Oncology Flashcards
1
Q
Cancer is the ____ leading cause of death in the US
A
2nd
2
Q
what are the 5 most common types of cancer
A
breast, prostate, lung, colon, lymphoma
3
Q
what are the 5 most common types of CANCER DEATH
A
lung, colon, breast, prostate and pancreas
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
5
Q
Why does cancer occur?
A
DNA is susceptible to changes
Exposure to chemical, radiation, viruses or unknown can cause mutations
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
7
Q
How is cancer named
A
after site of origin or tissue type
8
Q
what are the types of cancer
A
Solid tumors
Hematologic
9
Q
what is a primary tumor
A
original mass of cancer cells of a solid tumor in a body organ
10
Q
metastasize
A
spread of cancer from primary tumor to body sites
11
Q
benign tumor
A
are abnormal tumor growths but are not as invasive as malignant tumors and are not always fatal
12
Q
what are the 2 types of localized therapies?
A
surgery
radiation
13
Q
what are the types of systemic therapies
A
chemo traditional chemo monoclonal antibodies targeted agents Immunomodulation
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
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
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
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
18
Q
What are the targets of traditional chemotherapy
A
DNA,RNA, DNA polymerase, topoisomerases, spindle fiber formation
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
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
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
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
23
Q
what is 1st line primary therapy
A
used in advanced cancer cases in which other treatments would not be effective
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
25
what is adjuvant chemo
used after local therapies to improve their long term effect by eliminating any remaining undetected cancer cells
26
Why is dosing so important in chemotherapy use?
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
27
How is dose density used as a strategy of chemo used?
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
28
what are the 3 prognosis of cancer treatment
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
29
what is remission/complete response
unable to detect cancer
30
what is a cure in terms of cancer
prolonged period of remission usually 5 years
31
what is a partial response
reduction in tumor burden but cancer still present
32
what is treatment failure/ progressive disease
cancer continues to grow despite treatment
33
how is response to Tx determined
PE
Radiographic test
tumor markers
Biopsies
34
what is chemotherapy resistance
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
35
what are options if primary tx is not working
salvage Tx- uses other combinations of chemo drugs
| stem cell transplant
36
what is an Autologous SCT
high dose chemo is followed by re-infusion of pts stem cells
37
what is alloogeneic SCT
use of chemotherapy and immune modulation infusion of donor stem cells where pt get a new immune system
38
How do older chemo agents work
use various mechanism to block cell division
39
how do newer chemo agents work
taget specific functions of cancer cells that make the cancer cells cancerous
40
What do Alkylating agents target
DNA/RNA
| they tranfer an alkylating group to other molecules
41
which molecules do alkylating agents target
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
42
Which drugs are part of the alkylating agents class
Cyclophosphamide
Melphalan
Procarbazine
43
what types of cancer is cyclophosphamide used to treat
alkylating agent
| Breast cancer, Leukemia, Lymphoma, Myeloma
44
what is meplhalan used to treat
Myeloma
45
what is procarbazine used to treat
lymphoma
46
what are the adverse effects of Alkylating agents
```
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
```
47
what is the MOA of platinum analogs
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
48
what drugs are part of Platinum analogs
all have "platin" in their name
Oxaliplatin
Cisplatin
Carboplatin
49
what cancers do Cisplatin and Carboplatin analogs treat
Lung, Esophagus, Testicular, Ovary, Neck, Bladder, Head
50
what cancer does Oxaliplatin treat
Think of a PEC like a kiss and you sign a card "XO"
| pancreatic, esophageal, colorectal
51
What are the side effects of Cisplatin?
Renal toxicity, Ototoxicity
52
Carboplatin S/E
Myelosupression
53
Oxaliplatin s/e
neurotoxic, myelosupression
54
What are antimetabolites?
are molecules that substitute for actual components of metabolic process
55
Are antimetabolites cell cycle specific?
S-phase sepcific
56
what drugs are part of the antimetabolites
```
some end in "abine"
Fludarabine, Capecitabine, Cytarabine, Gemcitabine,
Others
Methotrexate
5-FU
6-mercaptupurine or 6-MU
Leucovorin
```
57
What is special about leucovorin?
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
What are adverse effects of antimetabolites
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
where do Vinca alkaloids come from
periwinkle plant
60
where do Taxanes come from
yew trees
61
where do Epipodophyllotoxins come from
mayapple root
62
where does camptothecins come from
camptothecin tree
63
what is the MOA of vinca alkaloids?
inhibit tubulin polymerization required for microtuble assembly
-prevents microtuble formation
64
What drugs are vinca alkaloids?
| what cancers do they treat?
Vincristine-Neuroblastoma, Wilms tumor, Rhabdomyosarcoma
Vinblastine-Kaposi sarcoma, germcell cancer
Vinorelbine-ovary cancer
65
What are the adverse effects of Vinca alkaloids
```
Think "VAN"
Vesicant (blisters) upon extravasation
Alopecia
Neurotoxic
Constipation
Myelosupression
```
66
what is the MOA of the Taxanes
promoting microtubule formation
prevents spindle fibers from retracting
preventing disassembly of microtubules blocks completion of cell division and leads to cell death
67
What drugs are part of Taxanes drug class?
```
A taxane will always have an "A" before or after an "X"
Think PID C
Paclitaxel
Ixabepilone
Docetaxel
Cabazitaxel
```
68
What cancers are Taxanes used for?
think "x" as in Sex since it treats both Ovary and Prostate
| head, neck, esophagus, bladder, breast, lung
69
what are the adverse effects of Taxanes?
Hypersensitivity reactions
Fluid retention
Peripheral neuropathy
myelosuppresison
70
What is the MOA of Epipodophyllotoxins
inhibit DNA topoisomerase II
| prevents proper unwinding of DNA resulting in blockade of DNA synthesis and cell division
71
what drugs are part of the epipodophyllotoxins
Etoposide
| Teniposide
72
what cancer do epipodophyllotoxins treat
Etoposide: gastric, lung cancer, germ cancer
Teniposide: pediatric leukemia,
73
what are the adverse effects of epipodophyllotoxins
hypotension
alopecia
myelosuppression
74
what is the MOA of antitumor antibiotics
compounds derived from micro-organisms to compete with with other micro-organisms for resources
75
what are examples of antitumor abx?
```
Anthracyclines:
doxorubicin, daunorubicin
epirubicin, Idarubicin
Anthracenedione:
Mitoxantrone
mitocyin
bleomycin
```
76
What is the MOA of anthracyclines?
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
what is DNA intercalation
drug binds on both strands preventing DNA from being replicated
78
how do free radicals work
very damaging to tissues by binding to metabolic products and disrupting cellular function
79
what cancers do anthracyclines treat?
Doxorubicin
Epirubicin
Mitoxantrone
Doxorubicin: myeloma, breast, leukemia, lymphoma
Epirubicin: breast GI
Mitoxantrone: multiple sclerosis, prostate
80
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?
Cardiotoxicity, Vesicant, Alopecia
Mucositis, Myleosupression
Mitoxantrone turns urine blue/green
Doxo/dauno/ido/Epi- rubicins turn urine reddish orange
81
what 2 forms of cadiotoxicity are there from anthracyclines
Acute: arrhythmias, pericarditis, myocarditis
Chronic: dose dependent causes cardiomyopathy increases with each dose
82
What is the MOA of bleomycin
bind DNA and forms free radicals that destroy DNA and prevent DNA replication
83
what cancer does bleomycin treat?
squamous cell cancer, germ cell tumors, head and neck cancer, lymphoma
84
what is the MOA for Tyrosine kinases inhibitors?
inhibit tyrosine kinases and block specific regulatory pathway and promote cancer cell death through apoptosis
85
what drugs are part of the TKI?
anything that ends in "inib"
86
what are the differences between TKI?
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
How is there resistance to TKI
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
What cancers do TKI treat
```
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
What are the adverse effects of TKI
```
CHF
Myalgias
Fluid retention
Diarrhea
fatigue
rash & myelosuppression
```
90
What type of drug interactions do TKI inhibitors have
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
Immunomodulators MOA
may alter tumor necrosis factor levels
may increase activity of NK cells, IL-2 and interferons
may promote apoptosis
92
What cancer are immunomodulators used to treat?
multiple myeloma
93
what drugs are part of the immunomodulator class
end in "alidomide"
Thalidomide
Lenalidomide
Pomalidomide
94
what are the adverse effects of immunomodulators
```
Thromboembolism
Peripheral neuropathy
Myelosuppression
Rash
Fatigue
```
95
what is the MOA of proteasome inhibitors?
inhibit complexes of proteins that would other wise break down unneeded or damaged proteins
-promoted activation of signaling pathways that trigger apoptosis
96
what are proteasome inhibitors used to treat
myltiple myeloma
97
what drugs are parts of the proteasome inhibitor class?
Bortezomib
| Carfilzomib need antiviral prophylaxis for both drugs
98
what are the adverse drug Rxn of protaesome inhibitors
```
Avtivation of herpes zoster
Heart failure
Pulmonary toxicity
Peripheral neuropathy
Neuralgia
```
99
what is the MOA of monoclonal antibodies?
specially designed antibodies target specific proteins in cancer cells and block their standard function, bind to EGFR, HER2, CD antigens
100
what drugs are part of monoclonal antibodies?
end in "mab"
101
what is the target subsystem if the monoclonal antibodies have -t(u), c(i)
zu?, mu?
t(u)= tumor
c(i)=circulatory
zu= humanized
mu=mouse
102
what is rituximab used to treat?
CD20+ lymphoma
103
what does Tarstuzumab treat?
| side effect?
HER2/neu overexpressing breast cancer
| Heart Failure
104
what does cetuximab treat?
| Side effect?
colorectal cancer, head & neck cancer, lung cancer
| hypomagnesmia, interstitial lung dz
105
what does panitumumab treat?
| side effects
colorectal cancer
| hypomagnesmia, interstitial lung dz
106
what does bevacizumab treat?
| side effects
Renal cell cancer, breast, lung, colorectal
| arterial thromboembolic events, delayed wound healing, GI perforation
107
what is the MOA of asparaginase?
enzyme antineoplastic agent
breaks down asparagine to aspartate
it deprives tumor of the amino acid asparagine leading to cell stress and apoptosis
108
what are the forms of asparaginase?
E coli asparaginase (MC)- daily
PEG-aspargase (bound to antifreeze) every 2 wks
ERwinia asparaginase (from erwinina yeast) when allergic to ecoli tx
109
what cancer do asparaginase treat?
ALL
110
what are the adverse effects of asparaginase
Pancreatitis
clotting/ bleeding disorders
Neuro tox
Hypersensitivity
111
what are key points about chemo?
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
what is the goal of Phase I of a trial?
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
what is the goal of Phase II of a clinical trial?
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
what is the goal of Phase III of a clinical trial
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
ALL quick hits
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
AML quick hits
more common in adults
2 stages (induction&consolidation)
7+3 regimen Cytrabine +daunorubicin/idarubicin
consolidation used to kill any remaining cancer
117
CML quick hits
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
CLL quick hits
seen in elderly pts
no tx till symptoms progress
Tx aimed at controlling symptoms and prolonging survival
119
Hodgkins lymphoma
B-cell with presence of reed sternberg
might be related to EBV
B-symptoms-fever, night sweats, weight loss, lymphadenopathy
AVBD regimen
120
non-hodgkins quick hits
B symptoms lyphadenopathy with NO REED STERNBERG CELLS
CHOP or RCHOP
only use rituximab if CD20+
121
myltiple myeloma quick hits
```
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
Breast cancer quick hits
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
prostate cancer quick hits
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
Colorectal cancer quick hits
most common GI cancer
Tx regimens: FOLFOX: 5-FU, leucovorin and oxaliplatin
FOLFIRI: 5-FU, leucovorin and irinotecan
125
lung cancer quick hits
types small cell and non-small cell
Tx options surgery,XRT, chemo
Chemo choices: cisplatin or Carboplatin with paclitaxel, vinorelbine, pemetrexed, gemcitabine, bevacizumab
126
ovarian cancer quick hits
```
typically slow growing and difficult to detect until later stages of dz
Chemo option:
paclitaxel with cisplatin/carboplatin
topotecan
Altertamine
Lipsomal doxorubicin
```
127
testicular cancer quick hits
```
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
malignant melonoma quick hits
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
brain cancer quick hits
multiple types: glioblastoma multiforme, oligodendroglioma, astrocytoma
Tx options: surgery, XRT, chemo
Chemo must be able to cross BBB: carmustine, lomustine, temozolomide
130
secondary malignancies quick hits
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
