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SEM3: PATH30210 Endocrine Health/Disease > L8 Endocrine Physiology of the Ovary > Flashcards

L8 Endocrine Physiology of the Ovary Flashcards

1
Q

Granulosa Cell (Ovary) Hormone Production?

A

FSH Responsive => Increased Estradiol

Granulosa Cells are Analogous to Sertoli cells in Males

Estrogen

  • Essential for normal reproductive function: Follicular Growth, Endometrial growth
  • Development of Reproductive Tissue
  • Secondary Sexual Characteristics
  • Mammary Gland Development

Inhibin: Negative feedback regulation of FSH

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2
Q

Luteal Cells (Ovary) Hormone Production?

A

Progesterone

  • Essential for normal reproductive function: Endometrial Development
  • Maintains pregnancy (till placental competency)
  • Mammary Gland Development
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3
Q

Ovarian Follicles Stages?

A

Primordial Follicles

  • Have entered first stage of meiosis , further progress arrested
  • Hormones cause meiosis I to resume in several follicles =>Meiosis II by ovulation
  • Penetration by sperm causes the final stage of meiosis to occur

Growing Follicles

Early Primary Follicle

  • Primary oocyte surrounded by unilinear granulosa
  • Follicle separated by basal lamina

Late Primary Follicle

  • Granulosa cells separated by distinct basement membrane
  • Surrounding stroma cells differentiate into Theca Interna and Theca Externa

Secondary (Antral) Follicle

  • Fluid-filled Antrum develops (DEFINING FEATURE OF SECONDARY FOLLICLES)

Mature (Graafian/Tertiary) Follicles

  • Influenced by FSH and LH some secondary follicles develop into Graafian Follicles
  • Completes First phase of Meiosis (previously arrested)
  • Oocytes is now secondary oocyte => secondary meiotic division begins
  • Oocyte, Zona Pellucida and Attached granulosa cells are expelled at ovulation
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4
Q

Importance of Theca Interna?

A

Theca Externa: Darker Staining- Fibrous

Theca Interna: Larger and paler staining - Endocrine

Theca Interna is an important endocrine cell secreting androgens that are converted to estrogen by granulosa cells (requires BOTH pituitary gonadotropins FSH and LH)

  • LH => Androgen synthesis in Thecal Cells
  • FSH => Conversion of Androgens to estrogen in Granulosa Cells
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5
Q

Thecal Cells (Ovary) Hormone Production?

A

LH responsive=> Increased Androgens

Analogous to Leydig Cells

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6
Q

Female Endocrine Cell analogous to the Leydig Cell?

A

Thecal Cells (responsive to LH) => Androgen Production

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7
Q

Female Endocrine Cell analogous to the Sertoli Cell?

A

Granulosa Cells (Responsive to FSH) => Estradiol/Inhibin Production

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8
Q

KEY ENZYMES of Ovarian Steroid Hormone Synthesis

A

Estradiol: produced in the Ovarian Follicle (by Granulosa Cells)

  • 17b hydroxysteroid dehydrogenase required to convert Estrone => Estradiol

Progesterone: produced in the Corpus Leuteum

  • 3b hydroxysteroid dehydrogenase required

Aromatase (Granulosa Cells) converts androgens to Estradiol

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9
Q

Endocrine Cells of the Ovary?

Hormones they Respond to?

Hormones they synthesize?

A

Thecal cells:

  • Respond to LH (Anterior Pituitary)
  • Synthesizes Androgens => output to granulosa cells for conversion to estrogen
  • DO NOT produce aromatase: cannot convert androgens to estrogen

Granulosa cells:

  • Respond to FSH (Anterior Pituitary)
  • Limited capacity to synthesize Estrogen from cholesterol
  • HIGH levels of aromatase: able to convert androgens (thecal cells) to Estrogen
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10
Q

Endocrine Cells of The Corpus Luteum (Luteal Cells)?

A

Corpus Luteum: Transient endocrine gland of the postovulatory ovary

Cell types:

Thecal Lutein Cells: Cholesterol => Androstenedione (converted to estradiol in Granulosa)

Granulosa Lutein Cells: Produces mainly PROGESTERONE, also ESTRADIOL

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11
Q

Life Cycle of Corpus Luteum (Fertilization vs. No Fertilization)

A

Under influence of pituitary gonadotrophins (FSH, LH) => Corpus Luteum begins to secrete progesterone (lesser amounts of estrogen)

NO Fertilization

Sufficient levels of Estrogen and Progesterone reached => LH secretion inhibited by negative feedback regulation
=>Lack of LH triggers demise of CL=> degenerates into non-functional Corpus Albicans

Fertilization/Implantation of Ovum rescues Corpus Luteum

After implantation embryo secretes LH like hormone (Chorionic gonadotropin hCG) => acts upon CL => continued progesterone production

CL remains a significant source of progesterone till the developing placenta takes over in the late 1st semester

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12
Q

_________ is major ovarian steroid before menopause

Effects?

A

Estradiol is major ovarian steroid before menopause

  • decelerates linear growth
  • closes epiphyseal growth plate
  • increases bone density
  • promotes adipose tissue deposition
  • stimulates growth of reproductive tissues
  • stimulates breast development
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13
Q

Control of Ovarian Endocrine Function?

A

GnRH released by Neuroendocrine cells in arcuate nucleus of hypothalamus => Stimulates LH and FSH Section (Gonadotroph cells of Anterior Pituitary)

  • LH => Thecal Cells
  • FSH => Granulosa Cells
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14
Q

Regulation of the Early Follicular Phase of Ovarian Cycle?

A
  • Feedback inhibition of LH by estrogen is WEAK => stimulation remains constant/increases during follicular phase despite rising estrogen levels
  • Feedback inhibition of GnRH secretion from hypothalamus by estrogen => SMALL effect on LH secretion from the pituitary
  • Feedback Inhibition of FSH secretion by estrogen is STRONG

Negative Feedback Requires both Estrogen AND Progesterone

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15
Q

Regulation of the Late Follicular Phase/Ovulation of Ovarian Cycle?

A

Presence of Progesterone means Corpus Leuteum or Placenta is secreting it indicating pregnancy (Mechanism of Birth Control )!!

Absence of Progesterone + high levels of estrogen stimulate pituitary LH (not FSH) production in POSITIVE FEEDBACK => LH surge=> OVULATION

Estrogen also acts on the hypothalamus to stimulate GnRH secretion => accentuates pituitary LH secretion and causes a modest rise in FSH

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16
Q

Regulation of Luteal Phase of Ovarian Cycle?

A

Only when both estrogen and progesterone levels are high (during luteal phase of cycle) is feedback inhibition of LH effective

Corpus luteum absolutely dependent on LH for continued survival

  • Falling LH => demise of Corpus Luteum
  • Implantation=> actions of hCG (Chorionic gonadotropin) from fetus after implantation can sustain Corpus Luteum
17
Q

Oral Contraception Options?

A

Progesterone only pill

  • low dose/short acting
  • long acting/slow release
  • main effects on cervix and gonadotrophin production

Combined OCP

  • synthetic estrogen and progesterone (both required for maximum efficacy)
  • primary action is to inhibit LH and FSH (no ovulation)
  • secondary action on endometrium and cervix

Emergency Contraception (morning after pill)

  • high dose Progesterone and/or Estrogen

mechanisms of action:

  • delay/prevent ovulation
  • alter endometrium to impair implantation
  • RU486 (Mifepristone)
  • Progesterone agonist that blocks action of Progesterone only pill
18
Q

GnRH Deficiency (aka._______________) Pathogenesis/Symptoms

A

GnRH Deficiency: Kallman Syndrome

Inherited disorder of deficient GnRH production (GnRH triggers FHS/LH release from anterior pituitary gland)

Mutations in KAL1 gene interpheres with migration of GnRH secreting neurons to hypothalamus in development

Deficient GnRH production=> Lack of FSH/LH Production

Symptoms:

  • Hypogonadotropic Hypogonadism (HH)
  • Infertility
  • Absent/Incomplete Pubertal Maturation
  • 50% cases have Anosmia (Lack of Smell) - distinguishes from other HH
19
Q

Hypopituitarism (aka. ______________) Pathogenesis/Symptoms/Treatment

A

Hypopituitarism: Sheehan’s Syndrome

Pathogenesis:

Postpartum hemorrhage => infarction and necrosis of pituitary gland => Less FSH and LH

Symptoms:

Present immediately or asymptomatic until additional insult/trauma:

  • cessation of lactation
  • amenorrhea/oligomenorrhea
  • fatigue
  • adrenal insufficiency

Treatment: Hormone replacement therapy

  • T4
  • cortisone
  • gonadotrophins or estrogen + progesterone if resumption of normal ovarian cycling desired
20
Q

Secondary Hypercortisolism (aka. ________________) Pathogenesis/Symptoms?

A

Secondary Hypercortisolism: Cushing’s Disease

Pathogenesis:

Secondary hypercortisolism due to ACTH excess=> ACTH stimulates cortisol AND androgen production=> increased negative feedback regulation by adrenal androgens in hypothalamus and pituitary => reduces LH and FSH production

Symptoms:

  • Fertility Impaired: Amenorrhea
  • Hirsutism (Facial Hair Growth)
21
Q

Hyperprolactinemia Pathogenesis/Symptoms?

A

Pathogenesis

  • 40% due to benign pituitary adenomas
  • Other due to tumor/pathologies that lower dopamine levels

More stimulation of luteal cells than granulosa:

  • Stimulates lactation
  • Interferes w/ gonadal function (hypogonadism) by suppressing LH and FSH

Symptoms:

Females: Galactorrhea, Amenorrhea

Males: Decreased libido, Infertility

22
Q

Congenital Adrenal Hyperplasia (CAH) Pathogenesis/Symptoms?

A

21a hydroxylase deficiency=> Excessive buildup of Androgens =>

  • sexual ambiguity in females
  • adrenal androgens limit FSH and LH=> prevents/delays puberty and ovulation

Sexual Development and Fertility in CAH: due to increased adrenal androgens

Males

  • precocious puberty in men (accelerated sexual development)
  • high incidence of infertility

Women - Masculinization (virilization)

  • ambiguous genitalia
  • excessive facial hair, virilization
  • menstrual irregularity in adolescence
  • anovulation in adulthood
23
Q

Most common form of chronic anovulation (ovaries don’t release oocyte) in women of reproductive age?

A

Polycystic Ovary Syndrome (PCOS)

24
Q

Polycystic Ovary Syndrome (PCOS) Associations and Hormonal Implications?

A

Most common form of chronic anovulation in women of reproductive age

Associated with Obesity and Type II diabtes

Hyperandrogenism => Insulin resistance (COMMON)

Altered GnRH Pulse Rate

  • LH INCREASED
  • FSH - DECREASED (More stimulation of luteal than granulosa)
  • Estrogen INCREASED
  • Androgens INCREASED
  • Insulin INCREASED
25
Q

Pathogenesis of Menopause?

A

Natural process caused by aging and depletion of finite amount of oocytes

Ovarian follicles become unresponsive to pituitary gonadotrophins

  • Lack of negative feedback by estrogen and inhibin leads to increased FSH and LH
  • Aromatase (in adipose tissues) continues to convert androgens to estradiol, still a big drop off from prior levels

SEM3: PATH30210 Endocrine Health/Disease (25 decks)

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