Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Oncology Pharmacology > Flashcards

Oncology Pharmacology Flashcards

1
Q

Azathioprine (imuran)

A

AZa, immunosuppressant medication used in organ transplantation and to treat autoimmune disorders

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

Methotrexate

A

Ok

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

Fluorouracil (5-FU)

A

Antimetabolite medication which works by inhibiting thymidylate synthase, leading to decreased DNA synthesis.

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

Indications flor 5-FU

A

Slow growing solid tumours

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

What is 5-FU coadministered with to treat gastric adenocarcinoma

A

Leucovorin

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

Why may 5-FU be used topically

A

Nasal cell carcinoma

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

Side effects fluorouracil

A

Myelosuppression, which is not reversible with leucovorin, as it is with methotrexate

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

MOA 5-FU

A

Antimetabolite that interferes with the cells normal metabolic functioning, inhibiting DNA synthesis. It is a pyramidine analog which competes with thymidylate synthetase to inhibit DNA synthesis

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

5-FU is a pyramidine analog

A

Causes thymidylate less death.
It decreases dTMP, as 5-FU competes with dUMP for thymidylate synthase, inhibiting its action.

Blocks synthesis of the pyramidine thymidine which is a nucleoside required for DNA synthesis and replication.

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

Without DNA synthesis

A

Tumor cells undergo apoptosis

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

Indications for 5-FU

A

Slow growing solid tumors (with leucovorin for stomach cancer)
Basal cell carcinoma (topical)

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

Examples of slow growing solid tumours

A

Stomach, colorectal, breast, ovarian, pancreatic

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

Side effects 5-FU

A

Myelosuppression —> megaloblastic anemia, neutropenia, and thrombocytopenia

Mucositis-inflammatory lesions of mucosa in oral, nasal and alimentary tract

Severe diarrhea-GI mucositis

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

Is myelosuppression of 5_FU with lev reversible

A

No

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

Is myelosuppression with methotrexate reversible

A

Yup

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

Bleomycin

A

Antitumour antibiotic which is used to treat testicular cancer and Hodgkin lymphoma, and squamous cell carcinoma

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

MOA bleomycin

A

Inducing free superoxide and hydroxide radicals, which cleave DNA, leading to breaks in cancerous DNA strands.

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

Side effects bleomycin

A

Pulmonary fibrosis, skin changes, and mucositis

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

Indications for bleomycin

A 
Testicular cancer (germ cell tumours)
Hodgkin lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

For treating testicular cancer,what is bleomycin typically combined with

A

Etoposide and cisplatin bc they have complimentary effects on inhibiting cancerous DNA

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

For Hodgkin lymphoma what are the drug regimes

A

ABVD or BEACOPP

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

MOA bleomycin

A

Chelates metal ins , leading to pseudoenzyme which converts oxygen to superoxide and hydroxide free radicals which can cleave DNA

break DNA strands (incision too)

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

Side effects bleomycin

A

Pulmonary fibrosis (also oxygen toxicity which may play a role in lung injury)

Skin changes (rash, alopecia, hyperpigmentation, and rayneuads, dermatographism)

Mucositis (typically mouth)

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

Actinomycetes (actinomycetes D)

A

Antitumour antibiotic for childhood tumours.

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

Indication for dactinomycin

A

Wilms, Ewing sarcoma, rhabdomyosarcoma, and gestational trophoblastic malignancy

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

MOA dactinomycin (actinomycetes D)

A

Intercalated DNA, halting the replication process in tumors.
Bind DNA transcription initiation complex, preventing RNA chain elongation.

Gets in the way physically blocking DNA replication

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

Side effect dactinomycin

A

Myelosuppression->leading to decreased red and white blood cell production

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

Doxorubicin (adriamycin)

A

Anthracycline antibiotic used in cancer therapy.

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

MOA doxorubicin

A

Intercalating DNA, preventing new cell growth in tumors, but leads to heart damage

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

Side effects doxorubicin

A

Cardiotoxic

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

How can you decrease cardiotoxic side effects of doxorubicin

A

Give with dexrazoxane

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

Indications for doxorubicin

A 
Solid tumors (bladder, breast, stomach, ovaries, lungs, thyroids, soft tissue sarcomas)
Lymphomas and leukemia’s (leukemia’s and hodgkins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MOA doxorubicin

A

Increases free radical production in tumor cells, leading to cytotoxicity
-inhibits biosynthesis of new cells as it intercalated DNA (once topoisomerase has split the DA to be replicated, doxorubicin intercalated the DNA, preventing the double helix from being resealed…stopping replication)

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

Side effects doxorubicin

A

Cardiotoxicity

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

Why does doxorubicin cause cardiotoxicity (leading to CHF)

A

Myocardial apoptosis, Dow Regulation of contractile proteins and oxidative stress on myocardial cells.

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

How can we decrease cardiotoxicity with doxorubicin

A

Give with dexrazoxane which is a cardioprotective agent

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

How does dexrazoxane work

A

Chelates iron ions, decreasing the amount of superoxide radicals that can harm the heart

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

Busulfan

A

Alkylation anticancer agent that is used to treat CML, and as a conditioning agent prior to bone marrow transplantation

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

MOA busulfan

A

Cross links DNA, preventing DNA replication, as these cross links cannot be repaired by cellular machinery, causing the cancer cell to undergo apoptosis

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

Indications for busulfan

A

CML

Bone marrow ablation (conditioning agent prior to bone marrow transplant, espicially in patients with CML)

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

What is the gold standard treatment for CML

A

Imatinib

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

Side effects busulfan

A 
Myelosuppression
Pulmonary fibrosis (busulfan lung)
Hyperpigmentation (mimics Addison disease, affecting the joints and skin creases as bronzing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Cyclophosphamide

A

Alkylation agent, which works by cross linking DNA at the guanine N7 position, causing cell apoptosis.

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

Before becoming active, cyclophosphamide is bioactivated by __ in the liver

A

Cp450

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

Indication for cyclophosphamide

A

Lymphomas (hodgkin and non Hodgkin))
Leukemia’s
Solid malignancies(breast, ovarian, cervical, testicular soft tissue sarcomas)
SLE, RA, MS, amyloid light chain amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Side effects cyclophosphamide

A

Myelosuppression (decrease r and w bc, + thrombocytes)

Hemorrhagic cystitis(which can be treated with mesna)

SIADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

MOA cyclophosphamide

A

Pro drug—>4 hydroxy cyclophosphamide (chemotherapeutic activity from over conversion)

Alkylation agent that cross links DNA (adds to alkyl group at guanin N7 position) inhibiting replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Indication for cyclophosphamide

A

Autoimmune disorders (depresses leukocyte replication)
Leukemias (kids too)
Lymphomas
Solid tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Side effects cyclophosphamide

A

Myelosuppression

Hemorrhagic cystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How does cyclophosphamide cause hemorrhagic cystitis

A

Produces acrolein

Which is toxic to the bladder epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How treat hemorrhagic cystitis

A

Mensa

Adequate fluid intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Risk with cyclophosphamide

A

TCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How does Mensa work

A

Binds to acrolein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Vincristine (once in)

A

Antineoplastic medicationt hat prevents cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Indication for vincristine

A

Leukemia’s, lymphomas, solid tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Side effects vincristine

A

Peripheral neuropathy

Paralytic ileus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Unlike __, vincristine does not cause bone marrow suppression

A

Vinblastine (velban)

58
Q

MOA vincristine

A

It is a vinca alkaloid that blocks mitosis during the metaphase of cell division. This action prevents the replication of cells and stops cellular growth
Inhibits microtubuels from moving chromosomes during metaphase of cell division. It binds to tubules, a component of microtubles to prevent synthesis and trigger apoptosis. Yb inhibiting microtubules, it causes cell death

59
Q

Indications vincristine

A

Leukemia’s

Lymphomas

60
Q

CHOP

A

Cyclophosphamide, hydroxydaunorubicin, and prednisone.

61
Q

Vincristine and lymphomas

A

Used with other chemos and causes apoptosis of tumour cells and prevents spread of cancer

62
Q

Side effects vincristine

A

Peripheral neuropathyparalytic( toxic to peripheral nerves. Disrupts neurotubules by binding to the protein tubules. Injures neurons by inhibiting the structures required for atonal transport of anzymes and organelles.

ileus (injure autonomic nerves and autonomic transmission between brain and the intestines)

63
Q

Why are there minimal CNS side effects with vincristine

A

Does not enter the brain

64
Q

Why is vincristine only given via IV

A

Not absorbed. Can cause severe skin irritation.

65
Q

Cisplatin

A

Chemo which triggers apoptosis in tumor cells by crosslinking their DNA.

66
Q

How is cisplatin administered

A

IV

67
Q

Indications for cisplatin

A

Solid malignancies, carcinomas—-ovarian, pulmonary, bladder and testicular carcinomas.

68
Q

Side effects cisplatin

A

Nephrotoxicity and ototoxicity

69
Q

Indications for cisplatin

A

Carcinoma-bladder, ovarian, lung, testicular

70
Q

MOA cisplatin

A

Interferes with mitosis, crosslinking DNA. Crosslinked DNA are unable to be replicated and are considered damage. The damage is irreperable, activation apoptosis

71
Q

Side effects cisplatin

A

Ototoxicity-acoustic nerve damage…from reactive oxygen species that damage the stria vascularis of the inner ear.

Nephrotoxicity-creates ROS that damage kidney

72
Q

Why should cisplatin never be combined with aminoglycosides

A

Otoxicity

73
Q

How treat nephrotoxicity from cisplatin

A

Use amigos time, which scavenges free radicals and neutralizes them, along with chloride diuresis

74
Q

Etoposide

A

Cytotoxic chemo used in treating malignancies like small cell lung cancer and testicular cancers

75
Q

Off label indications for etoposide

A

Leukemia and lymphoma

76
Q

MOA etoposide

A

Inhibits topoisomerase II, inhibiting proper DNA replication which leads to cancer cell apoptosis.

77
Q

Side effects etoposide

A

Alopecia, myelosuppression, hypotension, nausea and vomiting

78
Q

Indications etoposide

A

Small cell lung cancer

Testicular cancer

79
Q

MOA etoposide

A

Inhibits topoisomerase II, which is crucial for DNA replication, working to cleave and unwind DNA supercoils and then to relegate them.

80
Q

By inhibiting topoisomerase II, etoposide leads to errors in DNA synthesis, causing what

A

Apoptosis

81
Q

Why do cancer cells rely on topoisomerase II more than health cells

A

They divide more

82
Q

Side effects etoposide

A

Myelosuppression

Alopecia

Hypotension

Nausea and vomiting

83
Q

Hydrozyurea

A

Antimetabolite medication which acts by suppressing ribonucleotide reductase, an enzyme that reduces ribonucleotides into deoxyribonucleoties which are necessary for DNA synthesis.

84
Q

MOA hydroxyurea

A

DNA replication halted in the S phase of the cell cycle

85
Q

Indication for hydroxyurea

A

Chronic myeloid our leukemia, melanoma, sickle cell disease

86
Q

Side effects hydroxyurea

A

GI distress, myelosuppression

87
Q

MOA hydroxyurea

A

Inhibits ribonucleotide reductase (which reduced ribonucleotides into deoxyribonucleotides, which are necessary for DNA synthesis)

Decrease DNA synthesis
Stuck in S phase-“activating the S phase checkpoint”

88
Q

Indications hydrozyurea

A

Melanoma
CML
Sickle cel disease (effectively reverses suckling of cells, causes an increase of HbF and inhibits HbS)

89
Q

Side effects hydroxyurea

A 
Myelosuppression
GI distress (acute mucocutaneous toxicity)
90
Q

Bevacizumab

A

Monoclonal antibody cancer therapy that targets vascular endothelial growth factor (VEGF)

91
Q

MOA bevacizumab

A

Monoclonal antibodies normally made by the body in that they attach to invasive cells. Targets VEGF, attaching to cancer cells that express VEGF signal protein, thereby signaling the immune system to kill these cancer cels.

92
Q

What does the VEGF ligand normally bind to

A

It’s receptors on endothelial cells to help stimulate formation of new blood vessels either from endothelial cells (vasculogenesis) or from existing blood vessels (angiogenesis)

93
Q

What does bevacizumab bind

A

VEGF extracellulary an preventing it from binding to VEGF receptors on the surface of endothelial cells

94
Q

Effect of bevacizumab from binding to VEGF

A

Inhibiting VEGF from stimulating angiogenesis which inhibits tumor growth while antivascular effects reduce tomour size

95
Q

Effect of bevacizumab on tumor

A

Anti-angiotensin effects inhibit tumour growth while antivascular effects reduce tumour size

96
Q

Indications bevacizumab

A 
Capillaries grow CORN (cc-CORN acronym)
Colorectal cancer
Glioblastoma
Cervical cancer
Ovarian cancer
Renal cell carcinoma
Non small cell lung cancer

Age related macular degeneration

97
Q

Off label uses of bevacizumab

A

Metastatic HER2 neg breast cancer
Endometrial cancer
Retinopathy of prematurity
Diabetic retinopathy

98
Q

Side effects bevacizumab

A

Impaired wound healing(inhibit growth of new bv, do not take before surgery-28 days before and after)
Hemorrhage (nosebleeds, cough vomit blood, vaginal, brain, spinal cord)
GI perforation(leak)
Thromboembolic event
Osteonecrosis of jaw(in conjunction with chemotherapy regimes)

99
Q

Contraindications for bevacizumab

A

Recent he opts is or hemorrhage

100
Q

Imatinib (gleevec)

A

Tyrosine kinase inhibiting med used for treating cancers, such as CML and GI stromal tumors.

101
Q

MOA imatinib

A

Inhibits BCR-ABL tyrosine kinase enzyme (which is found in cancer cells), which is necessary for cancer growth. Also inhibits C-kit, which is involved in cell proliferation and differentiation in the GI stroma

102
Q

Indications imatinib

A

CML (inhibitor of BCR-ABL tyrosine kinase)

GI stromal tumors (inhibitor fo C-kit tyrosine kinase)

103
Q

Philadelphia chromosome

A

One of the most common forms of CML arises from the Philadelphia chromosome which is 9:22 translocation. A fusion gene is created as a result of this translocation, elongating chromosome 9 and pairing the ABI gene with the BCR gene from chromosome 22

104
Q

What does C-kit do

A

Signaling role in cell survival, proliferation and differentiation leading to cancerous growth of the GI system

105
Q

Side effects imatinib

A

Fluid retention
Edema
CHF

Also nausea headaches, pancytopenia and growth delay in kids

106
Q

Rituximab

A

Monoclonal antibody medication targeting CD20

107
Q

CCD20

A

A protein expressed on B cells.

108
Q

Indications or rituximab

A

Disorders of B cell malignancy, dysfunction or excess

109
Q

Side effects of rituximab

A

Infusion reactions at the site of IV administration, and the development of skin and oral reactions

110
Q

Rituximab is associated with hte reactivation of what

A

Hepatitis B virus, along with the development of PML

111
Q

Indications for rituximab

A 
CLL
Non Hodgkin lymphoma
RA
Microscopic polyangiitis (MPA)
Wegeners (granulomatosis with polyangiitis)
112
Q

Rituximab and CLL

A

Treats previously untreated and previously treated CD20 positive CLL and combined with fludarabine and cyclophosphamide

113
Q

Rituximab and non hodgkin lymphoma

A

Destroys malignant and normal B cells with CD20

114
Q

Rituximab and RA

A

Combined with methotrexate

115
Q

MOA rituximab

A

Monoclonal antibody to CD20 (on B cells and causes conformational change making them visible to NK cells)

116
Q

Side effects rituximab

A

Infusion reactions
Skin and mouth reactions
Reactivation of hep b
PML

117
Q

PML

A

Rare , serious brain infection that can lead to severe disability and death. Symptoms can include difficulty thinking, loss of balance, changes in speech or walking, weakness on one side of the body or blurred or lost vision

118
Q

Tamoxifen

A

Selective estrogen receptor. Modulator which is a receptor antagonist in breast, but agonist in bone

119
Q

Indication for tamoxifen

A

Estrogen receptor positive breast cancers

120
Q

Beneficial side effect of tamoxifen

A

Decreased risk of osteoporosis is

121
Q

Side effects tamoxifen

A

Increased risk of endometrial cancer and increased risk of thromboembolic event

122
Q

MOA tamoxifen

A

SERM-antagonist for estrogen receptors in some tissues, while an agonist in others

123
Q

Tamoxifen is antagonistic in _ tissue and agonistic in _

A

Breast

Bone

124
Q

Indication for tamoxifen

A

ER positive breast cancer

125
Q

Side effects tamoxifen

A

Decreased osteoporosis

Endometrial cancer

Increased risk of venous thromboembolism (VTE)

126
Q

Trastuzumab/herceptin

A

Anticancer medicationt hat is a monoclonal antibody against HER2

127
Q

HER2

A

Tyrosine kinase receptor that is overexpressed by breast cancer cells

128
Q

Side efects treastuzumab

A

CHF and cardiotoxicity

129
Q

Indications for trastuzumab

A 
Her 2 positive breast cancer
Stomach cancer(HER2 positive gastric cancers)
130
Q

How many breast cancers are her2 positive

A

1/5

131
Q

HER2+ gastric cancer

A

Overexpresses HER2 tyrosine kinase receptor, and is more responsive to trastuzumab

132
Q

MOA trastuzumab

A

Monoclonal antibody against HER2 which binds to cancer class leading to antibody mediated killing HER2 positive cancer cells

Inhibits HER2 initiated cellular signaling.

Antibody mediated cytotoxicity

133
Q

Side effects trastuzumab

A

Cardiotoxicity

134
Q

Aroma rose inhibitors

A

Drugs used in women whoa re post menopausal with breast cancer

135
Q

MOA aromoatse inhibitors

A

Block the production of estrogen or block the action of estrogen receptors

136
Q

Indications aromatase inhibitors

A

ER+ breast tumors bc they require estrogen to grow.

Ovation tumors in postmenopausal women

Systemic metastasis of er positive breast tumors, which preferentially sprea to the liver, lungs, brain and bones.

Ovarian cancer and preventing gynecomastia in men

137
Q

Examples of reversible, non steroid aromatase inhibitors

A

Letrozole

Anastrozole

138
Q

Letrozole

A

For hormonal responsive breast cancer after surgery. Works via reversible inhibition

139
Q

Anastrozole

A

For breast cancer after surgery, or metastasis in both pre and post menopausal women

Reversible inhibition

140
Q

Irreversible, steroid aromatase inhibitors

A

Exemestane

141
Q

Exemestane

A

Oral steroidal aromatase inhibitor that is used in ER positive breast cancer in addition to surgery and/or radiation in post menopausal women

142
Q

Side effects aromatase inhibitors

A

Osteoporosis
Arthritis -estrogens have a positive effect on bone metabolism by stimulating bone growth and inhibiting bone resorption

Arthritis

Pharmacology (52 decks)

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