Transcript Fluid & Electrolyte Balance

Fluid & Electrolyte Balance
Fluid Balance
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homeostatic value-must be maintained
food & water are taken in
what is not needed is excreted
body is in constant flux
must be a balance between amount of water gained & amount lost
Ideally-should cancel each other out
digestive system-major source of water gain
urinary system-primary system for fluid removal
The Body as an Open System
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“Open System”. The body exchanges
material and energy with its
surroundings.
Electrolyte Balance
• homeostatic value-must be
maintained
• electrolytes-Cl, Na, K, etc. are
ingested everyday
• water & sodium regulation are
integrated defending body against
disturbances in volume &
osmolarity
• K imbalance
– trouble with cardiac & muscle
functioning
• Calcium imbalances
– problems with exocytosis,
muscle contraction, bone
formation & clotting
• H & HCO3- balance
– determines pH or acid-base
balance
The Body as an Open System
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“Open System”. The body exchanges
material and energy with its
surroundings.
Maintaining Fluid & Electrolyte
Balance
• homeostasis depends on
integration of respiratory,
cardiovascular, renal &
behavioral systems
• primary route for excretion
of water & ions-kidneys
– essential for regulating
volume & composition of
fluids
• lungs remove H+ & HCO3by excreting CO2
• behavioral mechanisms
– thirst & salt appetite aid
in fluid & electrolyte
balance
Osmolarity
• number of solute particles
dissolved in 1liter of water
• reflected in solution’s ability to
produce osmosis & alter
osmotic properties of a solvent
• depends only on number of
non penetrating solute particles
in solution
• 10 molecules of Na+ has same
osmotic activity as 10 glucose
or 10 amino acid molecules in
same amount of fluid
Osmolarity
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important to maintain water
balance since water can cross
most membranes freely
water balance determines
osmolarity
as osmolarity of ECF (extra
cellular fluid) changeswater
moves into or out of cells
changing intracellular volumes &
cell function
excess water intakeosmolarity
decreaseswater moves into
cells swell
Na intake (osmolarity increases)
water moves out of cellsshrink
changes in cell volume impairs cell
function
swelling
– may cause ion channels to
open
– changing membrane
permeability
Water
• major constituent of body
• all operations need water as
diffusion medium
– to distribute gas, nutrients &
wastes
• distributed differently among
various body compartments
• 63-65%-intracellular fluid (ICF)
• 35- 37%-extracellular fluid (ECF)
• ECF-composed of three parts
– interstitial or tissue fluid-25%
– plasma-8%
– transcellular fluid-2%
• miscellaneous fluids such
as CSF, synovial fluid, etc.
Water Balance
• obtained when daily gains & losses
are equal
• average intake and loss-2.5L each
day
• Gains
– metabolism (200ml/day)
– preformed water-food & drink
• Losses
– about 1.5L each day lost via urine
– 200ml elmininated with feces
– 300 ml is lost during breathing
– 100 ml in sweat
– 400ml in cutaneous transpiration
• water that diffuses through
epidermis & evaporates
• output through breath & cutaneous
transpiration is insensible water loss
Regulation of Intake
• Intake-governed mostly by
thirst
• Dehydration
– reduces blood volume & blood
pressure
– raises blood osmolarity
• Detected by thirst center
– hypothalamus
• salivate lessdry mouth
sense of thirst
• ingest water
• cools & moistens mouth
• rehydrates blood
• distends stomachinhibits
thirst
Regulation of Output
• only way to control water
output significantly is through
urine volume
• kidneys cannot completely
prevent water loss or replace
lost water or electrolytes
• changes in urine volume are
usually linked to adjustments
in sodium reabsorption
– where sodium goes water
follows
• ADH is one way to control
urine volume without sodium
• ADHcollecting ducts
synthesize aquaporins (water
channels) water can diffuse
out of ductwater reabsorbed
Electrolytes
• participate in metabolism
• determine membrane
potentials
• affect osmolarity of body
fluids
• major cations
– Na, K, Ca & H
• major anions
– Cl, HCO3 & P
• intracellular fluid contains
more K+
• extracellular fluid has more
Na+ & Cl-
Sodium
• crucial role in water & electrolyte balance
• involved in excitability of neurons &
muscle cells (resting membrane
potentials)
• major solute in extracellular fluid
• determines osmolarity of extracellular
fluids
Sodium Balance
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need about 0.5 grams of sodium each day
typical American consumes 3-7 g/day
kidneys regulate Na+ levels
hormonal mechanisms control Na
concentrations
• Aldosterone
– primary role
• ADH
• ANP
ADH
• NaCl added to body
increased
osmolarityADH
(vaopressin) secretion &
thirst increased
• thirstdrink
• osmolarity decreases
• ADHkidneys
• conserves water by
concentrating urine
• increased water
reaborption increases BP
• returned to normal with
cardiovascular reflexes
Aldosterone
• Na regulation also
mediated by aldosterone
– steroid hormone
produced by adrenal
cortex
• stimuli-more closely tied to
blood volume & pressure &
osmolarity than Na
• Hyponatremia &
hyperkalemiaadrenal
cortexaldosterone
• Hypotension
reninaldosterone
secretion
Aldosterone
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tells kidneys to reabsorb Na in distal
tubule & collecting ducts
primary target-last 3rd of distal tubule
increases activity of Na-K ATPase
target cell-principal cell
Apical membranes of P cells have Na &
K leak channels
Aldosterone enters by simple diffusion
 combines with membrane receptors
Na channels increase time they
remain open
as intracellular Na increasesNa-K
ATPase speeds up transport of Na into
ECFnet result-rapid increase of Na
reaborption that does not require
synthesis of new channels or ATPase
proteins
slower phase of actionnewly made
channels & pumps inserted into
epithelial cell membranes
Renin-Angiotensin-Aldosterone
• primary signal for
aldosterone releaseangiotensin II
– component of reninangiotensin system
• kidneys sense low blood
pressure triggers specialized
cells-juxtaglomerular cells
(JG cells) in afferent
arterioles to produce renin
•  angiotensinogen
angiotensin I  angiotensin
II by ACE-angiotensin
converting enzyme-found in
lungs & on endothelium of
blood vessels
Renin-Angiotensin-Aldosterone
Path
• Angiotensin IIadrenal cortex
aldosteronedistal tubule
reabsorbs Na
• ADH secretion is also
stimulatedwater reabsorption
increases
• because aldosterone is also
acting to increase Na
reabsorption, net effect-retention
of fluid that is roughly same
osmolarity as body fluids
• net effect on urine excretiondecrease in amount of urine
excreted, with lower osmolarity
• Aldosteronemore NaCl
reabsorbed in DCT & collecting
ductsreduces filtrate osmolarity
Renin-Angiotensin-Aldosterone
• stimuli that begin renin pathwayrelated directly or indirectly to
blood pressure
• JG cells are directly sensitive to
pressure & respond to low
pressure by releasing renin
• sympathetic neurons are
activated by cardiovascular
control center when blood
pressure dropsJG cellsrenin
release
• paracrine feedback from macula
densa cells in distal tubule
stimulate renin release
• if fluid flow in distal tubule is
highmacula densaNO-nitric
oxideinhibits renin release
• GFR or BP lowfluid flow low
macula densa cellsNO
loweredJG cellsrenin
released
Sodium & Blood Pressure
• Na reaborption does
not directly raise blood
pressure
• retention helps
stimulate fluid intake &
volume expansion
which increases blood
volume& blood
pressure
Angiotensin & Blood
Pressure
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Angiotensin II has other effects on blood
pressure
increases it directly & indirectly through 4
pathways
activates angiotensin II receptors in
brainincreases vasopressin
secretionfluid retained in kidneys
constricts blood vessels
Angiotensin II serves to stimulate
thirstexpands blood volume & increases
blood pressure
Vasoconstriction-also stimulated by
angiotensin II increases blood pressure
without changing blood volume
angiotensin II activates receptors in
cardiovascular control centerincreases
sympathetic output to heart & blood
vesselsincreases cardio output &
vasoconstriction  increases blood
pressure
ANP
• Na also regulated by ANP
– atrial natriuretic peptide
– peptide hormone made by
heart atrial cells
• released when walls of atria
are stretched
• ANP enhances Na excretion &
urinary water loss
• increases GFR by making
more surface area available for
filtration decreases Na &
water reabsorption in collecting
ducts
• indirectly inhibits renin,
aldosterone & vasopressin
release
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K Balance
most abundant cation of ICF
– must be maintained within narrow range
changes affect resting membrane potentials
decreased Khypokalemiaresting
membrane potential becomes more
negative
increased Khyperkalemiamore K inside
celldepolarization
Hypokalemiamuscle weakness
– more difficult for hyperpolarized neurons
& muscles to fire action potentials
– very dangerous
– respiratory & heart muscle might fail
Hyperkalemia
– more dangerous of two situations
depolarization of excitable tissues make
them more excited initiallycells unable to
repolarize fully
become less excitableaction potentials
smaller than normal may lead to cardiac
arrhythmias
Sodium & Water Balance
• Na & water
reabsorption are
separately regulated
in distal nephron
• water does not
automatically follow
Na reabsorption here
• vasopressin (ADH)
must be present
• proximal tubule
– water reabsorption
automatically follows
Na reaborption
Acid-Base Balance
• water must be strictly
monitored to keep it at a
certain pH
– not too acidic or too alkaline
• metabolism depends on
functioning enzymes
– very sensitive to changes in
pH
• pH changes also disrupt
stability of cell membranes
– alter protein structure
• normal pH range 7.35 7.45
• neutral side
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pH
measurement of hydrogen ion
concentration
– lower pH indicates higher
hydrogen concentration-higher
acidity
– higher pH indicates lower
hydrogen concentration-higher
alkalinity
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HNO2
H+ + NO2
pH-below 7.35-acidosis
pH-above 7.45-alkalosis
Strong acids dissociate readily in
water giving up H which lowers pH
Weak acids ionized slightly
– keep most of hydrogen bound
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bases accept hydrogen ions
– strong base has strong tendency
to bind hydrogen ions
– raises pH
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weak base binds less hydrogen
ions
– less effect on pH
HNO2
H+ + NO2
Disruptions of Acid-Base
Balance
• pH imbalances produce problems that
can be life threatening
• intracellular proteins comprising
enzymes, membrane channels, etc
• very sensitive to pH
• functions of proteins depend on 3-d
shape can become altered by pH
changes
• must balance gain & loss of H ions
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Compensations for Acid-Base
Imbalances
Buffers
– first line of defense
– always present
– attempt to suppress changes in
H+
• Kidneys
– change in rate of hydrogen ion
secretion by renal tubules
– greatest effect
– requires days to take effect
• Lungs
– can have rapid effect
– cannot change pH as much as
urinary system
– change pulmonary ventilationexpel or retaining carbon dioxide
Chemical Buffers
• any substance that can bind or release H
ions such that they dampen swings in pH
• three major chemical buffer systems of
body
• Bicarbonate System
• Phosphate System
• Protein System
Carbonic Acid-Bicarbonate
Buffer System
• most important extracellular buffer
system
• CO2 + H2OH2CO3
H+ + HCO3-__
• add H equation shifts to leftmore
HCO3 made increases CO2 & H2O
Phosphate Buffer System
• important in buffering ICF & urine
• H2PO4H + HPO4
• H + HPO4  H2PO4
Protein Buffer System
• involves amino acids accepting or
releasing H+
•  pH: COOH  COO- + H+
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•  pH: NH2 + H+ NH3 + amino group
accepts H
Respiratory Compensation
• change in respiratory rate
directly affects carbonic acidHCO3 buffer system
• any change in PCO2 affects H
ion & HCO3 concentrations
• increasing or decreasing rate
of respiration alters pH by
lowering or raising PCO2
• PCO2 increasespH
decreases
• PCO2 decreasespH
increases
• excess CO2 ventilation
increases to expel more
• low CO2 ventilation is reduced
Renal Compensation
• slower than buffers or lung
compensation
• changes rate of H & HCO3
secretion or reabsorption in
response to changes in pH
• directly-excretes or reabsorbs H
ions
• indirectly-changes reabsorption
or excretion of HCO3
• during times of acidosis renal
tubule secretes H+ into filtrate
• HCO3- & K+ blood pH increases
• pH levels-secretion of H ions
decreased & bicarbonates not
reclaimed
Disorders of Acid-Base Balance
• Acidosis
– low pHneurons less excitableCNS
depressionconfusion & disorientation
comadeath
• Alkalosis
– high pHneurons hyperexcitable numbness &
tinglingmuscle twitches tetanus
• Acid-base imbalances fall into two categories
• Respiratory
• Metabolic
Respiratory Acidosis
• respiratory system cannot
eliminate all CO2 made by
peripheral tissues
• accumulates in ECF
lowers its pH
• primary symptom of
hypercapnia-respiratory
acidosis
• typical cause
• Hypoventilation-low
respiratory rate
Respiratory Alkalosis
• uncommon
• usually due to
hyperventilation
(plasma PCO2
decreases)
• can be modulated by
breathing into paper
bag & rebreathing
exhaled CO2
Metabolic Acidosis
• due to drop in blood
bicarbonate levels drop
– lost due to renal dysfunction
– lost through severe diarrhea
• due to accumulation of nonvolatile acids-organic acid
• Lactic acidosis
• Ketoacidosis
– generation of large amount of
ketone bodies
• occurs during starvation &
diabetes
• may also be caused by
impaired ability to excrete H
ions at kidneys or by severe
HCO3 loss as occurs during
diarrhea or overuse of
Metabolic Alkalosis
• HCO3 ions become
elevated
• Rare
• can be due to non
respiratory loss of acid
• excessive intake of
alkaline drugs
• excessive vomiting
causes a loss of HCl.
Compensations for Decreased pH
Compensations for Increased pH