Control of Extracellular Osmolarity and Sodium Concentration Flashcards

1
Q

Sodium most abundant ion

A

extracellular fluid  Range 140 to 145 mEq/Liter  Average 142 mEq/Liter

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2
Q

osmolarity  Average

A

300 mOsm/Liter [282 mOsm/Liter – corrected for

interionic attraction]  Range 291 to 309 mOsm/Liter [± 2% to 3%]

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3
Q

precise control of sodium and osmolarity important because

A

they control distribution of water between intracellular and extracellular compartments

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4
Q

Sodium and associated anions (chloride and bicarbonate) account for

A

94% of all extracellular solute

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5
Q

Glucose and urea contribute

A

3 to 5% of total osmolarity  Urea able to permeate cells easily so exerts little effective osmotic force

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6
Q

Sodium not very permeable so

A

has big effect on fluid movement between extracellular and intracellular compartments

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7
Q

Plasma osmolarity =

A

2.1) x (Plasma concentration sodium)  Posm = (2.1) x (142 mEq/L) = 298 mOsm/L

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8
Q

Two systems control / regulate extracellular osmolarity and sodium concentration

A

 Osmoreceptor – ADH system  Thirst mechanism

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9
Q

Osmoreceptor Cells location, response, impulses, release, which does what?

A

 Located in anterior hypothalamus  Cells shrink in response to increased ECF [Na+] (i.e.
increased osmolarity)
 As cells shrink, number of impulses sent to other nerve cells in supraoptic nuclei
 Impulses passed to posterior pituitary  Impulses stimulate release of AHD 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

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10
Q

Osmoreceptor Cells

 Increased osmolarity results in increased water permeability which allows

A

water to be reabsorbed (conserved) while sodium continues to be excreted at normal rate

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11
Q

ADH release is tied into

A

the arterial baroreceptor reflexes (which respond to changes in blood pressure) and the cardiopulmonary reflexes (which respond to changes in blood volume)

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12
Q

Reflex pathways tied into

A

hypothalamic nuclei that control ADH production and release

 Decreased blood pressure and/or decreased blood volume results in an increase in ADH release

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13
Q

A 15 to 20% reduction in circulating volume produces a

A

HUGE increase in [ADH]

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14
Q

Circulating volume must decrease approximately 10% before

A

appreciable change in [ADH]

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15
Q

factors that Increase ADH Release

A
Increased plasma osmolarity
Decreased blood volume
Decreased blood pressure
Nausea
Hypoxia
Morphine, Nicotine, Cyclophosphamide
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16
Q

factors that decrease ADH release

A

increase BV, increase BP, decrease plasma osmolarity, alcohol, clonidine, haloperidol

17
Q

Thirst center

A

Anteroventricular region of third cerebral ventricle (AV3V region) (Also promotes ADH release)
 Upper portion contains subfornical organ  Inferior portion contains organum vasculosum of the lamina terminalis

18
Q

thirst center located Anterolaterally in

A

preoptic nucleus

19
Q

thirst center neurons within area respond to changes in

A

osmolarity (function like

osmoreceptors)

20
Q

thirst mechanism stimulated by Na conc. of

A

2 mEq/Liter higher than normal  Thresholdfordrinking

21
Q

increase thirst

A
Increased plasma osmolarity
Decreased blood volume**
Decreased blood pressure**
Increased angiotensin II**
Dryness of mouth
22
Q

decrease thirst

A
Decreased plasma osmolarity
iNCREASED BLOOD VOLUME
Increased blood pressure
Decreased angiotensin II
Gastric distention
23
Q

With both osmoreceptor-ADH and thirst mechanism intake, able to prevent

A

though sodium intake has increases 6-fold

 Even if one system is not functional, other system still maintain the sodium concentration

24
Q

If both systems fail, there is no other system that can

A

regulate sodium concentration so sodium concentration will show large swings depending on sodium intake

25
Angiotensin II and aldosterone play an important role controlling
SODIUM REABSORPTION
26
angiotensin II and aldosterone DO NOT play a role in controlling
SODIUM CONCENTRATION
27
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)
28
Extremely high levels of aldosterone will only produce an increase in sodium concentration of
3 to 5 mEq/Liter
29
Complete loss of aldosterone secretion can lead to a
significant decrease in sodium concentration
30
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