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Unit 3 Clin Med II > L20: AKI > Flashcards

L20: AKI Flashcards

1
Q

Acute renal failure

A

refers to severe AKI which requires dialysis

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2
Q

AKI diagnosis

A

One of the following

  1. Increase in serum creatinine by >.3 mg/dL in 48 hours
  2. Increase in serum creatinine 1.5X baseline within last 7 days
  3. Urine output*
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3
Q

Prerenal AKI

A

decreased renal perfusion

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4
Q

Intrinsic renal AKI

A

acute tubular necrosis

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5
Q

Postrenal AKI

A

obstructive

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6
Q

Prerenal disease can be caused by

A 
True volume depletion
Hypotension (Shock, Aggressive HTN tx)
Edema
Selective renal ischemia (Bilateral renal artery stenosis)
Medications affecting GFR
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7
Q

Medications affecting GFR

A

NSAIDS

ACE-I

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8
Q

Intrinsic renal disease can be caused by

A

Renal ischemia: from any severe prerenal disease

Sepsis: hypotension→ release of cytokines and activation of neutrophils

Nephrotoxins

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9
Q

Risk of AKI from IV contrast

A

Pre-existing renal disease: rare in normal renal function

Volume depletion

Repeated doses of contrast

DM, CHF, age

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10
Q

Nephrotoxic drugs to avoid for 48 hours after IV contrast

A

NSAIDS

Metformin

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11
Q

Nephrotoxins that may cause AKI

A 
Rhabdomyolysis→ Heme pigments
Cisplatin
HIV meds
IVIG
Mannitol
IV contrast
Aminoglycosides
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12
Q

Causes of postrenal AKI

A

Bilateral obstruction:

Prostatic disease: hyperplasia or cancer

Metastatic cancer

Neurological disease: neurogenic bladder→ urinary retention

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13
Q

Obstructive BPH tx

A

foley catheter

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14
Q

Nonoliguric

A

> 400 mL/24 hours

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15
Q

Oliguric

A

<400 mL/24 hours

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16
Q

Anuric

A

<100 mL/24 hours

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17
Q

Make sure urine from a urinalysis

A

Is at room temperature within 2 hours of collection (or refrigerated then rewarmed)

Foley catheter: get sample “fresh” from tubing, not bag

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18
Q

Pathognomonic for acute tubular necrosis

A

muddy brown casts

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19
Q

Normal serum creatinine levels by gender

A

Male: .6-1.2 mg/dL
Female: .5-1.1 mg/dL

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20
Q

How is serum creatinine related to GFR?

A

Inverse relationship

ex: doubled serum creatine would represent a halved GFR

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21
Q

Prerenal fractional excretion of sodium (FENa)

A

<1%

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22
Q

Intrarenal fractional excretion of sodium (FENa)

A

> 2%

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23
Q

fractional excretion of sodium (FENa) is between 1-2%

A

could be either prerenal or intrarenal causes

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24
Q

when is fractional excretion of sodium (FENa) unreliable

A

diuretics

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25
Q

fractional excretion of sodium (FENa) calculation

A

(Urine Na/Serum Na)/ (Urine Cr/Serum CR) x 100%

26
Q

Would diagnose post-renal cause of AKI if seen on ultrasound

A

hydronephrosis

27
Q

Indication for renal biopsy

A

To provide more definitive diagnosis when there is no clear explanation of AKI:

Creatinine is markedly elevated/significantly worsens

May allow therapeutic intervention to prevent end stage renal disease

28
Q

Contraindications for renal biopsy

A

Bleeding diathesis
Pyelonephritis
Renal tumor
Solitary native kidney

29
Q

When is dialysis indicated for AKI?

A

Life-threatening complications

Volume imbalance, metabolic acidosis, hyperkalemia, hypocalcemia, hyperphosphatemia, uremia, AMS (severe AKI)

30
Q

Fluid challenge

A

if fluid causes an increase in urine, the cause of AKI is prerenal

31
Q

Signs/symptoms of volume depletion

A

History of fluid loss: N/V

Hypotension, tachycardia, oliguria

32
Q

How to do a fluid challenge

A

1-3 L of .9 NS

Reassess

33
Q

How might a patient become volume overloaded?

A

Initial presentation
~OR~
Fluid retention from IV therapy + decreased ability to secrete sodium and water

34
Q

Volume overload treatment

A

Diuretics

I+Os

35
Q

What can volume overload eventually cause?

A

Fluid retention→ pulmonary edema→ respiratory failure

36
Q

If diuretics don’t increase urine output in a volume overloaded patient

A

stop diuretics

start dialysis

37
Q

Causes of metabolic acidosis

A

Excretion of acid and regeneration of bicarb impaired + Low GFR

Diarrhea→ lost bicarb→ worsens

Sepsis, trauma, multi-organ failure (lactic/keto acids)

38
Q

For whom is dialysis the preferred treatment of metabolic acidosis?

A

Severe oligo-anuric AKI + volume overload + pH <7.1 (hemodynamically unstable)

39
Q

For whom is bicarbonate administration not preferred in cases of metabolic acidosis?

A

volume overload: causes large sodium load that can contribute to volume overload

40
Q

2 ways to manage metabolic acidosis

A

Dialysis

Bicarbonate administrations

41
Q

When can bicarb be given for metabolic acidosis?

A 
not volume overloaded and:
Diarrhea
pH <7.1 awaiting dialysis
Rhabdomyolysis 
→ prevent further renal injury by myoglobin
→ Falling out of favor
42
Q

Hyperkalemia presentation

A

Has very few symptoms, but is fatal

Impaired neuromuscular transmission and cardiac conduction abnormalities

43
Q

Hyperkalemia treatment

A

Medical therapy + dialysis

→ Remove excess and drive extracellular K+ into cells

44
Q

If a patient is asymptomatic, hypocalemic, and hyperphostphatemic

A

correct hyperphosphatemia

45
Q

Why do Hypocalcemia and Hyperphosphatemia occur in AKI?

A

Reduced GFR→ increased phosphorus → decreased calcium

Common

46
Q

When is the total serum concentration of ionized calcium inaccurate?

A

Low albumin

47
Q

Signs of hypocalcemia

A

paresthesia, tetany (carpopedal spasm)
confusion
seizures
trousseau’s sign (carpal spasm after occlusion of brachial artery)
chvostek’s sign (tap facial nerve→ contraction)
QT prolongation

48
Q

Treatment of symptomatic hypocalcemia and hyperphosphatemia

A

IV calcium

→ Severe hypocalcemia: given while awaiting dialysis regardless of risk of calcification

49
Q

IV Calcium side effects

A

If severely hyperphosphatemic, IV calcium → calcium phosphate crystal deposition in vasculature/organs

50
Q

Hyperphosphatemia >6 mg/dL treatment

A

dietary phosphate binders

51
Q

If a hyperphosphatemic patient cannot tolerate oral intake

A

dialysis

52
Q

Hyperphosphatemia >12 mg/dL treatment

A

dialysis
→ faster than binders
→ more effective in preventing injury to to crystal precipitation

53
Q

Dietary phosphate binders if the patient is also hypocalcemic

A

Calcium acetate

Calcium carbonate

54
Q

Dietary phosphate binders if the patient is not hypocalcemic

A

Aluminum hydroxide

Lanthanum carbonate

55
Q

Severe uremia treatment

A

dialysis

56
Q

Severe uremia symptoms

A

pericarditis
neuropathy
decline in mental status

57
Q

When is severe uremia more common?

A

CKD

58
Q

An episode of AKI

A

greater risk of CKD and ESRD

59
Q

predictor poor prognosis for short term and long term mortality

A

serum creatinine increases by .3 mg/dL

60
Q

If a patient gets AKI during their ICU stay

A

there is a 50% mortality rate

61
Q

How many patients:
Have AKI on admission?
Develop AKI during hospitalization?
Develop AKI in the ICU?

A

1%
25%
60%

Unit 3 Clin Med II (8 decks)

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