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

(108 cards)

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
what is the “gold standard” test to diagnose white coat HTN?
ambulatory BP monitoring
26
ARB exposure during the second and third trimesters has been a/w
neonatal renal failure and death
27
can diuretics be continued during pregnancy?
yes, especially in women with sodium-sensitive HTN or edema and when they were already on them
28
treatment of resistant HTN
- lifestyle modifications - w/d of interfering meds - correction of secondary HTN causes - MR antagonists (spironolactone, amiloride, eplerenone)
29
a trial published in 2008 demonstrated that antihypertensive therapy in patients > 80 yoa is a/w
- decrease in stroke | - decrease in cardiovascular mortality
30
older patients with HTN are more likely to be salt-sensitive and responsive to what therapy?
diuretics
31
in pregnant women with DM what is associated with a high incidence of fetal malformations?
poor glycemic control in the first trimester
32
patients with AKI in the setting of decompensated liver disease may have HRS, but what must be ruled out first and how?
- intravascular volume depletion | - evaluating clinical response to IVF
33
- increased hemodynamic instability - worsening respiratory failure with increased airway pressures and increasing difficulty with oxygenation - tense abdomen on exam - oliguric kidney failure
abdominal compartment syndrome
34
diagnosis of intra-abdominal hypertension and abdominal compartment syndrome is accomplished by
transduction of bladder pressure
35
intervention a/w greatest reduction in the risk for contrast-induced nephropathy
isotonic crystalloids prior to and following iv contrast
36
acyclovir, methotrexate, ethylene glycol toxicity and TLS can all present with
crystalluria
37
needle shaped crystals
acyclovir crystals
38
amorphous brown-colored precipitates in urine
methotrexate
39
dumbbell and needle-shaped calcium oxalate monohydrate crystals, and envelope-shaped calcium oxalate dihydrate crystals
ethylene glycol toxicity
40
what is the probability that AKI is d/t AIN when urinary eosinophils are present?
30%
41
single most probable cause of secondary HTN is
fibromuscular dysplasia
42
fibromuscular dysplasia is most likely to be identified on
CT angiography
43
localized kidney ischemia and/or infarction from dissection/contusion of the kidney following trauma
Page kidney
44
pathophysiology of Page kidney
perinephric hematoma compressing renal parenchyma, causing renal ischemia and RAAS activation
45
treatment of Page kidney
RAAS blockade
46
most patients, 52%, with longstanding atherosclerotic renovascular disease have “stabilization” of creatinine; what is the most probable outcome of renal revascularization?
GFR remains unchanged
47
MOST useful data regarding the salvageability of renal function with renal revascularization
LOW resistive indices
48
what is the MOST helpful procedure post revascularization during annual f/u renovascular disease?
renal artery duplex US
49
how do NSAIDs cause hyperkalemia?
- inhibit PGs --> reduces renin --> inhibits RAAS pathway --> hypoaldosterone state --> hyperkalemia
50
how do NSAIDs cause hyponatremia?
- 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
drug toxicity | - protease inhibitors
nephrolithiasis
52
drug toxicity | - nucleoside reverse transcriptase inhibitors (eg, stavudine, didanosine)
- lactic acidosis | - hepatic steatosis
53
drug toxicity | - nucleotide reverse transcriptase inhibitors (eg, tenofovir)
- ATN | - Fanconi syndrome
54
drug toxicity | - interferon
nephrotic syndrome
55
best stain for calcium phosphate crystals
von Kossa stain
56
chronic lithium use can lead to which renal syndrome?
- nephrogenic DI - distal, type 1, RTA - CKD - MCD - FSGS
57
lithium nephrotoxicity may be prevented by use of
amiloride
58
a known, serious complication of stem cell transplantation
hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome
59
hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome clinical presentation
- similar to HRS - AKI - low BP - sodium retentive state
60
pathophysiology of hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syndrome
sinusoidal obstruction --> portal HTN --> microvascular intrahepatic portosystemic shunting
61
what is the mechanism of proteinuria following bevacizumab therapy?
loss of vascular endothelial growth factor (VEGF)
62
- HL - massive kidneys on CT scan - AKI
lymphomatous infiltration of kidneys
63
what is the MOST effective therapy to lower methotrexate levels in a patient with AKI?
glucarbidase
64
- bone marrow suppression - stomatitis (painful swelling and sores inside the mouth) - AKI
methotrexate toxicity
65
can dialysis remove methotrexate?
need high flux HD for 8-12 hours (otherwise, rebound)
66
MOST effective oral treatment to remove sustained release lithium from GI tract
polyethylene glycol (PEG)
67
- AKI - severe HTN - GI bleeding - following invasive vascular procedure
cholesterol embolization (AED)
68
- acute myelomonocytic leukemia (AMML); tissue invasive leukemia - large kidneys on US - AKI
leukemic infiltration of renal interstitium
69
- HTN - AKI - proteinuria - MAB against VEGF - decreased NO - increased endothelin
bevacizumab
70
enters proximal tubular cells via APICAL membrane megalin receptor pathway
genatmicin
71
enters cells via BASOlateral organic ANion transporter pathway
tenofovir
72
enter proximal tubular cells via BASOlateral organic CATion transporter pathway
- cimetidine - ifosfamide - trimethoprim - "CIT CAT"
73
tenofovir causes proximal tubular injury, AKI and Fanconi syndrome, through what mechanism?
mitochondrial dysfunction
74
drug that can cause AKI, Fanconi syndrome, and nephrogenic DI?
tenofovir
75
what medication is most likely to cause nephrolithiasis?
atazanavir
76
what urine pH is atazanavir most soluble in?
< 4.5
77
MCC of AKI in ecstasy (MDMA) ingestion
nontraumatic rhabdomyolysis
78
AKI in setting of; - overdosing of abx - alkaline urine - underlying kidney injury - old age
ciprofloxacin-associated crystalline nephropathy
79
fluid management strategy a/w increased risk of AKI in critically ill septic patient
hydroxyethyl starch (HES)
80
MOST common adverse effect of rasburicase therapy
hemolytic reaction in patients who have underlying G6PD deficiency
81
ethylene glycol metabolites
glycolic acid, glyoxalate, and oxalic acid
82
dose adjustment for rasburicase in renal and/or liver failure
none needed
83
rasburicase metabolism
peptide hydrolysis
84
which IV vasopressor can raise serum K+ concentration and potentially worsen hyperkalemia?
phenylephrine
85
how can phenylephrine cause hyperkalemia?
nonselective α-agonist that blocks cellular uptake of K+
86
which vasopressors can cause hypokalemia?
epinephrine and norepinephrine
87
how can epinephrine and norepinephrine cause hypokalemia?
β2 agonism increases cellular uptake of K+
88
why is CRRT the best option for a patient awaiting liver transplant?
slow removal of solutes --> decreased risk of osmotic disequilibrium and increase in ICP
89
MOST likely mechanism of HTN and proteinuria in preeclampsia
decreased VEGF (vascular endothelial growth factor)
90
what effect does tight glucose control with insulin therapy in critically ill patients with sepsis in the ICU have?
increased risk of hypoglycemia
91
- LOW PRA - high renin level - low AG2 - low PAC
aliskiren (renin inhibitor)
92
- HIGH PRA - high renin level - LOW AG2 - low PAC
ACEI
93
- HIGH PRA - high renin level - HIGH AG2 - low PAC
ARB
94
- HIGH PRA - HIGH renin level - HIGH AG2 - HIGH PAC - antagonize MR
spironolactone (aldosterone antagonist)
95
what type of replacement fluid for CVVH is a/w higher solute clearance?
POSTfilter
96
what is the most effective way to increase urea clearance in a patient on CVVH with a QB of 150 ml/min?
increase QB
97
first step in evaluation and management in a patient with a differential diagnosis of prerenal azotemia secondary to volume depletion, HRS, or ATN
adequate volume repletion with IV isotonic crystalloid
98
- AKI - anemia - hypercalcemia - low AG - discrepancy between urine dipstick (trace protein) and UPC
MM with light chain cast nephropathy
99
amyloidosis can also be associated with presence of paraprotein, like MM, but on urine studies what is different?
significant albuminuria and NO discrepancy between protein by urine dipstick and UPC
100
- decompensated cirrhosis - progressively worsening renal function - low BP - low urine Na+
HRS
101
pathophysiology of AKI in setting of heart failure
- venous congestion --> activates sympathetic and RAA systems --> intrarenal vasoconstriction - increased intraabdominal pressure
102
best initial treatment to reduce risk of intratubular cast formation and AKI in rhabdomyolysis
rapid infusion of IV 0.9% saline
103
antibiotics, plasmapheresis, antimotility agents, and antiplatelet agents are not recommended in what condition?
diarrhea-associated HUS
104
home BP measurements have been established to lead to
improved medication adherence
105
patients with renovascular disease treated with what have reduced morbidity and mortality as compared with treatment with other agents?
RAAS blockade
106
treatment in a patient with renovascular HTN with a solitary functioning kidney
endovascular stent placement of renal artery for functioning kidney
107
elevated renin levels represent a loss of perfusion pressure to the juxtaglomerular apparatus, not a
decrease in oxygen levels
108
best treatment for a pregnant patient with increase in BP 2/2 FMD
renal angiography and percutaneous transluminal renal angioplasty (PTRA)