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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
Q

Treatment of acute interstitial nephritis

A
  • discontinue offending agent

- glucocorticoid therapy (prednisone, methylprednisolone)

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26
Q

What is acute tubular necrosis

A

acute tubular cell injury

27
Q

What causes acute tubular necrosis

A
  • ischemia
  • sepsis
  • toxins (exogenous, endogenous)
28
Q

What are some nephrotoxins that can cause acute tubular necrosis

A
  • NSAIDs
  • chemotherapeutic agents
  • aminoglucosides
  • amphotericin
  • vanco
  • radiocontrast dye
29
Q

Acute tubular necrosis on urinalysis

A

pigmented granular casts (muddy browncasts)

30
Q

Lab findings with acute tubular necrosis

A
  • Cr/BUN elevation
  • FeNa >2%
  • hyperkalemia
  • hyperphosphatemia
  • hyperuricemia
31
Q

Treatment of acute tubular necrosis

A
  • aggressive volume replacement
  • high dose loop diuretic if oliguric and volume normal
  • protein restriction
  • dialysis
32
Q

What is post-streptococcal glomerulonephritis

A

immune complex containing strep Ag is deposited in affected glomeruli

33
Q

PSGN occurs __ days following ___

A

7-12 days following sore throat/impetigo

34
Q

Findings of PSGN

A
  • oliguria
  • cola colored urine
  • edema
  • hypertension
  • malaise, anorexia, flank pain
35
Q

Tx of PSGN

A
  • abx

- subbortive (anti HTN, salt restriction, diuretics)

36
Q

Urinalysis of PSGN

A
  • proteinuria
  • hermaturia
  • pyuria
  • +/- RBC casts
37
Q

What is necessary for a diagnosis of PSGN

A

recent group A beta-hemolytic strep infection

38
Q

What is IgA nephropathy

A

deposition of IgA in the glomerulus often following a URI

39
Q

How does IgA nephropathy present

A
  • red or cola colored urine

- spectrum of glomerulonephritis

40
Q

How do you diagnose IgA nephropathy

A

renal biopsy

41
Q

How do you treat IgA nephropathy

A
  • ACE/ARB
  • steroids
  • renal transplant
42
Q

What is Henoch Scholein purpura

A

small vessel vasculitis w/ IgA complex deposition

43
Q

How does HSP affects

A

children around 6

44
Q

Classic clinical presentation of HSP

A
  • rash on LE and buttocks
  • abd pain/vomiting
  • arthralgias (knees, ankles)
  • edema on hands, feet, scalp, ears
45
Q

Tx of HSP

A
  • mostly supportive

- immunosuppressants and/or plasmapheresis for worsening disease

46
Q

Three main findings with nephrotic syndrome

A
  • heavy proteinuria
  • hypoalbuminemia
  • peripheral edema
47
Q

Other findings in nephrotic syndrome

A

-lipiduria
-hypercholesterolemia
-hypertension
-hypercoagulable state
0blan urinary sediment

48
Q

What things can cause nephrotic syndrome

A
  • membranous nephropathy
  • minimal change disease
  • amyloidosis
  • lupus
  • membranoproliferative glomerulonephritis
  • focal segmental glomerulosclerosis
  • IgA nephropathy
49
Q

Characteristic histologic finding of minimal change disease

A

diffuse effacement of the epithelial cell foot processes on electron microscopy

50
Q

Signs of minimal change disease

A
  • abrupt onset edema and nephrotic syndrome
  • hypoalbuminemia
  • HTN
  • proteinuria (10g/day)
51
Q

inimal change disease causes patients to be more susceptible to what

A

infection with gram + organisms

52
Q

What is the most common cause of AKI in children

A

PSGN

53
Q

How do you treat minimal change disease

A

prednisone

54
Q

Causes of post renal AKI

A
  • bladder outlet obstruction
  • -neurogenic bladder
  • gynecologic surgery or abdominopelvic malignancy
  • pregnancy
  • medications
55
Q

Treatment of postrenal AKI

A

relief of obstruction (bladder cath, nephrostomy tube)

56
Q

What is polycystic kidney disease

A

progressive genetic disorder with cyst formation and enlargement of the kidney

57
Q

What other organs does polycystic kidney disease affect

A

pancreas, liver, spleen

58
Q

Patients with polycystic kidney disease are at a 2x greater risk for what

A

intracranial aneurysm

59
Q

Most patients with polycystic kidney disease require what

A

kidney transplant

60
Q

Signs and sx of polycystic kidney disease

A
  • pain (abd, flank, back)
  • hypertension
  • palpable flank mass
  • nodular hepatomegaly
61
Q

How do you diagnose polycystic kidney disease

A
  • ultrasound
  • elevated H/H
  • urinalysis
62
Q

How do you treat polycystic kidney disease

A
  • ACE/ARB
  • pain control (no nsaids), surgical cyst decompression, nephrectomy
  • treat recurrent infections
  • hydrate and possibly transfuse if hematuria
63
Q

Signs and sx of vascular AKI

A
  • LE rash
  • livedo reticularis
  • urine eosinophils
64
Q

When do you dialyze a patient

A

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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