The female genital tract Flashcards

1
Q

What is the fundamental reproductive unit in females?
What is it composed of?

What is it surrounded by?

A
  • single ovarian follicle
    • composed of one germ cell (oocyte)
    • surrounded by endocrine cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Avg age of menarche

A

11-13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Female monthly sex cycle controlled by?

A

gonadotropins

  • only single ovum released
  • endometrium prepared for implanation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the ovarian cycle?

A

follicular phase - 15 days

Ovulation -occurs day 14

Luteal phase -13 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Phases of endometrial growth and menstration

A

proliferative phase (11 days) (cells of endometrium are proliferating and becoming thicker)

secretory phase (12 days) (thicking even more)

menstrual phase (5 days) (shed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the Hierarchies of homrones of the female hormonal system?

A
  • Hypothalamus -GnRH
  • Anterior pituitary -FSH & LH
  • The ovarian hormones- Estrogen (FSH) and Progesterone (LH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A surge in LH is required for?

A

Ovulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when are estrogen and progesterone at their highest during the cycle?

A

estrogen: after menses → ovulation
progesterone: after ovulation → menses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when are FSH and LH high during the cycle?

A
  • FSH: early follicle maturation, a bit higher than LH on either side of ovulation, spikes but lower than LH at ovulation
  • LH: spikes at ovulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what hormone contributes to early follicular maturation?

A

FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what hormones contribute to late follicular maturation?

A

FSH, LH, estrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does LH surge cause ovulation?

A

causes granulosa and theca cells produce more progesterone → transition to luteal phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which anterior pituitary hormone stimulates estrogen and which progesterone?

A

FSH → estrogen
LH → progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Body temperature and ovulation?

A

-spikes to 98.6 at ovulation, slowly returns to 96.8 over the rest of the luteal phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what happens physiologically during the menstrual cycle?

A

6 - 12 follicles develop, but only 1 follicle matures → ovulation releases ovum → corpus lutem degrades → corpus albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is endometriosis?

A
  • chronic, estrogen-dependent, inflammation w/ varying degree of severity (can be all over or localized)
    • Characerized by the presence and growth of endometrial tissue outside the uterine cavity

uterine tissue outside the uterus

17
Q

what are the clinical features of endometriosis?

A

mod - severe pain, lower back pain, infertility, dysmenorrhea

18
Q

what are the most common sites of endometriosis?

A

ovaries, cul-de-sac, broad ligaments

⇒cul de sac refers to the rectouterine pouch (the pouch of Douglas)

can be anywhere in the peritoneum

19
Q

pathogenesis of endometriosis is:

A

multifactoral

-ectopic endometrial tissue, inflammation, imbalanced cell prolif/apoptosis, angiogenesis, genetic factors

20
Q

what are the 2 theories of endometriosis?

A

Sampson’s theory of retrograde menstruation: endometrial cells flow backwards thru fallopian tubes into peritoneal cavity during menses (can be due to obstruction)

Pre-Menarcheal endometriosis: undifferentiated mullerian cells seed the peritoneal cavity & differentiate into endometrial tissue

21
Q

what are the 3 main players in the pathogenesis of endometriotic pain?

A
  1. endometriotic lesions → directly stimulate sensory nerves → nociceptive pain signal
  2. innate immune system release → proinflamm mediators and pro-nociceptive mediators such as nerve growth factor (NGF )→ stimulate sensory nerve endings
  3. peripheral nervous system → spinal cord
22
Q

what are uterine leiomyomas?

A

fibroids: benign myometrial tumors (created from smooth muscle cells of the myometrium)

23
Q

what is the most common pelvic tumor in women?

A

fibroids (confined & non-malignant) from uterus

24
Q

what are the clinical presentation/clinical significance of fibroids?

A

alters function/structure → excessive bleeding in uterus

25
Q

How does an Uterine Leiomyoma form?

A

-transformation of normal myocytes (cells of the smooth muscle) into abnormal myocytes

-growth of abnormal myocytes into clinically apparent, confined tumors (affect structure and function- not malignant)

26
Q

which 5 factors contribute to leiomyomas?

A
  1. genetics
  2. steroid hormones (estradiol & progesterone) → mitogenic stimuli
  3. stem cells
  4. angiogenesis
  5. ↑ fibrotic factors (ECM, collagen, abnormal fibrotic GFs)
27
Q

what is PCOS?

A

intraovarian androgen excess & insulin resistance → polycycstic ovaries

28
Q

triad of insulin resistance to keep in mind with PCOS?

A

triad of insulin resistance to keep in mind with PCOS

  • DM2
  • Obesity
  • CVD
29
Q

what is the clinical triad of PCOS?

A
  1. an/oligovulation
  2. hirsutism - due to hyperandrogenism
  3. polycystic ovaries
30
Q

what causes PCOS?

A

2 Hit:

  • genetic/acquired predisposition (maternal drugs, nutritional disorders affecting fetus)
  • insulin resistant hyperinsulinism (obesity, t2dm)
31
Q

Unified Minimal Model of PCOS patho

A

-Functional Ovarian Hyperandrogenism (FOH): accounts for all features of PCOS, most important factor

-Hyperinsulinism and Obesity

-LH Excess: secondary to FOH, no negative feedback

32
Q

what does hyperinsulinism do to PCOS?

A

In the ovary hyperinsulism increas androgen production in theca cells by sensitizing them to LH AND prematurely luteinizes granulosa cells

Excess insulin combined w. LH excess, aggravates ovarian dysfunction

33
Q

what is PMS?

A

biopsychological disorder

physical/behavioral symptoms in second half of menstrual cycle (luteal phase) for at least 2 consecutive cycles

34
Q

what is the clinical triad of PMS?

A

tender breasts
abdominal bloating
headaches

35
Q

What is the pathogenesis of PMS?

What is the common treatment?

A
  • abnormal NT (serotonin) response to normal hormonal changes
    • normal flucuations in hormones through out the cycle, just abnormal response to hormones
  • SSRI’s
36
Q

Development of menopause

A

getting periods→ menopausal transition (irregular periods) → menopause (no period consectively for one year)

37
Q

which 3 things contribute to menopause?

A
  • hypothalamic & ovarian aging
  • environmental/genetic/lifestyle
  • systemic diseases
38
Q

what does hypothalamic aging have to do with menopause?

A

desynchronized GnRH production & an abnormal surge of LH→this leads to no ovulation