Regulation of Sodium Balance and Extracellular Fluid Volume Flashcards Preview

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Flashcards in Regulation of Sodium Balance and Extracellular Fluid Volume Deck (35)
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What are some important factors that are determined by ECFV regulation?

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


How is ECFV calculated?
• What is the relationship between ECFV and sodium?

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+


Why do we say that Pna (plasma sodium) is constant?
• when is this not true?

• 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


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

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+


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

• 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


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

150 mEq


What are some condition that may lead to sodium imbalance?

Excessive Sweating


How much Na+ passes through the glomerulus each day?
• what happens to it after that?

~ 25,000 mEq of Na/day

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%)

150-250 mEq/day

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


What are some key causes of Hypovolemia?
• what are some key signs that you're becoming hypovolemic?

• Diarrhea/Vomiting
• Severe Burns
• Excessive Sweating

• LOW SYSTOLIC and DIASTOLIC blood pressure


What are some key causes of Hypervolemia?
• associated signs?

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

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


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


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)


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

• Increased Urination (diuresis)
• Solutes are conserved


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

Ridding XS H2O:
• Happens in like 0.5 hrs

Ridding XS Na+:
• take 2-4 DAYS

**Water regulation is clearly much faster


What happens when a normal person ingests extra salt?
• what happens when they go off of this diet?

• 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

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


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

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


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

1. Neural Stretch Receptors - Large Veins

2. Atrial Stretch Receptors - Atrial Stretch Receptors

3. Arterial Baroreceptors - Arterial Baroreceptors


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

• Neural Stretch Receptors
• Atrial Stretch Receptors
• Arterial Baroreceptors

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


What does ANP do?

Stimulates Na Excretion from the kidney


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

High GFR:
• Rapid Na+ excretion

Low GFR:
• More Na+ Retention


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

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


What effect does aldosterone have on the kidney?
• where does it act?

• Aldosterone Increases Reabsorption of Na+
• Acts in the Distal Tubule and Collecting Duct


What effect does Natriuretic hormone have on the kidney?

• Less Na+ reabsorption


What effect does RAAS have on the kidney?

• Decreases ECFV and Increases Na+ reabsorption


Would you be able to detect a 10% increase in GFR?
• what would this do to sodium excretion?

• 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+


What is pressure Natriuresis?
• describe what is does in a kidney that is not in the in tact system

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.


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

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


How rapidly are the effects Aldosterone observed?

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


• Source
• Stimulus/Inhibition
• Actions

• Mineralcorticosteroid secreted by the adrenal cortex

• Plasma K+
• Angiotensin

• Na+

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

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


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?

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


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

• Cardiac Atria

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

• Renal Blood Vessels
• Several Renal Tubular Segments

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