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Flashcards in Tubular Transport III Deck (41):
1

Rapid K regulation is accomplished by

rapid movement from IC to EC spaces through the action of Insulin, Epinephrine, and Aldosterone

2

Which hormone can rapidly move K into cells?

Insulin: used to treat hyperkalemia

3

Which hormone is used to move K out of cells? OR out of the cell?

Epinephrine + alpha-adrenoreceptors moves K OUT
Epinephrine + beta-2 adrenoreceptors moves K IN

4

Which hormone promotes K uptake over hours?

Aldosterone: causes uptake of K INTO cells

5

What would happen if there was chronic elevation of aldosterone?

Hypokalemia due to excretion of K and uptake of K into cells

6

Where is K secreted if there is increased intake of K?

principal cell of distal tubule

7

Where is K reabsorbed?

proximal tubule, loop of Henle, and INTERCALATED cells

8

Main mechanism of K reabsorption in the proximal tubule?

solvent drag

9

What are the primary physiologic regulators of K secretion in principal cells?

Plasma K and Aldosterone

10

What else may alter K secretion?

Acid-Base balance and Tubular fluid flow rate

11

Aldosterone causes Na reabsorption and therefore

K secretion; ENaC conductance increases, NA/K ATPase increases, K channels increased to secrete K

12

ROMK channel

channel allowing passive diffusion on the apical membrane on the principal cell (gradient established by Na/K ATPase

13

What factors determine K secretion?

Na/K ATPase function, electrochemical gradient driving force, permeability to K (ROMK)

14

Aldosterone increases K secretion by:

increasing Na/K ATPases, increased Na reabsorption (increased ENaC through CAP1 and SGK1), increased # of ROMK channels

15

Plasma K levels - hyperkalemia is corrected by

K secretion (aldosterone, increased Na/K ATPase, and permeability to K)

16

Alkalosis has what effect on K secretion

INCREASES it via Na/K ATPase and ROMK; chronic alkalosis leads to hypokalemia

17

Acute Acidosis has what effect on K secretion

DECREASES K secretion by inhibiting Na/K ATPase

18

Chronic Acidosis has what effect of K secretion

INCREASES K secretion because aldosterone is stimulated

19

How does an increase in tubular flow effect K secretion?

INCREASES K secretion

20

How does a decrease in tubular flow effect K secretion?

DECREASES K secretion (hypovolemia)

21

How does tubular flow rate change K secretion

Epithelial tubular cells have mechanosensor, when flow increases, Ca entry increases, and K channels open; why? because increased flow has increased Na --> Na reabsorption occurs and K secretion occurs

22

Increased tubular flow rate causes ______ K secretion

Increases

23

If we drink large amounts of water what happens to our K secretion?

stays the same, tubular flow rate is high but ADH is absent meaning low secretion of K

24

Contradictory arguments for K secretion and tubular rate

Low ADH and high tubular flow (which can occur after ingestion of lg amounts of H2O), cancel each other out

25

Liddle Syndrome (constitutively active ENaC)

High amounts of Na reabsorbed followed by H2O = hypertension, K secretion is high [hypokalemia] high BP and low RAAS

26

Apparent Mineralcorticoid excess (AME)

licorice creates high levels of coritsol that mimics aldosterone; increased Na reabsorbed followed by H2O = hypertension, K secretion is high [hypokalemia] high BP and low RAAS

27

Psuedohypoaldosteronism (loss of ENaC function)

decreased Na reabsorption, H2O loss, low BP, little secretion of K [hyperkalemia], increased aldosterone

28

Bartter's Syndrome (Na/K/Cl symporter loss of function)

large amounts of Na excreted (Na wasting), but Na is reabsorbed in the collecting duct and K is secreted in large amounts leading to [hypokalemia] increased RAAS

29

Diuretics decreases ECF

by increased Na excretion, when ECF drops, RAAS is activated and Na reabsorption occurs elsewhere. ECF volume is established at a lower volume

30

Naturiuresis

increase in Na excretion

31

Kaliuresis

increase in K excretion

32

Osmotic Diuretics act where and by?

proximal tubule; UNREABSORBABLE solutes cause retention of H2O in the tubule and therefore there is a decreased solvent drag (Na reabsorption) and increased Na back flow

33

Example of osmotic diuretics

MANNITOL (large sugar); also diabetics with increased blood glucose experience this effect (polyuria, polydypsia)

34

Carbonic Anhydrase inhibitor diuretic

prevents the production of H+ necessary for the Na/H+ antiporter in the proximal tubule therefore decreasing Na reabsorption

35

Loop Diuretics

block the Na/K/Cl symporter in the thick ascending limb, this prevents the hypertonic medulla gradient from establishing and therefore reduced the ability of kidney to concentrate urine

36

Example of a loop diuretic

furosemide (lasix)

37

Thiazide diuretic

block the Na/Cl symport in the early distal tubule, decreasing Na reabsorption and decreasing the ability of the kidney to maximally dilute the urine

38

K+ sparing diuretics

work in the late distal tubule and cortical collecting duct (therefore do not effect medulla gradient) to either block ENaC channels or act as an aldosterone inhibitor to prevent Na reabsorption

39

Examples of K+ sparing diuretics

amiloride: blocks ENaC
Spironolactone: antagonizes aldosterone receptor

40

Only group of Diuretics that does not waste K (vis increased K secretions)

K+ sparing in the distal tubule and collecting duct

41

Only group of diuretics to not affect the ability of the kidney to maximally concentrate/dilute the urine

K+ sparing