. Potentiometric measurements:
Potentio-metry is to determine the difference in potential between
a working (an indicator) electrode and a counter (a reference)
electrode.
- Cathode is the working / indicator electrode.
- Anode is the counter / reference electrode.
Indicator Electrode:
Electrode that responds to analyte and donates / accepts electrons
Reference Electrode:
Second ½ cell at a constant potential
ell voltage is difference between the indicator and reference
electrode
Ecell = Ec ─ Ea
Where : Ec is the reduction potential at the cathode.
: Ea is the reduction potential at the anode.
15.
16. Serum: 135 – 145 mEq/L
Urine:
24 hr urine sample: 40-220 mEq/day
Note: For random, it is better to do FeNa .
Also used in calculation of Anion gap & Osmolality
Biological reference range
Panic value
Serum level >160 and <120 mEq/L
A. Sodium (Na+)
17. Errors affecting Na+ result
A. Pseudohyponatraemia :
1. Sample collection from IV site, thus the sample is diluted by the
hypotonic fluid (5% dextrose).- confirmed by dilution effect on
other parameters
2. High plasma glucose level: increase 100 mg/dl – lowering Na
1.6 mmol/L, after 400 mg/dl, every 100 mg/dl lowering 2.4
mmol/L
Corrected Sodium = [0.016 x (serum glucose – 100)] + serum
Na
3. Increased viscosity due to the Hyperproteinemia,
Hyperlipidemia due subsequent decreased watery portion of
plasma can thus cause false low sodium concentrations
A. Sodium (Na+)
18. B. Pseudohypernatraemia :
1. Sample collection from IV site - confirmed by measurements
of CL- and K+
2. Drugs – SSRI, sodium valproate etc.
Errors affecting Na+ result
A. Sodium (Na+)
19. S. Sodium level < 135 mEq/L
< 280 mOsm/Kg > 280 mOsm/Kg
(N or increase)
True Hyponatremia
Pseudohyponatremia
Hypo-
volemic
Eu-
volemic
Hyper-
volemic
Cause Investigation
Paraproteinemia s. protein,
electrophoresis
Hyperlipidemia S. Cholestrol,TG
Hyperglycemia S. Glucose
A. HyponatremiaA. Sodium (Na+)
20. < 20 mEq/L
Extrarenal causes
vomiting
Diarrhea
Third spacing of fluid
Burns
Decrease total body water
Decrease total body sodium (more deficit)
Measure urinary sodium
>20 mEq/L
Renal causes
Diuretics
Salt losing nephropathy
Mineralocorticoids Def.
Osmotic diuresis
Note : In vomiting, to compensate metabolic alkalosis urinary Na > 20
mEq/L, and urinary cl- < 10 mmol/L
A. HyponatremiaA. Sodium (Na+)
A. Hypovolemic hyponatremia
21. Increase total body water
No change in total body sodium
Urinary sodium > 20 mEq/L
Urine osmolality>100 moSm/Kg
Causes
Glucocorticoids deficiency
SIADH
Hypothyroidism
Drugs
A. Sodium (Na+)
B. Euvolemic hyponatremia
A. Hyponatremia
22. Increase total body water (More)
Increase total body sodium
Measure urinary sodium
< 20 mEq/L
Other causes
Cirrhosis
Cardiac failure
>20 mEq/L
Renal causes
AKI
CKD
A. Sodium (Na+) A. Hyponatremia
C. Hypervolemic hyponatremia
23. A. Sodium (Na+) B. Hypernatremia
S. Sodium level > 145 mEq/L
26. • Major intracellular cation.
• Total body K+ content in a normal adult 3000-
4000mEq.
• 98% Intracellular , 2% in ECF
B. Potassium (K+)
Introduction
27. Regulates neuromuscular excitability and
muscle contraction
As coenzyme - glycogen & protein synthesis
Correction of acid base imbalances
FUNCTIONS
B. Potassium (K+)
28. The primary mechanism maintaining this balance : the
Na-K – ATP phase pump
Na-K ATPhase pump actively transports Na+ out of the
cell and K+ into the cell in a 3:2 ratio
Renal excretion – Major route of excess K+
Approx 90% of K+ excretion occurs in the urine
less than 10% excreted through sweat or stool.
Regulation
B. Potassium (K+)
30. Serum: venous blood sample in gel vaccutainer
Urine:
24 hrs urine collection
No preservative is required
Store at 2-8 degree
Sample collection
Method of estimation
Ions Selective Electrode
B. Potassium (K+)
31. Serum: 3.5 – 5.5 mEq/L
Urine:
• 24 hr urine sample: 25-125 mEq/day
• Random urine: 13-101 mmol/g creat
Note: Also used in calculation of anion gap
Biological reference range
Panic value
Serum level <2.0 and >7.0 mEq/L
B. Potassium (K+)
32. Errors affecting K+ result
A. Pseudohyperkalemia :
1. Cleaning of puncture site:
The site for venipuncture is to be cleaned with povidone
iodine.
2. Tourniquet application:
• It should be released once the first blood flow was
established.
• More than 1 min of tourniquet : haemo-concentration
3. Clenching fist for longer time causes elevation potassium.
B. Potassium (K+)
33. B. Potassium (K+)
4. Needle or syringe:
Size of syringe / pushing of blood in vaccutainer.
5. Order of drawing tubes:
The blood collected in a specific order avoids cross
contamination of additives.
Examples of the common carryover problems observed
are the EDTA which is easily determined by marked
hyperkalemia, hypocalcemia, hypomagnesemia and
hypozincanemia.
6. Centrifugation and vigorous shaking of sample.
34. 1. Sterile-blood culture
2. Coagulation (light blue)/ Citrate
3. Non-additive (red top)/ Plain
4. Gel separator tube (red or gold)/ Plain
5. Heparin tube (green top)
6. EDTA (lavender/purple top)
7. fluoride tube (grey top)
8. All other tubes
Order of blood collection by CLSI
35. 7. Storage : store after separation of serum
8. Lymphocytosis and thrombocytosis: Hyper cellularity
9. Fluid containing potassium
B. Potassium (K+)
36. B. Pseudohypokalemia :
1. Sample collection from IV site, thus the sample is diluted by
the hypotonic fluid (5% dextrose).- confirmed by dilutional
effect on other parameters
2. High plasma glucose level: Dilution effect
3. Increased viscosity
Errors affecting K+ result
B. Potassium (K+)
42. A. hypokalemiaB. Potassium (K+)
III. Renal Tubular Acidosis type-1/2:
Type 1: dRTA : Decreased H+ Excretion in DCT
Type 2: pRTA: Decreased reabsorption of HCO3
-
43. 3. Shifting of K+ from ECF to ICF
A. hypokalemiaB. Potassium (K+)
a. In alkalosis,
H+ moves out of the cells, at the same time, K+ moves into the
cells.
For each 0.1 unit increase of pH in ECF, the [K+] of serum
decreases 0.7 mmol/L.
b. Insulin: stimulates Na+-K+ ATPase.
c. Hyperthyroidism: Over-dose thyroxin stimulates Na+-K+ ATPase.
44. Serum potassium level of >5.5 mEq/L
• Common Causes:
1. Intra- to extracellular shift:
Acidosis – Uptake of H+, efflux of K+
Hyperosmolality- Hypertonic dextrose, mannitol, - Solvent Drag effect
β2-Adrenergic antagonists (non-cardioselective agents): Suppresses
catecholamine stimulated renin release- in turn aldosterone synthesis
Digoxin and related glycosides : Inhibits Na/K ATPase
Succinylcholine: Depolarizes Muscle cells, Efflux of K
Rapid tumor lysis / Rhabdomyolysis
B. HyperkalemiaB. Potassium (K+)
45. 2. Inhibition of the renin-angiotensin-aldosterone axis:
(↑ risk of hyperkalemia when these drugs are used in combination)
Angiotensin-converting enzyme (ACE) inhibitors
Renin inhibitors; aliskiren
Angiotensin receptor blockers (ARBs)
Blockade of the mineralocorticoid receptor: spironolactone
Blockade of the epithelial sodium channel (ENaC): amiloride,
triamterene
B. HyperkalemiaB. Potassium (K+)
46. 4. Renal resistance to mineralocorticoids:
Tubulointerstitial diseases:
SLE, amyloidosis, sickle cell anemia, obstructive uropathy, post–
acute tubular necrosis
Hereditary:
pseudohypoaldosteronism type I; defects in the mineralocorticoid
receptor or the epithelial sodium channel (ENaC)
5. Advanced renal insufficiency:
Chronic kidney disease
End-stage renal disease
Acute oliguric kidney injury
B. HyperkalemiaB. Potassium (K+)
47.
48. Most abundant mineral in human beings.
Total calcium in an average adult is about 1,000 gm :
99% in bones & teeth.
Rest in various tissues and body fluids.
Calcium is present in bones mainly in the form of
calcium phosphate.
C. Calcium (Ca++)
Introduction
49. About 50% of this is bound to protein (protein-bound or
non-diffusible calcium).
About 5% with organic anions e.g. citrate, (diffusible)
The remaining 45%: free ionized calcium (freely
diffusible)
Ionized calcium: Active form
C. Calcium (Ca++)
50. Functions
Formation of bones and teeth
Excitability and conductivity of nerves
Neuromuscular transmission
Excitability and contractility of myocardium
Coagulation of blood
Action of hormones
C. Calcium
53. Serum: venous blood sample in gel vaccutainer
Urine:
24 hrs urine collection
No preservative is required
Store at 2-8 degree
Sample collection
Method of estimation
C. Calcium
1. T. Calcium: Arsenzo- III Spectrophotometric method
2. Ionized Calcium: ISE
Ca+ + + Arsenazo III Ca- Arsenazo III complex (purple)
55. Free calcium is useful index - provides the better indication
of calcium biologically active and tightly regulated by
calcium binding hormones.
Calcium is predominantly transported bound to serum
proteins, total calcium levels are greatly influenced by protein
concentration especially albumin.
Earlier no proper technique to measure. This problem is
now solved due to availability of ion-selective electrodes, for
free calcium measurements .
What is better Ionized or Total ???
56. Corrected calcium : Total calcium + 0.8 (4.0 – S. Alb)
For this patient = 8.1 + 0.8 (4 – 3.2) = 8.1 + 0.64=8.75
Corrected total calcium ? ?
57. A. Pseudohypercalcemia:
1. Cleaning the venipuncture site:
2. Tourniquet application:
3. Clenching fist
4. Needle or syringe:
5. Order of drawing tubes:
6. Centrifugation and vigorous shaking of sample
Errors affecting Ca++ level
C. Calcium
58. 7. Storage:
8. Sample type:
9. Lymphocytosis and thrombocytosis
Errors affecting Ca++ level
C. Calcium
B. Pseudohypocalcemia:
1. Sample collection from IV site
2. High plasma glucose level
3. Increased viscosity
59. Hyperparathyroidism
Hypervitaminosis D
Bone cancer
Multiple myeloma
Leukaemia
Polycythaemia
Milk-alkali syndrome
Sarcoidosis
Idiopathic infantile
hypercalcaemia
A. Hypercalcemia
C. Calcium
B. Hypocalcemia
Hypoparathyroidism
Rickets
Osteomalacia
Chronic renal failure
Nephrotic syndrome
60.
61. The total amount of chlorine in an average
adult is about 80 gm
Chlorine, in the form of chloride ions, is the
chief anion of extracellular compartment
Normal serum chloride level is 98-107 mEq/L
(355-375 mg/dl)
D. Chloride
62. The chloride content of cerebrospinal fluid is 120
to 130 mEq/L
The interstitial fluid contains about 110 mEq/L
The intracellular fluid contains only about 4
mEq/L
D. Chloride
64. Serum: venous blood sample in gel vaccutainer
Urine:
24 hrs urine collection
No preservative is required
Store at 2-8 degree
Sample collection
D. Chloride
Method of estimation
By Ion Selective Electrode
65. Abnormal serum chloride levels
Changes in serum chloride level are parallel to those in
serum sodium level.
Serum chloride level is raised (hyperchloraemia) in
dehydration, respiratory alkalosis, metabolic acidosis
and adrenocortical hyperactivity.
Serum chloride level is decreased (hypochloraemia) in
severe vomiting, prolonged gastric suction, respiratory
acidosis, metabolic alkalosis and Addison’s disease.
D. Chloride
67. Classification of Diuretics
(According to the site of action)
DRUGS USED IN RENAL DISORDERS
Drugs that modify Drugs that modify
salt excretion water excretion
PCT TAL DCT CCT Osmotic diuretics ADH ADH
agonist antagonist
K+-sparing
diuretics
Thiazides
Loop
diuretics
Carbonic
anhydrase
inhibitors
69. 1. PROXIMAL CONVULATED TUBULE
1. Direct entry of Na+
2. Na+/ K+ pump @ BL membrane : Transfer of Na+
and K+ along with glucose, amino acids and other
organic anions & PO4
-3
3. Exchange of H+ @ Luminal Membrane:
Proximal tubule cells secrete H+ with the help of
carbonic anhydrase.
4. Large amount of HCO3
-, amino acid, acetate
along with Cl-
73. 2a. LOOP OF HENLE
(DESCEDING LOOP OF HENLE)
• The filtrate entering: isotonic
• Water absorption thereafter
• Tubular fluid becomes concentrated (Hypertonic)
(Three fold increase in salt concentration).
2b. LOOP OF HENLE
(ASCENDING LOOP OF HENLE)
1. ASCENDING LOOP OF HENLE (Medullary part lined by
cuboidal cells).
• Unique, Impermeable to water
74. • Active reabsorption of Na+, K+ & Cl- is mediated by
a Na+/K+/2Cl- Cotransporter.
• Mg++ and Ca++ enter the interstitial fluid.
• 25% to 30% of tubular NaCl returns to the Fluid
(blood).
2. ASCENDING LOOP OF HENLE (Cortical part lined by
flattened cells).
• Impermeable to water
• Salt reabsorption continues through Na+
electrochemical gradient transport
75.
76. Diuretic acting on Thick Asc. Loop Henle
1. Na+ K+/ 2CL- symporter inhibitor
Furosemide
Effects on electrolytes:
• Hypo Na +
• Hypo K +
• Hypo Cl- -Hypochloremic Alkalosis
• Hypo Mg ++
• Hypo Ca++
Note: Magnesium and Calcium reabsorption in the thick
ascending limb is dependent on the positive lumen voltage
gradient set up by potassium recycling through renal outer
medullary potassium channel, loop diuretics also inhibit
their reabsorption
79. 3. DISTAL CONVULATED TUBULE
• Impermeable to water.
• 10% of NaCl is reabsorbed
• Na+/Cl- transporter (inhibited by Thiazide)
• Calcium reabsorption: Na+/Ca++ exchanger into
the interstitial fluid.
• Ca++ excretion: PTH
80. Diuretic acting on DCT
1. Na+/ CL- Symporter
Thiazide
Effects on electrolytes:
• Hypo Na +
• Hypo Cl- -Hypochloremic Alkalosis
• Hyper Ca++
Note: By lowering the sodium concentration within the
epithelial cells, thiazides increase the activity of the Na+/Ca2+
anti-porter on the basolateral membrane to transport more
Ca2+ into the interstitium. This, in turn, decreases the
intracellular Ca2+.
85. A. PCT
1. Na+: Direct entry
Na+/ K+ pump @ BL membrane
2. Glucose, amino acids, PO4
-3 & organic anions :
Active transport along with sodium
3. HCO3
-, acetate, Cl-: Passive diffusion
B. Loop of Henle:
a. Descending loop:
1. Water
b. Ascending loop:
1. Active reabsorption of Na+, K+ & Cl- :
Na+/K+/2Cl- Cotransporter.
2. Mg++ and Ca++: Gradient
3. Na+ electrochemical gradient transport
Summary of sites of renal reabsorption of filtrate
86. C. DCT
1. Na+/Cl- transporter (inhibited by Thiazide)
2. Calcium reabsorption: Na+/Ca++ exchanger
into the interstitial fluid.
D. Collecting Duct
1. Aquaporins: Water Absorption – ADH
dependent
2. Na+ absorption @ Luminal membrane:
aldosterone dependent (inhibited by
amiloride)
3. Na+/ K+-ATPase @ BL membrane: aldosterone
dependent