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Renal > Regulation of Sodium and Water Balance > Flashcards

Regulation of Sodium and Water Balance Flashcards

1
Q

Why do changes in Na+ balance alter ECF volume?

A

[Na+] affects osmolality, which determines fluid movement between ECF and ICF

Osmolality changes also alter thirst and ADH release, which alters volume

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2
Q

Effective circulating volume

A

Portion of ECF contained w/in vasculature that is perfusing tissues

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3
Q

How is ECV influenced by changes in Na+ balance?

A

ECV reflects the activity of volume receptors (heart), and thus Na+ balance

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4
Q

What are mechanisms by which the body monitors ECV?

A

Vasculature baroreceptors (low and high pressure)

Volume receptors (Atria and R ventricle)

Hepatic volume and [Na+] sensors

CNS [Na+] sensors (carotids and CSF

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5
Q

In low volume, what are the major signals acting on the kidneys to alter Na+ excretion?

A

Volume receptors (SNS)

Vascular baroreceptors (SNS and ADH)

TG Feedback (RAAS)

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6
Q

In high volume, what are the major signals acting on the kidneys to alter Na+ excretion?

A

Atrial distention (ANP)

Ventricular distention (BNP)

Vascular baroreceptors (less SNS and ADH, more parasympathetics)

TG feedback (?)

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7
Q

What are some major signals acting on the kidneys based on Na+ concentration to alter Na+ excretion?

A

Osmolality receptors (ADH)

Hepatic portal blood [Na+] receptors (SNS)

CNS [Na+] sensors (Ang2/NP’s)

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8
Q

How is NaCl intake/excretion related to ECF volume over time?

Why?

A

Over time, NaCl intake = isosmotic fluid intake (and vice versa)

Any changes in NaCl concentration will cause regulatory changes in water balance until ECF osmolarity is returned to normal, regardless of volume changes

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9
Q

When talking of ECF volume, what other volume-based concepts are directly related?

A

Vascular volume

Blood pressure

Cardiac output

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10
Q

CHF

A 
Decreased BP and CO
Baroreceptors cause ADH release
Excess NaCl and H20 retained
Increased ECF volume as a result
Excess volume overflows into interstitium
Edema
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11
Q

Hepatic cirrhosis

A 
Portal vein blockage
Venous return to heart decreased
Venous pressure increased
Decreased ECV and perfusion
Baroreceptors cause ADH release
NaCl/H20 retention causes edema
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12
Q

Unilateral renal artery atherosclerosis

A 
Reduced renal perfusion pressure
TG feedback
RAAS
Vasoconstriction
Increased systemic BP
Opposite kidney TG feedback (+Ang2 from 1st)
Renin cut off
Further water/Na loss
Drop in BP
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13
Q

Effects of increasing SNS in the kidney

A

Constriction –> decrease GFR

Granular cells –> renin

PCT –> NaCl reabsorption (Starling)

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14
Q

Invoking the SNS in the kidney has what overall goal?

A

Restore ECF volume to normal (euvolemia)

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15
Q

What causes renin release? (3)

A

Low afferent perfusion pressure

Beta-adrenergics on granular cells (SNS)

TG feedback (low NaCl delivery)

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16
Q

How to inhibit renin release?

A

Intracellular calcium, ANP, NO, PGI2

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17
Q

The release of renin has what overall goal?

A

Maintain systemic arterial pressure for tissue perfusion

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18
Q

Functions of Ang II (5)

A

Aldosterone release (adrenal)

Vasoconstriction (increase BP)

ADH secretion + thirst (SFO and OVLT in brain)

Increased SNS (receptors in brain)

PCT NaCl reabsorption

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19
Q

Overall goals of Ang II?

A

Increase BP, decrease RBF, maintain GFR

Increase reabsorption

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20
Q

What causes the release of aldosterone? (2)

A

Ang II

Increased plasma [K+]

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21
Q

Function of aldosterone

A

NaCl reabsorption in the DCT/CD

22
Q

Ionic exchange as a result of aldosterone

A

Cl- reabsorption

K+ / H+ secretion

23
Q

What ions are affected by aldosterone?

Why?

A

Na, Cl, H, K

Increased Na/Cl symporter abundance
Increased apical Na+ permeability
Increased apical K+ permeability
Increased H+ ATPase in intercalated cells

24
Q

What causes the release of natriuretic peptides?

What causes that?

A

Atrial/ventricular dilation

Volume expansion / heart failure

25
Q

Function of natriuretic peptides

A

Relax vascular smooth muscle

Promote NaCl/H2O excretion

26
Q

How do natriuretic peptides work?

A

Increase GFR and Na+ filtered load (afferent dilation, efferent const.)

Inhibit renin, aldosterone (direct and indirect), NaCl reabsorption (direct and indirect), ADH

27
Q

What is the goal of Na+ reabsorption early in the nephron?

A

Constant delivery to DCT/CD for regulation

28
Q

What is the goal of Na+ reabsorption in the late nephron?

A

Match NaCl intake, etc.

29
Q

How does the proximal nephron maintain constant Na+ delivery to the late nephron? (3)

A

Autoregulate GFR (thus filtered load)

GT balance (PT load ∆ = PT reabsorption ∆)

Load-dependent reabsorption in Loop

30
Q

In a volume expansion, what is the first goal of the body’s regulation?

What signal and effects start this?

A

Increase Na+ excretion

Volume sensors –> decrease SNS, increase NPs, inhibit ADH and renin and aldosterone

31
Q

Results of vascular volume sensor and downstream effects in volume expansion (4)

A

Increase GFR

Increase Na+ filtered load

Decrease Na+ reabsorption in PT (Starling)

Decrease Na+ reabsorption in DT/CD (NPs + saturation)

32
Q

When is ADH released?

A

Low volume (baroreceptors)

High osmolality (osmoreceptors)

Ang II stimulation in brain (SFO, OVLT)

33
Q

ADH is released in volume depletion and osmolality increase.

When both are present simultaneously, how is ADH release affected?

Function of this?

A

Volume depletion –> lower osmolality necessary for ADH to be released

So ADH is released at a level below normal osmolality RATHER than only in HYPERosmolality

FUNCTION = get ADH going SOONER

34
Q

Functions of ADH (4)

A

Vasoconstriction (SM)

Increased Na/K/Cl2 transporter action (TAL)

Increased urea reabsorption (CD)

Increased aquaporins (CD)

35
Q

SIADH

A 
Excess ADH release
Excess H2O retention
[Hyponatremia]
Increased Na+ excretion (Starling)
[MORE hyponatremia)
36
Q

A patient is hypernatremic or hyponatremic. What is ALWAYS the cause?

A

Volume contraction or expansion

37
Q

How does the body deal with excess sodium?

A

The excess causes a rise in ECF/ECV, which causes signal release for Na+ excretion

38
Q

Diabetes insipidus (3 types)

A

Neurogenic - ADH doesn’t release

Nephrogenic - aquaporins don’t form

Gestational - abnormally low ADH in pregnancy

39
Q

When is Na+ reabsorbed more than normal?

A

When ECF in decreased

40
Q

How does FENa relate to ECV volume?

So?

A

Directly related

Low volume = low excretion
High volume = high excretion

41
Q

What are the short term and long term effects of loop diuretics on renin release?

A

Short term – less Na reabsorption (TAL) = more delivery to DT = TG feedback = LESS renin

Long term – less delivery to DT because volume depletion = TG feedback = MORE renin

42
Q

For a general renal injury, what is an acute (short term) time span?

What is a chronic (long term) time span?

A

Acute 2 days

43
Q

Hyperaldosteronism

A

Increased Na+ reabsorption and K+ secretion = hypokalemia

Increased H+ ATPase (intercalated cells) = alkalosis

44
Q

In a chronic state, why would a patient with high aldosterone or Ang II have low renin?

A

Negative feedback mechanisms on renin (aldosterone OR Ang II)

45
Q

Urodilatin

A

Endogenous to kidney

Secreted by DT/CD due to increased ECF volume and arterial pressure

46
Q

Function of urodilatin

A

Suppresses Na/H2O reabsorption in CD

47
Q

How does urodilatin affect BP?

A

NO EFFECT

Local effect only

48
Q

Intrarenal PGs

A

Increase GFR by dilating renal arterioles

Decrease reabsorption by increasing capillary flow

49
Q

A patient has a disease in which an abnormal amount of intrarenal PGs are released (hyperactive COX-1). What is the renal danger of this disease?

A

Wash out medullary hyperosmolarity by inhibiting ion reabsorption

Trouble concentrating urine –> volume depletion

50
Q

What is the danger of taking drugs that increase RBF?

A

Can inhibit the ability to concentrate urine

Renal (11 decks)

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