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
Q

Angiotensin II and aldosterone play an important role controlling

A

SODIUM REABSORPTION

26
Q

angiotensin II and aldosterone DO NOT play a role in controlling

A

SODIUM CONCENTRATION

27
Q

increased levels of angiotensin II and aldosterone

A

will increase sodium reabsorption AND water reabsorption (Change in total amount of sodium and total amount of water, but no change in concentration)

28
Q

Extremely high levels of aldosterone will only produce an increase in sodium concentration of

A

3 to 5 mEq/Liter

29
Q

Complete loss of aldosterone secretion can lead to a

A

significant decrease in sodium concentration

30
Q

Sodium depletion leads to

A

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