334 Acute Kidney Injury Flashcards

(63 cards)

1
Q

Common diagnostic features of AKI

A

Increase in BUN and/or increase in serum crea, reduction in urine volume

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2
Q

ICU mortality rates in AKI

A

May exceed 50%

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3
Q

Causes of AKI

A

Prerenal Azotemia
Intrinsic renal Parenchymal disease
Post renal Obstruction

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4
Q

Most comon form of AKI

Inadequate renal plasma flow and intraglomerular hydrostatic pressure

A

Prerenal Azotemia

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5
Q

Common clinical conditions in Prerenal azotemia

A

Hypovolemia
Dec cardiac output
Medications: NSAIDs, ARBs, ACEi

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6
Q

Prolonged periods of prerenal azotemia may lead to ischemic injury termed as

A

Acute TUbular NEcrosis (ATN)

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7
Q

Renal blood flow accounts for _ % of cardiac output

A

20%

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8
Q

This maintains GFR despite decreased renal blood flow by renal efferent vasoconstriction

A

Angiotensin II

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9
Q

This leads to dilataion in the setting of low perfusion pressure therefor maintaining GFR

A

Myogenic Reflex, prostaglandins, kinins, NO

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10
Q

Renal autoregulation usually fails once SBP falls below __ mm Hg

A

80 mmHg

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11
Q

These limits renal afferent vasodilation:

A

Long standing hpn, hyalinosis, myointimal hyperplasia

NSAIDs

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12
Q

These limits renal efferent vasodilation

A

ACE inhibitors, ARBs

Bilateral renal artery stenosis, unilateral renal artery stenosis

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13
Q

This poses a particularly high risk for developing prerenal azotemia

A

NSAIDs + ACE inhibitors

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14
Q

Type of Hepatorenal syndrome in which AKI without an alternate cause PERSISTS despite volume administration and witholding of diuretics

A

Type 1 HRS

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15
Q

This type of Hepatorenal syndrome is less severe form - characterized by REFRACTORY ASCITES

A

Type 2 HRS

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16
Q

Most common causes of intrinsci AKI

A

Sepsis, ischemia, nephrotoxins

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17
Q

Pathophysiology of sepsis-induced AKI

A

Tubular injury, inflammation, mitochondrial dysfunction and interstitial edema

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18
Q

Hemodynamic effects of sepsis in AKI

A

Generalized arterial vasodilation, expression of NO synthase -> decreased GFR

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19
Q

Healthy kidneys recieve _% of cardiac output and account for _% of resting o2 consumption

A

20% of cardiac output

10% of o2 cosumption

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20
Q

One of the most hypxic regions in the body

A

Renal medulla - outer medulla

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21
Q

Most common procedures associated with AKI

A

Cardiac surgery with bypass, vascular procedures with aortic clamping, intraperitoneal procedures

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22
Q

Risk factors for post op AKI

A

CKD, old age, DM, CHF, Emergency procedures

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23
Q

AKI is a complication of burns affecting 25% of individuals with more than _% of Total body surface area

A

10%

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24
Q

Intraabdominal pressure of _mmHG lead to renal vein compression and reduced GFR

A

20 mmHg

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25
Leading cause of AKI
Iodinated contrast agents for CV and CT imaging
26
Clinical course of contrast nephropathy
Rise in SCr 24-48 hrs following exposure, peak of 3-5 days, resolving within 1 week
27
Antibiotics causing tubular necrosis
Aminoglycosides and amphotericin B, mainfests after 5-7 days of therapy
28
Common finding in antibiotic induced AKI
Hypomagnesemia
29
Amphotericin B causes AKI by
renal vasoconstriction from increased tubuloglomerular feedback AND direct tubular troxicity; dose and duration dependent
30
Clinical features of Amphotericin B nephrotoxicity
Hypomagnesemia, hypocalcemia, nongap metabolic acidosis
31
May cause hemorrhagic cystitis and tubular toxicity; type 2 RTA (Fanconi's syndrome), polyuria, hypokalemia and decline in GFR
Ifosfamide
32
Cause of chinese Herb Nephropathy and Balkan Nephropathy
Aristocholic acid
33
Uromodulin, the most common protein in urine and produced in thick ascending loop of henle
Tamm- Horsfall protein
34
Uric acid levels in Tumor lysis syndrome
>15mg/dl
35
Tumor lysis syndrome:electrolyte features
hyperkalemia and hyperphosphatemia and hypocalcemia
36
Occurs when normally unidirectional flow of urine is blocked
Post renal AKI
37
Diagnosis of AKI
Rise from baseline of at least 0.3mg/dl within 48 hours at least 50% higher than baseline wihtin 1 week or Reduction in UO less than 0.5ml/Kg /hr for longer than 6 hours
38
AKI with palpable purpura, pulmonary hemorrhage or sinusitis raises the possibility of
systemic vasculitis with glomerulonephritis
39
AKI from ATN due to ischemic injury, sepsis or certain nephrotoxins has characteristic urine sediment findings of :
"Muddy Brown" Granular casts and tubular epithelial casts
40
Oxalate crystals in AKI should prompt evaluation for
Ethylene glycol toxicity
41
A measure of both the kidney's ability to reabsorb sodium as well as endogenously and exogenously administired factors that affcet tubular reabsorption
Fractional excretion of Na (Fe Na)
42
A type 1 transmembrane protein abundant in proximal tubular cells injured by ischemia or nephrotoxins such as cisplatin/ ichemic or nephrotoxic injury
Kidney injury molecule-1 (KIM-1)
43
NGAL (lipocalin-2 or siderocalin) | Neutrophile gelatinase associated lipocalin
Biomarker of AKI, bind to iron siderophoere an dmay have tissue protective effects; detected in plasma and urine within 2h of Cardiopulmonary bypass- associated AKI
44
Hallmark of AKI
Buildup of nitrogenous waste products, elevated BUN
45
BUN level which causes metal status changes, bleeding complications
>100mg/dl
46
Most concerning complication of AKI
Hyperkalemia
47
Definitive treatment of hepatorenal syndrome
orthotopic liver transplantation
48
Scleroderma renal crisis should be treated with
ACE inhibitors
49
Idiopathic TTP-HUS should be treated promptly with
Plasma exchange
50
Patients with rhabdomyolysis may initially require _L of fluid per day
10L
51
Diuretics may be used if fluid repletion is adequate but unsuccesful in achieving urinary flow rates of _
200-300mL/hr
52
Metabolic acidosis is generally not treated unless severe at pH_ and bicarbonate of _mmol/L
pH <7.20 and bicarbonate at <15mmol/L
53
According to KDIGO, AKI patients should achieve total energy intake of
20-30kcal/kg/day
54
Protein intake in non severe AKI, no need for dialysis
0.8 to 1.0 g/kg/perday
55
Protein intake in patients on dialysis
1.0-1.5 g/kg per day
56
Protein intake if hypercatabolic and receiving CRRT
1.7 g/kg per day
57
Many nephro initiate dialysis for AKI empirically when BUN exceeds:
100 mg/dl
58
Most common form of renal replacement therapy for AKI
Hemodialysis
59
_% may develop ESRD - among survivors of AKI requiring temporary dialysis
10%
60
Case: 60 M with constitutional symptoms, bone pain Lab: Monoclonal spike in urine, low anion gap, anemia
Multiple myeloma
61
Case: Aminoglycosisde antibiotics, cisplatin, antivirals, ethylene glycol ingestion, melamin ingestion Lab: urine sediment: granular casts, renal tubular epithelial cell casts, FeNa >1%
Tubular injury
62
Case: Recent medication exposure with fever, rash , arthralgias Lab: Urine has eosinophilia, sterile pyuria, nonoliguric
Interstitial nephritis
63
Case: Neurologic abnormalities present, recent diarrhea, with AKI, use of calcineurin inhibitors, pregnancy or post partum Lab: schistocytes on PBS, elevated LDH, anemia and decreased plt, ADAMTS13 activity
TTP/HUS Typical HUS - AKI with diarrhea (Shiga toxin, E.coli) Atypical HUS- inherited or acquired complement dysregulation TTP HUS - sporadic cases