Regulation of Sodium Balance and ECFV (Rao) Flashcards

1
Q

Why is it important to regulate ECFV?

A

it determines PV which determines mean circulatory filling pressure = cardiac output

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2
Q

What determines ECFV?

A

Na balance/intake

ECFV is INDEPENDENT of Plasma [Na]

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3
Q

What keeps plasma [Na] constant?

A

AVP/vassopressin-mediated water excretion by kidney

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4
Q

When is the only time plasma [Na] will change?

A

when gain or loss of Na exceeds thirst mechanism and kidney’s ability to correct the situation

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5
Q

If a person retains 1 day’s worth of Na (150 mEq) how much weight will they gain?

A

1 kg (from 1 L of H2O retained)

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6
Q

What does change in BW over a short period of time indicate?

A

Na retention

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7
Q

Why is BW monitored on a daily basis for pts on dialysis/renal failure?

A

used to calculate how much dialysis is needed/how much fluid they are retaining

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8
Q

What can cause a Na+ imbalance?

A

excessive sweating
diarrhea
diuretics

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9
Q

Is sweat isotonic?

A

1/2 isotonic

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10
Q

Is vomit isotonic?

A

yes

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11
Q

How is most of the Na excreted?

A

renal

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12
Q

How many mmoles of Na is put into the body per L of saline?

A

150 mmole

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13
Q

How many mEq of Na are reabs at each part of the nephron?

glomerulus, PT, LOH, DT/CD

A

glomerulus: 25,000 mEq

PT: 16,000 (64%)
LOH: 7,000 (28%)
DT/CD: 1750 (7%)

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14
Q

How much Na is excreted/day?

A

150-200 mEq or 1.5%

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15
Q

What signs are seen with ECFV deficit?

A
  • hypotension (drop systolic and diastolic) with inc pulse

- dec orthostatic hypotension

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16
Q

What signs are seen with moderate to severe ECFV expansion?

A
  • edema
  • CHF or CRF
  • heart sounds = S3 gallop (from inc venous congestion)
  • venous distension in neck
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17
Q

What is a sign of a more severe inc in ECFV?

A

pulmonary edema = hearing ascultation of lungs or seen in CXR

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18
Q

What does hypo-albuminemia + edema with normal or low ECFV indicate?

A

liver disease

nephroptic syndrome

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19
Q

_____ determines the distribution of fluid between the ISF and plasma

A

starling forces

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20
Q

Why does dec plasma albumin cause edema?

A
  • > dec colloid pressure -> fluid goes into ISF –> edema

* *but with reduced PV

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21
Q

Are burn pts edematous?

A

yes, they have inc endothelial permeability which leads to a flux of albumin and fluid into ISF

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22
Q

Does the body react faster to changes in Na input or to changes in plasma osmolarity from water intake?

A

plasma osmolarity changes due to water intake

1-2 hrs vs 2-4 days

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23
Q

What mechanisms respond to inc water intake?

A

thirst and ADH or AVP

24
Q

What determines ECFV?

A

salt intake

25
Q

Will ECFV inc or dec with a higher salt intake?

A

inc

26
Q

Why are hypertensive pts recommended to restrict salt intake?

A

low salt intake decreases ECFV -> dec PV -> dec BP

27
Q

What are salt-sensitive hypertensives?

A

pts that cannot correct hypertension with salt restriction alone. They need diuretics

28
Q

How does our body sense an inc or dec in ECFV?

A

we have stretch and baroreceptors in large veins, atria, and arteries

29
Q

What are the 3 types of ECFV receptors?

where are they?

A

Neural stretch
atrial stretch
arterial baroreceptor

30
Q

Neural stretch receptors:

Where are they?
What specifically do they respond to?
Describe their response to this stimulus.

A

in large veins

respond to mechanical stretch due to venous distention

signals to pituitary gland to regulate AVP/ADH –> regulates Na+ excretion at NK2C channel of TALH

31
Q

Atrial stretch receptors:

Where are they?
What specifically do they respond to?
Describe their response to this stimulus.

A

in atria

respond to distension

Elevated arterial pressure

  • ->dec ADH secretion via parasympathetic nerve impulses.
  • ->secrete ANP when the sense distension (promotes Na and H2O excretion)
32
Q

Arterial baroreceptors:

Where are they?
What specifically do they respond to?
Describe their response to this stimulus.

A

in arteries

respond to inc pulse pressure or arterial BP

signals to pituitary to regulate AVP and renin

33
Q

Changes in GFR result in proportional changes in the filtered load of ___

A

Na (therefore changing GFR will change Na excretion)

34
Q

Why can small changes in GFR cause a big change in the amt if Na excreted?

A

if you inc GFR by 10%, you will inc the FL of Na. Without a change in reabs of Na, more Na will be delivered to the LOH which will be passed along to the DT and CD and be excreted

*however, glomerulotubular balance functions such that Na reabs will always inc–ensuring a constant FRACTION is reabs

35
Q

What is pressure natriuesis and how does it regulate ECFV?

A

When BP gets too high, pressure naturesis will cause and inc in GFR to inc Na excretion in urine to decrease BP and correct ECFV

It is a compensatory mechanism to maintain blood pressure within the normal range.

36
Q

How is the effect of pressure naturesis different in an isolated kidney vs an intact system?

A

isolated: has an acute effect (2-3 fold inc in Na output by 30 to 55mmHg change in arterial pressure) = independent of sympathetic and hormonal regulation

Intact system: very effective and is syndergized with reduced formation of renin, angiotensin II, and aldosterone

None of this made any sense to me, so I just copied the notes, so this could be wrong/incomplete

37
Q

What secretes aldosterone?

A

adrenal cortex

38
Q

What stimulates the release of aldosterone from the adrenal cortex?

A

inc plasma K+

angiotensin (dec in ECFV–> renin release –> ang made)

39
Q

What inhibits the release of aldosterone from the renal cortex?

A

inc plasma Na

40
Q

Where does aldosterone act?

A

DCT and CD

41
Q

T or F: Inc in aldo decreases Na reabsorption

A

F: aldo increases Na reabs

42
Q

What is the MOA of aldosterone?

A

Acts on minearalcorticorticoid receptors (MR) in principal cells of DCT and CD to alter gene expression…

  • inc apical Na channels (lumen -> cell)
  • inc basolateral Na-K ATPase
  • inc K apical channels (cell -> lumen)
  • inc kreb’s cycle enzymes to inc ATP synthesis (which is needed for the new NaKATPases)
  • inc NKA- to inc Na reabs and K+ secretion (charges?)
43
Q

Aldosterone (slowly or rapidly) affects the reabs of Na.

A

slowly

44
Q

Will aldosterone play a role in the rapid regulation of Na+ excretion?

A

no (it works slowly to cause Na reabs)

45
Q

What is the source of ANP?

A

cells in cardiac atria

46
Q

What stimulates the secretion of ANP?

A
atrial distention (directly)
inc plasma Na (indirectly)
47
Q

What is the target of ANP?

A

afferent and efferent arterioles

tubules

48
Q

What are the actions of ANP?

A

GOAL is to inc Na excretion by…

  • inhibits Na reabs in tubules
  • dilates afferent arteriole and constricts efferent arteriole to increase GFR and inc Na excretion
  • inhibits aldosterone secretion from adrenal cortex
49
Q

What stiulates the renin-angiotensin system?

A

dec BP
dec ECVF
inc sympathetic firing

50
Q

What is the MOA of renin and the renin-ang sys?

A

secreted by JG cells and converts alpha-2 globin to ang I which gets converted to Ang II by ACE in the PT

Ang II
1. inc aldo production in adrenal cortex
2. activates PT Na:H exchanger
= both inc Na reabs

Once the ECFV has exapanded enough, the BP has been restored and the JG cells stop making renin and system is turned off

51
Q

What inhibits the renin-ang sys?

A

high Na (bc ECFV is high –> JG cells sense that volume is not low anymore and stops making renin)

52
Q

How does sympathetic nerve action affect Na reabs/ECFV?

A

constricts/dialates arterioles to
dec GFR –> inc Na reabs
inc GFR –> dec Na reabs

53
Q

What effect does prostaglandins, bradykinin, and dopamine have on Na retention/ECFV? WHere are these made?

A

they diurese and natriurese

made in kidney

54
Q

What is quabain like factor?

A

inhibits NaK-ATPase to inc Na excretion
produced in the atrium and plants

*not well understood

55
Q

How are the receptors of ecfv similar and how are they different?

A

All 3 regulate AVP secretion for pituitary

Neural are in veins
Atrial are in atria and also secrete ANP
Arterial are in arteries