oncology

Question 1

cell cycle

Answer 1

sequence of growth stages for mitosis and regeneration
G0, G1, S, G2, M
check points: DNA check, cancer cells often dont have these

Question 2

G0

Answer 2

rest
cancer cells dont enter this at beginning cancer stage

Question 3

G1

Answer 3

DNA rep prep, protooncogenes activated (control cell rep)

Question 4

S

Answer 4

DNA rep + move to opposite ends with new nuclear membranes

Question 5

G2

Answer 5

prep to divide

Question 6

M

Answer 6

2 daughter cells

Question 7

cancer cells

Answer 7

DNA make up change over time -> makes treatment particularly difficult - tries to impact cell cycle in some way
disregard normal cell cycle rules
large number of dividing cells, large variably shaped nuclei, large nucleus to cytoplasm ratio, variable size and shape, loss of normal cell features, disorganized arrangement, poorly defined tumor boundary

Question 8

cancer cells: disregard normal cell cycle rules

Answer 8

constantly going through cycle -> not G0
no checkpoints -> DNA errors, apoptosis
disregard growth I released by neighboring cells
as they proliferate, they accumulate on top, around, beside each other, take over boundaries of organs, crowd normal cells, can break free and travel

Question 9

immune surveillance

Answer 9

constantly survey for self v non self
non self antigen -> initiate attack to destroy invading substance
decrease with age therefore tumor development is easier

Question 10

differentiation

Answer 10

well differentiated = function like cell or origin
extent that neoplastic cells resemble normal cells both structurally (shape and size) and functionally (normal cell cycle)
anaplasia = lack of differentiation -> cancer, total cellular disorganization, abn appearance, cell dysF
benign usually well differentiated

Question 11

cancer cells break rules

Answer 11

contact inhibition - invade
cohesiveness - break away
communication - little to none
proliferation control - immortal/die unpredictable
proliferation rate - unpredictable, depends on differentiation (anaplastic = fast)
“self” HELA antigens - non self markers, attack may be muted, avoid

Question 12

benign

Answer 12

well differentiated, resemble origin
progressive, slow growth
cohesive, well demarcated, often encapsulated (moveable)
no necrosis

Question 13

malignant

Answer 13

poor dif, dont resemble origin, anaplastic
erratic growth (slow - rapid)
invasive and infiltrating, surround normal tissue
freq metastasis -> lymph or blood
can have necrotic core -> esp as age and size increase
- hard to get treatment there

Question 14

tumor markers

Answer 14

biologic substances - shed by some tumors
measurable -> hormones, enzymes, antigens, genes
- blood, urine, CSF, tumor plasma membranes
- screen or dx (not always - some non malignant diseases also produce): follow course, treatment working?
ex: PSA, BRCA gene mutation

Question 15

TNM: malignant

Answer 15

1 = well diff
2 = mod diff
3 = poorly diff or anaplastic

Question 16

staging

Answer 16

classifies tumor according to size, invasiveness, spread
help to understand seriousness, survival, tm, trials
T = tumor size, location, involvement
N = lymph node involvement
M = metastasis to distant organs

Question 17

staging: T

Answer 17

0 = no evidence of primary tumor
TIS = tumor in situ
T1-4 = progressive increase in size or involvement
1 = 1cm, 2 = 2cm, etc.

Question 18

staging: N

Answer 18

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

Question 19

staging: M

Answer 19

0 = none
1 = yes

Question 20

4 stage classification

Answer 20

limited info
1 = confined to origin of organ
2 = locally invasive
3 = regional spread
4 = distant site

Question 21

carcinogenesis

Answer 21

origin of cancer -> no simple answer, issue of gene expression
genes, carcinogens, promoters

Question 22

carcinogenesis: phases - initiation

Answer 22

alteration, change, mutation of genes that arise spontaneously or are induced by exposure to carcinogen

Question 23

carcinogenesis: phases - promotion

Answer 23

reversible -> alter/affect growth rate
actively proliferating cells accumulate

Question 24

carcinogenesis: phases - progression

Answer 24

further mutation - more invasive with metastatic potential

Question 25

carcinogenesis: phases - metastasis

Answer 25

spread of cancer

Question 26

cancer genetics: mutations

Answer 26

hereditary or sporadic
sporadic = acquired during life
mutations dont = cancer, just increase risk

Question 27

cancer genetic mechanisms

Answer 27

tumor suppressor genes = break pedal, p53 gene = controls apoptosis
if inactivated: proliferate out of control
oncogenes -> gas pedal stuck
mutated protooncogenes -> gas pedal
growth signal permanently on

Question 28

carcinogens

Answer 28

can alter DNA, damage is cumulative, often require prolonged exposure
classify: known, probable, possible
known = tobacco, asbestos, estrogen therapy, OH, virus
probable = night shift F
possible = engine exhaust

Question 29

promoters

Answer 29

promote dev
diet (increased fat)
OH, tobacco
hormones - estrogen (early menses, late menopause, no preg, HRT)

Question 30

viral induced cancer

Answer 30

HIV = carcinoma
HPV = cervical cancer
insert into host which becomes manufacturer of virus
moa: always involve activation of growth promoting pathways or I of tumor suppressors in infected cells

Question 31

metastasis

Answer 31

secrete vascular endothelial GF -> dev new BV = angiogenesis
primary and secondary tumor
spread = seeding, implantation, metastasis (lymph/vascular)

Question 32

seeding

Answer 32

tumor erodes and sheds cells into body cavities

Question 33

implantation

Answer 33

direct expansion to adjoining tissue

Question 34

metastasis: lymph

Answer 34

1st stop, trapped in nodes
death, dormancy, flourish/proliferate

Question 35

metastasis: vascular

Answer 35

penetrate local veins
liver 1st stop -> receives most of blood, clump, trapped, proliferate

Question 36

secondary tumors

Answer 36

need nutrients and O2, access to blood (angiogenesis)
lung, bone, liver, brain

Question 37

secondary tumors: lung

Answer 37

bone, brain

Question 38

secondary tumors: colon

Answer 38

liver

Question 39

secondary tumors: breast

Answer 39

bone, brain, liver, lung

Question 40

secondary tumors: prostate

Answer 40

vertebrae

Question 41

secondary tumors: melanoma

Answer 41

brain

Question 42

lung cancer

Answer 42

leading cancer COD, dx early - most present with advanced or metastatic
>65, AA

Question 43

lung cancer: etiology

Answer 43

smoking - promoter and known carcinogen, increase risk with # smoked -> pack per yr
overload of carcinogen and genetic predisposition
other common causes: 2nd hand, CPOD (chronic inflam), asbestos (construction), radon (test homes), arsenic, genetics, other (radiation therapy, pulm fibrosis)
get good hx

Question 44

lung cancer: patho

Answer 44

carcinogen overload, genetic predisp -> paralyze cilia -> lesions -> cancer -> activate oncogenes and deactivate tumor suppressor genes -> rapid proliferation/destruction/invasion

Question 45

lung cancer: types

Answer 45

non small cell lung cancer = slow growing
small cell = rapid, metastasize quickly

Question 46

lung cancer: s/s

Answer 46

coincide with smoking
cough, hemoptysis, wheeze/stridor, chest pain, dyspnea, weight loss, excessive fatigue, weak, hoarsness (compression of larynx)
obstructive accumulation of secretions in bronchioles -> pna (appear as pna)
routine CRX, asymp, paraneoplastic S may be first sign -> secretion of hormone (too much) by tumor -> ACTH -> tan bc stim melanocytes

Question 47

breast cancer

Answer 47

lining in ducts
overexposed estrogen receptors
overexposed human epidermal growth factor receptor

Question 48

breast cancer: rf

Answer 48

> 50, prolonged reproductive life = early menses and late menopause, HRT, obese, late childbirth (30+), nulliparous, fam hx, jewish, BRCA1 +2 mutation (increased r/o breast, ovarian, colon, pancreatic, prostate (M))
can rest for presence of BRCA in high risk, genetic counseling, preventative mastectomy and oophorectomy (ovaries)

Question 49

breast cancer: s/s

Answer 49

promote mamograms
single tumor, non tender, firm, irreg boarder, adherence to skin or chest wall, upper-outer quad of breast, nipple d/c, swelling in 1, nipple or skin retraction
peal d’orange = thickening of skin like orange peel
paget = redness, crsuting, pruritus, nipple tenderness

Question 50

cervical

Answer 50

clinical course = long asymp phase, abn pap (q3 yr)

Question 51

cervical: rf

Answer 51

smoke, hx STD, HPV! (genital wart type -> condylomata; or cancer type -> persistent infection), 2+ lifetime sexual partners, immunosuppression, genetics

Question 52

colorectal

Answer 52

q10 yr after 50yr
start asymp (tumorous mass that projects into intestinal lumen) -> most are small and have low chance of malignancy
familial adenomatous polyposis = predispose
hereditary non polyposis coli HNPCC -> low chance of cancer

Question 53

colorectal: rf

Answer 53

obsese (inflam), tobacco (polyps), physical inactivity (obese), insulin resistance, low fiber, high animal fat, high processed meats, decreased vits A, C, E (antioxidants); ulcerative colitis (inflam), high OH use

Question 54

colorectal: s/s

Answer 54

fatigue, weak, weight loss, Fe def anemia (slow blood loss), change in bowel habits, melena, d, c
hematochezia (rectal bleed) and narrowing of stool caliber (ribbon life bc passing by tumor)