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oncology > Exam 2- 3/4/5 > Flashcards

Exam 2- 3/4/5 Flashcards

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1
Q

3 types of SMKI

A

tyrosine kinase, serine/threonine kinase, and lipid kinase inhibitors

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2
Q

tyrosine kinase inhibitors

A

acting on Bcr-Abl, EGFR,

imatinib and erlotinib

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3
Q

serine/threonine kinase inhibitors

A

acting on B-raf

vemurafenib and trametinib

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4
Q

lipid kinase inhibitor

A

acting on PI-3K

idelalisib

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5
Q

mechanisms of tyrosine kinase activation include

A

genetic alteration, gene amplification, point mutation, protein accumulation

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6
Q

irreversible inhibition

A

SMKI forms a covalent bond with the cysteine residues in the active site of a protein kinase

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7
Q

reversible inhibition

A

type inhibition I to IV

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8
Q

group 1: targeting Bcr-Abl oncoprotein in chronic myeloid leukemia

A

imatinib (1st generation), nilotinib (2nd generation)

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9
Q

major cause of CML

A

the philadelphia chromosome (fusion of 9 and 22)

- this one mutation leads to cancer

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10
Q

imatinib clinical indication

A
  • PH+ CML in blast crisis, accelerated phase or chronic phase after IFN therapy
  • pediatric patients with PH+ CML in chronic phase
  • PH+ ALL
  • Kit+ GI stromal tumors (GIST)
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11
Q

monitoring PH+ CML after treatment

A
  • hematologic tests: normal range of blood cell counts
  • cytogenic tests: numbers of cells with PH+ chromosome
  • molecular tests: q-RT-PCR: existence of PH+ DNA/mRNA
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12
Q

nilotinib is cabable of

A

overcoming imatinib reisistance resulting from Brc-Abl kinase mutations

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13
Q

Nilotinib clinical indication

A

chronic phase and accelerated phase PH+ CML resistant or intolerate to imatinib

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14
Q

effectiveness of nilotinib is based on

A

hematologic and cytogenetic response rates

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15
Q

do not use nilotinib is patients with

A

hypokalemia, long QT syndrome or hypomagnesemia.

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16
Q

gemfitinib

A

EGFR

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17
Q

erlotinib

A

EGFR
Tarceva
NSCLC, metastatic pancreatic cancer

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18
Q

lapatinib

A

EGFR/Her2
Tykerb
breast cancer

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19
Q

Afatinib

A

EGFR/Her2

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20
Q

cigarette smoking decreases

A

erlotinib plasma concentrations

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21
Q

severe ADRs of erlotinib

Study These Flashcards
A

GI bleeding or perforations, renal disorders, hepatic disorders, ocular disorders- abnormal eyelash growth

22
Q

common ADRs of lapatinib

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A

GI- diarrhea, dermatologic, fatigue

23
Q

severe ADRs of lapatinib

Study These Flashcards
A

cardiac toxicity, hepatic toxicity, interstitial lung disease/pneumonitis

24
Q

multiple tyrosine kinases

Study These Flashcards
A

sunitinib, sorafenib

25
sunitinib
VEGFR, PDGFR, etc Sutent GIST, metastatic renal cell carcinoma
26
sorafenib
mutiple tyrosine kinases/serine/threonine kinases VEGFR, PDGFR, raf, etc administer w/out food Nexavar hepatocellular carcinoma (HCC), renal cell carcinoma (RCC)
27
sorafenib drug interactions
decetaxel, fluorouracil, gemcitabine, oxaliplatin, paclitaxel, doxorubicine, irinotecan
28
sorafenib severe ADRs
wound healing complications
29
interferones (IFNs)
are cytokines produced by the cells of the immune system in response to various challengers, particularly virus with double stranded RNA
30
biological potency of IFNs are determined as
millium IU
31
specific activity of IFN alfa-2b
2.6 X10^8 IU/mg protein
32
potential MOA of IFN in tumor therapy (4)
- direct inhibition of cancer cell proliferation - enhancement of cytotoxic T cell activities that kill cancer cells - cell cycle regulation leading to tumor cells cytostasis and apoptosis - increased expression of cell surface antigen/protein which facilitates immune cell recognition and cytotoxicity
33
main site for catabolism of IFN?
kidney. No IFN in urine after administration
34
;abeled indications for IFN therapy
PH+ CML, hairy cell leukemia, follicular lymphoma, AIDS-related kaposi's sarcoma, melanoma 18 yo and up
35
IFN also has an unlabeled indiction for
renal cancer
36
IFN drug interaction
may potentiate risk of renal failure in combo with IL-2
37
acute ADRs of IFN
flu-like symptoms- fever, chills, HA
38
chronic ADRs of IFN
depression, fatigue/weakness (most dose-limiting)
39
incomplete Reiter's syndrom induced by
systemic IFN alpha | tongue ulcers
40
do not use IFN-alpha with
autoimmune hepatitis (positive anti-nuclear antibody)
41
interleukin-2
Proleukin
42
biological potency of IL-2 is shown as
international units (IU)
43
IL-2 receptor
1. requires binding to its IL-2 receptor 2. receptor belongs to class I cytokine receptor family 3. IL-2 receptor is composed of 3 units (alpha, beta and gammaC) 4. signaling is transmitted by members of JAK and STAT family
44
IL-2 MOAs
1. enhancing lymphocyte mitogenesis and stimulation of long-term growth of IL-2-dependent cells 2. enhancing lymphocyte cytotoxicity 3. inducing lymphokine-activated (LAK) and NK activity - pretty much increase number and function
45
IL-2 rapidly distributes to
extravascular space
46
IL-2 clinical indication
renal cell carcinoma, melanoma
47
IL-2 injection should be reserved for patients with normal
cardiac and pulmonary function
48
IL-2 and glucocorticoids
glucocorticoids reduce IL-2 induced side effects (Fever, renal insufficiency, hyperbilirubinemia, confusion and dyspnea) however, they also reduce the effectiveness and should be AVOIDED
49
IL-2 has been associated with
- capillary-leak syndrome (CLS) | - impaired neutrophil function and increased risk of sepsis and bacterial endocarditis
50
IL-2 ADRs
hypotension, pulmonary congestion, anemia, thrombocytopenia, capillary leak syndrome

oncology (6 decks)

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