Oncology

Question 1

the cell cycle

Answer 1

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

Question 2

cancer cells

Answer 2

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

Question 3

why does tumor development become easier as we age

Answer 3

strength of immune system decreases

Question 4

well-differentiated

Answer 4

a cancer cell that looks and functions like a normal cell

Question 5

anaplasia

Answer 5

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

Question 6

cancer cells break all these characteristics of normal cells

Answer 6

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

Question 7

TNM system of staging cancer

Answer 7

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

Question 8

T

Tumor size & location

Answer 8

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

Question 9

N

Spread to nodes

Answer 9

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

Question 10

M

metastasis

Answer 10

M0 - none

M1 - Yes

Question 11

four stages of carcinogenesis

Answer 11

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

Question 12

tumor suppression genes

Answer 12

these are the brakes

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

Question 13

oncogenes

Answer 13

these are mutated proto-oncogenes

gas pedal

growth signal on permanently, gas pedal is stuck

Question 14

p53 gene

Answer 14

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

Question 15

promoters

Answer 15

help the mutated gene proliferate

examples:

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

Question 16

viral induced cancer

Answer 16

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

Question 17

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

Answer 17

vascular endothelial growth factor

Question 18

cancer spread

Answer 18

seeding - tumor erodes & sheds into body cavities

implantation - direct expansion of tumor into adjoining tissue

metastasis - lymphatic & vascular

Question 19

Common secondary site

Answer 19

liver bc the way the blood flows

Question 20

lung cancer metastasizes to

Answer 20

bone - pain

brain - change in balance

Question 21

colon cancer metastasizes to

Answer 21

liver - develop bleeding problems; ↑ liver enzymes

Question 22

breast cancer metastasizes to

Answer 22

bone
brain
liver
lung - coughing, hemoptysis

Question 23

prostate cancer metastasizes to

Answer 23

vertebrae - back pain

Question 24

melanoma metastasizes to

Answer 24

brain

Question 25

lung cancer

Answer 25

``` 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 ```

Question 26

lung cancer etiology

Answer 26

85% of lung cancer pts are current or former smokers risk increases with higher "cigarette pack years"

Question 27

patho of lung cancer

Answer 27

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

Question 28

types of lung cancer

Answer 28

non-small cell lung cancer (NSCLC) - 85-90% of lung cancers, slow growing small cell lung cancer (SCLC) - rapidly growing and mets quickly

Question 29

S/S of lung cancer

Answer 29

``` 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 ```

Question 30

paraneoplastic ACTH in lung cancer

Answer 30

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

Question 31

breast cancer risk factors

Answer 31

``` > 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 ```

Question 32

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

Answer 32

``` breast ovarian colon pancreatic males ↑ risk of prostate ```

Question 33

anti-cancer agents

Answer 33

cytotoxic agents hormonal agents biologicals targeted drugs

Question 34

cytotoxic agents = cell _________

Answer 34

death

Question 35

hormonal agents →

Answer 35

block effects of hormones on tumor

Question 36

biologicis →

Answer 36

alter the body's response to cancer

Question 37

targeted drugs →

Answer 37

newer class, targets cancer cells ONLY

Question 38

growth fraction

Answer 38

the ratio of proliferating cells to resting cells chemos work better on cells that are actively growing, dividing

Question 39

malignant tumors initially grow ______________

Answer 39

very rapidly

Question 40

as tumor increases in size, rate of proliferation __________

Answer 40

decreases ie. low growth fraction

Question 41

Low growth fraction of tumors have what characteristics

Answer 41

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

Question 42

consequences of late detection

Answer 42

mets less responsive patient more debilitated by disease

Question 43

solid tumors respond poorly because

Answer 43

low growth fraction | limited blood supply

Question 44

as tumor ages, heterogeneity ___________

Answer 44

increases mutations become harder to treat

Question 45

intermittent chemo goal

Answer 45

100% CA cell death with limited normal cell injury try to strike a balance, letting normal cells recover but not too long

Question 46

combo therapy

Answer 46

advantages: -reduces drug resistance & normal cell injury (don't want overlapping toxicities) -increases cancer cell death

Question 47

optimal dosing

Answer 47

- 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

Question 48

regional drug therapy

Answer 48

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

Question 49

usual chemo toxicities

Answer 49

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

Question 50

hyperuricemia toxicity with chemo

Answer 50

excessive level of uric acid in blood cause: cell death/destruction of DNA

Question 51

drugs to deal with chemo toxicities

Answer 51

odansetron (Zofran) - serotonin receptor antagonist promethazine (phenergan) - H1 receptor antagonist dexamethasone magic mouthwash

Question 52

cell cycle phase specific

Answer 52

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

Question 53

cell-cycle phase non-specific

Answer 53

works on all stages (including G0) not as effective in injury to the proliferating cell

Question 54

cytotoxic agents

Answer 54

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. ```

Question 55

alkylating agent

Answer 55

cyclophosphamide cell cycle phase non-specific resistance ``` usual toxicities plus: vesicant hemorrhagic cystitis sterility discoloration of skin & nails ```

Question 56

antimetabolite

Answer 56

methotrexate moa: folate antagonist cell cycle specific (typlically S phase) resemble natural metabolites resistance usual toxicities plus: nephrotoxic hepatotoxic fetal death & abnormalities

Question 57

antitumor abx

Answer 57

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

Question 58

vinca alkaloids

Answer 58

vincristine cell cycle specific (blocks mitosis) usual toxicities plus: peripheral neuropathy vesicant no bone marrow suppression in some drugs of this class

Question 59

ondansetron

Answer 59

serotonin antagonist treats N/V blocks serotonin receptors on vagal nerve and in the CTZ AE: HA, D, dizziness efficacy improved with steroids

Question 60

promethazine

Answer 60

dopamine antagonist N/V blocks dopamine receptors in CTZ AE: respiratory depression, drowsiness, sedation, vesicant black box: resp depression < 2 yo, gangrenous extravasation

Question 61

biologics moa

Answer 61

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

Question 62

biologic types

Answer 62

- 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

Question 63

biologics | SE

Answer 63

``` 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

Question 64

CTZ

Answer 64

chemoreceptor trigger zone