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Block 1 Week 4 > Clinical Cancer 1 > Flashcards

Clinical Cancer 1 Flashcards

1
Q

What is Cancer?

A
  • a disease of uncontrolled cell proliferation with w/ invasion of adjacent & distant tissues
  • progressively impairs normal organ function
  • is many diseases (>100 distinct types)
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2
Q

What are the 4 broad types of cancer?

A

1) sarcomas: bone, connective tissue
2) carcinomas: epithelial tissues kidney, liver pancreas, breast
3) lymphomas: lymph node, thyroid, spleen
4) leukemias: blood

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3
Q

Why is cancer important?

A
  • 1 in 3 people develop cancer
  • cancer spending accounts for a lot of disease based health expenditures
  • second leading cause of death
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4
Q

Pancreatic cancer incidence vs death rate?

A
  • pancreatic cancer incidence= its death rate; this means that if you get pancreas cancer you will probably die
  • is because hard to catch early, typically when get diagnosed its too late to do anything
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5
Q

What is premolecular definition of Neoplasm?

A

-an abnormal mass of tissue, proliferation exceeds and is unrelated to that of the normal tissue, & persists in same excessive manner after cessation of the stimuli which evoked the change

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6
Q

What is modern era definition of Neoplasm?

A

-a disorder of cell growth that is triggered by a series of acquired mutations affecting a single cell & its clonal progeny

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7
Q

Hypertrophy

A

-increase cell mass by increasing cell number w/o increasing size

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8
Q

Hyperplasia

A
  • increase cell mass by increasing the number of cells

- still posses normal growth control mechanisms

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9
Q

Metaplasia

A

reversible change in which one differentiated cell type is replaced by another cell type, in response to chronic irritation

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10
Q

Atrophy?

A

cell adaptation

  • when cell shrinks in response to non-lethal stimulus
  • usually shrinkage of organs as well
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11
Q

Atypical Hyperplasia

A
  • precancerous cell changes that can (do not always) become malignant
  • `cells have abnormal appearance
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12
Q

Dysplasia

A
  • further increase (from atypical hyperplasia) in abnormal cell appearance and organization
  • due to faulty maturation of cells
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13
Q

In Situ Carcinomas

A
  • very abnormal appearing cells which have not acquired the ability to invade the local barriers like the basement membrane
  • pre-malignant/cancerous condition, not obligated to progress to malignancy
  • just for carcinomas (epithelium) not sarcomas
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14
Q

Carcinoma in situ in uterus, how does it look?

A
  • see that the epithelial is much thicker (supposed to be single cell, now multi-layered)
  • but basement membrane is intact, cancer can’t metastasize
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15
Q

Carcinoma in situ in uterus, malignant?

A
  • epithelia has no blood vessels, cancer cells would need to break through membrane to access blood/lymph to metastasize or invade adjacent tissue
  • in situ this hasn’t happened; so can’t spread there technically not malignant BUT treat as malignant since at any time this can become invasive
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16
Q

How treat carcinoma in situ?

A
  • 30% in situ cells become invasive, so treat everything as malignant
  • means over treat 7/10 people, but don’t want to risk invasive cancer
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17
Q

Neoplasia

A

an abnormal mass of tissue (tumor) that continues to grow because it has lost its responsiveness to normal growth control mechanisms

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18
Q

When does neoplasia occur?

A
  • usually one of the later occurrences after atypical hyperplasia, dysplasia and cancer in situ.
  • but many roadways to cancer, not all the same, but it is a later stage
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19
Q

Neoplasia composition?

A
  • neoplasia= the abnormal mass of tissue (tumor) within it have:
    1) parenchymal tissue
    2) reactive stromal tissue
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20
Q

Parenchymal Tissue

A
  • the transformed malignant cells in a tumor

- they determine the nomenclature, classification, &biologic behavior of the cancer

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21
Q

Reactive Stromal Tissue

A
  • non-neoplastic supportive connective tissue of the tumor
  • has blood/lymphatic vessels & cells of the immune system
  • determines tumor structure, a lot= harder tumor; less= softer tumor
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22
Q

Nomenclature of benign vs malignant tumor?

A 
-benign: "oma"
      Fibroma 
-malignant: "sarcoma"
      Fibrosarcoma
-EXCEPT lymphoma & melanoma 
-prefeix= location of tumor
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23
Q

What types of cells are most tumors comprised of?

A
  • most common: 1 parenchymal, neoplastic cell type, with benign and malignant counter parts
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24
Q

Tumors with more than 1 neoplastic cell types?

A
  • yes, less common but happens in 2 ways:
    1) more than 1 neoplastic parenchymal cell type derived form SAME germ layer
    2) derived from DIFFERENT germ layer
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25
Q

what does teratogenous mean?

A
  • when have more than 1 neoplastic parenchymal cell type derived form derived from DIFFERENT germ layers?
  • is a teratoma
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26
Q

where are teratomas and what do they do?

A
  • usually benign
  • found in gonads (ovaries/ testes) usually; can also be found in midline
  • can form any type of tissue ( skin, brain, lungs, etc)
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27
Q

benign neoplasias?

A
  • remain localized
  • don’t have ability to invade local tissues/ spread to distant sites
  • can usually be removed w/o significant harm to patient
  • may cause significant morbidity if in dangerous location
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28
Q

malignant neoplasias?

A
  • called cancers
  • invade adjacent tissues and/or organs
  • may metastasize [spread] to distant sites
  • cells which enter the circulation, travel and lodge in distant sites and grow into tumors (metastasis), cause 90% of all cancer deaths.
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29
Q

what does it mean to say cancer cells metastasize? risk of metastasizing?

A
  • cells which enter circulation, travel & lodge in distant sites and grow into tumors
  • cause 90% of all cancer deaths.
  • extremely fast progression to death when have extensive metastasis
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30
Q

How does cancer spread? 3 main pathways

A

1) Direct seeding of cancer cells in body cavities & surfaces
2) Lymphatic spread
3) Hematogenous spread

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31
Q

How do carcinomas usually spread? Sarcomas?

A

Carcinomas: by lymph (lymphatics)
Sarcomas: blood (hematogonis)

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32
Q

differentiation/ anaplasia in benign tumors?

A
  • high degree of differnetiaion, low anaplasia

- usually composed of differentiated cells, often look like origin tissue

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33
Q

differentiation/anaplasia in malignant tumors?

A
  • high degree of anaplasia, cells are not well differentiated
  • can look similar or completely different to tissue of origin
  • typically more anaplasia= worse diagnosis
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34
Q

rate of growth in benign tumors ?

A
  • slow rate of growth,
  • can come to a standstill or regress
  • mitotic figures (hyperchromatism) is rare
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35
Q

rate of growth in malignant tumors?

A
  • erratic; can be slow or rapid

- mitotic figures (hyperchromatism) often numerous & abnormal

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36
Q

local invasion in adjacent tissues in benign tumors?

A
  • usually don’t invade surrounding tissues
  • expansile & cohesive (pushes out past borders)
  • w/ well defined borders
37
Q

local invasion in adjacent tissues in malignant tumors?

A
  • locally invasive, infiltrating surrounding tissue

- misleadingly cohesive &expansile

38
Q

expansile

A

means that the tumor can push borders and expand

39
Q

metastasis in benign tumors?

A

NEVER

40
Q

metastasis in malignant tumors?

A
  • frequent

- most likely with large, undifferentiated primary tumors

41
Q

common progression of breast cancer?

A

1) normal breast lobule
2) epithelial hyperplasia
3) atypical hyperplasia
4) ductal carcinoma in situ
5) invasive ductal breast cancer

42
Q

what is ductal carcinoma in situ?

A
  • a benign breast neoplasm

- have cancer like cells but contained within duct, still have intact basement membrane

43
Q

invasive ductal breast cancer cell appearance and mechanism?

A
  • malignant
  • cells abnormal in appearance, vary in size & shape, have crossed basement membrane & growing in surrounding tissue that lacks the myoepithelial layer
44
Q

What is first thing malignant cells invade in breast cancer?

A

1) stroma

2) blood vessels

45
Q

ductal carcinoma in situ characteristics?

A
  • cells have larger nuclei, hyperchromatism, all morphologies of malignancy
  • have NOT broke through basement membrane
46
Q

how treat ductal carcinoma in situ vs invasive ductal breast cancer ?

A
  • small invasive carcinoma will do lumpectomy in breast w/ margins
  • if have extensive DCIS; will perform masectomy because if miss any cells they could be the ones to develop into invasive cancer, hard to tell which are in-situ and which aren’t
47
Q

atypical hyperplasia look like in breast cancer?

A
  • cells acquire abnormal appearance (much larger) & architecture
  • may have crowded nuclei or be hyper chromatic
48
Q

epithelial hyperplasia look like in breast cancer?

A
  • cells retain normal appearance & architecture
  • look like normal cells, just more of them
  • is benign and responding to normal growth/ death signals
49
Q

Why breast cancer prefer to travel through lymph nodes not blood?

A

-lymph vessel walls are very thin, easy for tumors to break into than veins (have smooth muscle wall) or arteries(are very hard)

50
Q

First step in metastasis?

A

-invading the vessels

51
Q

what called when have breast cancer cells in one region in the breast?

A

-local tumor

52
Q

what called when have breast cancer cells that spread to axial lymph node?

A
  • local regional spread

- don’t categorize as metastsis yet since still close by

53
Q

what called when have breast cancer cells that spread to superclavical lymph node?

A
  • metastatic

- have moved far enough way to be considered distant and metastasis

54
Q

Breast cancer spread through blood?

A
  • yes; it can but not common route
  • tumor can go to lung, bone, and liver this way
  • shows that these rules are not gospel
55
Q

where metastasis usually appear? where rarely appear?

A
  • usually: liver, lung, bone and brain

- unusually/never: heart, spleen, kidney

56
Q

How large does tumor (accumulation of cells) have to be to be detected?

A
  • tumor needs to be about 1g
  • 1g (1 billion cells) is about what you need, but often not diagnosed until 1kg
  • usually by this time that can see metastasis it is too late and cancer is spreading rampantly through body
57
Q

Carcinogenesis? where are they found?

A
  • cause non-lethal genetic damage (cell doesn’t die but is fucked up)
  • are a molecular basis of cancer

1) env exposires
2) germline inheritence
3) spontaneous & random

58
Q

how is a tumor formed?

A

by the clonal expansion of a single precursor cell that has incurred genetic damage
-tumors are clonal

59
Q

how do we know tumors are clonal?

A

-know are clonal because we see same translocation in all tumor cells or same virus etc

60
Q

What are the 4 classes of normal regulatory genes that are targets for cancer causing mutations?

A

1) proto-oncogenes
2) tumor suppressor genes
3) genes that regulate apoptosis
4) genes involved in DNA repair

61
Q

Carcinogenesis results from?

A

the accumulation of proliferation promoting mutations in a stepwise fashion over time

62
Q

2 ways epigenetics can lead to malignant cancers?

A

1) DNA methylation can silence gene expression

2) histone modifications can enhance/ stop gene expression

63
Q

How many diff genes are implicated across different types of cancer?

A
  • 291 (1% of entire human genome)

- oncogenes & tumor supressor genes most common

64
Q

do all genes need to be mutated to progress to abnormal cell proliferation & cancer?

A

-no, the unique characteristic of each type of cancer arises from the particular set of mutations in 5-7 genes (possibly fewer)

65
Q

What are the 4 things the critical genes that lead to cancer in control of

A

1) cell division
2) cell survival
3) genome integrity
4) cell-cell interaction

66
Q

what does it mean when say need multi-step carcinogens to cause cancer?

A
  • means that 1 oncogene can’t transform cells
  • multiple genetic alterations involving both the activation of many oncogene & loss of TSG are necessary for carcinogenesis `
67
Q

what do the cell and molecular hallmarks of cancer consist of?

A

A) 8 fundamental changes in cell physiology

B) 2 enabling characteristics that promote cell transformation & tumor progression

68
Q

3 ways get dysregulation of Cancer-Associated Genes?

A

1) chromosomal changes
(ex translocations)
2) Epigenetic changes
3) Noncoding RNAs

69
Q

tumor progression (5 general steps)

A

1) 1 normal cell transformed into tumor cell; replicates a lot (progression)
2) treatment, cells that survive proliferate
3) end up w/ pop of cells that have unique systems of evading death, bunch together to form tumor
4) tumor now have assembly of cells that contribute diff things to tumor survival, some are chemo resistant, others immune resistant etc
5) tumor like superman, can’t kill, spreading everywhere patient dies

70
Q

How does Cancer cause Harm?

A
  • w/o treatment, malignant tumors cause symptoms/death:
    1) destruction of vital organs (organ failure)
    2) immune system suppression (overwhelmed w/ infection)
    3) abnormal blood clotting/bleeding
71
Q

9 ways cancer can present?

A

1) new mass patient/physician feels or see
2) unexplained persistent fever, weight loss or pain
3) occlusion of essential conduit
4) ulceration of the skin/ epithelial surface
5) abnormal fluid collections (effusions)
6) perforation of a hollow viscus (organ)
7) endocrine hyperactivity syndromes
8) paraneoplastic syndromes
9 screening

72
Q

what could cause pain in cancer (x3)

A
  • most are initially painless but some are not
    1) tumor pressing on nerve
    2) tumor obstructing organ’s fluid movement
    3) brain tumors cause variety of head pains & personality symptoms
73
Q

what types of cancers can present with persistent fevers (x3)?

A

1) lymphoma
2) leukemia
3) kidney cancer

74
Q

Cachexia & mechanism?

A
  • progressive loss of body fat & lean body mass
  • anemia, weakness, anorexia
  • mechanisms not understood, could be something that cancer cells themselves are releasing sending signals that aren’t hungry
75
Q

What is cachexia associated with?

A

1) equal loss of fat & lean muscle
2) elevated BMR
3) evidence of systemic inflammation

76
Q

Occlusion of an Essential Conduit?

A

seen in lung, esophageal, and pancreatic cancer

-obstructions of their ducts/openings can lead to pain, difficult swallowing, build up of bilirubin & johndas

77
Q

Ulcerations?

A

can be in the skin, GI tract tumors, or GU tract (kidney, bladder)

78
Q

effusions

A
  • Abnormal fluid collections
    1) Fluid around the lung (pleural effusion)
    2) Fluid in the abdomen (ascites)
79
Q

Perforation of a hollow viscus (organ)?

A
  • Often leads to formation of abnormal channels between two separate organs (fistula)
    1) gastro-colonic fistula
    2) rectal-vesical (bladder) fistula
80
Q

Endocrine hyperactivity syndromes

A

1) Increased hormone production by tumors derived from endocrine organs
2) Tumors inappropriately secreting hormones

81
Q

Paraneoplastic Syndromes

A
  • symptoms that can’t be explained by location of tumor or by the hormones indigenous to the tissue the tumor is in
  • in 10% of patients
82
Q

why important to recognize paraneoplastic syndromes?

A

1) may be early manifestation of an occult neoplasm
2) can cause significant clinical problems
3) may even be lethal
4) may mimic metastatic disease &confound treatment

83
Q

occult neoplasm

A

a cancer that is found at metastatic stage at time of diagnosis, but a primary tumor can’t be IDed

84
Q

Hypertrophic osteoarthropathy

A

-paraneoplastic syndrome
seen in lung carcinomas
-called clubbing of the fingers

85
Q

Local Effects of tumors?

A
  • Location is critical determinant of the clinical effects of tumors
  • they can impinge upon vital tissues and impair function
  • cause necrosis of involved tissues
  • cause hormone insufficiency
86
Q

Screening

A
  • helps diagnose cancer before it causes symptoms

- increase probability of finding it in a precancerous or early stage (better outcomes)

87
Q

common screening procedures?

A
  • Uterine cervical cancer – PAP smears
  • breast cancer self exams and mammograms
  • Colon Cancer- colonoscopy
  • skin exams
  • prostate exams (but can cause impatience)
88
Q

screen everybody?

A
  • Pap smears & mammograms everyone cuz showed help a lot

- other ones more painful/risky only at risk populations who show high rate of familial cancers

89
Q

VINDICATUM

A

Mnemonic for all types of Diagnosis:

Vascular
Infectious / Inflammatory
Neoplastic
Drugs
Iatrogenic
Congenital
Autoimmune
Trauma
Unknown
Metabolic

Block 1 Week 4 (7 decks)

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