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Physiology > Physiology Block 3 Week 13 Female Reproductive Endocrine > Flashcards

Physiology Block 3 Week 13 Female Reproductive Endocrine Flashcards

1
Q

How is genetic sex determined?

A

Genetic sex is determined at conception

The lack of hormonal signals lead to female phenotype–required to develop male phenotype

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2
Q

What gene is leads to development of male phenotype?

A

H-Y antigen–encoded by SRY (sex-determining region of Y-chromosome)

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3
Q

In absence of testis, what is not developed?

A

In absence of testis, ovaries form

There is a lack of androgen production

  • no testosterone or its conversion to DHT in target tissues
  • no Mullerian inhibiting factor (induces regression of mullerian ducts)

Without these 2 hormones:
Wollfian ducts regress and Mullerian ducts develop into female reproductive tract

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4
Q

Follicle Growth in the ovary

A

Pre-antral follicle has ovum

Follicle developed inside Granulosa and Theca cells

Once developed ovulates egg and can be fertilized

What’s left after ovulation is the corupus luteum

  • -produces primarily progesterone
  • -if egg not fertilized and does not implant, corpus luteum dies
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5
Q

Atresia

A

At 6 months gestation, will have 7 million oognoia (potential ova)

Oogonia start to degenerate which continues until menopause

At birth, about 600,000 oogonia remaining

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6
Q

Pattern of hormones and oogonia from:

  • Gestation
  • Birth
  • Puberty
A

Middle of gestation (fetus):
A burst of FSH and LH
Human chorionic gonadotropin (hCG) wanes
–important for stimulating oogonia

Birth (2-6 months):
Lose hCG
Another burst of FSH and LH
-Males: stimulates testes to produce androgen
-Females: unknown

Before Menarche (puberty):
Pituitary secretion of FSH and LH
–induces ovarian function to produce estrogen
–stimulates growth spurt (Growth Hormone)

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7
Q

Female Steroidogenesis

A

3 Estrogens:

  • Estrone (E1)
  • Estradiol (E2): estrogen of non-pregnant women
  • Estriol (E3): estrogen of pregnant women

AROMATASE (A) necessary to convert androgen to estrogen

Androstenedione (A)–> E1

  • -> E2
  • -> E3 (liver)

Androstenedione–>Testosterone (A)–> E2

  • -> E1
  • -> E3 (liver)
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8
Q

Steroid Distribution in Plasma and Binding Proteins

A

Most steroids bound to a carrying protein–very little is free

Cortisol Binding Globulin (CBG)–cortisol only, no estrogen, some progesterone (cortisol precursor)

Sex-Hormone Binding Globulin (SHBG)–binds sex hormones (mainly androgens) testosterone and estrogen

Albumin–estrogen will bind albumin more than SHBG

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9
Q

What initiates puberty in females?

A

Hypothalamic GnRH and Pituitary gonadotropins (FSH and LH) are released in pulsatile manner

Body fat and intake of calories may stimulate puberty in girls
–Gymnasts, anorexic (refusal to eat), and bulemic girls fail to have menstrual cycle (amenorrhea)

Leptin (from adipose tissue) signals hypothalamus to increase GnRH pulses

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10
Q

Kisspeptin

A

Estrogen has negative feedback on hypothalamus and pituitary
–when high, prevents release of GnRH

Leptin (from adipose tissue) activates neurons that activate kisspeptin, which actives GnRH neurons to pulse

  • -leads to increased FSH and LH release
  • -leads to ovaries producing more estrogen
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11
Q

Female Puberty

A

Leptin activates kisspeptin, which activates pulsatile release of GnRH, which activates pituitary to make FSH (and a little later LH)

  • FSH wakes up ovary follicles
  • follicles increase estrogen production

Simultaneous development of breast/pubic hair and growth spurt

  • -peak growth velocity is earlier in girls than boys
  • -estrogen induces closure of growth plates in long bones

Last thing to develop is 28 day menstrual cycle
–If not having regular menstrual cycles by 16, need to be checked

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12
Q

Menstrual Cycle: Follicular Phase

A
  1. Death of corpus luteum due to:
    - -no pregnancy
    - -hCG not released by the trophoblast into maternal blood

Results in:

  • -decreased progesterone (necessary for secretory phase of uterine cycle)
  • -decreased estrogen
  1. Loss of progesterone and estrogen negative feedback

Results in:
–FSH (primarily) and LH

  1. FSH induces maturation of next group of follicles
    - -a dominant follicle develops (from 6-12) and autonomously releases estrogen

Results in:

  • -estrogen increase decreases FSH and LH via negative feedback
  • -dominant follicle can survive loss of FSH and LH –atresia of non-dominant follicles
  1. When estrogen peaks induces hypothalamic-pituitary switch to positive feedback
    - -estrogen stimulates a SURGE in LH (and to a lesser degree FSH)
    - -LH surge required for ovulation induction
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13
Q

Menstrual Cycle: Luteal Phase

A
  1. LH surge stimulates ovulation
    - -formation of corpus luteum (what’s left)
    - -dominant follicle stops making estrogen, terminating LH surge
  2. Corpus luteum produces progesterone
    - -inhibits FSH and LH secretion
  3. Corpus luteum dies if:
    - -no pregnancy
    - -no release of hCG from trophoblast into maternal blood
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14
Q

Generation of Positive Feedback-Induced LH surge

A

Early Follicular Phase:

  • dominant follicle produces estrogen that acts LOCALLY to stimulate induction of FSH receptors on granulosa cells
  • allows survival of FSH decrease

Mid-Follicular Phase:
Non-dominant follices have died due to FSH decrease
Local estrogen positive feedback induces:
-more FSH receptors
-LH receptors
-proliferation (division) of granulosa cells

Late Follicular Phase:

  • follicle loaded with granulosa cells (proliferation)
  • estrogen peaks in blood (due to increased granulosa cells), inducing positive feedback stimulation of LH and FSH leading to LH surge
  • LH surge stimulates follicle to expel egg

All the cells left behind form corpus luteum, which produces progesterone

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15
Q

Interaction of Follicular Theca and Granulosa Cells

A

Production of estrogens

Theca cell:

  • makes LH receptors
  • no aromatase

Granulosa Cell:

  • makes FSH receptors
  • expresses LH receptors mid-cycle
  • aromatase present
  1. LH binds receptor on theca cell
  2. Androgens produced
  3. Androgens diffuse into granulosa cell
  4. FSH acts on granulosa cell and stimulates aromatase activity
  5. Conversion of androgen to estrogen

When follicle becomes more dominant, granulosa cell expresses LH receptor

  1. LH binds receptor on granulosa cell
  2. Production of progesterone (from cholesterol)
  3. Progesterone shuttled into Theca cells
  4. In Theca cells, progesterone converted to androgen
  5. Androgen diffuses into granulosa cell for conversion into estrogen under FSH stimulation

Need both Theca and Granulosa Cells to produce estrogen

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16
Q

Effect of Estrogen on Reproductive Tract

A

Estrogen predominates during follicular (proliferative growth) phase

Oviduct

  • Lining: increased cilia formation and activity (want to be ready to transport egg if fertilized)
  • Muscular Wall: increased contractility

Uterus

  • Endometrium: increased proliferation (growth)
  • Myometrium: increased growth and contractility
  • Cervical Glands: watery secretion (allows sperm to get in)

Vagina:

  • increased epithelial proliferation
  • increased glycogen deposition
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17
Q

Effect of Progesterone on Reproductive Tract

A

Progesterone predominates during luteal (secretory–slow things down) phase

Oviduct

  • Lining: increased secretion (help get to uterus)
  • Muscular wall: decreased contractility

Uterus

  • Endometrium: increased differentiation and secretion (ready for implantation)
  • Myometrium: decreased contractility (want uterus quiet rather than pushed out)
  • Cervical Glands: Dense/viscous secretion (to prevent germs getting in or egg leaving)

Vagina

  • increased epithelia differentiation
  • decreased epithelial proliferation
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18
Q

Myometrial (Uterine) Cycle

A

Estrogen dominates proliferative (follicular) phase (11 days), so thickness of endometrium grows dramatically

Progesterone from corpus luteum (12 days) dominates secretory (luteal) phase and stimulates secretions so if fertilized egg comes along, endometrium is ready for implantation

If no implantation occurs or hCG present to rescue corpus luteum, it dies (end of luteal phase)
–progesterone and estrogen plummet

Menstrual phase (5 days)

  • -uterine spiral artery supplying blood to endometrium vasoconstricts
  • -endometrium dies and sloughed into menstrual bleed
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19
Q

Which of the following is an example of positive feedback?

A. Effect of progesterone on LH and FSH in luteal phase
B. Effect of estrogen on LH and FSH in the late follicular phase
C. Effect of estrogen on LH and FSH in early follicular phase
D. Effect of decreasing progesterone in the late luteal phase

A

B. Effect of estrogen on LH and FSH in the late follicular phase

20
Q

How is corpus luteum rescued by hCG?

A

Follicular phase, estrogen predominates
Positive feedback of estrogen results in LH surge
–ovulation in 24 hours
–fertilization in 24 hours

Fertilization usually in oviduct (fallopian tube)
–begins development as works way to uterus

At uterus, now a blastocyts (Day 5)

  • -implanted into myometrium (Day 7)
  • -makes blood connection to maternal circulation

Placenta/trophoblast begins making hCG

  • -looks like LH, FSH, TH due to alpha subunit (beta unit = activity)
  • -goes into maternal circulation and rescues corpus luteum

Corpus luteum continues making estrogen and progesterone
–keeping FSH and LH low inhibits next menstrual cycle

21
Q

hCG

A

Stimulates estrogen and progesterone release from corpus luteum
–inhibits GnRH (hypothalamus) and Anterior pituitary gonadotropin secretion (FSH and LH), which prevents next menstrual cycle during pregnancy

Stimulates continued growth of endometrium to nurture growing implanted embryo and fetus

22
Q

Steroidogenesis in Trophoblast

A

Trophoblast implants into endometrium

  • -takes up LDL (for cholesterol)
  • -cholesterol converted to pregnenolone (mitochondria)

Pregnenolone converted to progesterone (SER) and secreted into maternal circulation

Also, pregnenolone passed to fetus
–taken up by fetal adrenal to make adrenal steroid end-products

23
Q

Steroidogenesis in Plancenta

A

Placenta has lots of aromatase

Maternal adrenal testosterone converted to estradiol (E2) in trophoblast

Maternal adrenal DHEA converted to estrone (E1) in trophoblast

Fetal adrenal synthesizes DHEA (from trophoblastic prognenolone) and sulfates it in fetal zone

  • -in fetal liver, DHEAS converted to 16-OH-DHEAS
  • -converted to Estriol (E3)

Estriol used as a marker of fetal distress

  • Fetal Adrenal function
  • Fetal Livers function
24
Q

Why is estriol used as a marker for fetal distress?

A

Assesses:

  • Fetal Adrenal function
  • Fetal Livers function
25
Q

How do the concentrations change in pregnancy?

  • Estrogen
  • Progesterone
  • hCG
A

hCG peaks in the first trimester

Placenta makes most of the estrogen and progesterone during 2nd and 3rd trimester (unregulated production)
–hCG wanes because corpus luteum no longer necessary

Estrogen and Progesterone increase as placenta gets bigger

26
Q

Changes of Anterior Pituitary hormones during pregnancy:

  • GH
  • LH, FSH
  • ACTH
  • TSH
  • PRL
A

GH–no change

LH and FSH–low during pregnancy bc estrogen and progesterone inhibit menstrural cycle

ACTH–no change

TSH–wobbles because maternal TH important in developing fetus (1st trimester):

  • TBG increases
  • reaches nadir (1st trimester) then plateaus

Prolactin–increases steadily during pregnancy bc mammary glands stimulated so tissue is there to produce milk after parturition

27
Q

Changes of placental proteins during pregnancy:

  • hCG
  • hPL
  • CRH
A

hCG–(homology with FSH and LH) increases, then declines

hPL–(homology with GH) increases steadily.
-thought to contribute to insulin-resistant state bc want maternal blood glucose to go up a little to feed baby

CRH–burst at end may contribute to onset of parturition
–stimulates ACTH

28
Q

Changes of fetoplacental estrogen during pregnancy

A

All increase!

Estriol (E3) increases most
Estradiol (E2)
Estrone (E1)

29
Q

Changes of fetoplacental androgens during pregnancy:

  • Testosterone
  • DHEA
  • Androstenedione
A

Fetus and placenta can make androgens

Testosterone–increases
–most from maternal adrenal glands

DHEA–decreases

Androstenedione–small increase

30
Q

Changes in thyroid hormones during pregnancy:

  • Total T4
  • fT4
  • Total T3
  • fT3
A

Estrogen stimulates production of thyroid binding globulin (TBG)
As estrogen increases, amount of TBG increases

Total T4 and T3 increase because there are more binding sites
–happens SLOWLY
–reaches a new baseline/steady state
Ex. Person who gets packed RBC has same PO2. RBC suck up O2, BUT lungs suck in a little more O2. The moles O2 taken in is small compared to O2 bound to Hb

Free TH never really changes
–conceptually TH goes down, but happens so slowly over months that will never be able to detect it

31
Q

Changes in cardiovascular system during pregnancy:

  • HR
  • BP
  • SV
  • CO
  • Peripheral venous distention
  • TPR
A 
BP = CO x TPR
CO = HR x SV

Placenta needs more blood
–parallel resistance circulation lowers TPR
Ex. Less resistance if more doors open to escape room.

HR--inc
CO--inc dramatically
BP--dec (despite CO inc)
TPR--dec
SV--inc
32
Q

Changes in pulmonary system during pregnancy:

  • RR
  • Tidal Vol
  • Expiratory Reserve
  • Vital capacity
  • Respiratory minute vol
A

Placenta needs O2, so alveolar ventilation goes up–hypernea (inc in breath irrespective of metabolism)

RR--no change
Tidal Vol--inc
Expiratory Reserve--dec to increase lung efficiency--get more O2 exchange for same TV
Vital capacity--no change
Respiratory minute vol--inc
33
Q

Changes in blood during pregnancy:

  • Volume
  • Hematocrit
  • Fibrinogen
  • Electrolytes
A

If going to pump more blood (CO), need to make more blood

Volume–inc
Hematocrit–dec (Red cell mass/ Plasma volume)–plasma volume change is greater than red cell mass
Fibrinogen–inc
Electrolytes–no change

34
Q

Changes in gastrointestinal system during pregnancy:

  • Sphincter tone
  • Gastric emptying time
A

Sphincter tone–dec

Gastric emptying time–inc

35
Q

Changes in renal system during pregnancy:

  • Renal flow
  • GFR
A

Lots of metabolic waste being produced by fetus–need to get rid of this

Renal flow–inc
GFR–inc

36
Q

Changes in weight during pregnancy:

  • uterine weight
  • body weight
A

Uterus gets bigger to accommodate growing fetus

37
Q

Parturition

A

Fetus gets so big that it out lives its space

Something happens in the fetus that turns on fetal adrenal gland

Aromatize androgens to estradiol

Stimulates uterus contractility and sensitivity to oxytocin leading to parturition

38
Q

Theory for onset of strong labor contractions

A
  1. Baby’s head stretches cervix
  2. Cervical stretch excites fundic contraction
  3. Fundic contraction pushes baby down and stretch cervix some more
  4. Repeat
39
Q

Oxytocin

A

As fetus head presses on cervix, afferent nerves carry impulses to hypothalamus such that oxytocin released from posterior pituitary
–oxytocin stimulates uterine contractions that inc cervical stretch (positive feedback)

After placenta delivery, estrogen and progesterone decrease

  • -lots of milk produced, but not released due to progesterone
  • -suckling stimulates oxytocin release and stimulating milk let down
40
Q

Breast and Mammary Gland

A

Mammary gland:

  • secretory lobules
  • alveoli
  • lactiferous duct

Myoepithelial cells synthesize milk
–oxytocin forces contraction and pushes milk into ductules

41
Q

Rates of secretion after parturition:

  • estrogens
  • progesterone
  • prolactin
A

At parturition, no longer have placenta hooked to maternal circulation

Estrogen and progesterone plummet

  • -releases mammary glands from inhibition
  • -when baby suckles, stimulates oxytocin AND prolactin to maintain milk synthesis

2 months post-partum, prolactin levels are not high, but are stimulated every time baby suckles

Prolactin inhibits FSH and LH release
–burst of prolactin prevents onset of new menstrual cycle for a period of time

Even though suckling, normal menstrual cycles can resume

42
Q

Control of Prolactin release

A

Pregnancy or suckling reduces activity of dopoadrenergic nerves in hypothalamus

  • -releases lactotroph from dopamine inhibition
  • -lactotroph produces prolactin
43
Q

Estrogen secretion throughout the sexual life of female human being

A

Estrogen low in first 10 years of life because GnRH pulses are not there
–FSH and LH are low

Calories, leptin, etc. stimulates GnRH pulses in hypothalamus (kisspeptin)
–FSH and LH pulses increase

Ovaries stimulated (FSH), which start making follicles and begin menstrual cycle

45-50–menopause due to ovarian failure

  • -No more follicles left, can’t have a dominant follicle making estrogen
  • -Pituitary is normal, and no longer receives negative feedback from estrogen
  • –will have abrupt increase in gonadotropins from GnRH pulses

In men, gonadotropins increase a little

44
Q

Mechanisms of Osteoporosis Due to Reproductive Events/Disorders

A

Osteoporosis–loss of bone mass

Loss of gonadal steroids removes the anti-resorptive (bone break down) effect, allowing loss of bone mineral

Females:

  • oophrorectomy
  • Turner’s syndrome
  • ovarian failure
  • hyperprolactinemia (prolactin secreting tumor)–inhibits pituitary gonadotropin secretion leading to hypogonadism
  • Exercise associated amenorrhea
  • menopause

Males:

  • hypogonadism
  • advanced age
45
Q

Which of the following is usually decreased at the end of the 3rd trimester of pregnancy?

Maternal prolactin
Maternal hematocrit
Maternal TSH
Maternal respiratory minute volume
Maternal total T4
A

Maternal prolactin–inc

Maternal hematocrit–DEC–(Red cell mass /
Plasma volume)–more plasma volume than red cell mass

Maternal TSH–wobbles, nadir, then plateau

Maternal respiratory minute volume–inc

Maternal total T4–inc due to more TBG

Physiology (20 decks)

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