Unit 6 Turner Female Reproductive Tract

Front 1

Hormones responsible for follicle development

Back 1

FSH
estrogen contributes to effects of FSH

Front 2

hormones responsible for follicle maturation

Back 2

FSH and LH

Front 3

hormones responsible for ovulation

Back 3

LH and local progesterone

Front 4

hormone responsible for corpus luteum development and function

Back 4

LH

Front 5

Hormones present before ovulation

Back 5

FSH, LH, estrogen, and a small amount of progesterone

Front 6

length of the menstrual cycle determined by

Back 6

length of the follicular phase

Front 7

cells present in ovary in the follicular phase

Back 7

granulosa
theca interna
stroma

Front 8

cells present in ovary in luteal phase

Back 8

lutein
paralutein
both produce progesterone

Front 9

granulosa cells become ______ on ovulation

Back 9

lutein

Front 10

theca interna cells become ________ on ovulation

Back 10

paralutein

Front 11

stroma cells become ________ on ovulation

Back 11

paralutein

Front 12

function of theca interna cells

Back 12

produce androgen which act on granulosa cells causing estrogen production

Front 13

stroma cells produce

Back 13

estrogens and androgen

Front 14

ovary makes 60% of _____ and 45% of ______

Back 14

60% of androstenedione

45% of testosterone

Front 15

adrenal makes 40% of ______ and 55% of ______

Back 15

40% androstenedione

55% testosterone

Front 16

most androstenedione is converted to what in the periphery?

Back 16

testosterone

Front 17

testosterone levels in women

Back 17

are 6-8% of those of men and 60% comes from peripheral conversion of androstenedione

Front 18

these are 2-3x higher in women

Back 18

plasma levels of proteins that specifically bind androgens

Front 19

functions of the uterus

Back 19

prepare for implantation
nourish the conceptus
expel the fetus

Front 20

menstrual cramps are due to

Back 20

estrogen stimulating myometrial contraction

Front 21

this hormone is the dominant hormonal stimulus in the uterine proliferative phase

Back 21

estrogen

Front 22

this hormone is the dominant hormonal stimulus in the uterine secretory phase

Back 22

Progesterone
estrogen has some effect but is more mild

Front 23

hormone levels just prior to ovulation

Back 23

surge in LH
rapidly rising estrogen
small surge in FSH
some progesterone

Front 24

FSH and the menstrual cycle

Back 24

stimulates follicle growth and increase in estrogen

Front 25

initial rise in estrogen (effect on FSH and LH)

Back 25

decreases FSH
increases LH

Front 26

rapid rise in estrogen one week before ovulation

Back 26

causes a dramatic rise in LH and a rise in FSH, although the rise in FSH is physiologically insignificant

Front 27

ovulation requires the functional integrity of these 3 effector proteins

Back 27

P receptor (enabling P action)

cyclooxygenase (enabling PGE synthesis)

cyclin D2 (a cell cycle activator)

Front 28

PGE F2-alpha

Back 28

appears to be invovled in luteolysis

Front 29

hormonal response to CL degradation

Back 29

sharp decrease in LH but selective increase in serum FSH which initiates a new wave of follicle maturation

Front 30

how much of the endometrium is actually lost during the period

Back 30

20%, the other 80% undergoes remodeling during the next cycle

Front 31

this converts androgens into estrogen

Back 31

aromatase that is stimulated by estrogen

Front 32

LH surge

Back 32

positive feedback
requires optimum CNS input
GnRH increases FSH and LH, but only the LH is important for ovulation

Front 33

important participants in the atretic process

Back 33

TNF-alpha
androgens
Fas-activating ligand
IL-6

Front 34

Post LH surge events leading to ovulation

Back 34

oocyte maturation inhibitor neutralized --> completion of meiosis

increased progesterone and local PGE --> increased follicle proteolytic enzymes --> weakened follicle wall --> ovulation

Front 35

CL formation due to

Back 35

LH-induced conversion of follicular cells to lutein cells

Front 36

secretion of CL

Back 36

due to increasing number of lutein cells
small amt of LH needed for maintenance

Front 37

Luteolysis

Back 37

lifespan normally and reliably 14-16 days
possibly preprogrammed
increase in E/LH ratio may facilitate breakdown

Front 38

function of HCG from developing chorion

Back 38

prevents luteolysis
prolongs steroid production until placenta takes over
then CL degenerates

Front 39

Menses

Back 39

E&P from CL sustain endometrium
E&P withdrawal leads to hemorrhagic and degenerative change in endometrium
partial sloughing of endometrium occurs (menses)

Front 40

Menstrual flow contents

Back 40

endometrial cells
leukocytes
blood
mucus

Front 41

menstrual flow volume and duration

Back 41

20-200 ml volume
3-7 days long

Front 42

effects of estrogen on uterine tubes

Back 42

increase contractility, secrection (lubrication), and ciliated cells

Front 43

effects of progesterone on uterine tubes

Back 43

decrease contractility, secrection (lubrication), and ciliated cells

Front 44

effects of E on cervix

Back 44

increased volume, pH, and [Na+]
decreased viscosity

Front 45

effects of P on cervix

Back 45

decreased volume, pH, and [Na+]
increased viscosity

Front 46

effects of E on vagina

Back 46

increased cornification (maturation) (stratified squamos epi)
decreased sloughing of epi and pH

Front 47

effects of P on vagina

Back 47

decreased cornification (maturation)
increased sloughing of epi and pH

Front 48

ER-alpha receptors predominate in

Back 48

uterus, mammary glands, testes, and non-reproductive tissues

Front 49

ER-beta receptors predominate in

Back 49

ovary and prostate

Front 50

E and P relationship

Back 50

E effects usually dominate
P usually antagonizes E effects
E/P ratio can be as important as E or P alone in overall effect

Front 51

effects of E on skin

Back 51

prevents wrinkling, oiliness, and thinning of skin

Front 52

effects of E on skeleton

Back 52

female pelvic arrangement
prevents calcium loss from bone
inhibits growth of long bones

Front 53

effects of E on metabolism

Back 53

increased deposition of subcutaneous fat and protein anabolism
general weight gain
decreased glucose tolerance and serum cholesterol

Front 54

effects of E on GI tract

Back 54

nausea, vomiting, bloating

Front 55

effects of E on blood

Back 55

increased fibrinogen, platelet aggregation, thromboembolism, and binding proteins in plasma
decreased clotting time

Front 56

effects of E on renal-electrolyte

Back 56

increased water and sodium retention

Front 57

effects of E on CNS

Back 57

altered thermoreg
increased excitability of neurons and emotionality & irritability
depressed mood
headaches
altered libido

Front 58

circumstances evidencing estrogen related effects

Back 58

puberty- adolescence
menopause- climacteric
premenstrual syndrome
oral contraceptive SEs

Front 59

Non-reproductive effects of progesterone

Back 59

thermogenic
antinatriuretic via renin release
decreased excitability of neurons (euphoric in high dose)
hyperventilation

Front 60

premenstrual syndrome occurs

Back 60

late in the luteal phase

Front 61

premenstrual syndrome symptoms include

Back 61

occur in about 30% of women
anxiety
depression
headaches
spontaneous crying
etc.

Front 62

premenstrual syndrome etiology

Back 62

uknown but likely excess of hypersensitivity to E or deficiency of P

Front 63

treatment for PMS symptoms

Back 63

diet and exercise
relaxation therapy
P therapy --> good for anxiety
anti-inflammatory drugs
serotonin-enhancing anti-depressants
anxiolytic drugs

Front 64

most common cause of endocrinopathy and anovulatory infertility in women

Back 64

polycystic ovarian disease

Front 65

PCOD is a symptom complex associated with polycystic ovaries and characterized in >50% of cases by

Back 65

oligomenorrhea
anovulation
obesity
hirsutism

Front 66

physical signs of PCOD

Back 66

white, smooth, sclerotic ovaries with thickened capsule
thecal cell hyperplasia
chaotic follicle growth
numerous atretic follicles

Front 67

onset of chronic anovulation and hirsutism in PCOD

Back 67

anovulation- typical pubertal onset is normal-age menarche followed by a year or two of menstruation with periods then becoming irregular and ceasing
hirsutism- typically pubertal but can be in adulthood

Front 68

etiology of PCOS

Back 68

not ovarian
most likely related to hyperinsulinemia

Front 69

All PCOS patients are _____ and most are _______

Back 69

all are hyperinsulinemic and most are obese

Front 70

IGF-1

Back 70

agent through which GH promotes growth

Front 71

genetic predisposition to PCOS

Back 71

cytochrome P450c17alpha hydroxylase excess

allows overproduction of androgens in ovary and adrenal

Front 72

Therapy for PCOS in obese patients

Back 72

weight reduction which leads to decreased androgens and decreased insulin resistance

Front 73

Therapy for PCOS in non-hirsute patients not wishing pregnancy

Back 73

progestin

Front 74

Therapy for PCOS in hirsute patients not wishing pregnancy

Back 74

oral contraceptives
glucocorticoids
GnRH analogues
antiandrogens

Front 75

Therapy for PCOS in patients desiring pregnancy

Back 75

standard procedures for inducing ovulation in infertility