Block 3 Week 7

Front 1

describe the time course of menstrual cycle

Back 1

1. follicular phase (approx 14 days), 2. ovulatory phase, 3. luteal phase (always 14 days b/c dependent on secretion of hCG to survive)

Front 2

describe GnRH pulsatile secretions and E2 feedback between follicular and luteal phase

Back 2

follicular phase: E2 positive feedback; GnRH is high freq/low amplitude; after LH surge, changes to E2 negative feedback to inhibit GnRH/LH/FSH and switch uterus to secretory phase; GnRH is low freq/high amplitude enough to sustain CL for 8-12d

Front 3

what components does the corpus luteum secrete

Back 3

E2 and prg

Front 4

how does hypothalamus switch by to positive E2 feedback

Back 4

after CL dies, drop in E2/prg levels switch to positive feedback > increase in GnRH pulse > increase LH/FSH > stimulate new follicles > secrete more E2

Front 5

explain how graafian follicle initiates LH surge

Back 5

follicle that has most FSH receptors becomes graafian follicle; in late stage, graafian follicle is very sensitive to FSH, and makes lots of E2 > LH surge

Front 6

describe coordination between theca/granulosa cells for estradiol secretion

Back 6

LH > theca > stimulate desmolase to convert cholesterol to androstenedione >> this diffuses into granulosa cell; FSH > granulosa > stimulate aromatase to convert weak androgen to estradiol

Front 7

what is effect of E2 on granulosa cells

Back 7

increase FSH receptors and stimulate granulosa cell proliferation

Front 8

describe formation of corpus luteum

Back 8

1. FSH induces expression of LH receptors on granulosa cells > LH surge causes leutinization of theca/granulosa cells > CL secretes E2/prg > inhibits GnRH pulsatile secretion

Front 9

what happens during overstimulation of GnRH receptors

Back 9

receptors downregulate through endocytosis, cascade inhibition, and GnRH receptor transcription downregulation

Front 10

what is the current treatment for precocious puberty and mechanism of action

Back 10

administer GnRH to downregulate receptors and keep hormones at pre-puberty levels

Front 11

describe effects of E2/prg on female reproductive system during follicular/luteal phase

Back 11

1. follicular phase > only E2 > uterus: proliferation, uterine contractions; cervix: muscles relax, watery secretion; fallopian tube: cilia beat towards uterus, oviduct contractions toward ovary; 2. luteal phase > E2 > uterine vasculature; prg > uterine secretory phase; cervix: hardens with thick mucus; inhibit uterine contractions

Front 12

what is the role of hCS (human chorionic somatotropin)

Back 12

secreted from trophoblast, stimulates placenta wall growth

Front 13

describe timing of fertilization to implantation

Back 13

1d fertilization, 3d oviduct transport, 1d wait in uterus

Front 14

what is the effect of E2 on endometrium

Back 14

maintains endometrium and promotes expression of oxytocin

Front 15

at what time is hCG detectable

Back 15

d8 of implantation

Front 16

describe changes in endometrium necessary for parturition from pregnancy to late-pregnancy

Back 16

during pregnancy, prg > E2 receptor, so prg inhibits uterine contractions; late-pregnancy, there is elevated E2 and estrogen intermediates, and E2 > prg receptors > removes the inhibition on uterine contractions

Front 17

what hormone stimulates expression of oxytocin receptors

Back 17

estradiol

Front 18

what hormone inhibits uterine contractions during pregnancy

Back 18

progesterone (prg)

Front 19

describe mechanism of parturition

Back 19

1. expression of oxytocin receptors on uterine wall increases toward end of pregnancy; high release of oxytocin toward end of pregnancy induces labor; 2. CRH-binding protein produced during pregnancy prevents CRH from acting, but CRH-BP drops near end of pregnancy > CRH binding and prostaglandin release stimulate uterine contractions

Front 20

explain premature birth and CRH

Back 20

premature births/labor tend to have lower CRH-BP

Front 21

describe the types of dysmorphology: 1. variation of normal, 2. minor malformation, 3. major malformation

Back 21

1. normal variation in human population, >4%; 2. <4%, cosmetic problem; 3. <4%, cosmetic and functional problem

Front 22

define malformation, deformation, dysruption

Back 22

malformation: primary defect due to genetic problem; deformation: caused by external force; dysruption: interruption of developmental process

Front 23

define association, sequence, syndrome

Back 23

association: most common cause of multiple problems, where two diagnoses found together more often than coincidence; sequence: initialy problem causes all the rest; syndrome: features that run together and have common cause

Front 24

pathogenesis of pierre robin sequence

Back 24

primary defect is small jaw > pushes tongue backwards > disrupts closure of hard palate > cleft palate

Front 25

what do abnormalities of the hand hint at

Back 25

possible problem with organs

Front 26

pathogenesis of phocomelia and one pharmacological cause

Back 26

malformation of long bones, causing short limbs; can be caused by thalidomide (sedative that inhibits angiogenesis)

Front 27

what is the most sensitive time period of development

Back 27

wk3 to wk8

Front 28

what is most common congential defect of the mouth

Back 28

cleft lip/palate

Front 29

what do abnormalities of the ear signify

Back 29

high association with renal problems

Front 30

clinical signs of kleinfelter

Back 30

long legs, short trunk

Front 31

clinical signs of marfan

Back 31

long arms

Front 32

clinical signs of neurofibramatosis

Back 32

1. lisch nodules; 2. cafe au lait spots --- NF is autosomal dominant

Front 33

how does hormonal contraception work

Back 33

high dose of E2/prg inhibit LH/FSH secretion > inhibit ovulation

Front 34

list some general classes of female contraceptive

Back 34

1. high hormonal E2/prg to inhibit GnRH and ovulation; 2. IUD to maintain cervix in inflammatory state > prevent implantation; 3. long-term implantation/injection

Front 35

list risk factors for hormonal contraceptives

Back 35

1. increase breast cancer; 2. increase BP, stroke, MI; 3. increase chance of forming blood clots

Front 36

effects of prg on endometrium

Back 36

thins endometrium and places it into hibernative state > reduced risk of cancers here

Front 37

what state is the egg cell at during ovulation phases

Back 37

primary oocytes frozen in prophase i > stimulation of follicles > only graafian follicle makes it out to stop at metaphase ii and become secondary oocyte

Front 38

explain sperm from cervix to egg

Back 38

sperm bind to fallopian tube to be capacitated > penetrate corona radiata and bind to zona pellucida

Front 39

describe proliferation of trophoblast upon implantation

Back 39

splits into two cell types; 1. cytotrophoblast is inner layer, contains the stem cells for outer layer; 2. syncytiotrophoblast invades endometrium via proteolysis, receives nutrients via diffusion

Front 40

decidual reaction generates what three layers from the endometrium

Back 40

1. decidua basalis, 2. decidua capsularis, 3. decidua parietalis

Front 41

describe generation of three cavity/sac in embryo

Back 41

1. embryonic disc makes a. epiblast (amnion) and b. hypoblast (yolk sac); 2. extraembryonic mesoderm invades lower part of the 'shell' to make the chronic cavity

Front 42

what tissue secretes hCG

Back 42

syncytiotrophoblast

Front 43

how is uteroplacental circulation established

Back 43

1. after chronionic cavity is developed, syncytioblast continues to erode endometrium and form lacunae, will reach radial arteries and blood will spill into lacunae; 2. cytotrophoblast grow primary villi into syncytioblast, extraembryonic mesoderm (lining chorionic cavity) grow into secondary villi, then mesoderm grows blood vessels into the villi and connect to fetus

Front 44

what compounds can pass through the placental membrane

Back 44

HIV, some viruses, alcohol, antibodies, hormones

Front 45

describe blood vessel system of umbilical cord

Back 45

two arteries carry low pO2 blood; one vein carry high pO2 blood

Front 46

define chorion frondosum and cotyledon

Back 46

chorion frondosum -- part of the decidua capsularis not fused with parietalis; cotyledon -- villus on chorion to increase surface area

Front 47

during development, what does each give rise to: 1. pronephros, 2. mesonephros, 3. metonephros

Back 47

1. rudimentary/non-functional kidney; 2. most degenerate except mesonephric duct (wolffian duct), paramesonephric duct develops laterally; 3. uteric bud from cloaca penetrates blastema

Front 48

where is lining of bladder/urethra derived from; where is muscle/connective tissue from

Back 48

endoderm, mesoderm

Front 49

where is cervix and vaginal plate derived from

Back 49

cervix -- mesoderm; vaginal plate -- endoderm

Front 50

how is the vaginal plate formed

Back 50

from fusion of paramesonephric ducts

Front 51

how is menopause defined

Back 51

amenorrhea for at least one year; decreased E2/prg due to progressive failure of ovarian function

Front 52

explain hormone replacement therapy (E2 and prg)

Back 52

ovaries stop making hormones; give E2 to replace lost estrogen, but also give prg to prevent uterus/endometrium from proliferating, otherwise E2-only increases risk of endometrial and breast cancer (but reduce risk of heart disease)