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Flashcards in Exam 2 lecture 1 Deck (51):
1

anuria

100ml/day

2

oligouria

100-400mL/day

3

non-oligouria

>400mL/day

4

Steps in prevention of AKI

identify pts at high risk
eliminate/reduce exposure to nephrotoxic agents
hydration
drug therapy?
glycemic control

5

high risk patients

- pre-existing renal insufficiency
- chronic diseases (CHF, cirrhosis)
-DM
- age
- dehydration
- nephrotoxic drugs
- IV contrast dye
- critical illness

6

nephrotoxic agents

aminoglycosides, amphotericin B, cisplatin, carboplatin, IV contrast

7

drugs that have an impact on renal blood flow

NSAIDs, ACEI, cyclosporin, tacrolimus

8

volume expansion benefits

- maintain renal perfusion
- flush out toxins
- decreased RAAS activation
- minimizes decrease in renal production of nitric oxide & prostacycline (vasodilators)

9

goal of volume expansion is to maintain urine output

>150mL/hr

10

for volume expansion in critically ill pts

use isotonic crystalloids (NS) over colloids

11

NS dosing with IV contrast dye

1-1.5mL/kg/hr for 3-12 hours before & 6-12 hours after
- euro guidelines say a minimum of 6 hours prior & after

12

sodium bicarb dosing with IV contrast dye

3mL/kg/hr for 1 hour prior then 1mL/kg/hr for 6 hours after

13

drugs for prophylaxis for AKI

are NOT FDA approved

14

N-acetylcysteine brand name

mucomyst

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N-acetylcysteine (mucomyst)

- adjunct to IV isotonic crystalloids
- few side effects, inexpensive
- scavenges free oxygen radicals
- 600-1200mg BID on day before ad day of

16

drugs that are potentially beneficial for prophylaxis but are NOT recommended

throphylline
ascorbic acid
statins

17

fenoldopam

- AKI prophylaxis
- NOT recommended
- DA-1 agonist causes vasodilation & increased renal blood flow
- significant risk of hypotension

18

theophylline

- not recommended
-adenosine antagonist-> vasodilator & increased renal blood flow
- potentially harmful ADE & interactions

19

ascorbic acid

- not recommended
- antioxidant that scavengers free oxygen radicals

20

HMG Co-A reductase inhibitors (statins)

- not recommended
- maintain nitric oxide synthesis & reduces oxidative stress
- if already on it, stay on it

21

dopamine

- not recommended
- renal vasodilation increases renal blood flow
- increased urine output

22

prophylaxis that is not recommended and potentially harmful

- diuretics (mannitol & furosemide)
- over compensate

23

KDIGO glycemic guidelines

target: 110-149mg/dL
- insulin may have a direct protective effect

24

prerenal, intrinsic or postrenal AKI is determined by

urinalysis, labs, history and/or causitive agents

25

anuric, oliguric, or non-oliguric renal failure is determined by

urine output

26

treatment of postrenal AKI

- removal of obstruction
- supportive therapy (electrolytes & fluid)

27

prerenal & intrinsic AKI treatment

- electrolyte management
- maintain BP & CO
- monitor fluid status
- volume expansion
- diuretics
- renal replacement therapy

28

hypovolemic prerenal or intrinsic AKI treatment

- NS IV 250-500mL over 15-30 min then reassess

29

hypervolemic prerenal, intrinsic AKI treatment

- reduce IV fluids to keep vein open
- concentration of IV meds
- concentration of tube feeds

30

hypercolemic prerenal, intrinsic AKI treatment

- reduce IV fluids to keep vein open
- concentration of IV meds
- concentration of tube feeds

31

diuretic use in prerenal & intrinsic AKI

- reserved for HYPERVOLEMIC pts who make adequate urine in response to diuretics
- pros: diuresi & prevention of obstruction
- may be more beneficial in non-oliguric than oliguric

32

diuretics used

- loop diuretics
-furosemide (lasix)
-torsemide (demadex)
- bumetanide (bumex)
- ethacrynic acid (Edecrin): for sulfa allergy

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potency of loop diuretics

bumetanide> torsemide> furosemide

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diuretic with best bioavailability

bumetanide

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diuretic with longest duration

torsemide

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goal urine output with diuretics

>1mL/kg/hr until pt is euvolemic

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furosemide dosing

40-80mg IV/PO increase by 20-40mg/dose Q6-8H
- doses up to 1-3g/day have been used

38

torsemide dosing

10-20mg IV/PO, double dose Q2H if necessary

39

continuous diuretic administration

- fewer adverse rxns (myalgia/ototoxicity)
- more natriuresis occurs
- also more expensive & more monitoring

40

causes of diuretic resistane

- excessive Na intake
- inadequate dose or drug regimen
- reduced bioavailability
- nephrotic sydrome (protein binding)
- reduced renal blood flow (drugs, hypotension)
- increased Na resorption (cirrhosis, nephron adaptation)

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mechanism of resistance of loops

- increase delivery of Na to distal tubule & collecting duct
- kidney responds with increased reabsorption at those sires
- adding thiazides or k- sparing can help restore function

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mechanism of resistance of loops

- increase delivery of Na to distal tubule & collecting duct
- kidney responds with increased reabsorption at those sires
- adding thiazides or k- sparing can help restore function

43

diuretic combos for resistance

- thiazides loop
-k sparing loop
- if CrCl

44

dopamine in prerenal & intrinsic AKI treatment

- NOT recommended in prevention or treatment
- controlled studies show no benefit
- increase in urine output

45

treatment of AKI with renal replacement therapy (RRT)

- very pt specific
- most common non-pharm treatment
- continuous vs intermittent

46

RRT indications

- acid-base abnormalities
- electrolyte imbalance
- intoxication
- fluid overload
- uremia

47

normal BUN

5-20mg/dL

48

normal SCr

0.5-1.5mg/dL

49

normal BUN:SCr ration

10-15:1

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if ratio unchaged

intrinsic

51

if ratio is increased

prerenal