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renal Flashcards

1
Q

pazopanib selectivity and toxicities

A

more selective to VEGF, less fatigue mucositis, more LFT abnl; better QOL compared to sunitinib

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2
Q

COMPARZ trial

A

phase III pazopanib. v. sunitinib first line; 1100 pts, non-inferiority study; reached endpoint–> pazopanib 8.4mo v. 9.5mo; HR 1.047, falling within margin

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3
Q

tox with pazopanib

A

LFTs

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4
Q

second line therapy

A

sorafenib

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5
Q

everolimus toxicities

A

infections, stomatitis, 15% non-infectious pneumonitis

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6
Q

pneumonitis toxicity everolimus

A

treat with steroids

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7
Q

axitinib

A

potent VEGF inhibitor, more than pazopanib; treated in second line setting versus sorafenib; PFS improved PFS 6.7v4.7mo

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8
Q

sorafenib tox

A

more skin

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9
Q

axitinib tox

A

diarrhea

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10
Q

second line therapy

A

either axitinib or everolimus; sequence not so important

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11
Q

combinations v. monotherapy

A

no benefit of combine; temsirolimus + bev–> no added benefit, more toxicity

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12
Q

poor risk tx

A

temsirolimus

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13
Q

poor risk factors

A

anemia, poor PS,

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14
Q

interferon for renal cancer

A

improved survival compared to megace

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15
Q

IL-2 for renal

A

small proportion with durable complete response, 2.5%, high tox

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16
Q

cytoreductive nephrectomy- should you take primary out?

A

2 studies with improved survival with this approach: do if no brain mets and safe procedure before starting meds

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17
Q

MSKCC risk groups (prognostic)

A

KPS<80, short time to need for treatment 12mo, low Hgb, high Ca, high LDH. favorable 0, 1-2 int, 3-5 poor.

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18
Q

temsirolimus FDA approval

A

used for the poor risk group only

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19
Q

histotypes of RCC

A

75% clear cell, 15% papillary, 5% chromophobe, 5% oncocytoma, rare others

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20
Q

clear cell RCC

A

VHL mutation (70-70%), LOH (3p25), or hypermethylation

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21
Q

Type 1 papillary RCC

A

c-met mutation

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22
Q

Type 2 papillary RCC

A

FH mutation

23
Q

VHL gene

A

tumor supresssor that regulates angiogenesis and cell proliferation. turns off wit hypoxia–>allows HIFa–> (VEGF, PDGF, TGF/EGFR). Mutation is constitutively off

24
Q

sorafenib for RCC

A

improved PFS 5.9v 2.8mo compared to placebo, only 2% PR but 78% SD.

25
Q

sorafenib/nexavar tox

A

RASH, hand/food in high proportions.

26
Q

first line RCC

A

sunitinib (biggest trial), bev+IFN, pazopanib (smaller trial), temsiroliumus (poor risk). no comparatives with each other.

27
Q

high risk RCC first line

A

temsirolimus (better than IFN or IFN/tem), IV weekly. more SD, low ORR.

28
Q

tox, temsirolimus

A

rash, LE dema, stomatitis, hypergly, HL, thrombocytopenia, dyspnea. (borderline DM tips them over)

29
Q

sunitinib toxicity

A

fatigue is most common to require dose reduction. others include HTN, nausea, hand/food, 13% with EF cardiac function. get baseline TTE, and yearly TTE.

30
Q

pazopanib tox

A

less fatigue, hand food, stomatitis, but more liver toxicity

31
Q

pazopanib v. sunitinib (COMPARZ)

A

1100pts, NONINFERIOR. sunitinib more fatigue, count suppression. pazopanib has more LFTs, and hair color changes.

32
Q

pazopanib LFT ab

A

if prolonged, then switch to sunitinib

33
Q

everolimus versus placebo in RCC

A

approved for third line

34
Q

tox of everolimus

A

pneumonitis.

35
Q

axitinib for RCC

A

most selective for VEGF. improved PFS compared to sorafenib in 2nd line setting.

36
Q

tox of axitinib

A

diarrhea, HTN.

37
Q

when to give everolimus?

A

either second line or beyond, doesn’t really matter when

38
Q

nivolumab dosing in RCC

A

phase II, Motzer: measure PFS, ORR was 20% across all arms, and durable response, most of them more than year. OS for group, 24 month OSS. now a phase III nivo versus everolimus following progression on a VEGFR.

39
Q

Birt-Hogg-Dube

A

-ch1, -Y. associated with chromophobe and oncocytoma variation. also has pulmonary nodules/hamartomas.

40
Q

hereditary papillary RCC

A

associated with c-met activating mutation, or hydratase inactivating mutation

41
Q

Stauffer syndrome

A

paraneoplastic liver failure that reverses with nephrectomy for RCC

42
Q

VHL syndrome

A

RCC, retinal angiomas, hemangioblastomas of CNS, pheochromocytomas

43
Q

VHL genetics

A

loss of VHL–>loss of ubiquitinization of HIF1a–>increased HIF1a–> increased VEGF/PDGF

44
Q

medullary carcinoma of kidney

A

associated with sickle cell

45
Q

type I papillary RCC

A

good prognosis

46
Q

type II papillary RCC

A

associated with poor prognosis

47
Q

treatment of RCC with bev

A

bev+IFN better than IFN alone; monotherapy is not tested

48
Q

first line RCC, good risk

A

pazopanib or sunitinib; pazopanib- less fatigue/hand food, thrombocytopenia, mucositis; more LFT abnl

49
Q

high risk RCC

A

only temsirolimus approved. 3 or more of the following: LDH, Hgb, Ca,

50
Q

second line good risk RCC Tx

A

axitinib OR everolimus. sorafenib worse than axitinib

51
Q

IL-2 for RCC

A

can use if good PFS and clear cell variant, in first line

52
Q

chemotherapy for RCC

A

if sarcomatoid- gem/dox; if collecting duct- gem/cis; if clear cell- gem/5-FU(or xeloda)

53
Q

treatment of mTOR-associatead pneumonitis

A

grade 1- ASx radiographic- monitor and continue; grade 2- Sx mild- hold and give steroids, then dose reduce.

GU (4 decks)

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