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Renal > AKI > Flashcards

AKI Flashcards

1
Q

Definition of azotemia

A

Elevation in nitrogenous waste products and creatinine

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2
Q

Uremia definition

A

Symptoms associated with accumulation of metabolic by-products and endogenous toxins in the blood caused by azotemia

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3
Q

Uremia symptoms

A 
Fatigue
Anorexia
N/V
Pruritus
Mental status changes
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4
Q

Normal urine output

A

1 - 1.5L per 24 hours

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5
Q

Urine output in non-oliguria

A

> 500 mL/day in patients with renal insufficiency

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6
Q

Urine output in oliguria

A

< 400-500 mL/day

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7
Q

Urine output in anuria

A

< 50-100 mL/day

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8
Q

What is pre-renal AKI?

A

Hypoperfusion of the renal cells

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9
Q

What are pre-renal causes of AKI?

A

Intravascular volume depletion
Reduced effective circulating volume
Occlusion of pre-renal vasculature
Drug induced

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10
Q

What is intrinsic AKI?

A

Direct damage to the renal cells

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11
Q

What are vasculature causes of intrinsic AKI?

A

Thrombotic thrombocytopenia purpura
Hemolytic uremic syndrome
Renal artery thrombosis

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12
Q

What are causes of intrinsic AKI due to the glomerulus?

A

SLE
Glomerulonephritis
Post-infection

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13
Q

What is AIN?

A

Acute, allergic interstitial nephritis

Inflammatory, immunologic reaction within the renal interstitium

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14
Q

What are the causes of AIN?

A

Drugs
Infections
Autoimmune disorders

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15
Q

What is ATN?

A

Acute tubular necrosis

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16
Q

What are the 3 phases of ATN?

A

Initiation
Maintenance
Recovery

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17
Q

What is the initiation of ATN?

A

Damage and decrease in GFR

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18
Q

What is the maintenance of ATN?

A

Toxin or ischemia has been removed but the kidney stays in the state

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19
Q

What is the recovery of ATN?

A

Building new epithelial

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20
Q

What can cause ATN?

A

Extending pre-renal states or exposure to toxins

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21
Q

What causes post-renal AKI?

A

Caused by an obstruction in the urinary collection system

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22
Q

What are causes bladder outlet obstruction?

A

Prostatic hypertrophy
Cancer
Improperly placed bladder catheter

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23
Q

What are causes of ureteral obstruction?

A

Cervical cancers
Retroperitoneal fibrosis
Nephrolithiasis

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24
Q

What are causes of renal pelvis/tubules obstruction?

A

Nepholithiasis (crystal deposition from medications)

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25
Q

What are RF for AKI?

A 
Age (> 65 yo)
Pre-existing renal dysfunction
Volume depletion
Serious infections
Comorbidities 
Exposure to nephrotoxins
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26
Q

What are comorbidities associated with AKI?

A

HF
CV issues
DM
Liver disease

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27
Q

What is AKIN stage 1 SCr criteria?

A

Increased SCr >/= 0.3
OR
Increased >/= 1.5- to 2-fold from baseline

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28
Q

What is AKIN stage 1 UO criteria?

A

< 0.5 ml/kg/hr x > 6 hours

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29
Q

What is AKIN stage 2 SCr criteria?

A

Increased SCr to > 2- to 3-fold from baseline

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30
Q

What is AKIN stage 2 UO criteria?

A

< 0.5 ml/kg/hr x > 12 hours

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31
Q

What is AKIN stage 3 SCr criteria?

A

Increase SCr to > 3-fold from baseline or SCr >/= 4.0 with an acute increase of at least 0.5

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32
Q

What is AKIN stage 3 UO criteria?

A

< 0.3 ml/kg/hr x 24 hours
OR
Anuria x 12 hours

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33
Q

What is KDIGO stage 1 SCr criteria?

A

1.5-1.9 times baseline
OR
>/= 0.3 increase

34
Q

What is KDIGO stage 1 UO?

A

< 0.5 ml/kg/h for 6-12 hours

35
Q

What is KDIGO stage 2 SCr criteria?

A

2.0-2.9 times baseline

36
Q

What is KDIGO stage 2 UO criteria?

A

< 0.5 ml/kg/h >/= 12 hours

37
Q

What is KDIGO stage 3 SCr criteria?

A 
3.0 times baseline
OR
Increase in SCr >/= 4.0
OR
Initiation of renal replacement therapy
OR
In patients < 18 years, decrease in eGFR < 35 ml/min/m2
38
Q

What is KDIGO stage 3 UO criteria?

A

< 0.3 ml/kg/h x >/= 24 hours
OR
Anuria for >/= 12 hours

39
Q

What are the limitations of diagnosis and staging AKI?

A

Need a baseline SCr level
May be 1-2 day delay to SCr increase after injury
UP can be variable
Primarily studied/validated in critically ill population

40
Q

What are some diagnostic procedures for AKI?

A 
Renal ultrasound
Catheter
Kidney-ureter-bladder (KUB) x-ray
Cystoscopy with retrograde pyelography
Renal biopsy
41
Q

What are types of Intrinsic AKI?

A

AIN

ATN

42
Q 
How to differentiate causes of AKI: Pre-renal
Physical Exam
Urine Sediment
Urine RBC
Urine Na
FEna
BUN:SCr ratio
A 
PE: Hypotension, dry mucous membranes, decreased CO, edema, ascites
Urine sediment: Normal
Urine RBC: None
Urine WBC: None
Urine Na: < 20
FEna: < 1
BUN:SCr ratio: >/=20:1
43
Q 
How to differentiate causes of AKI: Intrinsic
Physical Exam
Urine Sediment
Urine RBC
Urine WBC
Urine Na
FEna
BUN:SCr ratio
A 
PE: Variable
Urine Sediment: GRanular and epithelial casts
Urine RBC: 2-4+
Urine WBC: 2-4+
Urine Na: > 40
FEna: > 2
BUN:SCr ratio: <20:1
44
Q 
How to differentiate causes of AKI: Post-renal
Physical Exam
Urine Sediment
Urine RBC
Urine WBC
Urine Na
FEna
BUN:SCr ratio
A

PE: Prostatic enlargement, bladder distension
Urine sedment: Variable, cellular debris, RBCs, crystals possible
Urine RBC: variable
Urine WBC: 1+
Urine Na: > 40
FEna: Variable
BUN:SCr ratio: 15:1

45
Q

What are non-pharmacologic strategies for prevention of AKI?

A

Avoidance of nephrotoxins

Maintain hemodynamic stability to avoid hypotension, hypovolemia

46
Q

What are pharmacologic strategies for prevention of AKI?

A

Prevention of contrast media-induced nephrotoxicity (CIN)
Sodium bicarbonate + hydration
Loops

47
Q

What is the dose of sodium bicarbonate in AKI?

A

Alkalinizing agent
Dose - 154 mEq sodium bicarbonate in 1L D5W infuse at 3 mL/kg/h x 1 hr before procedure, then 1 mL/kg/h during procedure and 6 hours after procedure

48
Q

What are the desired goals of AKI treatment?

A 
Rapid identification of cause
Removal or reduction of causative agents
Prevent further kidney injury
Prevent complications
Regain renal function
49
Q

What is the mainstay of AKI treatment?

A

Supportive care

50
Q

What is supportive care for AKI treatment?

A

Stop nephrotoxic drugs
Maintain adequate hemodynamic status
Maintain glucose control
Manage complications

51
Q

What are indications for renal replacement therapy in AKI?

A 
A - acid-base abnormalities
E - Electrolyte imbalances (hyperkalemia usually)
I - Intoxications
O - Overload of fluids
U - Uremia
52
Q

What are the types of renal replacement therapy?

A

Intermittent HD (IHD)
Continuous renal replacement therapy (CRRT)
Hybrid

53
Q

What are the causes of diuretic resistance?

A 
Excessive sodium intake
Inadequate diuretic dose or inappropriate regimen
Reduce bioavailability
Reduced renal blood flow
Increased sodium reabsorption
54
Q

What are the complications of AKI?

A 
Fluid overload
Hyperkalemia
Hypernatremia
Infection
CV
GI
Neurologic
55
Q

What are the treatments for fluid overload?

A

Minimize fluid intake
Loop diuretics
Reduction of diuretic resistance

56
Q

What is the most commonly used loop for fluid overload?

A

Furosemide

57
Q

What is the IV bolus dosing of furosemide in fluid overload?

A

40-80 mg x 1 (caution - high doses are associated with ototoxicity)

58
Q

Strategies to reduce diuretic resistance

A

Identify and eliminate/reduce potential cause
Increase dose or use continuous infusion
Add an additional diuretic with a different mechanism

59
Q

Drugs to reduce diuretic resistance

A 
Thiazide diuretics (Chlorothiazide 250-500 mg IV q12h)
Thiazide-like diuretics (Metolazone 5-10 mg PO q24h))
60
Q

Hyperkalemiain AKI

A

Most common complication

61
Q

Clinical symptoms of hyperkalemia

A

Usually asymptomatic
May have palpitations or skipped heartbeats
EKG changes: peaked T waves, prolongation of PR and QRS intervals, disappearance of P wave/merger with QRS and T waves

62
Q

Drugs to treat hyperkalemia

A

Calcium gluconate (give every pt this)
Insulin (plus glucose)
Albuterol
Sodium polystyrene sulfonate (Kayexalate)

63
Q

Calcium gluconate MOA

A

Cardioprotection: stabilizes membrane voltage (not a true treatment, does not contribute to K levels at all)

64
Q

Calcium gluconate onset

A

1-3 minutes

65
Q

Calcium gluconate duration

A

30 minutes

66
Q

Calcium gluconate comments

A

May potentiate digoxin toxicity
Give over slow 20-30 minute infusion if patient is on dig
Calcium and bicarb are incompatible

67
Q

Insulin (plus glucose) and Albuterol MOA

A

Redistribution: increases cellular K uptake to decrease plasma K level

68
Q

Insulin (plus glucose) and Albuterol onset

A

10-30 min

69
Q

Insulin (plus glucose) Duration

A

2-6 hours

70
Q

Albuterol duration

A

2-4 hours

71
Q

Insulin (plus glucose) comments

A

Glucose given to avoid hypoglycemia
Glucose is unnecessary if BS > 250
Monitor glucose levels closely

72
Q

Albuterol comments

A

Works better when combined with insulin and glucose
25% of patients do not respond
Tachycardia is common

73
Q

Sodium polystyrene sulfonate MOA

A

Removal: eliminates K from the gut in exchange for Na

74
Q

Sodium polystyrene sulfonate Onset

A

1-3 hours

75
Q

Sodium polystyrene sulfonate duration

A

4-6 hours

76
Q

Sodium polystyrene sulfonate comments

A

Sorbitol used to minimize constipation
Quicker onset with rectal route
Sorbitol associated with bowel necrosis
May lead to Na retention

77
Q

Hypernatremia treatment

A

Sodium restriction

78
Q

What is the most common cause of death in AKI?

A

Infection

79
Q

How can infections cause AKI?

A

Sepsis can lead to AKI

80
Q

What are CV complications of AKI?

A

HTN with intermittent hypotension

CHF, arrhythmias, and pulmonary edema

81
Q

What are the GI complications of AKI?

A

Increased risk of bleeding
Stress ulceration
N/V

82
Q

What are neurologic complications in AKI?

A

Altered mental status
Seizures
Somnolence

Renal (8 decks)

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