Regulation of Sodium Balance and Extracellular Fluid Volume Flashcards

1
Q

What are some important factors that are determined by ECFV regulation?

A

ECFV Determines:
• Plasma Volume which determines…
• Circulatory Filling Pressure
• Cardiac Output

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2
Q

How is ECFV calculated?

• What is the relationship between ECFV and sodium?

A

ECFV = Amount of ECF Na+ / Pna

At constant Plasma Na concentration ECFV is proportional to total body Na

**Note: Pna = Plasma Concentration of Na+; is pretty constant so ECFV is really only dependent on Amt. of ECF Na+

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3
Q

Why do we say that Pna (plasma sodium) is constant?

• when is this not true?

A
  • Pna is kept constant by AVP(ADH)-mediated water regulation by the kidney
  • Pna change only occurs when gain or loss of Na+ exceeds thirst Mechanism and Kidney’s ability to correct the situation
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4
Q

T or F: Plasma sodium is a god reflection of ECFV.

A

False, Plasma Na is always kept CONSTANT by ADH-mediated regulation of water reabsorption in the kidney

**ECFV is the main thing that changes with increased Na+

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5
Q

How do healthy individuals respond to changes in salt intake?
• what about someone with renal dysfunction?

A

Normally:
• We just increase salt output (takes 2-4 days for kidney to make adjustment)

Renal Pathology:
• They Cannot adjust to secrete more so they just increase ECFV to dilute salt in the body back to a normal level

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6
Q

How much salt do you have to retain to gain 1kg (2.2lbs)?

A

150 mEq

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7
Q

What are some condition that may lead to sodium imbalance?

A

Diarrhea
Excessive Sweating
Diuretics

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8
Q

How much Na+ passes through the glomerulus each day?

• what happens to it after that?

A

~ 25,000 mEq of Na/day

Reabsorption: 
Proximal Tubule: 16,000 mEq/day (64%) 
Ascending LOH: 7,000 mEq/day (28%) 
Distal CT: 2000 mEq/day (8%) 
Collecting Duct: 1750 mEq (7%) 

Excretion:
150-250 mEq/day

**NOTE: the rate of excretion should be equal to our daily intake

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9
Q

What are some key causes of Hypovolemia?

• what are some key signs that you’re becoming hypovolemic?

A

Causes:
• Diarrhea/Vomiting
• Severe Burns
• Excessive Sweating

Signs:
• LOW SYSTOLIC and DIASTOLIC blood pressure
• ORTHOSTATIC HYPOTENSION

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10
Q

What are some key causes of Hypervolemia?

• associated signs?

A

Causes:
• Congestive Heart Failure (may be the cause or the 2º)
• Chronic Renal Failure

Signs:
• JVD - 2-3 liters of fluid
• S3 Gallop
• Pulmonary Edema

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11
Q

In what cases might you see edema with normal ECFV or even Low ECFV?

A

HYPOALBUMINEMIA

Caused by:
• Liver Disease - prot. never produced
• Nephrotic Syndrome - loss of prot. in urine.
• Burns (may loose lots of protein in add’n to fluid)

**Less protein in vessel means less fluid is in the vascular system and more is in the interstitial fluid (increased ISF)

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12
Q

How does your body compensate when you drink too much water?

A
  • Increased Urination (diuresis)

* Solutes are conserved

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13
Q

What is the difference in response time of increased H2O in the system and increased Na+?

A

Ridding XS H2O:
• Happens in like 0.5 hrs

Ridding XS Na+:
• take 2-4 DAYS

**Water regulation is clearly much faster

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14
Q

What happens when a normal person ingests extra salt?

• what happens when they go off of this diet?

A

ADDITION:
• It takes 2-4 days for the output to catch up to and match the intake

**During this time of increased Na+ intake you will gain H2O wt. - this is corresponds with the adjustment of the kidney.

**Note: even in a properly functioning kidney you gain wt. because you are constantly putting in more Na+ at the same high rate

REMOVAL:
• When Na+ is removed, it take 2-4 days for balance to be restored as well

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15
Q

How does your therapy differ for salt sensensitive and salt insensitive hypertensive patients?

A

Salt Sensitive:
• Not Good at filtering salt so you MUST GIVE DIURETIC to help them clear salt

Salt Insensitive:
• Will reduce ECFV naturally as they excrete salt

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16
Q

What 3 types of receptors are involved in detection of ECFV?
• location

A
  1. Neural Stretch Receptors - Large Veins
  2. Atrial Stretch Receptors - Atrial Stretch Receptors
  3. Arterial Baroreceptors - Arterial Baroreceptors
17
Q

What do the following receptors respond to?
• how do they modulate the bodies defense against stretch?

  • Neural Stretch Receptors
  • Atrial Stretch Receptors
  • Arterial Baroreceptors
A

Neural Stretch Receptors:
• Responds to stretch due to VENOUS DISTENTION
• DOWNREGULATES ADH/AVP to increase water and Na+ excretion

Atrial Stretch Receptors:
• Parasympathetic fibers in VAGUS NERVE affect centers involved in:
–> AVP secretion
–> Sympathetic Firing to Kidney
–> CV centers
• ALSO ANP (atrial neurogenic peptid is released)

Arterial Baroreceptors:
• Arteries
• Controls AVP/ADH secretion

18
Q

What does ANP do?

A

Stimulates Na Excretion from the kidney

19
Q

What effect does Increased Glomerular Filtration have on Sodium Excretion?
• decreased?

A

High GFR:
• Rapid Na+ excretion

Low GFR:
• More Na+ Retention

20
Q

What are 5 key factors that regulate SODIUM excretion in the kidney?

A
  1. Changes in GFR
  2. Aldosterone
  3. Natriuretic Hormone
  4. Renin-Angiotensin System
  5. Sympathetic nn. Prostaglandins, etc.
21
Q

What effect does aldosterone have on the kidney?

• where does it act?

A
  • Aldosterone Increases Reabsorption of Na+

* Acts in the Distal Tubule and Collecting Duct

22
Q

What effect does Natriuretic hormone have on the kidney?

A

• Less Na+ reabsorption

23
Q

What effect does RAAS have on the kidney?

A

• Decreases ECFV and Increases Na+ reabsorption

24
Q

Would you be able to detect a 10% increase in GFR?

• what would this do to sodium excretion?

A
  • 10% increase would not be detectable because serum creatinine is not a sensitive enough measure to see this change.
  • Sodium excretion will still be bumped up big time because much you will be pushing much more fluid through the nephrons

E.g. Eating a lot of pizza will increase Na+ and ECFV and you will get thirsty. Increased arterial pressure will result and you’ll increase GFR and pee out Na+

25
Q

What is pressure Natriuresis?

• describe what is does in a kidney that is not in the in tact system

A

Pressure natriuresis is a feedback regulatory mechanism for an increase in arterial pressure. If the systolic BP is increased by 50% there will be a 3-5 fold increase in Na excretion in the urine, thus reducing ECFV and reduction of BP. Of course smaller changes in BP will not significantly change GFR due to auto regulation.
However, an abnormal pressure natriuresis may contribute to chronic hypertension.

26
Q

What is the role of pressure natriuresis in the intact system?

A

• It synergizes with other factors such as those involved int DOWNregulation of RAAS to RAPIDLY respond to changes in pressure

27
Q

How rapidly are the effects Aldosterone observed?

A

Aldosterone - involved in Na+ up-regulation via several Na+ channels

• Knowing that it takes 2-4 days to respond to Na+ increases and that Aldosterone works through GENE EXPRESSION

28
Q
Aldosterone: 
• Source 
• Stimulus/Inhibition
• Actions
• MOA
A

Source:
• Mineralcorticosteroid secreted by the adrenal cortex

Stimulus:
• Plasma K+
• Angiotensin

Inhibition:
• Na+

Actions:
• Acts Exclusively in DCT and CD
• INCREASES Na+ Reabsorption

MOA:
• Increased Na+/Cl- cotransporter
• Increased NKA (on basolateral surface)
• Increased Krebs Cycle enzymes from increased ATP synthesis

29
Q

Would you expect aldosterone to respond to play a role in rapid regulation of Na+ excretion in the case of bolus administration of isotonic saltine and hemorrhage?

A

No, because it works on gene expression it has a relatively SLOW effect on Na+ reabsorption

30
Q
Natriuretic Peptides (ANP,ANF, ANH) 
• Source
• Target 
• when is it excreted? 
• Actions
A

Source:
• Cardiac Atria

When is it excreted?
• Direct stimulation via atrial distintion and Increases when Pna increases

Target:
• Renal Blood Vessels
• Several Renal Tubular Segments

Actions:
• Tubule - Inhibits Na+ reabsorption
• Renal Vessel - Increases GFR and Na+ excretion
• Adrenal Cortex: inhibits aldosterone secretion

31
Q

What cells are responsible for kicking off the RAAS cascade?
• what are the active products of this cascade?
• Effect on ECFV?

A

• Juxtaglomerular Cells sense DROP in ECFV and release Renin

Angiotensin II = Active:
• 1st directly Sodium/Hydrogen Exchanger in the Proximal Tubule to increase Na reabsorption

• 2nd stimulates ALDOSTERONE secretion from the adrenal cortex which in turn increases Na reabsorption via Na channels in the Distal Tubule

Overall, increases ECFV!

32
Q

T or F: sympathetic nerves really only effect GFR under non-physiologic conditions.

A

True, GFR gets decreased from Vessel Constriction and Sodium Reabsorption is increased

33
Q

What effect do Prostaglandins, Bradykinin, and Dopamine have on kidney?
• where are they produced?

A
  • Produced in Kidney

* cause Diuresis and Natriuresis

34
Q

***What is the effect of Ouabain like factor?

A
  • Produced in atrium

* Diuresis and Natriuresis

35
Q

Important Note on Aldosterone, ANP, and GFR.

A
  • Aldosteropne produces slow effect. Takes few days to adjust change in total body Na content and ECFV.
  • ANP has moderate effect. Works only under conditions of volume expansion. Only 3-5 fold increase in Na excretion
  • GFR can produce a rapid effect, but autoregulation can be a problem.