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pathology spring > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

neoplasms

A

1) tumor or swelling
2) new growth
- abnormal mass of tissue which is uncoordinated with normal tissues and persists in same excessive manner after cessation of stimuli

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2
Q

fundamental to neoplasm

A

1) loss of responsiveness to normal growth controls
2) and compete with normal cells and tissues for metabolic needs

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3
Q

oncology

A

1) study of tumors

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4
Q

tumors have 2 components

A

1) parenchyma
- transformed or neoplastic cells
2) stroma
- non neoplastic CT and blood vessels

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5
Q

benign tumors

A

1) suffix -oma
2) lipoma, adenoma, polyp, cystadenomas
- designated by cell type and pattern

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6
Q

know the roots

A

:(
fibroma
lipoma
rhabdomyoma = skeletal muscle
leiomyoma = smooth muscle
angioma
hemangioma
lymphangioma
neuroma
chrondroma
osteoma

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7
Q

squamous epithelium

A

1) squamous papilloma
- reactive?

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8
Q

glandular epithelium

A

1) adenoma

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9
Q

connective tissue

A

fibroma
- reactive, not uncontrolled

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10
Q

lymphoid

A

lymphoid hyperplasia
- reactive

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11
Q

melanocytic

A

1) nevus, mole

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12
Q

-oma misnomers that are NOT benign

A

1) hematoma
2) hamartoma
- usually controlled
3) choristoma
- abnormal location
4) teratoma
- tumors, benign or malignant
- all three germ cell layers
5) lymphoma, melanoma, mesothelioma, seminoma
- all malignant

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13
Q

cancer

A

1) can invade and destroy adjacent tissues and metastasize to cause death
- carcinoma (epithelium)
- sarcoma (soft tissue or bone)
- lymphoma (lymphoid)

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14
Q

villous adenoma

A

1) polyp of the colon
2) can become cancer

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15
Q

pleomorphic adenoma

A

1) benign mixed tumor of salivary glands

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16
Q

cystic teratoma

A

1) all three germ cells
2) can be taken out of ovary
3) hair and tooth

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17
Q

uterine leiomyoma

A

1) common in uterus
2) spindle cells

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18
Q

thyroid adenoma

A

1) lots of thyroid follicles

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19
Q

monoclonality and divergent differentiation

A

1) tumor from one cell
2) monoclonal origin
3) stem cell may undergo divergent differentiation
- tumor of mixed cell population
- mixed tumors

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20
Q

differentiation

A

1) extent to which tumor cells resemble tissue of origin
- well vs poorly
2) grading
- morphologically and functionally
- pleomorphic (look different)
- mitotic activity
- infiltration
- necrosis

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21
Q

anaplasia

A

1) lack of differentiation
2) if its anaplastic YOU WILL DIE
3) mitotic rate super high, pleomorphic, nucleus to cytoplasm ratio high, don’t mature and polarize

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22
Q

rhabdomyosarcoma

A

1) often in children
2) the cells look very different from others
- pleomorphic, deadly tumor

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23
Q

anaplastic tumor cell

A

1) hard to tell what it is
2) antibody stain
3) high NC ratio

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24
Q

dysplasia

A

1) precursor
2) intraepithelial neoplasia
3) can have it in the skin, epithelial
4) increased NC ratio, pleomorphism, not much mitosis (so it is malignant potential)

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25
Q

rate of growth

A

1) benign - slow
2) malignant - faster
- correlated with level of differentiation, if it is poorly diff. it is faster
3) cancers take years to evolve
4) rapidly growing tumors may contain areas of ischemic necrosis
- need blood supply, so if it outgrows it

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26
Q

local invasion

A

1) benign is typically localized with capsule
2) but if there is pleomorphic with no room, it will look slightly invasive
3) cancers grow by progressive infiltration

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27
Q

fibroadenoma of the breast

A

most common tumor of the breast
- likely benign
- fibrous component and ductal structures

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28
Q

invasive ductal carcinoma of the breast

A

1) extensions because it invades and can get into blood vessel

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29
Q

metastasis

A

1) neoplasm will be MALIGNANT
2) not all cancers have same ability to metastasize
- the more anaplastic, the more potential
3) 30% with solid tumors will metastasize

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30
Q

three modes of metastasis

A

1) seeding
- seeding into cavity
2) lymphatic spread
- carcinomas tend to do this
3) hematogenous spread
- favored by sarcomas
- liver and lungs

31
Q

comparison of beign and malignant

A

1) benign is well differentiated and slow, well demarcated
2) malignant is anaplastic, erratic growth, locally invasive, often metastasize

32
Q

epidemiology of cancer

A

1) dietary fat and fiber in africa and western societies
2) preneoplastic diseases
3) cigarette smoking and lung cancer

33
Q

incidence rates of cancers by sex

A

1) men with lung cancer is coming down
- stopped smoking
2) breast cancer is rising

34
Q

heredity

A

1) predisposition to a few uncommon cancers
- childhood retinoblastoma
- colon, ovary, prostate, uterus, and sometimes melanoma cancer
- xeroderma pigmentosum (sunburn damage)
- adenomatous polyposis coli (familial)

35
Q

preneoplastic disorders

A

1) in the setting of these disorders, more tumors
- persistent regenerative cell replication
- hyperplastic and dysplastic proliferation
- chronic atrophic gastritis
- leukoplakia
- villous adenoma of the color

36
Q

carcinogenesis

A

1) nonlethal genetic damage lies at the heart of cancer
- 4 genes
a) growth promoting proto-oncogenes
b) growth inhibiting cancer suppressor genes
c) genes that regulate apoptosis
d) genes involved in DNA repair

37
Q

molecular basis of cancer

A

1) failure of DNA repair
2) mutations in genes can then activate growth promoting oncogenes or alteration of genes that suppress cancer
3) malignant cell can become clonal and acquire mutations

*p53 is the guardian of the genome (DNA damage repair and halts cell cycle)

38
Q

oncogenes

A

1) discovered through transforming animal retroviruses
2) 2 points
- normally, they promote cell proliferation
- mutations promote UNCONTROLLED proliferation
3) DNA of spontaneously arising cancers contain these

39
Q

growth factors

A

1) mutations can make them oncogenic
2) PDGF necessary, but it can make tumors
2) ras over expression of GF genes
- TGF-alpha which bind to GF receptor to promote growth

40
Q

growth factor receptor

A

1) mutations can mean overexpression of continuous signals
2) EGR receptor family
- c-erb B-1 / B-2 (her-2-neu is seen in 15-20% of breast cancer)
- targets for new treatments

41
Q

c-ras and c-abl

A

1) 30% of all tumors contain mutated ras
- which tell nucleus to keep replicated
2) activated downstream kinases that flood signals to continue replication
3) lives on chromosome 9
- normal
- translocation to chromosome 22 is bad

42
Q

brc-c-abl

A

1) mutations also keeps signaling just like ras

43
Q

myc

A

1) causes cell cycle progression
2) active in nucleus
- binds to DNA causing transcriptional activation of growth genes
- overexpression contributes to overproliferation
3) part of chromosome 8
- translates to chromosome 14 which is BAD

44
Q

activation of oncogenes

A

1) mutations cuause inappropriate production of growth promoting protein
a) point mutation
- ras oncogene and seen in many tumors
b) chromosomal translocations
c) gene amplification

45
Q

brc-abl

A

1) potent tyrosine kinase => proliferation

46
Q

N-myc

A

1) can be amplified in neuroblastoma

47
Q

antioncogenes

A

1) apply brakes to cell-proliferation
2) retinoblastoma
- gene that prevents DNA synthesis by binding to TFs
- on chromosome 13
- if it is inactivated (cyclin phosphorylation) will cause tumor to form
- mutant must occur on both alleles

48
Q

TP53

A

1) cancer suppressor gene that inhibits cell cycle when DNA is damaged by chemicals or radiation
2) if no repair possible, APOPTOSIS
3) homozygous loss of P53 for malignant transformation
- seen in almost every types of cancer
4) mutation reduces efficacy of anti-cancer therapy

49
Q

bcl-2

A

1) prototypic anti apoptosis gene
- mutation t(18;14)
- seen in 80% of B cell lymphomas

50
Q

bax

A

1) opposes bcl-2 and accelerated cell death
- transcription is influenced by p53 (upregulated)

51
Q

BRCA1 gene

A

1) mutations predispose to breast cancer

52
Q

xerodoma pigmentosum

A

1) UV light causes DNA damage and prevent normal replication

53
Q

multistep oncogenesis

A

1) no single oncogene can transform cells
2) several must be activated
3) loss of 2 or more cancer suppressor genes are necessary for cancer to form

54
Q

adenoma - carcinoma sequence

A

1) normal epithelium is hyperproliferative
- loss of APC locus
- loss of DNA methylation
2) early adenoma => intermediate => late
- loss of tumor supressor, loss of p53
3) carcinoma

55
Q

angiogenesis

A

1) tumors cannot enlarge beyond 1-2 mm without vessels
- cannot metastasize without this
2) tumor cells secrete basic fibroblast GF and vascular endothelial GF cause vessel to grow

56
Q

tumor progression

A

1) more aggressive over time

57
Q

mechanisms of local and distant spread

A

1) migration to vessel
2) tumor embolus
3) extravasion at different site
4) make new blood supply for them

58
Q

classes of carcinogenic agents

A

1) chemical carcinomas
2) radiation
3) viral

59
Q

chemicals

A

1) highly reactive electrophiles and can be augmented by promoters
2) can act in concert with other carcinogens
3) direct
- weak
4) indirect
- metabolic conversion required

60
Q

radiation

A

1) chromosomal breakage, translocation, point mutation
2) latent period is long, which can accumulate additional mutations
- UV
- x-rays
- nuclear fusion

61
Q

ionizing

A

1) means of clinical diagnosis and curative mode of therapy for some tumors
- mutagen and destroyer of cells
2) electromagnetic or high energy neutrons and charged particles
3) both forms displace electrons
4) DNA (direct and indirect damage), cell membranes

62
Q

DNA damage is survivable

A

1) if cell is remained in the intermitotic phase
2) depends on repair and effect of oxygen
3) effect of radiation is cumulative

63
Q

molecular

A

1) formation of pyrimidine dimers

64
Q

cellular

A

chromatin clumping

65
Q

cytoplasmic

A

mitochrondria and cell swelling

66
Q

radon

A

1) short range DNA damage
2) certain US region with uranium in the soil

67
Q

total body radiation

A

1) 50-100 rads can cause nausea
2) 700 rads can cause death

68
Q

viral oncogenesis

A

1) can get into DNA
2) RNA oncogenic viruses
- human T-cell leukemia virus
3) DNA oncogenic
- HPV
- epstein barr
- hepatitis B

69
Q

burkitts lymphoma

A

1 )EBV get on lymphocytes and proliferate
2) translocation mutations from getting into the DNA

70
Q

tumor antigens

A

1) tumor treatment
2) immunohistochemistry is used to classify neoplasms
3) S-100 is on all neuroectodermally derived
- LCA on leukocytes
- cytokeratins
-PSA
- actin

71
Q

effects of tumors on the host

A

1) location is very improtant
2) hormone production in endocrine tumores
3) cachexia
- metabolic rate is increased despite decreased food intake
4) paraneoplastic syndromes
- hypercalcemia
- cushings

72
Q

grading of cancer

A

1) grade I
- differentiated
2) grade 4
- undifferentiated, spreading rapidly

73
Q

staging

A

1) T1 - T4 (tumor size and expansion)
2) N1-N3 (cancer in lymph nodes)
3) M0-M1 (metastasis)

73
Q

tissue sampling

A

1) tissue diagnosis of any mass is necessary before therapy is implemented
2) biopsy
3) fine needle aspiration
4) cytologic smears

pathology spring (7 decks)

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