AKI Flashcards

1
Q

what is an AKI

A

abrupt decline in renal function (GFR) occurring over hours to days, sometimes over weeks, with the inability to maintain and regulate fluid, electrolyte and acid-base balance

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2
Q

what labs are associated with AKI

A

associated with accumulation of waste products (urea and creatine)

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3
Q

normal urine output

A

> =1200ml/d

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4
Q

anuria urine output

A

<50ml/d

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5
Q

oliguria urine output

A

<500ml/d

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6
Q

non-oliguria urine output

A

> 500ml/d

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7
Q

KDIGO definition of AKI

A
  • SCr increase by >=26.5 mmol/L within 48h or
  • SCr increase to >=1.5x baseline within 7d or
  • Urine Vol <0.5ml/kg/h for >=6h
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8
Q

causes of AKI

A
  • intravascular volume depletion
  • drugs (NSAIDs, ACEi, ARBs, Contrast media, ahminoglycosides, amphotericin B, antivirals, Chemo)
  • infections
  • cardiac
  • surgery
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9
Q

pre renal AKI

A

resulting from decrease renal perfusion (most common in hospital) due to:
- volume depletion; or
- reduced cardiac output; or
- renal hypo perfusion

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10
Q

intrinsic AKI

A

result of structural damage within kidney due to:
- acute tubular necrosis (most common)
- acute interstitial nephritis
- glomerular damage
- vascular damage

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11
Q

post renal AKI

A

caused by obstruction of urine flow

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12
Q

risk factors for AKI

A
  • > 60yo
  • female
  • acute infection
  • pre existing chronic respiratory or CVD
  • dehydration / vol depletion
  • preexisting CKD -> AoCKD
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13
Q

clinical presentation of AKI

A
  • reduced urine output
  • peripheral edema
  • flank pain
  • abnormal labs (elevated SCr, BUN, K; presence of WBC, RBC, crystals in urine; abnormal SG, FeNA, urine osmolarity)
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14
Q

possible causes of volume depletion

A
  • hemorrhage
  • GI losses (vomit/diarrhea)
  • Urinary losses (over diuresis, DI)
  • burns, peritonitis
  • decrease effective volume (cirrhosis)
  • peripheral vasodilation (sepsis, vasodilator)
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15
Q

possible causes of reduced cardiac output

A
  • sepsis
  • CHF
  • MI
  • Pericardial tamponade
  • Acute PE
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16
Q

possible causes of renal hypoperfusion

A
  • Bilateral renal artery occlusion (thrombosis, emboli, stenosis)
  • medications (ACEi, NSAIDs, calcineurin inhibitors, radiocontrast media, vasopressors)
17
Q

diagnosis and evaluation for pre renal AKI

A
  • pt hx (GI loss, diuresis)
  • physical exam (orthostatic hypotension, tachycardia, poor skin turgor)
  • central venous pressure (volume status of heart)
  • urine test (SG, osmolarity, FeNa)
18
Q

Management of AKI

A
  • reverse etiologic factors (treat pre-renal causes)
  • use vasopressors with fluids in pt w vasomotor shock
  • supportive care
19
Q

possible causes of acute tubular necrosis

A
  • ischemic (hypotension, vasoconstriction)
  • nephrotoxins (contrast dyes, heavy metals, amphotericin B, Aminoglycosides, organic solvents)
  • endogenous toxins (hemoglobin, myoglobin)
20
Q

possible causes of acute interstitial nephritis

A
  • drugs (penicillin, ciprofloxacin, sulphonamides)
  • infections (viral and bacterial)
21
Q

possible causes of glomerular damage

A
  • SLE (lupus, nephritis)
  • rapidly progressive glomerulonephritis (GN)
  • post streptococcal GN
22
Q

possible causes of vascular damage

A
  • Vasculitis, polyarteritis, nodosa
    haemolytic uremic syndrome
    thrombotic thrombocytopenia purport, accelerated HTN
    emboli (thrombotic, atherosclerotic)
23
Q

4 phases of ATN

A
  1. initiating
  2. oliguric
  3. diuretic
  4. recovery