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Renal > Pathophysiology of Sodium Balance > Flashcards

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
Q

What is the BUN:Plasma creatinine ratio in a state of volume contraction? Why?

A

It will rise higher than 20:1, since sodium will be reabsorbed and urea will passively follow OUT of the urine

26
Q

Metabolic ACIDOSIS in the context of other volume depletion symptoms is indicative of what?

A

LOWER GI loss of fluid

27
Q

Metabolic ALKALOSIS in the context of other volume depletion symptoms is indicative of what?

A

UPPER GI loss of fluid

28
Q

What would you expect to see in a urinary sodium during volume depletion?

A

Low. Since the kidney will work to retain fluid/sodium

29
Q

What should be administered to treat hypovolemic shock?

A

Blood, ideally. If not available, albumin or dextran solutions are alternative choices.

30
Q

Why give blood and/or albumin in hypovolemic shock?

A

Because they preferentially increase the intravascular volume, since the large molecules do not leave the capillaries.

31
Q

Isotonic normal saline preferentially expands which compartment?

A

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
Q

Extravascular volume expansion is most classically associated with what finding?

A

Edema

33
Q

In SIMPLE terms, when does volume expansion occur?

A

When renal and extrarenal fluid losses do not match water and salt intake.

34
Q

Name three pathologies during which disturbed Starling forces can leaf to a decreased EABV and edema.

A
  1. Congestive heart failure
  2. Cirrhosis
  3. Nephrotic syndrome
35
Q

In SIMPLE terms, what is the treatment for volume expansion?

A
  1. Treatment of the underlying condtition.
  2. Salt restriction.
  3. Diuretics
36
Q

T/F: Diuretics should be used primarily to control the cosmetic appearance of edema

A

F. They should be used to treat the cardio/pulm problem, not for those vapid hoes to look better.

37
Q

Where does acetazolamide work?

A

The proximal tubule.

Easy to remember, since the proximal tubule comes first, and acetazolamide starts with an A.

38
Q

How does acetazolamide function?

A

Acetazolamide Blocks Carbonic anhydrase.

A-B-C

39
Q

What acid/base abnormality does acetazolamide cause?

A

Metabolic Acidosis.

Acid starts with an A as well.

40
Q

Where do furosemide, bumetanide, and torsemide act?

A

LoH

41
Q

How do furosemide, butenamide, and torsemide function?

A

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
Q

Where do thiazide diuretics work?

A

At the distal convoluted tubule.

43
Q

How to thiazide diuretics function?

A

They block entry of sodium across the apical membrane.

44
Q

Where do triamterene and amiloride work?

A

Collecting duct.

45
Q

How do triamterene and amiloride function?

A

They block the sodium channels

46
Q

Where does spironolactone work?

A

Collecting duct

47
Q

How does spironolactone function?

A

It’s a competitive inhibitor of aldosterone.

48
Q

Which diuretics are calcium-sparing?

A

The ones that function at the collecting duct.

Renal (14 decks)

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