Tubular Transport III Flashcards

1
Q

Rapid K regulation is accomplished by

A

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

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2
Q

Which hormone can rapidly move K into cells?

A

Insulin: used to treat hyperkalemia

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3
Q

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

A

Epinephrine + alpha-adrenoreceptors moves K OUT

Epinephrine + beta-2 adrenoreceptors moves K IN

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4
Q

Which hormone promotes K uptake over hours?

A

Aldosterone: causes uptake of K INTO cells

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5
Q

What would happen if there was chronic elevation of aldosterone?

A

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

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6
Q

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

A

principal cell of distal tubule

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7
Q

Where is K reabsorbed?

A

proximal tubule, loop of Henle, and INTERCALATED cells

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8
Q

Main mechanism of K reabsorption in the proximal tubule?

A

solvent drag

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9
Q

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

A

Plasma K and Aldosterone

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10
Q

What else may alter K secretion?

A

Acid-Base balance and Tubular fluid flow rate

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11
Q

Aldosterone causes Na reabsorption and therefore

A

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

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12
Q

ROMK channel

A

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

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13
Q

What factors determine K secretion?

A

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

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14
Q

Aldosterone increases K secretion by:

A

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

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15
Q

Plasma K levels - hyperkalemia is corrected by

A

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

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16
Q

Alkalosis has what effect on K secretion

A

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

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17
Q

Acute Acidosis has what effect on K secretion

A

DECREASES K secretion by inhibiting Na/K ATPase

18
Q

Chronic Acidosis has what effect of K secretion

A

INCREASES K secretion because aldosterone is stimulated

19
Q

How does an increase in tubular flow effect K secretion?

A

INCREASES K secretion

20
Q

How does a decrease in tubular flow effect K secretion?

A

DECREASES K secretion (hypovolemia)

21
Q

How does tubular flow rate change K secretion

A

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
Q

Increased tubular flow rate causes ______ K secretion

23
Q

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

A

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

24
Q

Contradictory arguments for K secretion and tubular rate

A

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