Female GT and Breast Flashcards Preview

Patho 2 > Female GT and Breast > Flashcards

Flashcards in Female GT and Breast Deck (71)
Loading flashcards...
1
Q

fundamental reproductive unit of FGT

A
  • ovarian follicle

- composed one one germ cell surrounded by endocrine cells

2
Q

menarche

A
  • beginning of menstrual cycle

- average age 11-13

3
Q

female monthly sexual cycle

A
  • controlled by gonadotropins
  • only single ovum released
  • endometrium is prepped for implantation
4
Q

ovarian cycle

A
  • follicular phase- 15 d
  • ovulatory phase- ends with ovulation
  • luteal phase- 13d
5
Q

female hormonal system

A
  • GnRH from hypothalamus
  • FSH and LH from pituitary
  • estrogen and progesterone from ovaries
6
Q

what is the predominating hormone during the follicular phase

A
  • estrogen

- low levels of FSH, LH and progesterone

7
Q

what happens around day 14

A
  • LH surge

- ovulation occurs

8
Q

what is the predominating hormone during the luteal phase

A
  • progesterone that is released by corpus luteum
9
Q

oogenesis

A
  • germ cells in ovary differentiate to oogonia
  • divide by mitosis
  • mature into primary oocytes
  • enclosed in primordial follicles
10
Q

what happens at puberty

A
  • periodic secretions of FSH triggers meiosis
  • only one completes meiosis I
  • produces polar bodies and secondary oocytes
11
Q

when is meiosis II completed

A

after fertilization of ovum by sperm

12
Q

cells of the follicle

A
  • theca cells= outer portion

- granulosa cells= inner portion that provide nourishment

13
Q

estrogen

A
  • steroid hormone
  • comes from androgenic precursors
  • transformed by aromatase from testosterone to estrogen
  • have E1-3
14
Q

E1

A
  • predominant estrogen after menopause
15
Q

E2

A
  • produced in theca and granulosa cells

- predominant estrogen in premenopausal women

16
Q

E3

A

estrogen of the placenta during pregnancy

17
Q

types of estrogen receptors

A
  • ER alpha
  • ER beta
  • GPER (g-protein coupled estrogen receptor)
18
Q

ER alpha

A
  • predominant in uterus, mammary glands, and may places throughout body
  • sustained exposure to estrogen and activation of ER alpha -> cancer of breast and endometrium
19
Q

ER beta

A
  • predominantly expressed in ovaries and prostate

- activates anti-proliferative and pro-apoptotic pathways in cancers

20
Q

GPER

A
  • mediates rapid estrogen signaling by stim adenylyl cyclase
  • expressed in normal ovary
  • regulates physiological processes like follicle maturation
21
Q

clinical disorders associated with estrogen

A
  • endometriosis
  • fibroids
  • PCOS
22
Q

endometriosis

A
  • chronic hormone dependent inflammatory disease
  • growth of endometrial tissue outside uterus
  • pathogenesis is multifactorial
23
Q

clinical sx of endometriosis

A
  • moderate to severe pain
  • dysmenorrhea
  • low back pain
  • infertility
24
Q

most common anatomic site for endometriosis

A
  • ovaries*
  • anterior and posterior cul de sac
  • broad ligaments
25
Q

Sampson’s theory of retrograde menstruation

A
  • during menses
  • endometrial cells flow backwards through fallopian tubes into peritoneal cavity
  • results in endometriosis
26
Q

pre-menarcheal endometriosis

A
  • undifferentiated cells of mullerian origin in peritoneal cavity differentiate into endometrial tissue
  • results in endometriosis
27
Q

major causes of endometriotic pain

A
  • endometriotic lesions -> stimulate nociceptors
  • innate immune system -> NGF
  • peripheral NS
28
Q

uterine leiomyomas

A
  • aka fibroids
  • benign tumors of myometrium
  • most common pelvic tumor
29
Q

leiomyoma significance

A
  • effects function and structure of endometrium

- causes excessive bleeding in uterus

30
Q

leiomyoma pathogenesis

A
  • genetics- trisomy 12 and point mutations
  • Steroid hormones cause mitogenic stimuli
  • increased vascularity and venular ectasia
  • fibrotic factors
31
Q

polycystic ovarian syndrome (PCOS)

A
  • intraovarian androgen excess
  • closely associated with insulin resistance
  • predisposes pts to metabolic dysfunction and type 2 DM
32
Q

presentation of PCOS

A
  • hirsutism
  • menstrual irregularities
  • infertility due to infrequent or absent ovulation
33
Q

PCOS etiology

A
  • first hit- inherited predisposition
  • second hit- postnatal provocative hit
  • second hit is usually insulin resistant hyperinsulinemia
34
Q

steroidogenesis and PCOS

A
  • down regulation of thecal androgen production is flawed
  • hyper-responsive to LH
  • excess androgen -> anovulation and polycystic ovaries
35
Q

summary of issues in PCOS

A
  • ovarian hyperandrogenism
  • insulin resistant hyperinsulinemia
  • LH excess
  • obesity
36
Q

premenstrual syndrome (PMS)

A
  • physical and/or behavioral sx in second half of menstrual cycle
  • abdominal bloating
  • breast tenderness
  • HA
37
Q

pathogenesis of PMS

A
  • normal serum estrogen or progesterone
  • abnormal neurotransmitter response to hormonal changes
  • assoc with low serotonin
38
Q

what is the more severe version of PMS?

A

Premenstrual dysphoric disorder (PMDD)

39
Q

processes that contribute to menopause

A
  • hypothalamic and ovarian aging
  • environmental, genetic, and lifestyle factors
  • systemic diseases
40
Q

result of hypothalamic aging

A
  • desynchronized GnRH production

- impaired LH surge

41
Q

what are the two major structures of the breast

A
  • ducts

- lobules

42
Q

what are the two types of epithelial cells

A
  • luminal

- myoepithelial

43
Q

breast structural changes in 1st half of menstrual cycle

A
  • lobules are quiescent
44
Q

breast structural changes after ovulation

A
  • cell proliferation and number of acini per lobule increases
  • intralobular stroma becomes edematous
45
Q

breast structural changes on menstruation

A
  • regression of lobules and disappearance of edema
46
Q

breast tissue at puberty

A
  • estrogen and progesterone induces branching of ductal sys and dev of lobules
47
Q

breast tissue during pregnancy

A
  • progesterone and prolactin high
  • permanent increase in number/size of lobules
  • oxytocin -> proliferation
  • after lactation, apoptosis of epithelium and lobule atrophy
48
Q

breast tissue during aging and menopause

A
  • atrophy
  • decrease in CT
  • increase in adipose
49
Q

cancers of lobule and terminal ducts

A

carcinoma

50
Q

cancers of intralobular stroma

A

fibroadenoma

51
Q

major classifications of benign breast lesions

A
  • non-proliferative
  • proliferative without atypia
  • atypical hyperplasia
52
Q

non-proliferative benign breast lesions

A
  • not associated with increased risk of cancer

- simple breast cyst- fluid filled mass

53
Q

fibroadenomas

A
  • proliferative benign tissue without atypia
  • associated with small increased risk of breast cancer
  • can be either simple or complex
54
Q

atypical hyperplasia

A
  • substantial increased risk in developing breast cancer
55
Q

simple fibroadenomas

A
  • likely hormonal
  • contain glandular and fibrous tissue
  • no increased risk of breast cancer
56
Q

complex fibroadenomas

A
  • slight increased risk of breast cancer when multicentric changes present
57
Q

pathophys of fibroadenomas

A
  • can be stimulated by estrogen, progesterone, and lactation
  • some have receptors that respond to epidermal growth factor and growth hormone
  • rarely seen in older pts
58
Q

fibroadenomas in elderly

A
  • increased stromal growth

- necrosis

59
Q

what is the most common type of breast cancer

A
  • adenocarinoma

- usually ductal

60
Q

what does HER2 stand for

A

human epidermal growth factor receptor 2

61
Q

HER2 oncogene

A
  • encodes HER2 receptors
  • type of EGFR receptor
  • controls cell growth and differentiation
  • possibly controls angiogenesis
62
Q

major genetic pathways of carcinogenesis

A
  • ER+, HER2-
  • HER2+
  • ER-, HER2-
63
Q

ER+, HER2-

A
  • 50-65% of cancers arise from this pathway
64
Q

HER2 and ER cross-talk

A
  • ER and HER2 are main drivers of cell proliferation and survival in breast caner
  • if positive for both must target both pathways
  • if you dont target both get a resistance to thearpy
65
Q

ductal carcinoma in situ (DCIS)

A
  • malignant proliferation of epithelial cells limited to ducts by basement membrane
  • nuclear grade and/or presence of necrosis
  • low, intermed, or high grade
66
Q

high grade DCIS

A
  • lacks estrogen and progesterone reeptors
  • high proliferative rates
  • over expression of HER2, p53 and angiogenesis
67
Q

low grade DCIS

A
  • estrogen and porgesterone positive
  • low proliferative rate
  • rarely show abnormalities in HER2 or p53
68
Q

ER+ HER2- invasive breast carcinoma

A
  • low proliferatoin
  • responds best to hormonal treatment
  • incomplete response to chemotherapy
69
Q

ER+ HER2- invasive breast cancer

A
  • high proliferation

- some respond to chemotherapy

70
Q

most common familial mutations in breast cancer

A
  • BRCA1 and BRCA2

- tumor suppressor proteins that normally repair DNA damage

71
Q

sporadic breast cancer

A
  • major risk factor= hormone exposure
  • age of menarche and menopause
  • reproductive history
  • breastfeeding
  • exogenous estrogens
  • radiation exposure