Renal: Salt and Water Balance Flashcards
What is the definition of osmo and volume regulation?
Osmoregulation: water regulation in the body to maintain constant ECF osmolarity.
Volume regulation: blood volume and pa regulation to ensure effective circulating volume
This is accomplished by regulating total amount (not conc) of Na in the ECF. The amount of Na determines volume bc where Na goes, water follows
What is the aim and mechanism of administering saline to a patient?
You add salt and water in equal proportion (isotonic saline), so ECF osmolarity will not change.
Since the cell membrane is impermeable to salts no habra change in osmotic gradient between ICF and ECF compartments.
Hence the added volume of isotonic saline will be retained in the ECF, expanding the volume of this compartment only.
Starling forces distribute this volume between plasma and ISF, increasing circulating volume.
How is renal Na excretion controlled?
Most filtered salt and water is reabsorbed in the PT – RAAS activity increases this
Much smaller fraction reabsorbed from DT and CD, under separate control by aldosterone and ADH.
Aldosterone mediated Na reabsorption increases plasma osmolarity.
This increases ADH secretion and water reabsorption.
Result is increased Na and water in ECF with little or no change in plasma [Na] or osmolarity- similar to iv saline
RAAS is the volume regulation system, ADH is the osmoregulation system.
What is the effect of aldosterone?
Acts on principal cells lining CD:
Increases Na/K ATPase
Increases expression of ENaC channels on luminal membrane, increasing Na+ reabsorption, K+ secretion
Acts on intercalated cells of CD
Increases H+ ATPase, causing increased H+ secretion and HCO3- reabsorption
What would happen if we added pure water to the ECF fluid compartment?
Adding pure water to the ECF compartment dilutes it. This forms an osmotic gradient, which means water shifts between the ECF and ICF by osmosis til eqm is re-established.
The net result is both the ECF and the ICF would be expanded.
So basically, changes in solute conc (osmolarity) of the ECF will cause shifts of water between ECF and ICF, and hence volume changes. Large shifts must be avoided, so osmolarity of the ECF must be regulated
The osmolarity of the ECF must be regulated to stay within safe limits. How is this done?
The osmolarity of the ECF is adjusted by adding or removing water, not solute.
This means dehydration will show as an increase in ECF osmolarity and too much water (overhydration) will show as a decrease.
How does ADH work as a defence against dehydration?
Net water loss increases ECF osmolarity (normal range 285-295 mOsm/kg)
Changes detected by osmoreceptors in anterior hypothalamus
PVN and SON neurons release ADH from their axon terminals in posterior pituitary
Threshold for ADH release is 280-285 mOsm/kg
Above this range small changes in osmolality produce large changes in ADH secretion
How does thirst defend against dehydration?
Osmoreceptors in anterior hypothalamus detect increased ECF osmolarity
Project to centres mediating thirst, drinking
Strong desire to drink when plasma osmolality ≥295 mOsm/kg
Oropharyngeal and upper GI receptors reduce thirst on drinking
Thirst is also stimulated by large drops in bp, Ang 2 acting on hypothalamus
What is the definition of hypernateraemia?
Hypernatremia does not mean too much Na; it means too little water!
The increase in Na concentration means there is a relative water deficit
Hypernatremia (Na > 145) always means hyperosmolality of ECF
What are the causes of hypernateraemia?
Gain of sodium (rare). Loss of water: Can occur in conditions associated w fluid loss (water loss> Na loss)
Extra-renal losses: dehydration, infection
Renal losses: osmotic diuresis: kidneys don’t dilute tubular fluid enough, reducing osmotic gradient between the tubular and ISF, impairing water reabsorption
Diabetes: glucose is left in the tubular fluid so is less dilute. This would impair the osmotic gradient for water reabsorption and lead to increased water loss.
How does diabetes insipidus cause hypernaterameia?
Renal water loss (inability to concentrate the urine) due to lack of effective ADH, either: Central (failure of secretion). Nephrogenic (lack of renal response)
Presents with polydipsia and polyuria
Thirst mechanism normally enough to prevent significant hypernatremia, but will rapidly develop if water access is restricted
What is hypoosmotic hyponaturaemia?
Water excess. ECF osmolality decreases (hypoosmolality). (Na < 135)
This can occur through fluid loss (hypovolemia) but only if net Na loss> water. There must be a dilution of ECF (hence check plasma osmolarity).
How can ADH pathology cause hyponaturaemia?
Continued ingestion of water without reducing ADH secretion will always lead to hyponatremia
Hyponaturaemia can be caused by Syndrome of inappropriate ADH secretion (SIADH). This syndrome also causes high urine osmolarity
Many causes of SIADH inc: CNS damage. Ectopic ADH production by tumour
How can the body send conflicting signals with regards to ADH release?
Low BP signals tell the hypothalamus to release ADH.
But al mismo tiempo, water retention lowers osmolarity, which signals to reduce ADH.
Here, circulation protection takes priority – ADH is released to restore volume, even at the cost of osmolarity.
So the normal role of ADH is osmoregulation. But, in a circulatory emergency it’s a last line of defence against volume depletion, temporarily ignoring the osmoregulatory function.
How can you get hypervolemia and hyponaturaemia?
Can occur when total sodium is increased, but total water is increased more Eg: congestive heart failure
RAAS ‘thinks’ body is hypovolemic, so you have Na/water retention (volume expansion)
Volume expansion is ineffective bc u have excess capillary filtration: oedema
Low volume signals activate ADH, causing hyponatremia
