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Patho 2 > Female GT and Breast > Flashcards

Female GT and Breast Flashcards

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1
Q

fundamental reproductive unit of FGT

A
  • ovarian follicle

- composed one one germ cell surrounded by endocrine cells

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2
Q

menarche

A
  • beginning of menstrual cycle

- average age 11-13

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3
Q

female monthly sexual cycle

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

ovarian cycle

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

female hormonal system

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

what is the predominating hormone during the follicular phase

A
  • estrogen

- low levels of FSH, LH and progesterone

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7
Q

what happens around day 14

A
  • LH surge

- ovulation occurs

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8
Q

what is the predominating hormone during the luteal phase

A
  • progesterone that is released by corpus luteum
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9
Q

oogenesis

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

what happens at puberty

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

when is meiosis II completed

A

after fertilization of ovum by sperm

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12
Q

cells of the follicle

A
  • theca cells= outer portion

- granulosa cells= inner portion that provide nourishment

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13
Q

estrogen

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

E1

A
  • predominant estrogen after menopause
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15
Q

E2

A
  • produced in theca and granulosa cells

- predominant estrogen in premenopausal women

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16
Q

E3

A

estrogen of the placenta during pregnancy

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17
Q

types of estrogen receptors

A
  • ER alpha
  • ER beta
  • GPER (g-protein coupled estrogen receptor)
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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
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19
Q

ER beta

A
  • predominantly expressed in ovaries and prostate

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

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20
Q

GPER

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

clinical disorders associated with estrogen

A
  • endometriosis
  • fibroids
  • PCOS
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22
Q

endometriosis

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

clinical sx of endometriosis

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

most common anatomic site for endometriosis

A
  • ovaries*
  • anterior and posterior cul de sac
  • broad ligaments
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25
Sampson's theory of retrograde menstruation
- during menses - endometrial cells flow backwards through fallopian tubes into peritoneal cavity - results in endometriosis
26
pre-menarcheal endometriosis
- undifferentiated cells of mullerian origin in peritoneal cavity differentiate into endometrial tissue - results in endometriosis
27
major causes of endometriotic pain
- endometriotic lesions -> stimulate nociceptors - innate immune system -> NGF - peripheral NS
28
uterine leiomyomas
- aka fibroids - benign tumors of myometrium - most common pelvic tumor
29
leiomyoma significance
- effects function and structure of endometrium | - causes excessive bleeding in uterus
30
leiomyoma pathogenesis
- genetics- trisomy 12 and point mutations - Steroid hormones cause mitogenic stimuli - increased vascularity and venular ectasia - fibrotic factors
31
polycystic ovarian syndrome (PCOS)
- intraovarian androgen excess - closely associated with insulin resistance - predisposes pts to metabolic dysfunction and type 2 DM
32
presentation of PCOS
- hirsutism - menstrual irregularities - infertility due to infrequent or absent ovulation
33
PCOS etiology
- first hit- inherited predisposition - second hit- postnatal provocative hit - second hit is usually insulin resistant hyperinsulinemia
34
steroidogenesis and PCOS
- down regulation of thecal androgen production is flawed - hyper-responsive to LH - excess androgen -> anovulation and polycystic ovaries
35
summary of issues in PCOS
- ovarian hyperandrogenism - insulin resistant hyperinsulinemia - LH excess - obesity
36
premenstrual syndrome (PMS)
- physical and/or behavioral sx in second half of menstrual cycle - abdominal bloating - breast tenderness - HA
37
pathogenesis of PMS
- normal serum estrogen or progesterone - abnormal neurotransmitter response to hormonal changes - assoc with low serotonin
38
what is the more severe version of PMS?
Premenstrual dysphoric disorder (PMDD)
39
processes that contribute to menopause
- hypothalamic and ovarian aging - environmental, genetic, and lifestyle factors - systemic diseases
40
result of hypothalamic aging
- desynchronized GnRH production | - impaired LH surge
41
what are the two major structures of the breast
- ducts | - lobules
42
what are the two types of epithelial cells
- luminal | - myoepithelial
43
breast structural changes in 1st half of menstrual cycle
- lobules are quiescent
44
breast structural changes after ovulation
- cell proliferation and number of acini per lobule increases - intralobular stroma becomes edematous
45
breast structural changes on menstruation
- regression of lobules and disappearance of edema
46
breast tissue at puberty
- estrogen and progesterone induces branching of ductal sys and dev of lobules
47
breast tissue during pregnancy
- progesterone and prolactin high - permanent increase in number/size of lobules - oxytocin -> proliferation - after lactation, apoptosis of epithelium and lobule atrophy
48
breast tissue during aging and menopause
- atrophy - decrease in CT - increase in adipose
49
cancers of lobule and terminal ducts
carcinoma
50
cancers of intralobular stroma
fibroadenoma
51
major classifications of benign breast lesions
- non-proliferative - proliferative without atypia - atypical hyperplasia
52
non-proliferative benign breast lesions
- not associated with increased risk of cancer | - simple breast cyst- fluid filled mass
53
fibroadenomas
- proliferative benign tissue without atypia - associated with small increased risk of breast cancer - can be either simple or complex
54
atypical hyperplasia
- substantial increased risk in developing breast cancer
55
simple fibroadenomas
- likely hormonal - contain glandular and fibrous tissue - no increased risk of breast cancer
56
complex fibroadenomas
- slight increased risk of breast cancer when multicentric changes present
57
pathophys of fibroadenomas
- 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
fibroadenomas in elderly
- increased stromal growth | - necrosis
59
what is the most common type of breast cancer
- adenocarinoma | - usually ductal
60
what does HER2 stand for
human epidermal growth factor receptor 2
61
HER2 oncogene
- encodes HER2 receptors - type of EGFR receptor - controls cell growth and differentiation - possibly controls angiogenesis
62
major genetic pathways of carcinogenesis
- ER+, HER2- - HER2+ - ER-, HER2-
63
ER+, HER2-
- 50-65% of cancers arise from this pathway
64
HER2 and ER cross-talk
- 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
ductal carcinoma in situ (DCIS)
- malignant proliferation of epithelial cells limited to ducts by basement membrane - nuclear grade and/or presence of necrosis - low, intermed, or high grade
66
high grade DCIS
- lacks estrogen and progesterone reeptors - high proliferative rates - over expression of HER2, p53 and angiogenesis
67
low grade DCIS
- estrogen and porgesterone positive - low proliferative rate - rarely show abnormalities in HER2 or p53
68
ER+ HER2- invasive breast carcinoma
- low proliferatoin - responds best to hormonal treatment - incomplete response to chemotherapy
69
ER+ HER2- invasive breast cancer
- high proliferation | - some respond to chemotherapy
70
most common familial mutations in breast cancer
- BRCA1 and BRCA2 | - tumor suppressor proteins that normally repair DNA damage
71
sporadic breast cancer
- major risk factor= hormone exposure - age of menarche and menopause - reproductive history - breastfeeding - exogenous estrogens - radiation exposure

Patho 2 (15 decks)

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