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BRS YR2 > Renal Regulation of Water and Acid-Base Balance > Flashcards

Renal Regulation of Water and Acid-Base Balance Flashcards

1
Q

What is the relationship between osmotic pressure and the number of solute particles?

A

proportional

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2
Q

What is osmolarity?

A

concentration x number of dissociated particles (Osm/L, mOsm/L)

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3
Q

Where is the majority of body fluid found?

A

2/3 in the intracellular fluid

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4
Q

Where is the 1/3 of extracellular fluid found?

A

1/4 intravascular (plasma)

3/4 extravascular (95% - interstitial fluid, 5% - transcellular fluid)

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5
Q

What are the different forms of unregulated water loss?

A
  • sweat
  • feces
  • vomit
  • water evaporation from respiratory lining and skin
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6
Q

What are the different forms of regulated water loss?

A

renal regulation (urine production)

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7
Q

What are the 2 different forms of renal regulation?

A

positive and negative water balance

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8
Q

What is positive water balance?

A
  • high water intake
  • increased ECF volume
  • reduced Na+ concentration
  • reduced osmolarity
  • hypoosmotic urine production
  • osmolarity normalises
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9
Q

What is the first compartment of the body where new fluid is put?

A

ECF

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10
Q

What is negative water balance?

A
  • low water intake
  • reduced ECF volume
  • increased [Na+]
  • increased osmolarity
  • hyperosmotic urine production
  • thirst induced
  • osmolarity normalizes
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11
Q

Where is the majority (67%) of water reabsorbed?

A

the DCT

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12
Q

What is absorbed in the ascending limb of the loop of Henle?

A
  • Thin: passive NaCl
  • Thick: active NaCl
    no water
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13
Q

What is absorbed in the descending limb of the loop of Henle?

A
  • passive water

-

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14
Q

Why is water reabsorbed first in the loop of Henle?

A
  • since water is reabsorbed through the passive process of osmosis, a gradient is required
  • the medullary interstitium needs to be hyperosmotic for water reabsorption to occur from LoH and CD
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15
Q

What process causes the gradient in the medullary interstitium?

A

countercurrent multiplication

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16
Q

What transports urea from the collecting duct to the medullary interstitial?

A

UT-A1, UT-A3

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17
Q

What are the 2 possible locations for urea to go to once in the medullary interstitial?

A
  • the descending loop of Henle

- the Vasa-Recta

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18
Q

What transporters allows for the movement of urea into the Vasa Recta?

A

UT-B1

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19
Q

What transporters allows for the movement of urea into descending LoH?

A

UT-A2

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20
Q

What is the purpose fo urea recycling?

A

to increase the interstitial osmolarity

  • causes urine concentration
  • urea excretion needs less water (high concentrations can be excreted)
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21
Q

How is vasopressin involved in urea recycling?

A

boosts UT-A1 and UT-A3 numbers

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22
Q

What is the main function of ADH/vasopressin?

A

promote water reabsorption from the collecting duct

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23
Q

Where is ADH produced?

A
  • hypothalamus

- neurons in the supraoptic and paraventricular nuclei

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24
Q

Where is ADH stored?

A

the posterior pituitary gland

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25
Q

What detects fluctuation in plasma osmolarity?

A

osmoreceptors in the hypothalamus

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26
Q

What factors stimulate ADH production and release?

A
  • increased plasma osmolarity
  • hypovolemia (reduced BP)
  • nausea
  • angiotensin II
  • nicotine
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27
Q

What factors inhibit ADH production and release?

A
  • low plasma osmolarity
  • hypervolemia (increased BP)
  • ethanol
  • ANP,BNP
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28
Q

What detects changes in BP?

A

baroreceptors to the hypothalamus

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29
Q

What is required in order for baroreceptors to detect BP changes?

A

5-10% change

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30
Q

What receptor binds ADH?

A

V2 receptor

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31
Q

What happens when ADH binds to a V2 receptor?

A
  • activates the G protein mediated signalling cascade
  • activating protein kinase A
  • increasing the secretion of Aquaporin 2 channels that are transporters of water on apical membrane
32
Q

What happens in diuresis?

A

increased dilute urine secretion (low/no ADH)

33
Q

What is absorbed/excreted in the collecting duct during diuresis?

A
  • NaCl reabsorbed

- water reabsorption in the inner medulla (even with absent ADH)

34
Q

What is the type of fluid that enters the LoH?

A

Isosmotic

35
Q

What is the type of fluid that enters the DCT?

A

Hypoosmotic

36
Q

What is reabsorbed in the DCT during diuresis?

A
  • active NaCl

- water channels closed in DCT

37
Q

What is the type of fluid that exits the CD?

A

hypoosmotic

38
Q

How is sodium reabsorbed in the collecting duct?

A
  • Na+/K+/ATPase Pump

- sodium channels

39
Q

What is antidiuresis?

A
  • concentrated urine in low volume excretion

- high ADH

40
Q

How does ADH increase salt reabsorption in the thick ascending limb?

A

increased number/action of the Na+/K+/2Cl- symporter

41
Q

How does ADH increase salt reabsorption in the DCT?

A

increased number/action of the Na+/Cl- symporter

42
Q

How does ADH increase salt reabsorption in the CD?

A

increased Na+ channels

43
Q

What is reabsorbed in the DCT during antidiuresis?

A
  • active NaCl

- water through AQP2

44
Q

What is reabsorbed in the CD during antidiuresis?

A
  • water reabsorbed increases as passing into the medulla
45
Q

What are some examples of ADH related clinical disorders?

A
  • central diabetes insipidus
  • syndrome of inapropriate ADH secretion (SIADH)
  • Nephrogenic Diabetes Insipidus
46
Q

What is the cause of central diabetes insipidus?

A

decreased/negligent production/release of ADH

47
Q

What are the clinical features of central diabetes insipidus?

A
  • polyuria

- polydipsia

48
Q

What is the treatment given for central diabetes insipidus?

A

external ADH

49
Q

What is the cause of SIADH?

A

increased production and release of ADH

50
Q

What are the clinical features of SIADH?

A
  • hyperosmolar urine
  • hypervolemia
  • hyponatremia
51
Q

What is the treatment given for SIADH?

A

Non-peptide inhibitor of ADH receptor

- (conivaptan and tolvaptan)

52
Q

What mechanisms neutralise excess metabolic acids?

A
  • bicarbonate buffering mechanism
53
Q

What is the role of kidneys?

A
  • secretion and excretion of H+
  • reabsorption of HCO3-
  • production of new HCO3-
54
Q

How much of bicarbonate ions are reabsorbed in the PCT?

A

80%

55
Q

How much of bicarbonate ions are reabsorbed in the ascending LoH?

A

10%

56
Q

What mechanisms neutralise excess metabolic acids?

A
  • bicarbonate buffering mechanism

- phosphate buffering system

57
Q

How much of bicarbonate ions are reabsorbed in the CD?

A

4%

58
Q

How is bicarbonate reabsorbed in the PCT?

A
  • CO2 from the tubule enters the cell
  • reacts with water to form HCO3-
  • Na/HCO3- symporter into the blood
59
Q

Where are intercalated cells found?

A
  • DCT

- CD

60
Q

What is the role of the alpha-intercalated cells?

A
  • HCO3- reabsorption

- H+ secretion

61
Q

What is the role of the beta-intercalated cells?

A
  • HCO3- secretion

- H+ reabsorption

62
Q

What happens in the alpha-intercalated cell?

A
  • H+ back into tubule via H+ATPase and H+/K+ ATPase

- HCO3- into blood by Cl-/HCO3- antiporter

63
Q

What happens in the beta-intercalated cell?

A
  • HCO3- into tubule by Cl-/HCO3- antiporter

- H+ ATPase pump for H+ into the blood

64
Q

Where are new bicarbonate ions produced

A

PCT

65
Q

How is new bicarbonate produced?

A
  • glutamine into 2 ammonia and one divalent ion

- 2 HCO3- ions that are reabsorbed

66
Q

What happens if ammonia reaches the blood and eventually back to the liver?

A
  • ammonia = one urea and one H+

- then uses up another HCO3- for neutralisation

67
Q

How do you prevent ammonia from reentering the blood stream and reaching the liver?

A
  • Na+/H+ antiporter (NH4+ replacing H+)

- Ammonium gas that binds with a H+ to produce ammonia that is excreted

68
Q

What happens to the excess proton when HCO3- is produced (from CO2 in the tubule) in the DCT and CD?

A

it is neutralised by phosphate in the tubule

69
Q

What are the characteristics of metabolic acidosis?

A
  • low [HCO3-]

- low pH

70
Q

What are the characteristics of metabolic alkalosis?

A
  • high [HCO3-]

- high pH

71
Q

What is the compensatory response to metabolic acidosis?

A
  • increased ventilation

- increased [HCO3-] reabsorption and production

72
Q

What is the compensatory response to metabolic alkalosis?

A
  • hypoventilation

- increased [HCO3-] excretion

73
Q

What are the characteristics of respiratory acidosis?

A
  • high Pco2

- low pH

74
Q

What is the compensatory response to respiratory acidosis?

A

acute
- intracellular buffering
chronic
- increase [HCO3-] reabsorption and production

75
Q

What are the characteristics of respiratory alkalosis?

A
  • low Pco2

- high pH

76
Q

What is the compensatory response to respiratory alkalosis?

A

acute
- intracellular buffering
chronic (more carbonic acid production)
- increase [HCO3-] excretion and reduced [HCO3-] production

BRS YR2 (70 decks)

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