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AND ELECTROLYTES
Plasma (6.6%)
Interstitial fluid (26.4%)
Lymph
Cerebrospinal fluid
Synovial fluid
Serous fluids
Aqueous humour
Fluid Balance
Maintained by regulating the osmolarity of
the ECF
Output (2500ml)
Urination 1200ml
Defecation 150ml
Sensible perspiration 750ml
Insensible perspiration 400ml
Regulation of Water
Dehydration more water is lost than is
gained
Under conditions of excess water loss
without comparable electrolyte loss the ECF
becomes hypertonic
Water moves from the ICF to the ECF
Both ECF and ICF are now more relatively
concentrated and contain less water
Regulation of Water
Dehydration (contd)
Hypernatremia develops
Severe thirst, dryness and wrinkling of the skin
If plasma volume decreases and bp decreases shock
may develop
Regulation of Water
Dehydration (contd)
Homeostatic Responses
ADH and Renin Secretion
Increased fluid Intake
ECF volume increases fluid shifts to ICF
Regulation of Water
Excess Water Gains
When ECF volume increases due to
increased water intake without
corresponding increases in electrolytes
ECF becomes hypotonic
Water shifts to ICF
Both ECF and ICF volumes larger than normal
and lower osmotic concentrations
Regulation of Water
Excess Water gains (contd)
Homeostatic Responses
ADH secretion decreases urine volume
increases
Regulation of Water
Excess Water Gains
If not corrected
Overhydration
Cells become distorted
Solute concentration around enzymes change
Cell function is disrupted
Regulation of Water
Overhydration is caused by
Ingestion of large volumes of freshwater
Inability to eliminate excess water due to chronic renal
failure or heart failure
Endocrine disorders excess ADH production
Signs of Overhydration
Hyponatremia
Drunken behavior, confusion, hallucinations,
convulsions, coma and then death
Regulation of Water
Treatment of Overhydration
Administration of Diuretics and
Infusion of a concentrated salt solution causing
a fluid shift from ICf to ECF
Electrolyte Balance
When the rates of gain and loss of each
electrolyte are equal in the body
Electrolyte Balance
Sodium (Na)
Gain and lose 1.1 3.3g each day
When there is a change in the gain or loss of Na
from the ECF there is no change in the
concentration of Na because there is always a
corresponding shift in water (ie osmosis occurs)
Electrolyte Balance
Sodium
If we eat a salty meal without adequate fluid
intake
Concentration of Na in the plasma increases
Fluid leaves the ICF and enters the ECF lowering Na
concentrations
Secretion of ADH due to osmoreceptors in pharynx
and hypothalamus
Electrolyte Balance
Sodium
In cases of dehydration where sodium is also
lost
Renin and Aldosterone are secreted
Overhydration
Plasma volume increases
Electrolyte Balance
Potassium (K)
1.9 5.8g each day
Higher in the cell
Concentration in the ECF is controlled by the
rate of secretion along the DCT and collecting
system
Electrolyte Balance
Potassium
Rate of secretion at the DCT depends on:
Changes in K concentration in the ECF
Changes in pH (if ECF pH decreases H is secreted in
exchange for Na instead of K)
Aldosterone levels
Aldosterone acts on Na/K pumps causing reabsorption of
Na in exchange for K
When K is high in the ECF aldosterone is also secreted
Electrolyte Balance
Calcium (Ca)
0.8 -1.2g
Maintained by Parathyroid hormone,
calcitriol and calcitonin
PTH and Calcitriol increase calcium levels
Calcitonin decreases calcium levels
Electrolyte Balance
Calcium
Hypercalcemia caused by:
Hyperparathyroidism
Cancers of the breast, lungs, kidneys and bone
marrow
Excessive calcium or vitamin D supplements
Electrolyte Balance
Calcium
Hypocalcemia due to
Hypoparathyroidism
Vitamin D deficiency
Chronic renal failure
Electrolyte Balance
Magnesium (Mg) Balance
Magnesium is higher in the ICF than the ECF
0.3-0.4 g of Mg need to be consumed daily to
maintain balance
Mg is reabsorbed along the PCT
Electrolyte Balance
Phosphate
0.8 1.2 g needed each day
Reabsorbed along the PCT stimulated by
calcitriol
Electrolyte Balance
Chloride
Most abundant anion in the ECF
1.7 5.1 g needed each day
Absorbed along the digestive tract with sodium
and reabsorbed with sodium along the renal
tubule
Acid-Base Balance
pH of the ECF is 7.35 7.45
We are unable to survive if the pH goes
below 6.8 or above 7.7
Acidosis the physiological state that
results from plasma pH falling below 7.35
Alkalosis the physiological state that
results from plasma pH rising above 7.45
Acid-Base Balance
Acidosis and Alkalosis both affect most
greatly the cardiovascular and nervous
systems
Homeostatic control of pH is, therefore, of
great importance
Acidosis is more prevalent as the body
produces several acids through its cellular
activities
Mechanisms of pH Control
Acid-base balance is achieved by balancing
hydrogen ion gains and losses
i.e. that gained at the digestive tract and
through metabolic activities must equal that
produced in the urine and produced at the lungs
Mechanisms of pH Control
H+ are transported from their site of
production to their site of elimination by a
buffer
This prevents damage to tissues
Mechanisms of pH Control
There are three types of acids
Organic Acids participants in or by-products
of aerobic metabolism eg lactic acid
Volatile Acids can leave solution and enter
the atmosphere eg. Carbonic acid
Fixed Acids do not leave solution; remain in
body fluids until eliminated at the kidneys eg.
Sulphuric and phosphoric acids (produced by
catabolism of amino acids, phospholipids and
nucleic acids
Buffer Systems
Types of Buffer Systems
Protein
Carbonic Acid Bicarbonate
Phosphate
Respiratory Compensation
A change in the respiratory rate that helps to
stabilize the pH of the ECF
When respiration rate increases or decreases the
pH is altered by increasing or decreasing CO2
levels
Recall that when CO2 increases the pH decreases
and visa versa
Recall also that when CO2 increases the
respiratory centre is stimulated and respiratory
rate increases
Renal Compensation
A change in the rates of H+ and HCO3- secretion
and reabsorption by the kidneys in response to
changes in plasma pH
Renal Compensation
The buffers involved in renal compensation
are:
Carbonic acid-bicarbonate
Phosphate
placed in the
tubule by filtration
Renal Compensation
1.
2.
3.
4.
Secretion of H+
Buffer activity in tubules
Removal of CO2
Reabsorption of NaHCO3
Renal Compensation
1. H+ secretion decreases
2. Tubular cells do not reclaim the
bicarbonates in the tubular fluid
3. HCO3- secreted and a strong acid such as
HCl is reabsorbed along the collecting duct
Respiratory Acidosis
Develops when the respiratory system
cannot eliminate all the CO2 generated by
tissues
Primary sign is low plasma pH due to
hypercapnia (elevated plasma CO2)
BUT the usual cause is
HYPOVENTILATION (abnormally low
respiratory rate) CO2 increases and pH
declines
Respiratory Acidosis
The body normally responds by increasing
respiratory rate
If respiratory rate does not increase
because the chemoreceptors fail to respond
to the decline in pH, breathing rate does not
increase or circulatory supply to the lungs is
inadequate pH will continue to decline
causing Acute Respiratory Acidosis
Respiratory Acidosis
Chronic Respiratory Acidosis
Develops when normal respiratory function is
compromised but the compensatory
mechanisms have not failed completely
Eg. Persons who have CNS injury and persons
whose respiratory centres have become desensitised
by alcohol or barbiturates
Respiratory Alkalosis
Occurs when respiratory activity lowers
plasma CO2 to below normal levels
(Hypocapnia)
Hypocapnia is caused by Hyperventilation
Respiratory Alkalosis
When pH increases (low CO2) due to
hyperventilation the condition corrects itself
by the chemoreceptors not being stimulated
so we do not get the urge to breathe
Respiratory Alkalosis rarely persists to
cause a clinical emergency
Respiratory Alkalosis
Respiratory Alkalosis
Initial Symptoms:
Tingling of hands, lips and feet
Light-headedness
Metabolic Acidosis
CAUSES
1. Production of a large number of fixed or
organic acids eg. Lactic Acidosis and
Ketoacidosis
2. Impaired ability to excrete H+ at the kidneys
due to glomerulonephritis or diuretics which
inhibit the Na/H transport system
3. Severe bicarbonate loss due to diarrhea
Metabolic Acidosis
Compensatory Mechanisms:
1. Respiratory Mechanism H+ interacting with
HCO3- CO2 and H2O
2. Renal Mechanism H+ secreted and HCO3reabsorbed
Metabolic Alkalosis
Results when HCO3- increases
HCO3- binds with H+ H2CO3
The resulting decline in H+ produces
symptoms of alkalosis
Metabolic Alkalosis
Can develop when HCl
is secreted by the
stomach causing
HCO3- to increase in
the ECF (Alkaline
Tide)
Metabolic Alkalosis
The temporary increase in pH due to the
release of HCO3- is not serious
BUT serious metabolic alkalosis can occur
due to bouts of repeated vomiting
Vomiting removes stomach acids, therefore,
the parietal cells are stimulated to produce
more HCl and therefore more HCO3-
Metabolic Alkalosis