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URN Biweekly 2 > AKI- Bessette > Flashcards

AKI- Bessette Flashcards

1
Q

a rapid decline in the GFR resulting in retention of nitrogenous wastes, primarily creatinine and blood urea nitrogen

A

Acute Kidney Injury (AKI)

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2
Q

associated w/ increased mortality and increased length of hospital stay

A

AKI

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3
Q

______ nephrology consultation leads to increased mortality and increased length of ICU stays

A

delayed

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4
Q

an increase in serum creatinine of _____ within 48 hours (AKI criteria)

A

0.3 mg/dl

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5
Q

______ baseline increase in serum creatinine w/in 7 days (AKI criteria)

A

> /= 1.5x baseline

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6
Q

a reduction in urine output(<______ for >6 hours) (AKI criteria)

A

<0.5 ml/kg/hr for > 6 hrs

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7
Q

ultimately a decrease in GFR and urine output and an increase in creatinine

A

AKI

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8
Q

<500 ml urine output/24 hours

A

oliguric

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9
Q

> 500 ml urine output/24 hours

A

nonoliguric

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10
Q

<100 ml/24 hrs

A

anuric

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11
Q

age >75
chronic kidney disease
cardiac failure
liver disease
diabetes
nephrotoxic medications
hypovolemia

A

risk factors for developing AKI

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12
Q

mismatch b/t oxygen or nutrient delivery and energy demand

A

pathogenesis of AKI

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13
Q

direct toxicity to tubular cell or vascular endothelium

A

pathogenesis of AKI

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14
Q

an AKI biomarker that you need to look back a day or two b/c its not sensitive

A

creatinine

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15
Q

small changes in _______ may reflect large changes in GFR

A

creatinine

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16
Q

1-1.5 is a ______ decrease in renal function

A

huge

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17
Q

another AKI biomarker that can be used; send off test

A

Cystatin C

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18
Q

AKI may lead to_____

A

CKD

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19
Q

CKD predisposes ____

A

AKI

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20
Q

the more you have an AKI +/or the worse it is= higher risk for _____

A

CKD

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21
Q

this type of AKI deals with hypovolemia (decreased CO and decreased perfusion of kidneys)

A

prerenal AKI

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22
Q

type of AKI that deals with glomerular, tubules and interstitium, and vascular

A

intrinsic AKI

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23
Q

type of AKI that deals with bladder outlet obstruction

A

postrenal AKI

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24
Q

physiologic response to renal hypoperfusion w/out tubular injury

A

prerenal AKI

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25
kidney is normal and there is reduced renal perfusion
prerenal AKI
26
urine Na+ decreased urine osmolality increased
prerenal AKI
27
fractional excretion of urea <35% BUN to creatinine ratio > 20:1
prerenal AKI
28
% of sodium filtered by kidney is excreted in the urine
fractional excretion of Na+
29
helps distinguish prerenal AKI from ATN
fractional excretion of Na+
30
<1% fractional excretion of Na+
prerenal AKI
31
>2% fractional excretion of Na+
ATN
32
(Urine Na+/Plasma Na+)/ (urine creatinine/plasma creatinine) x100
fractional excretion of Na+
33
fractional excretion of Na+ formula
(urine Na+/plasma Na+)/(urine creatinine/plasma creatinine) x 100
34
% of urea filtered by the kidney that is excreted in the urine
fractional excretion of urea
35
fractional excretion of urea formula
(urine urea/plasma urea)/(urine creatinine/plasma creatinine) x 100
36
low FE of urea (<35%)
prerenal AKI
37
high FE of urea (>50%)
intrinsic AKI (tubular damage)
38
what is less affected by diuretics than fractional excretion of Na+
fractional excretion fo urea
39
conditions that affect glomeruli, tubules, interstitium, or vasculature
intrarenal AKI (intrinsic)
40
__85__% of intrarenal AKI is due to what
tubular damage
41
can be due to ischemic or nephrotoxic causes
intrinsic AKI (tubular damage)
42
does not improve with volume repletion
intrinsic AKI
43
Involves inflammation and damage to the glomerular basement membrane, mesangium and capillary endothelium
acute glomerulonephritis
44
has high FENa+ (>2%) and high FEurea (>50%)
intrinsic AKI
45
usually immune mediated, RBC casts
nephritic
46
proteinuria, HTN, edema
nephrotic
47
kidney biopsy needed for diagnosis of what (that is causing AKI)
acute glomerulonephritis
48
RBC casts
49
urine findings include: dysmorphic RBCs RBC casts proteinuria (mild)
nephritic
50
RBC casts
51
maltese crosses nephrotic
52
this intrinsic AKI is mainly due to medications (antibiotics)
acute interstitial nephritis
53
key to diagnosis is hx of exposure and may have rash, fever, eosinophils
Acute interstitial nephritis
54
WBC and WBC casts hematuria mild proteinuria (rxn to medicine)
acute interstitial nephritis
55
eosinophils (acute interstitial nephritis)
56
most common type of AKI in hospitalized patients
Acute Tubular Injury
57
2 main causes of acute tubular injury
ischemic nephrotoxic
58
muddy brown casts seen with this (due to sloughed cells)
acute tubular necrosis
59
Mechanism of tubular injury:
1. ischemia/toxins 2. loss of cell polarity 3. cell necrosis/apoptosis 4. sloughing of cells 5. viable cell migration and proliferation 6. viable cell differentiation into normal epithelium
60
muddy brown casts (ATN)----intrinsic AKI
61
muddy brown casts (ATN)
62
this type of AKI is due to obstruction of urinary outflow
postrenal AKI
63
obstruction of parenchyma; bilateral or unilateral kidney obstruction; reduced UOP/anuria; bladder outlet obstruction
postrenal AKI
64
on US, could see hydroureter or hydronephrosis
postrenal AKI
65
can see distended bladder on physical exam
postrenal AKI
66
steps to diagnose AKI:
hx physical labs renal US biopsy
67
GFR/Cr clearance not useful unless what
serum [Cr] is in steady state
68
pre or post renal easiest to correct and how
foley catheter saline
69
management of AKI
supportive care
70
what to avoid if you have AKI
nephrotoxic agents (ex. NSAIDs)
71
first sign of recovery from AKI in oliguric and anuric patients
increased urine output (UOP)
72
recovery from AKI is seen when serum_______ stabilizes and decreases
creatinine
73
early recognition and treatment is essential for what
AKI
74
intact renal functional reserve (RFR) to deficient RFR leads to what
CKD

URN Biweekly 2 (15 decks)

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