Chapter 20 Fluid Balance

Chapter 20 Fluid Balance - Ch 20: Integrative Physiology II...

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Unformatted text preview: Ch 20: Integrative Physiology II Ch Fluid & Electrolyte Balance Objectives Explain homeostasis (remember Explain homeodynamics) of homeodynamics) 1. 1. Water Balance (ECF/ICF volumes) (ECF/ICF Water 2. Electrolyte Balance (Na+ and K+) 3. Acid-Base Balance (pH) Fig 20-18 Introduction to Fluid and Electrolyte Balance Balance • Intake must = Exhaust – Water, ‘lytes – ECF or ICF – O2 and CO2 • Many systems involved – Kidneys most important • BP Plays a role • Hydrostatic and osmotic Hydrostatic gradients gradients Kidneys maintain H2O balance by Kidneys balance regulating urine concentration regulating Fig 20-2 • Daily H2O intake balanced intake by H2O excretion (ins by excretion and outs) and • Kidneys react to changes Kidneys in osmolarity, volume, and blood pressure and Fig 20-1 Urine Concentration Urine Concentration Established by LOH, CD and Established vasa recta → reabsorption of varying amounts of H2O of and Na+ and Key player: ADH (= ADH Vasopressin) Vasopressin) Urine concentration, cont’d Urine • Often expressed in osmolarity Often mM/L or osmolality mM/kg mM/L – Blood: 300 mOsm – Filtrate in Bowman’s Capsule: Filtrate 300 mOsm – Bottom of LOH: 1200 mOsm – Urine: 50-1200 mOsm • Regulated by ADH Regulated (vasopressin) (vasopressin) – Osmoreceptors in Osmoreceptors hypothalamus hypothalamus – BP and blood volume, too Fig. 20-4 Effect of ADH Effect • Controls Urine concentration Controls via regulation of water reabsorption from the filtrate in the collecting duct in • Osmoreceptors in Osmoreceptors hypothalamus hypothalamus • ↑ADH caused by: – ↑Na+ and/or osmolality in the ECF ECF – H2O deprivation – ↓ renal blood flow renal Fig 20-5 Hi [ADH] Lo [ADH] Effect of ADH, cont’d Effect •ADH Receptors in CD cells •Luminal CM is generally impermeable to H2O •Aquaporins (remember Ch. 5) on cell membranes of CD are variably active, dependent on ADH •“Membrane Recycling” via exocytosis of AQP2 •Allows osmosis of H2O into vasa recta Troubles with ADH? Troubles ADH deficiency: •Diabetes insipidus •Central •Nephrogenic •Nocturnal enuresis ADH Excess: •AKA Inappropriate ADH secretion •XS H2O retention Review: Concentrated vs. Dilute Urine Concentrated In presence of ADH: Insertion of H2O pores Insertion pores into tubular luminal CM into At maximal H2O permeability: Net H2O permeability: movement stops at equilibrium equilibrium Maximum osmolarity of Maximum urine up to 1200 mOsm urine No ADH: DCT & CD DCT impermeable to H2O Osmolarity can Osmolarity plunge to ~ 50 mOsm mOsm Countercurrent Exchange Countercurrent • For temperature For exchange: exchange: – Pampiniform plexus: Pampiniform testicular A. and V are in close proximity close • For solute exchange, a For countercurrent multiplier countercurrent – LOH and vasa recta are in LOH close proximity close Fig. 20-9 LOH: Countercurrent Countercurrent Multiplier Multiplier leads to leads Hyperosmotic IF in medulla in Hyposmotic fluid Hyposmotic leaving LOH leaving Regulation of BP: Regulation Na+ Balance and ECF Volume • [Na+] affects plasma & ECF osmolarity affects – (Normal [Na+]ECF ~ 140 Mosm) • [Na+] affects blood pressure & ECF volume – [ ] Gradients • Aldosterone stimulates Na+ reabsorption and K+ reabsorption excretion in last 1/3 of DCT and CD – Type of hormone? Where produced? Type of mechanism? ↑ Aldosterone secretion ⇒ ↑ Na+ absorption from DCT – Secretion of aldosterone by two mechanisms ∀ ↑ K+ in ECF • ↓ BP BP – The signal to release aldosterone is via angiotensin II The angiotensin • Opposite of Aldosterone? – ANP (from the atria) causes loss of Na+ Fig 20-13 Fig 20-13 Aldosterone Mechanism Aldosterone Here (unlike normally) H2O does not necessarily follow Na+ absorption. This only happens in presence of . . . Na+/K+ ATPase activity ↑ ⇒ K+ secretion ↑ Regulation of BP: Regulation RAAS Pathways • • RAAS = renin-angiotensinaldosterone system JG cells release renin in JG response to ↓ BP BP – Renin converts Renin Angiotensinogen to Angiotensin I Angiotensin – ANG I converted to ANG II by ANG ACE ACE RAAS Pathways, cont’d RAAS ANG II causes ↑ BP via ↑ ADH Secretion ADH Thirst Vasoconstriction Sympathetic stimulation of heart ⇒ Sympathetic ↑ HR and CO HR ACE inhibitors will ↓ BP ACE BP Potassium Potassium • Recall that Recall – 2% of K+ is in ECF – Major contributor to resting membrane potential • Hypokalemia – MP more negative (weakness) • Hyperkalemia – MP more positive (poor AP and cardiac MP arrhythmias arrhythmias Maintaining the Balance Maintaining • Behavioral – Thirst – Salty foods – Avoidance behaviors • Osmolarity – Alsosterone Alsosterone – ADH Fig 20-18 Acid–Base Balance Acid–Base • Normal blood pH ? – ↑ pH = Alkalosis pH – ↓ pH = Acidosis pH • Enzymes & NS very sensitive to pH changes • [H+] is the same in ECF and ICF is – – • Kidneys have K+/H+ antiport Importance of hyperkalemia and Importance hypokalemia hypokalemia CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3– • pH can be altered by respiration Renal Compensation – H+ excretion, e.g., NH3 + H+ ⇌ NH4+ excretion, – 2HPO42- + H+ ⇌ HPO4HPO Fig 20-21 Body deals with pH changes by 3 mechanisms mechanisms CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3NH3 + H+ ⇌ NH4+ HPO42- + H+ ⇌ HPO4Buffers 1st defense, immediate response response Ventilation 2nd line of defense, can handle ~ 75% of most pH disturbances most Renal regulation of H+ & HCO3final defense, slow but very effective very Fig 20-21 Acidosis Acidosis Respiratory acidosis due to alveolar hypoventilation (accumulation of CO2) (accumulation Possible causes: Respiratory depression, increased Possible airway resistance (?), impaired gas exchange (emphysema, fibrosis, muscular dystrophy, pneumonia) pneumonia) Metabolic acidosis due to gain of fixed acid or loss of bicarbonate Possible causes: lactic acidosis, ketoacidosis, diarrhea Possible Buffer capabilities exceeded once pH change appears in Buffer plasma. Options for compensation? Options Alkalosis Alkalosis Respiratory alkalosis due to alveolar hyperventilation (excessive loss of CO2) (excessive Possible causes: Anxiety, excessive artificial ventilation, aspirin toxicosis, fever, high altitude aspirin Metabolic alkalosis due to loss of H+ ions or shift of H+ into the intracellular space. Alkali administration. Possible causes: Vomiting or nasogastric (NG) suction; hypokalemia; antacid overdose hypokalemia; Buffer capabilities exceeded once pH change appears in plasma. Buffer Options for compensation? Options ...
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This note was uploaded on 12/24/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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