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Pathopharm 326 > Oncology > Flashcards

Oncology Flashcards

1
Q

the cell cycle

A

G0 - cell is at rest

G1 - cell enters cell cycle, prepare for DNA replication, proto-oncogenes are activated

S - synthesis of structure and move to opposite poles; nuclear membranes develop around the separate sets of 23 pairs

G2 - cells prepare to divide

M - mitosis is completed and 2 daughter cells are created

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2
Q

cancer cells

A

No checkpoints - no DNA errors recognized, no apoptosis

disregard growth inhibitors of neighboring cells

they accumulate on top, around, and beside each other, crowding out, taking over normal cells and may break free and travel elsewhere

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3
Q

why does tumor development become easier as we age

A

strength of immune system decreases

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4
Q

well-differentiated

A

a cancer cell that looks and functions like a normal cell

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5
Q

anaplasia

A

indicates total cellular disorganization, abnormal cell appearance, & cell dysfunction

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6
Q

cancer cells break all these characteristics of normal cells

A 
Contact inhibition
Cohesiveness - "I'm out of here"
Communication - little to none
Proliferation control
Proliferation rate
"Self" HLA antigens
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7
Q

TNM system of staging cancer

A

T - tumor size, location, involvement
N - lymph node involvement
M - metastasis

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8
Q

T

Tumor size & location

A

T0 - no evidence of primary tumor
TIS - tumor in situ
T1-4 - progressive increase in size or involvement

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9
Q

N

Spread to nodes

A

N0 - no spread to regional lymph nodes
N1 - spread to closest or small number of regional lymph nodes
N2 - spread to most distant or numerous regional lymph nodes

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10
Q

M

metastasis

A

M0 - none

M1 - Yes

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11
Q

four stages of carcinogenesis

A

initiation - alteration of genes that arise spontaneously

promotion - actively proliferating cells accumulate → reversible

progression - cells undergo further mutation → tend to be more invasive w/ metastatic potential

metastasis

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12
Q

tumor suppression genes

A

these are the brakes

if these become inactivated, cells proliferate because there are no brakes

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13
Q

oncogenes

A

these are mutated proto-oncogenes

gas pedal

growth signal on permanently, gas pedal is stuck

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14
Q

p53 gene

A

tumor suppression gene in cells that controls cellular apoptosis (natural death of cells with damaged DNA)

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15
Q

promoters

A

help the mutated gene proliferate

examples:

  • diet (high fat)
  • ETOH
  • tobacco
  • hormones (long-term exposure to estrogen)
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16
Q

viral induced cancer

A

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

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17
Q

cancer cells secrete ________________, a substance that gives them the capability to develop new blood vessels (angiogenesis)

A

vascular endothelial growth factor

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18
Q

cancer spread

A

seeding - tumor erodes & sheds into body cavities

implantation - direct expansion of tumor into adjoining tissue

metastasis - lymphatic & vascular

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19
Q

Common secondary site

A

liver bc the way the blood flows

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20
Q

lung cancer metastasizes to

A

bone - pain

brain - change in balance

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21
Q

colon cancer metastasizes to

A

liver - develop bleeding problems; ↑ liver enzymes

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22
Q

breast cancer metastasizes to

A

bone
brain
liver
lung - coughing, hemoptysis

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23
Q

prostate cancer metastasizes to

A

vertebrae - back pain

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24
Q

melanoma metastasizes to

A

brain

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25
Q

lung cancer

A 
leading cause of cancer-related deaths (men & women)
70% present with advanced, or mets
early diagnosis key to treatment
most often > 65 yo
blacks more often affected
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26
Q

lung cancer etiology

A

85% of lung cancer pts are current or former smokers

risk increases with higher “cigarette pack years”

27
Q

patho of lung cancer

A 
carcinogen overload
genetic predisposition
paralyze the cilia
lesion development progresses to CA
activation of oncogenes
deactivation of tumor suppressor genes
rapid proliferation, destruction, invasion
28
Q

types of lung cancer

A

non-small cell lung cancer (NSCLC) - 85-90% of lung cancers, slow growing

small cell lung cancer (SCLC) - rapidly growing and mets quickly

29
Q

S/S of lung cancer

A 
cough
hemoptysis
wheeze or stridor
chest pain
dyspnea
wt loss
excessive fatigue
weakness
hoarseness
obstructive accumulation of secretions in the brochioles that appear as PNA
30
Q

paraneoplastic ACTH in lung cancer

A

tumor secretes ACTH, which resembles MSH, stimulating melanocytes, giving pt tanned appearance

31
Q

breast cancer risk factors

A 
> 50
prolonged reproductive life
hormone replacement therapy
obesity
late childbirth (after 30)
nulliparous (no pregnancies)
family hx of breast or ovarian cancer
ashkenazi jewish women
BRCA1 & BRCA2 mutation
32
Q

individuals with BRCA1 & BRCA2 mutations have an increased risk of what cancers?

A 
breast
ovarian
colon
pancreatic
males ↑ risk of prostate
33
Q

anti-cancer agents

A

cytotoxic agents
hormonal agents
biologicals
targeted drugs

34
Q

cytotoxic agents = cell _________

A

death

35
Q

hormonal agents →

A

block effects of hormones on tumor

36
Q

biologicis →

A

alter the body’s response to cancer

37
Q

targeted drugs →

A

newer class, targets cancer cells ONLY

38
Q

growth fraction

A

the ratio of proliferating cells to resting cells

chemos work better on cells that are actively growing, dividing

39
Q

malignant tumors initially grow ______________

A

very rapidly

40
Q

as tumor increases in size, rate of proliferation __________

A

decreases ie. low growth fraction

41
Q

Low growth fraction of tumors have what characteristics

A
  • large tumors have a necrotic core
  • ↓ nutrient supply at core
  • more cells in resting phase (G0)
  • more difficult to treat
42
Q

consequences of late detection

A

mets
less responsive
patient more debilitated by disease

43
Q

solid tumors respond poorly because

A

low growth fraction

limited blood supply

44
Q

as tumor ages, heterogeneity ___________

A

increases

mutations become harder to treat

45
Q

intermittent chemo goal

A

100% CA cell death with limited normal cell injury

try to strike a balance, letting normal cells recover but not too long

46
Q

combo therapy

A

advantages:
-reduces drug resistance & normal cell injury (don’t want overlapping toxicities)

-increases cancer cell death

47
Q

optimal dosing

A
  • maximize results
  • cell-cycle specific agents
  • keep active drug present in body long enough to hit the cells when they enter the specific phase the drug is targeting
48
Q

regional drug therapy

A

access to tumors
high drug concentrations
decrease systemic toxicity
examples: intraarterial, intrathecal, intravesical

49
Q

usual chemo toxicities

A 
N/V for several days after tx
1-2 weeks after first round:
     ↓ WBC, RBC, platelets
      Diarrhea
      alopecia
      fatigue
50
Q

hyperuricemia toxicity with chemo

A

excessive level of uric acid in blood

cause: cell death/destruction of DNA

51
Q

drugs to deal with chemo toxicities

A

odansetron (Zofran) - serotonin receptor antagonist

promethazine (phenergan) - H1 receptor antagonist

dexamethasone

magic mouthwash

52
Q

cell cycle phase specific

A

work only at a specific phase in cell cycle

does not affect G0 phase

prolonged infusion bc must capture each cell entering the phase it’s targeting

53
Q

cell-cycle phase non-specific

A

works on all stages (including G0)

not as effective in injury to the proliferating cell

54
Q

cytotoxic agents

A

largest class of chemo drugs (targets high growth fraction cells)

moa: disrupt dna synthesis, disrupt mitosis

Examples: 
alkylating agents
antimetabolites
antitumor abx
mitotic inhibitors
misc.
55
Q

alkylating agent

A

cyclophosphamide

cell cycle phase non-specific

resistance

usual toxicities plus:
vesicant
hemorrhagic cystitis
sterility
discoloration of skin & nails
56
Q

antimetabolite

A

methotrexate

moa: folate antagonist

cell cycle specific (typlically S phase)

resemble natural metabolites

resistance

usual toxicities plus:
nephrotoxic
hepatotoxic
fetal death & abnormalities

57
Q

antitumor abx

A

doxorubicin

cell cycle phase nonspecific

usual toxicities plus:
cardiotoxic (sometimes fatal); acute and delayed
harmless red color to urine/sweat

58
Q

vinca alkaloids

A

vincristine

cell cycle specific (blocks mitosis)

usual toxicities plus:
peripheral neuropathy
vesicant

no bone marrow suppression in some drugs of this class

59
Q

ondansetron

A

serotonin antagonist

treats N/V

blocks serotonin receptors on vagal nerve and in the CTZ

AE: HA, D, dizziness

efficacy improved with steroids

60
Q

promethazine

A

dopamine antagonist

N/V

blocks dopamine receptors in CTZ

AE: respiratory depression, drowsiness, sedation, vesicant

black box: resp depression < 2 yo, gangrenous extravasation

61
Q

biologics moa

A

uses body’s immune system to kill CA cells

stimulates body’s own immune system response by turning on or off the signals CA cells use to allude the immune system

62
Q

biologic types

A
  • immune checkpoint inhibitors - allow immune system to respond more strongly
  • T-cell transfer therapy - boosts natural abilities of T-cells to fight CA
  • monoclonal antibodies - mark CA cells
  • treatment vaccines - boosts immune system’s response
  • immune system modulators - enhance body’s immune response
63
Q

biologics

SE

A 
pain, swelling, soreness
flu-like sxs
weight gain/fluid retention
diarrhea
risk of infection

many SEs are d/t the revving up of immune response which can then also act on non-CA cells

64
Q

CTZ

A

chemoreceptor trigger zone

Pathopharm 326 (16 decks)

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