Renal Acid/Base Flashcards

1
Q

HCO3- reabsorption

A

99.9%

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2
Q

ESRD effects

A

decr plasma HCO3-
incr plasma K+
incr BP
decr Hct
incr Po4-

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3
Q

what typically triggers dialysis

A

high K+

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4
Q

why does Hct decreases in ESRD

A

decr EPO production

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5
Q

why does Po4- increase in ESRD

A

kidney is primary route of PO4- excretion

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6
Q

vital pH limits

A

6.8-7.8

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7
Q

how do we lower volatile acid

A

expiration

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8
Q

how much volatile acid do we produce

A

15,000 mEq /day

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9
Q

how much non volatile acid do we produce

A

70 mEq/day

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10
Q

how do we remove non volatile acid

A

secreted/excreted by kidney

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11
Q

foods that cause alkalosis

A

fruit
veg

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12
Q

food that cause acidosis

A

meats
grains
dairy

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13
Q

SAD results in

A

net endogenous acid production

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14
Q

pH ~

A

pH ~ renal function/pulm function

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15
Q

respiratory disturbance

A

kidney changes total HCO3-

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16
Q

renal disturbances

A

lungs change total PCO2

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17
Q

acute disturbance

A

less time for compensation
= more acidodic

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18
Q

chronic disturbance

A

more time for compensation
= less acidodic

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19
Q

how much HCO3 do we reabsorb daily

A

4320 mEq/day

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20
Q

how much H+ do we secrete daily

A

4390 mEq/day

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21
Q

what does the excess H+ bind to?

A

other renal bases

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22
Q

where is most of the bicarb reabsorbed?

A

PT (80%)

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23
Q

where is the highest pH in nephron

A

PT/DT
pH ~ 6.7

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24
Q

where is the lowest pH in nephron

A

IMCD (prior to urine excretion)
pH ~ 4.6 - 8

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25
Q

what promotes H+ secretion/HCO3- reabsorption?

A

acidosis
Ang2
aldosterone
decr ECFV
- incr RAAS
hypokalemia
- type A cells
- ammoniagenesis

26
Q

principle cells

A

incr K+ secretion
incr NHE
- incr H+ secretion
- incr HCO3- reabsoption

27
Q

Type A cell

A

incr K+ reabsorb
incr H+ secretion
incr HCO3- reabsorb

28
Q

ammoniagenesis will ____ HCO3-

A

incr HCO3-

29
Q

hypokalemia

A

increase H/K+ ATP pump
- incr K+ reabs
- incr H+ secretion
** incr HCO3- reabs

30
Q

ammoniagenesis

A

NH3 secreted OUT
or
NH3 + H+ -> NH4
- NH4 secreted out

31
Q

incr Ang2

A

metabolic alkalosis
incr NHE
- Na+ reabs
- H+ secreted
- HCO3- reabsorbed

32
Q

incr acid load is found in

A

PT/TAL

33
Q

incr acid load causes

A

incr HCO3- transporters
== incr HCO3- reabs

34
Q

CD effects

A

incr H/K ATPase
aldosterone
hyperkalemia

35
Q

H/K ATPase

A

incr H+ secretion
incr HCO3- reabs

favors metabolic alkalosis

36
Q

aldosterone effects

A

incr K+ secretion
incr K+ excretion

incr BK/ROMK
incr ENAC
incr Na/K ATPase

37
Q

in acidosis states we upregulate what in the CD

A

H/K ATPase
H ATPase

38
Q

when does H/K+ ATPase become more active

A

hypokalemia

39
Q

hypokalemia causes

A

incr H+ secretion
incr HCO3- reabsorption

40
Q

does aldosterone favor hypo or hyperkalemia

A

hyperkalemia

41
Q

hyperkalemia means

A

there is way more K+ than the H/K+ ATPase can reabsorb, so more will be excreted out

you will reabsorb more K+ than in normal conditions

42
Q

______ is permissive of acid base disturbances

A

aldosterone

43
Q

primary hyperaldosteronism

A

incr met alkalosis
- incr H+ secretion
- incr HCO3- reabs

44
Q

21/11 beta deficiency

A

incr met acidosis

45
Q

K+ channels in acidic state

A

decreased open probabilioty

46
Q

K+ channels closer to physiologic pH

A

incr open probability

47
Q

alkalosis: chronic

A

incr K+ channel open prob
incr K+ secretion

HYPOkalemia

48
Q

acidosis: acute

A

decr Na+/K+
decr K+ channel perm

HYPERkalemia

49
Q

acidosis: chronic effect in sk muscl

A

incr HKE
incr plasma K+
incr aldosterone

50
Q

acidosis: chronic effect in PT

A

incr ECFV
- incr RAAS/aldo
incr tubular flow
- incr K+ secretion

HYPOkalemia

51
Q

what factors cause incr H+ secretion/incr HCO3- reabs?

A

incr PCO2
incr H+
decr HCO3-
decr ECFV
- incr ANG2
- incr aldosterone
- incr NHE
- incr H/K ATP

52
Q

“new HCO3-“

A

some other base for H+ to bind to

H+ + renal base

70mEq/day

53
Q

max free [H+] in urine

A

0.03 mmol/L

54
Q

renal bases

A

phosphate
sulfate
ammonia

55
Q

primary buffer

A

phosphate

56
Q

what is different about ammoniagenesis?

A

generates 2 extra HCO3-

57
Q

what is broken down in ammoniagenesis

A

glutamine

58
Q

kidney function

A

excrete metabolic acids
regulate plasma [HCO3-]
prevent bad buffering

59
Q

when do you have an incr risk of metabolic acidosis

A

with low GFR

60
Q

if you want to excrete acid:

A

free filter HCO3- at glom
reabso 80% filtered HCO3- in PT
reabsb 19% HCO3- in TAC/DT/CD
secrete in DT/CD
H+
H2PO4-
NH4+
excrete acidic urine
H2PO4-
NH4+

61
Q

if you want to excreted base

A

free filter HCO3-
reabs 80% HCO3- in PT
reabs less HCO3- in TAF/DT/CD (10%)
secrete HCO3- in DT/CD
excrete alkaline urine with more HCO3- than normal