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_Physiology Exam 5 > 4/18: Renal Regulation of Potassium Secretion and Diuretics > Flashcards

4/18: Renal Regulation of Potassium Secretion and Diuretics Flashcards

1
Q

Describe the regulation of potassium

A

ECF K+ is tightly regulated (at 4.2 meq/L) because an increase of only 3 to 4 mEq/L can cause cardiac arrythmias, cardiac arrest, or fibrillation

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2
Q

Where is the regulation of potassium higher?

A

In ICF than in ECF

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3
Q

What are mechanisms controlling K+ homeostasis?

A
  1. Control of K+ distribution between the ECF and ICF
  2. To keep [K] constant; rate of K+ excretion must equal rate of K+ input
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4
Q

What is high K+?

A

Hyperkalemia

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5
Q

What is low K+?

A

Hypokalemia

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6
Q

What do factors that shift K+ into cells do?

A

Decreases [K]ECF
Increases secretion

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7
Q

What are examples of factors that shift K+ into cells?

A

Hyperkalemia
Insulin
Aldosterone
B2-adrenergic stimulation
Alkalosis
Decrease in ECF Osm

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8
Q

What do factors that shift K+ out of cells do?

A

Increase [K]ECF

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9
Q

What are examples of factors that shift K+ out of cells?

A

Hypokalemia
Insulin deficiency
Aldosterone deficicency (addisons disease)
B2 adrenergic antagonists
Acidosis
Increase ECF osm
Strenuous exercise
Cell lysis

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10
Q

What does an increase in Na/K ATPase activite do to the ICF?

A

Dilutes ICF and decreased gradient for diffusion of K+ out of the cell

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11
Q

What does a decrease in Na/K ATPase activite do to the ICF?

A

concentrates ICF and increases gradient for diffusion of K+ out of the cell

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12
Q

What is the mechanism of potassium traffic?

A

Intracellular protein content is high. Proteins are negatively charged and attract K and H to bind to them. Increase in hydrogen concentration in cell (acidosis) causes the hydrogen to displace some of the K and allow for more K to exit the cell

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13
Q

What happens when H levels inside the cell are low?

A

Na/K ATPase pump activity goes up and more K is bound to proteins. Functions to reduce ECF K levels

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14
Q

What creates balance?

A

Secretion in the collecting duct
(hyperkalemia is excess potassium secretion in the CF)
Hypokalemia is less potassium secretion in CD

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15
Q

What does the amount secreted dependent on?

A

Concentration of K+
- if high more will be secreted and if low, less will be secreted

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16
Q

What is day to day regulation of potassium concentration a function of?

A

Late distal tubule/collecting duct

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17
Q

What does high K+ intake do?

A

Increases K+ secretion (principal cells)

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18
Q

What does low K+ intake do?

A

Increases K+ reabsorption (alpha intercalated cells)

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19
Q

What are factors that control principal cell K+ secretion result in?

A

increased K+ secretion

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20
Q

What are examples of factors that control principal cell K+ secretion?

A
  1. Increased [K]ECF
  2. Increased aldosterone
  3. Increase distal tubule flow rate
  4. Alkalosis (acidosis would decrease K+ secretion_
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21
Q

What are mechanisms of increasing K concentration?

A

o Na/K ATPase activity (more activity results in more K into the cell and high gradient is created which favors diffusion of K across the apical membrane/secretion)
o Transepithelial potential difference (TEPD) between blood and lumen (negative TEPD will support K secretion into the cell)
o Permeability of apical membrane for K+ (increased probability of channels being open more K will be moved across apical membrane)
o When potassium levels go above set point levels, it will stimulate aldosterone secretion

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22
Q

What are the effects of aldosterone?

A

increases potassium secretion

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23
Q

When is aldosterone secreted as a result of?

A

Increased K ECF concentration

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24
Q

What cells are the target for aldosterone?

A

Principal cells of collecting duct

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25
Q

What happens under the influence of aldosterone?

A

Na/K ATPase pump increases in activity which raises K+ inside the cell and creates bigger gradient for K+ exit across the membraneW

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26
Q

What does aldosterone increase?

A

Number and activity of Na/K ATPase in basolateral membrane and increase activity of potassium channel in the apical membrane

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27
Q

What is aldosterone important in?

A

maintaining potassium homeostasis.
Normally, increase in K+ intake would not leave to an increase in [K+]ECF because of aldosterone

28
Q

What does an increase in distal tubule flow rate lead to?

A

Increase in K+ secretion

29
Q

What are factors that increase DT flow rate?

A

o High ECF volume (stimulates atrial pressure receptors to produce ANP. Which increases GFR and decreases sodium and water reabsorption. This increases distal tubular flow rate)
o Na+ loading (excrete excess sodium and water will follow)
o Diuretics (some)

30
Q

What does increasing the flow rate do?

A

Keep the luminal K+ lower (by washing away the secreted K) maintaining gradient for secretion

31
Q

What does an increase in tubular flow rate cause?

A

Increase the number of potassium channels in the membrane

32
Q

What is hyperkalemia caused by?

A
  • renal failure (inability to secrete)
  • decrease distal nephron flow
  • decreased aldosterone or decreased effect of aldosterone
  • metabolic acidosis (decreases K secretion)
  • diabetes (patients exhibit decrease in insulin, acidosis, and kidney disease)
33
Q

What do NSAIDs do for nephron flow?

A

inhibit prostaglandin production (dilate afferent arterioles) so afferent arterioles constrict and decrease GFR and distal nephron flow

34
Q

What causes decreased aldosterone or decreased effect of aldosterone?

A

adrenal insufficiency/Addison’s disease, resistance to aldosterone, K+ sparing diuretics (spironolactone, aldosterone receptor antagonist)

35
Q

What are causes of hypokalemia?

A

o Very low intake of K+
o GI loss of K+ due to diarrhea
o Metabolic alkalosis
o Excess insulin (increases Na/K ATPase which moves K into cells)
o Increased distal tubular flow (increases K secretion)
i.e. salt wasting nephropathies, osmotic diuretics, loop diuretics
o Excess aldosterone (Conn’s Syndrome)

36
Q

What are diuretics?

A

Drugs that increase urine volume output

37
Q

What is the most common reason for diuretic use?

A

To reduce ECFV (extracellular fluid volume)

38
Q

What does a reduction in ECFV cause?

A
  • reduces edema
  • reduces MAP
39
Q

What are the mechanisms of diuretics?

A
  1. Decreasing Na reabsorption from some part of the nephrone
  2. Decreasing H2O reabsorption
40
Q

What does natriuresis cause?

A

Diuresis by an osmotic mechanism

41
Q

What does natriuresis affect?

A

Reabsorption of Cl, K, and other electrolytes

42
Q

What is aquaresis?

A

Increases H2O secretion
- may affect the excretion of other solutes

43
Q

What are the functions of diuretics?

A

increase solute and water excretion until compensatory mechanisms re-establish balance

44
Q

What happens with diuretic therapy?

A

excretion rates increase so output (red) > input and ECF volume drops (purple)
- Both levels flatten out when other compensatory mechanisms (blood pressure, ang II/renin, ADH, etc.) create new normal steady state

45
Q

What is a target for many diuretics?

A

Na+ transport

46
Q

What do osmotic diuretics target?

A

Inhibits H2O reabsorption all along nephron

47
Q

What substances are filtered by osmotic diuretics?

A

Nonabsorbable substances (mannitol, glycerin)

48
Q

What do osmols in tubular fluid require?

A

Water

49
Q

What are osmotic diuretic effects similar to?

A

Effects of endogenous substances (glucose; diuresis caused by hyperglycemia)

50
Q

What results in diuresis?

A
  • due to aquaresis
  • to a lesser extend it increases Na and K secretion
51
Q

Where do carbonic anhydrase inhibitors function?

A

Proximal tubule and contains enzyme carbonic anhydrase

52
Q

How is bicarbonate reabsorbed in the proximal tubule via?

A

Na/H secondary active transporter

53
Q

What do carbonic anhydrase inhibitors block?

A

Na reabsorption and H+ secretion into cell
ex: acetazolamide

54
Q

What gradient do carbonic anhydrase inhibitors create?

A

Larger gradient to get H+ out of the cell so it slows down the Na/H transporter activity not allowing Na to be reabsorbed

55
Q

What are results of carbonic anhydrase inhibitors?

A

Natriuresis
Aquaresis
Acidosis

56
Q

Where do loop diuretics function?

A

Thick ascending limb

57
Q

What do loop diuretics inhibit?

A

Na/K/2Cl secondary active transporter on apical membarne
ex: furosemide, ethacrynic acid, bumetanide

58
Q

What happens when Na/K/2Cl cotransporter is inhibited?

A

Reduces sodium reabsorption, retain water and sodium in the filtrate and diaresis occurs

59
Q

Where do thiazide diuretics function?

A

In early distal tubule

60
Q

What do thiazide diuretics block?

A

Na/Cl cotransport mechanism (normally functions to pump sodium into cell down its gradient providing energy to put Cl into the cell. . Raises Cl concentrations inside setting up gradient for passive movement of Cl across basolateral membrane
ex: hydrochlorothiazide, chlorthalidone

61
Q

What does inhibition of the secondary active Na/Cl symporter do?

A

Reduces Na reabsorption
Na and H2O will be retained in the filtrate and increase excretion rate

62
Q

What can many diuretics cause?

A

K+ loss (hypokalemia) by increasing flow rate of filtrate through distal tubule nephrone increases K+ secretion
- Keeps luminal K+ concentrations low, supporting secretion

63
Q

What do K+ sparing diuretics function in?

A

principle cells. alter water excretion without altering solute excretion

64
Q

What do aldosterone antagonists do? (spironolactone)

A

reduce levels of Na/K ATPase, ENaC, K channel

65
Q

What do ENaC blockers do? (triameterene)

A

reduce Na uptake, Na/K ATPase activity and K secretion

_Physiology Exam 5 (10 decks)

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