Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology and MuscSkel > Antineoplastics and angiogenesis > Flashcards

Antineoplastics and angiogenesis Flashcards

1
Q

What are the rationale for anti-neoplastic drugs?

A

kill all tumor cells
suppress growth of tumor cells but not normal cells
improve ability of normal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cancer stem cells are what?

A 
small compartment of tumor
often quiescent
resistant to chemo and radiation
can regenerate tumor
one mechanism for drug resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

At what size is a tumor visible on X-ray?

A

at 1 cm in diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When is a tumor first palpiable?

A

at 1 gram; when first become symptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of kinetics does killing tumor follow?

A

first-order kinetics; so a constant dose of drug kills a constant fraction of tumor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Tumor size predicts what with respect to chemotherapy use?

A

not hte dose but duration of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What must the chemotherapy regimen must be like to be curative?

A

have a 2-4 log kill efficiency and be repeated 4-12 times

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Class II drugs target what type of tumor/cell?

A

target cells in specific stage of cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do class III drugs target what type of tumor/cell?

A

targets cells in cell cycle relatively specific for cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do class I drugs target?

A

target and kill all cells regardless of what sage they are at

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are targets-target therapies for antineoplastics?

A

targeting molecular targets taht are more specific for the cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is angiogenesis?

A

extension of capillaries or blood vessels from existing blood supplies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is vasculogensis?

A

formation of capillaries or blood vessels independently of old blood vessels and eventually join

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the difference between vessels in tumor vs normal vessels?

A

tumor vessels lack smooth muscle all the way around them; and much more chaotic, holes used for mestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is it difficult for drugs to enter tumor?

A

itnratumor pressure due to damaged lymphatic vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the role of VEGF in permeability of vessels?

A

50,000 times more potent than histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is NOTCH?

A

when it is cleaved and enters nucleus it is important in early angiogenisis by transcription increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the benefits of anti-angiogenic therapy?

A

target genetically stable population
naturally occuring-high tolerance low side effects
ease accessibility
**this is the ideal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is tumor doubling timea function of?

A

cell cycle time
growth faction
cell loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are are the four principles of tumor growth curve?

A

tumor mass generally first detectable at 10^9 cells
as a tumor grwos more cells enter G0
tumor cells are generally mores sensitivie to chemo agents during early growth periods
a palable tumor is large enought to have metastasized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the four stages of tumor growht?

A

I: tumor contained in organ of orgin
II: tumor metastasized regionally but is totally removable
III: metastasized regionally but no longer totally removable
IV: tumor is metastasized beyond local area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What log-kill rate is needed to double the expected lifespan of a patient?

A

2-4 log-kill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the total-kill concept?

A

one surviving cell can regenerate the tumor

the lifespan of the host is inversely related to the number of cells that survive therapeutic measures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are two antineoplastic drugs that are class I?

A

non-specific cytotoxicity:
mechlorethamine
carmustine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What drug is a class II that focuses on cells in the G1 phase?

A

prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What drugs are pyrimidine analogs that kill cells in the S phase greatest activity, class II?

A

Cytarabine, fluorouracil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What drug is an antimetabolite that is a folic acid analog that kills cells in the S phase? Class II

A

methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What drug is an antimetabolite, purine analog, class II, S phase ?

A

mercaptopurine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What drug is a class II, substituted urea, kill cells S phase?

A

hydroxyurea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What drugs are antibiotics, that are class II drugs, G 2 phase?

A

bleomycin, etoposide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the taxane, G2 phase, Class II?

A

Paclitaxel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What drug is Class II, m phase focused, a mitotic nhibitor?

A

vinblastine, vincristine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What drug is a class III alkylating agent?

A

cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What drug is a miscellaneous metal salt, class III drug?

A

cisplatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What drug is an antibitoic, class III drug?

A

doxorubicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the dosing frequency for one cycle of treatment of class I agents?

A

given as a single dose for each cycle of therapy?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the dosing frequency for one cycle of treatment of class III agents?

A

given as a single dose for each cycle of therapy?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the dosing frequency for one cycle of treatment of class II agents?

A

given by continuous infusion or frequent small doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the optimal intervals for cycles of treatments?

A

optimal intervals are those which deliver the next cycle of treatment when there is the greatest difference between recovery of normal tissue and recovery of tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the toxic effects of the alkylating agen mechlorethamine?

A

nausea vommiting, myelosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the mechanism of action of alkylating agents as anti-neoplastic rugs?

A

introduce alkylgroups into DNA

cause DNA crosslinks, strandbreaks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the toxic effects of cyclophosphamide, an alkylating agen?

A

nasuea and vomitting
limited myelosuppression
alopecia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the toxic effects of carmustine?

A

nasuea and vommitting

delayed myelo suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is mechlorethamine used to treat?

A

hodgkin’s and non-hodgkins lymphoma*

breast, lung and ovarian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is cyclophosphamide used to treat?

A 
very broad spectrum, mostly widely used
Hodgkins and non-hodgkins lymphoma
multiple myeloma
neuroblastoma
leukemias
carcinoma of endometrium, breast lung
46
Q

What is a unique side effect of cyclophosphamide?

A

may cause sterile hemorrhagic cytitis

47
Q

What are the properties of carmustine?

A

alkylating agent, extensively metabolized in liver

highly lipophilic, rapidly crosses blood brain barreir

48
Q

What is carmustine used to treat?

A

treatment of brain tumors, multiple myeloma, melanoma

49
Q

What is the mechanism of action of methotrexate?

A

metabolized to polyglutamates which binds to dihydrofoloate reductase and prevent formation of tetrahydrofolate

50
Q

What does methotrexate bind to?

A

serum albumin

51
Q

What are the toxicities associated with methotrexate?

A

intestinal epithelium, bone marrow suppression

renal tubular necrosis

52
Q

What is methotrexate used to treat?

A

acute lymphocytic leukemia; choriocarcinoma

53
Q

What si teh mechanism of action of fluorouracil?

A

activated in cells to FUTP which inhbiits RNA synthesis and FdUMP whihc interferes with DNA synthesis

54
Q

What is flurouracil used to treat?

A

carcinoma of the stomach, colon, pancreas, ovary, head and neck, breast, bladder
topical cream for basal cell carcinoma

55
Q

What is the toxicity of fluorouracil?

A

nausea, anorexia, diarrhea, delayed myelosuppression

56
Q

What is the mechanism of action of cytarabine?

A

cytidine analog
competes with cytidine for all 3 phosphorylation steps to dCTP
cytarabine tri-phosphate competes with dCTP for incorporation into DNA and causes DNA chain termination

57
Q

What is the toxicity of cytarabine?

A

marked myelosuppression and neurotoxicity

58
Q

What is cytarabine used to treat?

A

acute leukemia

59
Q

What is the mechanism of mercaptopurine?

A

purine analog that is converted in cells to ribonucleotide that inhibits RNA and DNA synthesis

60
Q

What is mercaptopurine used to treat?

A

acute leukemia and chronic granulocytic leukemia

61
Q

What is mercaptopurine toxicity?

A 
gradual bone marrow depression
vomiting
nausea
anorexia
jaundice
62
Q

What is the mechanism of action of hydroxyurea?

A

substituted urea that inhbiits ribonucleotide reductase blocking DNA synthesis; arrest at G1 to S pahse

63
Q

What is hydroxyurea used to treat?

A

granulocytic leukemia, head and neck cancer

64
Q

What is the toxicity associated with hydroxyurea?

A

hematopoietic depression, GI disturbances

65
Q

What are the mechanism of action of vina alkaloids?

A

binds to tubuline, inhibiting proper formation of microtubules and miotic spindle, arresting cellls in metaphase
M phase-specific

66
Q

What is Vinblastine used to treat?

A

hodgkins and non-hodgkins lymphoma

breast cancer

67
Q

What is vinblastine toxicity?

A

strongly myelosuppressive
epithelial uclerations
neurological disturbance and bronchospasm

68
Q

What is vincristine used to treat?

A

acute lymphocytic leukemia, hodgkins and non-hodgkins lymphomas, wilms tumor, neuroblastoma and rhabdomyosarcoma

69
Q

What is the toxicity of vincristine?

A

alopecia
neuromuscular abnoramlities (peripheral neuropathy incl)
significantly less bone marrow suppression than vinblastine

70
Q

What is the mechanism of action of taxanes?

A

blocks late in G2 phase; enhances assembly and stability of microtubules by binding to Beta0subunit of tubulin

71
Q

What is paclitaxel usedd to treat?

A

refactory ovarian cancer; breat cancer

72
Q

What is toxicity associated with Paclitaxel?

A

dose-limiting leukopenia, peripheral neuropathy, myalgia/arthalgia

73
Q

What is the doxorubicin mechanism of action?

A

prevents DNA and RNA synthesis by intercalating between DNA base pairs, dostorting DNA helix
causes lipid peroxidation and free radical generation
binds to DNA and topo II

74
Q

What is the Doxorubicin used to treat?

A

Hodgkin’s and non-hodgkin’s lymphoma, breast, ovary, small cell lung and other cancers

75
Q

What toxicity is assoicated with doxorubicin?

A

cardiomyopathy

bone marrow depression, alopecia, GI disturbance

76
Q

What is the mechanism of bleomycin?

A

a mixture of glycopeptides that bind to DNA
causes oxidative-like damage to DNA which leads to DNA strand breaks
phase specific for G2 and M

77
Q

What is bleomycin used to treat?

A

germ cell tumors of testes and ovaries

head, neck, lung, lymphomas

78
Q

What toxicitiy is associated with Bleomycin?

A

dose-related pulmonary toxicity
vesiculation of the skin, skin hyperpigmentation
minimal myelosuppression adn immunosuppresion

79
Q

What is the mechanism of action fo Etoposide?

A

stabilizes DNA topo II complexes resulting in double strand DNA breaks
maximal effect in late G2 phase

80
Q

What is used to treat with etoposide?

A

lymphomas, acute nonlymphocytic leukemia, small cell carcioma of lung, testicular tumor

81
Q

What is the mechanism of Filgastrim?

A

stimulates granulocyte production by marow

82
Q

What is Filgastrim used for?

A

given after myelosuppressive agent to speed neutrophil recovery;
bone pain major side effect

83
Q

What is the mechanism of Trastuuzumab?

A

humanized monoclonal antibody that binds to HER2 receptor

84
Q

Wha is trastuzumab used to treat?

A

breast cancer that overezpress HER2

85
Q

What is the toxicity of Trastuzumab?

A

cardiomyopathy
hypersensitivity
infusion reacctions

86
Q

What is the mechansim of cisplatin?

A

platinum coordination complex, hydrolysis leads to an activated species which causes DNA crosslinks, also promotes apoptosis

87
Q

What is cisplatin used to treat?

A

wide antitumor spectrum, testis of cancer, ovary, head, neck bladder, esophoagus small cell lung

88
Q

What is the toxicity associated with cisplatin?

A 
nephrotoxicity
ototoxicity
peripheral neuropathy
electrolyte disturbance
nausea, vomitting, myelosuppression
89
Q

What is procarbazine mechanism of action?

A

poorly understood, but activated in vivo to a methylating agent which causes chromsomal damage

90
Q

What is procarbazine used to treat?

A

hodgkins

91
Q

What is the toxicity associated with procarbazine?

A

myelosuppression, nausea, vomitting

92
Q

What is the mechanism of action of tamoxifen?

A

nonsteroidal antiestrogen that blocks estrogen receptors thereby reducing tumor cell renewal

93
Q

What is tamoxifen activatedd by?

A

CYP2D6

94
Q

What is tamoxifen used for?

A

ajuvant therapy in post-menopausal breast cancer
pre-menopausal metastic breast cancer
treatment of certain endometrail and ovarian cancers
breast cancer prophylaxis***

95
Q

What is tamoxifen toxicity?

A

hot flashes, fatigue, nausea, bone and other musculoskeletal pain

96
Q

What is letrozole mechanism of action?

A

non-steroidal aromataase inhibitor, inhibitis conversion of androgens to estrogens

97
Q

What is this treatment for letrozole?

A

breast carcinoma in post menopausal women

98
Q

What are the side effects of letrozole?

A

bone paina nd other musculoskeletal pain, hot flashes, nausea, fatigue

99
Q

What is the mechanism of action of leuprolide?

A

synthetic peptide analog oof gonadotropin-releasing horomone (GnRH)
after 2-4 weeks it desensitizes GnRH signaling inhibiting LH/FSH secretion decreasing testosterone synthesis to castration levels

100
Q

What is leuprolide used to treat?

A

advanced horomonally rsponsive prostate cancer

101
Q

What is leuprolide toxicity?

A

hot flashes, impotence

102
Q

What is the mechanism of action of Flutamide?

A

potent nosteroidal antiandrogen that blocks androgen receptors

103
Q

What is flutamide used to treat?

A

metastatic prostate cancer, often with GnRH analog

104
Q

What is the toxicity of flutamide?

A

gynecomastia, diarrhea, hepatotoxicity

105
Q

What is the reason for resistance to chemotherapy?

A

resting cells
dose limited by toxic effects on sensitive tissues
spontaneous mutations
clinical resistance
selectiona nd overgrwoth-major cause of chemotherapic failure

106
Q

What is multi-drug resistance medaited by?

A

ATP-dependent drug efflux pumps
pump out a variety of drugs from cells
simultaneous resistance to many drugs

107
Q

What are strategies to circumvent resistance?

A

increase dose
multi-drug regimens
co-admin agens that defeat resistance
recruit cells out of resting phase

108
Q

What is the advantages of combination therapy?

A

provide maximal cell kill within range of toxicity tolerated by host of each drug
provide a braoder range of coverage
prevent development of new resistant lines

109
Q

What is sequential blockade?

A

simultaneousl action of two inhibitors acting on different enzymes of a linera metablic pathway

110
Q

What is concurrent inhibition?

A

inhibitors block two separate pathways that lead to the same end product

111
Q

What is complementary inhibition?

A

one of the inhibitors affects the function of an end product the other inhbiitor affects the syntehsis of that end product

112
Q

What is rescue?

A

rescues teh normal cells from treatment

Pathology and MuscSkel (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions