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Unit 7: Physiology > Regulation of Plasma Sodium and ECF Volume (13) > Flashcards

Regulation of Plasma Sodium and ECF Volume (13) Flashcards

1
Q

Where are the osmolarity sensors?

Where are the volume sensors?

A

Osmolarity sensors: Hypothalamus

Volume sensors: Carotid sinus, aortic arch, renal afferent arteriole, atria

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2
Q

How are changes in ECF volume “sensed”?

A

Volume receptors that sense stretch

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3
Q

True or False: You can consume Na+ much faster than your kidney can get rid of it.

A

True

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4
Q

What is a rapid increase in body weight a measure for?

A

It is a measure of rapid increase in ECF volume (which shows an abrupt increase in NaCl)

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5
Q

What is positive Na balance?

A

Not excreting as much as consuming.

It is an increase in the amount of NaCl in the ECF, resulting in an acute increase in an isosmotic expansion of the ECF volume

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6
Q

What is negative Na balance?

A

Not consuming as much as excreting

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7
Q

With an abrupt increase in Na consumption, what happens to plasma osmolarity and ADH levels?

A

Both increase

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8
Q

What is the effective circulating volume?

A

A functional, not an anatomical, blood volume reflecting the extent of tissue/ organ where blood pressure is sensed

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9
Q

True or False: The effective circulating volume normally parallels the total ECF volume

A

True

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10
Q

Regulation of sodium excretion is induced by….Changes in Effective circulating volume or the total ECF volume?

A

Changes in the effective circulating volume

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11
Q

When there is decreased circulating volume, what happens to renal perfusion?

A

It decreases, which leads to activation of the RAA system (which then further increases Na retention and edema)

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12
Q

Which edematous disease states are associated with increased capillary hydrostatic pressure?

A

CHF, and Pulmonary edema

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13
Q

Which edematous disease states are associated with decreased plasma oncotic pressure?

A

Liver disease and nephrotic syndrome

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14
Q

Which is more important, low pressure sensors or high pressure sensors?

A

Low pressure sensors

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15
Q

What are the systems of feedback control of effective circulating volume?

A
  1. RAA hormonal system
  2. Increased renal sympatheic nerve activity
  3. The posterior pituitary releases ADH
  4. Reduced ECF volume also decreases the release of ANP
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16
Q

What is angiotensinogen?

A

Synthesized by liver and relseased into systemic circulation, it is the substrate of renin

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17
Q

What is renin?

A

Synthesized and stored in granular cells of the JG apparatus of the kidney

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18
Q

What is angiotensin I?

A

Substrate of ACE

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19
Q

What is the action of angiotensin II?

A

1- Induces aldosterone release from adrenal cortex

2- Acts on hypothalamus to increase thirst and release ADH

3- Vasoconstricts renal and other systemic vessels

4- Enhances Na/H exhange in the proximal tubule, which increases sodium reabsorption

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20
Q

What are the three renal mechanisms regulating renin release?

A

1- local real baroreceptors in afferent arterioles respond to low pressure and increase secretion of renin by granular cells

2- decreased systemic arterial blood pressure stim baroreceptor reglec which caused release of renin by JG apparatus stimulation

3- Cells of macula densa sense tubular fluid Na concentration….if low it causes the release of renin from granular/ JG cells

21
Q

What is aldosterone?

A

A mineral corticoid secreted into circulation by the adrenal cortex

22
Q

What is the primary long term regulator of salt balance and extracellular fluid volume and therefore BP?

A

Aldosterone

23
Q

What does aldosterone do to the kidney tubules?

A

Increases the reabsorption of Na and increases the secretion and excretion of K+

24
Q

Which cells does aldosterone act on?

A

Principal cells in the distal tubule and early collecting duct of the renal cortex

25
Q

How does aldosterone increase Na reabsorption?

A

Increased basolateral membrane Na/K pumps

Increased apical Na channels

Increased mitochondrial enzymes (ATP)

26
Q

True or False: Soulte reabsorption in cortical nephron segments participates in the counter current multiplication of the corticomedullary solute concentration gradient

A

False…it is actually rapidly returned to the general circulation and DOES NOT participate in the counter current multiplication of the cortico-medullary solute concentration gradient

27
Q

WHen in Na balance, what percentage of filtered Na is excreted?

A

0.4%

28
Q

Can sodium be secreted?

A

No…only filtered and reabsorbed (and then excreted)

29
Q

Where is the majority of Na reabsorbed?

A

The proximal tubule

30
Q

In the distal tubule/ collecting duct, what is Na reabsorption coupled to?

A

The secretion of K+

31
Q

What is hypernatremia?

A

An increase in plasma sodium concentration to a level above normal range

32
Q

What is normal sodium range?

A

135-145 mEq/L

33
Q

What are the symptoms of hypernatremia?

A

Lethargy, weakness and irritability

34
Q

What are the severe symptoms of hypernatremia and when is it seen?

A

Seizures and coma may occur at levels above 158 mEq/L

35
Q

In general, what is hypernatremia caused by?

A

A loss of water in excess of solutes from th eplasma due to inadequate consumption of water in excess of solute

and/ or

An inappropriate renal excretion of water in exces of solute

36
Q

The following are causes of what condition?

Inadequate water consumption
Extreme sweating
Severe diarrhea
Excessive renal excretion of water (polyuria)

A

Hypovolemia Hypernatremia

37
Q

What two medical conditions are associated with excessive renal excretion of water?

A

Diabetes mellitus and diabetes insipidis

38
Q

In central diabetes insipidus, what is the cause of polyuria?

A

Inadequate release of ADH from the posterior pituitary in response to an increase in plasma osmolariy

39
Q

What is the cause of polyuria in nephrogenic diabetes insipidus?

A

An inability of the collecting tubule and collecting duct to respond to ADN by increasing water permeability despite adequate release of ADH in response to increased plasma osmolarity

40
Q

What are the causes of hypervolemic hypernatremia?

A

Excessive hypertonic fluid consumption (seawater)

IV infusion of hypertonic saline

Hyperaldosteronism

41
Q

What is hyponatremia?

A

Decrease in sodium concentration to a level below the normal range

42
Q

What are the symptoms of hyponatremia?

A

Nausea, vomiting, headache, lethargy, fatigue, loss of appetite, restlessness and irritability, muscle weakness, spasms or cramps

43
Q

What are the symptoms of severe hyponatremia and what level are they seen at?

A

Neuro deficits, brain swelling, seizures, coma

Na levels below 125 mEq/L

44
Q

In general, what is the cause of hyponatremia?

A

Caused by a gain of water in excess of solutes in the plasma due to:

An extreme, excess consumption of water and an inappropriate increase in “free water” reabsorbed by the kidney

45
Q

What are the causes of hypervolemic hyponatremia?

A

In appropriate reab or water in excess of solutes from the tubular fluid to the plasma effectively increases plasma volume and dilutes plasma Na

46
Q

What are some diseases associated with hypervolemic hyponatremia?

A

CHF, kidney failure, liver failure, Syndrome of Inappropriate Anti-Diuretic Hormone, Polydispia

47
Q

What are some causes of hypovolemic hyponatremia?

A

May occur in a clinical setting where plasma volume reduction is extreme where consumption of water as well as increased “water in excess of solute” reabsorption by the kidney is insufficient to correct volume depletion by is sufficient to decreases plasma Na

48
Q

What clinical conditions are associated with hypovolemic hyponatremia?

A

Addison’s disease (adrenal insifficiency)

Severe vomiting or diarrhea

Unit 7: Physiology (19 decks)

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