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Therapeutics P3 Semester 1 > Final Exam - Cancer (Intro) > Flashcards

Final Exam - Cancer (Intro) Flashcards

1
Q

noeplasm

A

new growth, benign or malignant

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2
Q

tumor

A

nonspecific term meaning lump or swelling

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3
Q

cancer

A

malignant neoplasm

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4
Q

types of -plasias

A

hyperplasia
metaplasia
dysplasia
anaplasia

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5
Q

hyperplasia

A

increase in organ or tissue size due to increase in the number of cells

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6
Q

metaplasia

A

a substitution of one type of adult tissue for another

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7
Q

dysplasia

A

abnormal proliferation in which there is loss of normal architecture

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8
Q

anaplasia

A

Loss of structural differentiation. Cells dedifferentiate.

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9
Q

types of -omas

A

carcinoma
adenocarcinoma
sarcoma
lymphoma/leukemia
melanoma
blastoma
teratoma

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10
Q

carcinoma

A

malignant neoplasm, squamous epithelial cells

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11
Q

adenocarcinoma

A

malignant neoplasm, glandular tissue

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12
Q

sarcoma

A

malignant neoplasm, mesenchymal tissue

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13
Q

lymphoma/leukamia

A

malignant neoplasm, hematopoietic tissue

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14
Q

melanoma

A

cancer of pigment cells (skin or eye)

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15
Q

blastoma

A

malignancy in precursor cells (blasts)
-more common in children

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16
Q

teratoma

A

germ cell neoplasm of several different types of tissues

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17
Q

numerical staging

A

worse prognosis with increasing stage #

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18
Q

TNM staging

A

more involvement and higher numbers mean worse prognosis and worse outcomes in general

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19
Q

hallmarks of cancer

A
  1. sustaining proliferative signaling
  2. avoid immune destruction
  3. enable replicative immortality
  4. invasion and metastasis
  5. accessing vasculature
  6. resisting cell death
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20
Q

oncogenes

A

promote tumor growth
-v-Src
-EGFR
-Ras or Kras
-PI3K

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21
Q

tumor supporessors

A

suppress tumor growth
-RB1
-BRCA1 and BRCA2
-p16
-p53

22
Q

all CML have this

A

bcr-abl translocation

23
Q

15-30% of NSCLC have this mutation

A

EGFR

24
Q

EGFR is a ______ mutation

A

activating (cells begin to grow unchecked)

25
Q

drugs used to target EGFR mutation

A

tyrosine kinase inhibitors

26
Q

BRCA mutations in breast cancer are susceptible to what therapy

A

PARP inhibitors
-olaparib
-any other -paribs

27
Q

olaparib MOA

A

Binds PARP to DNA so that it cannot go to other DNA strand breaks. This leads to more and more DNA damage until eventually the cell dies.

28
Q

drug class and area of cell cycle it targets
-5 categories
-9 drug classes

A

DNA damaging agents (non-specific)
-alkylators
-intercalaters

DNA replication (S phase)
-anti-metabolites
-anti-folates
-topo1 inhibitors

sister chromatid separation (G2 phase)
-topo 2 inhibitors

chromosome segregation (M phase)
-microtubule inhibitors

mitogenic signaling (G1 phase)
-kinase inhibitors
-hormone inhibitors

29
Q

regulators of cell cycle steps

A

CDC2 - M phase/G2 phase

CDK4/6 - G1 phase

CDK2 - G1 phase at replication point/S phase

30
Q

CDK4/6 inhibtors

A

ribociclib
palbociclib
abemaciclib

31
Q

palbociclib AE

A

neutropenia
N/V/D
fatigue

32
Q

palbociclib MOA

A

approved for BRCA1/2 mutations

33
Q

are alkylating agents dependent on the cell cycle stage

A

no, they can damage DNA in G0 resting phase and cells that are progressing through the cell cycle

34
Q

cell cycle non-specific drugs

A

alkylating agents and DNA intercalating agents

35
Q

majority of SE from chemo occur to what cells in the body

A

rapidly dividing cells
-GI tract (N/V, loss of appetite)
-WBCs (infections)
-RBCs (anemia)

36
Q

major dose limiting toxicity in chemo drugs

A

myelosuppression

37
Q

most common SE in chemo drugs

A

N/V

38
Q

drugs that work at G1 stage

A

asparaginase
steroids (prednisone)

39
Q

drugs that work at S stage

A

folic acid analogs
methotrexate
cytarabine
gemcitabine
capecitabine
fluorouracil
mercaptopurine
irinotecan
topotecan

40
Q

drugs that work at G2 stage

A

bleomycin
etoposide

41
Q

drugs that work at M stage

A

docetaxel
paclitaxel
vinblastine
vincristine
vinorelbine

42
Q

drugs in CHOP

A

cyclophosphamide
doxorubicin
vincristine
prednisone

43
Q

mechanisms of drug resistance

A
  1. altered drug metabolism
  2. changes in drug target or fxn
  3. physiological changes that promote resistance
  4. cell survival mechanisms
44
Q

altered drug metabolism examples

A
  1. increased transport of drugs out of the cell through efflux pumps
    -PgP
    -MRP: multidrug resistant proteins
  2. reduced transport into the cell
    -loss of drug importer, decreased membrane permeability
  3. decreased activation of prodrug
  4. increased detoxification of drug molecule
45
Q

changes in drug target or fxn examples

A
  1. increased expression of drug target through gene amplification or expression
    -upregulation of target makes it harder to inhibit
  2. emergence of mutant, structurally altered target
46
Q

cell survival mechanisms examples

A
  1. activation of anti-apoptotic regulators
  2. increased repair of damage caused by chemotherapies
47
Q

microtubule inhibitors

A

vincristine
paclitaxel
docetaxel

48
Q

topoisomerase inhibitors

A

etoposide (topo 2)
irinotecan (topo 1)
doxorubicin (topo 2, DNA damage)
bleomycin (topo 2, DNA damage)

49
Q

alkylators/platinum compounds

A

chlorambucil
cyclophosphamide
mitomycin C
cisplatin

50
Q

anti-metabolites

A

6-mercaptopurine
methotrexate
5-fluorouracil
cytarabine

Therapeutics P3 Semester 1 (22 decks)

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