Chapter 11: Oncology Flashcards

1
Q

2 cause of death in the United States

A

Cancer

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2
Q

MC Ca in women

A

Breast cancer

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3
Q

MCC cancer related death in women

A

Lung cancer

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4
Q

MC Cancer in men

A

Prostate cancer

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5
Q

Used to identify metastases; detects fluorodeoxyglucose molecules

A

PET (positron emission tomography)

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6
Q

Need MHC complex to attack tumor

A

Cytotoxic T cells

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7
Q

Can independently attack tumor cells

A

Natural killer cells

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8
Q

Are random unless viral-induced tumor

A

Tumor antigens

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9
Q

Increased numbers of cells

A

Hyperplasia

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10
Q

Replacement of one tissue with another (GERD squamous epithelium in esophagus changed to columnar gastric tissue; e.g. Barrett’s esophagus)

A

Metaplasia

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11
Q

Altered size, shape, and organization (e.g., Barrett’s dysplasia)

A

Dysplasia

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12
Q

Tumor marker: colon ca

A

CEA

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13
Q

Tumor marker: liver CA

A

AFP

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14
Q

Tumor marker: pancreatic CA

A

CA 19-9

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15
Q

Tumor marker: Ovarian ca

A

CA 125

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16
Q

Tumor marker: testicular Ca, choriocarcinoma

A

Beta-HCG

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17
Q

Tumor marker: prostate CA

A

PSA

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18
Q

Prostate CA: thought to be tumor marker with the highest sensitivity, although specificity is low

A

PSA

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19
Q

Tumor marker: small cell lung CA, neuroblastoma

A

NSE

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20
Q

Tumor marker: breast CA

A

BRCA I and II

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21
Q

Tumor marker: carcinoid tumor

A

Chromogranin A

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22
Q

Tumor marker: thyroid medullary CA

A

Ret oncogene

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23
Q

Half life: CEA

A

18 days

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24
Q

Half life: PSA

A

18 days

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25
Half life: AFP
5 days
26
Two components of cancer transformation
1. Heritable alteration in genome and; | 2. Loss of growth regulation
27
Oncogenesis: time between exposure and formation of clinically detectable tumor
Latency period
28
Three phases of latency period
1. Initiation (carcinogen acts with DNA) 2. Promotion (then occurs) 3. Progression (cancers cells to clinically detectable tumor)
29
What can neoplasms arise from?
Carcinogenesis (e.g. smoking) Viruses (eg, EBV) Immunodeficiency (eg HIV)
30
What do retroviruses contain?
Oncogenes
31
Associated with Burkitt's lymphoma (8:14 translocation) and nasopharyngeal CA (c-myc)
Ebstein-Barr Virus
32
Human genes with malignant potential
Proto-oncogenes
33
Infectious agent: cervical cancer
Human papillomavirus
34
Infectious agent: gastric cancer
Helicobacter pylori
35
Infectious agent: hepatocellular carcinoma
Hepatitis B and hepatitis C viruse
36
Infectious agent: nasopharyngeal carcinoma
EBV
37
Infectious agent: Burkitt's lymphoma
EBV
38
Infectious agent: various lymphomas
HIV
39
Most vulnerable stage of cell cycle for XRT
M phase
40
Radiation therapy: what causes most of the damage?
Most damage done by formation of oxygen radicals -> maximal effect with high oxygen levels
41
Main target of radiation therapy
DNA: oxygen radicals and XRT itself damage DNA and other molecules
42
How does high-eneregy radiation have a skin--preserving effect?
Maximal ionizing potential not reached until deeper structures
43
What do fractionate XRT doses allow?
- Repair of normal cells - Re-oxygenation of tumor - Redistribution of tumor cells in the cell cycle
44
Very radiosensitive tumors
Seminomas, lymphomas
45
Very radio resistant tumors
Epithelial, sarcomas
46
Less responsive to XRT due to lack of oxygen in the tumor
Large tumors
47
Source of radiation in or next to tumor (Au-198, I-128); delivers high, concentrated doses of radiation
Brachytherapy
48
Chemo Agent: exhibit plateau in cell-killing ability
Cell cycle-specific agents (5FU, methotrexate)
49
Chemo Agent: Linear response to cell killing
Cell cycle-nonspecific agents
50
Chemo Agent: Decreases short-term (5 year) risk of breast CA 45%
Tamoxifen (blocks estrogen receptor)
51
Complications: tamoxifen therapy
1% risk of blood clots | 0.1 % risk of endometrial cancer
52
Chemo Agent: promotes microtubule formation and stabilization that cannot be broken down; cells are ruptures
Taxol
53
Chemo Agent: can cause pulmonary fibrosis
Bleomycin | Busulfan
54
Chemo Agent: nephrotoxic, neurotoxic, ototoxic
Cisplatin (platinum alkylating agent)
55
Chemo Agent: bone (myelo) suppression
Carboplatin (platinum alkylating agent) *and* | Vinblastine (microtubule inhibitor)
56
Chemo Agent: peripheral neuropathy, neurotoxic
Vincristine (microtubule inhibitor)
57
Chemo Agent: transfer alkyl groups; forms covalent bonds to DNA
Alkylating agents
58
Chemo Agent: Acrolein is the active metabolite. | - Side effects: gonadal dysfunction, SIADH, hemorrhagic cystitis
Cyclophosphamide
59
Tx: hemorrhagic cystitis s/t cyclophosphamide
Mesna
60
Chemo Agent: antihelminthic drug though to stimulate immune system against cancer
Levamisole
61
Chemo Agent: inhibits dihydrofolate reductase (DHFR), which inhibits purine and DNA synthesis - Side effects: renal toxicity, radiation recall
Methotrexate
62
Reverses effects of methotrexate by re-supplying folate
Leucovorin rescue (folinic acid)
63
Chemo Agent: inhibits thymidylate synthetase, which inhibits purine and DNA syntehsis
5-fluorouracil (5FU)
64
Increases toxicity of 5-fluorouracil
Leucovorin (folinic acid)
65
Chemo Agent: DNA intercalator, oxygen radical formation
Doxorubicin
66
Side effects: doxorubicin
Heart toxicity secondary to oxygen radicals at total doses > 500 mg/m^2.
67
Chemo Agent: inhibits topoisomerase (which normally unwinds DNA)
Etoposide (VP-16)
68
Chemo Agents: least myelosuppression
Bleomycin, vincristine, busulfan, cisplatin
69
Used for neutrophil recovery after chemo; side effects - Sweet's syndrome (acute febrile neutropenic dermatitis)
GCSF (granulocyte colony-stimulating factor
70
Acute febrile neutropenic dermatitis
Sweet's syndrome
71
When to consider resection of a normal organ to prevent cancer -> breast
BRCA I or II with strong family history
72
When to consider resection of a normal organ to prevent cancer -> thyroid
RET proto-oncogene with family history thyroid cancer
73
Tumor suppressor gene: chromosome 13; involved in cell cycle regulation
Retinoblastoma
74
Tumor suppressor gene: chromosome 17; involved in cell cycle
p53
75
Normal gene induces cell cycle arrest and apoptosis; abnormal gene allows unrestrained cell growth
p53
76
Tumor suppressor gene: chromosome 5, involved with cell cycle regulation and movement
APC
77
Tumor suppressor gene: chromosome 18; involved in cell adhesion
DCC
78
Tumor suppressor gene: involved in apoptosis (programmed cell death)
bcl
79
Chromosome: p53
17
80
Chromosome: APC
5
81
Chromosome: DCC
18
82
Proto-oncogene: G protein defect
ras proto-oncogene
83
Proto-oncogene: tyrosine kinase defect
src proto-oncogene
84
Proto-oncogene: platelet-derived growth factor receptor defect
sis proto-oncogene
85
Proto-oncogene: epidermal growth factor receptor defect
erb B proto-oncogene
86
Proto-oncogene: proto-oncogenes - transcription factors
myc (c-myc, n-myc, l-myc)
87
Defect in p53 gene -> patients get childhood sarcomas, breast CA, brain tumors, leukemia, adrenal CA
Li-Fraumeni syndrom
88
- Gene involved in development include APC, p53, DCC, and K-ras - APC though to be initial step in evolution - Does not usually go to bone
Colon cancer
89
Carcinogens: coal tar
Larynx, skin, bronchial CA
90
Carcinogens: beta-naphthylamine
Urinary tract CA (bladder CA)
91
Carcinogens: benzene
Leukemia
92
Carcinogens: asbestos
Mesothelioma
93
DDX: suspicious supraclavicular node
Neck, breast, lung, stomach (Virchow's node), pancreas
94
DDX: suspicious axillary node
Lymphoma (#1), breast, melanoma
95
DDX: suspicious periumbilical node
Pancreas (Sister Mary Joseph's node)
96
DDx: ovarian metastases
Breast (#1), prostate
97
DDx: skin metastases
Breast, melanoma
98
DDx: small bowel metastases
Melanoma (#1)
99
Clinical trials: - Phase 1 - Phase 2 - Phase 3 - Phase 4
- Phase 1: Is it safe and at what dose? - Phase 2: Is it effective? - Phase 3: Is it better than existing therapy? - Phase 4: implementation and marketing
100
What is induction therapy?
Sole treatment; use for advanced disease or when no other treatment exists
101
What is primary therapy?
(Neoadjuvant) - chemo give 1st (usually), followed by another (secondary) therapy
102
What is adjuvant therapy?
Combined with another modality; given after other therapy is used
103
What is salvage therapy?
For tumors that final to respond to initial chemotherapy
104
Have poor barrier function -> better to view them as signs of probably metastasis
Lymph nodes
105
Can be attempted for some tumors (colon into uterus, adrenal into liver, gastric into spleen); aggressive local invasiveness is different from metastatic disease
En bloc multiorgan resection
106
Tx: tumors of hollow visit causing obstruction or bleeding (colon Ca), breast CA with skin or chest wall involvement
Palliative surgery
107
No role in patients with clinically palpable nodes; you need to get after and sample these nodes
Sentinel lymph node biopsy
108
35% 5-year survival rate if successfully resected
Colon metastases to the liver
109
Prognostic indictors for survival after resection of hepatic colorectal metastases
Disease-free interval > 12 months, tumor number
110
Most successfully cured metastases with surgery
Colon CA in liver, sarcoma to the lung, but survival still low overall for these
111
One of the few tumors for which surgical debunking improves chemotherapy (not seen in other tumors)
Ovarian CA
112
Curable solid tumors with chemotherapy only
Hodgkin's and non-Hodgkin's lymphoma
113
T cell lymphomas
``` HTLV-1 (skin lesions) Mycosis fubgoides (Sezary cells) ```
114
HIV related malignancies
Kaposi's sarcoma, non-Hodgkin's lymphoma
115
Causes angiogenesis; involved in tumor metastasis
V-EGF (Vascular epidermal growth factor)