Intro to Oncology Flashcards

1
Q

Top 3 new cases of CA for men and women?

A
  1. Prostate/Breast
  2. Lung and bronchus
  3. Colon and rectum
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2
Q

Top 3 CA deaths for men and women?

A
  1. Lung and bronchus
  2. Prostate/Breast
  3. Colon and rectum
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3
Q

What accounts for at least 30% of cancer deaths?

A

30%

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4
Q

What are some CA prevention strategies?

A
  1. Smoking cessation
  2. Smoking prevention
  3. Sun avoidance
  4. Dietary modifications
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5
Q

What % of American smokers began before age 18?

A

Over 80%

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6
Q

What % of high school students have tried smoking?

A

58%

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7
Q

Do people who quit smoking regardless of age live longer than those who continue to smoke?

A

YES

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8
Q

Qutting before age 50 cuts the risk of dying in the next 15 years by what?

A

50%

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9
Q

What cancers are 85-90% preventable with appropriate screening?

A
  1. Colorectal: Fecal occult blood testing and colonoscopy
  2. Cervical: Pap and pelvis
  3. Breast: Self-exams and mammography
  4. Prostate: DRE and PSA
  5. Oral Cavity: Visits
  6. Skin: Physical exam
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10
Q

What 4 things are part of the approach to CA dx?

A
  1. Careful history
  2. Careful physical exam
  3. Radiological imaging
  4. Tissue biopsy
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11
Q

What 4 things should be assessed when taking history?

A
  1. Underlying diseases
  2. Smoking and alcohol
  3. Occupational exposures
  4. Family history
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12
Q

How much tissue should be taken for biopsy?

A

As much as is safely possible

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13
Q

What 4 things are determined from a tissue biopsy?

A
  1. Histology
  2. Grade
  3. Degree of invasiveness
  4. Molecular diagnostic and prognostic information
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14
Q

What is it called when the entire tumor mass is removed with a margin of normal tissue surrounding the mass?

A

Excisional biopsy

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15
Q

What is it called when a wedge of tissue is removed trying to include the majority of the cross-sectional diameter of the tumor?

A

Incisional biopsy

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16
Q

How is a core needle biopsy usually done?

A

With endoscope or CT… smaller tissue sample

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17
Q

What gets a cell suspension from within the mass and is very limited sample… usually CT guided or direct palpation of mass?

A

Fine needle aspiration

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18
Q

What 3 things are used for clinical staging?

A
  1. Physical examination
  2. Imaging procedures like XR, CT, Isotope scans
  3. BM examination for some tumors
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19
Q

What is done to determine pathologic staging?

A

Histologic examination of all tissues removed at surgery

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20
Q

What does higher clinical stage correlate with?

A

Higher tumor burden and less curability

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21
Q

What does the stage usually dictate or mandate?

A

Specific treatments

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22
Q

What 2 things must be taken into account with prognosis and planning treatment?

A

Physiological reserve of the patient (age and karnofsky and ECOG performance scores) and molecular markers

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23
Q

Where is hematopoiesis week 2 to 12 of gestation?

A

Yolk sac

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24
Q

What is produced from the yolk sac?

A

Only RBC for oxygenation

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25
Q

Where is hematopoisis from week 6 of gestation until postnatal week 1?

A

Fetal liver and spleen

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26
Q

When does hematopoiesis peak in the fetal liver and spleen?

A

Months 3-6

-Declines after month 6 and ends shortly after birth

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27
Q

When does hematopoesis begin in the BM?

A

2-4 months gestation

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28
Q

What is the major site of hematopoiesis after month 6 gestation?>

A

BM

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29
Q

In infancy, where is hematopoeisis?

A

All bones

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30
Q

What happens to hematopoeisis in childhood and adolescence?

A

Progressive decrease of hematopoetic marrow in the long bones

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31
Q

At age 25 where is the extent of hematopoesis in long bones?

A

Only in the proximal quarter of femoral and humeral shafts

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32
Q

In adults, where is hematopoesis?

A

Central skeleton and proximal ends of the long bones

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33
Q

Why do we have hematopoeisis?

A

To replace normal losses and maintain hemostasis

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34
Q

What does the diversity of blood cells reflect?

A

Need for cells with highly specialized functions

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35
Q

What is the process that involves the development of unique biochemical, structural, and functional characteristics known as?

A

Differentiation

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36
Q

True or False: Differentiation is a one-way process

A

TRUE

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37
Q

What is for the replacement of normal loss of blood cells and amplification of the number of mature blood cells during times of stress?

A

Proliferation

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38
Q

What 4 things does differentiation result in?

A
  1. Oxygen carrying capacity: red blood cells/hemoglobin
  2. Hemostasis: platelets
  3. Innate Immunity: neutrophilic granulocytes and NK cells
  4. Adaptive Immunity: T- and B- lymphocytes
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39
Q

What is it called when there is inadequate production and too few blood cells develop?

A

Cytopenias

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40
Q

What is it called when there is excessive production or if there is replacement of marrow by tumor or fibrosis to too many blood cells develop?

A

Cytosis

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41
Q

What are 2 ways cytosis can happen?

A
  1. Expansion of hematopoiesis down the shaft of the long bones
  2. Extramedullary hematopoiesis in liver, spleen, lymph nodes
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42
Q

What cell initiates hematopoiesis?

A

Hematopoietic stem cell

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43
Q

What 2 things is a hematopoietic stem cell?

A
  1. Multipotent

2. Self-Renewing

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44
Q

Define multipotent

A

Can give rise to all other hematopoietic cells by differentiating into committed progenitor cells

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45
Q

Define self-renewing

A

Can replace itself. When a HSC divides at least one of the progeny cells remains a HSC.

46
Q

What differentiates a stem cell from any other cell?

A

Self-renewal capacity

47
Q

What is the ability to self-renew dependent on?

A

Intrinsic characteristics of the stem cell and on its interaction with the bone marrow microenvironment: the bone marrow niche.

48
Q

What is essential to confer self-renewal capacity to stem cells?

A

Both direct cell-cell contact between bone marrow microenvironment and the stem cell, as well as stimulation of stem cell receptors by cytokines and growth factors

49
Q

Are HSC normally quiescent?

A

YES

-This protects multipotency and acquisition of mutations that could lead to malignant transformation

50
Q

True or False: In extreme circumstances, HSC can leave marrow and migrate to other organs

A

TRUE

51
Q

What is the first commitment step resulting in lymphoid or myeloid progenitor cell (from a HSC)?

A

Lineage commitment

52
Q

What is further differentiation of a committed progenitor cell?

A

Differentiation commitment

53
Q

What has the capacity to self-replicate, proliferate, and differentiate to increasingly specialized progenitor cells which in turn generate the mature cells of the peripheral blood?

A

Common primitive stem cell

54
Q

What do progentior cells resemble?

A

Lymphocytes (they are difficult to recognize morphologically and proliferate in culture and form colonies)

55
Q

What is hematopoeisis regulated by?

A

Growth factors that usually act synergistically

56
Q

Early lineage division is between what?

A

Lymphoid and myeloid cells

57
Q

The early stages of hematopoeisis is confined where for both myeloid and lymphoid cells?

A

Bone marroe

58
Q

Where do myeloid cells undergo almost the entire maturation process?

A

Inside the BM

59
Q

Where to lymphoid cells undergo functional maturation?

A

Lymph nodes, thymus, and other sites

60
Q

What are the 4 WHO Classifications of Myeloid Neoplasms?

A
  1. Acute Myeloid Leukemia (AML)
  2. Myelodysplastic Syndromes (MDS)
  3. Myelodysplastic/Myeloproliferative Neoplasms (MDS/MPN)
  4. Myeloproliferative Neoplasms (MPN)
61
Q

Which myeloid neoplasm is mostly a problem of abnormal differentiation (qualitative)?

A

MDS

62
Q

Which myeloid neoplasm is excessive proliferation with normal differentiation (quantitative)?

A

MPN

63
Q

Which myeloid neoplams is excessive proliferation and maturation arrest (qualitative and quantitiative)?

A

AML

64
Q

Weight loss, night sweats, splenomegaly, leukocytosis with mature and immature granulocytes, BM biopsy 100% cellular, BM aspirate shows increase in granulocytic and eosinophilic precursors?

A

Chronic myelogenous leukemia

65
Q

Had large B cell NHL, high-dose chemo and autologous stem cell trasnplant, complete remission….now has pneumonia, pancytopenia, 2% blasts, and BM with abnormal granulocytic maturation with hyposegmentation of nuclei and increases blasts?

A

Myelodysplastic syndrome, refractory anemia with excess blasts

66
Q

What is a combination of neutropenia with thrombocytopenia and anemia/reticulicytopenia?

A

Pancytopenia

67
Q

What is required to establish diagnosis of pancytopenia?

A

BM examination

68
Q

What causes hypercellular BM?

A

Usually hematologic malignancy, rarely a B12 deficiency

69
Q

What causes hypocellular BM?

A

BM failure disorder

70
Q
  • PBS with immature monocytes and blasts
  • Hypercellular marrow (95% cellular)
  • Myeloblasts = 25%
  • Monoblasts, immature monocytes, and mature monocytes = 42%
  • Abnormal eosinophils
A

Acute myeloid leukemia

71
Q

What do pro-B cells do first in the BM to rearrange their germline immunoglobulin genes?

A

Re-arrange the heavy chain genes

72
Q

What do pro-B cells do after rearranging their heavy chains?

A

Rearrange the light ones

73
Q

Once they rearragnce heavy and light chains, what are pro-B cells?

A

Immature B cells that have a unique IgM or IgD immunoglobulin that is expressed on the cell survace

74
Q

Were do immature B cells live for a long time and are quiescent?

A

Lymph Nodes

75
Q

Resting B cells are stimulated by what to develop into a plasma cell or memory B cell?

A

Antigen via APC with help from a T-cell

76
Q

When antigen-stimulated B cells eventually enter the germinal center what do they do?

A

Somatic hypermutation of the variable region genes

77
Q

The germinal center B-cells that survive can do what?

A

Heavy chain class switching to be IgG, IgA, IgD, or IgE

78
Q

What do plasma cells do once they move to the BM?

A

Produce highly specific immunoglobulin

79
Q

Where do pre-T-CElls undergo T-Cell receptor gene rearrangement?

A

Thymic cortex

80
Q

T cells that express high-affinity receptors for self-antigens undergo what?

A

Negative selection (clonal deletion) by apoptosis

81
Q

Where do T-cells undergo further maturation to become either a CD4 or CD8 Tcell?

A

Thymic medulla

82
Q

What is required for stimulation of T-cell receptors?

A

Antigen presentation on an APC via HLA
4- MHC II
8- MHC I

83
Q

What happens in the presence of a co-stimulatory signal?

A

T-cell activation

84
Q

What happens in the absence of a co-stimulatory signal?

A

T-cell Anergy

85
Q
  • Phenotype: CD10+, CD19+, CD20+, kappa +

- Genetics: t(14;18)(q32;q21)

A

Follicular lymphoma

86
Q

What causes follicular lymphoma?

A

Rearragement of the Bcl-2 gene at 18q21 adjacent to IgH gene at 14q32 results in BCL-2 OVEREXPRESSION

87
Q
  • Phenotype: CD10+, CD19+, CD20+, kappa +, bcl-6+, Ki-67 + 100%
  • Bcl-2 - , EBERs -
  • Genetics: t(8;14)(q24;q32)
A

Burkitt Lymphoma

88
Q

Bone Marrow Failure can arise as a result of disease processes that do what 2 things?

A
  1. compromise the bone marrow microenvironment

2. Injure stem cells directly

89
Q

What are prototype disorders for Bone Marrow Failure?

A
  1. Myelophthisis

2. Aplastic anemia

90
Q

What does myelophthisis do?

A

Compromises the bone marrow environment

91
Q

Pancytopenia due to marrow replacement can be caused by what 4 things?

A
  1. Fibrosis
  2. Metastatic tumors: Breast, prostate, lung, lymphoma
  3. Primary tumors: Acute leukemia, myeloproliferative neoplasms
  4. Granulomas: Tuberculosis, fungal infections, sarcoid
92
Q

What is seen in a peripheral blood smear with bone marrow failure?

A

-Nucleated RBCs, tear drop RBCs, myeloid precursors (leukoerythroblastic)

93
Q

What results if you injure stem cell directly?

A

Aplastic Anemia

94
Q

What are 2 causes of acquired bone marrow failure?

A
  1. Idiopathic
  2. Secondary to injury by radiation, drugs (chemotherapy, chloramphenicol), toxins (hydrocarbons, benzene), viral infections (non-A, non-B, non- hepatitis)
95
Q

What can cause congenital bone marrow failure?

A

Fanconi anemia (AR, defect in DNA repair)
Others
THIS IS RARE

96
Q

What is aplastic anemia?

A

A rare disorder with probable auto-immune etiology causing direct impairment of the ability of HSC to proliferate and differentiate

97
Q

What is likely a cause of aplastic anemia?

A

-Induction of antigen expression triggering immune destruction by cytotoxic T-cells.

98
Q

What can trigger the immune response in aplastic anemia?

A

Various stimuli (drugs, toxins, infections)

99
Q

True or False: v) Severe AA (ANC < 0.5) and very severe AA (ANC < 0.2) have high mortality if untreated.

A

TRUE

100
Q

What is mortality almost always due to in aplastic anemia?

A

Infections (fungal ones especially)

101
Q

What are 2 treatment options for aplastic anemia that have a high response rate?

A
  1. Allogeneic bone marrow transplantation (young patients with HLA-identical sibling).
  2. T-cell immune suppressive agents like anti-thymocyte globulin and cyclosporin (older patients and patients without HLA-identical sibs).
102
Q

What must you consider in treatment options for CA?

A

Curative or Palliative

-Surgery, Chemo, Radiation, Hormones, Immunotherapy

103
Q

What are some types of supportive care for CA treatment?

A

Pain, nausea, infections, nutrition, psychosocial issues

-Don’t forget about end of life care

104
Q

How does cancer grow?

A

Angiogenesis

105
Q

What are some terms for vascular access?

A
  1. Mediport
  2. Hickman
  3. PICC
106
Q

What is done through those vascular access sites?

A
  1. Infusions: Chemo or stem cell
  2. Blood draws
  3. Stem cell collection
107
Q

When a growth factor starts the signal for a cell to divide, what can a single tyrosine kinase inhibitor do?>

A

Stop the signal

108
Q

What can a multi-tyrosine kinase inhibitor do?

A

Block signal for the cell to divide (via growth factor) and block the signal for the cell to make blood vessels (via growth factor)

109
Q

Novel therapies?

A

He put in a picture with drugs that we covered in pharm…

110
Q

Why is it important to understand hemonc concepts?

A

So you can…

(1) Contribute to proper care
(a) Screening and Prevention
(2) Treat Complications of disease
(3) Treat Complications of treatments
(4) Contribute to your patient’s quality of life

111
Q

What does cancer do?

A

SCARES EVERYONE…