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Reproductive System I > Female Reproductive Physiology Lecture (Dr. Lopez) > Flashcards

Female Reproductive Physiology Lecture (Dr. Lopez) Flashcards

1
Q

Major differences between Male & Female reproductive systems

A

MALE:
- Gonads (testes) reside outside of abdominal cavity, in scrotum

  • Gonad is continuous with reproductive tract
  • Release of gametes (sperm) from gonads is continuous
  • Gametic reserve is replenished throughout life
  • Testosterone exerts negative feedback on secreNon of pituitary LH & FSH
  • Male tract serves only male gamete transport & maturaNon & delivery
  • Activity of male tract does not show rhythm
  • Testosterone is always the primary gonadal steroid
  • The male reproductive system does not prepare for newborn

FEMALE:
- Gonads (ovaries) reside within abdominal cavity

  • Gonad is not continuous with reproductive tract
  • Release of gamete (egg) from gonads occurs once per month
  • Gametic reserve is finite & exhausted by menopause
  • Estrogen exerts both negative & positive feedback on secretion of pituitary LH and FSH
  • Female tract serves male & female gamete transport & maturation, fertilization, placentation, & gestation
  • Activity of female tract is based on the monthly menstrual cycle, or on the length of a pregnancy (normally about 9 months)
  • Estrogen is the primary gonadal steroid in the first half of the monthly cycle, & progesterone in the second half
  • The female reproductive system prepares for newborn with breast development & milk production & is involved in breastfeeding of the newborn
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2
Q

Anatomy of the female reproductive system

A
  • The female reproductive system is composed of the Ovaries, & the Female Reproductive tract
  • The Mammary Glands (breasts) are also part of the Female Reproductive system
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3
Q

Anatomy of the female reproductive system

A
  • The ovary can be divided into an Outer Cortex & an Inner Medulla
  • NEUROVASCULAR elements run into the Medulla

• The Cortex is composed of a Densely Cellular Stroma
– Ovarian follicles reside within the Stroma

– Ovarian follicles contain a Primary Oocyte surrounded by follicle cells

– Cortex is covered by a layer of Simple Epithelium – Ovarian Surface Epithelial cells

  • Highly Mitogenic population of cells; gives rise to more than 80% of cases of ovarian cancer
  • The process of Ovulation involves an Inflammatory event that ERODES the Wall of the Ovary & Follicle
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4
Q

The ovarian follicle is the functional unit of the ovary

A
  • Performs both Gametogenic & Endocrine functions
  • Contains Follicular structures at many different points of their development (in Premenopausal cycling women)

• A follicle goes through the following stages:
– Resting primordial follicle

– Growing Preantral (1ry & 2ry) follicle

– Growing Antral (tertiary) follicle

– Dominant (Preovulatory, Graafian) follicle

– Dominant Follicle within the Periovulatory period

– CORPUS LUTEUM (of Menstruation or of pregnancy)

– Atretic Follicles (degenerate before coming to maturity)

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5
Q

Overview of the ovarian follicle maturation

A

• Oocyte maturation: production of a HAPLOID female gamete capable of fertilization by a sperm
– Begins in the fetal ovary

• Follicles mature in stages from Primordial to Graafian (or preovulatory) follicles

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6
Q

Primordial follicle

A

• Throughout reproductive life, some 90% to 95% of all follicles are the primordial (i.e., “nongrowing”) follicles
– Represent the Ovarian Reserve of Follicles

• Represent the Earliest & Simplest follicular structure in the ovary
– Consists of the Primary Oocyte with a surrounding SINGLE layer of Pregranulosa cells

– The Granulosa cells remain intimately attached to the Oocyte throughout its development

– Granulosa cells provide Nutrients such as Amino Acids, Nucleic Acids, & Pyruvate to support oocyte maturation

• First Primordial Follicle usually appears ∼6 weeks into intrauterine life; the generation of primordial follicles is complete by ∼6 months after birth

• Growing follicles restrain development of too many Primordial Follicles by release
of ANTI-MÜLLERIAN HORMONE (AMH)

• Primordial Follicles are lost primarily from death due to FOLLICULAR ATRESIA; a small subset of primordial follicles will enter follicular growth in WAVES
– The rate at which resting Primordial Follicles die or begin to develop will determine the reproductive LIFE Span of a woman

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7
Q

Fate of the ovarian reserve in women

A

• ~ 7 million follicles are produced of which less than 300,000 reach maturity & about 450 are OVULATED between Menarche & Menopause

• Only limited numbers of follicles are selected for ovulation, whereas the rest undergo ATRESIA at various stages of development
– ATRESIA: degenerative process involving the immature ovarian follicles

– Some studies indicate that the death of Granulosa cells triggers Atresia of the follicles (mechanisms are not completly understood yet)

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8
Q

Primordial follicle

A

• GAMETE
– The gamete in Primordial Follicles is derived from OOGONIA that have entered
the First Meiotic Division & are now called PRIMARY OOCYTES

– These Primary Oocytes progress through most of PROPHASE I over a 2-week period & then ARREST in the DIPLOTENE stage (sometimes up to 50 yrs.)

– The Nucleus of the Oocyte – GERMINAL VESICLE – remains intact at this stage
*** Endocrine function:
A) Release Paracrine Factors; do not produce Ovarian Steroid Hormones
• There is evidence that follicle cells stimulate Oocyte Growth by release of KIT LIGAND (Stem Cell Factor)
1) Is a Cytokine that binds to the C-KIT Receptor

2) Other functions include Guiding Cells to their appropriate locations in the Body

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9
Q

Growing Preantral follicle

A

• Development that occurs before the formation of a fluid-filled astral cavity

• One of the first visible signs of follicle growth is the appearance of CUBOIDAL GRANULOSA CELLS – at this point follicle is known as PRIMARY Follicle
– Contains a larger Primary Oocyte than the one in the Primordial follicle

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10
Q

Growing Prenatal follicle Cont 1

A

***As granulosa cells proliferate, they form a MULTILAYERED epithelium around the oocyte – at this point follicle is known as SECONDARY Follicle:
1) Contains a PRIMARY Oocyte surrounded by several LAYERS of Cuboidal Granulose cells
• Once a Secondary Follicle acquires 3 – 6 layers of Granulosa cells, it secretes PARACRINE factors that induce nearby Stromal Cells to differentiate into Epithelioid THECAL cells

2) Stromal cells differentiate, surround the follicle , & become the THECA cells
• Theca cells are on the OUTSIDE of the follicle’s Basement Membrane

3) Once a theca layer forms, the follicle is referred to as a Mature Prenatal follicle
• It takes SEVERAL months for a 1ry follicle to reach the mature Preantral stage

4) As the 2ry follicle grows in size, the number of Granulosa cells Increases to ∼600, & the THECA cells show Increasing differentiation

5) The progression to Secondary follicles involves the formation of capillaries & an Increase in the vascular supply to developing follicular units
• Movement of the follicle from the Outer Cortex to the Inner Cortex, CLOSER to the Vasculature of the Ovarian Medulla
• Follicles release ANGIOGENIC Factors that induce the development of 1 or 2 arterioles, which generate a Vascular Wreath around the follicle

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11
Q

Growing Prenatal Follicle Cont 2

A

1) GAMETE:
– In Preantral follicles, the Oocyte FAILS to complete MEIOSIS I because of a lack of
specific Meiosis-associated proteins

– The Oocyte begins to grow & produce cellular & secreted proteins
a) Initiates secretion of extracellular matrix GLYCOPROTEINS (ZP1 , ZP2 , & ZP3) that form the ZONA PELLUCIDA

b) The Zona Pellucida provides a species-specific binding site for sperm during fertilization
c) Granulosa cells & the Oocyte project CELLULAR EXTENSIONS through the Zona Pellucida & maintain GAP JUNCTIONAL contacts

2) ENDOCRINE FUNCTION
– Granulosa cells express the FSH RECEPTOR during this period but are dependent primarily on Factors from the Oocyte to GROW
a) DO NOT produce Ovarian Hormones at this stage

– THECAL cells are analogous to Testicular Leydig cells

a) The major product of the thecal cells is Androstenedione, as opposed to Testosterone
- Thecal cells DO NOT express high levels of a 17β-HYDROXYSTEROID DEHYDROGENASE

b) Androstenedione production at this stage is Absent or Minimal

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12
Q

Growing Antral follicles

A

• MATURE Preantral follicles develop into EARLY Antral follicles; takes ~ 25 days
– Once the granulose epithelium increases to 6 or 7 layers, fluid-filled spaces appear between cells & come together into the ANTRUM

• Over about 45 days, Antral follicles will continue to grow to Large, recruitable Antral follicles, with a 100x INCREASE in Granulosa cells

• During this stage there is also SWELLING of the antral cavity, which increasingly divides the granulosa cells into 2 discrete populations:
a) MURAL Granulose cells (STRATUM GRANULOSUM)

b) CUMULUS cells (CUMULUS OOPHORUS or CORONA RADIATA)

• Early Antral follicles are DEPENDENT on FSH for normal growth; Large Antral follicles become HIGHLY DEPENDENT on FSH for their growth & sustained viability

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13
Q

Growing astral follicles Cont 1

MURAL GRANULOSA CELLS

A

• MURAL GRANULOSA CELLS:
– Form the outer wall of the follicle

– Close to outerlying Thecal layers

– Become highly Steroidogenic

– Remain in the ovary after ovulation to differentiate into the CORPUS LUTEUM

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14
Q

Growing astral follicles Cont 2

CUMULUS CELLS­

A

• CUMULUS CELLS
­- INNER cells surrounding the Oocyte

­- The Innermost layer (relative to the oocyte) of Cumulus cells maintains GAP & ADHESION Junctions with the Oocyte

­- During Ovulation, Cumulus cells are released from the ovary with the Oocyte (cumulus- oocyte complex)

­- Crucial for the ability of the FIMBRIATED End of the oviduct to grab & MOVE the Oocyte along the length of the Oviduct to the site of fertilization

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15
Q

Growing Antral follicles Cont 3

A

• GAMETE
1) Oocyte grows rapidly in the early stages of Antral follicles; growth then SLOWS in Larger follicles

2) At the Antral stage, the Oocyte becomes competent to complete MEIOSIS I at ovulation
a) The Oocyte Synthesizes sufficient amounts of Cell Cycle Components (e.g. cyclin- dependent kinase-1 & cyclin B)

b) Larger Antral follicles, GAIN Meiotic competence but still maintain Meiotic arrest until the midcycle Luteinizing Hormone (LH) SURGE
- Meiotic ARREST is achieved by the MAINTENANCE of ELEVATED cAMP levels in the Mature Oocyte

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16
Q

Growing Antral follicles Cont 4

A

• ENDOCRINE FUNCTION
– Thecal cells of Large Antral follicles produce SIGNIFICANT amounts of Androstenedione & testosterone (to a much lesser extent )

– Androgens are converted to Estradiol-17β by the MURAL GRANULOSA CELLS

– FSH stimulates proliferation of Granulosa Cells & induces the expression of CYP19- AROMATASE

– The Mural Granulosa cells of the large Antral follicles produce Increasing amounts of INHIBIN (inhibin B) during the EARLY Follicular Phase

– LOW levels of Estrogen & Inhibin exert a NEGATIVE FEEDBACK effect on FSH Secretion, thereby contributing to the SELECTION of the follicle with the most FSH-responsive cells

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17
Q

Dominant Follicle

A

• At the end of the monthly cycle, several Large Antral follicles are recruited to begin RAPID development which is dependent on gonadotropins
a) The total number of Recruited follicles in both ovaries can be as high as 20 in a younger woman (

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18
Q

Dominant Follicle Cont 1

GAMETE

A

• GAMETE
– Oocyte continues to grow at a SLOWER rate, but remains
Arrested in Meiosis I

– STALK of Cumulus Cells attaching them to Granulosa Cells becomes THIN

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19
Q

Dominant follicle Cont 2

ENDOCRINE FUNCTION

A

• ENDOCRINE FUNCTION:
– Steroid hormone production requires Thecal & Granulosa cells
a) THECAL CELLS: express LH Receptors & Produce Androgens
- Basal LH levels stimulate production of Steroidogenic Enzymes (3β-HSD, CYP17,
CYP11A1), LDL Receptors in the Thecal cells

  • Androstenedione (primarily) & Testosterone released from Thecal cells can diffuse into the Mural Granulosa cells or can enter the vasculature surrounding the follicle

b) GRANULOSA CELLS: Express FSH receptors
– The Mural Granulosa cells of the selected follicle have a HIGH number of FSH Receptors & are very Sensitive to FSH signaling

– FSH up-regulates Aromatase gene expression & activity
» AROMATASE converts Androstenedione to Estrone & Testosterone to Estradiol-17β

– Granulosa cells express activating Isoforms of 17β-HSD, which DRIVES Steroidogenesis toward the production of Estradiol-17β

– FSH also induces the expression of INHIBIN B during the Follicular phase

– FSH also induces the expression of LH Receptors in the Mural Granulosa cells during
the 2nd half of the follicular phase
» Mural granulosa cells become Responsive to BOTH FSH & LH, allowing these cells to maintain HIGH levels of CYP19 in the Face of Declining FSH levels
» Acquisition of LH Receptors also ensures that Mural Granulosa cells will RESPOND to the LH SURGE

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20
Q

The Dominant Follicle during the Periovulatory period

A

• Periovulatory period can be defined as the time from the onset of the LH SURGE to Ovulation
– This process lasts 32 – 36 hours in women

• Starting at the same time, & superimposed on the process of ovulation, is a change in the Steroidogenic function of the THECA & MURAL GRANULOSA Cells (aka LUTEINIZATION)
– Luteinization culminates in the formation of a CORPUS LUTEUM, which is capable of producing large amounts of Progesterone, along with Estrogen, within a few days after ovulation

• The LH surge induces dramatic Structural CHANGES in the Dominant Follicle that involve its Rupture, Ovulation of the cumulus-oocyte complex, & the biogenesis Corpus Luteum from the remaining Thecal Cells & Mural Granulosa Cells

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21
Q

The Dominant Follicle during the periovulatory period Cont 1

A

• Major Structural Changes associated with the LH SURGE:

1) BEFORE OVULATION, follicle presses AGAINST wall of ovary to form bulge called STIGMA
• The LH surge induces the release of Inflammatory Cytokines & Hydrolytic enzymes from the Theca & Granulosa cells
a) These secreted components lead to the BREAKDOWN the Follicle Wall, Tunica Albuginea, & Surface Epithelium in the vicinity of the Stigma

b) At the END of this process, the Antral Cavity becomes CONTINUOUS with the Peritoneal cavity

2) CUMULUS CELLS DETACH from Granulosa Cells and Oocyte is FREED within the Antral cavity
• As an INDIRECT Response to the LH Surge (i.e. in response to LH-dependent paracrine factors), the Oocyte Releases the TRANSFORMING GRWOTH FACTOR-β (TGF-β)-related factor, GDF9
a) GDF9 stimulates the Cumulus Cells to SECRETE Hyaluronic Acid & other extracellular matrix components
» These secreted components causes EXPANSION of the Oocyte complex, making it Easier for CAPTURE by the oviduct & easier for Sperm to LOCATE (Sperm produce HYALURONIDASE to allow PENETRATION into the Cumulus-Oocyte complex)

» The Cumulus-Oocyte complex is released through the ruptured Stigma in a Slow, Gentle process

3) The BASAL LAMINA of the Mural Granulosa Cells is enzymatically Degraded, &
Blood vessels & Outer-lying Theca can PUSH INTO the Granulosa Cells
• Granulosa Cells also produce ANGIOGENIC Factors to INCREASE Blood Supply to the new CORPUS LUTEUM
a) Example of released angiogenic factors: Vascular Endothelial Growth Factor (VEGF), Angiopoietin-2, & Basic Fibroblast Growth Factor (bFGF)

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22
Q

The dominant follicle during the periovulatory period Cont 2

A

• GAMETE
– BEFORE OVULATION, the Primary Oocyte is competent to COMPLETE Meiosis but is ARRESTED in Prophase I as a result of HIGH cAMP levels

– LH SURGE induces release from arrest & completion of Meiosis I with extrusion of the first polar body

– Secondary Oocyte then progresses to Metaphase II where it arrests again until fertilization

• ENDOCRINE FUNCTION
– Both Thecal & Mural Granulosa cells express LH receptors at the time of the LH surge

– The LH surge induces Luteinization of the Granulosa Cells—a process that will continue for several days after ovulation

– During the PERIOVULATORY period, the LH surge induces shifts in the Steroidogenic activity of the Mural Granulosa Cells
a) Transiently INHIBITS Aromatase expression &, consequently, Estrogen production
– Rapid decline in Estrogen helps to TURNS OFF the POSITIVE FEEDBACK on LH secretion

b) Causes Vascularization of Granulosa cells to make Cholesterol available for Steroid Synthesis & INCREASE expression of LDL/HDL receptors
c) Increases expression of Proteins & Enzymes to produce Progesterone

23
Q

During the Luteal Phase

A
  • The major products of the corpus luteum are the PROGESTINS, although Estradiol synthesis is still substantial
24
Q

The Corpus Luteum

A
  • AFTER OVULATION, Antral cavity fills with Blood from Ruptured vessels (CORPUS HEMORRHAGICUM)
  • The Corpus Luteum is formed & the Granulosa Cells now become Granulosa Lutein cells which enlarge & fill with CHOLESTEROL ESTERS
  • These cells Collapse & Fill in the Antral Cavity

• The human Corpus Luteum is programmed to live for ~ 14 days (Corpus Luteum of menstruation), unless rescued by HUMAN CHORIONIC GONADOTROPIN (hCG), which originates from an implanting embryo
a) hCG is the protein that is DETECTED in Pregnancy Tests

b) If rescued, the Corpus Luteum of pregnancy will remain VIABLE for as long as the Pregnancy

25
Q

Corpus Luteum Cont

A

• GAMETE
– LH surge induces two parallel events, Ovulation & Luteinization
• If Ovulation occurs normally, the Corpus Luteum is devoid of a gamete

• ENDOCRINE FUNCTION
– Progesterone production by the Corpus Luteum INCREASES Steadily from the onset of the LH surge & peaks during the Midluteal Phase

– Estrogen production transiently DECREASES in Response to the LH SURGE but then Rebounds & also Peaks at Midluteal phase
• The ELEVATED Estrogen levels at Midluteal phase may be Responsible for the DECREASE in the Sensitivity of the Corpus Luteum to LH
a) Progesterone & Estrogen levels DECLINE during the 2nd half of the Luteal Phase unless an Increase in circulating hCG compensates for the decreased sensitivity to LH

– Luteal hormonal output is absolutely DEPENDENT on basal LH levels
• Progesterone output is closely correlated with the Pulsatile Pattern of LH release

• Both FSH & LH are reduced to basal levels during the luteal phase by the Negative Feedback from Progesterone & Estrogen

– Granulosa Lutein cells secrete INHIBIN A which further Suppresses FSH Secretion

26
Q

Follicular Atresia

A
  • Demise of an ovarian follicle
  • PREDOMINANT process in the ovary
  • Can occur at any time during development
  • During Atresia, the Granulosa cells & oocytes undergo Apoptosis

• Thecal cells Persist & Repopulate the cellular Stroma of the ovary
– Thecal cells retain LH Receptors & the ability to produce Androgens; collectively are referred to as the interstitial gland of the ovary

27
Q

Summary

A

• FOLLICULAR PHASE:
– Recruitment/growth of Antral follicles
– Selection of one dominant follicle
– Growth of dominant follicle until ovulation

• LH SURGE – Ovulation

• LUTEAL PHASE:
– Hormonal secretion by the Corpus Luteum

28
Q

Puberty marks the transition to cyclic, adult reproductive function

A

• Puberty in girls involves:
– MENARCHE: beginning of menstrual cycles

– THELARCHE: Breast development

– ADRENARCHE: increase in Adrenal Androgen secretion

29
Q

The menstrual cycle includes both the Ovarian & Endometrial cycles

A
  • The menstrual cycle actually involves cyclic changes in 2 organs: the Ovary & the Uterus
  • The menstrual cycle comprises parallel Ovarian & Endometrial cycles

• Ovarian cycle:
– FOLLICULAR Phase (coincides with PROLIFERATIVE Phase of endometrial cycle)

– LUTEAL Phase (coincides with SECRETORY Phase of endometrial cycle)

• Endometrial cycle:
– 3 phases: MENSES (Menstrual phase), PROLIFERATIVE phase, SECRETORY phase

30
Q

Ovarian cycle

Follicular phase

A

• Dependent upon normal Hypothalamic & Pituitary function

• FOLICULAR PHASE
1) FSH stimulates a follicle to
complete its development

2) Begins with onset of Menses & ends on day of LH Surge (≈ 14 days)
3) Granulosa Cells of the follicles Increase production of the Estrogen Estradiol, which stimulates the Endometrium to undergo REPID & CONTINUOUS Growth & Maturation

4) Coincides with PROLIFERATIVE phase of endometrial cycle
• Rapid rise in Ovarian Estradiol secretion eventually triggers a Surge in LH, which causes Ovulation

31
Q

Ovarian cycle

LUTEAL PHASE

A

• LUTEAL PHASE
1) Follicle transforms into
a Corpus Luteum

2) Luteal cells produce Progesterone &
Estrogen, which stimulate further endometrial growth & development

3) Begins on day of LH Surge & ends at onset of next Menses (≈ 14 days)
4) Coincides with the SECRETORY phase of the endometrial cycle

32
Q

Hypothalamic- Pituitary- Ovarian Axis

A
  • Neurons in the hypothalamus synthesize, store, & release GnRH
  • GnRH binds to receptors on the surface of gonadotrophs, resulting in the Synthesis & Release of FSH & LH
  • LH & FSH, stimulate the ovary to Synthesize & Secrete the sex steroids Estrogens & Progestins
  • Ovaries also produce peptides called INHIBINS & ACTIVINS
  • Ovarian steroids & peptides exert both Negative & Positive feedback on both the Hypothalamus & the Anterior pituitary
33
Q

Pulsatile release of GnRH & pulsatile secretion of LH

A
  • GnRH neurons release GnRH in RHYTHMIC PULSES
  • Early in the follicular phase of the cycle, when the Gonadotrophs are NOT very GnRH sensitive, each Burst of GnRH elicits only a small rise in LH
  • LATER in the Follicular Phase, when the Gonadotrophs in the Anterior Pituitary become much MORE SENSITIVE to the GnRH in the portal blood, each burst of GnRH triggers a much LARGER Release of LH
34
Q

GnRH stimulates gonadotrophs in the anterior pituitary to secrete FSH & LH, which stimulate Ovarian Cells to secrete Estrogens & Progestins

A

• Before ovulation, the LH & FSH secreted by the gonadotrophs act on cells of the developing follicle
– THECA cells of the follicle have LH Receptors, whereas the GRANULOSA cells have BOTH LH & FSH receptors

– BOTH LH & FSH are REQUIRED for Estrogen production because neither the theca cell nor the granulosa cell can carry out all the required steps

• After ovulation, LH acts on the cells of the Corpus Luteum

35
Q

Ovaries also produce Inhibins, which inhibit FSH secretion, & Activins, which activate it

A

• The INHIBINS are produced by the GRANULOSA cells of the follicle
– FSH specifically stimulates the granulosa cells to produce INHIBINS

– Estradiol may stimulate INHIBIN Production through an INTRAOVARIAN mechanism

– Just before ovulation, after the Granulosa cells acquire LH receptors, LH also stimulates the production of INHIBIN by GRANULOSA cells

– INHIBINS INHIBIT FSH production by gonadotrophs!!!!!!

• The ACTIVINS are produced in the same Tissues as the Inhibins, but they stimulate FSH release from Pituitary Cells

36
Q

Feedback on the hypothalamic-pituitary axis: Ovarian Steroids

A

• NEGATIVE FEEDBACK
– Throughout most of the menstrual cycle, the estrogens & Progestins feed back NEGATIVELY on BOTH the Hypothalamus & Pituitary

– The net effect is to REDUCE the Release of BOTH LH & FSH

– ESTROGENS exert Negative Feedback at BOTH LOW & HIGH concentrations, whereas the PROGESTINS are effective only at HIGH concentrations

• POSITIVE FEEDBACK
– Exert Positive feedback at the end of the Follicular Phase

– Levels of Estrogen (ESTRDIOL) rise gradually during the First half of the Follicular Phase of the ovarian cycle & then STEEPLY during the Second half

– After the Estradiol levels reach a certain threshold for a minimum of 2 days, HP axis REVERSES its sensitivity to estrogens, now exert POSITIVE FEEDBACK!!!!!!!

– Switch to Positive Feedback promotes the LH SURGE

– Rising levels of Progesterone during the Late Follicular phase also produce a Positive Feedback response & thus Facilitate the LH SURGE

37
Q

Feedback on the hypothalamic-pituitary axis: Inhibins & Activins

A

• NEGATIVE Feedback by the INHIBINS
– Inhibit FSH Secretion by the Gonadotrophs of the Anterior
Pituitary

– Inhibins also have the Intraovarian effect of Decreasing Androgen production, which can have Secondary effects on Intrafollicular Estrogen production

• POSITIVE feedback by the ACTIVINS
– The stimulatory effect of acNvins on FSH release is
independent of GnRH action

– Activins also have the intraovarian action of stimulating the Synthesis of Estrogens

38
Q

Cyclic hormonal changes during the menstrual cycle

A

• Positive Feedback of estrogens, Progestins, & Activins on the HP axis is involved in the induction of the LH SURGE

• As the Luteal Phase of the menstrual cycle begins, circulating levels of LH & FSH RAPIDLY DECREASE
– This fall-off in Gonadotropin levels reflects Negative Feedback by Estradiol, Progesterone, & Inhibit

– As gonadotropin levels fall, so do the levels of Ovarian Steroids

• During the Luteal Phase, the rise in concentration of Estradiol, Progesterone, & Inhibin causes— in typical Negative Feedback fashion—the continued Decrease of Gonadotropin levels MIDWAY through the Luteal Phase

39
Q

Cyclic hormonal changes during the menstrual cycle Cont

A
  • Circulating levels of LH slowly fall during the luteal phase
  • During the LATE Luteal Phase, the gradual demise of the Corpus Luteum leads to DECREASES in the levels of Progesterone, Estradiol, & Inhibit
  • Aner the onset of Menstruation, the HP axis returns to a Follicular-Phase pattern of LH Secretion (i.e. a gradual Increase in the frequency of GnRH pulses)
40
Q

The ovary synthesizes Estradiol, the major Estrogen, & Progesterone, the major Proges-n

A
  • Estrogens in female humans are derived from the ovary & the adrenal gland & from PERIPHERAL conversion in Adipose Tissue
  • In a Nonpregnant woman, Estradiol, the PRIMARY circulating Estrogen, is secreted principally by the OVARY
  • Ovarian cells can synthesize their OWN CHOLESTEROL DE NOVO
  • Cells in the Ovaries are different because, they have an AROMATASE that can convert Androstenedione to Estrone & Testosterone to Estradiol
  • Estrone can be converted into the more powerful Estrogen Estradiol, & vice versa, by 17β-HYDROXYSTEROID DEHYDROGENASE (17β-HSD)
  • The liver can convert BOTH Estradiol & Estrone into the weak estrogen ESTRIOL
  • Progesterone is the more Important progestin, and it has HIGHER circulating levels
41
Q

During the Follicular Phase, the Major Product of the Follicle is ESTRADIOL

A
  • In the Follicular Phase of the menstrual cycle, the FOLLICLE synthesizes ESTROGENS, whereas in the Luteal Phase, the CORPUS LUTEUM does the synthesis
  • Estradiol synthesis requires the contribution of 2 distinct cell types: the THECA & GRANULOSA cells within the Follicle & the THECA-LUTEIN & GRANULOSA-LUTEIN cells within the Corpus Luteum
42
Q

During the Luteal Phase

A
  • The Major products of the Corpus Luteum are the Progestns, although Estradiol synthesis is still substantial
43
Q

Hormonal regulation of basal body temperature (BBT) during the monthly cycle

A

• The higher levels of Estrogen present during the Pre-ovulatory (Follicular) phase of the menstrual cycle lower BBT

• The higher levels of Progesterone released by the Corpus Luteum after ovulation raise BBT!!!!!
– The rise in temperatures can most commonly be seen the Day AFTER ovulation, but this varies

• If pregnancy does NOT occur, the disintegration of the Corpus Luteum causes a DROP in BBT that roughly coincides with the onset of the next Menstruation

44
Q

The endometrial cycle

MENSTRUAL PHASE

A

• MENSTRUAL PHASE: if the oocyte was not Fertilized & Pregnancy did NOT occur in the previous cycle, a sudden diminution in Estrogen & Progesterone secretion will signal the DEMISE of the Corpus Luteum
– As hormonal support of the endometrium is withdrawn, the endometrium degenerates, the tissue breaks down, & Menstrual BLEEDING ensues; this moment is defined as day 1 of the menstrual cycle

45
Q

The endometrial cycle

PROLIFERATIVE PHASE

A

• PROLIFERATIVE PHASE: after menstruation, the Endometrium is restored by about the fifth day of the cycle
– Proliferation of the BASAL STROMAL cells in the ZONA BASALIS

– Proliferation of Epithelial Cells from other parts of the Uterus

– The Stroma gives rise to the connective tissue components of the Endometrium

– The Thickness of the endometrium INCREASES from ∼0.5 to ~ 5 mm during the Proliferative Phase

– Proliferation & differentiation of the endometrium are stimulated by Estrogen, which is Secreted by the developing follicles

– Levels of Estrogen RISE early in the Follicular phase & PEAK just before Ovulation
• Estrogen causes the Stromal components of the Endometrium to become HIGHLY developed
• Estrogen also induces the synthesis of Progestin receptors in Endometrial tissue

– Progesterone OPPOSES the action of Estrogen on the epithelial cells of the endometrium & functions as an ANTIESTROGEN
• INHIBITS epithelial cell proliferation but Promotes proliferatoon of the Endometrial STROMA
• Stimulates 17β-HSD & Sulfotransferase, enzymes that convert Estradiol to WEAKER compounds

46
Q

The endometrial cycle

SECRETORY PHASE

A

• SECRETORY PHASE: final phase of the Uterine cycle; corresponds to the LUTEAL PHASE of the Ovarian cycle
– Early Secretory phase of the menstrual cycle: Characterized by the development of a network of interdigitating tubes within the Nucleolus of the Endometrial Epithelial Cells (nucleolar channel system); stimulated by Progesterone

– Middle to Late Secretory Phase:
a) Vascularization of the Endometrium INCREASES, the Glycogen content Increases, & the thickness of the endometrium INCREASES to 5 to 6 mm

b) Endometrial glands become engorged with secretions
c) Progesterone promotes the differentiation of the STROMAL cells into PREDECIDUAL CELLS, which must be prepared to form the DECIDUA of Pregnancy, or to orchestrate menstruation in the absence of pregnancy

47
Q

Contraception: The oral contraceptive pill (OCP)

A
  • Hormonal contraception is the most commonly used method of contraception in the US
  • Numerous COMBINATION (i.e. Estrogen & Progestin) oral contraceptives & progestin-only pills are available
  • The woman takes the OCP daily for 21 days out of the 28-day cycle; she takes no pill, a placebo, or an iron pill during days 22 – 28
48
Q

Contraception: The oral contraceptive pill (OCP)

A

CONTRACEPTIVE EFECTIVENESS OF OCPs IS DUE TO:
1) Contraceptive Steroids feed back both DIRECTLY at the level of the Hypothalamus (Decreasing secretion of GnRH) & at the level of the Gonadotrophs in the Anterior Pituitary
• Net effect is SUPPRESSED SECRETION of FSH & LH
a) Low FSH levels are INSUFFICIENT to Stimulate Normal FOLLICULOGENESIS; the low LH levels obviate the LH Surge & therefore INHIBIT Ovulation

• In the commonly used doses, contraceptive steroids do NOT completely abolish either Gonadotropin Secretion or Ovarian function

2) The Progestin effect of the OCP causes the Cervical Mucus to THICKEN & become STICKY & insufficient
• These actions INHIBIT sperm Penetration into the Uterus

• Progestins also IMPAIR the MOTILITY of the Uterus & Oviducts & therefore DECREASE Transport of both ova & sperm to the normal site of fertilization in the DISTAL Fallopian tube

• Progestins also produce changes in the Endometrium that are not conducive for implantation of the embryo
a) Decreased Glandular production of Glycogen & thus diminished energy for the Blastocyst to survive in the uterus

• Progestin-only OCPs DO NOT effectively INHIBIT Ovulation, as do the combination pills; HIGHER Failure Rate than does the combined type of OCP

49
Q

Disorders of menstruation

A

• RelaNvely common

• Include:
– MENORRHAGIA: loss of > 80 mL of blood

– DYSMENORRHEA: Painful periods

– OOLIGOMENORRHEA: existence of Few, Irregular periods

– AMENORRHEA: absence of periods

– OLIGOMENORRHEA & AMENORRHEA often are due to dysfunction or cessation of the hypothalamus-pituitary- ovarian axis, as Opposed to local pelvic pathophysiology

50
Q

Pathophysiology of the uterus: ENDOMETRIOSIS

A
  • Most commonly affects women of Reproductive Age
  • Common Cause of female STERILITY

• Painful disorder in which tissue that normally grows INSIDE the Uterus Grows OUTSIDE it
– Presence of Endometrial Glands & Stroma OUTSIDE the uterus

• The areas of ENDOMETRIOSIS Bleed each month which results in Inflammation & Scarring
– Endometriosis most commonly involves the Ovaries, Bowel or the tissue Lining the Pelvis
– Rarely, Endometrial tissue may spread beyond the pelvic region

• Clinical presentation: Chronic pelvic Pain linked to Menses; Dysmenorrhea (painful, sometimes disabling cramps during the menstrual period) & Dyspareunia (painful sex); Rectal pain & constipation; INFERTILITY

51
Q

Ovarian pathophysiology: Polycystic ovarian syndrome (PCOS)

A
  • MOST COMMON CAUSE OF INFERTILITY IN WOMEN
  • Frequently becomes manifest during Adolescence
  • The essential components of the syndrome are the various combinations of otherwise unexplained Hyperandrogenism, Anovulation, & a Polycystic ovary
  • Ovarian dysfunction is characterized by Abnormal Ovarian Steroidogenesis & Folliculogenesis that are manifested clinically by Androgen Excess & Anovulation
  • Enlarged polycistic ovaries are known to be associated with INCREASED Androgen levels (DHEA)
  • High Androgens promotes ATRESIA in developing Follicules & DISRUPT Feedback relationships
  • PRESENTATION: young, Obese, Hirsute females of reproductive age; Oligomenorrhea or Secondary Amenorrhea; infertility
  • ELEVATED LH, LOW FSH, Elevated testosterone
52
Q

Other pathophysiologies: Turner syndrome

A

• Most common cause of Congenital hypogonadism

• In about 50% of cases, it results from the COMPLETE
ABSENCE of the Cecond X Chromosome
– Internal & External Genitalia typically are Female

  • Germ cells DO NOT develop, & each Gonad consists of a connective tissue-filled streak
  • CLINICAL PRESENTATION: Short stature, a characteristic WEBBED NECK, low-set ears, a shield-shaped chest, SHORT FOURTH Metacarpals, & Sexual Infantilism
53
Q

Menopause

A
  • Defined as occurring 12 months after the last menstrual period; marks the end of menstrual cycles
  • Occurs at 51.4 yrs of age (average)
  • Due to REDUCTION in Estrogen, LOW levels of Inhibin, there is NO NEGATIVE Feedback of LH & FSH; therefore, HIGH levels LH & FSH
  • Can occur naturally, Prematurely (premature ovarian failure), due to Surgery, or as a result of Chemotherapy
54
Q

Menopause Cont

A 
•  In the months or years leading up to menopause (Perimenopause), SIGNS & SYMPTOMS can include:
–  Irregular periods 
–  Vaginal dryness 
–  Hot flashes
–  Night sweats
–  Sleep problems
–  Mood changes
–  Weight gain and slowed metabolism 
–  Thinning hair & dry skin
–  Loss of breast fullness

• TREATMENTS focus on Relieving the signs & symptoms & preventing or managing Chronic conditions that may occur with aging: Estrogen Therapy, Vaginal Estrogen, low-dose antidepressants, Gabapentin (for treatment of hot flashes), etc.

Reproductive System I (18 decks)

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