Osmotic and Volume Regulation (B2: W5) Flashcards

1
Q

How do chages in volume affect ADH release?

A

E.g. Hemorrhage

  • Plasma volume goes down, so vascular pressure drops
    • Reflexes mediated by cardiovascular baroreceptors send a message
  • ADH release increases
    • Plasma ADH goes up
    • Tubular permeability to water goes up
  • Water is reabsorbed
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2
Q

How does the body respond to the consumption of 1 liter of saline?

A
  • Extracellular fluid goes up
  • ADH release goes down
    • Water is excreted
  • Plasma osmolarity increases
  • ADH increases

Initially ADH goes down, but eventually is increased again

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3
Q

How does the body respond to the consumption of 1 liter of distilled water?

A
  • Plasma osmolarity decreases
  • ADH is decreased
    • Want to raise Posm
  • Water is excreted
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4
Q

How is extracellular fluid volume regulated?

A

By regulating sodium reabsorption

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5
Q

Where is sodium reabsorbed along the neprhon?

A
  • 67% reabsorbed in the proximal tubule
  • More is reabsorbed in the ascending limb
    • 8% remaining
  • Additional reabsorption in distal tubule, convoluted collecting tubule, and collecting duct
  • 0.5% is usually excreted
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6
Q

When juxtaglomerular cells sense less stretch, they release ______.

A

Renin

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7
Q

What factors are associated with moving sodium back into the body to control extracellular fluid volume?

A

Kidney is in control of sodium retention

Affected by

  • GFR
  • Aldosterone
  • Natriuretic hormone
  • Peritubular pressure
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8
Q

When regulating volume, which is regulated first: sodium or water?

A

Regulation of volume requires first regulating sodium followed by regulating water

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9
Q

What is the relationship between filtered load and sodium reabsorption in the proximal tubule?

A

As the filtered load of Na goes up, a constant proporiton is reabsorbed in the proximal tubule - 67%

  • In the case of hypovolemia
    • Shifts graph to be more efficient and save salt
    • Slope goes up - maybe 69% instead
  • In the case of hypervolemia
    • Slope goes down and less salt is saved
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10
Q

Why does excess sodium consumption lead to an increase in extracellular fluid volume?

A
  • Plasma [Na] goes up
    • Plasma osmolarity increases
  • Shifts water from inside of cells OUT
  • Increase ADH to save water
    • Water reabsorption and consumption
  • Extracellular volume increases again

This process is slower than just drinking water

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11
Q

How does aldosterone affect collecting duct principal cells?

A
  • Aldosterone released in response to BP decrease (Angiotensin II) or in response to hyperkalemia
  • Aldosterone gets into cell to intracellular receptor where it affects the synthesis of proteins
    • Makes more Na channels
    • Enhances ATP generation
    • Makes more Na/K ATPases
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12
Q

How does aldosterone affect hydrogen atoms?

A

Enhances H+ secretion in the collecting duct

  • Becomes more acidic
  • More Na is reabsorbed back into the body
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13
Q

What are the two primary regulators of aldosterone release?

A
  1. Increased angiotensin II
  2. Increased plasma potassium concentration

Two minor regulators that are not as important

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14
Q

What three effects does aldosterone have on the kidneys?

A
  1. Increased Na reabsorption
  2. Increased K excretion
  3. Increased H excretion
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15
Q

What are the effects of hypoaldosteronemia (e.g. adrenal insufficiency - Addison’s disease)?

A
  1. Acidosis
  2. Hyperkalemia
  3. Hypotensin (salt wasting)
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16
Q

What are the effects of hyperaldosteronemia?

A
  1. Alkalosis
  2. Hypokalemia
  3. Hypertension (usually not overt volume expansion
17
Q

What are the two types of hyperaldosteronemia, and what distinguishes the two?

A
  • Primary: producing too much aldosterone
    • Tumor
    • Hypetension
    • Renin release is decreased - more stretch
  • Secondary: something else caused aldosterone to increase
    • Renal artery stenosis
    • Renin release is increased - less stretch

Both are associated with hypertension

18
Q

What effect does Atrial Natriuretic Factor have on aldosterone?

A

ANF is the “anti-aldosterone”

  • Released under opposite conditions - atrial stretch (increased volume)
  • Acts via membrane receptors coupled to guanylate cyclase
  • Decrease in sodium reabsorption in the collecting duct
  • Increase in GFR
  • Decrease effects of renin, angiotensin II, and aldosterone
19
Q

What is natriuresis?

A

Excretion of excess sodium in the urine

20
Q

What is the main regulator for sodium handling in the kidneys?

A

Arterial baroreceptors maintain effective cirulating volume (ECV - in the arterial system)

21
Q

Why do patients with heart failure exhibit markedly positive and progressively increasing sodium balance?

A

Baroreceptors in arteries sense a drop in the volume and save sodium, which in turn saves water

  • Shift in volume to venous system is sensed as a decreased volume
  • Message to kidneys: save more sodium
22
Q

What are the stages of kidney disease?

A
  1. Stage 1: kidney damage with normal or increased kidney function
  2. Stage 2: kidney damage with mild decreased kidney function
  3. Stage 3: moderate decreased kidney function
  4. Stage 4: severe decreased kidney function
  5. Stage 5: kidney failure
    1. GFR ~15
23
Q

How do you keep sodium reabsorption the same, even with fewer nephrons?

A
  • Losing GFR and filtered load
    • Matched by increased fractional excretion of sodium
    • Remaining nephrons dump more sodium out
  • Normally, 0.6% excreted
    • With 1/10 the amount of functioning nephrons, 6% excreted
24
Q

What happens to plasma and urine chemistry with nephron loss?

A
  • Patient becomes more acidotic with progressive loss of nephrons
  • Plasma creatinine and BUN increase
    • These are produced every day - must go out in kidneys
    • With fewer nephrons, less can leave
25
Q

How can a patient remain in creatinine balance with progressive nephron loss?

A
  • 1 mg/min produced every day
    • Need to excrete this amount per day in nephrons
  • 10 times as much in each mL
    • Can get 1/10 of the nephrons to excrete what we need
26
Q

What stimulates the kidneys to generate and release erythropoietin?

A

Reduced tissue oxygenation