Acute Kidney Injury Flashcards

1
Q

contrast media assoc with lower incidence of aki

A

Low osmolar, isosmolar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

acute decline in gfr in cin occurs in ___ and peak crea concentration in ____

A

24 to 48 hours

3 to 5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

most nephrotoxic amino glycosides

A

neomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

kidney hypoperfusion resulting from reductions in actual or effective arterial blood volume

A

prerenal AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

autoregulation works only to a mean sytemic MAP of

A

75 to 80 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

idiosyncratic allergic response to different pharmacologic agents

A

Acute interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hallmark of AIN

A

inflammatory infiltrates within the interstititium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2nd most common cause of intrinsic AKI

A

nephrotoxic ATN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pathophysiology of CIN
(3)

A

hypoxic and renal tubular damage +
endothelial dysfunction +
altered microcirculation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

to limit cast formation and preventive measure in tubular disease with endogenous nephrotoxins
(2)

A

volume expansion, alkalinization of urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what will accelerate and aggravate light chain cast nephropathy

A

reduction in GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

most common cause for post renal azotemia

A

structural or functional obstruction of the bladder neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

major and most commonly injured epithelial cell involved in AKI related to ischemia, sepsis and or nephrotoxins

A

proximal tubular cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

most susceptible to ischemic injury

A

S3 proximal tubule in the outer stripe of the medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

primarily responsible for the extension phase of AKI

A

endothelial cell injury and dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

passive non-energy dependent process that develops secondary to severe ATP depletion from toxic or ischemic insult

A

epithelial cell necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

form of regulated nonapoptotic cell death in ischemic/cisplatin induced AKI

A

necroptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Folic acid induced AKI

A

ferroptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

highly inflammatory form of regulated cell death

A

pyroptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

facilitate the restoration of normal function by assisting in the refolding of denatured proteins/appropriate folding of newly synthesized proteins

A

heat shock proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

significant reduction in blood vessel density after ischemic injury

A

vascular dropout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

One of the major risk factors for the development of dialysis requiring AKI

A

Preexisting kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

iodinated contrast agents

What type of aki

A

prerenal acute kidney injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

history of atrial fibrillation or recent MI, nausea, vomiting, flank or abdominal pain; mild proteinuria occasional rbcs; elevated LDH, normal transaminase levels

A

renal artery thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
recent manipulation of aorta, retinal plaques, subcutaneous nodules, purpura, livedo reticularis; eosinophiluria; eosinophilia, hypocomplementemia
atheroembolism
26
nephrotic syndrome; pulmonary embolism; flank pain; proteinuria, hematuria
Renal vein thrombosis
27
typical urinalysis findings in HUS/TTP (3)
RBCs, mild proteinuria, rarely RBC or granular casts
28
urine findings in rhabdomyolysis, hyperK, hyperphos, hypocalcemia, increased CK, myoglobin
positive for heme in absence of RBCs
29
urine findings in hemolysis, hyperK, hyperphos, hypocal, hyperuricemia and free circulating hgb
pink and positive for heme in absence of RBCs
30
urine findings in tumor lysis, myeloma, ethylene glycol (3)
urate crystals, dipstick proteinuria, oxalate crystals
31
Intoxication from what would cause calcium oxalate crystals
ethylene glycol intoxication
32
lafbp is detected in the urine within how many hours to ischemic or nephrotoxic injury
6 hours
33
mL of post void residual volume indicative of bladder outlet obstruction
100-150 ml
34
Cairo Bishop definition of tumor lysis syndrome (4)
2 of the following achieved in the same 24h interval from 3 days before to 7 days after chemo: uric acid > 8, K >6, phos > 4.6, calcium < 7 mg/dL
35
Diagnostic criteria for HRS (5)
1. cirrhosis with ascites 2. AKI 3. no improvement of AKI after 2 days of diuretic withdrawal and volume expansion 4. absence of shock 5. absence of parenchymal kidney disease
36
definitive therapy for abdominal compartment syndrome
surgical laparotomy
37
at risk hospitalized patients for contrast associated AKI rate of isotonic sodium chloride
1 ml/kg per hr for 6-12 hours prior and after procedure
38
at risk outpatients for contrast associated AKI, rate of isotonic sodium chloride
3 ml/kg 1 hour prior to procedure then 6 ml/kg per hr over 2-6 hours after procedure
39
used to limit uric acid generation with acute urate nephropathy
allopurinol 100 mg/m2 every 8 hours (max 800 mg/day)
40
effective prophylaxis and treatment for acute uric acid mediated tumor lysis syndrome
rasburicase
41
corticosteroids in AIN if considered dose
Methlypred 250-500 mg/day for 3-4 days then oral pred 1 mkd over 8-12 weeks
42
if the duration of AKI is short, not extremely catabolic and does not require RRT; dietary protein requirement is
0.8-1 g/kg bw/day
43
If duration of AKI is prolonged, with hypercatabolism or on RRT, dietary protein intake
1-1.5 kg/bw/day
44
total caloric intake with prolonged AKI
20-30 kcal/kg/by/day
45
transfusion threshold
7 g/dL
46
Kt/V recommended for RRT in AKI
3.9/week
47
effluent volume during CRRT
20-25 ml/kg/hr
48
FeNa in Radio Contrast Induced Nephrotoxicity
<1%
49
AKI resolves within
1-2 weeks
50
biomarker of AKI associated with reducing apoptosis and enhancing normal proliferation of renal tubular cells
NGAL
51
Diagnosis of Clinical Tumor lysis syndrome
laboratory + at least one of the ff: 1. Crea more than 1.5x, cardiac arrhythmia/sudden death, seizure
52
acute worsening of heart function leads to AKI Crs type?
Acute CRS Type 1
53
chronic abnormalities in heart function result in kidney dysfunction
Chronic CRS Type 2
54
AKI precedes cardiac dysfunction Crs type?
Acute renocardiac (Type 3)
55
CKD leads to cardiac dysfunction
Chronic renocardiac (Type 4)
56
Systemic conditions result in simultaneous cardiac and renal dysfunction
secondary CRS (Type 5)
57
rapid progressive AKI with doubling of the serum crea to > 2.5 in < 2 weeks
Type 1 HRS
58
Moderate renal dysfunction (Crea 1.5-2.5) with steady or slowly progressive course
Type 2 HRS
59
initial management of volume resuscitation
isotonic saline 0.9%
60
amount of albumin per Liter of ascites drained when paracentesis volume exceeds 5L
6 to 8 g albumin
61
vasoconstrictive agent combined with volume expansion that may improve kidney function in hrs
terlipressin
62
Early Goal Directed therapy for sepsis(4)
MAP > 65, CVP 10-12, UO > 0.5 ml/kg/hr, CVO2 > 70%
63
Relative indications for RRT in AKI
progressive azotemia without uremic manifestations, persisitent oliguria
64
cardinal manifestation of AKI
decreased urine output
65
nonoliguric uo
uo > 400 ml/day
66
oliguric uo
UO < 400 ml/day
67
anuric
uo < 100 ml/day
68
AKI RIFLE
increase of > 50% developing over 7 days
69
AKI AKIN (2)
Increase of > 0.3 mg/dL or > 50% developing over < 48 hours
70
KDIGO AKI (2)
Increase of > 0.3 mg/dL over <48 hours or an inc of > 50% developing over < 7 days
71
urine output in AKI definition
< 0.5 ml/kg/hr for > 6 hours
72
More than 50% (> 0.3 mg/dL) increase in crea stage
Risk, Stage 1
73
More than 100% increase in crea stage Rifle, Akin
Injury, Stage 2
74
More than 200% increase in crea stage
Failure Stage 3
75
need for RRT for >4 weeks stage of AKI
Loss
76
need for RRT for > 3 months stage of AKI
End Stage
77
UO in Risk or Stage 1 AKI
< 0.5 ml/kg/h for > 6 h
78
UO in Injury or Stage 2 AKI
< 0.5 ml/kg/h for > 12 h
79
UO in Failure or Stage 3 AKI
< 0.3 ml/kg/h for ? 24h or anuria for >12 h
80
most common cause of AKI
prerenal
81
hallmark feature in ATN
loss of the apical brush border of PTC
82
FeNa in ATN
>2
83
UNa in Prerenal vs ATN
<20 vs >40
84
Urine-Plasma Crea ratio Prerenal vs ATN
> 40 vs < 20
85
UOsm prerenal vs ATN
> 500 vs 300
86
Plasma BCr (pre renal vs renal)
>20 vs <10-15
87
organic thiophosphate to ameliorate cisplatin toxicity
Amifostine
88
limits acetaminophen induced renal injury if given within 24H of ingestion
NAC
89
Chelating agent that may prevent heavy metal nephrotoxicity
Dimercaprol
90
inhibits ethylene glycol metabolism to oxalic acid
Ethanol
91
inhibitor of alcohol dehydrogenase that decreases production of ethylene glycol metabolites
Fomepizole