Fluid and Electrolyte Balance

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Fluid and Electrolyte Balance

• Dr. Jena Hamra

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Homeostasis

• Body maintains balance of water and ions
• Loss Urine, feces, lungs, sweat
• Intake Drink, eat
• Osmolarity
• Decreases Cells swell
• Increases Cells shrink
• Integration of multiple systems
• Respiratory, cardiovascular
• Kidney

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Water Balance

• Input Output
• Water loss
• Urine, feces, sweat, lungs
• Water gain
• Drink, food, IV fluids
• Water conservation
• Kidneys

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Urine Concentration

• Kidneys can concentrate urine
• Without allowing osmotic water response
• Loop of Henle
• Urine becomes hyposmotic
• Cells in ascending loop impermeable to water
• Collecting duct
• Urine concentration determined by tubule
  permeability to water
• Impermeable Dilute urine
• Permeable Concentrated urine

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Vasopression (ADH)

• Causes collecting duct to insert water pores in
  apical membrane
• Water leaves by osmosis
• Concentrated urine
• No vasopressin
• Collecting duct impermeable to water
• Dilute urine

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Vasopressin

• Aquaporin
• Water channel regulated by vasopressin
• Found in
• Apical membrane of collecting duct
• Cytoplasmic vesicles
• Vasopressin
• Binds to receptors on basolateral membrane
• Activates G-protein/cAMP
• Causes aquaporin vesicles to move to apical
  membrane and fuse with it

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Vasopressin Secretion

• Stimuli for secretion
• Blood pressure and volume
• Volume decreases ?Atrial stretch receptors
  ?vasopressin release ?water conserved
• Pressure decreases ? Carotid, aortic
  baroreceptors ? vasopressin release
• ECF osmolarity!
• Osmoreceptors in hypothalamus
• Above 280 mOsm ? osmoreceptors fire ?vasopressin
  release
• Below 280 mOsm ? osmoreceptors dont fire ? no
  release

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Loop of Henle Countercurrent Exchange System

• High osmolarity of medullary intersititium
• Countercurrent exchange system
• Descending loop of Henle
• Permeable to water, not ions
• Ascending loop of Henle
• Permeable to ions, not water
• Transfer of solutes into ECF by ascending limb
  creates osmotic gradient for water movement in
  descending limb

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Vasa Recta

• Peritubular capillaries
• Pass into renal medulla
• Flow opposite tubule flow
• Descending vasa recta
• Solutes enter, water leaves
• Ascending vasa recta
• Water enters to dilute
• Urea
• Increases osmolarity in medullary interstitium

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Sodium Balance

• Main ECF solute
• Regulation through renin-angiotensin-aldosterone
  system (RAAS)
• Aldosterone
• Regulates sodium reabsorption in distal tubule
• Also causes potassium secretion
• Synthesized in adrenal cortex
• Acts on principal cells
• Distal tubule and collecting duct

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Principal Cells

• Na-K ATPase pumps on basolateral side
• Channels and transporters on apical side
• Na, K leak channels
• Aldosterone
• Fast response
• Apical Na channels increase open time
• Na-K ATPase pump speeds up
• Slow response
• Diffuses in, binds to cytoplasmic receptors
• Directs synthesis of new protein channels and
  Na-K ATPase pumps

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Control of Aldosterone Secretion

• Potassium concentration
• Increased K Acts on adrenal cortex ? stimulates
  aldosterone secretion
• Increased osmolarity Acts on adrenal cortex ?
  inhibits aldosterone secretion
• Indirect stimuli
• Angiotensin II
• Decreased blood pressure
• Decreased GFR

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Renin-Angiotenisn-Aldosterone Pathway

• Angiotensin II (ANGII)
• Primary control of aldosterone release
• Pathway
• JG cells secrete renin
• Renin converts angiotensin to angiotensin I
• Converted to angiotensin II by ACE
• Lungs, blood vessel endothelium
• ANGII stimulates aldosterone release by adrenal
  cortex

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Stimuli for RAAS Pathway

• Low renal arteriole pressure
• JG cells secrete renin
• Low blood pressure
• Sympathetic neurons stimulate renin secretion
• Low distal tubule flow
• Macula densa secretes paracrines
• Signals JG cells
• High flow ? NO release ? Inhibits renin release

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Angiotensin and Blood Pressure

• Activation of brain ANGII receptors
• Vasopressin secretion
• Increased water reabsorption
• Stimulates thirst
• Vasoconstrictor
• Increases blood pressure
• ANGII receptors in CVCC
• Sympathetic output to heart and blood vessels

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Atrial Natriuretic Peptide

• Released by atrial myocardial cells
• Response to stretch
• Causes sodium and water excretion
• Increases GFR
• More surface area
• Decreases sodium and water reabsorption in
  collecting duct
• Inhibits renin, aldosterone and vasopressin
  release
• Affects CVCC ? Lower BP

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Potassium Balance

• Hyperkalemia
• Decreases concentration gradient across membranes
  ? Depolarization
• Hypokalemia
• Increase concentration gradient ?
  Hyperpolarization
• Increased potassium
• Aldosterone secretion ? K secretion

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Behavioral Mechanisms

• Drinking water
• Replaces fluid loss
• Hypothalamic osmoreceptors (gt 280 mOsm)
• Oropharynx receptors
• Eating salt
• Low plasma Na ? stimulates craving for salt
• Hypothalamic salt appetite center
• Avoidance behaviors

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Integrated Control

• Osmolarity and ECF volume can change
  independently
• Each has 3 possible states
• Normal
• Increased
• Decreased

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Compensation

• Increased volume, increased osmolarity
• Excrete hypertonic urine
• Increased volume, unchanged osmolarity
• Excrete isotonic urine equal in volume
• Increased volume, decreased osmolarity
• Excrete dilute urine
• Normal volume, decreased osmolarity
• Conserve solutes, ingest more solutes

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Compensation

• Decreased volume, increased osmolarity
• Thirst, fluid ingestion
• Decreased volume, no osmolarity changes
• Blood transfusion, isotonic fluid replacement
• Decreased volume, decreased osmolarity
• Uncommon
• Table 20-2

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Dehydration

• Decreased volume, increased osmolarity
• Adrenal cortex
• Secrete and not secrete aldosterone
• Fix osmolarity first!
• Baroreceptors
• Decrease firing
• ? PSNS, ? SNS output ? ? blood pressure
• ? HR, CO, vasoconstriction, ? GFR ? ? renin
• Renin secretion
• SNS stimulation
• ? BP, ? GFR
• Thirst, vasoconstriction, ? vasopressin

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Compensatory Mechanisms

• Cardiovascular response
• Angiotensin II
• Vasopressin
• Thirst
• Net result
• Restoration of blood volume
• Maintenance of blood pressure
• Restoration of normal osmolarity

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Acid-Base Balance

• pH homeostasis
• Closely regulated
• Proteins sensitive
• Enzymes, membrane channels, nervous system
• Acidosis Decreased neuron excitability
• Alkalosis Neuron hyperexcitability
• Regulation linked to K balance
• K-H-ATPase antiporter

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Acid-Base Sources

• Acid input
• Organic acids
• Metabolic intermediates, foods
• Lactic acidosis
• CO2 and aerobic respiration
• HCO3 and H
• Base input
• Few significant sources

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PH Homeostasis

• Controlled by
• Buffers
• Ventilation
• Renal regulation
• Buffer systems
• Intracellular buffers
• Proteins, phosphate ions, hemoglobin
• Extracellular buffers
• Bicarbonate ion

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Ventilation

• PCO2 reflects CO2 content of blood
• Changes in PCO2 alters H and HCO3
• Hyperventilation ? CO2 ? ? H and HCO3
• Hypoventilation ? CO2 ? ? H and HCO3
• Control of ventilation
• Carotid, aortic chemoreceptors H
• Central chemoreceptors PCO2

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Renal Regulation

• Direct
• Retaining or excreting H
• Indirect
• Reabsorption or excreting HCO3
• Acidosis
• Kidney secretes H into proximal and distal
  tubules
• Ammonia and phosphate buffers in urine
• HCO3 reabsorbed
• Alkalosis
• Kidney secretes HCO3, reabsorbs H

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Renal Regulation

• Cellular mechanisms
• Apical Na-H antiporter
• Indirect active transporter
• Basolateral Na-HCO3 symporter
• Indirect active transporter
• H-ATPase
• Secretes H against concentration gradient
• H-K-ATPase
• H into urine, K reabsorbed
• Na-NH4-ATPase

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Proximal Tubule

• Most HCO3 reabsorbed here
• 2 pathways
• Secretion of H into tubule (Na-H antiport)
• Combines with filtered HCO3 ? CO2
• CO2 diffuses into proximal cell and dissociates
  to H and HCO3
• H secreted and HCO3 transporter out by HCO3-Na
  symporter

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Proximal Tubule

• Glutamine pathway
• Glutamine loses 2 amino groups
• Become ammonia
• Buffers H ? NH4
• NH4 transported into lumen in exchange for Na
• a-ketoglutarate metabolized to HCO3
• Transported into blood with Na

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Distal Nephron

• Fine regulation of acid-base balance
• Intercalated cells
• Between principal cells
• Type A Acidosis secrete H, reabsorb HCO3
• H-ATPase, H-K-ATPase
• HCO3-Cl- antiporter
• Type B Alkalosis secrete HCO3, reabsorb H
• Same transporters, opposite polarity
• Carbonic anhydrase
• Potassium balance

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Acid-Base Disturbances

• Respiratory Acidosis
• Ventilation inadequate to remove CO2
• ? plasma pH, ? HCO3
• Compensation Renal ONLY
• Secrete H, Reabsorb HCO3
• Metabolic Acidosis
• Dietary and metabolic acid input exceeds acid
  excretion
• ? HCO3
• Compenstion
• Renal Excrete H, Reabsorb HCO3
• Respiratory Increase ventilation

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Acid-Base Disturbances

• Respiratory Alkalosis
• Increased alveolar ventilation without increase
  in CO2
• ? HCO3 and ? pH
• Compensation
• Renal ONLY HCO3 excreted and secreted, H
  reabsorbed
• Metabolic Alkalosis
• Acid excretion exceeds acid input
• ? HCO3
• Compensation
• Respiratory Decreased ventilation
• Renal HCO3 excreted, H reabsorbed