Tubular Transport Flashcards

1
Q

Changes in body Na content will result in

A

changes in the ECF volume

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2
Q

Na balance occurs when

A

Na input = Na output

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3
Q

(-) Na balance =

A

loss of Na content and loss in ECF volume

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4
Q

(+) Na balance =

A

increase in Na content and gain of ECF volume

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5
Q

a problem in Na balance would show up as a

A

altered ECF volume

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6
Q

What happens during Hyperaldosteronism

A

increased Na reabsorption, increased ECF volume, hypertension

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7
Q

Small changes in Na and H2O reabsorptive mechanisms result in

A

large changes in Na an dH2O excretion

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8
Q

Transport mechanisms for solutes

A

active, diffusion (transcellular or paracellular), facilitated diffusion (transporter)

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9
Q

Solvent drag

A

H2O reabsorption allows solutes dissolved in the H2O to be reabsorbed via paracellular diffusion (Na, K, Cl, Mg, Ca)

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10
Q

Aquaporin-1

A

present in the proximal tubule, allows H2O to move rapidly from the tubule to the interstitium

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11
Q

Aquaporin-2

A

present in the collecting duct; under control of vasopressin (ADH)

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12
Q

Proximal tubule

A

main reabsorption of Na due to leaky epithelial junctions

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13
Q

Back-leak of Na

A

in the proximal tubule, Na can leak out or back into the tubule decreasing the amount of Na reabsorbed (always a net reabsorption of Na)

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14
Q

Transporters

A

transporters can become saturated, and therefore there is a maximum rate of transport for that solute

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15
Q

Maximum transport of a solute via a transporter protein (Tm)

A

Tm = #of transporters x rate of transport

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16
Q

For reabsorption, if filtered load > Tm then

A

solute will appear in the urine

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17
Q

Na-Glucose symport in the proximal tubule has a Tm of 375

A

if GFR = 100 and plasma [glucose] = 4 than filtered load FL= 400; meaning that 25mg/min of glucose would appear in the urine

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18
Q

Na-glucose symport inhibitor will

A

decrease the reabsorption of glucose by decreasing the Tm of the symporter, increasing excretion of glucose in urine

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19
Q

SGLT2

A

Na-glucose symporter in the proximal tubule; targeted inhibition for treatment of Type II diabetes

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20
Q

When filtration of glucose exceeds the transporters ability to transport Tm then

A

glucose will be excreted to account for the difference

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21
Q

If delivery of solute to the peri-tubular capillaries > Tm of secretory transport proteins, then

A

solute will be in the blood

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22
Q

Secretory transporters are non-specific for

A

organic anions, organic cations

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23
Q

Organic Anions compete for the same non-specific transporters

A

penicillin, PAH, probenecid, diuretics (furosemide and acetazolamide)

24
Q

Organic cations compete for the same non-specific transporters

A

cimetidine, procainamide, histamine, and NE

25
Co-administration of 2 drugs that compete for the same secretory transporter will
increase the plasma concentration and time for excretion drastically for both drugs, may result in drug toxicity
26
the Na/K ATPase sets the stage for ALL solute transfer in the proximal tubule
all solutes are carried by the passive movement of Na into the tubular cells down its gradient
27
Location of reabsorption
67% in proximal tubule, 20% in thick ascending limb, veyr little "fine-tuned" in distal and collecting duct
28
How does K differ from other solutes?
K can be SECRETED in the distal tubule if there is elevated intake of K
29
Transporters located in the early proximal tubule
Na-H+ antiport, Na-solute (glucose, aa, lactate, phosphate) symport
30
What is reabsorbed in the late proximal tubule?
Cl and Na via paracellular pathway
31
What is reabsorbed in the proximal tubule?
Na, Cl, aa, glucose, lactate, and phospahte
32
Methods for Na reabsorption in the proximal tubule
Na/H antiport, Na/solute symport, passive diffusion of Na and Cl, and solvent drag
33
What is the osmolarity of the filtrate at the end of the proximal tubule?
isotonic to plasma (300), even though 67% of the Na and H2O have been reabsorbed
34
How does the H+ secretion effect acid/base?
The more H+ that leaves the more CO2 + H2O that is converted into HCO3 and H+ and the more HCO3 is reabsorbed. Decreasing the acidity
35
Transporters located in the thick ascending limb
Na/K ATPase, Na/K/2Cl symport, Na/H antiport
36
Methods of Na reabsorption in the thick ascending limb of Loop of Henle
Na/Cl/K symport, Na-H antiport, Na paracellular diffusion
37
The rate of the Na transport in the thick ascending limb is __________
LOAD-DEPENDENT; more Na delivered, more Na reabsorbed (constant Na arrives at distal tubule)
38
What transporters are located in the early distal tubule?
Na/Cl symporter, Ca and Pi are also reabsorbed
39
Loop diuretics block
Na/K/2Cl symporter in the thick ascending limb
40
Thiazides block
Na/Cl symporter in the distal tubule
41
Aldosterone mechanism
increased Na reabsorption in the thick ascending limb, distal tubule, and principal cells of distal tubule and collecting duct; by increasing Na/K ATPase, Na/K/Cl symporters, and Na/Cl
42
Principal cells of the late distal tubule and collecting duct
reabsorb Na and H2O and secrete K
43
Intercalated cells if the late distal tubule and collecting duct
reabsorb K and secrete H or HCO3
44
Where is the main side of action for aldosterone?
principal cell of late distal tubule and collecting duct where Na is reabsorbed and K secreted
45
How does aldosterone accomplish this effect on the principal cells?
synthesis of ENaC proteins or Na/K ATPase, cell signaling, increased ENaC conductance (via CAP1) and increased # of ENaC channels on surface (SGK1)
46
Aldosterone is stimulated by
Ang II, high serum K, and plasma acidosis
47
What 2 signalling molecules increase the conductance of ENaC due to Aldosterone?
CAP1 and SGK1
48
Amiloride diuretic acts by
blocking the ENaC channel in the distal tubule and collecting duct to prevent Na reabsorption
49
The charge in the tubular lumen is ______ in the thick ascending limb and __________ in the distal tubule
positive; negative (allowing secretion of K)
50
Fractional excretion of Na (FENa) is the
fraction of the filtered Na load that is excreted
51
FENa =
Na excreted / Na filtered = ((Una x Pcreat) / (Ucreat x PNa))
52
FENa = ~
1%
53
FENa > 1
excreting more Na than expected
54
FENa < 1
retaining more Na than expected
55
FENa < 1 in acute renal injury means
retaining more Na - reabsorptive function is intact, may mean decreased RBF and GFR = ischemia called PRE-RENAL
56
FENa > 1 in acute renal injury means
excreting more Na than expected, reabsorptive function is impaired and INTRA-RENAL
57
Pre-renal causes of acute renal injury result from
derangement in hemodynamics; volume depletion, decreased RBF (hemorrhage, vomiting, diarrhea, CHF)