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clin med II, exam 3 > AKI > Flashcards

AKI Flashcards

1
Q

define acute kidney injury

A
  • abrupt loss of kidney function resulting in
    • retention of urea and other nitrogenous waste products
    • dysregulation of volume status and electrolytes
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2
Q

GFR

A

estimates how much blood passed through the glomeruli each minute to be filtered

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3
Q

what are the criteria for diagnosis of acute kidney injury

A
  1. serum creatinine levels
  2. decrease in urine output
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4
Q

can you still use serum creatinine to assess kidney function in patient undergoing dialysis

A

no, creatinine is removed by dialysis

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5
Q

Define the RIFLE acronym

A
  • Risk
  • Injury
  • Failure
  • Loss
  • ESRD
  • *first three are levels of severity; last two are outcome measures
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6
Q

what three groups have come up with ways to define AKI

A
  • RIFLE
  • AKIN
  • KDIGO
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7
Q

what is RIFLEs definition of AKI using serum creatinine

A
  • increase in serum creatitine > 50% developing over 7 days
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8
Q

what is AKIN’s definition of AKI using serum creatinine

A
  • increase in serum creatinine of 0.3 mg/dL pr > 50% developing over 48 hours
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9
Q

AKI can be classified into what 3 categories

A
  1. Prerenal: decreased renal perfusion
  2. Intrinsic renal: pathology of vessels, glomeruli, or tubules-interstitium
  3. Postrenal: obstructive
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10
Q

What are some causes of Prerenal AKI

A
  1. True volume depeletion
    • V/D; burns, third spacing from crush injury
  2. Hypotension
    • shock or aggressive tx of HTN
  3. Edematous status
    • heart failure, cirrhosis
  4. Bilateral renal artery stenosis
  5. Drugs affecting GFR
    • NSAIDs
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11
Q

What are some causes of Intrinsic renal AKI

A
  • renal ischemia
    • from all causes of severe prerenal dz
  • sepsis
  • nephrotoxins
    • aminoglycosides, IV contrast, rhabdomyolysis
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12
Q

How does IV contrast affect kidneys

A
  • causes renal tubular epithelial cell toxicity and renal medullary ischemia
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13
Q

risk factors for kidney damage by IV contrast

A
  • pre-existing renal disease
  • volume depletion
  • repeated doses of contrast
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14
Q

prevention of kidney damage by IV contrast

A
  • hydration
  • avoidance of nephrotoxic drugs for at least 48 hours after exposure
    • e.g metformin
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15
Q

define Nonoliguric

A

>400 mL/24 hours

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16
Q

Define Oliguric

A

<400mL/24 hr

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17
Q

define Anuric

A

<100mL/24 hr

18
Q

important labs to get when evaluating AKI

A
  • UA
  • creatinine
    • calculation of GFR
    • calculatoin of fractional excretion of sodium (FENa)
19
Q

first line imaging to get when evaluating AKI? what are you evaluating for

A
  • renal US
  • assess for urinary tract obstruction
20
Q

most dipsticks permit the analysis of the following core urine parameters

A
  • Heme
  • Leukocyte esterase
  • Nitrite
  • Albumin
  • Hydrogen ions (pH)
  • specific gravity
  • Glucose
21
Q

muddy brown casts are pathognomonic for

A

Acute tubular necrosis

22
Q

What are the two most commonly used equations for calculating GFR

A
  • Crockcroft-Gault
  • Modification of Diet in renal disease (MDRD)
23
Q

how is the fractional excretion of sodium (FENa) used

A
  • measures urine sodium
  • in an oliguric patient, the FENa may help to distinguish prerenal AKI from intrinsic renal pathology
24
Q

what is the equation for fractional excretion of sodium (FENa)? What values suggest prerenal and ATN?

A

FENa = (urine Na / Serum Na) / (Urine Cr / Serum Cr) x 100

  • < 1% suggests prerenal etiology
  • >2% suggests intrarenal (ATN)
25
Q

when can you not rely on the fractional excretion of sodium (FENa) equation

A
  • cannot be used in patients on diuretics
  • can’t be used with chronic renal failure
    • only useful in acute renal failure
26
Q

When is a renal biopsy indicated

A
  • for patients who have no clear explanation for AKI
  • if the creatinine is markedly elevated or if it significantly worsens over the course of days
  • biopsy will provide more definitive tissue diagnosis
27
Q

contraindications to getting a renal biopsy

A
  • solitary native kidney
  • bleeding diathesis
  • hydronephrosis
  • pyelonephritis
  • renal tumor
28
Q

List the life-threatening complications that can come from AKI

A
  • volume imbalance: depletion or overload
  • metabolic acidosis
  • hyperkalemia
  • hypocalcemia
  • hyperphosphatemia
  • uremia
  • **generally require hemodialysis
29
Q

if patient has a h/o consistent with fluid loss (V/D), a physical exam consistent with hypovolemia (hypotension, tachycardia) and/or oliguria, treatment is

A
  • IV fluids
    • fluid challenge attempts to identify prerenal failure
    • crystalloid isotonic fluid (0.9 nml saline) is preferred
30
Q

how much fluid is given

A
  • begin with 1-3 liters of fluid with careful and repeated clinical assessment
    • pts who do not respond to fluids are unlikely to have prerenal disease
31
Q

if patient becomes volume overloaded or develops fluid retention from IV fluid therapy then treatment is

A
  • diuretics (typically furosemide) = temporizing measure
    • should not be prolonged therapy
    • dialysis offers most efficient method of volume removal
32
Q

how does AKI lead to metabolic acidosis

A
  • excretion of acid and regeneration of bicarbonate is impaired with a low GFR
  • causes of AKI such as sepsis, trauma, and multi-organ failure produces increased amount of acid
33
Q

how does diarrhea worsens metabolic acidosis

A

causes net loss of bicarbonate

34
Q

treatment options for metabolic acidosis from AKI

A
  1. dialysis
  2. bicarbonate administration
    • choice depends on presence of volume overload and the underlying cause of acidosis
35
Q

when should a patient with metabolic acidosis from AKI be dialyzed

A
  • patients with severe oligo-anuric AKI who are volume overloaded and have severe metabolic acidosis ( pH <7.1)
    • bicarb adminstration results in large sodium load that may cause or increase volume overload
36
Q

when should a patient with metabolic acidosis from AKI be given bicarbonate

A
  • patients with AKI who are not volume overloaded and
    • acidosis is related to diarrhea
    • pH < 7.1 and awaiting dialysis
    • AKI due to rhabdomyolysis
  • goal: serum bicarb 20-22 mEq/L and pH > 7.2
37
Q

hyperkalemia can cause

A
  • impaired neuromuscular transmission
  • cardiac conduction abnormalities (arrhythmias)
38
Q

how does AKI cause hypocalcemia and hyperphosphatemia

A
  • increases in serum phosphorus levels is caused by reduced GFR
    • phosphorus binds to calcium -> hypocalcemia
  • **serum ionized calciu, should be measured
39
Q

what is the tx for patients who are symptomatically hypocalcemic but whose phosphate levels are very high?

A
  • dialysis
    • if you give IV calcium, it may result in deposition of calciu, phosphate into vasculature and organs
  • however, give IV calcium while waiting for dialysis if pt has tetany, QT prolongation, Chvostek sign
40
Q

Name signs/symptoms of severe hypocalcemia

A
  • tetany
  • confussion, sz
  • Trousseau’s sign
  • Chovstek sign
  • QT prolongation
41
Q

patients with serum phosphate levels > 6 mg/dL should be treated with

A

dietary phosphate binders

  • if serum ionized ca2+ is low => calcium acetate or calcium carbonate
  • if serum ionized ca2+ is high => aluminum hydroxide
42
Q

dialysis should be initiated in patients with severe uremia. what are some signs of severe uremia

A
  • pericarditis
  • neuropathy
  • unexplained decline in mental status

clin med II, exam 3 (6 decks)

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