Guyton - Chapter 29: Renal Regulation Of Potassium Flashcards

1
Q

How much of the body’s potassium is in the cells and how much is in the extracellular fluid?

A

98% of the total body potassium is contained in the cells and only 2% is in the extracellular fluid.

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2
Q

How does insulin affect potassium?

A

Insulin stimulates potassium uptake into cells.

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3
Q

How is aldosterone and potassium connected?

A

Increased potassium intake stimulates secretion of aldosterone which increases cells potassium uptake.

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4
Q

How is catecholamines and potassium connected?

A

Catecholamines especially epinephrine can cause movement of potassium from the extracellular to the intracellular fluid mainly by activation of B-adrenergic receptors.

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5
Q

How is acid-base abnormalities connected to potassium distribution?

A

Metabolic acidosis increases extracellular potassium concentration in part by causing loss of potassium from the cells whereas metabolic alkalosis decreases extracellular fluid potassium concentration.

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6
Q

How is increased extracellular fluid osmolarity connected to potassium?

A

Increased extracellular fluid osmolarity causes osmotic flow of water out of the cells. The cellular dehydration increases intracellular potassium concentration, thereby promoting diffusion of potassium out of the cells and increasing extracellular fluid potassium concentration. Decreased extracellular fluid osmolarity has the opposite effect.

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7
Q

What happens to potassium in the tubules?

A

Potassium is reabsorbed in the proximal tubule and in the ascending loop of Henle so only about 8% of the filtered load is delivered to the distal tubule. Secretion of potassium into the late distal tubules and collecting ducts adds to the amount delivered. Therefore the daily excretion is about 12% of the potassium filtered at the glomerular capillaries.

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8
Q

Where is the most important site for regulating potassium excretion?

A

The principal cells of the late distal tubules and the cortical collecting tubules. In these tubular segments, potassium can at times be reabsorbed or at other times be secreted depending on the needs of the body.

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9
Q

Where does most of the day-to-day regulation of potassium excretion occurs?

A

It occurs in the late distal and cortical collecting tubules where potassium can be either reabsorbed or secreted depending on the needs of the body.

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10
Q

Describe the two-step process of secretion of potassium from the blood into the tubular lumen.

A

It begins with uptake from the interstitium into the cell by the sodium-potassium ATPase pump in the basolateral cell membrane: this pump moves sodium out of the cell into the interstitium and at the same time moves potassium to the inferior of the cell. The second step of the process is passive diffusion of potassium from the inferior of the cell into the tubular fluid. The luminal membrane of the principal cells is highly permeable to potassium.

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11
Q

What are the primary factors that control potassium secretion by the principal cells of the late distal and cortical collecting tubules?

A
  1. The activity of the sodium-potassium ATP:ase pump
  2. The electrochemical gradient for potassium secretion from the blood to the tubular lumen.
  3. The permeability of the luminal membrane for potassium.
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12
Q

Which cells can reabsorb potassium during potassium depletion?

A

Intercalated cells in the late distal and collecting tubules.

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13
Q

What are the 3 most important factors that stimulate potassium secretion by the principal cells?

A
  1. Increased extracellular fluid potassium concentration
  2. Increased aldosterone
  3. Increased tubular flow rate

One factor that DECREASES potassium secretion is increased hydrogen ion concentration (acidosis).

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14
Q

What are the 3 mechanisms that makes increased extracellular fluid potassium concentration to raise potassium secretion?

A
  1. Increased extracellular fluid potassium concentration stimulates the sodium-potassium ATPase pump thereby increasing potassium uptake across the basolateral membrane. This in turn increases intracellular potassium ion concentration causin diffusion to diffuse across the luminal membrane into the tubule.
  2. Increased extracellular potassium concentration increases the potassium gradient from the renal interstitial fluid to the interior of the epithelial cell, this reduces back leakage of potassium ions from inside the cells through the basolateral membrane.
  3. Increased potassium concentration stimulates aldosterone secretion by the adrenal cortex which further stimulates potassium secretion.
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15
Q

How does aldosterone stimulate active reabsorption of sodium ions and how is the effect mediated?

A

Aldosterone stimulates active reabsorption of sodium ions by the principal cells of the late distal tubules and collecting ducts. This effect is mediated through a sodium-potassium ATP:ase that transports sodium outward through the basolateral membrane of the cell and into the blood at the same time that it pumps potassium into the cell.

A second effect of aldosterone is to increase the permeability of the luminal membrane for potassium further adding to the effectiveness of aldosterone in stimulating potassium secretion.

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16
Q

What does aldosterone do more than add to a stimulatory effect on renal secretion of potassium?

A

Aldosterone also increases cellular uptake of potassium.

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17
Q

What happens with potassium when there is a rise in distal tubular flow rate?

A

It stimulates potassium secretion.

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18
Q

What happens with potassium secretion in acute acidosis and alkalosis?

A

Acute increases in hydrogen concentration of the extracellular fluid (acidosis) reduces potassium secretion whereas alkalosis increases potassium secretion.

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19
Q

What is the primary mechanism by which increased hydrogen concentration inhibits potassium secretion?

A

By reducing the activity of the sodium-potassium ATP:ase pump. This in turn decreases intracellular potassium concentration and subsequent passive diffusion of potassium across the luminal membrane into the tubule.

20
Q

What happens to potassium in a chronic acidosis?

A

With more prolonged acidosis lasting over a period of several days, there is an increase in urinary potassium excretion. The mechanism for this effect is due in part to an effect of chronic acidosis to inhibit proximal tubular sodium chloride and water reabsorption which increases distal volume delivery thereby stimulating the secretion of potassium. This effect overrides the inhibitory effect of hydrogen ions on the sodium-potassium ATP:ase pump.

21
Q

What is the difference in effect on potassium from acute acidosis and chronic acidosis?

A

Chronic acidosis leads to a loss of potassium whereas acute acidosis leads to decreased potassium excretion.

22
Q

In what different forms are calcium in the body?

A

50% of the total calcium in the plasma exists in the ionised form which is in the form that has biological activity at the cell membranes.
40% is bound to plasma proteins
10% is complexed in the non ionised form with anions such as phosphate and citrate.

23
Q

How is calcium bound to plasma proteins in acidosis and alkalosis?

A

With acidosis, less calcium is bound to the plasma proteins and in alkalosis, a greater amount of calcium is bound to the plasma proteins.

24
Q

How is calcium stored?

A

99% is stored in the bone
0,1% in the extracellular fluid
1% in the intracellular fluid and organelles

25
Q

How does PTH regulate plasma calcium concentration?

A
  1. By stimulating bone reabsorption
  2. By stimulating activation of Vitamin D which then increases intestinal reabsorption of calcium
  3. By directly increasing renal tubular calcium reabsorption
26
Q

What happens with calcium in the kidneys?

A

Calcium is both filtered and reabsorbed in the kidneys but not secreted. Therefore the rate is renal calcium excretion is calculated as:

Renal calcium excretion = calcium filtered - calcium reabsorbed

27
Q

How much calcium is reabsorbed in the kidneys and where is it reabsorbed?

A

Normally about 99 % of the filtered calcium is reabsorbed by the tubules.
65% is reabsorbed in the proximal tubule
25-30% is reabsorbed in the loop of Henle
4-9% is reabsorbed in the distal and collecting tubules.

28
Q

How much of the calcium is reabsorbed through the transcellular pathway and describe the steps.

A

Only about 20% of the proximal tubular calcium reabsorption occurs through the transcellular pathway in 2 steps:

  1. Calcium diffuses from the tubular lumen into the cell down an electrochemical gradient due to the much higher concentration of calcium in the tubular lumen compared with the epithelial cell cytoplasm and because the cell interior has a negative relative to the tubular lumen.
  2. Calcium exits the cell across the basolateral membrane by a calcium ATP-ase pump and by sodium calcium counter transporter.
29
Q

How does most of the calcium reabsorption in the proximal tubule occur?

A

Through the paracellular pathway dissolved in water and carried with the reabsorbed fluid as it flows between the cells.

30
Q

Where does calcium reabsorption take place in the loop of Henle?

A

It’s restricted to the thick ascending limb.

Approximately 50% of calcium reabsorption in the thick ascending limb occurs through the paracellular route by passive diffusion.

The remaining 50% of calcium reabsorption in the thick ascending limb occurs through the transcellular process that is stimulated by PTH.

31
Q

How is calcium reabsorbed in the distal tubule?

A

Occurs almost entirely by active transport through the cell membrane.

32
Q

What is the primary controller of renal tubular calcium reabsorption?

A

PTH. Increased levels of PTH stimulates calcium reabsorption in the thick ascending loops of Henle and distal tubules which reduces urinary excretion of calcium.

33
Q

How does calcium reabsorption occur in the proximal tubule?

A

In the proximal tubule, calcium reabsorption usually parallels sodium and water reabsorption and is independent of PTH.

34
Q

How does phosphate influence calcium reabsorption?

A

Increased plasma phosphate stimulates PTH which increases calcium reabsorption by the renal tubules thereby reducing calcium excretion.

35
Q

How does acidosis and alkalosis affect calcium reabsorption?

A

Calcium reabsorption is stimulated by metabolic acidosis and inhibited by metabolic alkalosis.

36
Q

How is phosphate handled in the tubules?

A

The proximal tubule normally reabsorbs 75-80 percent of the filtered phosphate. The distal tubule reabsorbs about 10% of the filtered load and only very small amounts are reabsorbed in the loop of Henle, collecting tubules and collecting ducts. Approximately 10% of the filtered phosphate is excreted in the urine.

37
Q

What is the mechanism for phosphate reabsorption in the proximal tubule?

A

It occurs mainly through the transcellular pathway. Phosphate enters the cell from the lumen by a sodium-phosphate co-transporter and exits the cell across the basolateral membrane by a process that is not well understood.

38
Q

How does PTH play a significant role in regulating phosphate concentration?

A
  1. PTH promotes bone resorption thereby dumping large amounts of phosphate ions into the extracellular fluid from the bone salts.
  2. PTH decreases the transport maximum for phosphate by the renal tubules so a greater portion of the tubular phosphate is lost in the urine.
39
Q

Where does the primary reabsorption of magnesium occur and how much is usually reabsorbed?

A

The proximal tubule usually reabsorbs only about 25% of the filtered magnesium and the primary site of reabsorption is the loop of Henle where about 65% of the filtered load of magnesium is reabsorbed.

40
Q

What is pressure diuresis?

A

The effect of increased blood pressure to raise urinary volume excretion.

41
Q

What is pressure natriuresis?

A

It refers to the rise in sodium excretion that occurs with elevated blood pressure.

42
Q

How can the blood volume remain almost exactly constant despite extreme changes in daily fluid intake?

A
  1. A light change in blood volume causes marked changes in cardiac output.
  2. A slight change in cardiac output causes a large change in blood pressure and
  3. A slight change in blood pressure causes a large change in urine output.
43
Q

What are the principal factors that can cause accumulation of fluid in the interstitial spaces?

A
  1. Increases capillary hydrostatic pressure
  2. Decreased plasma colloid osmotic pressure
  3. Increased permeability of the capillaries
  4. Obstruction of lymphatic vessels
44
Q

What happens in the kidney when blood volume is reduced by hemorrhage, pressures in the pulmonary blood vessels and other low pressure regions of the thorax decrease, causing reflex activation of the sympathetic nervous system?

A

This in turn increases renal sympathetic nerve activity which has several effects to decrease sodium and water excretion:
1. Constriction of the renal arterioles with resultant decreased GFR of the sympathetic activation if severe.
2. Increased tubular reabsorption of salt and water.
3. Stimulation of renin release and increased angiotensin II and aldosterone formation both of which further increase tubular reabsorption.

45
Q

What is one of the body’s most powerful controllers of sodium excretion?

A

Angiotensin II

46
Q

How is atrial natriuretic peptide (ANP) stimulated and what does it do?

A

The stimulus for release of this peptide appears to be increased stretch of the atria (which can result from excess blood volume). Once released by the cardiac atria, ANP enters the circulation and acts on the kidneys to cause small increases in GFR and decreases in sodium reabsorption by the collecting ducts. These combined actions of ANP lead to increased excretion of salt and water which helps to compensate for the excess blood volume.