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Nephrology Board Review Pearls > ASN QBank Pearls - AKI, ICU Nephrology, HTN, and Pharmacology > Flashcards

ASN QBank Pearls - AKI, ICU Nephrology, HTN, and Pharmacology Flashcards

1
Q

what filtration fraction is associated with increased clotting on CVVH?

A

> 25-30%

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2
Q

how do you calculate filtration fraction for POSTfilter CVVH?

A

(QR + UF)/(QB x (1-Hct)) x 60 min/hr

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3
Q

how do you calculate filtration fraction for PREfilter CVVH?

A

(QR + UF)/((QB x (1-Hct)) x 60 min/hr) + QR

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4
Q

total body water (TBW)

A

weight x % body water

  • male 0.6, elderly male 0.5
  • female 0.5, elderly female 0.45
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5
Q

Na+ requirement formula

A

TBW x (desired Na+ - serum Na+)

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6
Q

infusion rate formula for hyponatremia

A

(Na+ requirement x 1000)/(infusate Na+ x time)

  • Na+ requirement = TBW x (desired Na+ - serum Na+)
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7
Q

Na+ concentration in 3% saline

A

513 meq/l

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8
Q

total water deficit formula

A

TBW x (1 - desired Na+/serum Na+)

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9
Q

electrolyte-free water clearance (EFWC) formula

A

urine volume × (1 − ((UNa+ + UK+)/SNa+))

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10
Q

free water clearance (FWC) formula

A

urine volume × (1 − (Uosm/Sosm)

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11
Q

indications for HD in lithium toxicity

A
  • > 5 withOUT CKD
  • > 4 WITH CKD
  • > 2 with neurologic or cardiac effects and AKI
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12
Q

clearance rate formula

A
  • equal to effluent rate

- (QR + UF) x 1 hr/60 min

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13
Q

fluid overload at time of dialysis initiation has been a/w increased risk of

A

mortality

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14
Q

have any RRT modalities shown that removal of myoglobin can shorten or prevent the course of AKI from rhabdomyolysis?

A

no

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15
Q
  • in a patient with acute brain injury, what dialysis modality should be avoided?
  • why?
  • how?
A
  • iHD
  • may worsen neurological status
  • compromises cerebral perfusion pressure d/t hypotension and disequilibrium
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16
Q
  • in a patient with acute brain injury, what dialysis modality should be used?
  • why?
A
  • CRRT

- slow removal of fluids and solutes decreases risk of worsening acute brain injury

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17
Q

what is the MC acid-base disturbance in the immediate postoperative period and is most prominent during the first 24-48 hours after surgery?

A

metabolic alkalosis

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18
Q

why is metabolic alkalosis the MC acid-base disturbance immediately post-op?

A

large citrate load from stored PRBC and FFP that’s metabolized to bicarbonate

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19
Q

what are the benefits of using bicarbonate as a buffer in the dialysate or replacement fluid of AKI patients with circulatory problems or liver dysfunction?

A
  • better correction of acidosis
  • lower lactate levels
  • improved hemodynamic tolerance
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20
Q

expected effect on systolic and diastolic BP after using CPAP

A

-3/-2 mmHg

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21
Q

what is the likelihood of identifying adrenal cancer or a hyperfunctioning lesion (pheochromocytoma, primary aldosteronism, Cushing’s) in the setting of discovering an adrenal “incidentaloma” mass?

A

10-20%

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22
Q

what is the BEST way to dose antibiotics for a patient on CRRT at 25 ml/kg/hr?

A

measure effluent UF and dialysate and calculate a CrCl

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23
Q

what is an independent risk factor for AKI in a patient undergoing surgery?

A

obesity

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24
Q

what is the most important risk factor for AKI in a patient undergoing surgery?

A

CKD

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25
Q

what is the “gold standard” test to diagnose white coat HTN?

A

ambulatory BP monitoring

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26
Q

ARB exposure during the second and third trimesters has been a/w

A

neonatal renal failure and death

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27
Q

can diuretics be continued during pregnancy?

A

yes, especially in women with sodium-sensitive HTN or edema and when they were already on them

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28
Q

treatment of resistant HTN

A
  • lifestyle modifications
  • w/d of interfering meds
  • correction of secondary HTN causes
  • MR antagonists (spironolactone, amiloride, eplerenone)
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29
Q

a trial published in 2008 demonstrated that antihypertensive therapy in patients > 80 yoa is a/w

A
  • decrease in stroke

- decrease in cardiovascular mortality

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30
Q

older patients with HTN are more likely to be salt-sensitive and responsive to what therapy?

A

diuretics

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31
Q

in pregnant women with DM what is associated with a high incidence of fetal malformations?

A

poor glycemic control in the first trimester

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32
Q

patients with AKI in the setting of decompensated liver disease may have HRS, but what must be ruled out first and how?

A
  • intravascular volume depletion

- evaluating clinical response to IVF

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33
Q
  • increased hemodynamic instability
  • worsening respiratory failure with increased airway pressures and increasing difficulty with oxygenation
  • tense abdomen on exam
  • oliguric kidney failure
A

abdominal compartment syndrome

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34
Q

diagnosis of intra-abdominal hypertension and abdominal compartment syndrome is accomplished by

A

transduction of bladder pressure

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35
Q

intervention a/w greatest reduction in the risk for contrast-induced nephropathy

A

isotonic crystalloids prior to and following iv contrast

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36
Q

acyclovir, methotrexate, ethylene glycol toxicity and TLS can all present with

A

crystalluria

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37
Q

needle shaped crystals

A

acyclovir crystals

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38
Q

amorphous brown-colored precipitates in urine

A

methotrexate

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39
Q

dumbbell and needle-shaped calcium oxalate monohydrate crystals, and envelope-shaped calcium oxalate dihydrate crystals

A

ethylene glycol toxicity

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40
Q

what is the probability that AKI is d/t AIN when urinary eosinophils are present?

A

30%

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41
Q

single most probable cause of secondary HTN is

A

fibromuscular dysplasia

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42
Q

fibromuscular dysplasia is most likely to be identified on

A

CT angiography

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43
Q

localized kidney ischemia and/or infarction from dissection/contusion of the kidney following trauma

A

Page kidney

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44
Q

pathophysiology of Page kidney

A

perinephric hematoma compressing renal parenchyma, causing renal ischemia and RAAS activation

45
Q

treatment of Page kidney

A

RAAS blockade

46
Q

most patients, 52%, with longstanding atherosclerotic renovascular disease have “stabilization” of creatinine; what is the most probable outcome of renal revascularization?

A

GFR remains unchanged

47
Q

MOST useful data regarding the salvageability of renal function with renal revascularization

A

LOW resistive indices

48
Q

what is the MOST helpful procedure post revascularization during annual f/u renovascular disease?

A

renal artery duplex US

49
Q

how do NSAIDs cause hyperkalemia?

A
  • inhibit PGs –> reduces renin –> inhibits RAAS pathway –> hypoaldosterone state –> hyperkalemia
50
Q

how do NSAIDs cause hyponatremia?

A
  • reduces PGE2 –> increased ADH effect –> increased H2O reabsorption
  • counteract effect of diuretics by reducing RBF –> increased proximal urine Na+ reabsorption –> and increased urine concentrating ability
51
Q

drug toxicity

- protease inhibitors

A

nephrolithiasis

52
Q

drug toxicity

- nucleoside reverse transcriptase inhibitors (eg, stavudine, didanosine)

A
  • lactic acidosis

- hepatic steatosis

53
Q

drug toxicity

- nucleotide reverse transcriptase inhibitors (eg, tenofovir)

A
  • ATN

- Fanconi syndrome

54
Q

drug toxicity

- interferon

A

nephrotic syndrome

55
Q

best stain for calcium phosphate crystals

A

von Kossa stain

56
Q

chronic lithium use can lead to which renal syndrome?

A
  • nephrogenic DI
  • distal, type 1, RTA
  • CKD
  • MCD
  • FSGS
57
Q

lithium nephrotoxicity may be prevented by use of

A

amiloride

58
Q

a known, serious complication of stem cell transplantation

A

hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome

59
Q

hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome clinical presentation

A
  • similar to HRS
  • AKI
  • low BP
  • sodium retentive state
60
Q

pathophysiology of hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome

A

sinusoidal obstruction –> portal HTN –> microvascular intrahepatic portosystemic shunting

61
Q

what is the mechanism of proteinuria following bevacizumab therapy?

A

loss of vascular endothelial growth factor (VEGF)

62
Q
  • HL
  • massive kidneys on CT scan
  • AKI
A

lymphomatous infiltration of kidneys

63
Q

what is the MOST effective therapy to lower methotrexate levels in a patient with AKI?

A

glucarbidase

64
Q
  • bone marrow suppression
  • stomatitis (painful swelling and sores inside the mouth)
  • AKI
A

methotrexate toxicity

65
Q

can dialysis remove methotrexate?

A

need high flux HD for 8-12 hours (otherwise, rebound)

66
Q

MOST effective oral treatment to remove sustained release lithium from GI tract

A

polyethylene glycol (PEG)

67
Q
  • AKI
  • severe HTN
  • GI bleeding
  • following invasive vascular procedure
A

cholesterol embolization (AED)

68
Q
  • acute myelomonocytic leukemia (AMML); tissue invasive leukemia
  • large kidneys on US
  • AKI
A

leukemic infiltration of renal interstitium

69
Q
  • HTN
  • AKI
  • proteinuria
  • MAB against VEGF
  • decreased NO
  • increased endothelin
A

bevacizumab

70
Q

enters proximal tubular cells via APICAL membrane megalin receptor pathway

A

genatmicin

71
Q

enters cells via BASOlateral organic ANion transporter pathway

A

tenofovir

72
Q

enter proximal tubular cells via BASOlateral organic CATion transporter pathway

A
  • cimetidine
  • ifosfamide
  • trimethoprim
  • “CIT CAT”
73
Q

tenofovir causes proximal tubular injury, AKI and Fanconi syndrome, through what mechanism?

A

mitochondrial dysfunction

74
Q

drug that can cause AKI, Fanconi syndrome, and nephrogenic DI?

A

tenofovir

75
Q

what medication is most likely to cause nephrolithiasis?

A

atazanavir

76
Q

what urine pH is atazanavir most soluble in?

A

< 4.5

77
Q

MCC of AKI in ecstasy (MDMA) ingestion

A

nontraumatic rhabdomyolysis

78
Q

AKI in setting of;

  • overdosing of abx
  • alkaline urine
  • underlying kidney injury
  • old age
A

ciprofloxacin-associated crystalline nephropathy

79
Q

fluid management strategy a/w increased risk of AKI in critically ill septic patient

A

hydroxyethyl starch (HES)

80
Q

MOST common adverse effect of rasburicase therapy

A

hemolytic reaction in patients who have underlying G6PD deficiency

81
Q

ethylene glycol metabolites

A

glycolic acid, glyoxalate, and oxalic acid

82
Q

dose adjustment for rasburicase in renal and/or liver failure

A

none needed

83
Q

rasburicase metabolism

A

peptide hydrolysis

84
Q

which IV vasopressor can raise serum K+ concentration and potentially worsen hyperkalemia?

A

phenylephrine

85
Q

how can phenylephrine cause hyperkalemia?

A

nonselective α-agonist that blocks cellular uptake of K+

86
Q

which vasopressors can cause hypokalemia?

A

epinephrine and norepinephrine

87
Q

how can epinephrine and norepinephrine cause hypokalemia?

A

β2 agonism increases cellular uptake of K+

88
Q

why is CRRT the best option for a patient awaiting liver transplant?

A

slow removal of solutes –> decreased risk of osmotic disequilibrium and increase in ICP

89
Q

MOST likely mechanism of HTN and proteinuria in preeclampsia

A

decreased VEGF (vascular endothelial growth factor)

90
Q

what effect does tight glucose control with insulin therapy in critically ill patients with sepsis in the ICU have?

A

increased risk of hypoglycemia

91
Q
  • LOW PRA
  • high renin level
  • low AG2
  • low PAC
A

aliskiren (renin inhibitor)

92
Q
  • HIGH PRA
  • high renin level
  • LOW AG2
  • low PAC
A

ACEI

93
Q
  • HIGH PRA
  • high renin level
  • HIGH AG2
  • low PAC
A

ARB

94
Q
  • HIGH PRA
  • HIGH renin level
  • HIGH AG2
  • HIGH PAC
  • antagonize MR
A

spironolactone (aldosterone antagonist)

95
Q

what type of replacement fluid for CVVH is a/w higher solute clearance?

A

POSTfilter

96
Q

what is the most effective way to increase urea clearance in a patient on CVVH with a QB of 150 ml/min?

A

increase QB

97
Q

first step in evaluation and management in a patient with a differential diagnosis of prerenal azotemia secondary to volume depletion, HRS, or ATN

A

adequate volume repletion with IV isotonic crystalloid

98
Q
  • AKI
  • anemia
  • hypercalcemia
  • low AG
  • discrepancy between urine dipstick (trace protein) and UPC
A

MM with light chain cast nephropathy

99
Q

amyloidosis can also be associated with presence of paraprotein, like MM, but on urine studies what is different?

A

significant albuminuria and NO discrepancy between protein by urine dipstick and UPC

100
Q
  • decompensated cirrhosis
  • progressively worsening renal function
  • low BP
  • low urine Na+
A

HRS

101
Q

pathophysiology of AKI in setting of heart failure

A
  • venous congestion –> activates sympathetic and RAA systems –> intrarenal vasoconstriction
  • increased intraabdominal pressure
102
Q

best initial treatment to reduce risk of intratubular cast formation and AKI in rhabdomyolysis

A

rapid infusion of IV 0.9% saline

103
Q

antibiotics, plasmapheresis, antimotility agents, and antiplatelet agents are not recommended in what condition?

A

diarrhea-associated HUS

104
Q

home BP measurements have been established to lead to

A

improved medication adherence

105
Q

patients with renovascular disease treated with what have reduced morbidity and mortality as compared with treatment with other agents?

A

RAAS blockade

106
Q

treatment in a patient with renovascular HTN with a solitary functioning kidney

A

endovascular stent placement of renal artery for functioning kidney

107
Q

elevated renin levels represent a loss of perfusion pressure to the juxtaglomerular apparatus, not a

A

decrease in oxygen levels

108
Q

best treatment for a pregnant patient with increase in BP 2/2 FMD

A

renal angiography and percutaneous transluminal renal angioplasty (PTRA)

Nephrology Board Review Pearls (10 decks)

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