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AKI Flashcards

1
Q

diagnostic criteria for AKI

A

Increase in SCr by >/= 0.3

increase in Scr to >/= 1.5 x baseline

urine volume <0.5 mL/kg/hr for 6 hours

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2
Q

what is an AKI

A

abrupt decline (<7 daysZ) in renal function
characterized by inability to excrete metabolic waste, maintain acid-base balance

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3
Q

nonoliguria

A

> 400 ml/day

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4
Q

oliguria

A

50-440 ml/day

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5
Q

anuria

A

<50 ml/day

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6
Q

measurements for AKI diagnosis

A

urine output
SCr (lag time 24-48 hrs behind)

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7
Q

4 classifications of AKI

A

prerenal azotemia
functional acute renal failure
acute intrinsic renal failure
post renal obstruction

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8
Q

what is prerenal azotemia

A

resulting from decreased renal perfusion

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9
Q

what is functional acute renal failure

A

decline in glomerular ultrafiltration production

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10
Q

what is acute intrinsic renal failure

A

structural damage to the kidney

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11
Q

what is post renal obstruction

A

obstruction of urine flow from the kidney

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12
Q

when is urine sodium concentration helpful?

A

to identify acute tubular necrosis from a pre-renal cause (effective volume depletion)
FENa< 1% is pre-renal cause
FENa >2% is acute tubular necrosis

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13
Q

how is FENa calculated

A

% FENa = (UNa x PCr)/(PNa x UCr) x 100

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14
Q

what causes pre-renal azotemia

A

decreased renal perfusion, hypotension
decreased blood volume
renal vessel occlusion
volume depletion

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15
Q

lab indicators of pre-renal azotemia

A

FENa< 1%
urine sodium < 20
urine osmolality > 500

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16
Q

what is the clinical presentation of pre-renal azotemia?

A

AKI hypotension present: causes decline in intravascular volume– hemorrhage, dehydration, decline in effective blood volume
can also be without hypotension

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17
Q

what causes functional acute renal failure

A

a decline in glomerular ultrafiltrate production WITHOUT DAMAGE TO THE KIDNEY. secondary to a reduced glomerular hydrostatic pressure— from changes in glomerular arteriolar circumference (vasoconstriction or vasodilation).

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18
Q

what are things that may cause vasoconstriction or vasodilation causing functional acute renal failure

A

vasoconstriction: hypocalcemia, cyclosporine, NSAIDs,, hepatorenal syndrome
vasodilation: ACEi/ARBs

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19
Q

what may be some causes of intrinsic renal failure

A

remember this is from DAMAGE to the kidney: may be from
-acute tubular necrosis (toxin exposure- contrast dye)
-ischemia (hypotension, pressors)
-Acute interstitial nephritis
-tubular damage
-small vessel disease

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20
Q

what is the clinical presentation of intrinsic AKI?

A

urine osmolality <250
urine sodium >20
FENa>1%

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21
Q

what are the medications causing intrinsic renal failure

A

antibiotics
anticonvulsants
loop diuretics
NSAIDs

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22
Q

structural areas of the kidney for potential damage in intrinsic renal failure

A

vasculature (small blood vessels)
glomeruli
renal tubules
interstitium

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23
Q

what is VASCULAR intrinsic renal failure

A

occlusion of a part of the vasculature that supplies the kidney with oxygenated blood.
can be caused by thrombotic emboli

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24
Q

what is acute tubular necrosis

A

death of tubular cells that form the tubule that transports urine to the ureters
causes muddy brown casts in the urine

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25
Q

FENa in ATN

A

usually >3%

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26
Q

what is GLOMERULUS intrinsic renal failure

A

inflammation of the glomeruli (caused by lupus, poststreptococcal infection, hepatitis C, etc) which is the 3rd most common cause of renal disease behind diabetes & HTN

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27
Q

difference between toxic ATN and ischemic ATN

A

toxic: characterized by proximal tubular epithelium necrosis due to a toxic substance (caused by meds like aminoglycosides, amphotericin B, cisplatin, contrast)

ischemic: caused when kidneys are not sufficiently perfused for a long period of time, or during shock

28
Q

what is INTERSTITIUM intrinsic renal failure

A

interstitium provides the structural support, environment to establish concentration gradients
caused by infection in the kidneys (pyelonephritis) or medication reaction (PCN, Ceph, NSAIDs)

29
Q

______ must involve both kidneys for injury

A

post renal obstruction
(remember this is obstruction of urine flow from the kidney)

30
Q

causes of post renal obstruction

A

bladder outlet obstruction (prostate hypertrophy)
crystal deposits in the tubules (uric acid, methotrexate, acyclovir)
urethral obstruction

31
Q

commonly implicated agents in drug induced AKI

A

antimicrobials (aminoglycosides, acyclovir, amphotericin)
chemo (cisplatin, cyclophosphamide)
calcineurin inhibitors (cyclosporine, tacrolimus)
NSAIDs
IV contrast

32
Q

what are some possible MECHANISMS for drug induced AKI

A

direct renal toxicity (aminoglycosides, cisplatin, amphotericin)
crystallization/obstruction (acyclovir, ganciclovir, methotrexate)
reduction in glomerular blood flow (NSAID, ACEi, ARB)

33
Q

what to do if a nephrotoxic drug is needed?

A

utilize renal-protective therapies
ensure patient is not dehydrated prior to nephrotoxic medication administration

34
Q

what is the diagnosis when there are muddy brown casts

A

ATN

35
Q

what is the diagnosis when urinalysis shows + hemoglobin without RBC

A

rhabdomyolysis

36
Q

what is the diagnosis when urinalysis shows WBCs, bacteria, nitrates; and microscope findings are WBC casts

A

pyelonephritis

37
Q

what is the diagnosis when urinalysis shows WBCs and no bacteria, proteinuria, hematuria

A

Acute interstitial nephritis

38
Q

what is the diagnosis when urinalysis shows hematuria, proteinuria. microscope shows RBC casts, dysmorphic RBC

A

glomerulonephritis

39
Q

possible treatments for AKI

A

remove the offending agent/correct underlying cause
avoid nephrotoxic agent
fluid bolus if prerenal cause
possibly diuretics
dialysis (AEIOU)
don’t recommend dopamine receptor agonists

40
Q

what are some alternative drugs to the commonly nephrotoxic drugs

A

lipid based ampho b vs conventional
extended interval aminoglycoside dosing vs traditional
low osmolality contrast medium vs higher osmolality dyes
acetaminophen vs nsaids

41
Q

how to treat if prerenal cause (FENa<1%)

A

fluid bolus of a crytalloid; rapid fluid resuscitation can improve renal perfusion and rescue hypoxic tubules

42
Q

______ test is helpful to see if fluid resuscitation is beneficial

A

furosemide

43
Q

who to trial furosemide test?

A

patients thought to be fully resuscitated
persistent oliguria (50-440)
clinicians unsure what would help

44
Q

what if outcome of furosemide test is urine output >200 mL in 2 hours?

A

pre-renal oliguria: replace output with IV crystalloid; attempt hemodynamic strategy to improve urine output

45
Q

what if outcome of furosemide test is urine output <200 mL in 2 hours?

A

intrinsic kidney failure; more fluid, pressors, or inotropes are unlikely to help.

46
Q

t/f: diuretics speed up recovery and improve prognosis

A

false

47
Q

when are diuretics useful

A

fluid management (pulmonary edema, reduce need for dialysis, increase K elimination)

48
Q

diuretic strategies

A

furosemide 80 mg IV x 1: if no increase in urine output, can double.
can also try continuous infusion of loops instead of intermittent.
can also try synergy with thiazide + loop (thiazides aren’t useful as monotherapy)
mannitol: use caution, hyperosmolar result

49
Q

____ are paired for additive effect with loop diuretics but are not useful as monotherapy in AKI

A

thiazide diuretics

50
Q

dopamine and fenoldopam for AKI

A

don’t recommend

51
Q

indications for dialysis

A

AEIOU
Acid base
Electrolyte imbalance
Intoxication
Overload (of fluid)
Uremia

52
Q

major disadvantage of hemodialysis

A

hypotension
(not tolerated in the hemodynamically unstable)

53
Q

advantages/disadvantages of CRRT

A

advantage: continuous removal, better tolerated
disadvantage: nursing time, DOSING SUCKS

54
Q

AKI results in _____ clearance of renally eliminated drugs

A

decreased

55
Q

with iHD, when to administer drugs?

A

after session

56
Q

3 common causes of AKI in the ICU

A

sepsis
rhabdomyolysis
drug induced

57
Q

why does sepsis cause AKI

A

hypotension: causes decreased renal perfusion

58
Q

treating sepsis/AKI

A

immediate administration of antibiotics is necessary; renal dose adjustments must be made

59
Q

rhabdomyolysis is characterized by

A

leakage of muscle-cell contents (electrolytes, myoglobin) into the circulation.
patient will present with pigmented granular casts, reddish-brown urine supernatant, rased CPK >20,000

60
Q

what are common causes of rhabdomyolysis in ICU

A

trauma (crush)
muscle hypoxia (person found down, limb compression during prolonged loss of consciousness)
drugs/toxins (statins, fibrates, alcohol, heroin, cocaine, daptomycin)
infections (viral, bacterial)

61
Q

why is there AKI in rhabdomyolysis

A

myoglobin is released from muscle
iron released from myoglobin generates ROS which damages the kidney
AND blood flow is decreased to the kidney

62
Q

treating rhabdomyolysis/AKI

A

if a drug is involved, d/c it.
adequate fluid hydration starting with 1-2 L of fluid/hr and goal urine output is 200-300 mL/hr
raise urine pH>6.5 (urine alkalinization prevents heme-protein precipitation) with sodium bicarbonate
maybe dialysis

63
Q

what are some preventative strategies prior to nephrotoxins???

A

hydration of sodium loading
0.9% NaCl most effective
1-2 mL/kg/hr starting 4 hours before nephrotoxin
goal urine output is at least 0.5 mL/kg/hr

64
Q

who gets prophylaxis for contrast dye

A

patients with high risk: AKI, GFR<30 and not on dialysis

65
Q

what is prophylaxis regimen for contrast induced nephropathy

A

0.9% NS 1 mL/kg/hr for 6-12 hrs PREPROCEDURAL
1 mL/kg/hr during and 6-12 hrs POSTPROCEDURAL

advanced nephrology (7 decks)

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