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FHB Hormone/Repro > 85 - Female Reproduction (cont'd) > Flashcards

85 - Female Reproduction (cont'd) Flashcards

1
Q

Define primary amenorrhea.

A

Absence of menses in a phenotypic female by age 17

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2
Q

Define secondary amenorrhea.

A

Cessation of menstruation for longer than 6 months

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3
Q

Define oligomenorrhea.

A

Infrequent periods (cycle length >35 days)

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4
Q

Define dysmenorrhea.

A

Painful menses (often involves abd cramps) related to uterine contractions

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5
Q

What are some common causes of primary amenorrhea?

A

Disorders of sexual differentiation

  • Turner’s syndrome (XO, no ovary)
  • Complete androgen resistance (XY, no ovary)
  • Hormonal disorders in ovaries, adrenals, thyroid, pituitary/adrenal/hypothalamic axis
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6
Q

What are some common causes of secondary amenorrhea?

A
  • Most common causes: pregnancy, lactation, menopause

- Others: prolactinoma, panhypopituitarism (causes cell death in pit that could affect gonadotrophs)

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7
Q

Why would pregnancy or prolactinoma cause secondary amenorrhea?

A

PRL inhibits GnRH

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8
Q

What are some common causes of oligomenorrhea?

A
  • Most common: changes due to functional abnormalities in CNS mechanisms that regulate GnRH release including stress and illness
  • Changes in body fat composition: very low levels (female athletes)
  • Intense exercise, extreme weight loss, anorexia nervosa – no consistent changes in plasma gonadotropins or ovarian steroids
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9
Q

What are the sx and causes of dysmenorrhea?

A
  • May involve pelvic pain radiating to back and thighs, nausea, vomiting, diarrhea.
  • Prostaglandin synthesis is promoted by E2 followed by progesterone. Prostaglandins released during menses cause uterine contraction, which may be severe enough to cause ischemia and pain.

(- Single most common cause of female work/school absenteeism.)

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10
Q

What are 2 ways to treat dysmenorrhea?

A
  • Prostaglandin synthesis inhibitors (NSAIDs)

- Oral contraceptives

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11
Q

During what phase of the ovarian cycle does pre-menstrual syndrome (PMS) occur?

A

Late luteal phase

  • Both physical and behavioral symptoms that interfere with normal life.
  • Moderate to severe: 30% of females with normal cycles.
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12
Q

What are the sx of PMS?

What is the cause?

A

Abdominal bloating, extreme sense of fatigue,
breast tenderness, labile mood – irritability, tension, depression
- Unclear cause, but clearly related to the cycle

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13
Q

What is considered the 1st line tx for PMS when socioeconomic disfunction is present?

A

SSRIs and oral contraceptives to suppress ovulation

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14
Q

Define hirsutism.
What is the cause?
What are the signs/sx?

A
  • Inappropriately heavy hair growth in androgen sensitive areas.
  • Causes: excessive androgen production
  • Virilization: clitoral hypertrophy, deepening voice, temporal balding, male pattern skeletal muscle development
    (Virilization includes hirsutism and more pronounced evidence of androgen stimulation)
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15
Q

What is a root cause of Polycystic Ovarian Syndrome (PCOS)? (*PCOS causes these as well!)

A

Insulin resistance, obesity

*PCOS is a leading cause of infertility

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16
Q

During Polycystic Ovarian Syndrome (PCOS), high insulin stimulates _____________ production (causing infertility), then abnormal conversion of them to ______________.

A
  • Androgen

- Estrogens (they are high due to the weight gain, although E is anorexogenic)

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17
Q

Because of the increase in androgens and estrogens in PCOS, what occurs that leads to the cyst formation?

A
  • Follicle development impaired, ovulation is not completed, follicles degenerate into cysts.
  • Ovaries can double in size.
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18
Q

Besides the insulin resistance (which can be causes of results of PCOS), what other symptoms do PCOS pts show?

A

Sleep apnea, menstrual irregularity, obesity, acne, decreased HDL and increased triglycerides, hirsutism.

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19
Q

What are some tx’s for PCOS?

2 behavior changes, 2 drugs

A

Weight loss, smoking cessation, metformin (for insulin resistance).

  • Metformin alone is often sufficient to restore fertility.
  • Clomiphene is also effective: 70% ovulation induction in PCOS cases.
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20
Q

What does metformin do that could help w/PCOS?

A

Decreases insulin sensitivity (Main effect is to increase GNG in the liver)

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21
Q

What are the 3 forms of estrogen? (name and abbreviation)

A

E1 – estrone - produced in higher amounts after menopause; lower binding affinity for estrogen receptors

E2 – 17β-estradiol – primary circulating estrogen during reproductive years

E3 – estriol (weak) – produced by the placenta. Also converted from estrone in the liver

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22
Q

Which form of estrogen is produced by the placenta?

A

E3, estriol

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23
Q

Which form of estrogen is the primary circulating estrogen during the reproductive years?

A

E2, 17β-estradiol

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24
Q

Which form of estrogen is produced in higher amounts after menopause?

A

E1, estrone (has a lower binding affinity for E receptors)

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25
Q

How is E transported in the blood?

what is it similar to?

A

Similar to T
38% bound to SHBG
60% bound to albumin
2-3% free

(High conversion in target tissues by aromatase&raquo_space; high local concentrations)

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26
Q

What are some dz’s associated w/estrogen imbalance?

A

Alzheimer’s dz, osteoporosis (review OPG), CV dz, ovarian Ca, Breast Ca, Uterine Ca

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27
Q

What are the names of the 2 receptors that E binds?

Which does it bind w/stronger affinity?

A

ERα, ERβ

- Binds both w/ equal affinity

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28
Q

ERα mediates which effects of E? What about ERβ?

Answer is reproductive or non-reproductive

A
  • ERα: reproductive

- ERβ non-reproductiveeffects (cardioprotection, neuroprotection, mood; but KO mice are sub-fertile…)

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29
Q

What is the purpose of using SERMs (selective estrogen receptor modulators)?

A
  • Synthetic compounds designed to specifically target the estrogen receptor
  • Can target ERα and/or ERβ
  • Can have tissue specific actions, e.g. Tamoxifen is an antagonist in breast and uterus, but an agonist in bone and brain.
30
Q

What is the original purpose of clomiphene, a SERM?
What receptor does it interact w/, and how?
What is it prescribed for, now?

A
  • Originally designed to treat women with oligomenorrhea
  • Selective antagonist for ERα, specific to hypothalamus (blocks negative feedback)
  • *Most highly prescribed drug to induce ovulation
31
Q

What are the names of the receptors for progesterone (P4)?

A

A and B

32
Q

What hormone upregulates the expression of progesterone receptors?

A

E2

33
Q

How is P4 xported in the blood?

A

Bound mostly to albumin; low affinity for SHBG

34
Q

What are the action (4) of P4?

  • Endometrium?
  • Myometrium?
  • Mammy glands?
  • Effect on E2?
A
  • Prepares endometrium for implantation of embryo (proliferation, synthesis of enzymes that lyse zona pellucida)
  • Inhibits myometrial contractions: maintains pregnancy (avoids premature birth)
  • Stimulates mammary gland development: preparation for lactation
  • Antagonizes actions of estrogen: important consideration for hormone replacement therapy
35
Q

What is menopause?

A

Age-related cessation of ovulation (usually starts at age 48-52)

36
Q

Peak fertility spans what ages?

A

18-25

- Female infertility quadruples b/w ages 20 and 40

37
Q

When can fertilization occur?

A

*W/in 24 hrs after ovulation, i.e. 12-16 days after onset of previous menses

38
Q

Fertilization requires rapid transit of germ cells to the ___________.

A

Oviduct

39
Q

How is gestational age calculated?

A

From first day of last menses.

40
Q

When is the best chance of fertilization for the ovum?

For the sperm?

A
  • Ovum: 24 hours post-ovulation
  • Sperm: 48-72 hours post-coitus

(Look at slide 31!!)

41
Q

What are (5) factors that assist sperm xport?

A
  1. Vaginal secretions become more alkaline
  2. Uterine and cervical contractions propel sperm forward
  3. Prostaglandin in seminal plasma induce muscle contractility
  4. Seminal “plug” – semen coagulates upon ejaculation
  5. Vaginal mucus less viscous
42
Q

Just 1 oocyte is released from ovary into peritoneal cavity. ___________ cells help fimbriae “capture” oocyte and direct towards oviduct.

A

Cumulus

43
Q

Where does fertilization usually occur??

A

Ampulla of oviduct

44
Q

Where are the 2 delays that occur once the sperm has reached the egg at the ampulla?
Why do they occur?

A
  1. Ampullary-isthmic junction delay (where fertilization occurs)
  2. Utero-tubal junction delay
    - Delay is to wait for uterine lining to be as receptive as possible
45
Q

How many sperm make it from the vagina, through the cervix, into the uterus, up the fallopian isthmus and into the distal oviduct?

A

Only ~50

46
Q

The former zygote enters the uterine cavity as a _________.

What day is this occuring?

A
  • Morula

- Day 3-4

47
Q

What is the name of the thing that the morula has developed into by the time it implants in the uterus?
What day does this occur?

A
  • Blastocyst

- Day 7

48
Q

What is sperm capacitation?

Where does it occur?

A

Refers to changes in functional properties of sperm acquired in the female tracts that allow for penetration of the zona pellucida of the egg (poorly understood, involves removal of protective protein coat)

49
Q

Capacitation makes the sperm competent to undergo the _________ reaction.

A

acrosomal

50
Q

What is the final step in sperm maturation?

A

Capacitation

51
Q

Explain the 3 steps of the acrosomal rxn, including the receptors involved.

A
  1. Sperm binds to ZP3 receptor (glycoprotein)
  2. Triggers increased calcium in sperm cell – leads to exocytosis of hydrolytic enzymes
  3. Sperm and oocyte membranes fuse – acrosome reacted sperm bind to ZP2 proteins
52
Q

Once the sperm penetrates the oocyte, there is a cortical reaction. The last step involves hardening of the _____________.

A

Zona pellucida

53
Q

During the cortical reaction of the sperm and ooxyte, spermatozoon penetration triggers (^ or v) Ca2+ in the oocyte, which releases chemicals that harden the z. pellucida.

A

Increase Ca2+

54
Q

*What are the 2 exocytosis events during fertilization?

A
  1. Exocytosis of the spermatozoon internal membrane contents

2. Exocytosis of the oocyte’s internal vesicles

55
Q

In terms of meiosis, what happens after sperm finally reaches the medulla of the egg?

A

The same increase in Ca2+ that triggered the cortical rxn also triggers completion of meiotic division! (recall, that oogenesis arrested at metaphase II)

(Second polar body is extruded – oocyte has haploid, unduplicated chromosomes)

56
Q

What combines to form the zygote, specifically?

A

Pronuclei of the egg and sperm

57
Q

“Hatching” of embryo – dissolution of zona pellucida by_____________ cells.

A

Trophoblast

58
Q

Blastocyst at implantation - trophoblast differentiates into _____________ and ______________.

A
  • cytotrophoblast

- syncytiotrophoblast

59
Q

What is the initial function of the cytotrophoblast?

A

Feeder for continually dividing cells (“cyto”)

60
Q

What are the 3 functions of the syncytiotrophoblast?

A

Adhesion, invasion, and endocrine

61
Q

Describe everything going on during embryo adhesion to endometrium. (hard, read at first)

A
  • Syncytiotrophoblasts secrete adhesive surface proteins (cadherins and integrins)
  • E2-dependent secretion of bridging molecules called osteopontin by uterine glands
  • Stromal cells form decidua (thick modified mucus membrane) and secrete nutrients. Later this structure becomes a barrier and endocrine organ.
62
Q

During embryo invasion (completely into the endometrium), there is a war going on b/w what 2 cells? (which is offense and which is defense?)

A

Decidual cells (defense) and trophoblast migration (offense)

63
Q

What are the 2 substances secreted by both the decidual cells (defense) and the trophoblasts (offense) during embryo invasion of the endometrium?

A
  • MMPs from trophoblasts vs. inhibitors of MMP from decidual cells
  • IGF-2 from trophoblasts vs IGF-bp’s from decidua
64
Q

What is the purpose of the battle b/w decidual cells and the trophoblast?

A

Balance prevents invasive trophoblasts from penetrating too deeply.

65
Q

When would you see lacuna?

What are they?

A
  • During placenta formation

- Fluid-filled spaces in the syncytium, make contact w/maternal bv’s

66
Q

During placenta formation, how is the chorionic villi formed?

A

Cytotrophoblasts proliferate and invade the syncytiotrophoblast

67
Q

What constitutes a mature villus?

A

Fetal tissue protruding into maternal blood, “brush border” of syncytiotrophoblast faces maternal blood

68
Q

How does fetal vasculature change during placenta formation?

A

Increase in volume, decrease in resistance

- Spiral aa. increase in diameter

69
Q

Failure to develop vasculature at site of implantation can result in _________________.

A

Placental ischemia

70
Q

What are the hallmark sx (3) of pre-eclampsia/eclampsia?

A
  • HTN
  • Proteinuria
  • Edema
71
Q

Explain the pathophysiology of pre-eclampsia/eclampsia?

A
  1. Relative placental ischemia leads to oxidative stress and endothelial cell damage
  2. Damaged endothelial cells decrease vasodilators and increase vasoconstrictors, results in worsening placental hypoperfusion
  3. Endothelial cell barrier between platelets and BM is breached: thrombosis (blood clot), which causes capillary leak -> edema and proteinuria
72
Q

What’s 1 major risk factor for pre-eclampsia/eclampsia?

A

Previous HTN in pregnancy

FHB Hormone/Repro (16 decks)

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