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PAtho > Unit 16 > Flashcards

Unit 16 Flashcards

1
Q

what is the most common ca in women

A

breast

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2
Q

et of breast ca

A

mutation of gene rt cell prolif

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3
Q

risk fact for breast ca 4

A

aging
genetic predispostion
inhereted gene def
hormones

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4
Q

how is aging a risk for breast ca

A

inc risk in older women rt to cumulativie exposure

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5
Q

how is genetic predisp a risk for breast ca

A

pt has inc susceptibility to risks, no identifiable gene

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6
Q

how many women does inherited gene def affect

A

5-10 out of every 100

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7
Q

what percent of the 5-10 out of every 100 women have an inherited gene that they pass onto offspring

A

75

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8
Q

what are the 2 inhereited gene defs in brst ca

A

brca1 on chr 17

brca2 on chr 13

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9
Q

what type of genes are brca1 and 2

A

tumor supressing genes

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10
Q

how do brca1 and 2 pass onto offpsring

A

autosomal dominatn

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11
Q

what hormone issue is the most important when looking at breast ca risks

A

excessive in the absense of P after menopause

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12
Q

when is E given to women without P

A

after menopause, normally given to tx the sudden drop in E prod by ovary to dec SEs of women

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13
Q

which conditions may lead to prolonged E exposure in women

A

early menarche, late menopause

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14
Q

how is early menarche determiend

A

based on population norms

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15
Q

what other ‘condition’ may lead to inc E exposure lt inc bc risk

A

nulliparity

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16
Q

why is nulliparity a risk for bc

A

uninterupted and repeated meneses means continuous E prod

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17
Q

what things break the E cycle

A

pregnancy
lactation
bc pill

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18
Q

where does 48% of bc occcur

A

near tail of spenec in outter upper q of breast

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19
Q

after tail of spence, in what areas does bc have inc incidence in

A

areola, UIQ, LOQ, ILQ

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20
Q

2 main types of bc

A

ductal carcinoma in situ

infiltrating ductal carcinoma

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21
Q

what type of cells are involved in ductal carcinoma in situ

A

inc in epith cells

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22
Q

“in situ” when speaking about ductal carcinomas

A

restricted, remains in site of origin, non invasive, good prognosis

23
Q

what fraction of all bc does ductal carcinoma in situ make up

A

1/5

24
Q

site of orgin of ductal carcinoma in situ

A

intraductal

25
Q

stage O in ductal carcinoma in situ

A

early stage that can progress to infiltrating ductal carcinoma if left untx

26
Q

where does infiltrating ductal carcinoma arise from

A

alone or from ductal carcinoma in situ

27
Q

what percent of bc does infiltrating ductal carcinoma make up

A

75%

28
Q

origin of infiltrating ductal carcionma

A

ductal origin

29
Q

what type of mass is in infiltrating ductal carcinoma

A

solid, irregular mass

30
Q

what are the 2 types of mets that arise from infiltrating ductal carcinoma

A

proximal

distal

31
Q

proximal mets in infiltrating ductal carcinoma

A

spreads short distance, axilla via lymph v

32
Q

distal mets in infiltrating dutal carcinoma

A

liver, bone, brain, via blood

33
Q

what does infiltrating ductal carcinoma do to breast tissue

A

destroys it

34
Q

what percent of bc is identified by pt

A

60-75%

35
Q

what mass is usually identifed by the pt

A

unilateral, immobile, hard, painless mass usually in uoq

36
Q

late mnfts of breast ca

A

nipple discharge and retraction

breast edema

37
Q

dx bc

A

px hx

mammography

38
Q

mammography

A

xray that can detect early tumors

39
Q

issues with mammograms

A

may have false + or -

limitations of age and freq of exams

40
Q

what happens if a mammogram is positiveee

A

biopsy to determine if its malignant or benign

remove mass

41
Q

what cell receptors do they look at in cell biopsys from bc

A

E and P

42
Q

what does the number of E and P receptors on a cell determine

A

how dependent a cell is on E and P

43
Q

why is e and p dependency helpful

A

we want to know what these malignant cells are receptive to

44
Q

tx for bc

A 
combo
H therapy with combo
sx
radition
chemo
45
Q

when do we use H thearpy to tx bc

A

if e and p receptor levels are inc on cell

46
Q

if E > P in cell r eceptors, what tx do we use

A

anti estrogen
inc dose of E without any P
androgens

47
Q

eg of an antiestrogen

A

tamoxefin

48
Q

why will inc an E dose without P tx E>P breast ca

A

inc E will down regulate the number of receptors for that H. Inc e -> damage to receptors killing them

49
Q

if P>E what tx do we use

A

progestins

50
Q

3 sx used in bc

A

lumpetctomy
qaudrectomy
mastectomy

51
Q

where do we radiate in bc

A

breast and axilla

52
Q

when do we use chemo in breast ca

A

pre and post sx, circumstantially

53
Q

what is prognosis of bc bsaed on

A

node involvement. a whole infected breast has better prognosis then a bit of breast and some lymph node

PAtho (31 decks)

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