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NUR 326 Exam 4 > Oncology > Flashcards

Oncology Flashcards

1
Q

proto-oncogenes

A

–genes that control cell replication
–result in cell growth and proliferation
–when mutated, proto-oncogenes become oncogenes that stimulate constant, unrelenting cell proliferation and cell cycling

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2
Q

difference between regular and cancer cell cycles

A

regular = checkpoints/rest phase
cancer = no checkpoints/rest phase

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3
Q

consequences of no checkpoints in cancer cell cycle

A

–no DNA errors recognized
–no apoptosis

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4
Q

growth in cancer cells

A

–cancer cells disregard the growth inhibitors released by neighboring cells
–as these cells proliferate, they stack on top of each other, take over boundaries of organs, crowd out normal cells, and may break free and travel to other sites in the body

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5
Q

differentiation

A

the extent that neoplastic cells resemble normal cells both structurally and functionally

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6
Q

anaplasia

A

total cellular disorganization, abnormal cell appearance, and cell dysfunction

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7
Q

anaplasia and proliferation

A

more anaplastic = faster proliferation

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8
Q

differentiation with benign and malignant tumors

A

benign = well-differentiated; resembles tissue of origin

malignant = poorly differentiated; does not resemble tissue of origin

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9
Q

rate of growth with benign and malignant tumors

A

benign = progressive, slow

malignant = erratic, slow to rapid

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10
Q

local invasion with benign and malignant tumors

A

benign = cohesive cells, well-demarcated tumor, often encapsulated making it movable

malignant = invasive and infiltrating, surrounding normal tissue

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11
Q

metastasis with benign and malignant tumors

A

benign = none

malignant = frequent

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12
Q

tumor care with benign and malignant tumors

A

benign = no necrosis

malignant = can have necrotic core

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13
Q

what are tumor markers?

A

biologic substances

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14
Q

what type of substances make up tumor markers?

A

hormones, enzymes, antigens, genes

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15
Q

where can tumor markers be found?

A

blood, urine, CSF, tumor plasma membrane

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16
Q

what are tumor markers useful for?

A

screening or diagnosis

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17
Q

are tumor markers diagnostic of cancer?

A

not always

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18
Q

examples of tumor markers

A

–prostate specific antigen
–BRCA gene mutation

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19
Q

grade I malignant tumor

A

cells are well-differentiated

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20
Q

grade II malignant tumor

A

cells are moderately differentiated

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21
Q

grade III malignant tumor

A

poorly differentiated or anaplastic cells

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22
Q

staging (T)

A

tumor size, location, and involvement

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23
Q

staging (N)

A

lymph node involvement

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24
Q

staging (M)

A

metastasis to distant organs

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25
Q

T0

A

no evidence of primary tumor

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26
Q

TIS

A

tumor in situ

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27
Q

T1-4

A

progressive increase in tumor size or involvement

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28
Q

N0

A

no spread to regional lymph nodes

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29
Q

N1

A

spread to closest or small number of regional lymph nodes

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30
Q

N2

A

spread to most distant or numerous regional lymph nodes

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31
Q

M0

A

none

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32
Q

M1

A

yes

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33
Q

stage 1

A

confined to organ of origin

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34
Q

stage 2

A

locally invasive (> 3 cm tumor)

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35
Q

stage 3

A

regional spread

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36
Q

stage 4

A

spread to distant sites

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37
Q

four phases of carcinogens

A

–initiation
–promotion
–progression
–metastasis

38
Q

initiation

A

mutation of genes, spontaneous or induced by carcinogenic agent

39
Q

promotion

A

actively proliferating cells accumulate; reversible

40
Q

progression

A

further mutation of cells; invasive with metastatic potential

41
Q

metastasis

A

spread of cancer

42
Q

tumor suppressor genes in cancer cells

A

–brake pedal
–normally function to restrain cell growth (apoptosis)
–can also become defective and lose the ability to inhibit cell growth and division = cancer formation

43
Q

oncogenes

A

–gas pedal
–mutated = gas pedal stuck
–growth signal permanently on

44
Q

p53 gene

A

tumor suppressor gene in cells that controls cellular apoptosis

45
Q

carcinogens

A

–substances that cause development of cancer
–can alter cell DNA
–damage = cumulative

46
Q

classification of carcinogens

A

–known
–probable
–possible

47
Q

promoters

A

agents that promote development of cancer

48
Q

examples of promoters

A

–diet
–alcohol
–tobacco
–hormones

49
Q

viral induced cancer

A

always involve the activation of growth-promoting pathways or inhibition of tumor suppressors in infected cells

50
Q

examples of viruses that can cause cancer

A

–HIV
–HPV
–Hep B
–Hep C

51
Q

vascular endothelial growth factor

A

a substance that gives cancer cells the capability to develop new blood vessels

52
Q

primary tumor

A

site of origin

53
Q

secondary tumor

A

anywhere that is not the site of origin
–need nutrients and oxygen
–need access to blood

54
Q

seeding

A

tumor erodes and sheds into body cavities

55
Q

implantation

A

direct expansion of tumor into adjoining tissue

56
Q

two primary routes of metastasis

A

(1) lymphatic
(2) vascular

57
Q

lymphatic spread

A

–cells trapped in lymph nodes
–three possible scenarios:
(1) death
(2) dormancy
(3) flourish/proliferate

58
Q

vascular spread

A

–spread by vascular drainage –> penetrate local veins
–first stop = liver

59
Q

why is the liver often the first stop in vascular spread?

A

because the liver receives the most blood through the portal vein before it circulates through the body

60
Q

what happens in the liver during vascular spread?

A

clumping, trapping, proliferating

61
Q

angiogenesis

A

complete own blood supply

62
Q

most common places for secondary tumors

A

–lungs
–bone
–liver
–brain

63
Q

lung cancer common site of metastasis

A

bone, brain

64
Q

colon cancer common site of metastasis

A

liver

65
Q

breast cancer common site of metastasis

A

bone, brain, liver, lung

66
Q

prostate cancer common site of metastasis

A

vertebrae

67
Q

melanoma common site of metastasis

A

brain

68
Q

lung cancer

A

–leading cause of cancer-related death
–early diagnosis is key to treatment
–most often in > 65 years
–African Americans more often affected

69
Q

lung cancer etiology

A

–cigarette smoking**
–passive smoke
–COPD
–asbestos
–radon
–arsenic
–genetics

70
Q

patho of lung cancer

A

–carcinogen overload
–genetic
–paralyze the cilia
–lesion development progresses to cancer
–activation of oncogenes
–deactivation of tumor suppressor genes
–rapid proliferation/destruction/invasion

71
Q

non-small cell lung cancer

A

makes up about 85-90% of all lung cancers; slow-growing

72
Q

small cell lung cancer

A

rapidly growing tumor that tends to metastasize quickly

73
Q

s/s of lung cancer

A

–cough
–hemoptysis
–wheeze or stridor
–chest pain
–dyspnea
–weight loss
–excessive fatigue
–weakness
–hoarseness
–pneumonia-like secretions
–often asymptomatic

74
Q

what might be the first sign of lung cancer?

A

paraneoplastic syndrome

75
Q

paraneoplastic syndrome

A

too much of a specific hormone showing up somewhere it shouldn’t be
–ACTH secretion from lung
–ACTH chemically resembles MSH
–stimulates melanocytes, giving patients with lung cancer a tanned appearance

76
Q

breast cancer

A

–most develop from lining in ducts
–overexpressed estrogen receptors
–overexpressed human epidermal growth factor receptor

77
Q

risk factors of breast cancer

A

–age > 50
–prolonged reproductive life
–hormone replacement therapy
–obesity
–late childbirth
–nulliparous
–family hx of breast or ovarian cancer
–Ashkenazi Jewish women
–BRCA1 and BRCA2 mutation

78
Q

procedures associated with BRCA genes

A

preventative mastectomy and oophorectomy

79
Q

cancer risks associated with BRCA genes

A

–breast
–ovarian
–colon
–pancreatic cancer
–prostate cancer

80
Q

s/s of breast cancer

A

–single tumor
–nontender tumor
–firm tumor
–irregular borders
–adherence to the skin or chest wall
–upper, outer quadrant of breast
–nipple discharge
–swelling in one breast
–nipple or skin retraction
–peau d’orange
–Paget’s disease of the breast

81
Q

peau d’orange

A

a thickening of skin that resembles an orange peel

82
Q

Paget’s disease of the breast

A

involves redness, crusting, pruritis, and tenderness of the nipple

83
Q

cervical cancer risk factors

A

–smoking
–history of STDs
–HPV infection
–two or more lifetime sexual partners
–immunosuppression
–genetics

84
Q

high risk HPV

A

causes persistent infection that progresses to cervical cancer

85
Q

low risk HPV

A

condylomata (genital warts) but does not cause cervical cancer

86
Q

cervical cancer clinical course

A

–long asymptomatic period
–abnormal pap = dx

87
Q

colorectal cancer screening

A

beginning at age 50, all adults should have a colonoscopy every 10 years

88
Q

polyps

A

tumorous mass that projects into the intestinal lumen

89
Q

familial adenomatous polyposis

A

well-defined hereditary disorder that predisposes an individual to intestinal polyps

90
Q

colorectal cancer risk factors

A

–obesity
–tobacco
–physical inactivity
–insulin resistance
–low fiber in diet
–high amount of animal fat in diet
–diets low in vit. A, C, and E
–UC
–heavy alcohol use

91
Q

s/s of colorectal cancer

A

–fatigue
–weakness
–weight loss
–iron deficiency anemia
–changes in bowel habits
–melena
–diarrhea
–constipation
–hematochezia (rectal bleeding) and narrowing of stool caliber

NUR 326 Exam 4 (5 decks)

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