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Physiology > Integrative Physiology II- Renal Regulation of Potassium Secretion and Diuretics > Flashcards

Integrative Physiology II- Renal Regulation of Potassium Secretion and Diuretics Flashcards

1
Q

what is the [K+]ECF

A

4.2 meq/L

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2
Q

what are the mechanisms controlling K+ homeostasis

A

-control of K+ distribution between ECF and ICF
- to keep [K]+ ECF constant, rate of K+ excretion=rate of K+ input

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3
Q

what are factors that shift K+ into cells thereby decreasing [K+]ECF

A

-insulin
-aldosterone
- beta2 adrenergic stimulation
- alkalosis
- low ECF Osm
- increased Na+/K+ ATPase activity
-dilute ICF
- low EC gradient for diffusion of K+ out of cell

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4
Q

what are factors that shift K+ out of cells thereby increasing [K+]ECF

A

-increased insulin deficiency in DM
- aldosterone deficiency in Addisons disease
-Beta2 adrenergic antagonists
-acidosis
-increased ECF Osm
-strenuous exercise
-Cell lysis
-decreased Na+/K+ ATPase activity
-concentrated ICF
- high EC gradient for diffusion out of cell

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5
Q

does acidosis cause hyperkalemia or hypokalemia

A

hyperkalemia

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6
Q

how does acidosis cause hyperkalemia

A

H+ inhibits Na+ K+ ATPase causing K+ to build up in the cell

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7
Q

what are the three factors in the tubular processing of K+

A

filtration, reabsorption and secretion

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8
Q

where is most K+ absorbed

A

in the PT

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9
Q

where is most K+ secreted

A

CD

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10
Q

what are the substances that go through all 3 processes in renal processing

A

urea and K+

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11
Q

what is day to day regulation of [K+] ECF a function of

A

late distal tubule/collecting duct

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12
Q

what does a high K+ intake cause

A

increased K+ secretion by principal cells

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13
Q

what does a low K+ intake cause

A

increased K+ reabsorption by alpha intercalated cells

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14
Q

what are the factors that determine rate of K+ secretion by principal cells

A
  • Na+/K+ ATPase activity
  • transepithelial potential difference (TEPD) between blood and lumen
  • permeability of apical membrane for K+
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15
Q

what are factors that control prinicpal cell K+ secretion

A
  • high [K+]ECF
  • high aldosterone
    -high distal tubule flow rate
  • acid/base status: if alkalosis: high K+ secretion and if acidosis: low K+ secretion
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16
Q

what are the mechanisms of how increased [K+]ECF increases K+ secretion

A

-increased Na+/K+ ATPase activity
-TEPD is more lumen negative due to increased Na+ reabsorption which favors K+ secretion
- increased number K+ channels in apical membrane
- stimulates aldosterone secretion

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17
Q

how does aldosterone increase K+ secretion

A

-increased K+ intake -> increased plasma K+ -> increased aldosterone secretion at the renal cortex -> increased plasma aldosterone -> increased K+ secretion at the CCD
-> K+ excretion

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18
Q

what causes increased distal tubule flow rate to increase K+ secretion

A
  • increased ECF volume
    -Na+ loading
    -some diuretics
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19
Q

what are the mechanisms of increased distal tubule flow rate increasing K+ secretion

A

-increased tubule flow rate keeps luminal K+ lower, maintaining chemical gradient for secretion
- increases #BK channels in apical membrane

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20
Q

what are the causes of hyperkalemia

A
  • renal failure
  • decreased distal nephron flow (CHF, NSAID)
  • decreased aldosterone or decreased effect of aldosterone (adrenal insufficiency, resistance to aldosterone, K+ sparing diuretics)
    -metabolic acidosis
  • diabetes
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21
Q

what are the causes of hypokalemia

A
  • very low intake of K+
  • GI loss of K+ from diarrhea
  • metabolic alkalosis
  • excess insulin
  • increased distal tubular flow: salt wasting nephropathies, osmotic diuretics, loop diuretics
  • excess aldosterone
22
Q

what are diuretics

A

drugs that increase urine volume output

23
Q

what is the most common reason for diuretics

A

to reduce ECFV which reduces edema and MAP

24
Q

what are the 2 mechanisms of action of diuretics and which is more common

A

-act by decreasing Na+ reabsorption from some part of the nephron - more common
- act by decreasing water reabsorption

25
Q

how do diuretics decrease Na+ reabsorption

A

natriuresis causes diuresis by an osmotic mechanism and affects reabsorption of Cl-, K+, and other ions

26
Q

how do diuretics decrease water reabsorption

A

by increasing water excretion through aquaresis

27
Q

what are drugs that modify salt excretion

A

-carbonic anhydrase inhibitors at the PCT
- loop diuretics at the TAL
- thiazides at the DCT
- K+ sparing diuretics at the CCT
-osmotic diuretics

28
Q

what are drugs that modify water excretion

A
  • osmotic diuretics
    -ADH agonists
  • ADH antagonists
29
Q

what do osmotic diuretics target

A

inhibits water reabsorption all along the nephron

30
Q

what is the result of osmotic diuretics

A
  • diuresis due to aquaresis
  • to lesser extent it increases Na+ and K+ excretion
31
Q

what do osmotic diuretics do

A

nonabsorbable substance is filtered

32
Q

what are osmotic diuretic effects similar to

A

effects of endogenous substances like glucose - diuresis caused by hyperglycemia

33
Q

what are the targets of carbonic anhydrase inhibitors and what does it do

A

-proximal tubule
- inhibits Na+ reabsorption by indirectly inhibiting Na+/H+ secondary active symporter

34
Q

what is an example of a carbonic anhydrase inhibitor

A

acetazolamine

35
Q

where does more than 80% of HCO3- reabsorption and H+ secretion occur

A

in the proximal tubule

36
Q

what do carbonic anhydrase inhibitors do

A

block Na+ reabsorption indirectly

37
Q

what are the results in diuresis by carbonic anhydrase inhibitors

A

-natriuresis
- aquaresis
- acidosis

38
Q

what are the targets of loop diuretics and what do they do

A

-TAL
- inhibits Na+ K+ 2Cl- secondary active symporter

39
Q

what are examples of loop diuretics

A

-furosemide, ethancrynic acid, bumetanide

40
Q

what are the results in diuresis of loop diuretics

A
  • natriuresis
  • aquaresis
  • overwhelm downstream absorptive capacity of DCT and CD
    -disrupt countercurrent multiplier
41
Q

what are the most powerful diuretics available

A

loop diuretics

42
Q

what is the target of thiazide diuretics and what do they do

A

-early DCT
- inhibit Na+ Cl- secondary active symporter
-block Na+ Cl- cotransport mechanism in early distal tubule

43
Q

what are examples of thiazide diuretics

A

hydrochlorothiazide, chlorthalidone

44
Q

what are the results in diuresis of thiazide diuretics

A

-natriuresis
- aquaresis
-overwhelm downstream absorptive capacity

45
Q

what are the K+ sparing diuretics

A

aldosterone antagonists and Na channel blockers

46
Q

what is the mechanism and site of action of aldosterone antagonists

A

-decreased Na+ absorption and K+ secretion
- late distal and collecting tubule

47
Q

what is the mechanism and site of action of ENaC blockers

A
  • block ENaC and decrease K+ secretion
  • late distal and collecting tubule
48
Q

how do some diuretics cause K+ loss/hypokalemia

A

-increasing flow rate of filtrate through distal nephron increases K+ secretion
- keeps luminal K+ concentration low supporting secretion

49
Q

what are examples of aldosterone antagonists

A

spironolactone and eplerenone

50
Q

what are examples of ENaC blockers

A

amiloride and triamterene

51
Q

what are the results in diuresis of K+ sparing diuretics

A
  • natriuresis
    -aquaresis
    -without hypokalemia

Physiology (41 decks)

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