Reproduction 4- Female Reproduction Continued Flashcards

1
Q

Define primary amenorrhea

A

The absence of menses in a phenotypic female by age 17

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2
Q

List three common causes of primary amenorrhea

A

Turner’s syndrome, Complete androgen resistance, and hormonal disorders of the ovaries, adrenals, thyroid, HPA axis

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3
Q

Define secondary amenorrhea

A

Cessation of menstruation for longer than 6 months

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4
Q

What are the most common causes of secondary amenorrhea?

A

Pregnancy, lactation, and menopause

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5
Q

Why would lactation cause amenorrhea?

A

Prolactin inhibits GnRH

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6
Q

Name two other causes of secondary amenorrhea

A

Prolactinoma, panhypopituitarism

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7
Q

Define oligomenorrhea

A

Infrequent periods (cycle length >35 days)

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8
Q

What are the most common causes of oligomenorrhea?

A

Changes due to functional abnormalities in CNS mechanisms that regulate GnRH release including stress and illness

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9
Q

Name a few other causes of oligomenorrhea

A

Changes in body fat composition (very low levels), Intense exercise, extreme weight loss, anorexia nervosa

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10
Q

What was Clomiphene originally used for? What is it used for now?

A

Clomiphene was first used to treat oligomenorrhea. Clomiphene blocks ER specifically in the brain. This turned out to be a very useful fertility drug due to the increased activation of the HPG axis from lack of negative feedback.

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11
Q

Define dysmenorrhea

A

Painful menses related to uterine contractions- may involved pelvic pain radiating to back and thighs, nausea, vomiting, and diarrhea.

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12
Q

What hormone is responsible for uterine contractions during menses?

A

Prostaglandins.

Prostaglandin synthesis is promoted by E2, followed by progesterone

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13
Q

What percent of women have moderate to severe PMS?

A

30%

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14
Q

What is virilization?

A

the development of male physical characteristics caused by excessive androgen production

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15
Q

What is the root cause of PCOS? Describe this.

A

Insulin resistance.

High insulin stimulates androgen production (causing infertility) and increased conversion to estrogens

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16
Q

Describe the formation of cysts in PCOS

A

Follicle development is impaired, ovulation isn’t completed, and follicles degenerate into cysts.

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17
Q

How does Metformin improve fertility in PCOS patients?

A

Metformin reduces insulin levels, and therefore decreases androgen levels

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18
Q

When is E1 the dominant estrogen?

A

Post-menopausal

19
Q

When is E3 produced?

A

E3 is produced by the placenta

20
Q

Describe how estrogens are transported through the blood

A

38% are bound to SHBG
60% bound to albumin
2-3% are free (similar to testosterone)

21
Q

Differentiate the roles of ER-alpha from ER-beta

A

ERalpha- mediates the reproductive effects of estrogens

ERbeta- mediates non-reproductive effects (cardioprotection, neuroprotection, mood).

22
Q

How does E2 regulate PR levels?

A

PR expression is upregulated by E2

23
Q

How is progesterone transported through the blood?

A

Mostly bound to albumin; low affinity for SHBG

24
Q

What are the actions of progesterone on the uterus?

A

Endometrium: prepares for implantation of embryo
Myometrium: Inhibits contractions (maintains pregnancy)

25
Q

What is the action of progesterone on the mammary gland?

A

Stimulates mammary gland development in preparation for lactation

26
Q

Why happens to FSH and LH levels in postmenopausal women?

A

They increase 3-4 fold due to lack of negative feedback from E2 and inhibin

FSH> LH

27
Q

What causes hot flashes during menopause?

A

Increased vasomotor activity synchronous with LH pulses.

This causes periodic increases in core temperature, causing reflex vasodilation, sweating and increase pulse rate

28
Q

When is peak fertility for women?

A

18-25

29
Q

Where does fertilization normally occur?

A

The ampulla of the fallopian tube

30
Q

When is the “window of opportunity” for fertilization?

A

24 hours post-ovulation for the ovum and 48-72 hours post-coitus

31
Q

What is sperm capacitation?

A

Sperm capacitation refers to changes in functional properties of sperm acquired in the female tract that allow for penetration of the zona pellucida of the egg.

Capacitation makes sperm competent to undergo the acrosomal reaction

32
Q

What initiates the acrosomal reaction?

A

Sperm binds to ZP3 receptor

33
Q

What happens following binding of sperm to the ZP3 receptor?

A

Binding triggers increased calcium in the sperm cell. This leads to exocytosis of hydrolytic enzymes –> sperm and oocyte membranes fuse and the acrosome reacted sperm binds to ZP2 proteins.

34
Q

Describe the cortical reaction

A

Spermatozoon penetration triggers increase in calcium concentration in the oocyte, resulting in fusion of cortical granules with the plasma membrane.

This releases enzymes that harden the glycoproteins of the zona pellucida and prevent more sperm from entering the oocyte

35
Q

How does E2 and progesterone affect transport of the blastocyst from the oviduct to the uterus?

A

E2 inhibits (causes constriction to allow time for the endometrium to prepare) and progesterone promote myometrial relaxation and transport of the blastocyst to the uterus

36
Q

Upon blastocyst implantation, the trophoblast differentiates into what two structures?

A

The cytotrophoblast and syncytiotrophoblast

37
Q

What is the role of the cytotrophoblast?

A

feeder for continually dividing cells

38
Q

What is the role of the syncytiotrophoblast

A

Adhesion
Invasion
Endocrine

39
Q

Embryo adhesion requires which fetal factors?

A

Syncytiotrophoblasts secrete adhesive surface proteins such as cadherins and integrins

40
Q

Embryo adhesion requires what maternal factors?

A

Uterine glands secrete estrogen-dependent substances like osteopontin which bind to surface proteins secreted by the blastocyst.

41
Q

Describe the balance between decidual cells and trophoblast migration

A

Matrix metalloproteinases from trophoblasts fight MMP inhibitors from decidual cells

42
Q

What are lacuna in the placenta?

A

Lacuna are fluid filled space in the syncytium that make contact with the maternal blood vessels

43
Q

What are the hallmark symptoms of preeclampsia?

A

Hypertension, proteinuria and edema

44
Q

Describe the pathophysiology of preeclampsia

A

Relative placental ischemia leads to oxidative stress and endothelial cell damage.

Damaged endothelial cells decrease vasodilators and increase vasoconstrictors- results in worsening placental hypoperfusion

The endothelial cell barrier between platelets and the basement membrane is breached- thrombosis causes capillary leak, which leads to edema and proteinuria