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X Clin Med II Exam 3 > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What does acute renal failure imply about severe AKI?

A

The need for dialysis

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2
Q

What is acute kidney injury?

A

Abrupt loss of kidney function resulting in retention of urea and other nitrogenous waste products and the dysregulation of vol status and electrolytes

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3
Q

Why can’t you use serum creatinine to diagnose AKI?

A

In early stages, creatinine may be low even though GFR is reduced (b/c it hasn’t accumulated yet)
Creatinine is removed by dialysis

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4
Q

KDIGO diagnostic criteria of AKi

A

Increase in serum creatinine by >.3 within 48 hrs
Increase in serum creatinine to >1.5 times baseline (within last 7 days)
Urine volume

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5
Q

Most common cause of AKI in the hospital

A

From prerenal disease or acute tubular necrosis (intrinsic)

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6
Q

Etiologies of AKI

A 
Prerenal (decreased perfusion)
Intrinsic renal (vessels, glomeruli, tubules)
Postrenal (obstructive)
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7
Q

Causes of prerenal AKI

A

True volume depletion
Hypotension (shock of aggressive tx of HTN)
Edematous states (HF, cirrhosis)
Selective renal ischemia (bilateral renal artery stenosis)
Drugs affecting GFR (NSAIDs, Ace-I)

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8
Q

What can cause intrinsic renal disease (like acute tubular necrosis)?

A 
Renal ischemia (from causes of severe prerenal)
Sepsis
Nephrotoxins (IV contrast, aminoglycosides, rhabdo, cisplatin etc)
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9
Q

What does IV contrast cause?

A

Renal tubular epithelial cell toxicity and renal medullary ischemia from vasoconstriction (usually reversible)

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10
Q

Risk factors of acute tubular necrosis from contrast?

A 
Preexisting renal disease
Vol depletion
Repeated doses of contrast
Comorbidities: diabetes, HF
Age
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11
Q

How to prevent ATN by IV contrast?

A 
Hydration (PO or IV)
Low-osmolal agents at low doses
Avoid repetitive doses
Avoid nephrotoxic drugs for 48 hrs after
(not recommend sodium bicard, NAC or renal replacement)
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12
Q

Most common cause of post renal AKI

A 
Prostatic disease (hyperplasia/cancer) or metastatic cancer
(might see neurological disease causing neurogenic bladder and urinary retention)
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13
Q

Description of post renal AKI

A

Reduction in GFR in pts without intrinsic renal disease that requires bilateral obstruction (or one if only one kidney)

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14
Q

How to classify urine output

A

Nonoliguric (>400ml/25 hrs) so normal
Oliguric (<400ml)
Anuric (<100)

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15
Q

Diagnostic tools for AKI

A

Urinalysis (also serum metabolic panel)
Renal US
Renal biopsy

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16
Q

What is pathognomic for ATN on urinalysis?

A

Muddy brown casts

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17
Q

Normal range of serum creatinine

A

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

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18
Q

General rule of thumb for creatinine and GFR

A

Creatinine 2xnormal means 1/2 normal GFR

Creatinine 3xnormal means 1/3 normal GFR

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19
Q

What is the fractional excretion of sodium?

A

Percent of filtered sodium that is excreted in the urine (can help distinguish prerenal from intrinsic in oliguric pt)

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20
Q

How to calculate FENa

A

(urine Na/serum Na)/(urine Cr/serum Cr) x 100

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21
Q

Values of FENa to distinguish

A

<1% is prerenal (reabsorption of almost all filtered soium represents appropriate response to decreased perfusion)
>2% suggests intrarenal
in between ay be either

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22
Q

Downside of FENa

A

Unreliable when on diuretics

Only useful in acute renal failure (not chronic)

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23
Q

Major reason for using renal imaging in AKI

A

Assess for urinary tract obstruction (so postrenal)-use renal US mostly

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24
Q

Sign of obstruction on renal US

A

Hydronephrosis (dilation of pelvis and calyces)

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25
Q

How to relieve urinary tract obstructions

A

BPH- place foley cath
Kidney stone- remove it
Mass- remove the mass

26
Q

When do you perform a kidney biopsy?

A

When creatinine is markedly elevated or it significantly worsens over course of a couple days

27
Q

What does a kidney biopsy do?

A

Provide more definitve tissue diagnosis and may allow a therapeutic intervention to prevent ESRD

28
Q

Contraindications of renal biopsy

A

Bleeding diathesis
Pyelonephritis
Renal tumor
Solitary native kidney

29
Q

Life threatening complications associated with AKI

A 
Volume imbalance
Metabolic acidosis (<7.4)
Hyperkalemia (>5.5)
Hypocalcemia
Hyperphosphatemia
Uremia
May also see altered mental status
30
Q

What must you do when the life threatening complications arise in AKI?

A

Hemodialysis (renal replacement therapy)

31
Q

What must be done when dialysis can’t be immediately provided>

A

Med management

32
Q

What must be performed in all pts with AKI?

A

Assessment of volume status (can be depletion of overload-correction might even reverse it)

33
Q

What to do when pt presents as volume depleted?

A

Administer IV fluids
Fluid challenge to ID prerenal failure
Crystalloid isotonic fluids preferred

34
Q

Whats good starting amount of fluid for volume depletion?

A

1-3 liters with repeated assessment (want to restore urine flow and improve function)

35
Q

What if pt doesn’t respond to the fluids?

A

They are unlikely to have prerenal disease and are more likely to have ATN or other intrinsic AKI

36
Q

What can fluid retention from vol overload or over IV fluid therapy with decreased excretion lead to?

A

Pulmonary edema and respiratory failure

37
Q

Diuretics in AKI

A

Temporizing measure
Dialysis offer the most efficient vol removal
If UOP doesnt increase after diuretics then they should be stopped)

38
Q

Why does metabolic acidosis happen in AKI?

A

Excretion of acid and regeneration of bicarb is impaired with low GFR (daily metabolism creates some acid but causes like sepsis, trauma etc can cause increased amounts of acid)

39
Q

What can worsen metabolic acidosis?

A

Diarrhea b/c causes net loss of bicarb

40
Q

Tx for metabolic acidosis

A

Dialysis or bicarb administration

*choice depends on absence or presence of vol overload and underlying cause and severity

41
Q

When to dialyze in metabolic acidosis?

A

Pts with severe oligo-anuric AKI who are volume overloaded and pH<7.1 (can lead to hemodynamic instability)

42
Q

Why dialysis preferred to bicarb administation in volume overloaded pt

A

B/c bicard cant result in large sodium overload that may cause or contribute to vol overload

43
Q

When to administer bicarb to AKI pt who has no indications for acute dialysis

A

IF acidosis related to diarrhea
pH,7.1 and awaiting dialysis
AKI due to rhabdo to prevent further renal injury

44
Q

Sxs of hyperkalemia

A

Very few sxs until die!!

45
Q

What can hyperkalemia cause?

A

Impaired neuromuscular transmission and cardiac conduction abnormalities (arrhythmias)

46
Q

Tx for hyperkalemia

A

Meds and dialysis-try to antagonize membrane effects of K by driving extracellular K into cells and removing excess

47
Q

Hypocalcemia in AKI

A

Common and is primarily related to increases in serum phosphorus levels caused by reduced GFR

48
Q

What to do when pt is asymptomatic and hyperphosphatemia is present

A

Correct it

49
Q

Tx of hypocalcemic symptomatic pts

A

IV calcium

50
Q

What happens when you administer Ca to pts who are severly hyperphosphatemic?

A

May result in deposition of Ca phosphate stones into vasculature and organs—need dialysis!

51
Q

Signs that indicated IV calcium is needed

A

Paresthesias, tetancy, confusion, seizures, Trousseau’s sign, Chvostek’s sign or QT prolongation

52
Q

Tx for pts with phosphate levels >6

A

Dietary phosphate binders (depends on level of serum ionized calcium concentration)

53
Q

What phosphate binder is used if serum Ca conc is low?

A

Calcium acetate or calcium carbonate

54
Q

What phosphate binder is used if serum Ca conc is high?

A

Aluminum hydroxide or lathanum carbonate (non calcium containing)

55
Q

What is the general level at which to dialyze pts with hyperphosphatemia?

A

> 12 (b/c it works faster than phosphate binders and may be more effective in preventing the injury due to precipitation)

56
Q

What kind of pt gets dialysis?

A

When cannot tolerate oral intake (hyperphosphatemia)

57
Q

When is uremia more common?

A

In CKD

58
Q

Dialysis and uremic syndrome

A

When severe uremia: pericarditis, neuropathy, unexplained decline in mental status

59
Q

What is uremia?

A

Associated with fluid, electrolyte, hormone imbalances and metabolic abnormalities that develop with decline in renal function

60
Q

Prognosis of AKI

A

Depends on cause and presence of pre-existing renal disease (will still have probs after)
Most pts recover renal function and UOP and creatinine normalize)

61
Q

Mortality rate for ICU pts with AKI is…

A

Higher

62
Q

What happens with pts that recover from AKi?

A

At greater risk to develop CKD and even ESRD (some even still have renal dysfunction)

X Clin Med II Exam 3 (6 decks)

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