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SF4 - Test 3 > 2 - Female Reproductive System > Flashcards

2 - Female Reproductive System Flashcards

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1
Q

What are the major roles o Estradiol and Progesterone in the female reproductive system?

What are roles of Inhibin A and B?

A
  • Act directly on the reproductive tract to regulate its functions
  • Feedback on Anterior Pituitary and Hypothalamus that regulate gonadotropin release
  • Inhibin A and B which inhibit FSH release by Anterior Pituitary
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2
Q

What is the primary source of estrogens in the non-pregnant adult?

What are the major estrogens?

What forms the basis of pregnancy tests?

A

The maturing follice

  • Estradiol (E2) - Principle ovarian estrogen, most potent
    • 99% comes from the ovary
  • Estrone (E1) - Weaker than estradiol; formed from estradiol by peripheral conversion via aromatase activity in fat via estrogen conversion of androgens
  • Estriol (E3) - Weak androgen; in non-pregnant woman, derived from metabolism of E1/E2;
    • Clinical: Measured in pregnancy; the placenta synthesizes high E3
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3
Q

What are the two cell types present in ovarian follicle cells to synthesize estrogen?

What hormones regulate this?

What are their principle secretory products?

Enzymes at each cell?

A
  • Thecal Cells - Regulated by LH - Androstenedione
    • ​Close proximity to blood vessels;ample supple ofLDL Cholesterol for steroid hormon synthesis
    • Site of enzymes for androgen synthesis
    • Do NOT possess aromatase activity; can NOT convert andogens to estrogens
    • Androstenedione is primary androgen secreted by Thecal Cells
  • Granulosa Cells - Regulated by FSH - E2 Primary Product
    • ​During Follicular Phase of ovarian cycle, granulosa cells have limited access to LDL cholesteol (separated from vascular supply)
    • Progesterone production limited during this phase
    • Do NOT have 17a-hydroxylase activity, unable to convert Pregnenolone / progesterone to androgens
    • Have high levels of aromatase/17B-HSD activity; can convert androgens from thecal cells to estrogens
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4
Q

What reeptors are loacted on thecal cells?

What pathway does thi activate?

A

LH Receptors induce androgen biosynthesis

Activate cAMP Signaling pathways within cell

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5
Q

What receptors are located on Granulosa cells?

What pathway is activated?

A

FSH recptors activate aromatase activity

Activate cAMP signaling pathway

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6
Q

What is promoted by progestins?

What are the major progestins?

What is the principle source of progesterone in the non-pregnant adult?

A
  • Progestins are steroids that promote gestation
  • The major progestins are:
    • Progesterone (most potent!)
    • 17a-hydroxyprogesterone
  • The principle source of progesterone in the non-pregnant adult is the corpus luteum
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7
Q

What is the principle circulating androgen in women?

What is its source?

What are other circulating androgens?

A

The principle circulating androgen in women is testosterone

Half is derived from peripheral conversion of steroid precursors

Half is produced by ovaries and adrenals

Other circulating androgens: Dihydrotestosterone, Androstenedione, DHEA, DHEA-sulfate

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8
Q

***Reproductive Cycle in Non-Pregnant Women***

Follicular Phase

Ovulatory Phase

Luteal Phase

A
  • Follicular Phase
    • Begins w/onset of menstrual bleeding
    • Variable in length
    • Corresponds to proliferative phase of endometrial cycle
  • Ovulatory Phase (~36 hrs)
  • Luteal Phase
    • Constant Length (13-14 days)
    • Corresponds to secretory phase of endometrial cycle
    • Ends with onset of next menses
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9
Q

What is developing during the follicular phase?

What is the primary hormone?

What does it correspond to in the endometrial cycle?

A
  • During the follicular phase the preovulatory follicle develops within the ovary
  • Estradiol is primary hormone
  • Corresponds to Menstrual / Proliferative phases of endometrial cycle
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10
Q

What does the ovulatory phase culminate in?

What are the primary hormones of the Luteal Phase?

What phase of the endometrial cycle correspond to?

What does it end with?

A

Ovulation

During the Luteal Phase, the Corpus Luteum secretes Progesterone/Estradiol

Luteal Phase corresponds to the secretory phase of th endometrial cycle

Ends with onset of next menses

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11
Q

What is the functional unit of the ovary?

What are its main actions (4)

A

The follicle is the functional unit of the ovary

  1. Sustains the oocyte
  2. Produces hormones to regulate reproductive function
  3. Spot of endocrine regulation to regulate hormone production and promote ovulation
  4. Differentiates into endocrine structure, Corpus Luteum after ovulation is complete
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12
Q

What are Primordial Follicles?

What type of junctions are formed?

What is the blood supply?

What stage of division is the oocyte arrested in?

A

Primary Oocyte surrounded by a single layer of poorly differentiated pregranulosa cells

Pregranulosa Cells form Gap Junctions with each other and the oocyte

The primordial follicle has no independent blood supply

Meiosis I - Prophase

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13
Q

When does primordial follicle formation begin?

What is their status for the duration of a woman’s life?

A

In the fetus, complete by 6 months old

Primordial Follicles remain dormant in the ovary until recruited to resume growth and development

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14
Q

What occurs in the ovaries in the absence of gonadotropin?

What is the main signaling mechanism for this?

What is the status before puberty?

A

Growth of Primordial Follicles, involves intraovarian signaling

Prior to puberty, follicular growth occurs but the process is arrested in an early stage of development, and the follicle undergoes atresia

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15
Q

At what stage does a primordial follicle become a primary follicle?

A

Formation of the Zona Pellucida; as the granulosa cells become cuboidal and begin to undergo mitosis.

Oocyte and granulosa cells increase in size.

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16
Q

What is the next stage of development for primary follicles?

What is this next stage surrounded by?

What surrounds this layer, and what induces its formation?

A

Growth of primary follicles leads to Preantal Follicles

In Preantral follicles, the oocyte is surrounded by multiple layers of granulosa cells enclosed within the basal lamina.

Surrounding the basal lamina is a thecal layer formed from stromal cells in response to paracrine factors produced by the granulosa cells

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17
Q

What proteins are secreted during the formation of mature preantral follicles?

What type of receptors do granulosa cells begin to express?

A
  • Oocyte grows and secretes the following into the Zona Pellucida:
    • ZP1
    • ZP2
    • ZP3
  • These provide species specific binding sites for sperm cells
  • Continued secretion of paracrine factors to stimulate:
    • growth/differentiation of granulosa cells (causing formation of multilayered structure)
    • Formation of thecal layer from stromal cells
  • Granulosa cells begin to express FSH and Estrogen Receptors, but still depend on paracrine factors to support growth!
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18
Q

What do follicles release to promotes formation of vascular supply?

What occurs in the granulosa layer wrt vascularization?

A

Follicles release angiogenesis factors that promote formation of a vascular supply

Granulosa Layer remains avascular until after ovulation

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19
Q

What do early antral follicles become responsive to?

Are they dependent on this?

How does thi change with larger antral follicles?

A

Early antral follicles become responsive to the growth-promiting effects of Follicle Stimulating Hormone (FSH)

No, considered independent of FSH for survival

Larger antral follicles become highly dependent on FSH for survival

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20
Q

What enhances the steroidogenic capacity of rapidly growing large antal follicles?

What do thecal cells express, and what is their major secretory product?

What does FSH stimulate expression of?

What secretion increases as follicle matures?

A

Responsiveness to gonadotropins

  1. Thecal Cells express LH receptors and enzymes for steroidogenesis, major secretory product is androstenedione
  2. FSH stimulates expression of aromatase in the granulosa cell, enables conversion of androgens to estrogens
  3. The gonadotropin sensitive thecal and granulosa compartments of follicle form functional unit capable of estrogen production in response to LH / FSH; as follicle matures the capacity to secrete estrogens increases
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21
Q

What populations of cells emerge from granulosa cells? (2x)

What becomes the corpus luteum?

What facilitates capture of oocyte by fallopian tubes?

A

Mural Cells: close contact with Thecal Layer, actively engaged in steroidgenesis; retained after ovulation, differentiate into corpus luteum

Cumulus Cells: Surround oocute; inner cells maintain gap junctions with oocyte; released with oocyte during ovulation and facilitate capture of oocyte by ciliated fallopian tubes

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22
Q

What is mainly affected by Atresia?

What is fate of Thecal Cells?

What opposes apoptosis of the follice?

What factors promote atresia?

A

Oocytes / Granulosa Cells

Thecal cells dedifferentiate and return to pool of stromal interstitial cells

FSH opposes apoptosis of the follice

TNFa, Androgens, IL-6 all promote atresia

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23
Q

What are four major changes in the growing preantral follicle?

What stimulation do early antral follicles respond to? What is their growth ultimately independent of though (early)?

Study These Flashcards
A
  1. Thecal Cells express LH Receptors and steroidogenic enymes
  2. Granulosa Cells acquire receptors for FSH and Estrogens
  3. FSH induces aromoatase activity in granulosa cells
  4. Early antral follices respond to FSH Stimulation–however follicular growth is still gonadotropin independent
24
Q

What is the process of cyclic recruitment?

How many survive?

What does this become?

What happens to the remainder that aren’t matured?

***What is survival of follicles at this stage dependent on?***

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A

~20 days before ovulation, cohort of growing antral follicles is recruited for final stage of rapid growth

Usually only one follicle survives as the dominant follicle, to become a mature graafian (preovulatory) follicle

They undergo atresia

Survival of follicles that enter this stage of rapid growth is dependent upon FSH

25
When does Cyclic Recruitment occur? What is the dominant follicle selected? What indicates a dominant follicle has been selected? When does ovulation occur?
Late Luteal Phase of **preceding cycle** During **early follicular phase of current cycle** Dramatic **increases in estradiol** indicates a dominant follicle is present ~ 10-14 days after follicle selected
26
What is the role of **FSH** in the selection process of cyclic recruitment? What does FSH stimulate? (2x) What inhibits FSH release and what is the major effect of this? What receptors does FSH induce in granulosa cells? What major effect does this have?
1. FSH Stimulates **granulosa cell proliferation** and **estradiol (E2) synthesis** 2. **E2 works synergistically with FSH** to promote granulosa cell proliferation 3. Estradiol and **inhibin** have **negative feedback effect** on **FSH release by anterior pituitary** (in this way _dominant follicle blocks development of other follicles, it has FSH supply of its own)_ 4. **_FSH induces expression of LH receptors_** in granulosa cells, so they are **able to respond to LH surge; E2 enhances the action of FSH/LH receptor induction**
27
How does the dominant follicle grow in presence of declining levels of FSH? 5 Reasons:
1. The rapidly proliferating dominant follicle has **more FSH receptors (FSHR) than** the other follicles that were recruited at the same time--due to increased granulosa cell population 2. Dominant follicle produces **growth factors**, such as **IFG-1;** locally produced, enhances FSH stimulus 3. FSH induces expression of LH receptors; enhanced by E2 4. Accumulation of FSH in antral fluid gives **higher FSH concentration in follicular fluid** 5. Better developed **vascular supply**
28
What is increased by the dominant follicle as it approaces the ovulatory phase? What is the stigma? What drives the cumulus expansion? What does this enable?
Antral Fluid Stigma - Poorly vascularized bulge caused by pressure of the follicle against the surface of the ovary Cumulus Expansion - Secretion of ECM components (hyaluronic acid) in response to **LH Stimulation** causes increase in size of cumulus-oocyte complex; enables **capture by fallopian tubes**
29
What do thecal and granulosa cells release in response to LH stimulation? What does this catalyze?
Proteolytic Enzymes catalyze the breakdown of ECM proteins in the thecal layer and surface of ovary at stigma This **gently releases cumulus-oocyte**
30
What is the signal required to induce ovulation? What triggers this? What cells respond to this?
**LH Surge** Triggerd by **positive feedback of estradiol on the pituitary and hypothalamus** Granulosa cells are able to respond to the LH surge because they start expressing LH receptor during the mid-follicular phase in response to FSH stimulation
31
What are the specific actions of LH on the preovulatory follicle?
1. Induces release of **inflammatory cytokines (TNF-a)** 2. Induces expression of **metalloproteinase enzymes** that beaks down wall of follicle, epithelial surface of the ovary at Stigma 3. Induces expression of **Cyclooxygenase-2 (COX-2) and progesterone receptors** in granulosa cells 4. **Resumption of meiosis**; release of growth factors; complete meiosis and extrude polar body (arrested at Metaphase II by cytostatic factor until fertilization) 5. Cumulus Expansion
32
What is the role of COX-2, and what is a clinical example of its inhibition?
COX-2 catalyzes the formation of prostaglandins from arachidonic acid COX-2 **inhibitors** have been shown to **inhibit ovulation**
33
How does LH alter the endocrine profile of the ovary?
LH Promotes reorganization of the postovulatory follicle into the corpus luteum
34
What is the basis for Corpus Luteum formation? What is the fate of granulosa and thecal cells?
The Corpus Luteum is formed from **remnants of the ruptured follicle** Granulosa and Thecal cells differentiated into granulose-lutein and theca-lutein cells
35
What occurs to the vascular supply of granulosa-lutein cells? What receptors do they posses, and key enzyme are they able to synthesize? What does LH induce in these cells?
Granulosa-Lutein cells become vascularized **and are able to obtain cholesterol from circulating LDL / HDL** Express **LH / FSH** receptors and synthesize **Aromatase Enzyme** **LH stimulates** ezpression of enzymes that promote conversion of cholesterol to **progesterone**
36
How does LH promote angiogenesis in granulosa-lutein cells? How can Granulosa-Lutein Cells obtain cholesterol from circulating LDL / HDL?
Secretes angiogenesis factors such as **Vascular Endothelial Growth Factor (VEGF)** **- - -** **1. LH** induces the breakdown of the basal lamina; this allows the newly formed vascular supply of the corpus lutein to vascularize the granulosa-lutein cells **2. LH** induces the expression of LDL / HDL Receptors
37
What does LH induce in the formation of the Corpus Luteum? Why do granulosa-lutein cells not complete androgen synthesis? What does progesterone production peak, and what does this correspond to?
LH induces the expression of **StAR** and **3B-HSD, stimulating conversion of pregnenolone to progesterone** in granulosa-lutein cells - They do **not** express enzymes that promote androgen synthesis, so **they release progesterone** - Progesterone production peaks at the mid-luteal phase; = the **blastula entering the uterine cavity in pregnant woman**
38
What enzyme is synthesized in granulosa-lutein cells via LSH/FSH receptors? What signaling mechanisms does this use?
Aromatase Enyme cAMP dependent mechanism
39
What does estrogen production by the corpus luteum require? (Cell types and actions of each)
_**Both** types of Lutein Cells_! **1. Theca-lutein** synthesize **androgens (LH stim)** **2. Granulosa-lutein** convert these to **estrogens, and secrete Inhibin A**
40
If pregnancy does not occur by day 9, what is the fate of the corpus luteum? What is rapidly declining at this stage? If preganncy does occur, what maintains the corpus luteum?
Luteolysis; rapid **decline** in **progesterone synthesis, due to decline in LH production** Human Chorionic Gonadotropin (hCG)
41
What are the hormonal changes (H-P-Ovarian) in the early follicular phase? How do the low levels of estradiol being produced affect FSH?
FSH promotes granulosa cell proliferation FSH / LH stimulate estradiol synthesis Low levels of estradiol being produced has a **negative feedback** on FSH release
42
What are the hormonal changes (H-P-Ovarian) in the late follicular phase?
Dramatic increase in **circulating levls of estradiol** due to rapid increase in number of **granulosa cells** in dominant follicle and **stimulatory of FSH / LH** As **_estradiol rises_** it acts on hypothalamus to **_increase GnRH pulse generator frequency and on pituitary to increase gonadotrope sensitivity GnRH stimulation_** (Positive Feedback Effect of Estradiol) Surge in LH triggers events in follicle that promote ovulation
43
What are the hormonal changes (H-P-Ovarian) in the late Luteal Phase? Secretory products? Feedback results?
LH Promotes the development and secretory activity of **corpus luteum** Secretory products of corpus luteum include progesterone, estradiol, inhibin A _Progesterone_ - **Negative feedback** on **gonadotropin release** at hypothalamus/pituitary _Estradiol/Inhibin A_ - **Negative feedback** on **anterior pituitary** **FSH** will increase as corpus luteum declines; coincides with start of rapid growth phase of cohort of follicles for next menstrual cycle
44
What are the hormonal changes (H-P-Ovarian) due to circulating inhibin levels? (Clinical Uses)
* Inhibin B * Clinical marker to assess **FSH mediated granulosa cell function** * Inhibin A * Clinical marker to asses **LH mediated corpus luteum function**
45
Where are the endometrium changes restricted to during the menstrual cycle? What strongly influences these changes? What is the Stratum Basalis involved in?
Upper 2/3, **Stratum Functionalis** Strongly influenced by **Ovarian Hormones** **Stratum Basalis** involved in **regenerating endometrium after menstruation**
46
Endometrium Proliferative Phase Hormone changes? Action of estradiol?
Begin several says after start of **Follicular Phase** **Estrogens increasing** Principle action of **Estradiol is to restore endometrial lining**
47
Endometrium Proliferative Phase How does estradiol restore the endometrial lining?
1. Causes dramatic increase in thickness of endometrium by increasing **proliferation of superficial epithelial/stromal cells; _mediated by growth factors produced by stromal cells_** 2. Induces **growth of uterine glands,** elongation of **spiral arteries** 3. Increases **expression of progesterone receptors**
48
Endometrium Secretory Phase Ovarian cycle phase? Hormones secreted?
Coincides with **Luteal Phase** of ovarian cycle **Progesterone/Estradiol** secreted by **Corpus Luteum**
49
Endometrium Secretory Phase Major role of Progesterone? What capacity is enhanced in the endometrium? What occurs to spiral arteries/capillaries? What is the net effect?
* Progesterone **inhibits** epithelial cell proliferation and regulates actions of estradiol * Promotes **differentiation of endometrium and enhance secretory capacity** * **​**Spiral Arteries become more coiled, capillaries increase in permeability * Stromal cells enlarge * **Net Effect: Provide cnutrients for the unattached embryo and prepare endomtrium for implantation and pregnancy**
50
Endometrium Menstrual Phase What characterizes this phase? What causes this to occur?
If implantation does not occur, the uterus enters the menstrual phase; characterized by **endometrial ischemia, tissue necrosis, and shedding of endometrium** **- - -** Sudden **drop in estrogen/progesterone** at end of luteal phase
51
Endometrium Menstrual Phase What is the vasomotor response of the spiral arteries, and what causes this? What is released in response to progesteron withdrawl? What aids expulsion of desquamated tissue?
Vessels undergo progressive rhythmic contractions and relacations; induced by **Prostraglandin F2a (PGF2a)--result is ischemia** Matrix metalloproteinases are released in response to progesterone withdrawal **Uterine Contractions**, induced by **PGF2a,** helps expel desquamated tissue
52
What are the hormonal changes associated with puberty in girls?
Trigger - **Increase** in pulsatile release of **GnRH by hypothalamus** **FSH / LH increase (FSH faster)** **17B-Estradiol increases** (promotes bone growth, breasts, female reproductive tract maturation)
53
What effect does estrogen have on progesteron receptors? What are the cardiovascular effects of estrogens? How does estrogen effect the skeletal system? Clinical?
Estrogens **stimulate progesterone receptor synthesis** Estrogens have **vasodilatory effect, and are nongenomic** (do not change gene expression); exert **longer-term effects, prevent atherosclerosis--these involve gene changes (genomic)** In the skeletal system, estrogens **inhibit bone resporption; \*\*Clinical: After menopause may need estrogen replacement therapy to attenuate age-related bone loss\*\***
54
What hormonal changes are associated with menopause? Symptoms?
* Hormonal Changes * Decreased estrogens (estrone) * Increased FSH/LH * Increased GnRH * HAVOC * H - Hot Flashes * A - Atrophy * V - of Vagina * O - Osteoperosis * C - Coronary Artery Disease
55
\*\*What estrogen receptors have been identified?\*\*
* ERa , ERb * Can induce genomic or nongenomic effects (steroid mechanism)
56
What are major hormonal hallmarks at the following stages? LH and puberty? Gonadotropin release and reproductive years? LH / FSH ratio and reproductive years? Gonadotropin and menopause?
* **LH** displays **nocturnal** release associated with **puberty** * Gonadotropin shows **cyclic** pattern during reproductive years * LH / FSH ratio changes during reproductive years (LH increase, FSH decrease @ puberty) * LH / FSH increase w/menopause; flip back vs reproductive years
57

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