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Patho 1 > Oncology > Flashcards

Oncology Flashcards

1
Q

How does the cell cycle catch mistakes in DNA?

A

has checkpoints

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2
Q

Order of cell cycle

A

G0, G1, S, G2, M

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3
Q

G0 phase

A

rest phase

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4
Q

G1 phase

A

enter cell cycle and prep for DNA replication–proto-oncogenes are activated

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5
Q

S phase

A

synthesis of chr and chr move to opp poles to prep for division into 2 cells (23 chr at end each with nuclear mem around each)

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6
Q

G2 phase

A

cells prep to divide

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7
Q

Mitosis phase

A

2 daughter cells develop

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8
Q

Immune surveillance

A
  • our immune sys surveys bod for foreign subs or “no-self” antigens to attach
  • with age, system worsens and reaction declines–mutated cells escape easier
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9
Q

Patho of cancer cells

A
  • rapid rep w/o G0 and checkpoints
  • altered DNA keeps reproducing; no apoptosis
  • constant move thru cycle
  • ignore growth inhibitors released by neighboring cells so nothing stops them from going where they want
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10
Q

Differentiation

A

how neoplastic cells resemble normal cells with structure and function

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11
Q

anaplasia

A

lack differentiation
- often malignant cells
- total cell disorganization, abnormal appearance, cell dysfxn

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12
Q

Which tumors are more well-differentation?

A

Benign

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13
Q

Rules that cancer cells BREAK

A
  • contact inhibition–push others aside
  • not cohesive (mets)
  • little communication
  • proliferation w/o apoptosis
  • avoid “non-self” markers so the sys doesn’t attach
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14
Q

Cancer cells are…

A

UNORGANIZED
VARIABLE SHAPE
MAY DIVIDE
VARIABLE NUCLEUS

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15
Q

Benign tumor characteristics

A
  • well-differentiated
  • local
  • cohesive
  • no mets
  • no necrotic core–living
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16
Q

Malignant tumor char

A
  • poor diff or anaplastic
  • break free easily
  • slow or rapid growth
  • neurotic core esp with age–harder to tx bc can’t get tx in
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17
Q

Tumor markers

A
  • hor, enzymes, genes, or antigens in blood, urine, or CSF
  • let us follow the clinical course (dec w/ tx)
  • can also be present w/o cancer (ex: PSA)
18
Q

Phases of cancer cell grwoth

A
  • initiation–alt of genes (spon) or induced by contract with (carcinogen)
  • promotion–cells accum
  • progression–more mutate with met potential
  • metastasis
19
Q

Cancer genetics

A

gene mutations are sporadic or hereditary (BRCA)

20
Q

tumor suppressor genes

A

genes that normally “brake” cell division but can mutate and become inactive, inhibiting the brake

21
Q

Oncogenes

A

Proto-oncogenes that normally tell the cell to grow and mutate to be permanently “on”–prolif

22
Q

Carcinogens

A

Substances that cause the development of cancer–start mutations
- can alter DNA
- damage accums

23
Q

3 classes of carcinogens

A
  • known–HPV, HIV, alcohol, virus, tobacco
  • probable–nightshift
  • possible–insuff evidence; exhaust engine
24
Q

promoting agents

A

help genes proliferate and encourage further mutation
- hi fat diet
- alc
- tobacco
- hor (estrogen)

Reversible

25
Q

viral-induced cancer

A
  • malignancies assoc with virus–HIV, HPV, Hep B and C
  • insert gene into host cell and host cell begins manufacturing virus
  • activate growth - promo paths or inhibit tumor supp in infected cells
26
Q

3 ways cancer can spread

A
  • seeding - tumor erodes and sheds into body cavity
  • implantation - exposure to adjoining tissue
  • mets - travel thru lymph or vasc
27
Q

Primary tumor

A

origin tumor

28
Q

Secondary tumor

A

metastasis; loos like cells from original site
- site depends on location of primary tumor
- can make own blood supply and secrete vascular endo Grwoth factor

29
Q

most common sites of secondary tumors

A

lung, bone, liver, brain

30
Q

Where does colon cancer often met to

A

liver

31
Q

Where does lung cancer often met to

A

bone and brain

32
Q

Where does breast cancer met to

A

everywhere

33
Q

Where does prostate cancer met to

A

vertebrae

34
Q

Where does melanoma met to

A

the brain

35
Q

Why is the liver a common site for mets?

A

all blood flow thru the liver

36
Q

intraperitoneal seeding

A

Spreads thru the peritoneum to other ab organs

37
Q

lymph spread of cancer

A

cells can get trapped and die, go dormant, or flourish

38
Q

vasc spread of cancer

A

penetrate BVs and drain local veins; first stop often liver

39
Q

Classifications of malignancy

A

1 - well diff
2 - mod diff
3 - poor dif

40
Q

Layman class of tumors

A

1 - confined to organ of origin
2 - locally invasive
3 - regional spread
4 - spread to distal sites

41
Q

TNM classifications

A

T - tumor size, location, involvement
N - lymph node involvement
M - metastasis (N0 none, M1 yes)

42
Q

P53

A

a tumor suppressor gene that triggers apoptosis

Patho 1 (37 decks)

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