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Renal Exam 2 > Regulation of Sodium and Water Balance > Flashcards

Regulation of Sodium and Water Balance Flashcards

1
Q

Major body fluid compartments

-Main substances exerting osmotic pressure in compartments-Cells?

A

Potassium

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2
Q

Major body fluid compartments

-Main substances exerting osmotic pressure in compartments-Interstitial fluid?

A

Sodium

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3
Q

Major body fluid compartments

-Main substances exerting osmotic pressure in compartments-plasma?

A

Protein (usually albumin)

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4
Q

Electrolyte composition of ECF (compared to ICF)?

A

High-Na, Cl, Ca, bicarb, pH

-Low-K, phosphate

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5
Q

ECF volume is determined by?

A

Total body Na

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6
Q

Why are water and Na balance regulated independently?

A

To prevent large changes in plasma osmolality

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7
Q

Effects of increased Na in the body?

-Can be compensatory for?

A
  • Increased ECF volume and ECV

- Can be compensatory for hypovolemia

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8
Q

Sodium balance

  • Total body sodium compared to plasma sodium
  • Plasma Na (and therefore osmolarity) is primarily regulated by?
  • Major cause of hyponatriemia?
A
  • Total body sodium is different from plasma sodium:
    • Plasma sodium is affected by water balance
  • Major cause of hyponatriemia is too much water (not low sodium)
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9
Q

Total body Na content=?

A

dietary intake-urinary Na excretion

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10
Q

Dietary Na intake

A
  • Not regulated in humans

- Kidneys control body Na content by adjusting urinary excretion

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11
Q

Increased ECF volume activates mechanisms that have what effect?

A

-Increase Na excretion

decreased ECF causes Na to be conserved

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12
Q

Reabsorption of filtered Na load

  • Bulk of reabsorption occurs in?
  • Fine tuning occurs in?
A
  • Bulk of reabsorption of filtered Na in proximal tubule, loop of Henle
  • Fine tuning occurs in the distal nephron
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13
Q

Neurohormonal factors controlling renal Na handling

-Factors that promote Na reabsorption?

A
  • Activation of renal sympathetic nerves
  • Activation of renin/angiotensin system
  • Secretion of aldosterone
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14
Q

Neurohormonal factors controlling renal Na handling

-Factors that promote Na excretion?

A
  • Release of ANP and BNP (brain natriuretic peptide)
  • Release of urodilatin
  • Intrarenal prostaglandins
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15
Q

Increased activity of renal sympathetic nerves has what effects:

  • on GFR?
  • reabsorption of water and sodium?
  • granular cells?
A
  • Decreased GFR
  • Increased proximal reabsorption of Na and H2O
  • Direct stimulation of granular cells (beta-adrenergic receptors)
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16
Q

Increased activity of renal sympathetic nerves has what effects
-Decreased GFR and increased proximal reabsorption of Na and H2O lead to?

A

Decreased rate of fluid delivery to the macula densa

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17
Q

Increased activity of renal sympathetic nerves has what effects
-Decreased rate of fluid delivery to the macula densa and direct stimulation of granular cells (beta-adrenergic receptors) lead to?

A

Increased renin secretion

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18
Q

Factors that promote renin secretion?

A
  • Renal sympathetic stimulation
  • Tubuloglomerular feedback
  • Intrarenal baroreceptor afferent arteriolar vasoconstriction
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19
Q

Factors that promote renin secretion

  • Renal sympathetic stimulation
    • Due to?
    • Directly stimulates?
A
  • Renal sympathetic stimulation (due to decreased perfusion pressure through the cardiopulmonary baroreceptors)
  • Directly stimulates renin secretion via beta-1 receptor activation in the JG apparatus
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20
Q

Factors that promote renin secretion

-Tubuloglomerular feedback stimulated by?

A

-Decreased NaCl delivery to macula densa causing increased renin secretion

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21
Q

Factors that promote renin secretion

-Intrarenal baroreceptor afferent arteriolar vasoconstriction stimulated by?

A

Decreased pressure at granular cells causing increased renin secretion

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22
Q

Loop diuretics MOA?

A

Inhibit the Na-K-2Cl pump

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23
Q

What effect would loop diuretics have on renin secretion?

A

They would increase renin secretion

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24
Q

Angiotensin II stimulates?

A
  • Systemic arteriolar constriction
  • Renal arteriolar constriction
  • Na reabsorption
  • Thirst
  • ADH and aldosterone secretion
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25
Q

Angiotensin II stimulates

  • Renal arteriolar constriction
    • Afferent compared to efferent?
    • How would this affect GFR?
    • How would this affect RBF?
A
  • Efferent > afferent
  • Maintain or slightly increase GFR
  • Decrease RBF-stopping flow and backing up pressure
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26
Q

Angiotensin II stimulates

-Na reabsorption occurs in? Via?

A

-Na reabsorption in the PCT (via increased Na-H exchanger activity) > TAL, CCD (cortical collecting duct?)

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27
Q

Where is ADH secreted from?

A

Posterior pituitary

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28
Q

Where is aldosterone secreted from?

A

Adrenal cortex

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29
Q

Renal effects of angiotensin II?

A
  • Decreased renal blood flow
  • Proportionately increased efferent arteriolar resistance
  • Glomerular mesangial cell contraction
  • Decreased medullary blood flow
  • Increased tubular sodium reabsorption–>sodium retention
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30
Q

Renal effects of angiotensin II

-Proportionately increased efferent arteriolar resistance–>?

A

-Proportionately increased efferent arteriolar resistance–>increased glomerular capillary hydrostatic pressure–>increased filtration

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31
Q

Renal effects of angiotensin II

-Glomerular mesangial cell contraction–>?

A

-Glomerular mesangial cell contraction–>Decreased glomerular capillary surface area available for filtration–>decreased filtration (offsets increased filtration)

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32
Q

Slide 17/18

A

flow charts

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33
Q

Where do aldosterone’s actions take place?

-What are the cells called?

A

Late DCT and CD (principal cells)

34
Q

Aldosterone stimulates sodium reabsorption resulting in?

A

lumen negative potential difference

35
Q

Aldosterone stimulates sodium reabsorption

-Electroneutrality maintained by?

A

Passive Cl-reabsorption and K+/H+ secretion

36
Q

Aldosterone

  • Potassium is secreted by what type of cell?
  • In what part of the nephron?
A

Principal cells of the DT and the CCD

37
Q

Aldosterone

  • Hydrogen is secreted by what type of cell?
  • In what part of the nephron?
A

H+ ATPase activity in intercalated cells of CCD

38
Q

What would happen to K and H secretion in a patient with hyperaldosteronism?

A

Increased secretion of K and H-hypokalemic and metabolic alkalosis

39
Q

Factors that stimulate aldosterone secretion?

A
  • Increased plasma K concentration
  • Increased plasma ACTH
  • Volume depletion–>ANG II conc
40
Q

Feedback control of aldosterone secretion

-Aldosterone–>decreased Na and water excretion leads to?

A

-Increased ECF volume–>increased renal arterial mean pressure, decreased discharge of renal nerves–>inhibits renin

41
Q

ANP-How does it affect:

  • Na, H2O excretion?
  • GFR?
  • Na reabsorption?
  • Renin, aldosterone, ADH?
  • Overall effect?
A
  • Increases Na, H2O excretion
  • Increases GFR
  • Inhibits Na reabsorption
  • Suppresses renin, aldosterone, and ADH secretion
  • Systemic vasodilator
42
Q

ANP response to increased ECF volume flow chart

-ANP is released in response to?

A
  • ANP is released in response to an increased right atrial pressure
  • Slide 22 and 23
43
Q

Urodilatin

-What is it?

A

Endogenous renal natriuretic peptide

44
Q

Urodilatin

  • Secreted by?
  • Secreted in response to?
  • Suppresses?
A
  • DCT and CD in response to increased arterial pressure and ECF volume
  • Suppresses Na and water reabsorption by medullary CD
45
Q

Urodilatin

-Difference between urodilatin and ANP/BNP?

A

Urodilatin has NO EFFECT on systemic circulation

46
Q

Prostaglandins

-Compare their effects to those of sympathetics

A

Prostaglandins oppose sympathetics

47
Q

Effect of intrarenal prostaglandins

  • on Na excretion/Na reabsorption?
  • GFR?
A
  • Intrarenal prostaglandins increase Na excretion and suppress Na reabsorption
  • Increase GFR
48
Q

Effect of intrarenal prostaglandins

-How do they increase GFR?

A

By dilating renal arterioles

49
Q

Effect of intrarenal prostaglandins

-Where is the Na reabsorption suppressed?

A

thick ascending limb and cortical CD

50
Q

What effect will intrarenal prostaglandins have on the solute concentration in the renal medullary tissue?

A

Decreased osmolarity, won’t concentrate urine as you would normally

51
Q

Major regulatory hormones of each segment of the nephron

-PCT?

A

Ang II, norepi, epi, dopamine

52
Q

Major regulatory hormones of each segment of the nephron

-Loop of Henle and DCT?

A

Aldosterone and Ang II

53
Q

Highest percentage of NaCl is reabsorbed in what portion of the nephron?

A

PCT

54
Q

Mechanisms of Na entry across apical membrane?

-PCT

A

Na-H antiporter, Na symporter with aa, Na-H-Cl antiporter, paracellular

55
Q

Mechanisms of Na entry across apical membrane?

-Loop of henle?

A

Na-K-2Cl symporter

56
Q

Mechanisms of Na entry across apical membrane?

-DCT?

A

NaCl symporter

57
Q

Mechanisms of Na entry across apical membrane?

-Late DCT and CD?

A

epithelial sodium channel

58
Q

Major regulatory hormones of each segment of the nephron

-Late distal tubule and CD?

A

Aldosterone, ANP/BNP, urodilatin, Ang II

59
Q

2 types of receptors that control ADH secretion?

A

Osmoreceptors (hypothalamic > hepatic) and baroreceptors

60
Q

Two major stimuli for ADH release?

A
  • Hyperosmolarity
  • Volume depletion
  • These two arms are separate but they interact
61
Q

Plasma AVP vs osmolality (graphs)

A
  • Normal plasma osmolality corresponds to maximum ADH

- Need thirst and resulting hydration to overcome any extra osmolarity

62
Q

Plasma AVP vs blood volume (graphs)

A

Volume receptors not as sensitive but once they are activated they are powerful

63
Q

Changes in blood volume modulate osmolality-dependent changes in plasma AVP

A
  • Volume depletion potentiates ADH response to hyperosmolality
  • Volume depletion prevents inhibition of ADH release normally induced by a fall in plasma osmolality
  • VOLUME ALWAYS TRUMPS OSMOLARITY
64
Q

Renal response to increased NaCl intake flow chart

A

Slide 33

65
Q

Integrated response to volume expansion flow chart

A

Slide 34

66
Q

Clinical manifestations of impaired regulation

-Too much water?

A

Hyponatriemia (low plasma Na)

67
Q

Clinical manifestations of impaired regulation

-Too little water?

A

Hypernatriemia (high plasma Na)

68
Q

Clinical manifestations of impaired regulation

-Too much Na?

A

Edema

69
Q

Clinical manifestations of impaired regulation

-Too little Na?

A

Volume depletion

70
Q

Activation of Ang II in response to hemorrhage flow charts

A

slide 36, 37, 38

71
Q

Integrated response to volume contraction flow chart

A

slide 39

72
Q

Increased renal tubular Na reabsorption in response to volume contraction

A

slide 40

73
Q

Summary table
Sensors and effectors of osmoregulation and volume regulation
-Osmoregulation-What is sensed?

A

Plasma osmolarity

74
Q
  • Osmoregulation

- sensors?

A

Hypothalamic osmoreceptors

75
Q
  • Osmoregulation

- Effectors?

A

ADH and thirst

76
Q
  • Osmoregulation

- What is affected?

A

Urine osmolarity and water intake

77
Q

Volume regulation

-What is sensed?

A

Adequate tissue perfusion

78
Q

Volume regulation

-Sensors?

A

Macula densa, afferent arterioles, atria, carotid sinus

79
Q

Volume regulation

-Effectors?

A

RAAS, ANP, NE, ADH

80
Q

Volume regulation

-What is affected?

A

Urinary sodium and thirst

Renal Exam 2 (6 decks)

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