Ch 20 Integrative Physiology II Fluid & Electrolyte Balance
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Transcript of Ch 20 Integrative Physiology II Fluid & Electrolyte Balance
Ch 20 Integrative Physiology II
Fluid & Electrolyte Balance
Explain homeostasis ofExplain homeostasis of
1.1. Water Balance Water Balance (ECF/ICF volumes)(ECF/ICF volumes)
2. Electrolyte Balance (osmolarity),
3. Acid-Base Balance (pH)
ObjectivesObjectives
Kidneys maintain H2O balance by regulating urine concentration
• Daily H2O intake balanced by H2O excretion
• Kidneys react to changes in osmolarity, volume, and blood pressure
Fig 20-1
CD AnimationUrinary System: Early Filtrate Processing
Fig 20-2
H2O excretion in kidneys controlled
primarily by vasopressin
(= antidiuretic hormone = ADH)
Fast response !
ADH
Fig 20-1
Nephron Recycling: Overview
At beginning of LOH: ~ 65 % of H2O & solutes are reabsorbed (filtrate isosmotic with IF)
Urine concentration can vary between 50 – 1200 mOsM How does Nephron
Establish Urine Concentration ?
Urine ConcentrationEstablished by LOH and CD
reabsorption of varying amounts of H2O and Na+
Key player: ADH (= Vasopressin)
Fig 20-4
Fig 20-4
ADH - Vasopressin Released from? when?
Controls water permeability of last section of DCT and all of CD
Regulates AQP2 channel
2nd messenger mechanism transduces ADH signal to cell interior Insertion of water pores in apical membrane
Fig 20-6
ADH MechanismADH Mechanism
Fig 20-6
Regulation of ADHADH release regulated via 1. ECF osmolarity 2. Blood pressure and volume
Diabetes insipidus – central vs. nephrogenic
Nocturnal enuresis
Fig 20-7
ADH RegulationADH Regulation
Fig 20-7
Concentrated vs. Dilute UrineIn presence of ADH:
Insertion of H2O pores
At maximal H2O permeability: Net H2O movement stops at equilibrium
Maximum osmolarity of urine?
No ADH:DCT & CD
impermeable to H2O
Osmolarity can plunge to ~ 50 mOsm
Review:
Fig 20-5
Fig 20-5 ADH No ADH
LOH:Countercurrent
Multiplier
leads to
Hyperosmotic IF in medulla
Hyposmotic fluid leaving LOH
Na+ Balance and ECF Volume• [Na+] affects plasma & ECF osmolarity (Normal [Na+]ECF
~ 140 mosmol)
• [Na+] affects blood pressure & ECF volume (?)
Aldosterone regulates Na+ (and K+) excretion in last 1/3 of DCT and CD– Type of hormone? Where produced? Type of mechanism?
– Aldosterone secretion Na+ absorption
Fig 20-13
Aldosterone MechanismAldosterone Mechanism
Na+/K+ ATPase activity K+ secretion
Here (unlike normally) H2O does not necessarily follow Na+ absorption. This only happens in presence of . . .
Fig 20-13
Acid–Base Balance• Normal blood pH ?
• Enzymes & NS very sensitive to pH changes
• Kidneys have K+/H+ antiporter
• Importance of hyperkalemia and hypokalemia
• Acidosis vs. alkalosis
Fig 20-19
AcidosisRespiratory acidosis due to alveolar
hypoventilation (accumulation of CO2)Possible causes: Respiratory depression, increased
airway resistance (?), impaired gas exchange (emphysema, fibrosis, muscular dystrophy, pneumonia)
Metabolic acidosis due to gain of fixed acid or loss of bicarbonate
Possible causes: lactic acidosis, ketoacidosis, diarrhea
Buffer capabilities exceeded once pH change appears in plasma. Options for compensation?
Body deals with pH changes by 3 mechanisms
Buffers 1st defense, immediate response
Ventilation 2nd line of defense, can handle ~ 75% of most pH disturbances
Renal regulation of H+ & HCO3-
final defense, slow but very effectiveFig 20-21
Renal Compensation for AcidosisRenal Compensation for Acidosis
Fig 20-21
Alkalosis much rarer
Respiratory alkalosis due to alveolar hyperventilation in the absence of increased metabolic CO2 production
Possible causes: Anxiety with hysterical hyperventilation, excessive artificial ventilation, aspirin toxicity, fever, high altitude
Compensation?
Metabolic alkalosis due to loss of H+ ions or shift of H+ into the intracellular space.
Possible causes: Vomiting or nasogastric (NG) suction; antacid overdose
Compensation?
Buffer capabilities exceeded once pH change appears in plasma.