The female genital tract Flashcards

(38 cards)

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
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2
Q

Avg age of menarche

A

11-13

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3
Q

Female monthly sex cycle controlled by?

A

gonadotropins

  • only single ovum released
  • endometrium prepared for implanation
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4
Q

Describe the ovarian cycle?

A

follicular phase - 15 days

Ovulation -occurs day 14

Luteal phase -13 days

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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)

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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)
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7
Q

A surge in LH is required for?

A

Ovulation

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8
Q

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

A

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

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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
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10
Q

what hormone contributes to early follicular maturation?

A

FSH

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11
Q

what hormones contribute to late follicular maturation?

A

FSH, LH, estrogen

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12
Q

How does LH surge cause ovulation?

A

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

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13
Q

which anterior pituitary hormone stimulates estrogen and which progesterone?

A

FSH → estrogen
LH → progesterone

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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

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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

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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
How does an Uterine Leiomyoma form?
-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
which 5 factors contribute to leiomyomas?
1. genetics 2. steroid hormones (estradiol & progesterone) → mitogenic stimuli 3. stem cells 4. angiogenesis 5. ↑ fibrotic factors (ECM, collagen, abnormal fibrotic GFs)
27
what is PCOS?
intraovarian androgen excess & insulin resistance → polycycstic ovaries
28
triad of insulin resistance to keep in mind with PCOS?
triad of insulin resistance to keep in mind with PCOS - DM2 - Obesity - CVD
29
what is the clinical triad of PCOS?
1. an/oligovulation 2. hirsutism - due to hyperandrogenism 3. polycystic ovaries
30
what causes PCOS?
2 Hit: - genetic/acquired predisposition (maternal drugs, nutritional disorders affecting fetus) - insulin resistant hyperinsulinism (obesity, t2dm)
31
Unified Minimal Model of PCOS patho
**-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
what does hyperinsulinism do to PCOS?
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
what is PMS?
biopsychological disorder physical/behavioral symptoms in **second half of menstrual cycle (luteal phase)** for at least 2 consecutive cycles
34
what is the clinical triad of PMS?
tender breasts **abdominal bloating** headaches
35
What is the pathogenesis of PMS? What is the common treatment?
* abnormal NT **(serotonin)** response to normal hormonal changes * normal flucuations in hormones through out the cycle, just abnormal response to hormones * SSRI's
36
Development of menopause
getting periods→ menopausal transition (irregular periods) → menopause (no period consectively for one year)
37
which 3 things contribute to menopause?
* **hypothalamic & ovarian aging** * environmental/genetic/lifestyle * systemic diseases
38
what does hypothalamic aging have to do with menopause?
desynchronized GnRH production & an abnormal surge of LH→this leads to no ovulation