unit 6 osmolarity

8/10/2019 Unit 6 Osmolarity

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REGULATION OF FLUIDS

AND ELECTROLYTES


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Fluid Compartments of the Body

Intracellular Fluid (ICF)67%

Extracellular Fluid (ECF)33%

Plasma (6.6%) Interstitial fluid (26.4%)

Lymph

Cerebrospinal fluid

Synovial fluid Serous fluids

Aqueous humour


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Plasma And Interstitial Fluid

Separated by blood capillaries

Water and solutes move by passive

diffusion Components similar except for plasma

proteins and RBCs


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ECF & ICF

Separated by cell membrane

Components different

Cell proteins in ICF Unequal distribution of Na, K and their anions

due to the Na/K pump (pumps Na out and K into

cell)


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Fluid Balance

Maintained by regulating the osmolarity of

the ECF


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Fluid Input and Output

Input (2500 ml)

Eating1000ml

Liquids1200ml

Metabolic water300ml

Output (2500ml)

Urination1200ml

Defecation150ml Sensible perspiration750ml

Insensible perspiration400ml


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Regulation of Water

Dehydrationmore water is lost than is

gained

Under conditions of excess water losswithout 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


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Regulation of Water

Dehydration (contd) Hypernatremia develops

Severe thirst, dryness and wrinkling of the skin

If plasma volume decreases and bp decreases shockmay develop Hypotension (90 mmHg and less)

Pale, cool, moist skin

Confusion and disorientation

Heart rate increases, rapid , weak pulse Cessation of urination

A drop in pH of blood; due to lactic acid produced by O2deprived cells


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Regulation of Water

Dehydration (contd)

Homeostatic Responses

ADH and Renin Secretion

Increased fluid Intake

ECF volume increases fluid shifts to ICF


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Regulation of Water

Excess Water Gains

When ECF volume increases due to

increased water intake withoutcorresponding increases in electrolytes

ECF becomes hypotonic

Water shifts to ICF

Both ECF and ICF volumes larger than normal

and lower osmotic concentrations


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Regulation of Water

Excess Water gains (contd)

Homeostatic Responses

ADH secretion decreasesurine volumeincreases


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Regulation of Water

Excess Water Gains

If not corrected

Overhydration

Cells become distorted

Solute concentration around enzymes change

Cell function is disrupted


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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 disordersexcess ADH production

Signs of Overhydration

Hyponatremia

Drunken behavior, confusion, hallucinations,

convulsions, coma and then death


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Regulation of Water

Treatment of Overhydration

Administration of Diuretics and

Infusion of a concentrated salt solution causing

a fluid shift from ICf to ECF


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Electrolyte Balance

When the rates of gain and loss of each

electrolyte are equal in the body


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Electrolyte Balance

Sodium (Na)

Gain and lose 1.13.3g 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)


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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


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Electrolyte Balance

Sodium

In cases of dehydrationwhere sodium is also

lost

Renin and Aldosterone are secreted

Overhydration

Plasma volume increases

Atrial and ventricular walls stretch Natriuretic peptides secreted (ANP and BNP)

Thirst is reduced; ADH and Aldosterone secretion blocked

Salt and water losses increase at the kidneys


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Electrolyte Balance

Potassium (K)

1.95.8g each day

Higher in the cell

Concentration in the ECF is controlled by the

rate of secretion along the DCT and collecting

system


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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


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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


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Electrolyte Balance

Calcium

Hypercalcemia caused by:

Hyperparathyroidism

Cancers of the breast, lungs, kidneys and bone

marrow

Excessive calcium or vitamin D supplements


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Electrolyte Balance

Calcium

Hypocalcemia due to

Hypoparathyroidism

Vitamin D deficiency

Chronic renal failure


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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


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Electrolyte Balance

Phosphate

0.81.2 g needed each day

Reabsorbed along the PCT stimulated by

calcitriol


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Electrolyte Balance

Chloride

Most abundant anion in the ECF

1.75.1 g needed each day

Absorbed along the digestive tract with sodium

and reabsorbed with sodium along the renal

tubule


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Acid-Base Balance

pH of the ECF is 7.357.45

We are unable to survive if the pH goes

below 6.8 or above 7.7 Acidosisthe physiological state that

results from plasma pH falling below 7.35

Alkalosisthe physiological state thatresults from plasma pH rising above 7.45


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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


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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


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H+ are transported from their site of

production to their site of elimination by a

buffer

This prevents damage to tissues


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There are three types of acids

Organic Acidsparticipants in or by-productsof aerobic metabolism eg lactic acid

Volatile Acidscan leave solution and enterthe atmosphere eg. Carbonic acid

Fixed Acidsdo not leave solution; remain inbody fluids until eliminated at the kidneys eg.

Sulphuric and phosphoric acids (produced bycatabolism of amino acids, phospholipids andnucleic acids


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Buffer Systems

Types of Buffer Systems

Protein

Carbonic AcidBicarbonate

Phosphate


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Protein Buffer Systems

Depend on the ability of amino-acids to

respond to pH changes by accepting or

releasing H+

Contribute to regulating ECF and ICF pH


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If pH increases theCOOH (carboxyl) group

on the amino acid loses its H+ to become a

COO-(carboxylate ion)

Some amino acids have an R group that can

also donate an H+ if the pH increases above

normal

If the pH decreases the COO-and NH2can

accept H+


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Proteins that can act as buffers include:

Plasma proteins

Extracellular protein fibres in interstitial fluid

Structural proteins in the ICF


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If pH of the ECF declines the H+ move into

the ICF where they are buffered

If pH increases in the ECF H+ move from

the ICF to the ECF in exchange for

potassium ions

This system is slow and cannot make rapid

and large-scale adjustments in the pH of the

ECF


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Haemoglobin Buffer System

The only intracellular buffer system that has an

immediate effect on the pH of the ECF and

helps prevent drastic changes in the pH whenthe partial pressure of CO2 in the plasma

increases or decreases


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Carbonic Acid-Bicarbonate Buffer

System

CO2 + H2O H2CO3 H++ HCO3

Prevents changes in pH caused by organic acidsand fixed acids in the ECF

If pH decreases the H+ will be removed by HCO3- H2CO3 CO2 + H2O

The CO2 and H2O are released at the lungs The reaction moves in the opposite direction if pH

increases ie H+ is released


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Phosphate Buffer System

H2PO4- H+ + HPO4

2-

i.e. Dihydrogen phosphate hydrogen +

monohydrogen phosphate

Supports the carbonic acid-bicarbonate

buffer system in the ECF but is of utmostimportance in the ICF

Also important in buffering urine


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Respiratory Compensation

A change in the respiratory rate that helps tostabilize the pH of the ECF

When respiration rate increases or decreases the

pH is altered by increasing or decreasing CO2levels

Recall that when CO2 increases the pH decreasesand visa versa

Recall also that when CO2 increases therespiratory centre is stimulated and respiratoryrate increases


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Renal Compensation

A change in the rates of H+ and HCO3-secretion

and reabsorption by the kidneys in response to

changes in plasma pH

The process of elimination of H+ is dependent on

the availability of buffers in the renal tubule

i.e. the secretion of H+ cannot continue if the tubular

fluid declines to 4.0-4.5. At this point the H+ will leak

out of the tubular fluid (back into the blood) as fast as it

is secreted


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Renal Compensation

The buffers involved in renal compensation

are:

Carbonic acid-bicarbonate placed in the

Phosphate tubule by filtration

Ammoniaproduced by tubular cells


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Renal Compensation

Renal Responses to Acidosis

1. Secretion of H+2. Buffer activity in tubules

3. Removal of CO2

4. Reabsorption of NaHCO3


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Renal Compensation

Renal Responses to Alkalosis

1. H+ secretion decreases2. Tubular cells do not reclaim the

bicarbonates in the tubular fluid

3. HCO3- secreted and a strong acid such asHCl is reabsorbed along the collecting duct


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Disturbances of Acid-Base Balance

Can occur under the following circumstances:

1. Cardiovascular Conditions eg heart failure and

hypotension

Affect pH of internal fluids by causing fluid shifts and bychanging glomerular filtration rates and respiratory efficiency

2. Disorders that affect circulating buffers, respiratory

performance or renal function eg emphysema or renal

failure

3. Conditions affecting the CNS

Will affect respiratory and cardiovascular reflexes


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Respiratory Acidosis

Develops when the respiratory systemcannot eliminate all the CO2 generated bytissues

Primary sign is low plasma pH due tohypercapnia (elevated plasma CO2)

BUT the usual cause is

HYPOVENTILATION (abnormally lowrespiratory rate)CO2 increases and pHdeclines


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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 declinecausing Acute Respiratory Acidosis


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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


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Respiratory Alkalosis

Occurs when respiratory activity lowers

plasma CO2 to below normal levels

(Hypocapnia)

Hypocapnia is caused by Hyperventilation


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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


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Common causes of Hyperventilation

1. Physical stresses eg pain

2. Psychological stresses eg extreme anxiety


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Initial Symptoms:

Tingling of hands, lips and feet

Light-headedness

If pH continues to increase one may become unconscious

which removes any psychological stimuli, therefore,

breathing rate decreases

Breathing into a paper bag is a simple treatment for

respiratory alkalosis


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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 system3. Severe bicarbonate loss due to diarrhea


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Metabolic Acidosis

Compensatory Mechanisms:

1. Respiratory MechanismH+ interacting with

HCO3- CO2 and H2O

2. Renal MechanismH+ secreted and HCO3-

reabsorbed

C bi d R i t & M t b li


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Combined Respiratory & Metabolic

Acidosis

Due to drowning

Lactic acid produced due to struggling muscles

CO2 increases if breathing stops

TreatmentArtificial and Mechanical Respiratory

Assistance along with intravenous infusion of

isotonic solutions such as sodium lactate,sodium gluconate or sodium bicarbonate

(release anions that can bind with the H+)


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Metabolic Alkalosis

Results when HCO3-increases

HCO3- binds with H+ H2CO3

The resulting decline in H+ producessymptoms of alkalosis


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Metabolic Alkalosis

Can develop when HCl

is secreted by the

stomach causing

HCO3- to increase inthe ECF (Alkaline

Tide)


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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-


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Metabolic Alkalosis

Compensation Mechanisms andTreatments

1. Breathing rate declinesCO2 increases pH

declines2. Increased loss of HCO3- from urine

3. Treatment of vomiting by using sodiumchloride or potassium chloride solutions

4. Acute cases treated with Ammonium Chloride Metabolism of ammonium chloride releases HCl

H+ lowers pH

unit 6 osmolarity

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