Renal 2 Flashcards

1
Q

High (99%) reabsorption

A

H2O
Ca2+
HCO3-
CL-
Na+
Glu

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2
Q

excretion equation

A

excretion = filtration - reabs + secretion

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3
Q

Low reabsorption

A

Urea
K+

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4
Q

urea reabsorption rate

A

44%

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5
Q

urea is an effective osmol in

A

the kidney

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6
Q

effective osmol

A

does not move freely in or out of cell

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7
Q

ADH effect in kidney

A

incr urea transporters in kidney
incr urea reabsorption
incr H2O reabsorption

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8
Q

K+ reabsorption rate

A

86%

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9
Q

why is K+ reabsorption rate lower

A

decr K+ reabsorption rate in order to favor Na+ reabsoprtion

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10
Q

Glomerulotubular balance

A

incr GFR results in incr reabsorption of filtrate

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11
Q

what % of PT filtrat is absorbed

A

67%

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12
Q

GTB prevents

A

washout
- minimizes large swings in urine volume when GFR is high

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13
Q

GTB pressures

A

incr colloid oncotic P
decr hydrostatic P

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14
Q

without GTB

A

urine volume increases significantly with high GFR

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15
Q

proximal tubule reabsorbs:

A

67% Na+/Cl-/K+/H2O
80% HCO3-
98% Glu/AA/Pi

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16
Q

most important transporters for Na+/H2O reabasorption

A

Na/K+ ATPase

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17
Q

carbonic anhydrase function

A

turns CO2 and H2O into carbonic acid

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18
Q

ANG2 renal function

A

incr NHE
incr Na+/K+ ATPase
incr HCO3- transporter

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19
Q

carbonic anhydrase inhibitors are

A

K+ wasting

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20
Q

TF/P > 1

A

substance reabsorbed less than H2O or secreted into PT

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21
Q

TF/P > 1 examples

A

creatine
urea

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22
Q

TF/P = 1

A

no reabsorption or secretion in PT

OR

reabsorption of H2O at same rate as substance

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23
Q

TF/P = 1 examples

A

Cl-
Na+

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24
Q

TF/P < 1

A

more substance reabsorbed than H2O in PT

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25
Q

TF/P <1 examples

A

HCO3-
Glu
AA

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26
Q

Tm or Tmax

A

Transport maximum
- the point when increasing concentration does not result in increased transport across membrane
- the point when excess will be excreted

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27
Q

filtered load

A

FL = [P Glu] x GFR

28
Q

threshold

A

[P Glu] when Glu begins to show up in urine

29
Q

threshold > Tm

A

incr Glu excretion

30
Q

counter current multiplier

A

nephron

31
Q

counter current exchanger

A

vasa rector

32
Q

what drives H2O reabsorption

A

counter current exchanger (vasa rector)

33
Q

blood flow in vasa rector

A

slow to give more time to pick up salts

34
Q

descending vasa rector

A

incr salts

35
Q

ascending vasa rector

A

incr H2O

36
Q

vasa recta function

A

bring salts/H2O back into circulation

37
Q

loop diurectics

A

disrupt the CCM and CCE
- decr H2O reabs
- incr excretion

38
Q

loop diuretics wasting

A

Ca2+ wasting
K+ wasting

39
Q

thiazide diuretics wasting

A

K+ wasting
(promote Ca2+ absorption)

40
Q

amelioride wasting

A

K+ sparing

41
Q

incr fraction of Na+ will _____ diuretics

A

increase power of diuretic

42
Q

principle cell regulation mechanism

A

high flow
incr cilia bending
incr 2d messengers
incr ROMK
K+ secreted via ROMK
incr K+ excretion

43
Q

if you increase K+ secretion, you

A

incr K+ excretion

44
Q

what causes higher flow

A

CA inhibitors
loop diuretics
thiazide diuretics

45
Q

diuretic effect

A

decr Na+ reabs
decr H2O reabs
incr naturesis
incr diuresis
decr ECF volume
decr HTN/edema

46
Q

causes of CKD

A

genetic
uncontrolled diabetes
HTN

47
Q

TGF impact on CKD

A

accelerates CKD

48
Q

plasma waste

A

Cr
urea

49
Q

plasma waste is dependent on

A

filtration

50
Q

decr GFR results in ______ [plasma]

A

decr GFR = incr [plasma]

51
Q

plasma acid/base

A

Pi
H+

52
Q

decr GFR = ____pi/H+

A

incr H+
incr Pi

53
Q

plasma electrolytes

A

Na+
Cl-

54
Q

decr GFR = _____ Na+/Cl-

A

minimal change to Na+/Cl-

55
Q

what increases ADH

A

incr [P Na+]
decr plasma volume

56
Q

ADH brings back a ______ volume

A

hypotonic

57
Q

block ADH

A

incr [Na+]

58
Q

block RAAS

A

no change to [Na+]

59
Q

ADH effects

A

incr NKCCs
incr Na+/K+
incr ENAC
incr AQP2
incr UTA1 (urea reabs)
EA constriction

60
Q

ADH ON

A

incr ADH = incr plasm osm

Small volume of high concentrated urine

61
Q

ADH OFF

A

decr ADH = decr plasm osm

large volume of dilute urine

62
Q

where is renin release

A

juxtaglomerular cells

63
Q

RAAS effects

A

vasoconstriction
EA constriction
incr NHE
incr aldosterone
incr ADH

64
Q

EA constriction

A

incr FF
- decr RBF
- incr GFR

65
Q

block aldosterone

A

still incr K+ excretion but not as much

can lead to hyperkalemia

66
Q

ANP/BNP effects

A

oppose RAAS
- decr ECFV

67
Q
A