Female Reproductive System Flashcards

1
Q

What is the fundamental reproductive unit?

A

Single ovarian follicle

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2
Q

What is an ovarian follicle composed of?

A

Oocyte (germ cell)

Surrounded by endocrine cells

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3
Q

What is menarche?

A

beginning of menstrual cycle around 11-13 years of age

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4
Q

What is the female monthly sexual cycle?

A

One ovum is released from ovaries/month

uterine endometrium is prepared for implantation of fertilized ovum

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5
Q

What are the three phases of the ovarian cycle?

A

Follicular phase
Ovulation
Luteal Phase

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6
Q

What releases hCG?

A

embryo trophoblasts

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7
Q

What does FSH do?

A

stimulates follicle to grow durign follicular stage

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8
Q

Where does estrogen come from and what does it do?

A

Comes from follicles

Causes female sexual chracteristics and thickening of endometrium

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9
Q

What doe luteinizing hormone do?

A

produces progesterone

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10
Q

What does progesterone do?

A

Maintains thickness of endometrium and keeps uterus from contracting too early in pregnancy

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11
Q

What causes ovulation?

A

LH surge at day 14

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12
Q

What is oogenesis?

A

Germ cells in the ovary differentiate into oogonia, which divide by mitosis, and mature into primary oocyte enclosed in primordial follicles

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13
Q

What happens to the primary oocyte during puberty?

A

It becomes a secondary oocyte by completing Meiosis I

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14
Q

When is Meiosis II completed?

A

After fertilization of ovum by sperm

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15
Q

Where does fertilization occur?

A

fallopian tube

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16
Q

What is estrogen?

A

a steroid hormone that is derived from androgenic precursors androstenedione and testosterone by means of aromatization

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17
Q

What are the three naturally occurring estrogens?

A

17 beta-estradiol (E2)
Estrone (E1)
Estriol (E3)

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18
Q

What is E2?

A

primarily produced by theca and granulosa cells of the ovary

Predominant form of estrogen found in PREMENOPAUSAL WOMEN

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19
Q

What is E1?

A

Predominant form of circulating estrogen after menopause

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20
Q

What is E3?

A

Estrogen the placenta secretes during pregnancy

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21
Q

What are the three estrogen receptors?

A

ER-alpha
ER-beta
GPER

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22
Q

Where is ER-alpha found?

A
Uterus
Mammary gland
Testis
Pituitary
Liver
Kidney
Heart
Skeletal Muscle
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23
Q

What does ER-alpha activation do?

A

Increases the risk and/or the progression of various cancers, including cancers in the breast and endometrium

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24
Q

Where is ER-beta found?

A

Ovary

Prostate

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25
Q

What does ER-beta activation do?

A

activates antiproliferative and pro-apoptotic pathways in many cancer cells

26
Q

What does G-protein coupled estrogen receptor activation do?

A

mediates rapid estrogen signaling via stimulation of adenylyl cyclase

Expressed in normal ovary

Regulates physiological processes such as follicle maturation

27
Q

What is endometriosis?

A

a chronic, hormone-dependent, inflammatory disease

28
Q

What is endometriosis characterized by?

A

presence and growth of endometrial tissue outside the uterine cavity

29
Q

What is endometriosis frequently associated with?

A

Moderate to severe pain
Dysmenorrhea
Low back pain
Infertility

30
Q

What are the most common sites that endometriosis occurs?

A

Ovaries
Anterior and Posterior cul-de-sac
Broad Ligaments

31
Q

What is the pathogenesis of Endometriosis?

A
Ectopic endometrial tissue
Altered immunity and inflammation
Imbalanced cell proliferation and apoptosis
Angiogenesis
Genetic factors
32
Q

What is Sampson’s theory of retrograde menstruation?

A

states that endometrial cells flow backwards through the fallopian tubes and into the peritoneal cavity during menses and that this is what causes endometriosis

33
Q

What is Pre-menarcheal endometriosis?

A

Undifferentiated cells of mullerian origin in the peritoneal cavity can differentiate to endometrial tissue

34
Q

What is MCP-1?

A
Monocyte chemotactic protein 1 that comes from ectopic endometrium and causes peritoneal macrophages to produce:
Inflammatory cytokines
Growth factors
Angiogenic factors
Oxidative stress
35
Q

What are the three things that cause endometriotic pain?

A

Endometriotic lesions
Innate immune system
Peripheral nervous system

36
Q

How is endometriotic pain caused?

A

Endometrial lesions produce mediators that activate Innate immune system

Innate immune system releases NGF which stimulates sensory nerve endings to generate nociceptive pain

37
Q

What are uterine Leiomymomas (Fibroids)?

A

benign tumors arising from the smooth muscle cells of the myometrium

Most common pelvic tumor in women

38
Q

What is the clinical significance of fibroids?

A

Effects the function and structure of the endometrium causing pathogenesis of excessive bleeding in uterus

39
Q

How do fibroids form?

A

Transformation of normal myocytes into abnormal myocytes

Growth of abnormal myoctyes into clinically apparent tumors

40
Q

What should you associate Uterine Leiomymomas with?

A

Fibrotic process with lots of ECM production

41
Q

What is the pathogenesis behind uterine leiomymomas?

A

Genetics
Steroid Hormones
Vascular abnormalities
Fibrotic factors

42
Q

What genetics cause Uterine Leiomymomas?

A

Abnormal karyotypes casing dysregulation of specific genes

Point mutation in regulatory genes

43
Q

What steroid hormones cause Uterine Leiomymomas?

A

Estradiol and Progesterone induce mature leiomymoma cells to release mitogenic stimuli to adjacent immature cells

44
Q

What vascular abnormalities cause Uterine Leiomymomas?

A

Increased numbers of arterioles and venules

Venular Ectasia (dilation)

45
Q

What fibrotic factors cause Uterine Leiomymomas?

A

Increase in extracellular matrix components and collagen

Fibrotic growth factors are also dysregulated

46
Q

What is Polycystic Ovarian Syndrome (PCOS)?

A

A disorder of intraovarian androgen excess

Closely associated with insulin resistance

47
Q

What does PCOS predispose patients to?

A

metabolic dysfunction

Increased risk of type 2 diabetes

48
Q

What are the clinical symptoms of PCOS?

A

Hirsutism due to the function of hypersecretion of ovarian androgens

Menstrual Irregularity and Infertility due to infrequent or absent ovulation

49
Q

What is the etiology of PCOS?

A

arises as a congenitally programmed predisposition = first hit

this becomes manifest in the presence of a provocative factor = second hit

50
Q

What are the congenital factors that cause PCOS?

A

Hereditary

Acquired = maternal drugs or nutritional deficits affecting the fetus

51
Q

What are the postnatal provocative factors that cause PCOS?

A

Insulin resistant hyperinsulinism

52
Q

What is the two-gonadotropin, two cell model of ovarian steroidogenesis?

A
  1. Theca cells, under the control of LH, produce androgens that diffuse into the granulosa cells
  2. in mature follicles, FSH acts on granulosa cells to stimulate conversion of androgens to estrogens
53
Q

What is the connection between ovarian steroidogenesis and PCOS?

A

Down-regulation of thecal androgen production is flawed

Ovaries are hypersensitive to LH stimulation

Excess intraovarian androgen causes the granulosa cell dysfunction

54
Q

What is the minimal model for the pathogenesis of PCOS?

A
  1. Ovarian Hyperandrogenism
  2. Insulin-resistant hyperinsulinism
  3. LH excess
  4. Obesity
55
Q

What is PMS/PMDD?

A

characterized by physical and/or behavioural symptoms in the second half of the menstrual cycle

56
Q

What are the physical manifestations of PMS/PMDD?

A

abdominal bloating
breast tenderness
headaches

57
Q

What are the risk factors for PMS/PMDD?

A

genetic factors

environmental influences

58
Q

What is the pathogenesis of PMS/PMDD?

A

Ovarian steroids = normal serum levels, but there is an abnormal neurotransmitter response to normal hormonal changes

Serotonin is low

59
Q

What processes contribute to decline ovarian function and development of menopause?

A

Hypthalamic and ovarian aging
Environmental, genetic, and lifestyle factors
Systemic diseases

60
Q

What does hypothalamic aging do?

A

leads to desynchronized GnRH production and an impaired surge of LH

61
Q

What is menopause?

A

CNS changes + ovarian aging + anovulation = cycle irregularities and FSH upregulation