fluid & electrolyte balance. fluid balance homeostatic value-must be maintained food & water...
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Fluid & Electrolyte Balance
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Fluid Balance• 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
T h e B o d y a s a n O p e n S y s t e mT h e B o d y a s a n O p e n S y s t e m
“ O p e n S y s t e m ” . T h e b o d y e x c h a n g e s m a t e r i a l a n d e n e r g y w i t h i t s s u r r o u n d i n g s .
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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
T h e B o d y a s a n O p e n S y s t e mT h e B o d y a s a n O p e n S y s t e m
“ O p e n S y s t e m ” . T h e b o d y e x c h a n g e s m a t e r i a l a n d e n e r g y w i t h i t s s u r r o u n d i n g s .
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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+ & HCO3- by
excreting CO2
• behavioral mechanisms– thirst & salt appetite aid in
fluid & electrolyte balance
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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
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Osmolarity• important to maintain water
balance since water can cross most membranes freely
• water balance determines osmolarity
• as osmolarity of ECF (extra cellular fluid) changeswater moves into or out of cells changing intracellular volumes & cell function
• excess water intakeosmolarity decreaseswater moves into cells swell
• Na intake (osmolarity increases) water moves out of cellsshrink
• changes in cell volume impairs cell function
• swelling– may cause ion channels to
open – changing membrane
permeability
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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.
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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
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Regulation of Intake• Intake-governed mostly by
thirst• Dehydration
– reduces blood volume & blood pressure
– raises blood osmolarity• Detected by thirst center
– hypothalamus• salivate lessdry mouth
sense of thirst• ingest water• cools & moistens mouth• rehydrates blood• distends stomachinhibits
thirst
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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
• ADHcollecting ducts synthesize aquaporins (water channels) water can diffuse out of ductwater reabsorbed
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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-
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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
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Sodium Balance• 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
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ADH• NaCl added to body
increased osmolarityADH (vaopressin) secretion & thirst increased
• thirstdrink• osmolarity decreases• ADHkidneys• conserves water by
concentrating urine• increased water
reaborption increases BP• returned to normal with
cardiovascular reflexes
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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 & hyperkalemiaadrenal cortexaldosterone
• Hypotension reninaldosterone secretion
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Aldosterone• 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 increasesNa-K ATPase speeds up transport of Na into ECFnet result-rapid increase of Na reaborption that does not require synthesis of new channels or ATPase proteins
• slower phase of actionnewly made channels & pumps inserted into epithelial cell membranes
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Renin-Angiotensin-Aldosterone• primary signal for
aldosterone release-angiotensin II– component of renin-
angiotensin 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
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Renin-Angiotensin-Aldosterone Path
• Angiotensin IIadrenal cortex aldosteronedistal tubule reabsorbs Na
• ADH secretion is also stimulatedwater 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 excretion- decrease in amount of urine excreted, with lower osmolarity
• Aldosteronemore NaCl reabsorbed in DCT & collecting ductsreduces filtrate osmolarity
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Renin-Angiotensin-Aldosterone• stimuli that begin renin pathway-
related 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 dropsJG cellsrenin release
• paracrine feedback from macula densa cells in distal tubule stimulate renin release
• if fluid flow in distal tubule is highmacula densaNO-nitric oxideinhibits renin release
• GFR or BP lowfluid flow low macula densa cellsNO loweredJG cellsrenin released
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Sodium & Blood Pressure
• Na reaborption does not directly raise blood pressure
• retention helps stimulate fluid intake & volume expansion which increases blood volume& blood pressure
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Angiotensin & Blood Pressure
• Angiotensin II has other effects on blood pressure
• increases it directly & indirectly through 4 pathways
• activates angiotensin II receptors in brainincreases vasopressin secretionfluid retained in kidneys constricts blood vessels
• Angiotensin II serves to stimulate thirstexpands 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 centerincreases sympathetic output to heart & blood vesselsincreases cardio output & vasoconstriction increases blood pressure
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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 Khypokalemiaresting
membrane potential becomes more negative
• increased Khyperkalemiamore K inside celldepolarization
• Hypokalemiamuscle 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 initiallycells unable to repolarize fully
• become less excitableaction potentials smaller than normal may lead to cardiac arrhythmias
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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
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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
• 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• bases accept hydrogen ions
– strong base has strong tendency to bind hydrogen ions
– raises pH• weak base binds less hydrogen
ions – less effect on pH
• HNO2 H+ + NO2
HNO2 H+ + NO2
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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 ventilation-
expel or retaining carbon dioxide
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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
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Carbonic Acid-Bicarbonate Buffer System
• most important extracellular buffer system
• CO2 + H2OH2CO3 H+ + HCO3-__
• add H equation shifts to leftmore
HCO3 made increases CO2 & H2O
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Phosphate Buffer System
• important in buffering ICF & urine
• H2PO4H + HPO4
• H + HPO4 H2PO4
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Protein Buffer System• involves amino acids accepting or
releasing H+
• pH: COOH COO- + H+
• pH: NH2 + H+ NH3 + amino group
accepts H
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Respiratory Compensation
• change in respiratory rate directly affects carbonic acid-HCO3 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 increasespH decreases
• PCO2 decreasespH increases
• excess CO2 ventilation increases to expel more
• low CO2 ventilation is reduced
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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
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Disorders of Acid-Base Balance• Acidosis
– low pHneurons less excitableCNS depressionconfusion & disorientation comadeath
• Alkalosis– high pHneurons hyperexcitable numbness &
tinglingmuscle twitches tetanus
• Acid-base imbalances fall into two categories• Respiratory• Metabolic
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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
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Respiratory Alkalosis• uncommon• usually due to
hyperventilation (plasma PCO2 decreases)
• can be modulated by breathing into paper bag & rebreathing exhaled CO2
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Metabolic Acidosis• due to drop in blood
bicarbonate levels drop– lost due to renal dysfunction– lost through severe diarrhea
• due to accumulation of non-volatile 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 laxatives
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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.
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Compensations for Decreased pH
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Compensations for Increased pH
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