Ch 26


Published on

water, electrolyte, pH balance

Published in: Technology, Business
  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Ch 26

  1. 1. EC questions• What does ICF stand for?• a chemical compound that dissociates into ions in water is called an______.• is sodium concentration higher in the ECF or ICF?• a sensation of thirst causes us to: 1
  2. 2. Describe the major fluidcompartments including intracellular,extracellular, intravascular andinterstitial.
  3. 3. Total body water Volume = 40 L 60% body weight Extracellular fluid (ECF) Volume = 15 L 20% body weightIntracellular fluid (ICF) Interstitial fluid (IF)Volume = 25 L Volume = 12 L40% body weight 80% of ECF Figure 26.1
  4. 4. • Describe the regulation of water intake and output
  5. 5. Regulation of Water Intake• Thirst mechanism is the driving force for water intake• The hypothalamic thirst center osmoreceptors are stimulated by – Plasma osmolality of 2–3% –Angiotensin II or baroreceptor input –Dry mouth –Substantial decrease in blood volume or pressure
  6. 6. Regulation of Water Intake• Drinking water creates inhibition of the thirst center• Inhibitory feedback signals include –Relief of dry mouth –Activation of stomach and intestinal stretch receptors
  7. 7. • Most of the body’s water is1. Intracellular2. Intravascular3. interstitial 7
  8. 8. Regulation of Water Output• Obligatory water losses –Insensible water loss: from lungs, skin, Feces –Minimum daily sensible water loss of 500 ml in urine to excrete wastes• Body water and Na+ content are regulated in tandem by mechanisms that maintain cardiovascular function and blood pressure
  9. 9. Regulation of Water Output: Influence of ADH• Water reabsorption in collecting ducts is proportional to ADH release• ADH dilute urine and volume of body fluids• ADH concentrated urine• Hypothalamic osmoreceptors trigger or inhibit ADH release
  10. 10. • Which of the following would stimulate thirst center osmoreceptors? 1. Plasma osmolality of 2–3% 2. Angiotensin II or baroreceptor input 3. Dry mouth 4. Substantial decrease in blood volume or pressure 5. All of these 10
  11. 11. • Which of the following is an electrolyte? 1. sodium chloride 2. Hydrochloric acid 3. Sodium hydroxide 4. glucose 5. 1,2, and 3 6. All of these 11
  12. 12. • Describe the regulation of the major electrolytes- salts, acids and bases
  13. 13. Central Role of Sodium• Most abundant cation in the ECF• Sodium salts in the ECF contribute 280 mOsm of the total 300 mOsm ECF solute concentration• Na+ leaks into cells and is pumped out against its electrochemical gradient• ECF Na+ concentration remains stable due to osmosis
  14. 14. Central Role of Sodium• Changes in plasma sodium levels affect – Plasma volume, blood pressure – ICF and IF volumes• Renal acid-base control mechanisms are coupled to sodium ion transport• No receptors are known that monitor Na+ levels in body fluids
  15. 15. Regulation of Sodium Balance: Aldosterone• Na+-water balance is linked to blood pressure and blood volume control mechanisms• Na+ reabsorption – 65% is reabsorbed in the proximal tubules – 25% is reclaimed in the loops of Henle• Aldosterone active reabsorption of remaining Na+• Water follows Na+ if ADH is present
  16. 16. Regulation of Sodium Balance: Aldosterone• Renin-angiotensin mechanism is the main trigger for aldosterone release –Granular cells of JGA secrete renin in response to • Sympathetic nervous system stimulation • Filtrate osmolality • Stretch (due to blood pressure)
  17. 17. Regulation of Sodium Balance: Aldosterone• Renin catalyzes the production of angiotensin II, which prompts aldosterone release from the adrenal cortex• Aldosterone release is also triggered by elevated K+ levels in the ECF• Aldosterone brings about its effects slowly (hours to days)
  18. 18. K+ (or Na+) concentration Renin-angiotensin in blood plasma* mechanism Stimulates Adrenal cortex Negative Releases feedback inhibits Aldosterone Targets Kidney tubules Effects Na+ reabsorption K+ secretion Restores Homeostatic plasma levels of Na+ and K+ Figure 26.8
  19. 19. Regulation of Sodium Balance: ANP• Released by atrial cells in response to stretch ( blood pressure)• Effects• Decreases blood pressure and blood volume: – ADH, renin and aldosterone production – Excretion of Na+ and water – Promotes vasodilation directly and also by decreasing production of angiotensin II
  20. 20. Influence of Other Hormones• Estrogens: NaCl reabsorption (like aldosterone) – H2O retention during menstrual cycles and pregnancy• Progesterone: Na+ reabsorption (blocks aldosterone) – Promotes Na+ and H2O loss
  21. 21. • The most abundant cation in the ECF is:1. Sodium2. Potassium3. Calcium4. chloride 21
  22. 22. • Changes in sodium ion concentration effect: 1. Blood Plasma volume 2. blood pressure 3. ICF volume 4. IF volume 5. All of these 22
  23. 23. Cardiovascular System Baroreceptors• Baroreceptors alert the brain of increases in blood volume and pressure – Sympathetic nervous system impulses to the kidneys decline – Afferent arterioles dilate – GFR increases – Na+ and water output increase
  24. 24. Regulation of Potassium Balance• Importance of potassium: – Affects RMP in neurons and muscle cells (especially cardiac muscle) • ECF [K+] RMP depolarization reduced excitability • ECF [K+] hyperpolarization and nonresponsiveness
  25. 25. Regulation of Potassium Balance• H+ shift in and out of cells – Leads to corresponding shifts in K+ in the opposite direction to maintain cation balance – Interferes with activity of excitable cells
  26. 26. Regulation of Potassium Balance• K+ balance is controlled in the cortical collecting ducts by changing the amount of potassium secreted into filtrate• High K+ content of ECF favors tubule cell secretion of K+• When K+ levels are low, cells reabsorb some K+ left in the filtrate
  27. 27. Regulation of Potassium Balance• Influence of aldosterone –Increased K+ in the adrenal cortex causes • Release of aldosterone • Potassium secretion
  28. 28. Regulation of Calcium• Ca2+ in ECF is important for –Neuromuscular excitability –Blood clotting –Cell membrane permeability –Secretory activities
  29. 29. Regulation of Calcium• Hypocalcemia- excitability and muscle tetany• Hypercalcemia- Inhibits neurons and muscle cells, may cause heart arrhythmias• Calcium balance is controlled by parathyroid hormone (PTH) and calcitonin
  30. 30. Influence of PTH• Bones are the largest reservoir for Ca2+ and phosphates• PTH promotes increase in calcium levels by targeting bones, kidneys, and small intestine (indirectly through vitamin D)
  31. 31. Hypocalcemia (low blood Ca2+) stimulates parathyroid glands to release PTH. Rising Ca2+ in blood inhibits PTH release. Bone 1 PTH activates osteoclasts: Ca2+ and PO43S released into blood. 2 PTH increases Kidney Ca 2+ reabsorption in kidney tubules. 3 PTH promotes kidney’s activation of vitamin D, which increases Ca2+ absorption from food. IntestineCa2+ ionsPTH Molecules Bloodstream Figure 16.12
  32. 32. Regulation of Anions• Cl– is the major anion in the ECF – Helps maintain the osmotic pressure of the blood – 99% of Cl– is reabsorbed under normal pH conditions• When acidosis occurs, fewer chloride ions are reabsorbed• Other anions have transport maximums and excesses are excreted in urine
  33. 33. • Which ion moves in and out of cells to maintain cation balance in response to hydrogen ion shifts?1. Sodium2. Potassium3. Calcium4. chloride 33
  34. 34. • Which hormone will increase sodium reabsorption?1. PTH2. ADH3. Aldosterone4. Estrogen5. Progesterone6. 3 and 4 34
  35. 35. • Describe buffer systems and their role in acid/base balance. what is a buffer?
  36. 36. Acid-Base Balance• pH affects all functional proteins and biochemical reactions• Normal pH of body fluids – Arterial blood: pH 7.4 – Venous blood and IF fluid: pH 7.35 – ICF: pH 7.0• Alkalosis or alkalemia: arterial blood pH >7.45• Acidosis or acidemia: arterial pH < 7.35
  37. 37. Acid-Base Balance• Most H+ is produced by metabolism –Lactic acid from anaerobic respiration of glucose –Fatty acids and ketone bodies from fat metabolism –H+ liberated when CO2 is converted to HCO3– in blood
  38. 38. Acid-Base Balance• Concentration of hydrogen ions is regulated sequentially by –Chemical buffer systems: rapid; first line of defense –Brain stem respiratory centers: act within 1–3 min –Renal mechanisms: most potent, but require hours to days to effect pH changes
  39. 39. Acid-Base Balance• Strong acids dissociate completely in water; can dramatically affect pH• Weak acids dissociate partially in water; are efficient at preventing pH changes• Strong bases dissociate easily in water; quickly tie up H+• Weak bases accept H+ more slowly
  40. 40. HCI H2CO3(a) A strong acid such as (b) A weak acid such as HCI dissociates H2CO3 does not completely into its ions. dissociate completely. Figure 26.11
  41. 41. • Something that resists changes in pH is a1. Strong acid2. Electrolyte3. Buffer4. hormone 41
  42. 42. • Which of the following dissociates completely in water?1. Strong acid2. Weak acid3. Weak base4. All of these 42
  43. 43. Bicarbonate Buffer System• Mixture of H2CO3 (weak acid) and salts of HCO3– (e.g., NaHCO3, a weak base)• Buffers ICF and ECF• The only important ECF buffer
  44. 44. Bicarbonate Buffer System• If strong acid is added: – HCO3– ties up H+ and forms H2CO3 • HCl + NaHCO3 H2CO3 + NaCl – pH decreases only slightly, unless all available HCO3– (alkaline reserve) is used up – HCO3– concentration is closely regulated by the kidneys
  45. 45. Bicarbonate Buffer System• If strong base is added – It causes H2CO3 to dissociate and donate H+ – H+ ties up the base (e.g. OH–) • NaOH + H2CO3 NaHCO3 + H2O – pH rises only slightly – H2CO3 supply is almost limitless (from CO2 released by respiration) and is subject to respiratory controls
  46. 46. Phosphate Buffer System• Action is nearly identical to the bicarbonate buffer• Components are sodium salts of: – Dihydrogen phosphate (H2PO4–), a weak acid – Monohydrogen phosphate (HPO42–), a weak base• Effective buffer in urine and ICF, where phosphate concentrations are high
  47. 47. Protein Buffer System• Intracellular proteins are the most plentiful and powerful buffers; plasma proteins are also important• Protein molecules are amphoteric (can function as both a weak acid and a weak base) – When pH rises, organic acid or carboxyl (COOH) groups release H+ – When pH falls, NH2 groups bind H+
  48. 48. • The most important ECF buffer system is:1. bicarbonate2. Phosphate3. Protein4. plasma 48
  49. 49. • The phosphate buffer system functions in:1. ECF2. ICF3. Urine4. 2 and 35. All of these 49
  50. 50. Describe the role of the respiratory system in acid/base balance. Describe the role of the urinary system in acid/base balance.
  51. 51. Physiological Buffer Systems• Respiratory and renal systems – Act more slowly than chemical buffer systems – Have more capacity than chemical buffer systems
  52. 52. Acid-Base Balance• Chemical buffers cannot eliminate excess acids or bases from the body – Lungs eliminate volatile carbonic acid by eliminating CO2 – Kidneys eliminate other fixed metabolic acids (phosphoric, uric, and lactic acids and ketones) and prevent metabolic acidosis
  53. 53. Respiratory Regulation of H+• Respiratory system eliminates CO2• A reversible equilibrium exists in the blood: – CO2 + H2O H2CO3 H+ + HCO3–• During CO2 unloading the reaction shifts to the left (and H+ is incorporated into H2O)• During CO2 loading the reaction shifts to the right (and H+ is buffered by proteins)
  54. 54. 54
  55. 55. Respiratory Regulation of H+• Hypercapnia activates medullary chemoreceptors• Rising plasma H+ activates peripheral chemoreceptors- breathing rate increases –More CO2 is removed from the blood –H+ concentration is reduced –CO2 + H2O H2CO3 H+ + HCO3–
  56. 56. Respiratory Regulation of H+• Alkalosis depresses the respiratory center – Respiratory rate and depth decrease – H+ concentration increases• Respiratory system impairment causes acid- base imbalances – Hypoventilation respiratory acidosis – Hyperventilation respiratory alkalosis – CO2 + H2O H2CO3 H+ + HCO3–
  57. 57. • The advantage of chemical buffer systems is1. They have a very high capacity2. Their effects are long lasting3. Their effects are rapid4. All of these 57
  58. 58. 2/3 of the body’s fluid is located where?1. ECF2. ICF3. IVF4. IF 58
  59. 59. Where is the thirst center?1. mouth2. hypothalamus3. cerebellum4. medulla 59
  60. 60. • What hormone regulates water balance1. Aldosterone2. PTH3. ADH4. Secretin5. aquaporin 60
  61. 61. • What hormone regulates calcium balance1. Aldosterone2. PTH3. ADH4. Secretin5. aquaporin 61
  62. 62. • What hormone regulates sodium balance1. Aldosterone2. PTH3. ADH4. Secretin5. aquaporin 62
  63. 63. • How do the lungs eliminate carbonic acid?1. Excreting it directly2. Eliminating carbon dioxide3. They don’t4. Sending hormones to the kidneys, which cause the kidneys to excrete it 63
  64. 64. • The advantage of physiological buffer systems is1. They have a very high capacity2. Their effects are short term3. Their effects are instantaneous4. All of these 64
  65. 65. • Rising plasma H+ concentration will do what to breathing rate?1. Increase2. Decrease3. Not change 65
  66. 66. Renal Mechanisms of Acid-Base Balance• Most important renal mechanisms –Conserving (reabsorbing) or generating new HCO3– –Excreting HCO3–• Generating or reabsorbing one HCO3– is the same as losing one H+• Excreting one HCO3– is the same as gaining one H+
  67. 67. Renal Mechanisms of Acid-Base Balance• Renal regulation of acid-base balance depends on secretion of H+• H+ secretion occurs in the PCT and in the collecting duct: –The H+ comes from H2CO3 produced in reactions catalyzed by carbonic anhydrase inside the renal tubule cells
  68. 68. Peri- PCT cell tubular capillary 2K+ 2K+ ATPase 3Na+ 3Na+ HCO3– + Na+ Cl– Cl– HCO3– H+ 3a H+ HCO3– 3b HCO3– 2 HCO3– 4 ATPase H2CO3 H2CO3 Na+ Na+ 5 * 1 6 H2O CO2 CO2 + CO2 H2OTight junction 68
  69. 69. Reabsorption of Bicarbonate• Tubule cell luminal membranes are impermeable to HCO3– – CO2 combines with water in PCT cells, forming H2CO3, which dissociates – H+ is secreted, and HCO3– is reabsorbed into capillary blood – Secreted H+ unites with HCO3– to form H2CO3 in filtrate, which generates CO2 and H2O• HCO3– disappears from filtrate at the same rate that it enters the peritubular capillary blood
  70. 70. Peri- PCT cell tubular capillary 2K+ 2K+ ATPase 3Na+ 3Na+ HCO3– + Na+ Cl– Cl– HCO3– H+ 3a H+ HCO3– 3b HCO3– 2 HCO3– 4 ATPase H2CO3 H2CO3 Na+ Na+ 5 * 1 CA 6 H2O CO2 CO2 + CO2 H2OTight junction 70
  71. 71. Bicarbonate Ion Secretion• When the body is in alkalosis, renal tubule cells – Secrete HCO3– – Reclaim H+ and acidify the blood
  72. 72. Abnormalities of Acid-Base Balance• Respiratory acidosis and alkalosis• Metabolic acidosis and alkalosis
  73. 73. Respiratory Acidosis and AlkalosisThe most important indicator of respiratoryfunction is PCO2 level (normally 35–45 mm Hg) – PCO2 above 45 mm Hg respiratory acidosis • Most common cause of acid-base imbalances • Due to decrease in ventilation or gas exchange • Characterized by falling blood pH and rising PCO2
  74. 74. Respiratory Acidosis and Alkalosis• PCO2 below 35 mm Hg respiratory alkalosis –A common result of hyperventilation due to stress or pain
  75. 75. Metabolic Acidosis and Alkalosis• Any pH imbalance not caused by abnormal blood CO2 levels• Indicated by abnormal HCO3– levels
  76. 76. Metabolic Acidosis and Alkalosis• Causes of metabolic acidosis –Ingestion of too much alcohol ( acetic acid) –Excessive loss of HCO3– (e.g., persistent diarrhea) –Accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure
  77. 77. Metabolic Acidosis and Alkalosis• Metabolic alkalosis is much less common than metabolic acidosis –Indicated by rising blood pH and HCO3– –Caused by vomiting of the acid contents of the stomach or by intake of excess base (e.g., antacids)
  78. 78. Effects of Acidosis and Alkalosis• Blood pH below 7 depression of CNS coma death• Blood pH above 7.8 excitation of nervous system muscle tetany, extreme nervousness, convulsions, respiratory arrest death
  79. 79. Respiratory and Renal Compensations• If acid-base imbalance is due to malfunction of a physiological buffer system, the other one compensates –Respiratory system attempts to correct metabolic acid-base imbalances –Kidneys attempt to correct respiratory acid-base imbalances
  80. 80. Respiratory CompensationIn metabolic acidosis –Blood pH is below 7.35 and HCO3– level is low –High H+ levels stimulate the respiratory centers –Rate and depth of breathing are increased –As CO2 is eliminated by the respiratory system, PCO2 falls below normal
  81. 81. Respiratory Compensation• Respiratory compensation for metabolic alkalosis is revealed by: –Slow, shallow breathing, allowing CO2 accumulation in the blood –High pH (over 7.45) and elevated HCO3– levels
  82. 82. Renal Compensation• Hypoventilation causes elevated PCO2• (respiratory acidosis) –Renal compensation is indicated by high HCO3– levels• Respiratory alkalosis exhibits low PCO2 and high pH –Renal compensation is indicated by decreasing HCO3– levels
  83. 83. • The respiratory system compensates for metabolic acidosis by1. Increasing breathing rate2. Decreasing breathing rateCO2 + H2O H2CO3 H+ + HCO3– 83
  84. 84. • The renal system compensates for respiratory acidosis by1. absorbing or generating bicarbonate2. Secreting more bicarbonateCO2 + H2O H2CO3 H+ + HCO3– 84