Endocrine Reproductive

Front 1

Describe the key hormone released from the hypothalamus that is important to consider in reproduction. What does constant secretion of this lead to?

Back 1

GnRH - released in pulsatile fashion and acts on pituitary to induce secretion of FSH and LH via phospholipase C signaling. constant GnRH leads to low FSH and LH due to down regulation of GnRH receptors

Front 2

What does LH do?

Back 2

acts on intersitial steroidogenic cells- Leydig cells of testis + theca cells of ovary.

Front 3

What does FSH?

Back 3

Acts on follicular cells: Sertoli cells of testis and granulosa cells of ovary

Front 4

Describe testosterone: production, and synthesis

Back 4

Produced Leydig cells of the testis. inhibits LH release by anterior pituitary + decreases GnRH. T is convereted to DHT by 5 alpha-reductase in target tissues

Front 5

Describe estrogen: production and synthesis

Back 5

Estrogens: estrone (E1), estradiol (E2), estriol (E3- fetal adrenal/liver placental). Androgen precursors (that make these) are made by theca cells of the ovary but converted to final products in granulosa cells by FSH induced enzyme aromatase.

Front 6

What do moderate, steady levels of estrogen inhibit and when?

Back 6

inhibits LH release early in menstrual cycle but rising levels of estrogen stimulate LH release before ovulation by increasing the number of GnRH receptors on gonadotropes.

Front 7

Describe progesterone: production and synthesis

Back 7

produced by corpus luteum after ovulation (and by placenta during pregnancy). synergistic w/ E2; P inhibits GnRH release

Front 8

How are sex steroids carried in the plasma?

Back 8

98% are bound. 2/3 of T is carried via gonadal steroid binding globulin (GBG or SHBG) and 1/3 by albumin.

P binds to albumin + corticosteroid binding globulin (CBG).

Front 9

What is androgen binding protein?

Back 9

produced by sertoli cells under stimulation of T and FSH + secretes in into seminiferous tubules, very high T levels.

Front 10

Inhibins?

Back 10

produced by FSH-stimulated Sertoli or granulosa cells and act on anterior pituitary to decrease FSH release.

Inhibin B - produced in male during follicular phase in female

Inhibin A is characteristic of luteal phase. All belong to TGFB superfamily.

Front 11

Activins?

Back 11

formed from 2 inhibin beta chains. Stimulate FSH release but a physiologic role for apparent positive feedback is uncertain.

Front 12

What induces testis development?

Back 12

Downstream action of SRY (sex-determining region of Y) gene product

Front 13

What is Turner syndrome?

Back 13

streak gonad, amenorrhea, short stature, webbed neck, lacking secondary sexual characteristics (XO).

Front 14

What's Jacob's syndrome?

Back 14

XYY (super male syndrome) seemingly normal male, said to have excess acne, taller than normal, more aggressive, but not supported statistically.

Front 15

Kleinfelter syndrome?

Back 15

XXY  Kleinfelter’s syndrome (seminiferous tubule dysgenesis): ~1 per 1,000; male genitalia but sterile; high FSH/LH/E2; feminization; retardation (XXX & XYY ~as frequent, normal)Seminferous tubule dysgenesis: male genitalia, increase FSH, LK, and E2 and decrease T sterility, feminization, retardation. "hypergonadotrpic hypogonadism"

Front 16

Triple X syndrome?

Back 16

typically normal female since only 1 x chromosome remains active

Front 17

Mullerian inhibiting hormone or substance or factor

Back 17

this causes regression of mullerian ducts (precursor of oviduct, uterus, vagina) while leydig cells produce testosterone supporting differentiation of Wolffian ducts.

Front 18

What does testerone help develop after conversion to DHT?

Back 18

induces development of prostate, urethra, penis, and scrotum

Front 19

Describe sexual development in the male.

1) When is testosterone synthesized?

2) When does testosterone increase again?

3) When do testosterone levels reach a maximum?

Back 19

1) testosterone is synthesized at near-adult levels toward the end of the first trimester (→ differentiation of internal and external genitalia) and again at about 2 months postpartum (function unknown).

2) The level then remains quite low until puberty, at which point the hypothalamus again becomes active, initially nocturnally, then constantly. The hypothalamus is thought to become less sensitive to testosterone inhibition: “resetting the gonado¬stat” → rising testos¬terone. Growth of the penis, sebaceous glands, long bones, and axillary and pubic hair characterize the adolescent period.

3) Testosterone levels reach a maximum in the mid/late-20s, and then fall gradually thereafter. There is no abrupt hormonal equivalent of menopause ("andropause").

Front 20

Describe sexual development in the female

1) When is estrogen synthesized?

2) What's the first defining event of estrogen release?

3) When do estrogen levels peak?

4) What happens post-menopause?

Back 20

1) estrogen synthesis is seen during gonadal develop¬ment toward the end of the first trimester, and FSH & LH (& E?) are high 2-3 months post-partum (function unknown), but estrogen levels do not rise again until puberty, control¬led as noted above.

2) The first defining event is breast development (thelarche), followed by the development of axillary and pubic hair (pubarche), and finally the first menstrual period (menarche).

3) Estrogen levels peak monthly after menarche (except during preg¬nancy), then periods become irregular (climac¬teric) and cease around the fifth decade (menopause).

4) Post-menopausal LH & FSH levels are high due to low estrogen and lack of inhibin.

Front 21

What is long bone growth augmented by?

What happens at 8-10 years?

Back 21

In both sexes, long bone growth is augmented by sex steroids (E in the female; T → E, in the male) but high levels of sex steroids near the end of puberty bring about cessation of long bone growth by epi¬physeal plate closure.

2) At 8-10 yrs, the adrenals increase their secretion of androgens (adren¬arche), without significant changes in cortisol or ACTH levels. These andro¬gens (from androsten¬dione) contribute to the early stages of the “growth spurt” and to pubic and axillary hair growth, independent of gonadal puberty.

Front 22

Testicular Feminization or androgen insensitivity syndrome (AIS)?

Back 22

XY genotype but female external genitalia. Cause: >200 known mutations in the androgen receptor (AR) gene; carried on the X chromosome; complete AIS is seen in ~1 in 20,000 births.

Y chromosome → testis → MIH and testosterone, therefore Mullerian ducts regress via MIH action but Wollfian ducts also regress since they can’t respond to testosterone. Leydig → T but Sertoli cells can’t function → no spermatogenesis. Later, without negative feedback from T, GnRH↑ → ↑LH → ↑A → ↑T → ↑E (peripheral aromatization) → breast development → female phenotype, even though T>E.

Front 23

5α-reductase-2 Deficiency Syn¬drome or “Penis at Twelve” (guevedoces)

Back 23

XY genotype, beginning life with a female phenotype but later reverting to a male phenotype.

Cause: one of the two 5α-reductase genes (type 2) is non-functional. An autosomal recessive, clusters have been found in isolated, inbred populations of the Dominican Republic, Papua New Guinea and Turkey. Y chromosome → testes and internal male ducts since T is present but no prostate, penis, or scrotum form since conversion to DHT is required. At puberty, ↑T may promote sufficient binding to the receptor, inducing development of external male genitalia and/or the normal 5α-reductase (type 1) present in the prostate and external genital tissues may suffice at very high T levels.

Front 24

Congenital Adrenal Hyperplasia (CAH):

Back 24

1) In females: masculinization, e.g. enlargement of the clitoris and fusion of the labia before birth; increased muscular development, facial hair (hirsuitism), irregular menses post-puberty.

2) In males: precocious puberty or super¬masculinization. Cause: hyper¬secretion of adrenal
androgens due to a defect in steroid biosynthesis. CAH is a group of autosomal recessive disorders. Most commonly, 21- or 11β-hydroxylase deficiencies reduce the formation of aldosterone and cortisol, resulting in accumulation of their androgen precursors. Defects in 21-hydroxylase account for >90% of cases, with a carrier frequency of about 1 in 60 in the general population but much higher in isolated clusters. Defects in 11β-hydroxylase account for >5% of cases. CAH is classified as salt-losing or salt-retaining, depending on the compromised pathway.

Front 25

Describe the cells of the testis:

1) spermatogonia
2) Leydig cells
3) Sertoli cells

Back 25

1) (= germ cells): The sperm-producing stem cell line.

2) (= interstitial cells): Stimulated by LH, they synthesize and secrete

3) (= follicular cells): Stimulated by FSH (and T, to produce ABP), they surround the developing sperm. Inter¬connected laterally by tight junctions, Sertoli cells form a “blood-testis barrier," thus protecting developing sperm cells. Sertoli cells contain abundant aromatase and can convert T to E2

Front 26

Components of the male reproductive system
1) seminiferous tubules
2) Rete testis
3) Efferent ductules
4) Epididymis
5) vas ductus deferens
6) Seminal vesicle
7) Prostate gland
8) Bulbourethral (Cowper's) gland
9) Urethra
10) Scrotum

Back 26

• Seminiferous tubules: formed by the above cells, for sperm production (combined length about 250 meters).
• Rete testis: collects sperm from multiple seminiferous tubules.
• Efferent ductules: conducts sperm to epididymis.
• Epididymis: passage wherein sperm undergo maturation (about 6 meters long).
• Vas (ductus) deferens: exit for sperm to seminal vesicles.
• Seminal vesicle: drains into vas deferens above the prostate, thus forming ejaculatory duct; produces fructose (major sperm nutrient) and prostaglandins (stimulate uterine/ovarian contractions); accumulates hormones and sperm-coat proteins.
• Prostate gland: joins ejaculatory ducts with the urethra; produces buffered secretions to aid sperm in motility and fertilization.
• Bulbourethral (Cowper’s) gland: drains into urethra; produces lubricating mucus.
• Urethra: the common urogenital passage through the penis.
• Scrotum: external pouch that suspends testes away from the body, the temperature of which is inhibitory to sperm dev

Front 27

Describe the pathway of the sperm

Back 27

seminiferous tubules → rete testis → efferent ductules → epididymis → vas deferens → ejaculatory ducts → prostate gland → urethra, inter¬sected along the way by ducts from the seminal vesicle, bladder, and bulbourethral gland.

Front 28

Describe the process of sperm maturation

Back 28

Spermatogonium → continual mitosis → primary spermatocyte (2n / 2DNA) → 1st meiotic division → 2 secondary spermato¬cytes (1n / 2DNA) → 2nd meiotic division → 4 spermatids (1n / 1DNA) → loss of cytoplasm → 4 spermatozoa (sperm).

Front 29

1) How long does the primary spermatocyte take to develop into fully formed spermatozoa?

2) How long does passage through the epididymis take?

Back 29

1) 2 months
2) Passage through the epididymis takes ~12 days for full maturation, during which size, shape, metabolic, and cell surface/acrosomal protein changes take place (but sperm can’t fertilize until they undergo capacitation in the female tract).

Front 30

How does testosterone effected during the following periods..

1) Fetal
2) Puberty
3) Adult

Back 30

1) induces the Wolffian-derived duct system directly; induces the prostate and the urethra / penis / scrotum via DHT (through 5α-reductase-2)

2) : induces facial, pubic and axil¬lary hair; sebaceous glands (all mainly via DHT); sperm production; larynx development; fat and muscle distribution; promotion of bone growth during puberty but cessation of bone growth with increasing T post-puberty (T likely acts indirectly on bone growth by aromatase-mediated conversion to E).

3) sex drive; muscle growth & maintenance (T is an anabolic steroid); ↑erythropoiesis (hence higher male hematocrit); ↑male pattern baldness (via DHT); ↑cholesterol, with its negative cardiovascular consequences.

Front 31

1) Oligospermia

2) Defective sperm
3) Male contraception?
4) Male impotence (erectile dysfunction)

Back 31

1) defined as having less than 20 million sperm per ml (i.e. <1/5 normal); Causes: decreased GnRH (e.g. because of anabolic steroid abuse; stress), poor nutrition, environmental factors (e.g. heat, toxic chemicals).
2) even with sufficient number, some sperm may be physically defective (e.g. double headed, short tailed), not sufficiently motile, or not able to undergo later capacitation, hyperactivation, or the acrosome reaction (see below). >50% defective is considered problematic.

3) Difficulties: 2-month period for sperm production and the sheer number of sperm. Possibilities: GnRH or gonadotropin antagonists; testosterone analogues; progesterone; inhibitors of sperm motility or function; blockage of sperm-egg recognition.

4) (erectile dysfunction) can have a psycho¬logical basis, but anticholinergic drugs, nerve damage, or aging can inhibit arteriolar dilation, which occurs via the NO pathway.
• Benign prostatic hyperplasia (BPH) and male pattern baldness: since T must be converted to DHT for p

Front 32

Female reproductive system

1) Oogonia (= germ cells)
2) Theca cells (= interstitial cells)
3) Granulosa cells (= follicular cells; surround and “nurse” developing oocytes

Back 32

1) The counterpart of ¬the spermatogonia in the testis, oogonia exist only during fetal life, generating a fixed number of primary oocytes by birth
2) The steroidogenic counter¬part of Leydig cells in the testis, they are stimulated by LH to produce androstenedione. Theca cells are low in aromatase and cannot effectively convert androgens to estrogens
3) The counterparts of Sertoli cells, granulosa cells are stimulated by FSH to produce abundant aromatase and thus can convert theca cell androstenedione to estrogen.

Front 33

1) fimbriae
2) oviduct
3) uterus
4) cervix
5) vagina

Back 33

1) ciliated finger-like structures on funnel like end of oviduct recieves ovum from the topologically seperate ovary
2) transports the ovum from the ovary to the uterus; provides an appropriate environ-ment for fertilization
3) site of implantation and growth of the embryo; lining renewed at each cycle
4) constricted base of uterus, separating it from vagina
5) accepts penis; with dilated cervix, forms the birth canal.

Front 34

Describe the creation of a zygote beginning with oogonia

Back 34

Oogonia → continual mitosis only until birth → fixed number of primary oocytes (2n / 2DNA); reduced 10-fold through atresia (= apoptosis = programmed cell death) by the time of puberty.
• Primary oocyte → 1st meiotic division → secondary oocyte (1n / 2DNA) plus polar body at ovulation.
• Secondary oocyte → 2nd meiotic division → “egg” (1n / 1DNA) plus polar body at
fertilization, at which point the haploid egg (ovum) and sperm nuclei fuse to produce the diploid zygote ("conceptus" → embryo → fetus)

Front 35

(primordial follicles

Back 35

Primary oocytes (25 μm) are each surrounded by a single layer of granulosa cells

Front 36

zona pellucida, primary follicles, gap junctions

Back 36

Secreting a clear, protective zona pellucida, a cohort of a dozen or so oocytes grows while granulosa cells multiply (→ primary follicles); granulosa cells are connected to each other and to the oocyte via gap junctions

Front 37

secondary follicles / preantral follicles

Back 37

Surrounding connective tissue differentiates into a theca cell layer as granulosa cells and oocytes grow further

Front 38

early antral follicles

Back 38

After oocytes reach their final size (~150 μm), granulosa cells secrete fluid, forming a fluid-filled space, the antrum

Front 39

dominant follicle; artetric follicles

Back 39

Typically, one follicle (dominant follicle) develops faster than the others, which undergo atresia , or apoptosis (artetric follicles), ~ day 7.

Front 40

cumulus oophorous; antral follicle

Back 40

The dominant follicle enlarges, mainly via an expanding antrum, and the oocyte, encompassed by a sphere of granulosa cells (cumulus oophorous), protrudes into the antrum (antral follicle).

Front 41

mature (“Graafian”) follicle; secondary oocyte

Back 41

After growth to 1-2 cm, the mature (“Graafian”) follicle is palpable at the surface of the ovary and ready for ovulation, ~day 14; As ovulation approaches, the first meiotic division concludes (→ secondary oocyte), cytoplasm matures, and the cumulus begins separating from the follicle wall.

Front 42

corpus hemmorhagicum; corpus luteum; corpus albicans

Back 42

Ovulation occurs when the adjacent walls of the follicle and ovary rupture (corpus hemorrhagicum), expelling the secondary oocyte (surrounded by the zona pellucida and cumulus of granulosa cells) onto the surface of the fimbriae.
• The remaining follicular cells (~80% granulosa + ~20% theca = "luteal" cells) enlarge and form a glandular structure, the corpus luteum (yellow body).
• If fertilization and implantation do not occur, the corpus luteum develops maximally by ~day 25, then rapidly degenerates by apoptosis (→ corpus albicans, white body); after ~28 days, a new cohort of primary oocytes begins to develop

Front 43

Early follicular

Back 43

Having been strongly inhibited by progesterone, estrogen and inhibin A in the previous cycle, LH and FSH rise as their respective inhibitors fall.
No longer supported by progesterone, the uterine lining degenerates → menstruation.
Stimulated by rising FSH, a new cohort of follicles begins to develop. Proliferating granulosa cells now secrete inhibin B

Front 44

Mid-follicular

Back 44

Rising inhibin B begins to suppress FSH release. As FSH decreases, one follicle becomes dominant while the others undergo atresia.

Estrogen levels increase as a result of LH-stimulated theca cell production of androgens and subsequent granulosa cell conversion of androgens to estrogen via FSH-induced aromatase.
Estrogen stimulates further growth of granulosa and theca cells via autocrine / paracrine actions.

Front 45

Late follicular

Back 45

Estrogen-induced growth of the follicle results in rapidly rising estrogen levels, which stimulate further follicular growth.
Rising estrogen renders the anterior pituitary increasingly more sensitive to GnRH by inducing more GnRH receptors on the gonadotropes, an apparent "positive" feedback.
Consequently, LH release increases dramatically (and GnRH may also increase).
Estrogen (+ FSH) induces LH receptors on the granulosa cells that encompass the oocyte.

Front 46

Ovulation

Back 46

The rapid increase in LH triggers ovulation through action on the now-LH-sensitive granulosa cells, which release lytic enzymes and prostaglandins to expel the oocyte.
There is passive release (co-secretion) of FSH and a subsequent inhibin B response.
The LH surge also induces completion of the oocyte’s first meiotic division, preparing it for fertilization

Front 47

Early luteal

Back 47

The LH surge and the loss of oocyte signaling to the follicle result in a metabolic shift, after which the remaining “luteal” cells produce less estrogen and inhibin B but increasing amounts of progesterone and inhibin A

Front 48

Mid-luteal

Back 48

As the corpus luteum grows under LH stimulation, progesterone, estrogen and inhibin A rise maximally.
But the resulting high progesterone, together with estrogen, inhibit both GnRH and LH release while inhibin A inhibits FSH

Front 49

Late luteal

Back 49

If implantation occurs, the trophoblasts of the embryo produce hCG (≈ LH), which maintains the corpus luteum through the first two months of pregnancy. If not…you get late luteal phase; The corpus luteum, lacking LH – the luteinizing hormone – degenerates.
Consequently, progesterone, estrogen and inhibin A levels fall rapidly, releasing both the hypothalamus and the anterior pituitary from inhibition

Front 50

End cycle/recycle

Back 50

Lacking inhibition, FSH and LH begin to rise, stimulating a new cohort of follicles.

Front 51

Name 3 uterine events (phases) during the menstrual cycle

Back 51

1) Menstrual phase (days 1-5): endometrium degenerates and flow begins
2) proliferative pahse (days 5-14): increased estrogen allows endometrium to regenerate, thicken and form glandular structure. Progesterone receptors appear on endo cells due to increased estrogen; myometrium also thickens + has progesterone receptors
3) secretory phase (14-28): glycogen synthesis + vascularization increase due to increase in progesterone; P also inhibits myomterial contraction to prepare for implantation

Front 52

What thickens and becomes acidic during the mid cycle of the menstrual phase?

Back 52

Under E's influence, cervical mucus is thin allowing sperm movement, but under P it thickens and becomes acidic which prevents sperm movement + bacterial invasion.

Front 53

Why does hemorrhage occur during the end cycle?

Back 53

P falls and deprives endo of support + blood vessels constrict, prostaglandin secretion, and death of tissue. P no longer inhibits myometrium contraction, and endometrial blood vessels will hemorrhage through weak capillary walls.

Front 54

What does E stimulate + inhibit, in terms of other systems in the body?

Back 54

Stimulate: growth + maintainence of F reproductive tract, F configuartion, bone growth + maintainence, epiphyseal plate closure, hair pattern, cervical mucus secretion, breast development, prolactin secretion, myometrial contractions

Inhibit: GnRH release (moderate E in early to mid-follicular; E+P in luteal); milk producing effects of prolactin + atherosclerosis

Front 55

What does P stimulate + inhibit?

Back 55

Stimulate: breast glandular growth,uterine secretion, cervical mucus thickening, and increase in body temp

inhibit: myometrial contractions, milk producing effects of prolactin

Front 56

Why do estrogens have different effects, at different times, on different tissues?

Back 56

Due to 2 estrogen receptors: ERalpa and ERbeta.

one of the 2 activation function domains overlaps ligand-binding doamin so receptor can distinguish sterically among E or analogues to produce different effects. Ex: Selective E receptor modulators (SERMs)- analogues for certain purposes (reduce osteoporosis) but minimize side effects (tumor promotion)

Front 57

Describe P receptors

Back 57

PR-B and PR-A both come from same gene but w/ 2 different initiation codons, so PR-B has one more activation function domain.
Share same inhibitory domain, DNA-binding, and ligand binding, and dimerization doamins.

Front 58

What are phytoestrogens?

Back 58

flavonoids + ligands part of HRT that may relieve menopausal symptoms.

Front 59

How does the vaginal mucus change before and after ovulation?

Back 59

before: its thin + stringy. a dried vaginal smear results in branching salt crystals

after: mucus is highly viscous + doesn't form salt crystals

Front 60

What are 3 ways to induce ovulation?

Back 60

1) clomiphene (E2 antagonist) leads to increase GnRH which increases FSH
2) hmG or FSH stimulation
3) use phased protocols: give FSH and block normal cycle with GnRH antagonist. Then do pulses of hcG (LH) to trigger multiple ovulations

Front 61

Name 2 assisted reproductive technologies

Back 61

IVF (in vitro fertilization) and ICSI (intracytoplasmic sperm injection) utilize multiple oocytes obtained by induction protocols, fertilized by capacitated or injected sperm, respectively

Front 62

How do progestin only birth controls work?

Back 62

Decrease FSH, LH, and E2 to early/mid follciular phase to suppress ovulation and produce thick cervical mucous and thin atrophic endometrium. Irregular bleeding may occur

Front 63

How do combination estrogen + progestin birth controls work?

Back 63

oral daily protocol: 21 days on, 7 days off. Can be monophasic with constant E/P ratio, biphasic 2 different E/P ratios, or triphasic: 3 different E/P ratios

Front 64

How does the morning after pill work?

Back 64

2 doses of progestin, 12 hrs apart w/in 72 hours of intercourse. work the same way as progestin only contraceptive depending on when its taken during menstrual cycle

Front 65

Name the following changes the sperm must undergo in the female reproductive system

Back 65

1) capacitation: epididymis derived proteins are removed, transmembrane proteins are rearranged, metabolism + motility increase

2) hyperactivation: Ca influx converts slow beating to rapid beating triggered by proximtiy to egg (paracrine signal)

3) acrosome reaction: sperm head binds to zona pellucida and triggers acrosin via exocytosis in order to clear a path for the sperm head to fuse w/ egg plasma membrane

Front 66

How long does it take the egg to reach the uterus after ovulation?

Back 66

4 days; travels from the fimbraie to the oviduct and finally reaches uterus

Front 67

how long is the egg viable? where does fertilization take place?

Back 67

Unless fertilized, its viable for 12-24 hrs. Takes place is distal portion of oviduct (ampulla) 1-2 days after ovulation.

Front 68

Describe the events that happen beginning from sperm-egg receptor binding to cleavage stage

Back 68

Specific sperm-egg receptor binding → membrane fusion → exocytosis of cortical granules releases enzymes beneath zona pellucida → block to poly¬spermy & egg activation; 2nd meiotic division → haploid female pronucleus → union with male pro¬nucleus → mitosis → beginning of cleavage stage

Front 69

1) morula
2) blastocyst stage
3) trophoblast
4) blastocoel
5) implanation stage
6) ectopic pregnancy

Back 69

The cleaving zygote passes through the oviduct and enters the uterus as a morula (no cavity), 3-4 days post-ovulation.

• The zygote differentiates to the blastocyst stage: an outer layer of cells (the trophoblast, destined to become the fetal portion of the placenta), an inner cell mass (destined to become the embryo/fetus), and a central, fluid-filled cavity (the blastocyst cavity, or blastocoel).

The zygote sheds its zona pellucida (~day 6) in preparation for implantation.


• The embryo implants in the uterine wall ~7 days post-ovulation (implantation stage), during a "window of receptivity" before or after which implantation may fail.

• If transport is delayed, implantation can occur in the oviduct wall or, if the fertilized egg escapes the fimbriae, in the abdominal wall (→ ectopic pregnancy)

Front 70

1) syncytiotrophoblasts
2) chorionic villi
3) decidua
4) chorion
5) placenta
6) amniotic cavity
7) amnio¬centesis

Back 70

Contact between blastocyst and endometrium triggers proliferation of an outer layer of syncytial trophoblast cells (syncytiotrophoblasts),

which penetrate between endometrial cells, aided by proteolytic enzymes, thus embedding the blastocyst in the uterine wall.

• The syncytiotrophoblasts form finger-like pro¬jections (chorionic villi) into the endo¬metrium; these develop extensive capillaries linked to the embryo’s circulatory system.

• Under the influence of an invading villus, the surrounding endometrial cells form a sinus of blood supplied by maternal arterioles. This modified maternal endometrial tissue (decidua) plus the fetal chorion (synctiotrophoblasts, mesoderm cells and the cytotropho¬blasts from which both arose) interlock to form the placenta.

• Umbilical arteries and veins form, in turn forming the umbilical cord attaching the developing embryo to the placenta.

• By 5 weeks, the fetal heart is functioning.

• Meanwhile, a fluid-filled space – the amniotic cavity – form

Front 71

chrorionic gonadotropin

Back 71

made by trophoblasts after their invasion into endometrium (signal that implantation has occurred).

similar to LH, maintains corpus luteum for up to 2 months strongly stimulating P and E + prevents more ovulation. peaks after 2 months, and declines to constant level during pregnancy.

Front 72

What is RU486 (French abortion pill)?

Back 72

a com¬petitive inhibitor of progesterone (binds to but doesn't activate P receptor), causing endo¬metrial degradation and myometrial contraction. If administered with a prosta¬glandin (misoprostol), it will result in expulsion of the fetus.

Front 73

Describe the development of DHEAS, E2, and E, and E3. What is the starting point?

Back 73

• maternal cholesterol → placenta → pregnenolone → fetal adrenal → DHEAS;
• fetal adrenal DHEAS → placenta → DHEA → androstenedione → E2 and E;
• fetal adrenal DHEAS → fetal liver → 16α-OH-DHEAS → placenta → 16α-OH-DHEA → E3.

Front 74

Placental Lactogen

Back 74

faciltates breast development, maintains positive protein balance, mobilizes fats for energy and promotes high glucose for tthe fetus. Level rises at near constant rate throughout preganncy

Front 75

After 8.5 months of pregnancy, what contributes to the softening and dilation of the cervix?

Back 75

mediated by estro¬gens, the ovarian/placental polypeptide hormone relaxin, (insulin/IGF-like) and prosta¬glandins.

Since E is increasingly synthesized by placenta, the efficacy of P in hibihibting contraction decreaase

Front 76

What is released from the posterior pituitary, that is stimulated by stretch receptors in the uterus/cervix?

Back 76

oxytocin! increases and synchornizes contractions more (positive feedback) and increases uterine prostaglandin relase.

Front 77

Describe 3 main relevant prolactin functions. What is prolactin release inhibited + stimulated by?

Back 77

1) mammogenesis – growth and development of mammary gland;
2) lactogenesis – initiation of lactation;
3) galactopoiesis – maintenance of milk production.

inhibited by dopamine, stim by prolactin releasing factor (PRF) .

Front 78

What can you measure as a good estimate of the fetal health?

Back 78

E3; if normal, this should increase as the fetus grows. E3 requires fetal precursors

Front 79

What rises right before birth?

Back 79

Inhibin A and Activin A both rise just before birth.

Front 80

What inhibits the actual production of milk?

Back 80

progesterone. PRL, E, and P promote alveoli to grow in early pregnancy. However, as long as P is high, there will be no milk production.

Front 81

What results in neural input to hypothalamus that inhibits dopamine release?

Back 81

suckling. inhibiting dopamine means prolactin can be secreted. May also result in increased PRF and TRH.

Oxytocin is also released by suckling