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Clin Med III Exam II > Acute Renal Failure > Flashcards

Acute Renal Failure Flashcards

1
Q

Acute kidney injury

A

abrupt decline in renal function manifesting as reversible acute increase in nitrogenous wastes over hours to weeks

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2
Q

What are the 3 graded levels of acute injury to the kidney (RIFLE criteria)

A

risk, injury, failure

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3
Q

What are the 2 outcome measures in the RIFLE criteria

A

loss of function and end stage renal disease

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4
Q

What is the RIFLE criteria based on

A

either degree of serum creatinine elevation or decrease in urine output

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5
Q

What conditions put a patient at a high risk of developing AKI

A
  • HTN
  • CHF
  • DM
  • multiple myeloma
  • chronic infection
  • myeloproliferative disorder
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6
Q

What are the three categories of causes of AKI

A
  • prerenal causes (low flow)
  • intrinsic causes (problem with actual kidney)
  • post renal cause (flow obstruction)
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7
Q

Prerenal causes of AKI

A
  • hypovolemia
  • decreased cardiac output
  • decreased effective circulating volume
  • impaired renal autoregulation (NSAIDs, ACE/ARB, cyclosporine)
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8
Q

What is azotemia

A

increased in BUN and creatinine

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9
Q

What causes most AKI

A

low flow state (prerenal cause)

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10
Q

Pre-renal AKI results from what? What can be done to reverse it?

A

results from poor renal perfusion

can be reversed with restoration of renal perfusion/glomerular pressure

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11
Q

BUN/Creatinine ratio would be what in pre-renal injury

A

20:1

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12
Q

What would a urinalysis show in pre- renal injury

A

hyaline casts

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13
Q

What is the breakdown of intrinsic causes of AKI

A
  • glomerular
  • tubules and interstitium
  • vascular
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14
Q

What does calculation of FeNa tell you

A

where the renal failure is occuring

<1% prerenal
>1% intrinsic
>4% post renal failure

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15
Q

When is the calculation of FeNA not accurate

A

when pt takes diuretics

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16
Q

What is the alternative to FeNa

A

FeUrea

<35% prerenal
>50% suggests acute tubular necrosis

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17
Q

Labs for prerenal AKI if due to volume depletion. Decreased CO.

A

Volume Depletion:

  • elevated H/H, albumin, calcium (hemoconcentration)
  • elevated Na, BUN, Cr

Decreased CO

  • edema
  • low Na, albumin

Urine

  • oliguria or anuria
  • high urine specific gravity
  • low urine Na
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18
Q

Treatment for prerenal AKI caused by volume depletion. Decreased CO.

A

Volume depletion:
-correct water deficit, NS

Decreased CO:

  • diuretics
  • nitrates
  • dobutamine
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19
Q

What are some intrinsic causes of AKI

A
  • acute interstitial nephritis
  • acute tubular necrosis
  • glomerular diseases
  • pyelonephritis
  • malignancy
  • renal artery embolism/thrombus
  • vasculitis
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20
Q

What is acute interstitial nephritis typically due to

A

allergic reaction to medication

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21
Q

What is the classic presentation of acute interstitial nephritis

A
  • recent new drug exposure
  • fever
  • skin rash
  • peripheral eosinophelia
  • oliguria
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22
Q

How do patients more commonly present with acute interstitial nephritis

A

found incidentally, rising serum creatinine after initiation of a new med

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23
Q

What medications are associated with acute interstitial nephritis

A
  • abx (b-lactams, sulfonamides, vanco, erythro, rifampin)
  • acyclovir
  • NSAIDs
  • anticonvulsants
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24
Q

Acute interstitial nephritis urinalysis

A
  • pyuria (WBC casts)

- hematuria

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25
Treatment of acute interstitial nephritis
- discontinue offending agent | - glucocorticoid therapy (prednisone, methylprednisolone)
26
What is acute tubular necrosis
acute tubular cell injury
27
What causes acute tubular necrosis
- ischemia - sepsis - toxins (exogenous, endogenous)
28
What are some nephrotoxins that can cause acute tubular necrosis
- NSAIDs - chemotherapeutic agents - aminoglucosides - amphotericin - vanco - radiocontrast dye
29
Acute tubular necrosis on urinalysis
pigmented granular casts (muddy browncasts)
30
Lab findings with acute tubular necrosis
- Cr/BUN elevation - FeNa >2% - hyperkalemia - hyperphosphatemia - hyperuricemia
31
Treatment of acute tubular necrosis
- aggressive volume replacement - high dose loop diuretic if oliguric and volume normal - protein restriction - dialysis
32
What is post-streptococcal glomerulonephritis
immune complex containing strep Ag is deposited in affected glomeruli
33
PSGN occurs __ days following ___
7-12 days following sore throat/impetigo
34
Findings of PSGN
- oliguria - cola colored urine - edema - hypertension - malaise, anorexia, flank pain
35
Tx of PSGN
- abx | - subbortive (anti HTN, salt restriction, diuretics)
36
Urinalysis of PSGN
- proteinuria - hermaturia - pyuria - +/- RBC casts
37
What is necessary for a diagnosis of PSGN
recent group A beta-hemolytic strep infection
38
What is IgA nephropathy
deposition of IgA in the glomerulus often following a URI
39
How does IgA nephropathy present
- red or cola colored urine | - spectrum of glomerulonephritis
40
How do you diagnose IgA nephropathy
renal biopsy
41
How do you treat IgA nephropathy
- ACE/ARB - steroids - renal transplant
42
What is Henoch Scholein purpura
small vessel vasculitis w/ IgA complex deposition
43
How does HSP affects
children around 6
44
Classic clinical presentation of HSP
- rash on LE and buttocks - abd pain/vomiting - arthralgias (knees, ankles) - edema on hands, feet, scalp, ears
45
Tx of HSP
- mostly supportive | - immunosuppressants and/or plasmapheresis for worsening disease
46
Three main findings with nephrotic syndrome
- heavy proteinuria - hypoalbuminemia - peripheral edema
47
Other findings in nephrotic syndrome
-lipiduria -hypercholesterolemia -hypertension -hypercoagulable state 0blan urinary sediment
48
What things can cause nephrotic syndrome
- membranous nephropathy - minimal change disease - amyloidosis - lupus - membranoproliferative glomerulonephritis - focal segmental glomerulosclerosis - IgA nephropathy
49
Characteristic histologic finding of minimal change disease
diffuse effacement of the epithelial cell foot processes on electron microscopy
50
Signs of minimal change disease
- abrupt onset edema and nephrotic syndrome - hypoalbuminemia - HTN - proteinuria (10g/day)
51
inimal change disease causes patients to be more susceptible to what
infection with gram + organisms
52
What is the most common cause of AKI in children
PSGN
53
How do you treat minimal change disease
prednisone
54
Causes of post renal AKI
- bladder outlet obstruction - -neurogenic bladder - gynecologic surgery or abdominopelvic malignancy - pregnancy - medications
55
Treatment of postrenal AKI
relief of obstruction (bladder cath, nephrostomy tube)
56
What is polycystic kidney disease
progressive genetic disorder with cyst formation and enlargement of the kidney
57
What other organs does polycystic kidney disease affect
pancreas, liver, spleen
58
Patients with polycystic kidney disease are at a 2x greater risk for what
intracranial aneurysm
59
Most patients with polycystic kidney disease require what
kidney transplant
60
Signs and sx of polycystic kidney disease
- pain (abd, flank, back) - hypertension - palpable flank mass - nodular hepatomegaly
61
How do you diagnose polycystic kidney disease
- ultrasound - elevated H/H - urinalysis
62
How do you treat polycystic kidney disease
- ACE/ARB - pain control (no nsaids), surgical cyst decompression, nephrectomy - treat recurrent infections - hydrate and possibly transfuse if hematuria
63
Signs and sx of vascular AKI
- LE rash - livedo reticularis - urine eosinophils
64
When do you dialyze a patient
acidosis electrolytes: hyperkalemia, hyperphosphatemia, hypocalcemia Ingestion of toxins Volume overload + anuria Symptoms of Uremia

Clin Med III Exam II (11 decks)

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