Pathophysiology of Sodium Balance Flashcards

1
Q

T/F: Fat people have a lower fraction of their body weight attributable to water.

A

T. Since fat contains less water than other tissue, an obeast will have a lower water weight percentage.

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2
Q

ICF and ECF compartments are in ______ equilibrium.

A

Osmotic

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3
Q

T/F: Urea and other freely permeable solutes effect the movement of water between ECF and ICF.

A

F. If they are allowed to move freely, they don’t contribute to a gradient.

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4
Q

When will the movement of water across a membrane cease?

A
  1. When the concentration gradient dissipates.

2. When the increase in hydrostatic pressure balances out the osmotic pressure.

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5
Q

Do osmotic gradients develop between the vascular and interstitial compartments? Why or why not?

A

No. The capillary walls are fenestrated and permeable to all sorts of stuff. That’s kind of their job, actually.

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6
Q

How quickly do IV infusions of albumin and dextran cross the capillary wall?

A

They don’t. They’re much too big to get through the fenestrations.

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7
Q

How quickly do IV infusions of normal saline (.9% NaCl) cross the capillary wall into the interstitial space?

A

Very quickly. The small molecules can easily cross the barrier.

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8
Q

Definition of effective arterial blood volume. (EABV)

A

The amount of blood that is detected by volume sensors.

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9
Q

Where are the low-pressure baroreceptors located?

A
  1. Cardiac atria
  2. Left ventricle
  3. Pulmonary vascular bedr
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10
Q

What role does the brain play in low-pressure baroreceptor control of blood pressure?

A

In the state of volume expansion, these stretch receptors in the sensory send signals to the medulla and hypothalamus, which then decrease renal SNS activity, leading to a loss of sodium and decreased ECF.

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11
Q

Where are the high-pressure baroreceptors located?

A
  1. Aortic arch

2. Carotid bodies at the bifurcation of the carotid.

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12
Q

What role does the brain play in high-pressure baroreceptor control of blood pressure?

A

In the state of volume contraction, these receptors send a signal to the brain to increase SNS signals to the kidneys. In SEVERE contraction, norepinephrine is also released.

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13
Q

Where are the intrarenal sensors located?

A

In the JGA that releases renin.

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14
Q

What are the 4 factors that influence renal sodium excretion?

A
  1. Glomerular filtration
  2. Physical factors at the level of the proximal tubule
  3. Humoral effector mechanisms
  4. Renal sympathetic nerves.
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15
Q

What is tubuloglomerular feedback? (TGF)

A

Increased distal delivery of NaCl to the JGA increases arteriolar tone to return GFR to a normal value

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16
Q

What is glomerulo-tubular balance?

A

Changes in GFR automatically induce proportional changes in tubular reabsorption.

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17
Q

What is “third-spacing?”

A

Accumulation of fluid in a cavity where it shouldn’t be, leading to ECF depletion

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18
Q

What are Bartter’s Syndrome symptoms?

A
  1. Hypokalemia
  2. Hypomagnesmia
  3. Metabolic alkalosis
  4. High renin and aldosterone
  5. Increased Ca+ excretion
  6. Normal blood pressure
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19
Q

When does Bartter’s syndrome present?

A

Early in life

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20
Q

What is the etiology of Bartter’s syndrome?

A

A mutation in the Na/K/2Cl cotransporter

21
Q

What is different between Bartter’s and Gitelman’s?

A

Gitelman’s Syndrome is accompanied by a REDUCED urinary excretion of calcium

22
Q

When does Gitelman’s present?

A

In older individuals

23
Q

What is the etiology of Gitelman’s?

A

A mutation in the NaCl cotransporter in the distal tubule.

24
Q

What are the two criteria for orthostatic hypotension?

A
  1. A difference greater than 10mmHg in SYSTOLIC pressure between supine and standing
  2. An increase of greater than 20bpm
25
What is the BUN:Plasma creatinine ratio in a state of volume contraction? Why?
It will rise higher than 20:1, since sodium will be reabsorbed and urea will passively follow OUT of the urine
26
Metabolic ACIDOSIS in the context of other volume depletion symptoms is indicative of what?
LOWER GI loss of fluid
27
Metabolic ALKALOSIS in the context of other volume depletion symptoms is indicative of what?
UPPER GI loss of fluid
28
What would you expect to see in a urinary sodium during volume depletion?
Low. Since the kidney will work to retain fluid/sodium
29
What should be administered to treat hypovolemic shock?
Blood, ideally. If not available, albumin or dextran solutions are alternative choices.
30
Why give blood and/or albumin in hypovolemic shock?
Because they preferentially increase the intravascular volume, since the large molecules do not leave the capillaries.
31
Isotonic normal saline preferentially expands which compartment?
The interstitial one. About 80% goes there because it is about 80% of the volume, and NaCl can move out of the capillary freely.
32
Extravascular volume expansion is most classically associated with what finding?
Edema
33
In SIMPLE terms, when does volume expansion occur?
When renal and extrarenal fluid losses do not match water and salt intake.
34
Name three pathologies during which disturbed Starling forces can leaf to a decreased EABV and edema.
1. Congestive heart failure 2. Cirrhosis 3. Nephrotic syndrome
35
In SIMPLE terms, what is the treatment for volume expansion?
1. Treatment of the underlying condtition. 2. Salt restriction. 3. Diuretics
36
T/F: Diuretics should be used primarily to control the cosmetic appearance of edema
F. They should be used to treat the cardio/pulm problem, not for those vapid hoes to look better.
37
Where does acetazolamide work?
The proximal tubule. Easy to remember, since the proximal tubule comes first, and acetazolamide starts with an A.
38
How does acetazolamide function?
Acetazolamide Blocks Carbonic anhydrase. A-B-C
39
What acid/base abnormality does acetazolamide cause?
Metabolic Acidosis. Acid starts with an A as well.
40
Where do furosemide, bumetanide, and torsemide act?
LoH
41
How do furosemide, butenamide, and torsemide function?
They inhibit the reabsorption of sodium, potassium, and chloride at the Na/K/2Cl transporter. Three drugs, LoH is three words, they effect the triple transporter. It's all threes
42
Where do thiazide diuretics work?
At the distal convoluted tubule.
43
How to thiazide diuretics function?
They block entry of sodium across the apical membrane.
44
Where do triamterene and amiloride work?
Collecting duct.
45
How do triamterene and amiloride function?
They block the sodium channels
46
Where does spironolactone work?
Collecting duct
47
How does spironolactone function?
It's a competitive inhibitor of aldosterone.
48
Which diuretics are calcium-sparing?
The ones that function at the collecting duct.