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Fluid and Electrolyte Balance

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Fluid and Electrolyte Balance Powered By Docstoc
					Fluid and Electrolyte Balance



    Dr. Jena Hamra
                 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
                Water Balance
 Input = Output
 Water loss
     Urine, feces, sweat, lungs
   Water gain
     Drink, food, IV fluids
   Water conservation
     Kidneys
         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
         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
                 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
       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 don’t
         fire  no release
    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
                 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
              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
               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
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
     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
     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
       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
      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
          Potassium Balance
   Hyperkalemia
     Decreases concentration gradient across
      membranes  Depolarization
   Hypokalemia
     Increase concentration gradient 
      Hyperpolarization
   Increased potassium
     Aldosterone secretion  K+ secretion
       Behavioral Mechanisms
   Drinking water
     Replaces fluid loss
     Hypothalamic osmoreceptors (> 280 mOsm)
          Oropharynx receptors
   Eating salt
     Low plasma Na+  stimulates craving for salt
     Hypothalamic salt appetite center
   Avoidance behaviors
           Integrated Control
 Osmolarity and ECF volume can change
  independently
 Each has 3 possible states
     Normal
     Increased
     Decreased
              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
               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
                 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
    Compensatory Mechanisms
 Cardiovascular response
 Angiotensin II
 Vasopressin
 Thirst
 Net result
     Restoration of blood volume
     Maintenance of blood pressure
     Restoration of normal osmolarity
           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
           Acid-Base Sources
   Acid input
     Organic acids
        Metabolic intermediates, foods
     Lactic acidosis
     CO2 and aerobic respiration
        HCO3 and H
                      +

   Base input
     Few significant sources
             PH Homeostasis
   Controlled by:
     Buffers
     Ventilation
     Renal regulation
   Buffer systems
     Intracellular buffers
        Proteins, phosphate ions, hemoglobin
     Extracellular buffers
        Bicarbonate ion
             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
               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+
            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
             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
            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+
             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
      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
        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

				
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posted:4/6/2013
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