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Renal Physiology > Regulation of Plasma Sodium and ECF Volume > Flashcards

Regulation of Plasma Sodium and ECF Volume Flashcards

1
Q

what does the hematocrit describe? what is it normally?

A

volume of red blood cells compared to total blood volume

normally about 45%

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2
Q

changes in fluid volume and composition of extravascular fluid reflects what?

A

changes in intravascular fluid (they are in equilibrium)

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3
Q

where is extra cellular fluid osmolarity and volume sensed? what types of cells are these?

A

osmolarity- hypothalamic osmoreceptors
volume- stretch receptors in the atria and vasculature (carotid sinus, aortic arch, renal afferent arterioles)
these cells are neuronal

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4
Q

what 4 “effector agents” (organs) cause the necessary changes to correct for change in ECF volume and osmolarity? which are short and which are long term?

A

the posterior pituitary (long), autonomic nervous system (short), the heart (short) and the kidney (long)

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5
Q

what is the role fo the autonomic nervous system in maintaining ECF volume and osmolarity?

A

it increases or decreases peripheral vascular resistance and heart rate to maintain blood pressure at a normal range

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6
Q

what does the renin-angiotensin-aldosterone axis regulate?

A

peripheral vascular resistance and renal Na excretion

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7
Q

what parameters are used to regulate ECF osmolarity? volume?

A

osm: renal free water excretion and water consumption
vol: blood pressure and sodium excretion

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8
Q

what determines the ECF volume?

A

total amount of sodium in the ECF

high sodium= larger ECF volume

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9
Q

how much water is in 1 kg? a 1 kg increase in weight reflects a positive Na balance of what?

A

1 L of water

140 mEq NaCl

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10
Q

expansion of ECF volume results in what in the kidney? volume contraction?

A

expansion- increase in output of sodium and water in urine

contraction- decrease in output of sodium and water

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11
Q

the initial absorption of Na after a salty meal has what effect?

A

induces increased release of ADH into the circulation
increases thirst and absorption of free water in the kidney
(maintains osmolarity and increases plasma volume)

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12
Q

how is the increase in plasma volume from a high salt diet reduced over time?

A

by gradually decreasing renal sodium resorption and increasing excretion

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13
Q

what is the initial effect in decrease of sodium consumption?

A

decrease in plasma osmolarity which decreases ADH

decrease in thirst and resorption of free water in the kidney (concentrates and decreases plasma)

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14
Q

how is the volume contraction of a low sodium diet reduced over time?

A

gradual regulatory increase in renal Na absorption and decreased excretion

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15
Q

an excess of salt in the diet can lead to what phenomenon? why is this important with increasing age?

A

has clinical effect of raising blood pressure

important because off loading excess sodium is more difficult with age

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16
Q

what is the kidney’s response to ECF volume expansion? volume contraction? what is the change in GFR?

A

expansion- decreasing Na and water resorption
contraction- increasing sodium and water resorption
no change in GFR unless severe volume contraction

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17
Q

how long does a change in sodium in the diet take to balance with sodium output? what is the detector for this correction?

A

4-5 days–very closely regulated

detected by baroreceptors that detect the secondary volume change that accompanies the salt intake

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18
Q

compare the osmolarity and volume that is achieved after a increased Na consumption with normal conditions.

A

there is an isosmotic expansion of ECF volume

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19
Q

what circumstance does the kidney react to to increase Na excretion?

A

in response to increase in ECF volume, not an increase in sodium concentration

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20
Q

what changes induce regulation of sodium excretion?

A

changes in effective circulating volume, not total ECF volume

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21
Q

what is the effective circulating volume?

A

functional blood volume reflecting extent of perfusion where blood pressure is sensed

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22
Q

when does the effective circulating volume not match total ECF?

A

may be less in disease states that cause edema (like congestive heart failure)

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23
Q

decrease in renal perfusion pressure does what? what does this lead to in the context of edema?

A

activates the renin- angiotensin- aldosterones system

further increases sodium retention and edema

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24
Q

name four edematous disease states.

A

conesive heart failure, pulmonary edema, liver disease and nephrotic syndrome

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25
Q

what do liver disease and nephrotic syndrome have in common?

A

both reduce plasma oncotic pressure by either failing to produce (liver) or allowing excretion of (kidney) albumin

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26
Q

what do diuretic drugs do? how does this impact edema?

A

decrease plasma volume by forcing the kidney to increase sodium and water excretion in the urine
favors absorption of edematous fluid

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27
Q

which central vascular sensors sense low pressure? which sense high pressure? which are more important?

A

low- atria and pulmonary vasculature (more important)

high- carotid sinus, aortic arch and juxtaglomerular apparatus in the renal afferent arteriole

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28
Q

how do receptors sense the ECF volume?

A

by sensing vascular pressure changes that occur with changes in volume

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29
Q

what four systems are activated with decrease in effective circulating volume?

A

renin-angiotensin-aldosterone system, increased renal sympathetic nerve activity, ADH release by the posterior pituitary and decrease in release of atrial natriuretic peptide

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30
Q

how does angiotensin II affect the kidney? aldosterone?

A

ang- promotes sodium retention by stimulating Na/H exchange in proximal tubule and decreases renal plasma flow promoting increased Na rebsorption
ald- increased sodium resorption by late distal tubule and collecting duct

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31
Q

what does renal sympathetic nerve activity do during decreased intravascular pressure?

A

induces renal vasoconstriction and increased Na reabsorption

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32
Q

what is the function of atrial natriuretic peptide?

A

it induces sodium excretion with high atrial pressures

33
Q

where is renin synthesized and stored? what is its function?

A

synthesized and stored in granular cells of the juxtaglomerular apparatus of the kidney
converts angiotensinogen to angiotensin I

34
Q

where is ACE located and what does it do?

A

on luminal surface of vascular endothelium, particularly in lungs. it converts angiotensin I to angiotensin II

35
Q

describe the deactivation of angiotensin II

A

has a short half life due to rapid degredation by aminopeptidases cleaving it into angiotensin III (less activity)

36
Q

what is the most important factor controlling angiotensin II levels?

A

renin release

37
Q

what are the three renal mechanisms that regulate renin release?

A

local renal baroreceptors in afferent arterioles
decreased systemic pressure influences sympathetic stimulation of the juxtaglomerular apparatus
cells of the macula densa sense tubular fluid sodium concentration

38
Q

what are the 5 actions of angiotensin II?

A

induces aldosterone release from adrenal cortex
hypothalamus- increases thirst and induces ADH release
vasoconstricts renal and systemic vessels
enhances Na/H exchange in proximal tubule
induces hypertrophy of renal tubule cells

39
Q

what is the purpose of renal vasoconstriction induced by angiotensin II?

A

constricts efferent more than afferent increasing GFR

increases starling forces favoring resorption of tubular fluid by peritubular capillaries

40
Q

what is the primary long term regulator of salt balance and ECF volume? where is it produced

A

aldosterone (a mineralcorticoid)

produced in the adrenal cortex

41
Q

what two effects does aldosterone have on the kidney?

A

increases resorption of sodium and therefore water

promotes potassium secretion by the distal nephron

42
Q

in what cells does aldosterone increase Na absorption and where are they? what distinguishes these cells?

A

principal cells in the late distal tubule and early collecting duct in the renal cortex
express of intracellular aldosterone receptors

43
Q

in what three ways does aldosterone increase sodium absorption?

A

increases basolateral Na/K pumps, increases apical membrane Na channels and increases mitochondrial enzymes to make more ATP

44
Q

what happens to sodium absorbed in the late distal tubule? how does it change the cortico medullary solute concentration gradient?

A

since it is in the cortex, it is returned to circulation and does not participate in the gradient

45
Q

how is cortical Na resorption separated from the counter current multiplication system?

A

there is separate venous circulation in the cortex and in the vasa recta of the medulla

46
Q

where is most filtered sodium absorbed in the nephron? where is most of the remaining sodium absorbed?

A

proximal tubule

thick ascending limb of the loop of henle

47
Q

how is the loop of henle split functionally? what is the difference?

A

into the cortical and medullary portions

only medullary portion contributes to the counter current multiplication

48
Q

how much of Na is reabsorbed in Na balance? what segments account for the variability in that number?

A

99% of filtered Na is reabsorbed

late distal tubule and early collecting tubule (aldosterone)

49
Q

what mechanism is not included in the renal handling of Na?

A

secretion of Na does not occur

50
Q

describe resorption of NaCl in principal cells of the cortical collecting tubule.

A

Na is passively absorbed into the cell and actively pumped into the blood via a Na/K pump. Cl follows transcellularly

51
Q

how is Na absorption coupled to K secretion in the late distal tubule and collecting duct?

A

increase in Na resorption occurs simultaneously with increase in transcellular K secretion through luminal channels

52
Q

in what two ways does aldosterone increase K secretion?

A

by increasing synthesis of the Na/K pump in the basolateral membrane and by increasing synthesis of K channels in the luminal membrane

53
Q

what is the driving force for paracellular resorption of Cl?

A

because 3 Na+/2K+ are transported, the transport of Na and K is electrogenic. the negative luminal voltage difference drives Cl movement

54
Q

how does aldosterone produce effects in the cell?

A

it binds to an intracellular receptor and induces transcription for membrane transport proteins

55
Q

what do hormone specific secretogogues refer to?

A

agents that increase release of hormones into circulation

56
Q

what secretogogues are there for aldosterone?

A

angiotensin II (induces ACTH release by anterior pituitary), increased plasma K+ and ACTH

57
Q

what is the normal plasma sodium concentration?

A

135-145 mEq/L

58
Q

what are the symptoms of hypernatremia? at what levels do they become severe?

A

lethargy, weakness and irritability

>158 mEq/L- seizures and coma may occur

59
Q

what can cause hypernatremia?

A

caused by loss of free water from plasma due to inadequate consumption in excess of solute or inappropriate renal excretion of water

60
Q

what are the possible causes of hypovolemic hypernatremia?

A

inadequate water consumption, extreme sweating, severe diarrhea and polyuria (like in diabetes mellitus and insipidus)

61
Q

how does diabetes mellitus cause hypernatremia?

A

glucose transport is maximized and there is still excess in tubular fluid. this opposes reabsorption in distal nephron segments and prevents water resorption

62
Q

what is central diabetes insipidus?

A

inadequate release of ADH from the posterior pituitary to an increase in plasma osmolarity. free water is not reabsorbed and is excreted in the collecting duct

63
Q

what is nephrogenic diabetes insipidus?

A

inability of the collecting tubule to respond to ADH despite adequate release

64
Q

when does hypervolemic hypernatremia occur?

A

with consumption of hypertonic NaCl solution (seawater) or from inappropriate IV infusionof hypertonic saline
may also occur from hyperaldosteronism

65
Q

in the case of hyperaldosteronism, how do central osmoreceptors change? how does this effect ADh release?

A

central osmoreceptors decrease sensitivity and for given increase in plasma osmolarity there is less ADH release

66
Q

what are the symptoms of hyponatremia? at what level do they get more severe?

A

nausea, vomiting, headache, lethargy, fatigue, loss of appetite, muscle weakness, spasm and cramps
<125 mEq/L neurological deficis, brain swelling, seizures and coma occur

67
Q

what are some causes of hyponatremia?

A

extreme excessive consumption of water and inappropriate increase in free water reabsorbed secondary to dysregulation of ADH (syndrome of inappropriate ADH release)

68
Q

what is SIADH?

A

syndrome of inappropriate ADH release when levels are elevated with plasma osmolarity is reduced

69
Q

is hyponatremia typically the result of water imbalance or salt imbalance?

A

water

70
Q

hypervolemic hyponatremia may result from what 5 conditions?

A

congestive heart failure, kidney failure, liver failure, syndrome of inappropriate anti diuretic hormone and polydypsia

71
Q

how does congestive heart failure lead to hypervolemic hyponatremia?

A

inadequate pumping of blood effectively decreases circulating volume, causing the release of ADH

72
Q

how does hypervolemic hyponatremia result from kidney failure?

A

Na reabsorption is not sufficient and there is an over compensation for plasma volume depletion by increasing free water reabsorption in excess of solutes

73
Q

how does liver failure cause hypervolemic hypernatremia?

A

effective circulating volume is decreased due to edema and ADH is released

74
Q

what is psychogenic polydipsia?

A

compulsive water consumption verging on intoxication. imbalance in consumption and excretion dilutes plasma and increases volume

75
Q

in what settings does hypovolemic hyponatremia occur?

A

severe vomiting or diarrhea, hemorrhage, prolonged exercise in heat, diuretic drug therapy and in addison’s disease

76
Q

how does diuretic drug use cause hypovolemic hyponatremia?

A

diuretics inhibit sodium reabsorption in the kidney but low plasma volumes increase water resorption in excess of solute

77
Q

what is addison’s disease? how does this lead to hypovolemic hyponatremia

A

the adrenal gland does not respond to angiotensin II. kidney is unable to increase sodium resorption in response to volume depletion but water may still be retained

78
Q

why does plasma volume trump plasma osmolarity?

A

plasma volume will be protected at the expense of osmolarity becuase adequate circulation must be maintained to deliver oxygen and nutrients

Renal Physiology (12 decks)

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