Regulation of Sodium Balance and ECFV (Rao) Flashcards Preview

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Flashcards in Regulation of Sodium Balance and ECFV (Rao) Deck (55):
1

Why is it important to regulate ECFV?

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

2

What determines ECFV?

Na balance/intake

***ECFV is INDEPENDENT of Plasma [Na]***

3

What keeps plasma [Na] constant?

AVP/vassopressin-mediated water excretion by kidney

4

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

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

5

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

1 kg (from 1 L of H2O retained)

6

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

Na retention

7

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

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

8

What can cause a Na+ imbalance?

excessive sweating
diarrhea
diuretics

9

Is sweat isotonic?

1/2 isotonic

10

Is vomit isotonic?

yes

11

How is most of the Na excreted?

renal

12

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

150 mmole

13

How many mEq of Na are reabs at each part of the nephron?
glomerulus, PT, LOH, DT/CD

glomerulus: 25,000 mEq

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

14

How much Na is excreted/day?

150-200 mEq or 1.5%

15

What signs are seen with ECFV deficit?

-hypotension (drop systolic and diastolic) with inc pulse
-dec orthostatic hypotension

16

What signs are seen with moderate to severe ECFV expansion?

-edema
-CHF or CRF
-heart sounds = S3 gallop (from inc venous congestion)
-venous distension in neck

17

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

pulmonary edema = hearing ascultation of lungs or seen in CXR

18

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

liver disease
nephroptic syndrome

19

_____ determines the distribution of fluid between the ISF and plasma

starling forces

20

Why does dec plasma albumin cause edema?

-> dec colloid pressure -> fluid goes into ISF --> edema
**but with reduced PV

21

Are burn pts edematous?

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

22

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

plasma osmolarity changes due to water intake
1-2 hrs vs 2-4 days

23

What mechanisms respond to inc water intake?

thirst and ADH or AVP

24

What determines ECFV?

salt intake

25

Will ECFV inc or dec with a higher salt intake?

inc

26

Why are hypertensive pts recommended to restrict salt intake?

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

27

What are salt-sensitive hypertensives?

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

28

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

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

29

What are the 3 types of ECFV receptors?
where are they?

Neural stretch
atrial stretch
arterial baroreceptor

30

Neural stretch receptors:

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

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

Atrial stretch receptors:

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

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

Arterial baroreceptors:

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

in arteries

respond to inc pulse pressure or arterial BP

signals to pituitary to regulate AVP and renin

33

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

Na (therefore changing GFR will change Na excretion)

34

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

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

What is pressure natriuesis and how does it regulate ECFV?

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

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

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

What secretes aldosterone?

adrenal cortex

38

What stimulates the release of aldosterone from the adrenal cortex?

inc plasma K+
angiotensin (dec in ECFV--> renin release --> ang made)

39

What inhibits the release of aldosterone from the renal cortex?

inc plasma Na

40

Where does aldosterone act?

DCT and CD

41

T or F: Inc in aldo decreases Na reabsorption

F: aldo increases Na reabs

42

What is the MOA of aldosterone?

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

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

slowly

44

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

no (it works slowly to cause Na reabs)

45

What is the source of ANP?

cells in cardiac atria

46

What stimulates the secretion of ANP?

atrial distention (directly)
inc plasma Na (indirectly)

47

What is the target of ANP?

afferent and efferent arterioles
tubules

48

What are the actions of ANP?

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

What stiulates the renin-angiotensin system?

dec BP
dec ECVF
inc sympathetic firing

50

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

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

What inhibits the renin-ang sys?

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

52

How does sympathetic nerve action affect Na reabs/ECFV?

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

53

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

they diurese and natriurese

made in kidney

54

What is quabain like factor?

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

*not well understood

55

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

All 3 regulate AVP secretion for pituitary

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