Exam 2-Cancer Flashcards

1
Q

2 basic components of tumor

A
  1. parenchyma-the proliferating neoplastic cells

2. stroma-supportive tissues made of connective tissue and blood vessels

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2
Q

Benign neoplasms

A

end in ‘oma’

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3
Q

malignant neoplasms

A
  • end in ‘sarcoma’ mesenchymal origin

- end in ‘carcinoma’ epithelial origin

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4
Q

Cancer prefixes-point to location

  • adeno
  • chondro
  • erythro
  • hemangio
  • hepato
  • lipo
  • lympho
  • melano
  • myelo
  • myo
  • osteo
A
  • gland
  • cartilage
  • red blood cell
  • blood vessels
  • liver
  • fat
  • lymphocyte
  • pigment cell
  • bone marrow
  • muscle
  • bone
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5
Q

Nomenclature of tumors

  • mesenchymal origin
  • epithelial
  • totipotential cells
A
  • mesoderm

- ectoderm or endoderm

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6
Q

Pasaway

A
  1. ‘OMA’ but malignant
    ex: hepatoma, lymphoma, glioma, melanoma
  2. 3 germ layers
    ex: teratoma
  3. non-neoplastic but “OMA”
    ex: choristoma-ectopic rest of normal tissue
    hamartoma-mass of disorganized but mature specialized cells or tissue indigenous to the particular site
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7
Q

Benign character

  • differentiation/anaplasia
  • rate of growth
  • local invasion
  • metastasis
A
  • well-differentiated (closely resembles cell of origin, shows signs of specialization)
  • usually progressive and slow
  • well circumscribed and have a capsule
  • absent
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8
Q

Malignant character

  • differentiation/anaplasia
  • rate of growth
  • local invasion
  • metastasis
A
  • poorly or completely undiff(lost signs of specialization of cell of origin)
  • erractic and may be slow to rapid
  • locally invasive, infiltrating the surrounding normal tissues
  • present
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9
Q

the extent to which a neoplastic cell resembles its normal cell of origin

A

differentiation

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10
Q

‘to form backwards’

  • tumor cells show no evidence of specialization
  • tumor cells primitive
A

anaplasia

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11
Q

cytologic characteristics of malignancy

A
  • overall enlargement of cell
  • nucleus: -enlargement -nuclear to cytoplasmic ratio 1:1 -hyperchromatism -pleomorphism -abnormal mitotic figures
  • cytoplasm more primitive
  • architecture altered
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12
Q

Age

A
  • frequency of cancer increases with age

- cancer deaths bet 55-75

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13
Q

Heredity

A
  • autosomal dominant: inherit mutation of cancer suppressor genes
  • autosomal recessive: defects in DNA repair
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14
Q

knudson’s 2-Hit hypothesis

A

-if cell receives damage on the 2nd chromo that cell can produce cancer

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15
Q

exposure to some etiologic agents

A

cellular transformation and derangement theory

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16
Q

all individuals possess cancer cells, however, cancer cells are recognized by the immune response system and they undergo destruction. the failure of the immune resp sys will lead to inability of the WBC to destroy cancer cells

A

failure of the immune response theory

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17
Q

mutant genes that cause multiple changes in the regulatory control of the cell

A

oncogenes

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18
Q

normal genes that affect cell growth and differentiation but have the potential to become oncogenic following mutations in their DNA sequences

A

proto-oncogenes

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19
Q

Rb gene

-P53 gene

A
  • governor of the cell cycle

- guardian of the genome

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20
Q

carcinogen alter the DNA of cell and will either die or repair

A

initiation

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21
Q

repeated exposure to carcinogens, abnormal gene will express latent

A

promotion

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22
Q

irreversible period, neoplastic transformation, malignancy

A

progression

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23
Q

E-cadherin function is lost in almost all epithelial cancers

A

1st step: loosening of intercellular junctions

24
Q

local degradation of the basement membrane and interstitial connective tissue

A

2nd step

25
Q

changes in attachment of tumor cells to ECM proteins

A

3rd step

26
Q

propelling tumor cells through the degraded basement membranes and zones of matrix proteolysis

A

final step: locomotion

27
Q

3 spread of cancer

*metastasis-identifies neoplasm as malignant

A
  1. lymphatic
  2. hematogenous
  3. direct spread
28
Q

lymphatic mode

*“sentinel lymph node”

A

initial mode of metastasis of carcinoma

  • invades lymphatic channel and breaks free into lymph fluid
  • the first regional lymph node that receives lymph flow from a primary tumor
29
Q
  • preferred mode of metastasis of sarcomas
  • invades blood vessel (vein) and breaks free into blood stream
  • occurs in rich blood supply-lungs, bone marrow, liver
  • direct venous extension
A

hematogenous spread

30
Q
  • neoplasm grows at/near surface of body cav
  • breaks free and floats in body cav
  • floating tumor cell implants/grows at new site on wall of same body cav
A

seeding

*ovarian cancer

31
Q
  • during surgery, may be carrier by scapel to another site

- rare mode

A

direct implantation

32
Q

classes of carcinogenic agents

A
  • chemicals
  • radiation
  • viruses and other microbes
33
Q

-highly reactive electrophiles which react w/ DNA, RNA, and other cellular proteins

A

chemical carcinogen

  • direct
  • indirect-acting
34
Q
  • may activate oncogenes and activate tumor suppressor genes
  • causes: -chromo breakage -translocation -point mutations
  • long latent period
    • suggests must be accumulation of mutations
    • suggests may be safe threshold of exposure
A

Radiation carcinogen

35
Q

sources of radiation

A
  • sunlight, local irradiation
  • therapeutic
  • diagnostic
  • occupational exposure
  • nuclear arms/ accidents
36
Q
  • animal models ex: feline leukemia virus
  • human RNA oncogenic viruses ex: human t-cell leukemia virus
  • human DNA oncogenic viruses ex: HPV, EBV, herpes virus 9, hepatitis B

*helicobacter pylori

A

viral carcinogenesis

*other microbial carcinogen

37
Q

body defenses against tumor

A
  1. t cell system
  2. b cell sys
  3. phagocytic
38
Q

effects of tumor on host

A
  1. location and impingment on adjacent structure
    - functional activity such as hormone synthesis
    - bleeding & secondary infection
    - initiation of acute symptoms-rupture or infarction
39
Q
  • a disease or symptom that’s the consequence of cancer in the body but is not due to the local presence of cancer cells
  • mediated by humoral factors excreted by tumor cells or immune response against the tumor
A

paraneoplastic syndrome

40
Q

p. syndromes

A
  1. anemia
  2. hypercalcemia
  3. DIC
  4. anorexia-cachexia syndrome
41
Q
  • includes acute leukemia, small cell lung CA, lymphomas

- responsive to chemotherapy

A

fast-growing neoplasm

42
Q
  • low grade

- surgical resection and radiation therapy are more effective treatment

A

slow-growing tumor

43
Q

cancer diagnosis

A
  1. biopsy
  2. CT, MRI
  3. tumor markers
44
Q
  • definitive diagnosing
  • provides histological proof of malignancy
  • involves the surgical incision of a small piece of tissue for microscopic examination
A

biopsy

45
Q

types of biopsy

A
  1. needle
  2. incisional
  3. excisional
  4. shave
  5. punch
46
Q
  • histologic classification
  • assigned by pathologist
  • estimates the aggressiveness of cancer based on cytologic features: -deg of differientiation -#mitotic figures per high power field -level of invasion
A

Grading of cancer

47
Q
  • clinical classification
  • determined by clinicians
  • based on extent of disease at initial diagnosis
  • aids in determination of best tx, expected patient survival, tumor behavior
A

Staging of cancer

T=size of primary tumor
N=lymph node involvement
M= distant metastasis

48
Q

T=size of primary tumor

0
IS
1-4

A
  • no tumor clinically evident
  • carcinoma in situ
  • range of size of primary tumor (large # large size)
49
Q

N=
0
X
1-3

A
  • no metastasis
  • regional lymph node cannot be assessed
  • range of increasing degrees of nodal involvemnt
50
Q

M=
0
1

A
  • no evidence of distant metastasis

- distant metastasis identified: liver, lungs, anywhere except regional lymph nodes

51
Q

promotive and preventive managment

A
  1. lifestyle modification
  2. nutritional management
  3. screening
  4. early detection
52
Q
  • reducing risks for healthy people
  • patient ed
  • avoidance of known carcinogen
  • diet/lifestyle mod
A

Primary Prevention

53
Q
  • early screening for strong fam Hx of cancer

- implementation of programs for early detection of programs

A

secondary prevention

54
Q
  • breast self exam: 20+, 7 days after mense
  • clinical breast exam: 20-39, every 3 yrs, 40+ yrly
  • mammogram: 35-40
  • pap smear: 18+ or sexually active
  • testicular self exam: 15+ monthly
  • digital rectal exam: 40+ yrly
  • stool blood occult: 50 yrly
  • sigmoidoscopy: 50+ every 3 yrs
A

early screening

55
Q
  • avoid obesity
  • cut down total fat intake
  • high fiber diet
  • vitamin ACE
  • broccoli, cabbage, cauliflower (benzypyryne hydroxylase)-inactivate carcinogens
  • moderation of alcohol consumption
  • mod in salt-cured and smoked foods
A

dietary recomm against cancer