Sodium

Distribution
In a 70 kg adult : approx 4000 mmol of sodium

75% exchangeable 25% non exchangeable

(majority in ECF ) (in bones)

135-145mmol/lit
• Dietary food sources
Table salt (NaCl) , salty foods , animal foods /milk,
baking soda , baking powder , some vegetables

• RDA
1-5g
5g NaCl /day : for adults without hypertension
1g NaCl /day : for adults with hypertension
• Absorption and Excretion
Sodium is readily reabsorbed in the blood stream
via the epithelial cells by an active transport .
Filtered Sodium is
70-80% :actively reabsorbed in the PT
20-25% : reabsorbed in the loop of Henle along
with Cl and water
5% -10%: distal tubules (this is influenced by
the hormone -Aldosterone )
Urinary sodium output is regulated by four
mechanisms

1. RAAS –Renin –angiotensin aldosterone system

2. Atrial natriuretic peptide
3. The GFR
4. Dopamine
• Renin Angiotensin Aldosterone system
Decreases or Increases blood Sodium levels
??? ?
 Secreted Stimulus Target site What does
by it achieve ??
Na+ /Blood
Volume

ALDOSTERONE

ADH

ANP

Dopamine
Functions
• Maintenance of osmotic pressure & normal
distribution of water in the extracellular
fluid compartment.
• Regulates the body’s acid base balance
  HCl + Na2HPO4 - - > NaH2PO4 + NaCl
• It maintains muscle and nerve excitability
• Sodium is involved in cell membrane
permeability
Clinical Conditions Related to Plasma Sodium
Level Alteration : HYPERNATREMIA
Is an increase in serum sodium concentration
above the normal range of 135mEq/Lit to 145
mEq/lit :
Causes : lack of water intake /loss of water
a. Dehydration (due to lack of H2O intake)
b. due to excessive Aldosterone secretion eg.
Cushings syndrome >> hyperactivity of adrenal
cortex . >> Aldosterone excess >> Increases
Sodium reabsorption in the kidney >>
retention of sodium
c. Diabetes Insipidus –involves inadequate
production of the hormone –ADH /Vasopressin
(from the pituitary gland ) >> increased H2O
excretion >> blood sodium unaffected =
hypernatremia (hyperosmolality )

Symptoms of hypernatremia
Lethargy , seizures , coma
If due to excess salt gain : those of hypertension and
edema
Osmolality :
Is the concentration of solution in terms of
osmoles of solute /lit of solution

Osmoles : A UNIT OF Osmotic pressure

equivalent to the amount of solute that
dissociates in soln to form 1mole of particles
Significance of Osmolality measurement
Helpful in
• Interpretation of low blood sodium
concnetration and,
• In water deprivation tests
• Patient suspected of having ingested subs like
ethanol or ethylene glycol = increases
Osmolality
Hyponatremia
Is a significant fall in serum sodium concentration
below the normal range 135mEq/Lit to 145 mEq/lit

Two types of Hyponatremia

True hyponatremia = Hypo Osmolality

Pseudo hyponatremia = Normal /High

Osmolality
Osmolality = 275 to 295 mOsm/kg.
Pseudo hyponatremia = Normal /High

Osmolality
Normal Osmolality : hyperlipidemia ,
hyperprotenemia
High Osmolality : Hyper glycemia
Plama sodium concn falls by 1.4mmol/lit for every
100mg/dl rise in plasma concn
1. Causes for Hyponatremia with Normal ECF
Volume = Normal ECF low Sodium
Example : SIADH (Syndrome of inappropriate
ADHsecretion) :
2. Causes for Hyponatremia with High ECF
Volume = High ECF Normal Sodium
Example : Congestive cardiac Failure ,
Cirrhosis and , Renal Failure
3. Causes for Hyponatremia with Low ECF
Volume = low ECF low Sodium
Causes : Renal and Non Renal
Non Renal loss
Vomiting and diarrhoea :
LOSS OF WATER >>Decrease of ECF
volume>> water and sodium are both
lost :
Sodium loss exceeds H2O=
(hypovolemic hyponatremia)
Renal Loss
• Diuretics Use : : Diuresis LOSS OF WATER
>> water is lost through kidney and so
together does Sodium = hypovolemic
hyponatremia
• Adrenal insufficiency : (e.g Addisons disease)
No Aldosterone =No reabsorption of Sodium
from the DT = hypovolemic hyponatremia
Symptoms of Hyponatremia :
Potassium
Distribution

Adult male =50 mEq/kg of body weight

Influenced by age , gender and muscle mass
(75% is seen in skeletal msles )
98% : is in cells (150-160 mEq/lit)
2% : is in ECF (3.5-5 mEq/lit )
Dietary food sources : coconut water
Vegs , fruits , whole grains , meat , milk , legumes
RDA : 2g-5g

Absorption : passive diffusion from the GIT

Excretion : through Urine
After formation of urine in glomerulus >> Pot is
reabsorbed in PT >>then actively secreted in DT .
Regulation : controlled by kidneys
Aldosterone and Corticosteroids increase the
excretion of Pot
Function :
1. Pot maintains the intracellular osmotic
pressure , water balance and acid –base
balance
2. Depolarisation and contraction of heart
require potassium
3. Transmission of nerve impulses ; = there is
sodium influx and potassium efflux ; with
depolarisation
4. Nuclear activity and protein synthesis are
dependent on potassium
 Serum Potassium
3.5 mmol/l to 5 mmol/l

Hypokalemia : < 3.5 mmol/l to 5 mmol/l

Causes :
a. Redistribution b. Excretion
Redistribution : Hypokalemia
a. Alkalosis : K+ moves into the cell in
exchange of H+
Redistribution : Hypokalemia
b. Insulin therapy for diabetic hyperglycemia :
Insulin enhances transport of Pot into the cell
causing the fall : Hence Hypokalemia
• Excretion Renal Causes
Non Renal Causes
Renal loss cause
a. Diuretic phase of ATNecrosis
b. Excess mineralocorticoid –Aldosteronism
or excess gluco corticoid –Cushings syndrome
c. Conn’s syndrome ( an aldosterone producing adrenal
adenoma)
Aldosterone increases Na+reabsorption =
obligatory K+ excretion
Non Renal Causes :
Gastrointestinal losses : due to vomiting ,
diarrhoea ,excessive sweating, purgative use

• Symptoms :
Muscular weakness , constipation and paralytic
ileus (common problems)
Cardiac arrythmias
Cardiac arrest (ECG changes –T wave is inverted
, ST segment is lowered )
 Hyperkalemia
Less common but is more dangerous

Causes :
a. Redistribution
b. Increased production
c. Decreased Excretion
Redistribution
a. Acidosis : transfer of intracellular K in ECF
occurs in Acidosis as H+ (shifts out to maintain
electrical neutrality .

b. Insulin deficiency /Resistance

Increased production
Massive intravascular hemolysis , burns , violent
muscular activity = [K+ spills into the blood]
Decreased Excretion
Renal Failure
Adrenocorticol insufficiency (e.g Addison’s
disease) No Aldosterone = No Na+
reabsorption = K+ retention
Symptoms : Hyperkalemia
In Skeletal muscle : weakness and flaccid paralysis
In Cardiac Muscle : Bradycardia and Cardiac arrest
(significant ECG changes )
Respiratory Depression
 Hyperkalemia
Less common but is more dangerous
Lowers the resting membrane potential
Results in depolaristion and,
 repolarisation cannot occur = cell is no
longer excitable
• A 67 year old woman presented with severe
muscle weakness .She had been in the habit of
taking large amount s of purgatives and
recently had been prescribed a thiazide
diuretic for mild heart failure .
Her Serum K+ = 2.4mmol/lit

Justify low serum potassium in the patient

Chloride
Dietary Food Sources :
Table salt , leafy veg , eggs and milk

RDA :
2-5g

Absorption : Rapidly and almost totally absorbed in

GIT

Excretion : via 3 routes

GI , Skin , and Urinary tract
Functions :

1.As a part of sodium chloride, chloride is

essential for water balance , regulation of
osmotic pressure , and acid base balance
2. Formation of HCL by the gastric mucosa and
3. For activation of enzyme amylase
Clinical conditions related to Plasma chloride
level alterations
Ref Range: 95-105mEq/l

Useful in the differential diagnosis of :

Acid Base disturbances
For calculating Anion Gap
 Anion Gap
Cations mM/L Anions mM/L
Na+ 142 95%
Cl -
103 85% Measured
K+ 4 HCO3- 27
Ca 2+ 5 HPO42- 2 Unmeasured

Mg2+ 2 12
SO 4
2-
1 24
Others 1 Org. anions 5
Proteins 16

Total 154 154

• Anion gap is defined as the difference between the
total concentration of measured cations and that of
measured anions.
Causes of hypochloremia and hyperchloremia =
Causes of hyponatremia and hypernatremia

Major clinical exceptions are :

With Metabolic Acidosis : hyperchloremia may
not be associated with hypernatremia
With Metabolic Alkalosis ; hypochloremia may
not be associated with Hyponatremia