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Pharm III Heme/Onc > Oncology > Flashcards

Oncology Flashcards

1
Q

Cancer is the ____ leading cause of death in the US

A

2nd

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2
Q

what are the 5 most common types of cancer

A

breast, prostate, lung, colon, lymphoma

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3
Q

what are the 5 most common types of CANCER DEATH

A

lung, colon, breast, prostate and pancreas

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4
Q

What is cancer

A

dz caused by accumulated mutations in DNA that alter cellular function
the mutation give cancer cells growth advantages over normal cells which allows the cancer cells to use bodies resources to grow

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5
Q

Why does cancer occur?

A

DNA is susceptible to changes

Exposure to chemical, radiation, viruses or unknown can cause mutations

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6
Q

Why is cancer bad

A

they invade other areas and organ of the body

as cancer grows and spreads, it becomes a burden to the body leading to organ failure and death

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7
Q

How is cancer named

A

after site of origin or tissue type

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8
Q

what are the types of cancer

A

Solid tumors

Hematologic

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9
Q

what is a primary tumor

A

original mass of cancer cells of a solid tumor in a body organ

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10
Q

metastasize

A

spread of cancer from primary tumor to body sites

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11
Q

benign tumor

A

are abnormal tumor growths but are not as invasive as malignant tumors and are not always fatal

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12
Q

what are the 2 types of localized therapies?

A

surgery

radiation

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13
Q

what are the types of systemic therapies

A 
chemo
traditional chemo
monoclonal antibodies
targeted agents
Immunomodulation
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14
Q

Surgery goals in cancer depend on what?

A 
tumor size, location and type of tumor 
complete removal of tumor
remove tumor and affected organs
remove troublesome metastases
Can't use in hematologic malignancies
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15
Q

Radiation

A

may be used alone or in combo with surgery and or chemo
involves exposing the pt to radioactive energy that destroys cancer cells
Also may damage healthy tissue

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16
Q

Chemotherapy

A

involves use of drugs with various mechanisms that disrupt cancer cell function
usually given IV or Oral which exposes drug to cancer and normal cells

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17
Q

why use chemotherapy

A

many types of chemo target mechanisms of cell function that block cancer cell growth and division
most active against rapidly growing tumors that activate growth mechanism

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18
Q

What are the targets of traditional chemotherapy

A

DNA,RNA, DNA polymerase, topoisomerases, spindle fiber formation

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19
Q

what are the targets of newer chemotherapy agents

A

target specific proteins receptor or their ligands that are required for various cancer cell function
CD antigent, tyrosine kinases

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20
Q

what is log cell kill kinetics

A

a given treatment kills a constant fraction of cells

subsequent doses reduce the cancer burden proportionally over time

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21
Q

what is the gompertzian model of tumor cell growth

A

growth of the tumor is not constant there for as a tumor gets larger the growth fraction decreased which is why later stages of cancer do not respond well to chemo because fewer cells are replicating so less susceptible to chemo

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22
Q

what are the principles of identifying drug combination

A

efficacy: each drug in a regimen must have some anticancer activity when used alone
Toxicity: select drugs to minimize overlapping tox.
Optimum Sched: each drug should be given in intervals to maximize its activity
MOA: multiple mechanisms of action help overwhelm cells ability to develop resistance

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23
Q

what is 1st line primary therapy

A

used in advanced cancer cases in which other treatments would not be effective

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24
Q

what is Neoadjuvant chemo

A

used prior to the use of local therapies to improve their effect by reducing the size of the tumor

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25
Q

what is adjuvant chemo

A

used after local therapies to improve their long term effect by eliminating any remaining undetected cancer cells

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26
Q

Why is dosing so important in chemotherapy use?

A

chemo typically kills in a dose dependent fashion. Higher doses kill more cells but they also have more side effects
SO knowing dose limiting toxicities of chemo helps determine the safe doses of meds

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27
Q

How is dose density used as a strategy of chemo used?

A

giving repeated doses of multiple chemo agents over a period of time
regular exposure to chemo provides was like approach to killing cancer cells over time
-a certain percentage of cancer cells are killed each time the patient gets chemo the time in between give the pt time to recover and less side effects

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28
Q

what are the 3 prognosis of cancer treatment

A

cure- sustained cancer free period
control-reduce cancer burden, prevent extension of cancer, extend survival but cure is unlikely
palliation- reduce symptoms of dz, improve quality of life and prolong survival

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29
Q

what is remission/complete response

A

unable to detect cancer

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30
Q

what is a cure in terms of cancer

A

prolonged period of remission usually 5 years

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31
Q

what is a partial response

A

reduction in tumor burden but cancer still present

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32
Q

what is treatment failure/ progressive disease

A

cancer continues to grow despite treatment

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33
Q

how is response to Tx determined

A

PE
Radiographic test
tumor markers
Biopsies

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34
Q

what is chemotherapy resistance

A

sometimes chemo does’t work because mutations within cancer cells could
block chemo actions
block uptake of chemo into cells
facilitate excessive transport of drug back out of the cells
drug interactions could decrease chemo conc. by increasing their metabolism

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35
Q

what are options if primary tx is not working

A

salvage Tx- uses other combinations of chemo drugs

stem cell transplant

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36
Q

what is an Autologous SCT

A

high dose chemo is followed by re-infusion of pts stem cells

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37
Q

what is alloogeneic SCT

A

use of chemotherapy and immune modulation infusion of donor stem cells where pt get a new immune system

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38
Q

How do older chemo agents work

A

use various mechanism to block cell division

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39
Q

how do newer chemo agents work

A

taget specific functions of cancer cells that make the cancer cells cancerous

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40
Q

What do Alkylating agents target

A

DNA/RNA

they tranfer an alkylating group to other molecules

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41
Q

which molecules do alkylating agents target

A

DNA/RNA
sulfhydryl, amino, hydroxyl, carboxyl and phosphate groups on DNA
this disrupts normal DNA structure by altering atomic interactions and prevents use of DNA as a blueprint for cell division
CELL CYCLE NON-SPECIFIC

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42
Q

Which drugs are part of the alkylating agents class

A

Cyclophosphamide
Melphalan
Procarbazine

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43
Q

what types of cancer is cyclophosphamide used to treat

A

alkylating agent

Breast cancer, Leukemia, Lymphoma, Myeloma

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44
Q

what is meplhalan used to treat

A

Myeloma

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45
Q

what is procarbazine used to treat

A

lymphoma

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46
Q

what are the adverse effects of Alkylating agents

A 
Think when you drink a little Alky your sperm goes down, your mouth is dry, you get N/V, it causes cancer
Sterility (usually temporary)
Mucositis 
Tissue damage from extravasation
N/V
Bone marrow toxicity
Risk of secondary malignancies
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47
Q

what is the MOA of platinum analogs

A

MOA unclear
thought to act similar to alkylating agents by binding DNA and form intra- and interstrand crosslinks
also binds cytoplasmic and nuclear proteins required for cell function

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48
Q

what drugs are part of Platinum analogs

A

all have “platin” in their name
Oxaliplatin
Cisplatin
Carboplatin

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49
Q

what cancers do Cisplatin and Carboplatin analogs treat

A

Lung, Esophagus, Testicular, Ovary, Neck, Bladder, Head

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50
Q

what cancer does Oxaliplatin treat

A

Think of a PEC like a kiss and you sign a card “XO”

pancreatic, esophageal, colorectal

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51
Q

What are the side effects of Cisplatin?

A

Renal toxicity, Ototoxicity

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52
Q

Carboplatin S/E

A

Myelosupression

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53
Q

Oxaliplatin s/e

A

neurotoxic, myelosupression

54
Q

What are antimetabolites?

A

are molecules that substitute for actual components of metabolic process

55
Q

Are antimetabolites cell cycle specific?

A

S-phase sepcific

56
Q

what drugs are part of the antimetabolites

A 
some end in "abine"
Fludarabine, Capecitabine, Cytarabine, Gemcitabine, 
Others
Methotrexate
5-FU
6-mercaptupurine or 6-MU
Leucovorin
57
Q

What is special about leucovorin?

A

special antimetabolite with NO anticancer action
reduced form of folic acid
2 Key uses:
reduces methorexate toxicity by rescuing normal cell
Increases 5-FU activity against colon cancer

58
Q

What are adverse effects of antimetabolites

A

capecitabine: hand and foot syndrome (PPE) use dexamethasone to treat PPE, Pulm toxicity, cerebellar toxicity
Mucositis, Myelosupression,
Pemetrexed: give B12 and folate to reduce adverse events

59
Q

where do Vinca alkaloids come from

A

periwinkle plant

60
Q

where do Taxanes come from

A

yew trees

61
Q

where do Epipodophyllotoxins come from

A

mayapple root

62
Q

where does camptothecins come from

A

camptothecin tree

63
Q

what is the MOA of vinca alkaloids?

A

inhibit tubulin polymerization required for microtuble assembly
-prevents microtuble formation

64
Q

What drugs are vinca alkaloids?

what cancers do they treat?

A

Vincristine-Neuroblastoma, Wilms tumor, Rhabdomyosarcoma
Vinblastine-Kaposi sarcoma, germcell cancer
Vinorelbine-ovary cancer

65
Q

What are the adverse effects of Vinca alkaloids

A 
Think "VAN"
 Vesicant (blisters) upon extravasation
Alopecia
Neurotoxic
Constipation
Myelosupression
66
Q

what is the MOA of the Taxanes

A

promoting microtubule formation
prevents spindle fibers from retracting
preventing disassembly of microtubules blocks completion of cell division and leads to cell death

67
Q

What drugs are part of Taxanes drug class?

A 
A taxane will always have an "A" before or after an "X"
Think PID C
Paclitaxel
Ixabepilone
Docetaxel
Cabazitaxel
68
Q

What cancers are Taxanes used for?

A

think “x” as in Sex since it treats both Ovary and Prostate

head, neck, esophagus, bladder, breast, lung

69
Q

what are the adverse effects of Taxanes?

A

Hypersensitivity reactions
Fluid retention
Peripheral neuropathy
myelosuppresison

70
Q

What is the MOA of Epipodophyllotoxins

A

inhibit DNA topoisomerase II

prevents proper unwinding of DNA resulting in blockade of DNA synthesis and cell division

71
Q

what drugs are part of the epipodophyllotoxins

A

Etoposide

Teniposide

72
Q

what cancer do epipodophyllotoxins treat

A

Etoposide: gastric, lung cancer, germ cancer
Teniposide: pediatric leukemia,

73
Q

what are the adverse effects of epipodophyllotoxins

A

hypotension
alopecia
myelosuppression

74
Q

what is the MOA of antitumor antibiotics

A

compounds derived from micro-organisms to compete with with other micro-organisms for resources

75
Q

what are examples of antitumor abx?

A 
Anthracyclines:
doxorubicin, daunorubicin
epirubicin, Idarubicin
Anthracenedione: 
Mitoxantrone 
mitocyin
bleomycin
76
Q

What is the MOA of anthracyclines?

A

Inhibit topisomerase 2
bind to DNA and interclate DNA strands
Generate free radicals
bind to cell membrane transport and alter fluid and ion transplant

77
Q

what is DNA intercalation

A

drug binds on both strands preventing DNA from being replicated

78
Q

how do free radicals work

A

very damaging to tissues by binding to metabolic products and disrupting cellular function

79
Q

what cancers do anthracyclines treat?
Doxorubicin
Epirubicin
Mitoxantrone

A

Doxorubicin: myeloma, breast, leukemia, lymphoma
Epirubicin: breast GI
Mitoxantrone: multiple sclerosis, prostate

80
Q

What are the adverse effects of anthracyclines?
What color does Mitoxantrone make your urine?
What color does Doxo/Dauno/Ida/Epi (icin) make your urine?

A

Cardiotoxicity, Vesicant, Alopecia
Mucositis, Myleosupression
Mitoxantrone turns urine blue/green
Doxo/dauno/ido/Epi- rubicins turn urine reddish orange

81
Q

what 2 forms of cadiotoxicity are there from anthracyclines

A

Acute: arrhythmias, pericarditis, myocarditis
Chronic: dose dependent causes cardiomyopathy increases with each dose

82
Q

What is the MOA of bleomycin

A

bind DNA and forms free radicals that destroy DNA and prevent DNA replication

83
Q

what cancer does bleomycin treat?

A

squamous cell cancer, germ cell tumors, head and neck cancer, lymphoma

84
Q

what is the MOA for Tyrosine kinases inhibitors?

A

inhibit tyrosine kinases and block specific regulatory pathway and promote cancer cell death through apoptosis

85
Q

what drugs are part of the TKI?

A

anything that ends in “inib”

86
Q

what are the differences between TKI?

A

target different TK that vary in level and activity in different cancers
differ in binding affinity to their targets making some more potent
differ in binding affinity to their targets allowing some to bind with less restriction

87
Q

How is there resistance to TKI

A

they are developed to bind to specific amino acids located on the tyrosine kinases so a mutation in the amino acid sequence could prevent TKI from binding and make the drug ineffective

88
Q

What cancers do TKI treat

A 
Imatinib/dasatini/nilotinib/bosutinib/ponatinib: Ph+ CML & ALL
Erlotinib: lung and pancreatic
Sorafenib: renal cell cancer
Sunitinib: renal cell cancer
Lapatinib: breast cancer
Crizotinib and Gefinitib: lung
89
Q

What are the adverse effects of TKI

A 
CHF
Myalgias
Fluid retention
Diarrhea
fatigue 
rash & myelosuppression
90
Q

What type of drug interactions do TKI inhibitors have

A

CYP450 metabolized
azoles can decrease metabolism and increase S/E
Phenytoin can Increase metabolism and decrease effectiveness
reduced bioavailability with use of PPI and H2

91
Q

Immunomodulators MOA

A

may alter tumor necrosis factor levels
may increase activity of NK cells, IL-2 and interferons
may promote apoptosis

92
Q

What cancer are immunomodulators used to treat?

A

multiple myeloma

93
Q

what drugs are part of the immunomodulator class

A

end in “alidomide”
Thalidomide
Lenalidomide
Pomalidomide

94
Q

what are the adverse effects of immunomodulators

A 
Thromboembolism
Peripheral neuropathy
Myelosuppression
Rash
Fatigue
95
Q

what is the MOA of proteasome inhibitors?

A

inhibit complexes of proteins that would other wise break down unneeded or damaged proteins
-promoted activation of signaling pathways that trigger apoptosis

96
Q

what are proteasome inhibitors used to treat

A

myltiple myeloma

97
Q

what drugs are parts of the proteasome inhibitor class?

A

Bortezomib

Carfilzomib need antiviral prophylaxis for both drugs

98
Q

what are the adverse drug Rxn of protaesome inhibitors

A 
Avtivation of herpes zoster
Heart failure
Pulmonary toxicity
Peripheral neuropathy
Neuralgia
99
Q

what is the MOA of monoclonal antibodies?

A

specially designed antibodies target specific proteins in cancer cells and block their standard function, bind to EGFR, HER2, CD antigens

100
Q

what drugs are part of monoclonal antibodies?

A

end in “mab”

101
Q

what is the target subsystem if the monoclonal antibodies have -t(u), c(i)
zu?, mu?

A

t(u)= tumor
c(i)=circulatory
zu= humanized
mu=mouse

102
Q

what is rituximab used to treat?

A

CD20+ lymphoma

103
Q

what does Tarstuzumab treat?

side effect?

A

HER2/neu overexpressing breast cancer

Heart Failure

104
Q

what does cetuximab treat?

Side effect?

A

colorectal cancer, head & neck cancer, lung cancer

hypomagnesmia, interstitial lung dz

105
Q

what does panitumumab treat?

side effects

A

colorectal cancer

hypomagnesmia, interstitial lung dz

106
Q

what does bevacizumab treat?

side effects

A

Renal cell cancer, breast, lung, colorectal

arterial thromboembolic events, delayed wound healing, GI perforation

107
Q

what is the MOA of asparaginase?

A

enzyme antineoplastic agent
breaks down asparagine to aspartate
it deprives tumor of the amino acid asparagine leading to cell stress and apoptosis

108
Q

what are the forms of asparaginase?

A

E coli asparaginase (MC)- daily
PEG-aspargase (bound to antifreeze) every 2 wks
ERwinia asparaginase (from erwinina yeast) when allergic to ecoli tx

109
Q

what cancer do asparaginase treat?

A

ALL

110
Q

what are the adverse effects of asparaginase

A

Pancreatitis
clotting/ bleeding disorders
Neuro tox
Hypersensitivity

111
Q

what are key points about chemo?

A

not all chemo is active against all cancers

multiple phases of in vitro, animal and human trial are required to determine that chemo is effective

112
Q

what is the goal of Phase I of a trial?

A

Assess Safety
Also assess dose ranges, chedule and efficacy. ~10-20 patients who have not responded to other treatments. Usually test agents in multiple cancer.

113
Q

what is the goal of Phase II of a clinical trial?

A

assess efficacy
also assess safety and dosing.
Larger trial with more patients (20-40 or more) focus effect in patient with specific cancers who have not responded to other therapy

114
Q

what is the goal of Phase III of a clinical trial

A

assess efficacy compared to standard treatment
Also assess safety
Larger than phase II trails enroll pts who are at the stage of a specific dz which approval will be sought

115
Q

ALL quick hits

A

more common in kids
3 stages of therapy (induction=remission, consolidation, maintenance)
uses intrathecal chemo for spread to CNS
good chance for a cure

116
Q

AML quick hits

A

more common in adults
2 stages (induction&consolidation)
7+3 regimen Cytrabine +daunorubicin/idarubicin
consolidation used to kill any remaining cancer

117
Q

CML quick hits

A

Philadelphia chromosome- think of the M-Maureen who is from philly
3 stages of dz (chronic, accelerated, blast crisis)
BRC-ABL d/t new chromosome
TKI used to control dz
SCT is only known cure

118
Q

CLL quick hits

A

seen in elderly pts
no tx till symptoms progress
Tx aimed at controlling symptoms and prolonging survival

119
Q

Hodgkins lymphoma

A

B-cell with presence of reed sternberg
might be related to EBV
B-symptoms-fever, night sweats, weight loss, lymphadenopathy
AVBD regimen

120
Q

non-hodgkins quick hits

A

B symptoms lyphadenopathy with NO REED STERNBERG CELLS
CHOP or RCHOP
only use rituximab if CD20+

121
Q

myltiple myeloma quick hits

A 
malignant plasma cells produce abnormal antibody fragments and ctokines
causes bone lesions, renal damage, and anemia
Only stage 2 and 3 get Tx
Common options: Immunomodulators
Protease inhibitors
Steroids
Traditional chemo
requires pain and anemia Tx
Use bisphosphonates to control lesions
122
Q

Breast cancer quick hits

A

affects both men and women
Tx is based on stage and pre/post menopausal status
Test for estrogen receptors on cancer due to hormone sensitive nature of the cancer cells
Cure is possible in all stages but IV
use trastuzumab only if HER2/neu overexpressed
Tx could include surgery/XRT/chemo or hormonal

123
Q

prostate cancer quick hits

A

common in elderly men
Tx options: Hormonal therapy( leuprolide, goserelin, degarelix, bicalutimide, flutamide)
Chemo (mitoxantrone, paclitaxel, docetaxel)
Brachytherapy (radioactive seeds implanted in prostate)
surgical castration
monitor PSA and androgen levels for response to therapy

124
Q

Colorectal cancer quick hits

A

most common GI cancer
Tx regimens: FOLFOX: 5-FU, leucovorin and oxaliplatin
FOLFIRI: 5-FU, leucovorin and irinotecan

125
Q

lung cancer quick hits

A

types small cell and non-small cell
Tx options surgery,XRT, chemo
Chemo choices: cisplatin or Carboplatin with paclitaxel, vinorelbine, pemetrexed, gemcitabine, bevacizumab

126
Q

ovarian cancer quick hits

A 
typically slow growing and difficult to detect until later stages of dz
Chemo option: 
paclitaxel with cisplatin/carboplatin
topotecan
Altertamine
Lipsomal doxorubicin
127
Q

testicular cancer quick hits

A 
younger pop than most solid tumor (20-40's)
Tx options surgery, radiation, chemo
Chemo combo's
BEP: bleomycin, eptoposide
ICE: Ifosfamide, cisplatin, eptoposide
128
Q

malignant melonoma quick hits

A

skin cancer
curable in early stages with surgery, early detection is very important
Chemo tx aim to prolong survival
dacarbazine, tenozolomide, cisplatin, aldesleukin (IL-2)

129
Q

brain cancer quick hits

A

multiple types: glioblastoma multiforme, oligodendroglioma, astrocytoma
Tx options: surgery, XRT, chemo
Chemo must be able to cross BBB: carmustine, lomustine, temozolomide

130
Q

secondary malignancies quick hits

A

occur d/t previous exposure tx
(XRT or chemo) for other caners
Acute leukemia or Lymphoma are most common secondary
harder to treat than de novo cancer
can occur years after cured of primary
Associated with alkylating agents and eptoposide

Pharm III Heme/Onc (2 decks)

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