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UTHSC M2016 CBD - Renal > Reg of Sodium Balance & Extracellular Fluid Volume (Rao) > Flashcards

Reg of Sodium Balance & Extracellular Fluid Volume (Rao) Flashcards

To know: 1. The importance of maintenance of constant extracellular fluid volume (ECFV). 2. How body sodium balance determines ECFV. 3. Daily balance between sodium intake and output. 4. Sodium reabsorption in different segments of nephron. 5. How sodium balance is different from water balance. 6. Different receptors of ECFV. 7. Kidney responses to change in ECFV.

1
Q

ECFV =

A

ECFV = ECF Na+ / PNa

At constant PNa, ECFV = ECF Na

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2
Q

PNa =

A

Amount ECF Na / ECFV

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3
Q

Change in body weight over a short period indicates what?

A

Na+ balance change

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4
Q

Output of Na+ (%ages)

A

Renal 80-90%
GI 0.5-10%
Skin 0-20%

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5
Q

Location and amounts of renal Na+ reabsorption (3 locations & % of 25000 mEq/day))

A

Proximal Tubule: Isotonic ~64%
Loop of Henle: ~28%
Distal tubule and CD: ~7%

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6
Q

S3 gallop & vein distension meaning

A

ECFV expansion

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7
Q

Decreased plasma albumin effect

A

reduced plasma colloid pressure -> edema

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8
Q

Time for recovery of diuresis after water intake

A

1-2 hrs

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9
Q

Time for recovery from input of Na+

A

2-4 days

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10
Q

Receptors for ECFV (location, action, result)

A

Neural stretch receptors - large veins - signals pituitary -> AVP/ADH -> regulates renal Na+ excretion

Atrial stretch receptors - atria - parasympathetic in vagus - AVP secretion -> sympathetics to kidney. Also ANP

Arterial baroreceptors - arteries - signals to pituitary -> AVP

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11
Q

5 regulators of Na excretion by kidney

A 
Changes in GFR
Aldosterone
Natriuretic hormone
Renin-Angiotensin system
Others (sympathetic nerves, prostaglandins)
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12
Q

Changes in GFR result on Na+ filtered load

A

Proportional to GFR

Small changes in GFR undetectible, marked change in Na+

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13
Q

Pressure natriuresis

A

BP up –> 3-5 fold increase in urine & Na+ excretion. Autoregulation doesn’t totally compensate

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14
Q

Arterial pressure increase:
Acute effect in isolated kidney
Chronic effect in intact system

A

Acute - 2-3 fold increase by 30-50 mmHg
Chronic - compensates until 100-110 mmHg

(clarify?)

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15
Q

Aldosterone

source, stimulated/inhibited by

A

mineralcorticoid from adrenal cortex
Release stim by K+, angiotensin
Release inhibited by Na+
Acts exclusively on DCT and CD to increase Na+ reabsorption

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16
Q

Aldosterone mechanism

A

upregulates genes for:
Apical membrane Na Chanel in DCT and CD
Luminal NaCl cotransporter (increase Na reabs)
NKA (increase Na abs, K sec)

Slow acting

17
Q 
Natriuretic peptide (ANP)
(source, stimulated/inhibited by)
A

Source - cardiac atrial cells (to plasma)
Stim by PNa increased or atrial distention
Renal tubular segments, renal blood vessels

18
Q

ANP actions

A

Tubule - inhibits Na reabsorption
Renal vessel - increases GFR and Na excretion
Adrenal cortex - inhibits aldosterone secretion

19
Q

Renin-Angiotensin

source, stimulated/inhibited by

A

Source - JG cells
Stim - Decreased ECF volume, increased sympathetic firing, decreased renal art BP
Inhib - expansion of ECF volume

20
Q

Renin-Angiotensin

actions, cascade, result

A

Renin activates alpha2-globulin ->
Angiotensin I (converted by ACE to)
Angiotensin II

Effects:
Adrenal cortex -> aldosterone
Na reabsorption in DCT and CD

21
Q

Sympathetic nervous effect on Na reabsorption

A

lowers GFR, incrases proimal sodium reabsorption

22
Q

Prostaglandins, bradykinin, dopamine effect on Na reabsorption

A

produced in kidney

diuresis and natriuresis

23
Q

Oubain-like factor

A

produced in atrium

diuresis & natriuresis

24
Q

Which takes precedence for regulation - hypovolemia or hyponatremia

A

hypovolemia causes a more rapid response

UTHSC M2016 CBD - Renal (7 decks)

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