Regulation of ECF Volume and Water Balance Flashcards
[…] is the major effective osmole in the ECF and determines the movement of water into/out of cells
NaCl
How can you estimate the plasma osmolality (Posm) of a patient?
Measure serum [Na+] and mulitply by 2 to account for equal parts Cl- for each Na+ molecule
Ex: serum Na+ = 145 mEq / L then Posm = 290 mEq / L
When a person is hyponatremic or hypernatremic, what is driving that change in [Na+]?
Water
Too much = hyponatremia
Too little = hypernatremia
The driving force for fluids to shift between the body’s fluid compartments is driven by what?
Most important take away - WATER MOVES across the membrane, not the Na+
What if there is isoosmotic volume change? Will there be shifts between body fluid compartments?
No
IMPORTANT: Fluid shifts occur ONLY IF […] osmolality changes.
ECF
Additional questions:
- Calculate TBW and ICF, ECF volumes before infusion.
- Calculate again after infusion.
- Does plasma volume (25% of ECFV) change?
ECF
Why does water balance change body fluid osmolality?
If you were to add 1L of pure water to a person’s body (i.e. ingestion or IV infusion):
- Where is this fluid added?
- What is the effect on osmolality?
- What will be the response of the kidneys?
- ECF
- Decreased
- Decrease reabsorption of water to increase excretion of water to restore normal osmolality
If you were to remove 1L of pure water from a person’s body:
- Where is this fluid removed from?
- What is the effect on osmolality?
- What will be the response of the kidneys?
- ECF
- Increase
- Increase reabsorption of water to restore normal fluid volume and osmolality
What will be the impact on levels of ADH and thirst in the two scenarios shown by this image?
Explain how the body senses changes in osmolality.
Explain what this graph is showing.
Explain how ADH leads to increased reabsorption of water in the kidney.
ADH in blood –> binds to V2 receptor on basolateral surface of cells in DCT and CD –> V2 is GPCR that stimulates AC to increase production of cAMP –> cAMP travels to nucleus and binds to cAMP response element which increases transcription of gene for aquaporin 2 channel –> AP2 loaded into membrane of vesicles and trafficked to membrane where vesicles fuse with membrane to deliver AP2 –> increased water reabsorption. This also by proxy increases Na+ reabsorption b/c Na+ travels with water. In the absence of ADH, CD does not have any aquaporins and thus does not reabsorb water unless in presence of ADH.
Given the case below:
- What will happen to fluid volume in her body compartments?
- What will happen to osmolality in her body compartments?
- How will the body respond?
- How would you describe her condition in one sentence?
- What will happen to her urine production?
- What will happen to levels of ADH?
- What will happen to her levels of thirst?
- What will be her urine flow rate and osmolality?
- ECF volume will decrease, which will drive decrease in ICF also
- Osmolality will increase because she’s losing more water than Na+. Although osmolality will increase relative to her starting osmolality, it will be isoosmotic across her body compartments (i.e. Osm of ECF = Osm of ICF, both will be hyperoosmotic)
- Correct osmolality and volume –> THESE ARE FIXED BY DIFFERENT MECHANISMS
- Hyperosmotic volume contraction due to excess water loss
- Decrease, need to increase volume
- ADH will be elevated
- 5% increase in plasma Osm so thirst will be elevated
- Flow rate decreased, concentrated urine so hyperosmotic urine
B
- Where in the nephron does ADH exert its effects?
- What are its effects at these locations?
Describe how the suppression of ADH leads to dilute urine at the different segments of the nephron.
Urine in the PCT and PST is isoosmotic because there is equal reabsorption of water and Na+. In thin decending limb, Osm increases as move down limb so water will be reabsorbed and removed from urine, making urine hyperosmotic. As urine travels up thick ascending limb, Na+ is removed which results in diluted urine. The Na+ that is removed helps maintain the gradient of interstitial Osm. In the absence of ADH, this process still occurs but that explains why in the presence of ADH the interstitial Osm gradient is much higher, since ADH increases Na+ reabsorption in the TAL. Urine leaving thick ascending limb is hypoosmotic due to removal of solute. When reaches collecting duct, in absence of ADH, no water is removed but more solute is removed so it becomes even more hypoosmotic and thus we get dilute urine.
Describe how the activation of ADH leads to concentrated urine.
Urine in the PCT and PST is isoosmotic because there is equal reabsorption of water and Na+. In thin decending limb, Osm increases as move down limb so water will be reabsorbed and removed from urine, making urine hyperosmotic. In the presence of ADH, the interstitial gradient is much higher due to icreased Na+ in interstitium, so even more water is removed from the urine so urine is very concentrated. Urine entering TAL is concentrated and now has a lot of Na+ removed b/c ADH is present so more solute is removed (Na+, K+, 2Cl- co transporter) leading to once again hypoosmotic urine in the DCT even in the presence of ADH which is supposed to concentrate the urine. When urine reaches the CD, ADH promotes increased aquaporins so there will be increased H2O reabsorption leading to increased Osm and thus ultimately concentrated urine.
Describe what ADH does to the cells of the thick ascending limb.
Increases activity of Na+/K+/2Cl- co-transporter to further dilute urine by removing solute. This makes the interstitium have a higher osmolality so the nephron can reabsorb more water in the thin descending limb.
