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Pathophysiology > Cancer Reading Guide- Mini Exam 4 (09/15) > Flashcards

Cancer Reading Guide- Mini Exam 4 (09/15) Flashcards

1
Q

How do we get cancer

A

environment, cell cycle, and genetics

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2
Q

some environmental agents associated with cancer are:

A

viruses, tobacco use, food, radiation, chemicals, pollution

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3
Q

types of genes within individual cells which may mutate to cause cancer

A

oncogenes, tumor suppressor genes, DNA repair genes

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4
Q

somatic mutations

A

alterations in the function of the DNA repair genes

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5
Q

oncogenes

A

-genes that regulate cellular growth

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6
Q

porto-oncogenes

A

normal state
initial state of oncogenes
as proto-genes promote cell growth that is self-regulated
mutation causes genes to become oncogenes, cell growth becomes unregulated

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7
Q

tumor suppressor genes

A

the genes normal function is to regulate cell division, both alleles need to be mutated or removed in order to lose the gene activity
the first mutation may be inherited or somatic
the second mutation will often be a gross event leading to loss effectiveness of gene

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8
Q

DNA repair genes

A

genes that detect mutations
normally will send protein to site of mutation and promote repair
mutation will cause slow reaction to mutations or will cause these genes to become dormant

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9
Q

cellular proliferation

A

the generation of new, daughter cells divided from progenitor (parent cells)
-stem cells play an important role in proliferation

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10
Q

stem cells

A
  • highly undifferentiated
  • have potential to divide into daughter stem cells
  • can mature into more differentiated units that have a specific function
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11
Q

cellular differentiation

A

refers to maturity, specificity, and functionality of cells

cellular differentiation normally takes place in an orderly process

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12
Q

three basic steps of cellular differentiation

A
  1. cells start out as undifferentiated (stem) cells that have the potential to mature into more specific cell types
  2. as a need arises the stem cells turn into progenitor (patron) cells that can reproduce daughter cells
  3. daughter cells then become highly differentiated cells that do not reproduce
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13
Q

most frequent problems with altered cellular proliferation and differentiation

A

most frequent problems: over-proliferation and lack of differentiation
neoplasia

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14
Q

neoplasia

A

the irreversible deviant development of cells that result in the formation of neoplasms

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15
Q

where do we see neoplasias

A

only in cells that have the ability to proliferate (esp. cells that undergo rapid mitosis)

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16
Q

where would we not see neoplasias

A

permeant cells that do not regenerate are not areas where neoplasia arises

  • cardiac myocytes
  • mature neurons
  • lens of the eye
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17
Q

why does cancer occur

A
  • at the level of the cell, cancer is genetic

- all cancer involves malfunction of genes that control cell functions (reproduction, growth, differentiation, death)

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18
Q

caretaker genes

A

genes taht repair mutated DNA and protect the genome

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19
Q

oncogenes

A

genes that code for proteins involved in cell growth and proliferation

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20
Q

tumor suppressor genes

A

genes that prohibit over-proliferation of cells and regulate apoptosis

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21
Q

what is the path of malfunction

A

called carcinogens

  1. initiating event
  2. promoters (internal and external)
  3. continued exposure and change in DNA)
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22
Q

carcinogens

A

cancer causing agent, agents that interfere with molecular pathways and can initiate or promote tumors to form in the body

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23
Q

types of carcinogens

A

radiation, hormones, tobacco, viral infections, chemicals

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24
Q

characteristics of neoplasms

A

autonomy and anaplasia

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25
Q

autonomy

A

unregulated cell growth

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26
Q

anaplasia

A

term used to describe the neoplasms loss of differentiation

the greater the degree of anaplasia, or the more undifferentiated the tumor cells, the more aggressive the tumor will be

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27
Q

the greater the degree of anaplasia, or the more undifferentiated the tumor cells, the ____ aggressive the tumor will be

A

more

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28
Q

neoplastic cells

A
  • lack cell-to-cell inhibiitions, cohesion, and adhesiveness
  • undergo extensive angiogenesis (development of new blood vessles)
  • deprive unaffected tissues of oxygen and other nutrients
  • secrete substances that can alter metabolic processes
29
Q

benign characteristics

A
  • remain localized
  • over-proliferate, but do not have significant loss of differentiation
  • can still be life threatening
  • can sometimes be a precursor to cancer
30
Q

malignant characteristics

A

invasive
destructive
spread to other sites
doesn’t resemble tissue of origin (undifferentiated)
can cause ischemia and necrosis of tissue
uses energy and nutrients that are needed by healthy tissue

31
Q

types of cancer spread

A

localized, invasion or direct extension, seeding, metastasis

32
Q

localized cancer spread

A

proliferation within the tissue of the organ
can still cause: obstruction, hemorrhage, necrosis
better prognosis

33
Q

invasion or direct extension cancer spread

A

tumor cells moving and growing into adjacent tissue and organs
travels to nearby structures
releases enzymes that degrades tissue walls that allows the tumor to grow

34
Q

seeding cancer spread

A

cancer cells in body fluids or along membranes
occurs many times within peritoneal or pleural cavities surrounding affected organ or tissue
gravity will pull the cells downward or cells will follow flow of fluid within the body cavity

35
Q

metastasis cancer spread

A

malignant neoplasms spread to distant sites: lymphatics and blood vessels
lethal aspect of cancer
detection and treatment become much more complex

36
Q

steps of metastases

A
  1. breaks through the basement membrane and/or extracellular membrane
  2. gains access to and begins to circulate within the blood vessels or lymph system
  3. leaves the blood vessels or lymph system and adheres to distant tissues
  4. establishes a new nutrient network through the process of angiogenesis
37
Q

organ tropism

A

desire of a primary tumor to relocate to a specific distant site

38
Q

factos that promote organ tropism

A

favorable environment for new growth, increased adherence capability, location of the distant organ in relation to the blood flow or lymphatic flow

39
Q

examples of organ tropism

A

colon cancer to liver
lung to brain
breast or prostate to bone

40
Q

-oma

A

benign tumor sufficiently attached to a root word

41
Q

carcinomas

A

cancer of epithelial tissue

42
Q

adenocarcinomas

A

cancer of glandular tissue

43
Q

sarcomas

A

cancer of connective tissue

44
Q

leukemias

A

hematopoietic (blood forming organs)

45
Q

lymphomas

A

tumors in lymphatic tissue

46
Q

gliomas

A

tumor of central nervous system

47
Q

carcinoma-in-situ

A

early stage cancer tumor that has not broken through the basement membrane of the organ

48
Q

TNM

A

size of tumor
involvement in the lymph system
metastasis (remember if this one is yes it is automatically stage 4)

49
Q

grade 1

A

well differentiated, cancer confined to organ of origin

50
Q

grade 2

A

moderately differentiated cells. cells invading locally

51
Q

grade 3

A

poorly differentiated cells, spread to regional structures

52
Q

grade 4

A

undifferentiated cells, spread to regional structures

53
Q

systemic effects of malignant tumors

A

weight loss and cachexia; anorexia, fatigue, pain, stress; anemia; severe fatigue; effusions; infections); bleeding); paraneoplastic syndrome

54
Q

cachexia

A

weakness and wasting of the body due to severe chronic illness

55
Q

CAUTION

A 
Change in bowel/bladder
A lesion that doesn't heal
Unusual bleeding or discharge
Thickening or lump in breast or elsewhere
Indigestion
Obvious change in wart or mole
Nagging cough or persistent hoarseness
56
Q

Diagnostic tests

A 
routine screening
self-examination
blood tests
radiographic, ultrasound, MRI, CT scans
Cytologic tests require biopsy or cell sample
57
Q

routine screening tests

A

essential for early detection

following treatment to detect any further tumors

58
Q

self-examination tests

A

early detection if done consistently

breast, testicular, and skin exams are important

59
Q

blood tests

A

measure blood cell levels during treatment, may detect tumor markers eg PSA test

60
Q

radiographic, ultrasound, MRI, CT scans

A

methods of visualizing changes in tissues or organs

61
Q

Cytologic tests require the biopsy or cell sample

A

histologic and cytologic examinations to determine degree of differentiation and tumor type
may be tested for growth promoter sensitivities, eg: estrogen-dependent tumors
most dependable confirmation of malignancy

62
Q

risk factors

A

genetic factors; radiation

63
Q

chemicals (risk factors)

A 
organic solvents 
asbestos
heavy metals
formaldehyde
chemotherapy agents
64
Q

biological factors of cancer

A

chronic irritation and inflammation
age
diet
hormones

65
Q

risk reduction

A

limit UV exposure from sun or tanning booths
regular medical and dental exams
self-examination
diet (increased fiber content, reduced fats, 5-10 servings of fresh fruits and vegetable, these foods contain antioxidants which reduce changes to DNA)

66
Q

immunity and cancer risk

A
  • cell-mediated immunity recognizes some tumor cells and destroys these
  • immunization for cervical cancer and hepatitis is recommended to reduce cancer risk from infection
67
Q

cancer-free state generally defined when

A

as a 5-year survival without recurrence

-some cancers such as childhood leukemias can be considered cured after a 10 year cancer free period

68
Q

remission

A

no clinical signs of cancer

-client may experience several remissions

69
Q

examples of malignant tumors

A

skin cancer, ovarian cancer and brain tumor

Pathophysiology (7 decks)

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