Lipid Profile and

Elctrolytes
Prof Shirani Ranasinghe
(Senior Prof. in Biochemistry, Prof of Biochemistry)
Department of Biochemistry
Faculty of Medicine
University of Peradeniya
Serum Electrolytes
 Sodium (Na+)
• Bulk cation of extracellular fluid  reflects change in total
body Na+
• Principle active solute for the maintenance of intravascular &
interstitial volume
• Absorption: throughout the GI system via active Na,K-ATPase
system
• Excretion: urine, sweat & feces
• Kidneys are the principal regulator 3
 Sodium (Na+)
• Kidneys are the principal regulator
• 2/3 of filtered Na+ is reabsorbed by the proximal convoluted tubule,
increase with contraction of extracellular fluid
• Countercurrent system at the Loop of Henle is responsible for Na+
(descending) & water (ascending) balance – active transport with Cl-
• Aldosterone stimulates further Na+ re-absorption at the distal
convoluted tubules & the collecting ducts
• <1% of filtered Na+ is normally excreted but can vary up to 10% if
necessary
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 Sodium (Na+)
• Normal SNa: 135-145
• Major component of serum osmolality
• Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18)
• Normal: 285-295
• Alterations in SNa reflect an abnormal water regulation

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 Measurement of serum sodium
1 Potentiometry
• Measurement of electrolytes with ion-specific electrodes.
• There are two types of potentiometry: direct and indirect.
• Direct potentiometry: Used by blood gas machines and no any sample
dilution.
• Indirect potentiometry: Used by automated chemistry analyzers, such as
the ones used at Cornell University, and involves sample dilution before
analysis.
 Sodium (Na+)
• Hypernatremia: Causes
• Excessive intake
• Improperly mixed formula
• Exogenous: bicarb, hypertonic saline, seawater
• Water deficit:
• Increased insensible loss
• Inadequate intake

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 Sodium (Na+)

• Hypernatremia: Causes
• Water and sodium deficit
• GI losses
• Cutaneous losses
• Renal losses
• Osmotic diuresis: mannitol, diabetes mellitus
• Chronic kidney disease

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 Sodium (Na+)
• Hypernatremia Clinical presentation
• Dehydration
• Irritability, lethargy, weakness
• Intracranial hemorrhage

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 Sodium (Na+)
• Hypernatremia Treatment
• Rate of correction for Na+ 1-2 mEq/L/hr
• Calculate water deficit
• Water deficit = 0.6 x wt (kg) x [(current Na +/140) – 1]
• Rate of correction for calculated water deficit
• 50% first 12-24 hrs
• Remaining next 24 hrs

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 Sodium (Na+)
• Hyponatremia
• Na+<135 mEq/L
• Seizure threshold ~125
• <120 life threatening

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 Sodium (Na+)
• Hyponatremia: Etiology
• Hypervolemic
• CHF Cirrhosis
• Nephrotic syndrome Hypoalbuminemia
• Septic capillary leak
• Hypovolemic
• Renal losses Cerebral salt wasting
• Extra-renal losses aldosterone effect
• GI losses
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 Sodium (Na+)
-
• Hyponatremia: Etiology
• Euvolemic hyponatremia
• Glucocorticoid deficiency
• Hypothyroidism
• Water intoxication
• Psychogenic polydipsia
• Diluted formula

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 Pseudo-hyponatremia
• It is a laboratory artefact
• When plasma contains protein and fat
• Hyperglycemia
 Sodium (Na+)

• Hyponatremia Clinical presentation

• Cellular swelling due to water shifts into cells
• Anorexia, nausea, emesis, malaise, lethargy, confusion, agitation,
headache, seizures, coma
• Chronic hyponatremia: better tolerated

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 Sodium (Na+)
• Hyponatremia Treatment
• Rapid correction  Goal 12 mEq/L/day
• Hyponatremic seizures
• Poorly responsive to anti-convulsants
• Hypertonic saline
• Need to bring Na to above seizure threshold

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 Potassium (K+)
• Normal range: 3.5-4.5 mEq/L
• Largely contained intra-cellular  SK does not reflect total
body K
• Important roles: contractility of muscle cells, electrical
responsiveness
• Principal regulator: kidneys

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 Potassium (K+)
• Daily requirement 1-2 mEq/kg
• Complete absorption in the upper GI tract
• Kidneys regulate balance
• 10-15% filtered is excreted
• Aldosterone: increase K+ & decrease Na+ excretion
• Mineralocorticoid & glucocorticoid  increase K+ & decrease
Na+ excretion in stool
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 Potassium (K+)
• Solvent drag
• Increase in Sosmo  water moves out of cells  K+ follows
• 0.6 SK / 10 of Sosmo
• Evidence of solvent drag in diabetic ketoacidosis
• Acidosis
• Low pH  shifts K+ out of cells (into serum)
• High pH  shifts K+ into cells
• 0.3-1.3 mEq/L K+ change / 0.1

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 Measurement of Serum Potassium
• Using a flame photometer or ion-selective electrode.
• The procedure is rapid, simple, and reproducible. I
 Potassium (K+)

• Hyperkalemia
• >6.5 mEq/L– life threatening
• Potential lethal arrhythmias

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 Potassium (K+)
• Hyperkalemia Treatment
• Lower K+ temporarily
• Calcium gluconate 100mg/kg IV
• Bicarb: 1-2 mEq/kg IV
• Insulin & glucose

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 Potassium (K+)

• Hyperkalemia Treatment
• Increase elimination
• Hemodialysis or hemofiltration
• Furosemide via urine

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 Potassium (K+)
• Hypokalemia
• <2.5 mEq/L: life threatening
• Common in severe gastroenteritis

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 Bicarbonate HCO3-
• It is a byproduct of your body's metabolism.
• Your blood brings bicarbonate to your lungs
• it is exhaled as carbon dioxide.
• Your kidneys also help regulate bicarbonate.
• Bicarbonate is excreted and reabsorbed by your kidneys.
• This regulates your body's pH, or acid balance.
 Bicarb (HCO3--)

• Normal range: 25-35 mEq/L

• Important buffer system in acid-base homeostasis
• Increased in metabolic alkalosis or compensated respiratory
acidosis
• Decreased in metabolic acidosis or compensated respiratory
alkalosis
• 0.15 pH change/10 change in bicarb in uncompensated
conditions
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 Decrease Bicarb (HCO3--)

• Metabolic acidosis Clinical presentation

• Chest pain, palpitation
• Kussmaul respirations
fast, deep breaths response to metabolic acidosis.
• Hyperkalemia
• Neuro: lethargy, coma, seizures
• Cardiac; arrhythmias, decreased response to Epinephrine, hypotension

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 Increase Bicarb (HCO3--)

• Metabolic alkalosis
• There is excess of bicarbonate in the body fluids.
• It can occur in a variety of conditions.
• It may be due to digestive issues, like repeated vomiting, that
disrupt the blood's acid-base balance.
• It can also be due to complications of conditions affecting the
heart, liver and kidneys.

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 Calcium

• Normal range: 8.8-10.1 mg/dl with half bound to albumin

• Ionized (free or active)calcium: 4.4-5.4 mg/dl – relevant for
cell function
• Majority is stored in bone
• Hypoalbuminemia  falsely decreased calcium

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 Calcium

• Roles:
• Coagulation
• Cellular signals
• Muscle contraction
• Neuromuscular transmission
• Controlled by parathyroid hormone and vitamin D

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 Calcium
• Hypercalcemia:
• Excess parathyroid hormone, lithium use
• Excess vitamin D
• Malignancy
• Renal failure
• High bone turn over
• Prolonged immobilization
• Hyperthyroidism
• Thiazide use, vitamin A toxicity
• Paget’s disease 31

• Multiple myeloma
 Calcium
• Hypercalcemia: Clinical presentation
• constipation
• fatigue, lethargy, depression
• bone pain
• Stones: kidney stones
• Psychiatric overtones: depression & confusion
• Fatigue, anorexia, nausea, vomiting, pancreatitis
• ECG: short QT interval, widened T wave
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 Calcium

• Hypercalcemia Treatments
• Fluid & diuretics
• Oral supplement: biphosphate or calcitonin
• Glucocorticoids
• Dialysis

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 Calcium
• Hypocalcemia Eating disorder
• Hungry bone syndrome
• Ingestion: mercury , excessive Mg
• Chelation therapy EDTA
• Absent of PTH
• Ineffective PTH:
• ineffective vitamin D
• Deficient in PTH:
• Blood transfusions 34
 Calcium

• Hypocalcemia: Clinical presentation

• Neuromuscular irritability
• Tetany (Chvostek & Trousseau signs)
• Laryngospasm
• Jittery, poor feedings or vomiting in newborns
• ECG changes: prolonged QT intervals

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 Calcium

• Hypocalcemia: Treatments
• Supplements
• IV: gluconate or chloride with ECG change
• Oral calcium with vitamin D

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 Calcium Balance
• What is calcium Balance?

• How we maintain calcium intake and output?

 Calcium Balance

• In adults it is 0 balance.
• Growing children + ve balance
 Menopause
• In women after menopause Ca excretion increase in urine.
• So it is advisable to take a glass of milk after menopause
 Magnesium
• Normal range: 1.5-2.3 meq/L
• 60% stored in bone
• 1% in extracellular space
• Necessary cofactor for many enzymes
• Renal excretion is primary regulation

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 Magnesium

• Hypermagnesemia: Causes
• Hemolysis
• Renal insuficiency
adrenal insufficiency, hyperparathyroidism, lithium intoxication

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 Magnesium

• Hypermagnesemia: Clinical presentation

• Weakness, nausea, vomiting
• Hypotension, hypocalcemia

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 Magnesium
• Hypermagnesemia: Treatments
• Calcium infusion
• Diuretics
• Dialysis

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 Magnesium
• Hypomagnesemia
• Alcoholism: malnutrition diarrhea; Thiamine deficiency

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 Magnesium

• Hypomagnesemia: Clinical presentation

• Weakness, muscle cramps
• Cardiac arrhythmias
• CNS: irritability, tremor, jerking,
• Hallucination, depression, epileptic fits, tachycardia, tetany

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 Magnesium

• Hypomagnesemia: Treatments
• Oral or IV supplement
• Correct on going loss

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 Phosphorus
• Normal range: 2.3 - 4.8 meq/L
• Most store in bone or intracellular space
• <1% in plasma
• Intracellular major anion, most in ATP
• Concentration varies with age, higher during early childhood
• Necessary for cellular energy metabolism

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 Phosphorus
• Hyperphosphatemia
• Hypoparathyroidism
• Chronic renal failure
• Osteomalacia
• Presentations
• Ectopic calcification
• Renal osteodystrophy
• Treatments
• Dietary restriction
• Phosphate binder 49
 Phosphorus

• Hypophosphatemia

• Respiratory alkalosis
• Alcohol abuse
• Malabsorption

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 Phosphorus

• Hypophosphatemia
• Clinical presentation
• Muscle dysfunction and weakness
• WBC dysfunction
• Instability of cell membrane
• Treatments
• supplementation

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 Chloride
• Anion in ECF
• It is distributed in the extracellular fluid compartment (ECF)
• blood/plasma (or serum) interstitial fluid compartment.
• Chloride is the major anion associated with sodium in the ECF . serum
chloride concentrations range from 96 -106 mEq/L.
 Estimation of Chloride
(1) the autoanalyzer (a colorimetric technique—SMA and ACA methods)
(2) a coulometric method
(3) chloride-specific ion electrodes.
 Maintenance of Chloride
• The kidney maintains total body chloride
• Part or all of the chloride filtered by the glomerulus
• Reabsorbed as a result of both active and passive transport processes
along the tubules
 Elevation of Serum Cl (hyperchloremia)
1 addition of excess chloride to the ECF compartment
2 loss of water from this compartment
 Hypochloremia
• By the loss of chloride from the ECF
• Addition of water to this compartment. This means that one cannot
evaluate total body chloride stores from the serum chloride concentration.
 Possible causes for Hypochloremia
• Extrarenal causes
• inadequate sodium chloride intake
• losses of certain gastrointestinal fluids
• vomiting
• nasogastric suction
• loss of fluids through the skin occurring as a result of trauma
• (e.g., burns).
 Contd.
• Renal causes
• diuretic abuse
osmotic diuresis (e.g., mannitol, diabetic ketoacidosis, or hyperosmolar
nonketotic coma)
interstitial nephritis
Iron
• Critical element for all cells

• Requirement varies by tissue type, growth and development

• Free iron is toxic, concentration balance is critically important

Iron Distribution

Adult male has

~4g total body
iron stores

Andrews NEJM, 23 DEC 1999 x VOLUME 341, Number 26

 Plasma Distribution of Iron in the body
• Transport iron-Transferrin Serum Transferrin-300 mg/dl
in plasma.

• This can bind 300 g Fe/dl (Total Iron Binding Capacity (TIBC)-
• Normally 1/3 is saturated.
• In Fe deficiency saturation decreases.
• In excess of Fe increases.
 Functions
Carry O2 and CO2 as Hemoglobin and storage function -Myoglobin

Critical for the function of iron containing enzymes

eg, cytochrome P450,myeloperoxidase (Lyzozomalenzyme), E transport
chain.
Heme enzymes-Catalase, Glutathione peroxidase All are antioxidant
enzymes involved in destruction of H2O2.
 Iron Absorption

• Maximum absorption at upper duodenum, stomach

• Heme is readily absorbed Fe form
 Physiological changes in the plasma
transferrin
• Requirement of iron increases in pregnancy, lactation, anemia, growth &
inflammation
• It increases
• At 28 the week of pregnancy
• Women with contraceptive
• Patients under oestrogen treatment
 Pathological changes in the plasma

• Increases
• In Fe deficiency

• Decreases
• Nephrotic syndrome –Loss in urine
Andrews NEJM, 23 DEC 1999 x VOLUME 341, Number 26
 Tests for Iron Deficiency
• Complete blood
• Low mean corpuscular volume (MCV)
• Low mean corpuscular hemoglobin concentration (MCHC)
• Peripheral blood smear-RBCs are microcytic and hypochromic in chronic cases
• Platelets usually are increased
• Serum ferritin- Low
• Serum iron-Low
• TIBC is elevated. Why?
• Bone marrow iron stain (Prussian blue)
 Treatment
• Most patients are treated initally with oral iron unless there is an
absorptive problem.
• Dietary sources + FeSo4 BID.
• TID is very constipating and causes gastric distress; commonest cause
for noncompliance
• Iv iron is no longer ‘dangerous’. The newer formulations such as iron
sucrose, lmw iron dextran and ferric gluconate have minimal risks of
infusion reactions
• In very severe cases, RBC transfusion
 Summary
• What are electrolytes?
• Role played by different elctrolytes
• What are the important cations and anions
Thank you!