test 9 part 2 Flashcards
(23 cards)
What is the most abundant ion in the ECF
Range 140 to 145 mEq/Liter
Average 142 mEq/Liter
osmolarity of ECF
Average 300 mOsm/Liter [282 mOsm/Liter – corrected for interionic attraction]
Range 291 to 309 mOsm/Liter [± 2% to 3%]
Sodium & Osmolarity of ECF
Precise control of both important because they control distribution of water between intracellular and extracellular compartments
Estimating Extracellular Osmolarity
Sodium and associated anions (chloride and bicarbonate) account for 94% of all extracellular solute
Glucose and urea contribute 3 to 5% of total osmolarity
Urea able to permeate cells easily so exerts little effective osmotic force
Sodium not very permeable so has big effect on fluid movement between extracellular and intracellular compartments
Plasma osmolarity = (2.1) x (Plasma concentration sodium)
Posm = (2.1) x (142 mEq/L) = 298 mOsm/L
H2O concentration controlled by
ADH
[Na] controlled by
- aldosterone
- angiotensin II
- amount of water (ADH)
Regulation of Osmolarity & [Sodium]
Multiple systems control sodium and water excretion via urine
Two systems control / regulate extracellular osmolarity and sodium concentration
Osmoreceptor – ADH system
Thirst mechanism
Osmoreceptor Cells
Located in anterior hypothalamus
Cells shrink in response to increased ECF [Na+] (i.e. increased osmolarity)
As cells shrink, increased number of impulses sent to other nerve cells in supraoptic nuclei
Impulses passed to posterior pituitary
Impulses stimulate release of ADH stored in secretory granules within nerve endings
Increased [ADH] of blood stimulates increased water permeability in late distal tubules, cortical collecting tubules, and medullary collecting tubules
Osmoreceptor-ADH Response
- water deficit results in increase in osmolarity -> increasing plasma ADH ->Increased water permeability of distal tubules/collecting ducts -> increasing water reabsorption -> decreasing water excreted
- Allows more water to be reabsorbed (conserved) while sodium continues to be excreted at normal rate
[ADH] Also Tied to Blood Pressure / CBV
ADH release is tied into the arterial baroreceptor reflexes
Which respond to changes in blood pressure
And the cardiopulmonary reflexes
Which respond to changes in blood volume
Reflex pathways tied into hypothalamic nuclei that control ADH production and release
Decreased blood pressure and/or decreased blood volume results in an increase in ADH release
Increase in [ADH] in response to
- increase in osmolarity
- decrease in CBV and BP
ADH Response to Osmotic vs Volume Changes
- A very small change (1%) in osmolarity caused a huge change in [ADH]
Circulating volume must decrease approximately 10% before appreciable change in [ADH]
A 15 to 20% reduction in circulating volume produces a HUGE increase in [ADH]
6 things that Increases ADH Release
- Increased plasma osmolarity
- Decreased blood volume
- Decreased blood pressure
- Nausea
- Hypoxia
- Morphine, Nicotine, Cyclophosphamide
4 things that Decreases ADH Release
- Decreased plasma osmolarity
- Increased blood volume
- Increased blood pressure
- Alcohol, Clonidine (antihypertensive), Haloperidol (dopamine blocker)
Thirst Mechanism
Controls fluid intake
Needed to replace fluid loss via sweating, breathing, GI tract
-input and output are equal and our overall CBV does not change
Thirst center
It is in the brain
when stimulated it promotes ADH release
- organum vasculosum is part of our thirst center
when thirst center is stimulated
causes immediate drive to drink
Drive continues as long as area is stimulated
Neurons within area respond to changes in osmolarity (function like osmoreceptors)
Stimulated by sodium concentration 2 mEq/Liter higher than normal
Threshold for drinking
Increased thirst caused by
- Increased plasma osmolarity
- Decreased blood volume (change in volume)**
- Decreased blood pressure (change in volume)**
- Increased angiotensin II**
- Dryness of mouth
- The mechanism for this response is probably driven by neural input from the baroreceptor and cardiopulmonary reflexes since circulating volume and blood pressure can change without changes in osmolarity
- ***Probably acts on organum vasculosum of lamina terminalis
- Takes 30 to 60 minutes to absorb and distribute ingested fluid. Gastric distension and relief of dry mouth quench the thirst drive so ingested water has time to be processed.
Decreased Thirst Caused By
- Decreased plasma osmolarity
- Increased blood volume
- Increased blood pressure
- Decreased angiotensin II
- Gastric distention
Tight Control of Sodium
- With both osmoreceptor-ADH and thirst mechanism intake, able to prevent large changes in sodium concentration even though sodium intake has increases 6-fold
Even if one system is not functional, other system still maintain the sodium concentration
If both systems fail, there is no other system that can regulate sodium concentration so sodium concentration will show large swings depending on sodium intake
Aldosterone and [Na+]
- Angiotensin II and aldosterone play an important role controlling SODIUM REABSORPTION
Angiotensin II and aldosterone DO NOT play a role in controlling SODIUM CONCENTRATION
Increased levels of angiotensin II and aldosterone will increase sodium reabsorption AND water reabsorption
Change in total amount of sodium and total amount of water, but no change in concentration
Extremely high levels of aldosterone will only produce an increase in sodium concentration of
3 to 5 mEq/Liter
Complete loss of aldosterone secretion
Complete loss of aldosterone secretion can lead to a significant decrease in sodium concentration
Sodium depletion leads to volume depletion and decreased blood pressure which activates thirst reflex and the cardiopulmonary reflex which results in further decrease in sodium concentration as volume is ingested and/or reabsorbed
