Renal 2

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  1. What 2 factors control body water concentration?
    fluid intake and renal excretion
  2. What is the range of urine osmolarity that the kidneys can excrete?
    50 mosm / L (very dilute) to 1400 mosm / L (very concentrated)
  3. What is the purpose of excreting a dilute urine?
    Get rid of excess water (body fluid osmolarity is reduced)
  4. What is the purpose of excreting a concentrated urine?
    Conserve water (body fluid osmolarity is increased)
  5. There is a decrease in what hormone when ECF concentration is low (excess body water in relation to solutes)?
    • ADH production and secretion (by post pit) is decreased
    • This causes decreased permeability of the DT and CT to water (water is not reabsorbed)
    • Water is then excreted
  6. Where are the osmoreceptors that control ADH secretion located?
    Hypothalamus
  7. When ADH secretion is decrease, what happens to cause decreased water reabsorption?
    Decreased number of aquaporins in the DT and CT, this causes water to NOT be reabsorbed, but secreted
  8. Explain how a dilute urine is created (differences in tubular reabsorption in the different tubules)
    • Tubular fluid remains isosmotic in PCT (solute and water reabsorbed equally)
    • Tubular fluid becomes concentrated (water is reabsorbed) in the desc LoH (in the medulla)
    • Tubular fluid becomes dilute in the asc LoH as solutes (Na, K, Cl) are reabsorbed, this portion is impermeable to water, so dilution occurs
    • More dilution occurs in the DT and CT (solutes reabsorbed, water is NOT reabsorbed)
  9. In the distal and collecting tubules, what affects water reabsorption?
    ADH
  10. T or F, the ascending LoH is very permeable to water due to the effect of ADH
    • F, this area is NOT affected by ADH levels
    • Even in the presence of high ADH levels, the ascending LoH is impermeable to water
  11. What is the stimulus for excreting a concentrating urine?
    Increased plasma ECF
  12. Obligatory urine volume
    • The minimum amount of urine that must be excreted to get rid of waste products from metabolism
    • For a 70 kg pt, 600 mosm of waste must be excreted
    • Max urine concentration is 1200 mosm/ L
    • 600/ 1200- 0.5 L / day
    • This is where min UO of 20-30 ml / hr is derived from
  13. What 2 factors allow us to produce a concentrated urine?
    • #1- Hyperosmolar medullary interstitial fluid (provides an osmotic gradient to allow water reabsorption)
    • #2- High levels of ADH (increase in # of aquaporins to allow increased reabsorption)
  14. What are the vasarecta?
    • Blood vessels to the LoH
    • Part of the peritubular capillaries
  15. What solutes are key contributors to a hyperosmolar medullary interstitial gradient?
    • Na Cl
    • Urea
  16. What is the only part of the LoH that's permeable to water?
    Descending limb
  17. In the thick ascending LoH, what solutes get reabsorbed (back into blood) and what get excreted?
    • Reabsorbed- Na, Cl, K, Ca, bicarb, Mg
    • Excreted- H
  18. What factors contribute to the build up of solute in the renal medulla to create a hyperosmolar medullary interstitial gradient?
    • Active transport of Na out of LoH and into medullary interstitial
    • Co-transport of K, Cl, and other ions with Na
    • Facilitated diffusion of urea into medullary interstitial
    • Limited diffusion of water from tubules into medullary interstitium
  19. Countercurrent mechamism
    process that allows creation of  hyperosmolar medullary interstitial gradient
  20. What is the driving force behind counter current mechanism?
    Osmolarity
  21. Explain the main activities occurring in counter current mechanism
    • Active pump in thick ascending LoH moves Na and Cl into medullary ISF (increased osm in ISF)
    • To balance this out, water moves out of desc LoH into medullary ISF
    • Solutes keep getting reabsorbed and tubular fluid gets more concentrated, and this process gets repeated
    • Concentration gradient established by active transport gets multiplied
    • Urine gets very concentrated as water gets reabsorbed to dilute medullary ISF
  22. ADH causes water to be reabsorbed, does it get reabsorbed in the medullary or cortical ISF?  Why?
    Water gets reabsorbed into the cortical ISF, if it got reabsorbed into the medullary ISF it would dilute it and counteract the hyperosmolar gradient (that serves to allow urine concentration)
  23. When a substance is reabsorbed, where is it going?
    Back into the blood
  24. What is the only part of the LoH that allows water reabsorption?
    Descending
  25. What percent of the hyperosmolar medullary interstitial gradient is urea?
    • 40-50%
    • 500-600 mosm / L
  26. Is urea passively or actively reabsorbed from the tubules?
    Passively
  27. What is the significance of urea ?
    • Urea cycles through the tubules multiple times before excretion
    • Urea contributes to the hyperosmolar medullary interstitial gradient (water gets reabsorbed from the collecting ducts and urea is concentrated, this allows facilitated diffusion to move urea from tubules into medullary ISF)
  28. Where does urea reabsorption occur?
    medullary collecting duct
  29. What happens after urea is reabsorbed into the medullary collecting ducts?
    • Contributes to hyperosmolar medullary interstitial gradient
    • Urea then diffuses into thin LoH and passes again thru the distal tubules
    • Process repeats a few times, until urea is finally excreted
  30. What 2 features of the renal medially blood flow contribute to preservation of hyperosmolarity?
    • 1) Low blood flow, < 5% of total renal BF, this minimizes solute loss from medullary interstitium
    • 2) Vasarecta serve as countercurrent exchanges, this minimizes washout of solutes
  31. T or F, the purpose of countercurrent exchange with VR is not to create hyperosm state in medullary interstitium but rather to prevent it from being dissipated?
    T
  32. How does the VR help to maintain medullary hyper osmotic state?
    • Desc LoH:
    • Solute leaves medullary ISF and goes into VR
    • Water goes from blood (VR) into medullary ISF
    • Asc LoH:
    • Solutes leave VR and go into medullary ISF
    • Water leaves medullary ISF and enters medulla
    • Both things make the blood less concentrated and the tubular fluid more concentrated
  33. What stimulates ADH secretion?
    Plasma osm, BP and BV (both mediated by baroreceptors, N/V, hypoxia, medications (morphine)
  34. What's an easy way to estimate plasma osm?
    Na x 2.1
  35. What happens to ADH secretion if plasma osm is increased?
    Increase in ADH secretion and insertion of aquaporins (to increase water reabsorption in DT and CD)
  36. Quantitatively, which has more of an effect on blood volume- blood volume or plasma osm?
    Plasma osm- a 1% increase stimulates ADH release vs. a 10% decrease in blood volume
  37. Is most K ICF or ECF?
    ICF
  38. Normal K concentration in the plasma?
    4 meq/L
  39. What factors will cause K to move from ECF to ICF?
    • Insulin (occurs after a meal)
    • Aldosterone
    • Catecholamines (beta 2 mechanism)
    • Metabolic alkalosis
  40. What factors will cause K to move from ICF to ECF?
    Metabolic acidosis, exercise, cell lysis, increased ECF osmolarity (causes cellular dehydration, water moves out of the cell, so does K)
  41. Why is a diabetic pt at particular risk for hyperkalemia?
    Impaired insulin release (insulin causes K to move into the cell), K levels are increased after a meal
  42. What % of K gets reabsorbed in the PCT?
    65%
  43. Where does the majority of K secretion (into tubular fluid) occur?
    principle cells of the DT and CCT
  44. What are the principle cells?
    • Special tubular epithelial cells 
    • Make up 90% of the tubular epithelial cells in the DT and CCT
  45. How do the principle cells of the DT and CCT secrete K?
    • 1) uptake of K into principle cells (Na/K/ATPase pump)
    • 2) passive diffusion of K from principle cell to tubular fluid (principle cells have unique channels that allow K diffusion into tubular fluid)
  46. What is the major stimulant for K secretion by the DT and CCT?
    Plasma K level
  47. T or F, an increase in plasma K will stimulate aldosterone secretion, that will in term cause K secretion?
    T
  48. Renal K excretion is determined by the sum of….?
    • Rate of K filtration (GFR x plasma K concentration)
    • minus rate of tubular reabsorption

    Plus rate of tubular secretion
  49. What does PTH do?
    • Increases plasma Ca levels by bone resorption and vitamin D activation
    • Also causes increased Ca reabsorption by the tubules and decreased Phos absorption
  50. What does calcitonin do?  Where is it released from?
    • Decreases plasma Ca levels
    • Thyroid
  51. Normal ionized Ca level
    2.4 meq/L
  52. What form of Ca can be filtered by the kidneys?
    The ionized as the rest is complexed to anions or protein bound
  53. What % of filtered Ca gets reabsorbed?  Where does most of the reabsorption occur?
    • 99%
    • PCT
  54. In what 3 locations in the tubules does Ca reabsorption occur?  What controls the reabsorption at each site?
    • PCT- 65%- volume status
    • LoH- 25-30%- PTH
    • DT and CT- 4-9%- PTH
  55. How does plasma phos level affect Ca levels?
    • Increased plasma Phos causes an increase in PTH
    • Ca reabsorption is increased
    • Ca excretion is decreased
  56. What effect will metabolic acidosis have on Ca reabsorption?
    • Increased reabsorption
    • Met alkalosis will do the opposite
  57. What factors cause decreased Ca excretion?
    Decreased ECF volume, decr blood volume, incr PTH, metabolic acidosis, incr Phos, vitamin D
  58. What effect does SNS stimulation have on the kidneys?
    • VC of renal arterioles
    • Decr GFR
    • Incr tubular reabsorption on Na
    • Increased renin release
    • Aldosterone and angio 2 release
  59. Aldosterone escape
    Increase in aldosterone causes Na and water retention and increased BP and ECF- pressure natruresis and diuresis occur
  60. ANP
    • released from atrial stretch receptors
    • causes an increase in GFR
    • decr Na reabs
    • incr water secretion
  61. Acid
    • substance that can donate a proton
    • Bronstead- Lowry theory of acids and bases
  62. Base
    • substance that can accept a proton
    • Bronstead- Lowry theory of acids and bases
  63. Acid base rxn
    rxn where a proton is transferred
  64. strong acid
    an acid that gives up H easily and is completely dissociated in water
  65. weak acid
    an acid that does not give up H easily and is less than 100% dissociated in water
  66. acid dissociation
    splitting apart of an acid in water to produce an H ion and an anion
  67. Why is regulation of H ion concentration (pH) so important?
    • optimal enzyme functioning
    • proper electrolyte distribution
    • optimize myocardial contractility
    • optimal Hgb saturation
  68. 2 sources of acid
    • volatile (able to be eliminated via the lungs)
    • non volatile or fixed (must be eliminated by the kidneys
  69. How much CO2 is produced / day from aerobic metabolism?  How much is eliminated via the lungs / day
    • 15-20 mols
    • 15-20 mols
  70. How much non volatile acid is produced each day?
    • 1 meq/ kg
    • (50-100 meq)
  71. What processes produce H ions?
    • Protein metab
    • Lactic acid (aerobic CHO metab)
    • Ketone bodies (triglycerides)
  72. Carbonic anhydrase
    • CO2 is hydrated to become carbonic acid
    • slow process in the plasma, but in the RBC carbonic anhydrase speeds it up
  73. Henderson- Hasselbalch equation
    • pHa= pK + log bicarb / 0.03 x PaCO2
    • =kidneys / lungs

    0.03 is the solubility coefficient of CO2 in the plasma
  74. buffer
    any substance that reversibly binds H ions
  75. How do the kidneys contribute to acid / base balance?
    • Produce an acid or basic urine depending on our needs
    • Balance of removing H and bicarb
  76. Is most bicarb reabsorbed or secreted?
    reabsorbed
  77. Quantitatively, which is more important- secretion of H ion or reabsorption of bicarb?
    Bicarb reabsorption
  78. Primary ECF buffer
    bicarb
  79. What will the kidneys do in response to acidosis?
    Reabsorb all filtered bicarb and produce more bicarb
  80. What will the kidneys do in response to alkalosis?
    • There's an excess of bicarb
    • Kidneys can't reabsorb all the filtered bicarb, so bicarb is excreted
    • This has the same effect as increasing the H ion concentration
  81. In what part of the tubules is H ion secreted?
    • PCT (80-90% occurs here) 
    • thick asc LoH
    • early distal tubule
  82. Mechanism for H ion secretion?
    Counter transport (a form of secondary active transport)
  83. T or F, slightly more H ions are secreted than bicarb reabsorbed
    T
  84. Where does primary active H ion secretion occur?
    • intercalated cells of the late distal tubule
    • collecting tubule
  85. T or F, in general, for every H ion secreted a bicarb is reabsorbed?
    T
  86. How can new bicarb be produced by the kidneys?
    • By the ammonia and phosphate buffers
    • Quantitatively the ammonia buffer is more significant

Card Set Information

Author:
 ariadne9
ID:
 247048
Filename:
 Renal 2
Updated:
2013-11-15 17:06:01
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BC Nurse Anesthesia PV3
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renal lecture 2
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