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Endo/Repro > Female Physiology > Flashcards

Female Physiology Flashcards

1
Q

Maturation of primary oocyte

A

During puberty, primary oocytes undergo change into secondary oocyte (arrested in metaphase II) –> dependent on the LH surge
- once fertilization occurs –> secondary oocyte undergoes Meiosis II and becomes an ovum

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2
Q

Corpus Luteum

A

produces progesterone –> silences the ovary and remains patent until either 2nd trimester of pregnancy or it involutes if no fertilization occurs

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3
Q

Summary of Ovarian Follicular Development

A
  1. Birth –> all oogonia developed into primary oocytes
  2. Primary oocytes surrounded by follicular cells = granulosa/thecal cells (primordial follicles)
  3. Primordial follicles slowly progress to primary follicles
  4. When follicles exhausted = menopause
  5. Each cycle, a cohort of follicles recruited and usually one becomes ovulatory follicle
  6. Recruitment refers to antral follicles stimulated by FSH
  7. Dominant follicle is largest and produces most hormones
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4
Q

Hypothalamo-Pituitary Ovarian Axis

A
  • Hourly GnRH pulses result in FSH and LH basal secretion
  • FSH stimulates follicle development
  • FSH/LH promotes estrogen synthesis
  • Estrogen feedbacks negatively to hypothalamus and pituitary –> reduces FSH and LH
  • Inhibin inhibits FSH secretion, no effect on LH
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5
Q

Feedback of estrogen and secretions

A
  • Feedback relationship between estrogen and secretions reverse when antral follicles are large –> high estrogen induces rapid GnRH pulses and ovulatory surge in LH
  • Inhibin levels increase as well to keep FSH in check –> reducing more follicle development
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6
Q

GnRH

A

polypeptide hormone

  • produced in arcuate nucleus of hypothalamus
  • pulsatile secretion
  • member of Gq –> increased Ca
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7
Q

FSH

A

follicular growth and estradiol secretion

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8
Q

LH

A

critical for inducing ovulation

ovulation required for formation of corpus luteum

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9
Q

hCG

A

1st trimester maintains the corpus luteum -> which keeps progesterone levels high to maintain pregnancy
- later in pregnancy the placenta takes over

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10
Q

FSH, LH, hCG

A

secretions are cyclical –> essential for normal gonadal response
- serum [ ] increase with removal of ovaries and when ovarian functions decrease

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11
Q

FSH, LH, hCG receptors

A

Gs protein coupled –> increase cAMP
LH/CH receptors are in thecal cells –> androgen production
FSH receptors are in granulosa cells -> converts androgens to estrogen (estradiol 17beta)

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12
Q

Estrogen receptor

A

ERalpha –> mediates HPO axis response to estrogen

- SHBG = steroid hormone binding globulin

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13
Q

Menstrual Cycle

A
  1. Small increases in LH and FSH lead to follicular growth –> increase synthesis and secretion of ovarian steroids
  2. High levels of estrogen provoke changes in GnRH to manifest rapid pulses
  3. Stimulates surge of LH which induces resumption of meiosis
  4. Ovulation induces luteinization –> corpus luteum
  5. If no conceptus -> spontaneous luteinolysis
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14
Q

Ovarian Cycle

A 
Estrogen = thickening and proliferation of endometrium
Progesterone = halts further growth of endometrium
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15
Q

Maternal recognition of pregnancy

A

hCG produced by chorion –> maintains/promotes maintenance of corpus luteum

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16
Q

Maintenance of pregnancy

A

accomplished by placenta

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17
Q

Endocrine control of pregnancy

A

Shifts from P>E to E>P
Progesterone causes hyperpolarization of myometrial cells –> prevent contractions, inhibits oxytocin receptor synthesis, inhibits ER synthesis
Estrogen causes increase oxytocin receptors, promotes uterine contractility, cervical ripening, increases local PG release from placenta

18
Q

Prostaglandins

A

PGF2 and PGE are predominant in reproduction

  • involved in rupture of Graafian follicle at ovulation
  • primes the uterus for real deal
19
Q

Oxytocin

A

secreted from posterior pituitary

  • main effects are on uterus and breast during childbirth and lactation
  • (+) autoregulation within hypothalamus during labor
20
Q

Breast Development

A

Puberty -> development of ductal tree (estrogen, glucocorticoids, and GH dependent)
Pregnancy -> mid-late preg (lobular-alveolar growth), post-partum (copious milk secretion, removal of placenta -> prolactin dependent)

21
Q

Lactation

A

Galactopoiesis -> presence of prolactin and removal of milk
Milk Ejection -> oxytocin
Involution -> lack of prolactin or suckling

22
Q

Folliculogenesis promotion

A 
FSH and LH for women with hypothalamic anovulatory function
Clomiphene citrate (estrogen antagonist) for women with endogeneous estrogen activity and normal HPO function
23
Q

Mimic gonadotropins

A

Menotropins -> pergonal with hCG given in sequence for ovulation in anovulatory women and production of multiple follicles
Urofolitropin -> metrodin with hCG given in sequence for induction of ovulation of patients with PCOD
Follitropin -> induce follicle development and when coupled with hCG -> induction of ovulation

24
Q

Clomiphene Citrate

A

Estrogen antagonist (Selective estrogen receptor modulator)

  • blocks ER signaling to hypothalamus and anterior pituitary -> stimulates release of GnRH and gonadotropins
  • used as fertility drug to induce ovulation
25
Q

2 Step ovulation induction

A
  1. Follicular Stimulation using combined FSH and LH

2. hCG stimulates LH surge -> follicular maturation and ovulation

26
Q

hCG (human chorionic gonadotropin)

A

isolated from urine in pregnant women

  • binds to LH/CG receptor -> LH-like induction of ovulation
  • stimulates estrogen primed follicle to induce meiotic resumption
27
Q

GnRH Agonists

A

Synthetic GnRH -> Leuprolide

  • nonpulsatile administration -> suppresses FSH and LH (AFTER initial transient rise) –> shuts down HPO
  • pulsatile administration -> release of FSH/LH -> inducing follicle development
28
Q

GnRH Antagonists

A

Ganirelix, Cetrorelix

  • competitive antagonist of GnRH -> suppressing gonadotropin release
  • used in fertility to prevent LH surge while promoting folliculogenesis
  • used in prostate and breast cancer therapy to inhibit steroid production
  • No transient rise in FSH, LH
29
Q

Effects of Estrogens

A

development, growth, maintenance of sex tissue
skeletal growth, body shape
key regulator of HPO axis and maintaing menstrual cycle

30
Q

Uses of estrogen

A

Oral contraceptives, HRT, dysmenorrhea

31
Q

Estradiol 17beta

A

PRINCIPAL NATURAL HORMONE

  • readily absorbed, 1st pass metabolism limits oral effectiveness –> addition of methyl at 17 reduces metabolism
  • injection, patch, gel, vaginal ring
32
Q

Tamoxifen

A

Estrogen antagonist in breast and vasculature
Agonist in uterus, bone, lipoproteins
SERM

33
Q

Raloxifene

A

SERM
Agonist - bone, lipoproteins
Antagonist - breast, uterus (ER+ breast cancer)

34
Q

Toremifene

A

SERM
Antagonist - breast
no effect in bone
Agonist - uterus

35
Q

Fulvestrant

A

SERD (down regulator)

- PURE estrogen antagonist -> blocks receptor binding and down regulates receptor in all tissues

36
Q

Aromatase inhibitors

A

steroidal and nonreversible -> exemestane
nonsteroidal and reversible -> anastrozole, letrozole
treat ER+ cancer

37
Q

Actions of progesterone

A

development and maintenance of secretory endometrium

  • promotes uterine relaxation during pregnancy
  • withdrawal during late pregnancy is part of partruition
  • prepares breast for lactation
38
Q

Uses of synthetic progestins

A

Oral contraceptives, HRT, dysmenorrhea, luteal supprt

39
Q

Synthetic Progestins

A

Progestanes -> medroxyprogesterone acetate
Estranes -> norethindrone
Gonanes -> levonorgestrel (more potent at lower doses)
- 17alpha substitution decreases 1st pass metabolism

40
Q

Emergency contraception

A

Levonogestrel -> progesterone agonist
Mifepristone (also abortefacient) and Ulipristal acetate -> progesterone antagonist
MOA - interferes with ovulation as emergency contraception

Endo/Repro (34 decks)

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