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ABSITE 2019-RM > Chapter 11: Oncology > Flashcards

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; defects 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
Q

Half life: AFP

A

5 days

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26
Q

Two components of cancer transformation

A
  1. Heritable alteration in genome and;

2. Loss of growth regulation

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27
Q

Oncogenesis: time between exposure and formation of clinically detectable tumor

A

Latency period

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28
Q

Three phases of latency period

A
  1. Initiation (carcinogen acts with DNA)
  2. Promotion (then occurs)
  3. Progression (cancers cells to clinically detectable tumor)
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29
Q

What can neoplasms arise from?

A

Carcinogenesis (e.g. smoking)
Viruses (eg, EBV)
Immunodeficiency (eg HIV)

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30
Q

What do retroviruses contain?

A

Oncogenes

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31
Q

Associated with Burkitt’s lymphoma (8:14 translocation) and nasopharyngeal CA (c-myc)

A

Ebstein-Barr Virus

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32
Q

Human genes with malignant potential

A

Proto-oncogenes

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33
Q

Infectious agent: cervical cancer

A

Human papillomavirus

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34
Q

Infectious agent: gastric cancer

A

Helicobacter pylori

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35
Q

Infectious agent: hepatocellular carcinoma

A

Hepatitis B and hepatitis C viruse

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36
Q

Infectious agent: nasopharyngeal carcinoma

A

EBV

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37
Q

Infectious agent: Burkitt’s lymphoma

A

EBV

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38
Q

Infectious agent: various lymphomas

A

HIV

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39
Q

Most vulnerable stage of cell cycle for XRT

A

M phase

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40
Q

Radiation therapy: what causes most of the damage?

A

Most damage done by formation of oxygen radicals -> maximal effect with high oxygen levels

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41
Q

Main target of radiation therapy

A

DNA: oxygen radicals and XRT itself damage DNA and other molecules

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42
Q

How does high-eneregy radiation have a skin–preserving effect?

A

Maximal ionizing potential not reached until deeper structures

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43
Q

What do fractionate XRT doses allow?

A
  • Repair of normal cells
  • Re-oxygenation of tumor
  • Redistribution of tumor cells in the cell cycle
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44
Q

Very radiosensitive tumors

A

Seminomas, lymphomas

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45
Q

Very radio resistant tumors

A

Epithelial, sarcomas

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46
Q

Less responsive to XRT due to lack of oxygen in the tumor

A

Large tumors

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47
Q

Source of radiation in or next to tumor (Au-198, I-128); delivers high, concentrated doses of radiation

A

Brachytherapy

48
Q

Chemo Agent: exhibit plateau in cell-killing ability

A

Cell cycle-specific agents (5FU, methotrexate)

49
Q

Chemo Agent: Linear response to cell killing

A

Cell cycle-nonspecific agents

50
Q

Chemo Agent: Decreases short-term (5 year) risk of breast CA 45%

A

Tamoxifen (blocks estrogen receptor)

51
Q

Complications: tamoxifen therapy

A

1% risk of blood clots

0.1 % risk of endometrial cancer

52
Q

Chemo Agent: promotes microtubule formation and stabilization that cannot be broken down; cells are ruptures

53
Q

Chemo Agent: can cause pulmonary fibrosis

A

Bleomycin

Busulfan

54
Q

Chemo Agent: nephrotoxic, neurotoxic, ototoxic

A

Cisplatin (platinum alkylating agent)

55
Q

Chemo Agent: bone (myelo) suppression

A

Carboplatin (platinum alkylating agent) and

Vinblastine (microtubule inhibitor)

56
Q

Chemo Agent: peripheral neuropathy, neurotoxic

A

Vincristine (microtubule inhibitor)

57
Q

Chemo Agent: transfer alkyl groups; forms covalent bonds to DNA

A

Alkylating agents

58
Q

Chemo Agent: Acrolein is the active metabolite.

- Side effects: gonadal dysfunction, SIADH, hemorrhagic cystitis

A

Cyclophosphamide

59
Q

Tx: hemorrhagic cystitis s/t cyclophosphamide

60
Q

Chemo Agent: antihelminthic drug though to stimulate immune system against cancer

A

Levamisole

61
Q

Chemo Agent: inhibits dihydrofolate reductase (DHFR), which inhibits purine and DNA synthesis
- Side effects: renal toxicity, radiation recall

A

Methotrexate

62
Q

Reverses effects of methotrexate by re-supplying folate

A

Leucovorin rescue (folinic acid)

63
Q

Chemo Agent: inhibits thymidylate synthetase, which inhibits purine and DNA syntehsis

A

5-fluorouracil (5FU)

64
Q

Increases toxicity of 5-fluorouracil

A

Leucovorin (folinic acid)

65
Q

Chemo Agent: DNA intercalator, oxygen radical formation

A

Doxorubicin

66
Q

Side effects: doxorubicin

A

Heart toxicity secondary to oxygen radicals at total doses > 500 mg/m^2.

67
Q

Chemo Agent: inhibits topoisomerase (which normally unwinds DNA)

A

Etoposide (VP-16)

68
Q

Chemo Agents: least myelosuppression

A

Bleomycin, vincristine, busulfan, cisplatin

69
Q

Used for neutrophil recovery after chemo; side effects - Sweet’s syndrome (acute febrile neutropenic dermatitis)

A

GCSF (granulocyte colony-stimulating factor

70
Q

Acute febrile neutropenic dermatitis

A

Sweet’s syndrome

71
Q

When to consider resection of a normal organ to prevent cancer -> breast

A

BRCA I or II with strong family history

72
Q

When to consider resection of a normal organ to prevent cancer -> thyroid

A

RET proto-oncogene with family history thyroid cancer

73
Q

Tumor suppressor gene: chromosome 13; involved in cell cycle regulation

A

Retinoblastoma

74
Q

Tumor suppressor gene: chromosome 17; involved in cell cycle

75
Q

Normal gene induces cell cycle arrest and apoptosis; abnormal gene allows unrestrained cell growth

76
Q

Tumor suppressor gene: chromosome 5, involved with cell cycle regulation and movement

77
Q

Tumor suppressor gene: chromosome 18; involved in cell adhesion

78
Q

Tumor suppressor gene: involved in apoptosis (programmed cell death)

79
Q

Chromosome: p53

80
Q

Chromosome: APC

81
Q

Chromosome: DCC

82
Q

Proto-oncogene: G protein defect

A

ras proto-oncogene

83
Q

Proto-oncogene: tyrosine kinase defect

A

src proto-oncogene

84
Q

Proto-oncogene: platelet-derived growth factor receptor defect

A

sis proto-oncogene

85
Q

Proto-oncogene: epidermal growth factor receptor defect

A

erb B proto-oncogene

86
Q

Proto-oncogene: proto-oncogenes - transcription factors

A

myc (c-myc, n-myc, l-myc)

87
Q

Defect in p53 gene -> patients get childhood sarcomas, breast CA, brain tumors, leukemia, adrenal CA

A

Li-Fraumeni syndrom

88
Q
  • 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
A

Colon cancer

89
Q

Carcinogens: coal tar

A

Larynx, skin, bronchial CA

90
Q

Carcinogens: beta-naphthylamine

A

Urinary tract CA (bladder CA)

91
Q

Carcinogens: benzene

92
Q

Carcinogens: asbestos

A

Mesothelioma

93
Q

DDX: suspicious supraclavicular node

A

Neck, breast, lung, stomach (Virchow’s node), pancreas

94
Q

DDX: suspicious axillary node

A

Lymphoma (#1), breast, melanoma

95
Q

DDX: suspicious periumbilical node

A

Pancreas (Sister Mary Joseph’s node)

96
Q

DDx: ovarian metastases

A

Breast (#1), prostate

97
Q

DDx: skin metastases

A

Breast, melanoma

98
Q

DDx: small bowel metastases

A

Melanoma (#1)

99
Q

Clinical trials:

  • Phase 1
  • Phase 2
  • Phase 3
  • Phase 4
A
  • 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
Q

What is induction therapy?

A

Sole treatment; use for advanced disease or when no other treatment exists

101
Q

What is primary therapy?

A

(Neoadjuvant) - chemo give 1st (usually), followed by another (secondary) therapy

102
Q

What is adjuvant therapy?

A

Combined with another modality; given after other therapy is used

103
Q

What is salvage therapy?

A

For tumors that final to respond to initial chemotherapy

104
Q

Have poor barrier function -> better to view them as signs of probably metastasis

A

Lymph nodes

105
Q

Can be attempted for some tumors (colon into uterus, adrenal into liver, gastric into spleen); aggressive local invasiveness is different from metastatic disease

A

En bloc multiorgan resection

106
Q

Tx: tumors of hollow visit causing obstruction or bleeding (colon Ca), breast CA with skin or chest wall involvement

A

Palliative surgery

107
Q

No role in patients with clinically palpable nodes; you need to get after and sample these nodes

A

Sentinel lymph node biopsy

108
Q

35% 5-year survival rate if successfully resected

A

Colon metastases to the liver

109
Q

Prognostic indictors for survival after resection of hepatic colorectal metastases

A

Disease-free interval > 12 months, tumor number

110
Q

Most successfully cured metastases with surgery

A

Colon CA in liver, sarcoma to the lung, but survival still low overall for these

111
Q

One of the few tumors for which surgical debunking improves chemotherapy (not seen in other tumors)

A

Ovarian CA

112
Q

Curable solid tumors with chemotherapy only

A

Hodgkin’s and non-Hodgkin’s lymphoma

113
Q

T cell lymphomas

A 
HTLV-1 (skin lesions)
Mycosis fubgoides (Sezary cells)
114
Q

HIV related malignancies

A

Kaposi’s sarcoma, non-Hodgkin’s lymphoma

115
Q

Causes angiogenesis; involved in tumor metastasis

A

V-EGF (Vascular epidermal growth factor)

ABSITE 2019-RM (33 decks)

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