Water And Electrolyte Homeostasis

written by
Dr J Onubi, MBBS , Msc , FMCPath.
Consultant chemical pathologist
Department of Pathology
Naval Hospital OJO
Lagos.

Introduction
Water and electrolyte homeostasis is one of the important components of chemical biochemistry.
Any derrangement in either of them could lead to life threatening situations that may require urgent attention .
Four major electrolyte . Na+. K+, cl- and Hco3- concentrations maintains water homoestasis.

Water Homeostasis
Homeostatic processes ensure that
Total water balance is maintained within narrow limits.
The distribution of water between the various body compartments is maintained.

Water Distribution
TBW = 42l in a 70kg man- this is about 60% total body weight < in women.
ICW = 24 L >1/2 TBW
ECW =18 L,=13L intestinal =5L intravascular
Each compartment of B W remains at constant volume .This implies that the rate of water loss must equal the rate of gains
Daily water gain = 1.5-2.5L
Daily water loss = 1.5-2.5L


The gains is through drinks and food while the loss is through ,urine , faeces, sweat and expired air.
= 200L of Water is filtered by the kidney each day.
= 10L of water enter the interstitial lumen.
In this case the whole of the ECW could be lost by passive filtration in little more than an hour, but ,under normal circumstances about 90% is reabsorbed . Consequently, the daily loss amounts to about 1.5 to 2.5 L in urine and 100ml in faeces.


=900 ml of water is loss through sweat daily . This volume is primarily controlled by skin temperature.
Respiratory water loss depends on the respiratory rate and bears no relation to the body ‘s needs for water.
Regulatory Meachanism
Normal plasma osmolality 275-295 M os/kg.

The regulatory meachanism is the osmolality of the body water which changes with either water over load or water deficit . The principal organs involved are the hypothalamus and the kidneyS.
Osmolality – Concentration of particles per Kg of water (w/w ) Mmol/ kg.
Osmolarity – Concentration of particles per volume of solution (w/V) Mmol/ L.
osmolarlity is more exact because solution concentrations expressed on a weight bases are temperature independent , where as those based on volume vary with temperature.

An increase in osmolarlity resulting from water loss, leads to:
- stimulation of thirst – increase water intake
Secretion of ADH - Increase reabsorption.
ADH – synthesized in the hypothalamus as fluids intake continues there is dilution of NA+ - decrese in ADH concentration.
If there is no counter meachanism to balance up, the cells will take the pure water leading to spatially cerebral oedema- tonsillar hermiation -
Increase in intracranial pressure ,fits and death.


However – when the osmolarlity drops the thirst center response shuts up and ADH also stops.
The kidney opens up and allows water loss.

ELECTROLYTES
They are ions capable of carrying an electric charge.
All electrolytes are dissolved in BW but distributed differently in the various compartments along concentration gradients.
Their functions include:

Volume and osmotic regulation.
Myocardial rhythm and contractility.
Cofactors in enzyme activation.
Acid – base balance.
Blood coagulation.

Four major ones, Na+, K+, Cl- and Hco-3 will be considered
Na+
Major cation of ECF.
Central role in maintaining the normal distribution of water and the osmotic pressure.
Regulation.
Amount of Na+ in the body is relatively constant.
= 3g/dly intake. Same quantity is excreted.
The kidneys have the ability to conserve or excrete large amounts of Na+, depending on the Na+ content of the ECF and the blood volume.
Approximately 80% of filtered Na+ is reabsorbed at PCT.
Small amount at Loop with water.
Remainder at the CD under influence of Aldosterone hormone secreted by adrenal cortex.
Disturbances
Lead to either Hypernatraemia or Hyponatraemia.

Hypernatraemia.
Causes - Cushing's syndrome (hyperadrenalism).
Dehydration.
Na+ intake/infusion of hypertonic Na+ solution.
DKA treated with insulin.
Hypothalamic insufficiency-loss of thirst mechanism.
Diabetes Insipidus.

Treatment
Slow infusion of hypotonic fluid.
Hyponatraemia.
Causes
GI loss – diarrhea, vomiting, fistulae.
DKA before coma stage. Large amount, of Na+ and K+ are excreted into the urine as salts of the ketoacids with replacement of water because of thirst.

Salt – losing nephritis.
Addison’s disease with depressed secretion of aldosterone and corticosteroids.
Diabetes Insipidus with compensatory intake of water.
K+
Is the major intracellular cation.
Regulation
Once tissue needs are met the remainder is excreted by the kidney.
Nearly all filtered K+ are reabsorbed at the PCT
Aldosterone aids secretion at the DT& CD in exchange for Na+.

Hyperkalaemia
Causes.
Anoxia
Metabolic acidosis
Renal tubular acidosis
Renal failure
Low urine output
Addison’s disease
artifacts

Hypokalaemia
Causes
Vomiting, diarrhea fistulae
Diuretics
Nephritis
Cushings’s syndrome
Alkalosis
Insulin overdose

Treatment
Oral or intravenous replacement of K+.
Food with high K+ content – dried fruits, bananas & orange juice.

Chloride Cl-
Major extracellular anion
Precise function in the body is not well understood; however, it is involved in maintaining osmolality, blood volume and electric neutrality.

Regulation
Filtered Cl- is reabsorbed passively with Na+ at PCT.
Excess is excreted in urine & sweat.
Na+ reabsorption is limited by the amount of Cl- available

Disorders of Cl-
Similar to Na+

Hyperchloraemia
Causes
Dehydration
ARF
Metabolic acidosis
Respiratory alkalosis

Hypochloraemia
Causes
Salt- losing nephrites
Addison’s disease
Bromide intoxication
SIADH
Renal failure
Prolonged vomiting

Bicarbonate HCO3 _
Second most abundant anion in the ECF
It is the major component of the buffering system in the blood.
It is produced following the dissociation of carbonic acid formed from CO2 and H2O
CD
CO2 + H2O H2CO3- H+ + HCO3-
CD – Carbonate dehydratase present in high concentrations in erythrocytes and renal tubular cells.
They remove H+ quickly from the plasma at the same time adding more HCO-3.
H2O is freely available

HCO3- generation is therefore accelerated if the concentration of:
CO2 raises
HCO3- falls.
H+ falls because it is either buffered by erythrocytes or excreted from the body by renal tubular cells.
An increase of intracellular PCO2, or a decrease in intracellular [ HCO3-] in the erythrocytes and renal tubular cells maintain the extracellular [HCO3-] by accelerating the production of HCO3-. thereby minimizes changes in the ratio of [HCO3-] to [CO2] = 20 : 1 and the PH. This can be calculated from Henderson- Hasselbalch equation:

PH = PK + Log [HCO3 -]
S * PCO2
S = solubility constant for CO2. If PCO2 is in mmHg , S = 0.03
PK of HCO3- system = 6.1

PH = 6.1 + Log [HCO3]
PCO2 * 0.03

Disturbances
Acidosis
Alkalosis

Acidosis occurs if there is a fall in the ratio of [HCO3-]: PCO2 in the
ECF. This is either metabolic, in which the primary abnormality in the bicarbonate buffer system is a reduction in [HCO3-]; or respiratory in which there is increase in PCO2. Compensatory change is vice versa.

Oedema

DEFINITION: The accumulation of abnormal amounts of fluid in the interstitium or body cavities.

CAUSES:

Increased hydrostatic pressure
A. Impaired venous return
B. Arteriolar dilatation

Reduced oncotic pressure of plasma
A. Reduced intake
B. Increased loss
C. Decreased production

Sodium retention
A. Excessive salt intake with reduced renal function
B. Increased tubular reabsorption of sodium

Lymphatic obstruction
A. Inflammatory
B. Neoplastic
C. Post surgical
D. Post irradiation

PATHOGENESIS
Arterial end oncotic pressure venous end
35mmHg 25mmHg 15mmHg

MORPHOLOGY

Subcutaneous tissue- localised or generalised (anasarca)

Body cavities- hydrothorax or pleural effusion; hydropericardium or pericardial effusion; hydroperitoneum or ascites

Organs- pulmonary oedema, cerebral oedema; Both can be fatal.

COR PULMONALE

Cor Pulmonale
1. Is pulmonary (left sided) HHD secondary to pulmonary hypertension induced by intrinsic disease of the lungs or pulmonary vasculature.
2. It is characterized by Left Ventricular Hypertrophy
3. Massive pulmonary embolism usually results in Chronic Cor Pulmonale
4. Acute Cor Pulmonale is a cause of sudden death
5. Systemic Hypertension can cause Cor Pulmonale
The following lung diseases can result in Cor Pulmonale
1. Chronic Obstructive Pulmonary Disease
2. Diffuse Pulmonary Interstitial Fibrosis
3. Pneumoconiosis
4. Cystic Fibrosis
5. Bronchiectasis
The following statements are true of Cor pulmonale
1. Primary Pulmonary Hypertension is a known cause
2. Kyphoscoliosis and marked obesity predispose to it
3. A nutmeg appearance of the liver is classical in acute cases
4. Haemosiderosis may be seen in the spleen
5. Severe pulmonary oedema is always present
In Chronic Cor Pulmonale these features may be present
1. Right ventricular wall thickening of >0.5cm.
2. Hypertrophied trabeculae
3. Thickened outflow tract
4. Ventricular septum bulges to the left compressing LV
5. Tricuspid regugitation