Repro - Chapter 81, Female; Watson; Kek

Front 1

in female fetal development, since there are no androgens, what regresses that must be present for male genitalia to develop?

Back 1

wolffian duct regresses since there is no testosterone (wolffian in male turns into male genitalia)

Front 2

without ____________, the mullerian duct turns into what in the female?

Back 2

antimullerian hormone from sertoli cells; the upper female reproductive tract

Front 3

without hormone ______________, the external genitalia will appear female.

Back 3

DHT (dihydrotestosterone); also a 5alpha reductase will cause external female genitalia (but that's an enzyme!)

Front 4

what layer of the uterus is sensitive to estrogen and progesterone?

Back 4

endometrium

Front 5

explain mitosis, meiosis I and II in the female.

Back 5

mitosis occurs in a female fetus where there is a production of ~7M oogonia; then the 1st meiosis occurs at 8-9weeks of gestation and the oogonia are called primary oocytes. for each primary oocyte that goes undergoes meiosis, only one functional oocyte is produced. the other two or three cells produced are called polar bodies. at birth there are about 2M primary oocytes present which will decrease to about 400,000 just before puberty and then decrease even more with each cycle/ovulation. a follicle that is mature and about to ovulate is called a graafian follicle. meiosis II won't occur unless fertilization occurs.

Front 6

explain what the ovarian follicle (reproductive unit) is made of.

Back 6

contains a single oocyte (ovum/egg) with a layer of granulosa cells enclosed in a thin layers of extracellular matrix (basal lamina) = ovarian follicle; once it grows larger and is ready for ovulation it is called a graafian follicle

Front 7

where does the oocyte get its estrogen from?

Back 7

thecal cells produce androgens which get converted to estradiol after it flows into the granulosa compartment (since granulosa cells have aromatase activity)

Front 8

the corpus luteum is the yellow body that is left over after the mature follicle is ovulated. what is it dependent on for survival? what does the corpus luteum secrete to maintain pregnancy?

Back 8

LDL cholesterol; corpus luteum secretes progesterone that allows the pregnancy to continue

Front 9

what hormone is higher in the system, estrogen or progesterone?

Back 9

progesterone is always higher; its just that estrogen has more active receptors

Front 10

there are two cycles to describe the female menstrual cycle. what are they and what do they describe?

Back 10

OVARIAN CYCLE: has a follicular phase (describes what happens to the oovum) and a luteal phase (maintains progesterone levels in case of fertilization and implantation); ENDOMETRIAL CYCLE: describes the menstrual, proliferative, and secretory phases (describes the endometrial lining changes)

Front 11

starting with menses, name the phases and the days that coorespond to the endometrial cycle.

Back 11

1) menstrual cycle (day 1-5); 2) proliferative phase (5-14); 3) secretory phase (after ovulation ~day 15 - day 28)

Front 12

what hormone surges to stimulate ovulation?

Back 12

estradiol increases stimulates LH surges around day 11-13; then estradiol has negative feedback on GnRH to reduce LH and FSH

Front 13

what hormone is the highest during the secretory phase?

Back 13

progesterone (lots from corpus luteum)

Front 14

in what phase is estradiol highest?

Back 14

spikes with LH surge around pre-ovulation and in the secretory phase

Front 15

changes in what hormones cause menses?

Back 15

decrease in estradiol and increase in FSH

Front 16

what is the purpose of the corpus luteum and what is it made of? what happens if no fertilization occurs?

Back 16

provides progesterone necessary for implantation of the zygote into the uterus. made of 80% granulosa cells (FSH stimulates to convert androgens (from thecal cells) to estradiol by aromatase) and 20% thecal cells; if its not fertilized it will regress in about 14 days and form a scar (corpus albicans)

Front 17

in what endometrial phase is the uterine lining the thickest?

Back 17

secretory phase

Front 18

what endometrial phase does sloughing occur?

Back 18

menstrual phase

Front 19

what two factors do the granulosa cells make that either negatively or positively feedback to the anterior pituitary?

Back 19

FSH stimulates the granulosa cells to produce either inhibin (negative feedback) or activin (positive feedback) to AP - this will decide whether to secrete more FSH

Front 20

what is needed to convert cholesterol to prenenolone in the production of steriod hormones?

Back 20

Side Chain Clevage (type of desmolase)

Front 21

there are 3 types of estrogens in the female at different times in the lifespan. Explain each of them.

Back 21

E1(estrone - a metabolite of 17B-estradiol): primary estrogen during menopause (results from the conversion of adrostenedione (from adrenals) converted by aromatase); E2(17B-Estradiol) pre-menopausal: occurs from conversion of testosterone -> estradiol by aromatase; E3(estriol): during pregnancy (conversion of androstenedione into E3 by aromatase - to elimate estrogen so fetus doesn't get too much estrogen; neonatal androgenation - disruption of normal cycling of GnRH)

Hint 21

None

Front 22

what does estradiol do to the body (outside of the repro system)?

Back 22

fat deposition (subc fat in women - hips, thighs, breast); increase vascularization of skin; increase in bone density (estrogen causes decreased osteoclastic activity)

Front 23

what does estradiol do to the female sex organs?

Back 23

at puberty, it increases the size of the fallopian tubes, uterus and vagina, external genitalia deposition of fat in the mons pubis; the epithelium changes from cuboidal to stratified squamous; proliferation of cells and endometrial glands; thinning of cervical mucous (progesterone will cause a thick cervical mucus)

Front 24

what type of receptors does estrogen have and what are the acute molecular effects of estrogen?

Back 24

nuclear receptors alpha and beta; acutely, they increase intracellular calcium, stimulate Nitrous oxide system to produce vasodilation; upregulates synthesis of estrogen and progesterone receptors; also an antioxidant

Front 25

what progesterone receptor antagonist causes abortion and inhibits hyperhydrocortisolism?

Back 25

mifepristone

Front 26

define puberty.

Back 26

transition from noncyclic, relatively quiescent reproductive endo system to a reproductive state that is cyclic. it begins with pulsatile GnRH/LH secretion during REM sleep

Front 27

what determines age at puberty?

Back 27

genetics, nutrition, geographic location, exposure to light, body composition, fat deposition, exercise (menarche has been occurring earlier in US and EU in the past few decades - i think increase in fat and hormones in diet); distance from the equator, higher altitudes: early onset

Front 28

Name the 4 phases in the female sexual response.

Back 28

1) excitement phase (parasymp. NO regulated); 2) plateau phase (increase HR, BP, respiratory rate, muscle tension) 3) orgasmic phase 4) resolution phase (faster than men's phase) don't require refractory time

Front 29

FSD (female sexual dysfxn) may be as high as 45% with many mechanisms. name some treatments.

Back 29

counseling, testosterone, viagra, avlimil (herbs- licorice, sage, black cohosh root, capsicum pepper, isoflavones)

Front 30

There are many methods of contraception in females. explain the rhythm method.

Back 30

calculating ovulation (day 13-15); temperature decreases and then increases slightly following ovulation. mucus discharge changes

Front 31

There are many methods of contraception in females. explain oral estrogens and progestins.

Back 31

the Pill is usually a combo of estrogens and progestins: ESTROGENS: (maintence) decrease androgenic effects, suppress GnRH, FSH, LH- prevent ovulation; PROGESTINS: increase cervical mucus and inhibit motility of sperm and the endometrium is not conducive to implantation

Front 32

There are many methods of contraception in females. explain implant contraceptives.

Back 32

norprogestins or "norplant" high dose progestins; last 5 years (goes under skin in the arm)

Front 33

There are many methods of contraception in females. explain Depoprovera, IUD, and barrier methods.

Back 33

Depo: shot, lasts 3 months, inhibits ovulation, implantation; IUD: small T device that is implanted in the uterus that prevents implantation of a zygote; BARRIER METHOD: diaphragm with spermidcidal jelly; condoms

Front 34

There are many methods of contraception in females. What is a postcoital contraceptive?

Back 34

RU-486 is used within 72 hours of unprotected sex; won't allow implantation into the uterus

Front 35

Define Menopause.

Back 35

ovaries become obsolescent; no estradiol production; no period for 12 months; average age 51.4; exogenous steroids can cause premature menopause

Front 36

explain the HERS study. what does it stand for?

Back 36

HERS: Heart and Estrogen/progestin Replacement Study: study looked at secondary prevention of CHD with estrogen replacement; study was 4.1 years duration; in first year, significant increase in coronary events; NO OVERALL DIFFERENCE in CHD endpoints with HRT or placebo over 4.1 yrs

Front 37

WHI (women's health initiative) agrees with the HERS study in saying...

Back 37

"HRT regimen should not be initiated or continued for primary prevention of CHD"

Front 38

WHat are SERMs?

Back 38

Selective Estrogen Receptor Modulators have both agonistic and antagonistic effects depending on tissue (ie. raloxiphene and tamoxiphen - anti-estrogen for Breast CA; actually a weak estrogen that inhibits the more active estrogen)

Front 39

name the term that refers to fibroids in the uterus; its a smooth muscle tumor that is estrogen dependent.

Back 39

Leiomyomas

Front 40

Name the term that refers to uterine tissue outside the uterus.

Back 40

endometriosis (painful, responds to E2(estradiol) Tx: give GnRH continuously to downregulate GnRH receptors but causes hypoestrogenism

Front 41

what is the condition that is characterized by an acute, life-threating illness caused by menstrual(tampons, barrier contraceptives) and non-menstrual methods(burns, insects, wounds).

Back 41

TOXIC SHOCK SYNDROME;the cause are exoproteins produced by staphyllocus A or B

Front 42

name the clinical symptoms that are associated with Toxic Shock syndrome.How would you treat it?

Back 42

hypotension, rash, multiorgan dysfunction (renal, myocardial), desquamation (flaking of the skin); Treat with: antibiotics (po or IV), drain wound, give fluids and vasopressors for hypotension

Front 43

what is the genotype and phenotype of turner's syndrome?

Back 43

XO, female phenotype; one sex chromosome being biologically active; ovary needs both active XX chromosomes - get streak gonads; normal until puberty

Front 44

what causes hyperprolactinemia?

Back 44

lack of suppressive dopamine on the anterior pituitary; increase in TRH (hypothyroid pt) can also cause prolactin release

Front 45

what are the clinical manifestations of hyperprolactinemia on the male and female?

Back 45

Female: 30-80% galactorrhea, menstrual irregularity, infertility; MEN: <30% galactorrhea, impotence, visual field abnormalities, headache, extraocular muscle weakness, anterior pituitary malfunction

Front 46

clinically, how would a woman present with polycystic ovarian syndrome and describe it?

Back 46

it is an insulin resistant problem; over production of androgens; pts present with acne and hirsutism